BioMedLib Search Engine
[ goto HOMEPAGE ]
Save time; Find better answers!
Skip to content
Advanced Search
Search History
MeSH Query
Page Format
Query is expanded
Login
Skip to content
Export Citations
Search Results
RSS
Email
Articles' Details
Start new query
Reset All
Refine your query
(more in Advanced-Search):
Search all of MEDLINE
Focus on the recent 5 years
Focus on the current year
Focus on the last 30 days
More choices ...
Focus on articles with free fulltexts
More choices ...
Do simple 'keyword' search (no query expansion)
[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click
here to
RESET
all values
Click
here to
GO BACK
without resetting any value
Advanced Search
Submit one or more of the following items, and they will be searched along with your query in the search box above.
Any submit button will submit all of the items you have changed.
+
Publication-Date
Published in the last:
30 days
60 days
90 days
6 months
12 months
this year
2 years
3 years
5 years
10 years
Or published in the following date range: From (yyyy/mm/dd - month and day are optional)
to ('to' is optional)
+
Full Text
Retrieve articles with hyperlinks to:
full text (either free or subscription)
free full text
subscription full text
no full text link
+
Sort-Order
Sort the retrieved articles by:
relevance
publication date
+
Language
And with languages:
English
French
German
Italian
Japanese
Russian
Spanish
More languages:
Afrikaans
Albanian
Amharic
Arabic
Armenian
Azerbaijani
Bengali
Bosnian
Bulgarian
Catalan
Chinese
Czech
Danish
Dutch
Esperanto
Estonian
Finnish
Georgian
Scottish Gaelic
Greek, Modern
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Kinyarwanda
Korean
Latin
Latvian
Lithuanian
Macedonian
Malayalam
Maori
Malay
Multiple languages
Norwegian
Persian
Polish
Portuguese
Pushto
Romanian
Sanskrit
Serbian
Croatian
Slovak
Slovenian
Swedish
Thai
Turkish
Ukrainian
Undetermined
Urdu
Vietnamese
Welsh
+
Publication-Type
And with publication types:
Clinical Trial
Editorial
Letter
Meta-Analysis
Practice Guideline
Randomized Controlled Trial
Review
More publication types:
Addresses
Bibliography
Biography
Case Reports
Classical Article
Clinical Conference
Clinical Trial, Phase I
Clinical Trial, Phase II
Clinical Trial, Phase III
Clinical Trial, Phase IV
Comment
Comparative Study
Congresses
Consensus Development Conference
Consensus Development Conference, NIH
Controlled Clinical Trial
Corrected and Republished Article
Dictionary
Directory
Duplicate Publication
English Abstract
Evaluation Studies
Festschrift
Government Publications
Guideline
Historical Article
Interactive Tutorial
Interview
Introductory Journal Article
In Vitro
Journal Article
Lectures
Legal Cases
Legislation
Multicenter Study
News
Newspaper Article
Overall
Patient Education Handout
Periodical Index
Portraits
Published Erratum
Retracted Publication
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Retraction of Publication
Scientific Integrity Review
Technical Report
Twin Study
Validation Studies
+
Species
And for:
Humans
Animals
+
Gender
And for:
Male
Female
+
Age
And for these age groups:
Newborn: birth to 1 month
Infant: 1 to 23 months
Preschool child: 2 to 5 years
Child: 6 to 12 years
Adolescent: 13 to 18 years
Adult: 19 to 44 years
Middle aged: 45 to 64 years
Aged: 65+ years
80 and over: 80+ years
+
Title
And for this query matching the titles:
+
Transliterated-Title
And for this query matching the title in original language:
+
Abstract
And for this query matching the abstratcs:
+
Major-Mesh
And for this query matching the MeSH-Major terms:
+
Mesh
And for this query matching any MeSH terms:
+
Journal
And for one or more of these journal abbreviated names:
OR
OR
(see
title abbreviations
)
+
Volume
And with journal volume number:
+
Issue
And with journal issue number:
+
Page
And with page number:
+
ISSN
And with ISSN:
+
Publication-Place
And with journal's country of publication:
+
Author
And for...
all these author names:
AND
AND
(see
help
)
one or more of these author names:
OR
OR
but not having any of these unwanted author names:
NOT
NOT
+
Affiliation
And with affiliation to:
+
Has-Abstract
Find MEDLINE records with the abstract status:
has abstract
does not have abstract
include both record types
include both record types but rank higher the records having abstract (the default BML behavior)
+
PMID
Show me only articles for these PMIDs (PubMed IDs):
+
Semantic-Type
And with semantic types:
A. Entity
A1. Physical Object
A1.1. Organism
A1.1.1. Archaeon
A1.1.2. Bacterium
A1.1.3. Eukaryote
A1.1.3.1. Animal
A1.1.3.1.1. Vertebrate
A1.1.3.1.1.1. Amphibian
A1.1.3.1.1.2. Bird
A1.1.3.1.1.3. Fish
A1.1.3.1.1.4. Mammal
A1.1.3.1.1.4.1. Human
A1.1.3.1.1.5. Reptile
A1.1.3.2. Fungus
A1.1.3.3. Plant
A1.1.4. Virus
A1.2. Anatomical Structure
A1.2.1. Embryonic Structure
A1.2.2. Anatomical Abnormality
A1.2.2.1. Congenital Abnormality
A1.2.2.2. Acquired Abnormality
A1.2.3. Fully Formed Anatomical Structure
A1.2.3.1. Body Part, Organ, or Organ Component
A1.2.3.2. Tissue
A1.2.3.3. Cell
A1.2.3.4. Cell Component
A1.2.3.5. Gene or Genome
A1.3. Manufactured Object
A1.3.1. Medical Device
A1.3.1.1. Drug Delivery Device
A1.3.2. Research Device
A1.3.3. Clinical Drug
A1.4. Substance
A1.4.1. Chemical
A1.4.1.1. Chemical Viewed Functionally
A1.4.1.1.1. Pharmacologic Substance
A1.4.1.1.1.1. Antibiotic
A1.4.1.1.2. Biomedical or Dental Material
A1.4.1.1.3. Biologically Active Substance
A1.4.1.1.3.1. Neuroreactive Substance or Biogenic Amine
A1.4.1.1.3.2. Hormone
A1.4.1.1.3.3. Enzyme
A1.4.1.1.3.4. Vitamin
A1.4.1.1.3.5. Immunologic Factor
A1.4.1.1.3.6. Receptor
A1.4.1.1.4. Indicator, Reagent, or Diagnostic Aid
A1.4.1.1.5. Hazardous or Poisonous Substance
A1.4.1.2. Chemical Viewed Structurally
A1.4.1.2.1. Organic Chemical
A1.4.1.2.1.5. Nucleic Acid, Nucleoside, or Nucleotide
A1.4.1.2.1.6. Organophosphorus Compound
A1.4.1.2.1.7. Amino Acid, Peptide, or Protein
A1.4.1.2.1.8. Carbohydrate
A1.4.1.2.1.9. Lipid
A1.4.1.2.1.9.1. Steroid
A1.4.1.2.1.9.2. Eicosanoid
A1.4.1.2.2. Inorganic Chemical
A1.4.1.2.3. Element, Ion, or Isotope
A1.4.2. Body Substance
A1.4.3. Food
A2. Conceptual Entity
A2.1. Idea or Concept
A2.1.1. Temporal Concept
A2.1.2. Qualitative Concept
A2.1.3. Quantitative Concept
A2.1.4. Functional Concept
A2.1.4.1. Body System
A2.1.5. Spatial Concept
A2.1.5.1. Body Space or Junction
A2.1.5.2. Body Location or Region
A2.1.5.3. Molecular Sequence
A2.1.5.3.1. Nucleotide Sequence
A2.1.5.3.2. Amino Acid Sequence
A2.1.5.3.3. Carbohydrate Sequence
A2.1.5.4. Geographic Area
A2.2. Finding
A2.2.1. Laboratory or Test Result
A2.2.2. Sign or Symptom
A2.3. Organism Attribute
A2.3.1. Clinical Attribute
A2.4. Intellectual Product
A2.4.1. Classification
A2.4.2. Regulation or Law
A2.5. Language
A2.6. Occupation or Discipline
A2.6.1. Biomedical Occupation or Discipline
A2.7. Organization
A2.7.1. Health Care Related Organization
A2.7.2. Professional Society
A2.7.3. Self-help or Relief Organization
A2.8. Group Attribute
A2.9. Group
A2.9.1. Professional or Occupational Group
A2.9.2. Population Group
A2.9.3. Family Group
A2.9.4. Age Group
A2.9.5. Patient or Disabled Group
B. Event
B1. Activity
B1.1. Behavior
B1.1.1. Social Behavior
B1.1.2. Individual Behavior
B1.2. Daily or Recreational Activity
B1.3. Occupational Activity
B1.3.1. Health Care Activity
B1.3.1.1. Laboratory Procedure
B1.3.1.2. Diagnostic Procedure
B1.3.1.3. Therapeutic or Preventive Procedure
B1.3.2. Research Activity
B1.3.2.1. Molecular Biology Research Technique
B1.3.3. Governmental or Regulatory Activity
B1.3.4. Educational Activity
B1.4. Machine Activity
B2. Phenomenon or Process
B2.1. Human-caused Phenomenon or Process
B2.1.1. Environmental Effect of Humans
B2.2. Natural Phenomenon or Process
B2.2.1. Biologic Function
B2.2.1.1. Physiologic Function
B2.2.1.1.1. Organism Function
B2.2.1.1.1.1. Mental Process
B2.2.1.1.2. Organ or Tissue Function
B2.2.1.1.3. Cell Function
B2.2.1.1.4. Molecular Function
B2.2.1.1.4.1. Genetic Function
B2.2.1.2. Pathologic Function
B2.2.1.2.1. Disease or Syndrome
B2.2.1.2.1.1. Mental or Behavioral Dysfunction
B2.2.1.2.1.2. Neoplastic Process
B2.2.1.2.2. Cell or Molecular Dysfunction
B2.2.1.2.3. Experimental Model of Disease
B2.3. Injury or Poisoning
Page Format
Any submit button will submit all of the items you have changed.
[theme]
Use this page design theme:
original
twenty ten
[shown]
Results per page:
5
10
20
50
100
200
500
[expand/collapse]
show these sections expanded by default:
Advanced search
MeSH query
Search history
Page format
Query expansion
Articles details
Export citations
Email
[text size]
use this font size for text:
25%
50%
75%
100%
125%
150%
200%
or enter your choice of font size:
[page width]
use this page width (relative to the default initial value):
25%
50%
75%
100%
125%
150%
200%
or enter your choice of page width:
[highlight color]
use this color to highlight query words in the articles:
red
green
blue
black
purple
yellow
orange
navy
olive
maroon
none
[query history]
maximum number of queries shown in the history section:
[annotate]
Annotate these parts of each article:
title
abstract
both
none
Reset all values
Find best MeSH terms for
Search History
1
adenoma sebaceum syndrome 2005:2010[pubdate] *count=100
13053 results
Searchbox
Export
PDF
RSS
Email
Delete
Email this search result to the following email address:
[X] Close
Expand the query
'
adenoma sebaceum syndrome
' expanded to all its synonyms;
details
Email the results to the following email address:
Export the checked citations in RIS format (RIS format is used by RefWorks, Endnote, among others).
Items 1 to 100 of about 13053
1.
Kothur K, Ray M, Malhi P:
Correlation of autism with temporal tubers in tuberous sclerosis complex.
Neurol India
; 2008 Jan-Mar;56(1):74-6
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Correlation of autism with temporal tubers in
tuberous sclerosis complex
.
Tuberous sclerosis complex
(
TSC
) is an inherited genetic
disorder
commonly associated with neuropsychiatric complications like
epilepsy
, mental retardation, autism and other behavioral problems and constitutes about 1-4% of the autistic population.
Patients of
TSC
with autism are more likely to have temporal tubers than those cases without autism.
We describe clinical and neuroimaging features of two such cases of
tuberous sclerosis
with autism.
[MeSH-major]
Autistic
Disorder
/ complications. Autistic
Disorder
/ pathology. Temporal Lobe / pathology.
Tuberous Sclerosis
/ complications.
Tuberous Sclerosis
/ pathology
Genetic Alliance.
consumer health - Autism
.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18310844.001).
[ISSN]
0028-3886
[Journal-full-title]
Neurology India
[ISO-abbreviation]
Neurol India
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
India
2.
Rahimi M, Meletis EI, You S, Nguyen K:
Formulation and characterization of novel temperature sensitive polymer-coated magnetic nanoparticles.
J Nanosci Nanotechnol
; 2010 Sep;10(9):6072-81
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Formulation and characterization of novel
temperature sensitive
polymer-coated magnetic nanoparticles.
To form these novel nanoparticles, silane-coated magnetic nanoparticles (MNPs) were used as a template for a free radial polymerization of three monomers, N-isopropylacrylamide, acrylamide, and allylamine (NIPA-AAm-AH), on the
surface
of MNPs.
To investigate the chemical composition and chemical
state
of our nanoparticles, FTIR and XPS were used.
Furthermore, bovine serum albumin (BSA) was used in order to investigate the protein release profile of the nanoparticles as a function of the
temperature
.
The protein release profile indicated that the NIPA-AAm-AH coated MNPs have a significantly higher percent release at 41 degrees C compared to those of 4 degrees C and 37 degrees C, which demonstrates their
temperature sensitivity
.
In the future, the release profile of therapeutic drugs from nanoparticles at various
temperatures
and pHs as well as targeted capability of the synthesized nanoparticles for possible applications in controlled and targeted delivery will be investigated.
[MeSH-minor]
Acrylamides / chemistry. Animals. Cattle. Coated Materials, Biocompatible. Drug Carriers / chemistry. Drug Delivery Systems. In Vitro Techniques. Magnetics. Microscopy, Electron, Transmission. Nanotechnology. Particle Size. Photoelectron Spectroscopy. Polymers / chemistry. Serum Albumin, Bovine / administration & dosage. Serum Albumin, Bovine / pharmacokinetics. Silanes / chemistry. Spectroscopy, Fourier Transform Infrared.
Temperature
. Vinyl Compounds / chemistry
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21133151.001).
[ISSN]
1533-4880
[Journal-full-title]
Journal of nanoscience and nanotechnology
[ISO-abbreviation]
J Nanosci Nanotechnol
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Acrylamides; 0 / Coated Materials, Biocompatible; 0 / Drug Carriers; 0 / Polymers; 0 / Serum Albumin, Bovine; 0 / Silanes; 0 / Vinyl Compounds; 0 / trimethoxyvinylsilane
3.
Spadavecchia C, Levionnois O, Kronen P, Andersen OK:
The effects of isoflurane minimum alveolar concentration on withdrawal reflex activity evoked by repeated transcutaneous electrical stimulation in ponies.
Vet J
; 2010 Mar;183(3):337-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The effects of isoflurane minimum alveolar
concentration
on withdrawal reflex activity evoked by repeated transcutaneous electrical
stimulation
in ponies.
The aim of this study was to quantify the effects of isoflurane at approximately the minimum alveolar
concentration
(peri-MAC) on the temporal summation (
TS
) of reflex activity in ponies.
TS
was evoked by repeated electrical
stimulations
applied at 5 Hz for 2 s on the digital nerve of the left forelimb of seven ponies.
Surface
electromyographic activity was recorded from the deltoid and common digital extensor muscles.
TS
thresholds and amplitude of response
to stimulations
of increasing intensities were assessed during anaesthesia at 0.85, 0.95 and 1.05 times the individual MAC, and after anaesthesia in standing animals.
Under isoflurane anaesthesia,
TS
thresholds increased significantly in
a concentration
-dependent fashion and at each isoflurane MAC, the responses increased significantly for increasing
stimulation
intensities.
A concentration
-dependent depression of evoked reflexes with a reduction in the
slopes
of the stimulus-response function was observed for both muscles.
[MeSH-minor]
Anesthesia, Inhalation / veterinary. Animals. Dose-Response Relationship, Drug. Electric
Stimulation
. Electromyography / veterinary. Horses / physiology. Male. Pain Threshold / drug effects
Hazardous Substances Data Bank.
Isoflurane
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
2009 Elsevier Ltd. All rights reserved.
(PMID = 19186084.001).
[ISSN]
1532-2971
[Journal-full-title]
Veterinary journal (London, England : 1997)
[ISO-abbreviation]
Vet. J.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Anesthetics, Inhalation; CYS9AKD70P / Isoflurane
Advertisement
4.
Thomas X:
The role of timed sequential chemotherapy in adult acute myelogenous leukemia.
Curr Hematol Malig Rep
; 2008 Apr;3(2):89-95
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Consecutive trials of timed sequential chemotherapy (
TSC
) have been conducted in adults with acute myelogenous leukemia.
The rationale for
TSC
was based on the observation that leukemic
cells
can be recruited synchronously into the
cell
cycle after initial intensive therapy, at which
time
they may become more susceptible to killing by chemotherapeutic agents.
Achieving complete remission is essential for prolonged
disease
-free survival and may affect long-term outcome.
TSC
has led to higher rates of complete remission and has improved long-term outcomes.
This article reviews the results of important trials in which
TSC
was used as an induction regimen in
de
novo, relapsed, or refractory acute myelogenous leukemia or as postremission therapy.
[MeSH-minor]
Adult.
Cell
Cycle / drug effects. Clinical Trials as Topic. Drug Administration Schedule. Humans
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Adult
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Blood. 1989 Jan;73(1):24-30
[
2910362.001
]
[Cites]
Lancet. 1977 Mar 5;1(8010):497-9
[
65605.001
]
[Cites]
Blood. 1996 Oct 15;88(8):2841-51
[
8874180.001
]
[Cites]
Blood. 1987 May;69(5):1441-9
[
3552076.001
]
[Cites]
Cancer Res. 1977 Jul;37(7 Pt 1):2138-46
[
266416.001
]
[Cites]
Cancer Treat Rep. 1986 Feb;70(2):285-6
[
3456272.001
]
[Cites]
Leuk Res. 2000 Nov;24(11):957-63
[
11086179.001
]
[Cites]
Blood. 1992 Jan 15;79(2):313-9
[
1730080.001
]
[Cites]
J Clin Oncol. 1996 Sep;14(9):2480-5
[
8823326.001
]
[Cites]
Leukemia. 1990 Mar;4(3):177-83
[
2179638.001
]
[Cites]
Am J Hematol. 1990 Sep;35(1):22-5
[
2202204.001
]
[Cites]
Leukemia. 1991 Jun;5(6):510-6
[
2056774.001
]
[Cites]
Leukemia. 2003 Jun;17(6):1078-84
[
12764371.001
]
[Cites]
Blood. 2004 Oct 15;104(8):2467-74
[
15142880.001
]
[Cites]
Br J Haematol. 1996 Jul;94(1):89-98
[
8757514.001
]
[Cites]
Blood. 1996 Jun 15;87(12):4979-89
[
8652810.001
]
[Cites]
Leuk Res. 1991;15(5):321-5
[
2046385.001
]
[Cites]
Blood. 1991 Nov 15;78(10):2520-6
[
1824249.001
]
[Cites]
Blood. 1991 Feb 15;77(4):700-11
[
1993213.001
]
[Cites]
Trends Mol Med. 2002;8(4 Suppl):S32-7
[
11927285.001
]
[Cites]
Cancer. 1980 Mar 1;45(5):859-65
[
6942904.001
]
[Cites]
Leukemia. 1999 Aug;13(8):1214-20
[
10450749.001
]
[Cites]
BMC Cancer. 2002 May 09;2:12
[
12019034.001
]
[Cites]
Blood. 1982 Aug;60(2):454-62
[
6953986.001
]
[Cites]
Cancer Res. 1997 Aug 15;57(16):3375-80
[
9269999.001
]
[Cites]
Leuk Res. 2004 Jun;28(6):571-7
[
15120933.001
]
[Cites]
Leukemia. 1993 Mar;7(3):372-7
[
8445942.001
]
[Cites]
Blood. 1987 Apr;69(4):1134-40
[
3470054.001
]
[Cites]
Blood. 1984 Nov;64(5):975-80
[
6487807.001
]
[Cites]
Leukemia. 1989 Feb;3(2):115-21
[
2911205.001
]
[Cites]
Leukemia. 2000 Jun;14(6):1006-13
[
10865965.001
]
[Cites]
Bone Marrow Transplant. 1994 Aug;14(2):293-8
[
7994245.001
]
[Cites]
Clin Cancer Res. 2001 Aug;7(8):2168-81
[
11489790.001
]
[Cites]
Cancer Res. 1986 Aug;46(8):4205-7
[
3731087.001
]
[Cites]
J Clin Oncol. 1992 Jul;10(7):1103-11
[
1607916.001
]
[Cites]
Blood. 1989 Oct;74(5):1499-506
[
2676014.001
]
[Cites]
J Natl Cancer Inst. 1981 Sep;67(3):529-38
[
6944525.001
]
[Cites]
J Clin Oncol. 1995 Jan;13(1):11-8
[
7799010.001
]
[Cites]
Blood. 2005 Jan 15;105(2):481-8
[
15213095.001
]
[Cites]
Cancer Res. 1983 May;43(5):2005-9
[
6572561.001
]
[Cites]
Blood. 1981 Dec;58(6):1203-12
[
6946847.001
]
[Cites]
Leuk Res. 2003 Apr;27(4):313-21
[
12531222.001
]
[Cites]
Leuk Lymphoma. 2005 Jul;46(7):1007-16
[
16019551.001
]
[Cites]
Blood. 1996 Mar 1;87(5):1710-7
[
8634416.001
]
[Cites]
Ann Hematol. 2005 Jun;84(6):376-82
[
15782343.001
]
[Cites]
Clin Cancer Res. 2003 Jan;9(1):307-15
[
12538483.001
]
[Cites]
Blood. 1991 May 1;77(9):1894-900
[
2018832.001
]
[Cites]
Cancer Chemother Pharmacol. 1996;39(1-2):109-12
[
8995507.001
]
[Cites]
N Engl J Med. 2003 Aug 21;349(8):743-52
[
12930926.001
]
[Cites]
Leukemia. 2007 Mar;21(3):453-61
[
17252021.001
]
(PMID = 20425452.001).
[ISSN]
1558-822X
[Journal-full-title]
Current hematologic malignancy reports
[ISO-abbreviation]
Curr Hematol Malig Rep
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
50
5.
Ackermans L, Temel Y, Visser-Vandewalle V:
Deep brain stimulation in Tourette's Syndrome.
Neurotherapeutics
; 2008 Apr;5(2):339-44
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Deep
brain stimulation
in Tourette's
Syndrome
.
Tourette's
Syndrome
(
TS
) is a neuropsychiatric
disorder
characterized by motor and vocal tics, often associated with behavioral disorders.
The pathophysiology of
TS
is still a matter of considerable debate.
Current
knowledge of cortico-basal ganglia-thalamocortical circuits provide explanations for the beneficial effects of deep
brain stimulation
(DBS) on tics.
When conservative treatment fails in patients with severe
TS
, DBS may be a therapeutic option.
In 1999, thalamic DBS was introduced for intractable
TS
.
Since then,
multiple
targets have been used in a small number of patients, including the globus pallidus pars interna and the nucleus accumbens.
[MeSH-major]
Deep
Brain Stimulation
/ methods. Tourette
Syndrome
/ therapy
MedlinePlus Health Information.
consumer health - Tourette Syndrome
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18394575.001).
[ISSN]
1933-7213
[Journal-full-title]
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
[ISO-abbreviation]
Neurotherapeutics
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
41
6.
Mort M, Ivanov D, Cooper DN, Chuzhanova NA:
A meta-analysis of nonsense mutations causing human genetic disease.
Hum Mutat
; 2008 Aug;29(8):1037-47
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A meta-analysis of nonsense mutations causing human genetic
disease
.
Nonsense mutations account for approximately 11% of all described gene lesions causing human inherited
disease
and approximately 20% of
disease
-associated single-basepair substitutions affecting gene coding regions.
Tumor suppressor (
TS
) genes exhibit a disproportionate number of nonsense mutations while most mutations in oncogenes are missense.
A total of 12% of somatic nonsense mutations in
TS
genes were found to occur recurrently in the hypermutable CpG dinucleotide.
In a comparison of somatic and germline mutational spectra for 17
TS
genes, approximately 43% of somatic nonsense mutations had counterparts in the germline (rising to 98% for CpG mutations).
Finally, the proportion of
disease
-causing nonsense mutations predicted to elicit nonsense-mediated mRNA decay (NMD) is significantly higher (P=1.56 x 10(-9)) than among nonobserved (potential) nonsense mutations, implying that nonsense mutations that elicit NMD are more likely to come to clinical attention.
[MeSH-major]
Codon, Nonsense. Databases, Genetic. Genetic
Diseases
, Inborn
MedlinePlus Health Information.
consumer health - Genetic Disorders
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18454449.001).
[ISSN]
1098-1004
[Journal-full-title]
Human mutation
[ISO-abbreviation]
Hum. Mutat.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0800509
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Codon; 0 / Codon, Nonsense
7.
Kamen BA:
The 3 ts of therapy: typing, tailoring, and targeting.
J Pediatr Hematol Oncol
; 2008 Nov;30(11):789-90
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The 3
ts
of therapy: typing, tailoring, and targeting.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18989153.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Introductory Journal Article
[Publication-country]
United States
8.
Liang S, Li A, Zhao M, Jiang H, Yu S, Meng X, Sun Y:
Epilepsy surgery in tuberous sclerosis complex: emphasis on surgical candidate and neuropsychology.
Epilepsia
; 2010 Nov;51(11):2316-21
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Epilepsy
surgery in
tuberous sclerosis complex
: emphasis on surgical candidate and neuropsychology.
PURPOSE: To discuss neuropsychological outcome and candidate of
epilepsy
surgery for
tuberous sclerosis complex
(
TSC
).
METHODS: To retrospectively analyze clinical data of 25 patients with
TSC
and
epilepsy
who underwent
epilepsy
surgery between 2001 and 2007.
Seizure reduction was analyzed at 1-year (1FU), 2-year (2FU), and 5-year (5FU) follow-up visits after surgery, and outcomes of
intelligence
quotient (IQ) and quality of life (QOL) were evaluated at 2FU.
RESULTS: Resective procedures included 14
tuber
resections, 9 lobectomies, and 2
tuber
resections and lobectomies.
Corpus callosotomies (CCTs) were performed as the adjunctive approach in eight cases with
low
IQ and behavioral problems.
Significant improvement was found in performance IQ in patients with preoperative
low
IQ or CCT.
Significant improvement in mean QOL score was observed in all patients, especially patients with preoperative
low
IQ and CCT but postoperative seizure freedom.
CONCLUSION: To be surgical candidates, patients with
TSC
and
epilepsy
should have identified epileptogenic tubers, and candidates should include patients with
low
IQ and
multiple
epileptogenic tubers.
CCT could be performed as an adjunctive approach to resective operation for
TSC
patients with
epilepsy
and
low
IQ and render improvement of performance IQ and QOL.
[MeSH-major]
Cognition Disorders /
diagnosis
.
Epilepsy
/ surgery. Neuropsychological Tests / statistics & numerical data. Patient Selection. Postoperative Complications /
diagnosis
.
Tuberous Sclerosis
/ surgery
[MeSH-minor]
Adolescent. Anterior Temporal Lobectomy. Child. China. Corpus Callosum / physiopathology. Corpus Callosum / surgery. Female. Follow-Up Studies. Frontal Lobe / physiopathology. Frontal Lobe / surgery. Humans.
Intelligence
/ physiology. Male. Neurosurgical Procedures. Occipital Lobe / physiopathology. Occipital Lobe / surgery. Patient Care Team. Quality of Life / psychology. Retrospective Studies. Young Adult
Genetic Alliance.
consumer health - Epilepsy
.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - After Surgery
.
MedlinePlus Health Information.
consumer health - Epilepsy
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Wiley Periodicals, Inc. © 2010 International League Against Epilepsy.
(PMID = 20633038.001).
[ISSN]
1528-1167
[Journal-full-title]
Epilepsia
[ISO-abbreviation]
Epilepsia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
9.
Wiśniewski A, Stupnicki R, Milde K, Szufladowicz-Woźniak J:
[Turner's syndrome: subjects with a normal body mass at birth grow taller than born small for gestational age].
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw
; 2006;12(2):131-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Turner's
syndrome
: subjects with a normal body mass at birth grow taller than born small for gestational age].
BACKGROUND: Body mass deficit at birth is one of the characteristic features observed in Turner's
syndrome
(
TS
).
Body mass is lower than expected for gestational age in about 90% of
TS
-babies, and is below -2 SD (i.e.
OBJECTIVES: The aim of the study was to compare the growth courses of
TS
-girls born with normal and deficient body mass.
PATIENTS: A group of 157
TS
-girls, delivered at term (> or =38 weeks of gestation), were studied.
METHODS: Turner's
syndrome
was confirmed by chromosome analysis.
Postnatal body height and mass values were related to Polish norms for females with Turner's
syndrome
and to the norms for healthy female population.
RESULTS: In the spontaneously growing
TS
-girls from the AGA group, a total of 275 measurements of body mass and height were carried out, the respective numbers for DSGA and PSGA groups were 176 and 100.
Mean differences between the actual and expected body height for the AGA, DSGA and PSGA groups amounted to 0.40+/- 1.02, -0.21+/-0.88 and -0.95+/-0.80 SD
TS
, respectively, all means differing highly significantly (p<0.001) from each other.
CONCLUSION: It may be concluded that spontaneously growing girls with Turner's
syndrome
, who had a normal (for gestational age) body mass at birth, attain a higher stature than girls with body mass deficit.
[MeSH-major]
Birth Weight. Body Height. Growth Disorders / epidemiology. Infant,
Low
Birth Weight / growth & development. Infant, Small for Gestational Age. Turner
Syndrome
/ epidemiology. Turner
Syndrome
/ physiopathology
Genetic Alliance.
consumer health - MASS syndrome
.
MedlinePlus Health Information.
consumer health - Birth Weight
.
MedlinePlus Health Information.
consumer health - Growth Disorders
.
MedlinePlus Health Information.
consumer health - Turner Syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16813719.001).
[ISSN]
1234-625X
[Journal-full-title]
Endokrynologia, diabetologia i choroby przemiany materii wieku rozwojowego : organ Polskiego Towarzystwa Endokrynologów Dziecięcych
[ISO-abbreviation]
Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw
[Language]
pol
[Publication-type]
Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Poland
10.
Piedimonte LR, Wailes IK, Weiner HL:
Tuberous sclerosis complex: molecular pathogenesis and animal models.
Neurosurg Focus
; 2006;20(1):E4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Tuberous sclerosis complex
: molecular pathogenesis and animal models.
Mutations in one of two genes, TSC1 and TSC2, result in a similar
disease
phenotype by disrupting the normal interaction of their protein products, hamartin and tuberin, which form a functional signaling
complex
.
Disruption of these genes in the
brain
results in abnormal cellular differentiation, migration, and proliferation, giving rise to the characteristic
brain
lesions of
tuberous sclerosis complex
(
TSC
) called cortical tubers.
The most devastating complications of
TSC
affect the central nervous
system
and include
epilepsy
, mental retardation, autism, and glial tumors.
Relevant animal models, including conventional and conditional knockout mice, are valuable tools for studying the normal functions of tuberin and hamartin and the way in which disruption of their expression gives rise to the variety of clinical features that characterize
TSC
.
In the future, these animals will be invaluable preclinical models for the development of highly specific and efficacious treatments for children affected with
TSC
.
[MeSH-major]
Disease
Models, Animal.
Tuberous Sclerosis
/ etiology.
Tuberous Sclerosis
/ genetics. Tumor Suppressor Proteins
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[RetractionIn]
Jane JA Sr. Neurosurg Focus. 2006;21(1):e17
[
16886289.001
]
(PMID = 16459994.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article; Retracted Publication; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; 4JG2LF96VF / tuberous sclerosis complex 2 protein
[Number-of-references]
64
11.
Ribeiro AS:
Effects of coupling strength and space on the dynamics of coupled toggle switches in stochastic gene networks with multiple-delayed reactions.
Phys Rev E Stat Nonlin Soft Matter Phys
; 2007 Jun;75(6 Pt 1):061903
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Effects of coupling strength and space on the dynamics of coupled toggle switches in stochastic gene networks with
multiple
-delayed reactions.
They have been interpreted as decision circuits in
cell
differentiation, a process long hypothesized to be bistable, or as cellular memory units.
Once a "decision" is made, the
system
must remain stable.
One way to gain stability is by duplicating the genes of
a TS
and coupling the two TSs.
For this, we introduce the coupling strength (C), a parameter to characterize the GRN
structure
, against which we compare the GRN stability (S).
We first show that
time
delays in transcription, associated to the promoter region release, ensure bistability of
a TS
, given no cooperative binding or self-activation reactions.
Three dynamical regimes are observed: (i) for weak coupling, high frequency synchronized oscillations, (ii) for average coupling,
low
frequency synchronized oscillations, and (iii) for strong coupling the
system
becomes stable after a transient, in one of two steady
states
.
The
system
stability, S, goes through a first order phase
transition
as C increases, in the average coupling regime.
After, we study the effects of spatial separation in two compartments on the dynamics of two coupled TSs, where spatial separation is modeled as normally distributed random
time
delayed reactions.
The phase
transition
of S, as C increases, occurs for lower values of C than when the two TSs are in the same compartment.
Finally, we couple weakly and homogeneously several TSs within a single compartment and observe that as the number of coupled TSs increases, the
system
goes through the phase
transition
in S, from oscillatory to stable and for C values lower than in the two previous cases.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17677296.001).
[ISSN]
1539-3755
[Journal-full-title]
Physical review. E, Statistical, nonlinear, and soft matter physics
[ISO-abbreviation]
Phys Rev E Stat Nonlin Soft Matter Phys
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
12.
D'Amato E, d'Annunzio G, Calcaterra V, Morsellino V, Larizza D, Lorini R:
Horseshoe kidney malformation in Turner syndrome is not associated with HNF-1beta gene mutations.
Pediatr Nephrol
; 2008 Jan;23(1):137-40
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Horseshoe kidney malformation in Turner
syndrome
is not associated with HNF-1beta gene mutations.
Mutations in hepatocyte nuclear factor-1beta (HNF-1beta) gene cause a subtype of maturity-onset diabetes of the young (MODY5), whose clinical features are pancreatic beta-
cell
dysfunction, renal malformations, and in some females, internal genital malformations.
Diabetes mellitus, horseshoe kidney, and X chromosome monosomy or mosaicism can be observed in Turner
syndrome
(
TS
).
To investigate whether mutations/polymorphisms of HNF-1beta and X monosomy influence horseshoe kidney development, we evaluated HNF-1beta gene sequence in 13 patients with
TS
and several kidney abnormalities.
We conclude there is no direct relationship between horseshoe kidney in
TS
and mutation or polymorphism of HNF-1beta gene, but we speculate that target gene(s) of HNF-1beta, likely mapped on the X chromosome, is/are responsible of the horseshoe kidney formation in
TS
.
[MeSH-major]
Hepatocyte Nuclear Factor 1-beta / genetics. Kidney / abnormalities. Mutation. Turner
Syndrome
/ genetics. Turner
Syndrome
/ pathology
Genetic Alliance.
consumer health - Horseshoe kidney
.
Genetic Alliance.
consumer health - Turner syndrome
.
MedlinePlus Health Information.
consumer health - Turner Syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Can J Urol. 2003 Jun;10 (3):1899-904
[
12892577.001
]
[Cites]
N Engl J Med. 2001 Sep 27;345(13):971-80
[
11575290.001
]
[Cites]
J Am Soc Nephrol. 2002 Sep;13(9):2384-98
[
12191984.001
]
[Cites]
Eur J Biochem. 2004 Sep;271(18):3715-28
[
15355349.001
]
[Cites]
Yonsei Med J. 2003 Aug 30;44(4):744-6
[
12950137.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4695-700
[
10758154.001
]
[Cites]
J Clin Endocrinol Metab. 2007 Jan;92(1):10-25
[
17047017.001
]
[Cites]
Eur J Pediatr. 2002 Apr;161(4):224-5
[
12014393.001
]
[Cites]
J Pediatr Endocrinol Metab. 2002 Sep-Oct;15(8):1183-90
[
12387517.001
]
[Cites]
Pediatr Nephrol. 1996 Aug;10 (4):498-500
[
8865252.001
]
[Cites]
J Am Soc Nephrol. 2003 Aug;14(8):2033-41
[
12874457.001
]
[Cites]
Ann Intern Med. 2004 Apr 6;140(7):510-7
[
15068978.001
]
[Cites]
Am J Physiol Renal Physiol. 2002 Oct;283(4):F839-51
[
12217876.001
]
[Cites]
J Exp Clin Cancer Res. 2002 Dec;21(4):613-6
[
12636110.001
]
[Cites]
Kidney Int. 2000 Mar;57(3):898-907
[
10720943.001
]
[Cites]
Pediatrics. 2005 Mar;115(3):732-5
[
15741379.001
]
[Cites]
Nat Genet. 1997 Dec;17(4):384-5
[
9398836.001
]
[Cites]
Nephrol News Issues. 2006 Dec;20(13):20-2
[
17168054.001
]
[Cites]
Diabetologia. 2002 Jan;45(1):153-4
[
11845237.001
]
[Cites]
Best Pract Res Clin Endocrinol Metab. 2002 Jun;16(2):243-61
[
12064891.001
]
(PMID = 17922147.001).
[ISSN]
0931-041X
[Journal-full-title]
Pediatric nephrology (Berlin, Germany)
[ISO-abbreviation]
Pediatr. Nephrol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
138674-15-4 / Hepatocyte Nuclear Factor 1-beta
13.
Hayashi T, Kawahara H, Kobayashi S, Kashiwagi H, Hirai K, Yanaga K:
Importance of thymidine phosphorylase, dihydropyrimidine dehydrogenase and thymidylate synthase expression at the invasive front of T3 rectal cancer as prognostic factors.
Hepatogastroenterology
; 2008 Mar-Apr;55(82-83):403-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
BACKGROUND/AIMS: We evaluated a relationship between postoperative recurrence and thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (
TS
) expression at the invasive front of T3 rectal cancer.
Paraffin-embedded sections of these patients were immunostained for TP, DPD and
TS
.
RESULTS: There was no relationship between expression of DPD or
TS
in the tumor
cells
and recurrences.
Although no relationship was present between expression of TP in the stromal
cells
around the invasive front of the tumor and postoperative recurrences, there was a strong correlation between expression of TP in the invasive front of the tumor and postoperative recurrence.
Moreover, by multivariate logistic regression analysis, TP expression in the tumor
cells
was the only independent contributory factor for postoperative recurrences (p = 0.021) with an odds ratio of 8.27.
Genetic Alliance.
consumer health - Rectal Cancer
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18613375.001).
[ISSN]
0172-6390
[Journal-full-title]
Hepato-gastroenterology
[ISO-abbreviation]
Hepatogastroenterology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.4 / Thymidine Phosphorylase
14.
D'Addio G, Cesarelli M, Corbi G, Romano M, Furgi G, Ferrara N, Rengo F:
Reproducibility of heart rate turbulence indexes in heart failure patients.
Conf Proc IEEE Eng Med Biol Soc
; 2010;2010:2573-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Reproducibility of heart rate
turbulence
indexes in heart failure patients.
Cardiovascular oscillations following spontaneous ventricular premature complexes (VPC) are characterized by a short-term heart rate fluctuation known as heart rate
turbulence
(HRT) described by the so-called
turbulence
onset (TO) and
slope
(
TS
).
A paired t
test
was used to assess the clinical stability of patients during the study period and the number of PVC in Holter recordings' couples.
Both TO and
TS
indexes were calculated for each isolated VPC, and due to their skewed distribution, reproducibility of median and mean TO and
TS
was studied by Bland-Altman technique.
Results showed that median HRT indexes might be preferred to commonly suggested mean values and that, although TO showed lower bias value than
TS
,
TS
can be considered much more reproducible than TO, comparing limits of agreements with normal values.
This preliminary results suggest the use of medians instead of mean HRT indexes values and a reliability of the
turbulence slope
greater than the
turbulence
onset index.
[MeSH-minor]
Aged. Humans. Male. Middle Aged. Models, Cardiovascular. Models, Statistical. Oscillometry / methods. Reproducibility of Results.
Time
Factors
MedlinePlus Health Information.
consumer health - Heart Failure
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21096173.001).
[ISSN]
1557-170X
[Journal-full-title]
Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
[ISO-abbreviation]
Conf Proc IEEE Eng Med Biol Soc
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
15.
Luya Schmidt A, Mach F:
[Takotsubo syndrome: myth or reality?].
Rev Med Suisse
; 2009 May 27;5(205):1184, 1186-8, 1190-2 passim
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Takotsubo
syndrome
: myth or reality?].
[Transliterated title]
Syndrome
de
Takotsubo: mythe ou réalité?
Takotsubo
syndrome
(
TS
) also named transient left ventricular apical ballooning
syndrome
is a particularly entity of the acute coronary
syndrome
with normal coronary arteries.
The aetiology and physiopathology of
TS
are subject to many hypothesis, sometime contradictory.
The typical image at the ventriculography is
a systolic
left ventricular apical ballooning reversible in a few days to weeks with an excellent prognostic.
The goal of this article is to review the actual knowledge about
TS to
help the general practitioner, aboard this entity in the management of an ACS.
[MeSH-major]
Electrocardiography. Takotsubo Cardiomyopathy /
diagnosis
. Takotsubo Cardiomyopathy / physiopathology
[MeSH-minor]
Adrenergic beta-Antagonists / therapeutic use. Biomarkers / blood. Creatine Kinase, MB Form / blood.
Diagnosis
, Differential. Diuretics / therapeutic use. Drug Therapy, Combination. Echocardiography. Female. Humans. Middle Aged. Prognosis. Risk Factors. Stress, Psychological / complications. Treatment Outcome. Troponin I / blood
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19517750.001).
[ISSN]
1660-9379
[Journal-full-title]
Revue médicale suisse
[ISO-abbreviation]
Rev Med Suisse
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Adrenergic beta-Antagonists; 0 / Biomarkers; 0 / Diuretics; 0 / Troponin I; EC 2.7.3.2 / Creatine Kinase, MB Form
[Number-of-references]
16
16.
Collepardo-Guevara R, Craig IR, Manolopoulos DE:
Proton transfer in a polar solvent from ring polymer reaction rate theory.
J Chem Phys
; 2008 Apr 14;128(14):144502
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
When the A-H distance is used as the reaction coordinate, the ring polymer trajectories are found to exhibit
multiple
recrossings of the
transition state
dividing
surface
and to give a rate coefficient that is smaller than the quantum
transition state
theory value by an order of magnitude.
This is to be expected on kinematic grounds for a heavy-light-heavy reaction when the light atom transfer coordinate is used as the reaction coordinate, and it clearly precludes the use of
transition state
theory with this reaction coordinate.
As has been shown previously for this problem, a solvent polarization coordinate defined in terms of the expectation value of the proton transfer distance in the ground adiabatic quantum
state
provides a better reaction coordinate with less recrossing.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18412454.001).
[ISSN]
0021-9606
[Journal-full-title]
The Journal of chemical physics
[ISO-abbreviation]
J Chem Phys
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
17.
Harris EL, McLaren CE, Reboussin DM, Gordeuk VR, Barton JC, Acton RT, McLaren GD, Vogt TM, Snively BM, Leiendecker-Foster C, Holup JL, Passmore LV, Eckfeldt JH, Lin E, Adams PC:
Serum ferritin and transferrin saturation in Asians and Pacific Islanders.
Arch Intern Med
; 2007 Apr 9;167(7):722-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
BACKGROUND: Asians and Pacific Islanders in the Hemochromatosis and Iron Overload Screening (HEIRS) Study had the highest prevalence of elevated serum ferritin (SF) and transferrin saturation (
TS
) levels, but to our knowledge, the reasons for this have not been investigated.
METHODS: Using
multiple
linear regression, we compared
TS
and SF distributions for 42 720 Asian, Pacific Islander, and white HEIRS Study participants recruited through 5 field centers in North America who did not have HFE C282Y or H63D alleles.
RESULTS: Compared with their white counterparts, Asian men had a 69-ng/mL (155-pmol/L) higher adjusted mean SF level and a 3% higher
TS
level (P<.001); Asian women had 23-ng/mL (52-pmol/L) higher adjusted mean SF level and a 3% higher
TS
level (P<.001).
The mean
TS
level of Asian women was higher than that of Pacific Islander women, and the mean SF level of Pacific Islander men was significantly higher than that of white men.
These differences remained significant after adjusting for self-reported history of diabetes or liver
disease
.
CONCLUSION: Higher
TS
and SF levels in persons of Asian or Pacific Island heritage may need to be interpreted differently than for whites, although the biological basis and clinical significance of higher levels among Asians and Pacific Islanders are unclear.
MedlinePlus Health Information.
consumer health - Asian American Health
.
MedlinePlus Health Information.
consumer health - Native Hawaiian and Pacific Islander Health
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17420432.001).
[ISSN]
0003-9926
[Journal-full-title]
Archives of internal medicine
[ISO-abbreviation]
Arch. Intern. Med.
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / M01 RR 00032; United States / NCRR NIH HHS / RR / M01 RR 000827; United States / NCRR NIH HHS / RR / M01 RR 10284; United States / NHLBI NIH HHS / HC / N01 HC 05185; United States / NHLBI NIH HHS / HC / N01 HC 05186; United States / NHLBI NIH HHS / HC / N01 HC 05188; United States / NHLBI NIH HHS / HC / N01 HC 05189; United States / NHLBI NIH HHS / HC / N01 HC 05190; United States / NHLBI NIH HHS / HC / N01 HC 05191; United States / NHLBI NIH HHS / HC / N01 HC 05192; United States / NHLBI NIH HHS / HL / UH1 HL 03679-05
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Transferrin; 9007-73-2 / Ferritins
18.
Damsa C, Borras L, Bianchi-Demicheli F, Andreoli A:
[Alpha-thalassemias and bipolar disorders: a genetic link?].
Encephale
; 2005 Jan-Feb;31(1 Pt 1):72-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
After a previous paper discussing the possible association between beta-thalassemias and bipolar
disorder
, this article considers a possible association between alpha-thalassemia and the bipolar
disorder
.
We report the case of a 36 year old woman with bipolar
disorder
and alpha-thalassemia.
The patient, native of Reunion Island, has a family history of bipolar
disorder
(both parents, one brother, and a paternal uncle).
The severity of the bipolar
disorder
type I in her family, is illustrated by the suicides of both parents, one brother and the paternal uncle, in intervals of only a few years.
Some genetic studies described the existence of possible genetic susceptibility for bipolar
disorder
on the short arm of chromosome 16, close to the gene involved in certain alpha-thalassemias, on the region 16p13.3.
An interesting
finding
is that the sequencing of 258 kb of the chromosome region 16p13.3 not only allowed the identification of genes involved in the alpha-thalassemia and in the vulnerability to bipolar disorders, but also the identification of genes implicated in
tuberous sclerosis
, in polycystic kidney
disease
, in cataract with microophtalmia, and in vulnerability genetic factors for ATR-16
syndrome
, asthma,
epilepsy
, certain forms of autism and mental retardation.
Numerous clinical descriptions and some familial studies on linkage suggested a possible relationship between
tuberous sclerosis
, polycystic kidney
disease
, cataract with microophtalmia, ATR-16
syndrome
, asthma,
epilepsy
, certain forms of autism, mental retardation and bipolar
disorder
, given the closeness of these vulnerability genes on the short arm of the chromosome 16.
Taking into account the methodological difficulties due to the clinical and genetic heterogeneity of bipolar
disorder
, we suggest that linkage techniques should be used to confirm the presence of susceptibility genetic factor for bipolar disorders on chromosome 16.
Thus a known genetic
disease
(alpha-thalassemia) could contribute to confirming the presence on the short arm of chromosome 16 of a susceptibility genetic factor for bipolar disorders.
Linkage studies should be performed in families with a strong association for both
diseases
.
Thanks to linkage techniques, one could hope for an improvement in understanding the physiopathology of bipolar
disorder
, with possible implications at a therapeutic level.
[MeSH-major]
Bipolar
Disorder
/ complications. Bipolar
Disorder
/ genetics. alpha-Thalassemia / complications. alpha-Thalassemia / genetics
MedlinePlus Health Information.
consumer health - Bipolar Disorder
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15971642.001).
[ISSN]
0013-7006
[Journal-full-title]
L'Encéphale
[ISO-abbreviation]
Encephale
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
19.
Jacobs J, Rohr A, Moeller F, Boor R, Kobayashi E, LeVan Meng P, Stephani U, Gotman J, Siniatchkin M:
Evaluation of epileptogenic networks in children with tuberous sclerosis complex using EEG-fMRI.
Epilepsia
; 2008 May;49(5):816-25
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Evaluation of epileptogenic networks in children with
tuberous sclerosis complex
using EEG-fMRI.
PURPOSE: Ninety percent of patients with
tuberous sclerosis complex
(
TSC
) have
epilepsy
.
METHODS: Five children with
TSC
and focal
epilepsy
were studied using simultaneous EEG and functional MRI recordings.
RESULTS: Thirteen different types of interictal epileptiform discharges (IED) were analyzed with 12 showing a BOLD response, all involving more than one
tuber
.
Five studies had tubers with activations exclusively within the lesion, three studies had lesional activations extending to perilesional areas, and two studies had activations involving exclusively perilesional areas of at least one
tuber
.
Deactivations exclusively within
a tuber
were found in six studies, lesional deactivations extending to perilesional areas were found in four studies, and tubers with exclusively perilesional deactivations were found in five studies.
A BOLD response was found in at least one
tuber
in the lobe of IED generation and presumed seizure onset (according to telemetry) in all patients.
DISCUSSION: These findings suggest extended epileptogenic networks in patients with
TSC
, which exceed networks described in PET and SPECT studies.
[MeSH-major]
Brain
Mapping / methods. Electroencephalography / methods.
Epilepsy
/ physiopathology. Magnetic Resonance Imaging / methods.
Tuberous Sclerosis
/ physiopathology
[MeSH-minor]
Age Factors.
Brain
/ physiopathology. Child. Child, Preschool. Female. Humans. Male. Neural Pathways. Oxygen / blood. Preoperative Care
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Epilepsy
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
OXYGEN
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18177362.001).
[ISSN]
0013-9580
[Journal-full-title]
Epilepsia
[ISO-abbreviation]
Epilepsia
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
S88TT14065 / Oxygen
20.
Zikou A, Ioannidou MC, Tzoufi M, Astrakas L, Argyropoulou MI:
Magnetization transfer ratio measurements of the brain in children with tuberous sclerosis complex.
Pediatr Radiol
; 2005 Nov;35(11):1071-4
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Magnetization transfer ratio measurements of the
brain
in children with
tuberous sclerosis complex
.
BACKGROUND: Magnetization transfer contrast and magnetization transfer ratio (MTR) in
brain
are mainly related to the presence of myelin.
Neuropathological studies of
brain
lesions in
tuberous sclerosis complex
(
TSC
) have demonstrated disordered myelin sheaths.
OBJECTIVE: To evaluate the MTR of the
brain
in children with
TSC
and to compare with that in controls.
MATERIALS AND METHODS: Four patients (aged 0.41-8.4 years, mean 2.5 years) with
TSC
and four age- and sex-matched controls were evaluated with classic MR sequences and with a three-dimensional gradient-echo sequence without and with magnetization transfer pre-pulse.
CONCLUSIONS: MTR measurements not only provide semiquantitative information for
TSC
lesions but also reveal more extensive
disease
.
[MeSH-major]
Brain
/ pathology.
Brain
Neoplasms / pathology. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Nerve Fibers, Myelinated / pathology.
Tuberous Sclerosis
/ pathology
[MeSH-minor]
Child. Child, Preschool. Female. Humans. Infant. Male. Reproducibility of Results.
Sensitivity
and Specificity. Severity of Illness Index
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
MedlinePlus Health Information.
consumer health - MRI Scans
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Pediatr Radiol. 2005 Dec;35(12):1294
[Cites]
Neuroradiology. 1999 Jun;41(6):428-32
[
10426218.001
]
[Cites]
Radiology. 2004 Aug;232(2):461-5
[
15215545.001
]
[Cites]
Mayo Clin Proc. 1989 Mar;64(3):305-11
[
2704253.001
]
[Cites]
Psychol Med. 2001 Nov;31(8):1437-46
[
11722158.001
]
[Cites]
Magn Reson Med. 1999 Dec;42(6):1128-36
[
10571935.001
]
[Cites]
Clin Neuropathol. 2003 May-Jun;22(3):119-28
[
12809354.001
]
[Cites]
Eur J Paediatr Neurol. 2002;6(1):15-23
[
11993952.001
]
[Cites]
Neurology. 1999 Oct 22;53(7):1384-90
[
10534239.001
]
[Cites]
J Magn Reson Imaging. 2001 Apr;13(4):534-46
[
11276097.001
]
[Cites]
Pediatr Radiol. 2004 May;34(5):387-92
[
15029464.001
]
[Cites]
Pediatr Neurol. 2003 Nov;29(5):404-9
[
14684235.001
]
[Cites]
J Magn Reson Imaging. 1998 May-Jun;8(3):548-53
[
9626867.001
]
[Cites]
Brain Dev. 2001 Nov;23(7):508-15
[
11701246.001
]
[Cites]
J Magn Reson Imaging. 1996 Jul-Aug;6(4):573-9
[
8835948.001
]
[Cites]
Neuroradiology. 2001 Apr;43(4):305-8
[
11338414.001
]
[Cites]
J Child Neurol. 1998 Dec;13(12 ):624-8
[
9881533.001
]
[Cites]
Arch Neurol. 2003 Nov;60(11):1580-4
[
14623730.001
]
[Cites]
Radiology. 1994 Sep;192(3):593-9
[
8058919.001
]
[Cites]
AJNR Am J Neuroradiol. 1999 May;20(5):907-16
[
10369365.001
]
[Cites]
J Comput Assist Tomogr. 1997 Jan-Feb;21(1):8-14
[
9022761.001
]
[Cites]
Am J Med Genet. 2002 Sep 1;111(4):435-9
[
12210306.001
]
(PMID = 16052334.001).
[ISSN]
0301-0449
[Journal-full-title]
Pediatric radiology
[ISO-abbreviation]
Pediatr Radiol
[Language]
eng
[Publication-type]
Controlled Clinical Trial; Journal Article
[Publication-country]
Germany
21.
Wu HP, Huang CC, Cheng TL, Tseng WL:
Sodium hydroxide as pretreatment and fluorosurfactant-capped gold nanoparticles as sensor for the highly selective detection of cysteine.
Talanta
; 2008 Jul 15;76(2):347-52
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Sodium
hydroxide as pretreatment and fluorosurfactant-capped gold nanoparticles as sensor for the highly selective detection of cysteine.
When adding NaOH
to a
solution of HCys, the five-membered ring
transition state
is formed through intramolecular hydrogen abstraction.
By contrast, it is difficult for Cys to form a four-membered ring
transition state
after Cys has been pretreated with NaOH.
As a result, the HCys-induced aggregation of the FSN-capped AuNPs is suppressed because the five-membered ring
transition state
exhibits relatively larger steric hindrance and has stronger interaction with the FSN molecules.
Note that HCys and Cys have very similar
structure
and pK(a) value.
[MeSH-major]
Cysteine / analysis. Metal Nanoparticles.
Surface
-Active Agents
[MeSH-minor]
Fluorescent Dyes. Gold. Homocysteine / analysis. Homocysteine / urine. Humans. Kinetics. Methods.
Sodium
Hydroxide
Hazardous Substances Data Bank.
SODIUM HYDROXIDE
.
Hazardous Substances Data Bank.
CYSTEINE
.
Hazardous Substances Data Bank.
GOLD, ELEMENTAL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18585288.001).
[ISSN]
1873-3573
[Journal-full-title]
Talanta
[ISO-abbreviation]
Talanta
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
England
[Chemical-registry-number]
0 / Fluorescent Dyes; 0 / Surface-Active Agents; 0LVT1QZ0BA / Homocysteine; 55X04QC32I / Sodium Hydroxide; 7440-57-5 / Gold; K848JZ4886 / Cysteine
22.
Igartúa-Nieves E, Ocasio-Delgado Y, Torres-Castillo MD, Rivera-Betancourt O, Rivera-Pagán JA, Rodriguez D, López GE, Cortés-Figueroa JE:
Electrochemistry and [60]fullerene displacement reactions of (dihapto-[60]fullerene) pentacarbonyl metal(0) (M = Cr, Mo, W).
Dalton Trans
; 2007 Apr 7;(13):1293-9
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
A Jahn-Teller type distortion of the spherical
surface
of [60]fullerene promoted by [60]fullerene-metal pi-backbonding may explain the observed positive shifts.
Analysis of the activation parameters for the metal-[60]fullerene dissociation, the metal-[60]fullerene bond enthalpies (from DFT computations), and metal-solvent (benzene) bond enthalpies (from DFT computations) suggests appreciable solvent contribution to the
transition state
leading to formation of the intermediate species solvent-M(CO)(5).
Appreciable
transition state
stabilization due to solvation of the intermediate species is inferred for M = Mo and W.
For M = Cr, stabilization of the intermediate species due to solvation is not accompanied by the corresponding
transition state
stabilization.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17372644.001).
[ISSN]
1477-9226
[Journal-full-title]
Dalton transactions (Cambridge, England : 2003)
[ISO-abbreviation]
Dalton Trans
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
23.
Klingenberg M:
Ligand-protein interaction in biomembrane carriers. The induced transition fit of transport catalysis.
Biochemistry
; 2005 Jun 21;44(24):8563-70
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Ligand-protein interaction in biomembrane carriers. The induced
transition
fit of transport catalysis.
A transition state
is invoked in which the binding site assumes the best fit to the substrate, whereas in the two ground (internal and external)
states
, the fit is poor.
The maximum binding energy released in the
transition state
provides catalytic energy to enable the large carrier protein transformations associated with transport.
This "induced
transition
fit" (ITF) of carrier catalysis provides a framework of rules, concerning specificity, unidirectional versus exchange type transport, directing inhibitors to the ground
state
instead of the
transition state
, and excluding simultaneous chemical and transport catalysis (vectorial group translocation).
The analysis of the
structure
-function relationship based on new carrier
structures
may be challenged to account for the workings of the ITF.
[MeSH-major]
Carrier Proteins / chemistry. Carrier Proteins / metabolism.
Cell
Membrane / metabolism. Enzymes / metabolism. Ligands
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15952762.001).
[ISSN]
0006-2960
[Journal-full-title]
Biochemistry
[ISO-abbreviation]
Biochemistry
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Carrier Proteins; 0 / Enzymes; 0 / Ligands; 9068-80-8 / Mitochondrial ADP, ATP Translocases
24.
Debes NM, Skov L, Hjalgrim H:
[Tourette syndrome. Genetics, neuroanatomy and neurotransmitters].
Ugeskr Laeger
; 2008 Aug 25;170(35):2695-700
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Tourette
syndrome
. Genetics, neuroanatomy and neurotransmitters].
[Transliterated title]
Tourettes
syndrom
. Genetik, neuroanatomi og neurotransmittere.
The etiology and pathophysiology of Tourette
syndrome
(
TS
) have not yet been clarified.
The inheritance of
TS
is unknown; the etiology seems to be polygenic.
The basal ganglia are probably smaller in patients with
TS
.
ADHD results from a decreased
concentration
of dopamine and an increased
concentration
of noradrenaline.
[MeSH-major]
Tourette
Syndrome
[MeSH-minor]
Adolescent. Animals. Attention Deficit
Disorder
with Hyperactivity / genetics. Attention Deficit
Disorder
with Hyperactivity / metabolism. Attention Deficit
Disorder
with Hyperactivity / physiopathology. Basal Ganglia / anatomy & histology. Basal Ganglia / physiology.
Brain
/ anatomy & histology.
Brain
/ metabolism.
Brain
/ physiology. Child. Dopamine / metabolism. Female. Genetic Predisposition
to Disease
. Humans. Male. Norepinephrine / metabolism. Obsessive-Compulsive
Disorder
/ genetics. Obsessive-Compulsive
Disorder
/ metabolism. Obsessive-Compulsive
Disorder
/ physiopathology. Serotonin / metabolism. Tics / genetics. Tics / metabolism. Tics / physiopathology
Genetic Alliance.
consumer health - Tourette Syndrome
.
MedlinePlus Health Information.
consumer health - Tourette Syndrome
.
Hazardous Substances Data Bank.
Norepinephrine
.
Hazardous Substances Data Bank.
DOPAMINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18761860.001).
[ISSN]
1603-6824
[Journal-full-title]
Ugeskrift for laeger
[ISO-abbreviation]
Ugeskr. Laeg.
[Language]
dan
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Denmark
[Chemical-registry-number]
333DO1RDJY / Serotonin; VTD58H1Z2X / Dopamine; X4W3ENH1CV / Norepinephrine
[Number-of-references]
40
25.
Yoshida S, Hayashi T, Ishii N, Yoshinaga A, Ohno R, Terao T, Watanabe T, Yamada T, Osada H:
Bilateral renal angiomyolipoma coexistent with pulmonary lymphangioleiomyomatosis and tuberous sclerosis.
Int Urol Nephrol
; 2006;38(3-4):413-5
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Bilateral renal angiomyolipoma coexistent with pulmonary lymphangioleiomyomatosis and
tuberous sclerosis
.
A case of bilateral renal angiomyolipoma coexistent with pulmonary lymphangioleiomyomatosis and
tuberous sclerosis
was described, being in shock with massive hematuria.
Lymphangioleiomyomatosis has been suggested to be an incomplete expression of
tuberous sclerosis
.
Although coexisting renal and pulmonary involvement in
tuberous sclerosis
is rare, it is important to recognize lymphangioleiomyomatosis as a pulmonary involvement of angiomyolipoma with
tuberous sclerosis
.
[MeSH-major]
Angiomyolipoma / complications. Kidney Neoplasms / complications. Lung Neoplasms / complications. Lymphangioleiomyomatosis / complications. Neoplasms,
Multiple
Primary / complications.
Tuberous Sclerosis
/ complications
Genetic Alliance.
consumer health - Lymphangioleiomyomatosis
.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Kidney Cancer
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Radiology. 2002 Oct;225(1):78-82
[
12354988.001
]
[Cites]
J Urol. 1994 Jun;151(6):1612-5
[
8189576.001
]
[Cites]
Radiographics. 2002 Oct;22 Spec No:S185-98
[
12376610.001
]
[Cites]
Cancer. 1983 Sep 1;52(5):851-5
[
6871826.001
]
[Cites]
J Urol. 1987 Sep;138(3):477-81
[
3625844.001
]
[Cites]
Int Urol Nephrol. 2000;32(2):219-22
[
11229634.001
]
[Cites]
Urology. 2002 Jan;59(1):138
[
11796307.001
]
(PMID = 17111084.001).
[ISSN]
0301-1623
[Journal-full-title]
International urology and nephrology
[ISO-abbreviation]
Int Urol Nephrol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
26.
Tutaj M, Szczepanik M:
Epicutaneous (EC) immunization with myelin basic protein (MBP) induces TCRalphabeta+ CD4+ CD8+ double positive suppressor cells that protect from experimental autoimmune encephalomyelitis (EAE).
J Autoimmun
; 2007 Jun;28(4):208-15
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Epicutaneous (EC) immunization with myelin basic protein (MBP) induces TCRalphabeta+ CD4+ CD8+ double positive suppressor
cells
that protect from experimental autoimmune encephalomyelitis (EAE).
Multiple sclerosis
(MS) is a central nervous
system
(CNS) chronic inflammatory autoimmune
disease
with limited treatment modalities.
Oral tolerance is one of the experimental methods that protects from autoimmune
diseases
.
In our previous work we found that epicutaneous (EC) immunization with protein antigen induced
a state
of profound immunosuppression that inhibited inflammatory response in contact
sensitivity
, in experimental autoimmune encephalomyelitis (EAE) and in allogeneic skin graft rejection.
In our
current
work, we precisely determined the phenotype of EC induced T suppressor (
Ts
)
cells
that reduce the progress of EAE.
Employing TCRdelta-/-, CD1d-/- mice, we showed that EC induced
Ts cells
do not belong either to the population of TCRgammadelta
cells
or CD1d restricted NKT
cells
.
This might suggest that NKT
cells
could interfere with the induction of
Ts cells
.
Using beta2m-/- mice, negative selection and positive selection of EC induced
Ts cells
, we showed that
Ts cells
protecting from EAE belong to the population of TCRalphabeta+ CD4+ CD8+ double positive lymphocytes.
[MeSH-major]
CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology.
Multiple Sclerosis
/ prevention & control. Myelin Basic Protein / immunology. Receptors, Antigen, T-
Cell
, alpha-beta / immunology
[MeSH-minor]
Animals. Antigens, CD1 / genetics. Antigens, CD1 / immunology. Antigens, CD1d. Encephalomyelitis, Autoimmune, Experimental / genetics. Encephalomyelitis, Autoimmune, Experimental / immunology. Encephalomyelitis, Autoimmune, Experimental / pathology. Female. Guinea Pigs. Immunization. Inflammation / genetics. Inflammation / immunology. Inflammation / pathology. Inflammation / prevention & control. Killer
Cells
, Natural / immunology. Killer
Cells
, Natural / pathology. Mice. Mice, Knockout. Receptors, Antigen, T-
Cell
, gamma-delta / deficiency. Receptors, Antigen, T-
Cell
, gamma-delta / immunology. Skin Transplantation. Transplantation, Homologous. beta 2-Microglobulin / deficiency. beta 2-Microglobulin / immunology
MedlinePlus Health Information.
consumer health - Multiple Sclerosis
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17442539.001).
[ISSN]
0896-8411
[Journal-full-title]
Journal of autoimmunity
[ISO-abbreviation]
J. Autoimmun.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Myelin Basic Protein; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / beta 2-Microglobulin
27.
Ram R, Rosenbach A:
Effects of ambient room temperature on cold air cooling during laser hair removal.
J Cosmet Dermatol
; 2007 Sep;6(3):203-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Effects of ambient room
temperature
on cold air cooling during laser hair removal.
Forced air cooling is a well-established technique that protects the epidermis during laser heating of deeper
structures
, thereby allowing for increased laser fluences.
The goal of this prospective study was to identify whether an elevation in ambient room
temperature
influences the efficacy of forced air cooling.
Skin
surface temperatures
were measured on 24 sites (12 subjects) during cold air exposure in examination rooms with ambient
temperatures
of 72 degrees F (22.2 degrees C) and 82 degrees F (27.8 degrees C), respectively.
Before cooling, mean skin
surface temperature
was 9 degrees F (5 degrees C) higher in the warmer room (P < 0.01).
Immediately after exposure to forced air cooling (within 1 s), the skin
surface temperature
remained considerably higher (10.75 degrees F, or 5.8 degrees C, P < 0.01) in the warmer room.
We conclude that forced air cooling in a room with an ambient
temperature
of 82 degrees F (27.8 degrees C) is not as effective as in a room that is at 72 degrees F (22.2 degrees C).
[MeSH-major]
Hair Removal / methods. Laser Therapy / methods. Skin
Temperature
.
Temperature
[MeSH-minor]
Air. Cold
Temperature
. Humans. Lasers, Solid-
State
/ therapeutic use. Prospective Studies
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17760700.001).
[ISSN]
1473-2165
[Journal-full-title]
Journal of cosmetic dermatology
[ISO-abbreviation]
J Cosmet Dermatol
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
28.
Montoya A, Sendt K, Haynes BS:
Gas-phase interaction of H2S with O2: A kinetic and quantum chemistry study of the potential energy surface.
J Phys Chem A
; 2005 Feb 17;109(6):1057-62
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Gas-phase interaction of H2S with O2: A kinetic and quantum chemistry study of the potential energy
surface
.
The basic mechanism, the rates of reaction, and the potential energy
surface
were calculated.
Isomers and
transition states
that connect the reactants with intermediates and products of reaction were identified using the G2 method and B3LYP/6-311+G(3df,2p) functional.
Hydrogen abstraction to form HO2 + SH is the dominant product channel and proceeds through a loose
transition state
well-described at the level of calculation employed.
The
temperature
dependence of the rate coefficient in the range 300-3000 K has been determined on the basis of the ab initio potential energy
surface
and with variational
transition
-
state
theory.
The reaction is 169.5 kJ mol(-1) endothermic at 0 K with a rate constant given by 2.77 x 10(5) T(2.76) exp(-19 222/T) cm3 mol(-1) s(-1) and should proceed slowly under atmospheric thermal conditions, but it offers a route to the initiation of H2S combustion at relatively
low temperatures
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16833414.001).
[ISSN]
1089-5639
[Journal-full-title]
The journal of physical chemistry. A
[ISO-abbreviation]
J Phys Chem A
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
29.
Lin H, Zhang HF, Jiao HC, Zhao T, Sui SJ, Gu XH, Zhang ZY, Buyse J, Decuypere E:
Thermoregulation responses of broiler chickens to humidity at different ambient temperatures. I. One week of age.
Poult Sci
; 2005 Aug;84(8):1166-72
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Thermoregulation responses of broiler chickens to humidity at different ambient
temperatures
. I. One week of age.
Three trials were conducted to investigate the effect of RH (35, 60, and 85%) on thermoregulation of 1-wk-old broiler chickens at different
temperatures
(35, 30, and 25 degrees C).
The response to humidity in rectal
temperature
and plumage
temperature
at the back and breast within 24 h after exposure were recorded at 5
time
points (1,4,8,16, and 24 h).
Humidity affected the thermoregulation of 1-wk-old broiler chickens by redistributing heat within the body at high,
low
, and thermoneutral
temperatures
.
The redistribution of heat resulted in decreased rectal
temperature
and increased peripheral
temperature
, which were, respectively, beneficial and unfavorable at high and
low temperatures
.
These results suggested that feedback effects of
surface temperature
on core
temperature
also exist in poultry, as already observed in mammals, and could be induced not only by changed ambient
temperature
but also by the changes in humidity at high
temperature
.
The disturbance of thermal equilibrium could not be established solely by changes in RT, but rather core and
surface temperatures
had to be considered.
The daily rhythms in rectal and
surface temperatures
were affected by humidity.
[MeSH-major]
Body
Temperature
Regulation / physiology. Chickens / physiology. Humidity.
Temperature
[MeSH-minor]
Aging. Animals. Housing, Animal.
Time
Factors
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16156198.001).
[ISSN]
0032-5791
[Journal-full-title]
Poultry science
[ISO-abbreviation]
Poult. Sci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
30.
Hougland JL, Kravchuk AV, Herschlag D, Piccirilli JA:
Functional identification of catalytic metal ion binding sites within RNA.
PLoS Biol
; 2005 Sep;3(9):e277
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
In the Tetrahymena group I intron, previous work using atomic mutagenesis and quantitative analysis of metal ion rescue behavior identified three metal ions (MA, MB, and MC) that make five interactions with the ribozyme substrates in the reaction'
s transition state
.
Our findings establish a direct connection between the ribozyme core and the functionally defined model of the chemical
transition state
, thereby extending the known set of
transition
-
state
interactions and providing information critical for the application of the recent group I intron crystallographic
structures to
the understanding of catalysis.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Annu Rev Biochem. 1985;54:367-402
[
2411211.001
]
[Cites]
Biochemistry. 1999 Aug 24;38(34):10958-75
[
10460151.001
]
[Cites]
Mol Cell. 2004 Nov 5;16(3):351-62
[
15525509.001
]
[Cites]
RNA. 1999 Nov;5(11):1399-407
[
10580468.001
]
[Cites]
Chem Rev. 1998 May 7;98(3):1067-1088
[
11848925.001
]
[Cites]
J Biol Chem. 1997 Oct 24;272(43):26822-6
[
9341112.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):8924-8
[
8799129.001
]
[Cites]
Biochemistry. 2003 Apr 15;42(14):4265-76
[
12680781.001
]
[Cites]
J Mol Biol. 1992 Dec 5;228(3):743-58
[
1469712.001
]
[Cites]
Nat Struct Biol. 1999 Apr;6(4):318-21
[
10201397.001
]
[Cites]
J Mol Biol. 2000 Jun 23;299(5):1303-11
[
10873454.001
]
[Cites]
Biochemistry. 1997 Mar 4;36(9):2465-77
[
9054551.001
]
[Cites]
J Biol Chem. 1978 Jul 25;253(14):4823-5
[
670166.001
]
[Cites]
Science. 1996 Dec 20;274(5295):2065-9
[
8953035.001
]
[Cites]
RNA. 2001 Oct;7(10):1454-63
[
11680850.001
]
[Cites]
Biochemistry. 2002 Mar 19;41(11):3667-75
[
11888283.001
]
[Cites]
RNA. 1997 Nov;3(11):1352-63
[
9409625.001
]
[Cites]
RNA. 2000 Jun;6(6):795-813
[
10864040.001
]
[Cites]
Biochemistry. 1997 Oct 14;36(41):12477-85
[
9376352.001
]
[Cites]
Biochemistry. 1999 Oct 26;38(43):14363-78
[
10572011.001
]
[Cites]
RNA. 2002 Jul;8(7):933-47
[
12166648.001
]
[Cites]
Curr Opin Chem Biol. 1999 Oct;3(5):578-83
[
10508668.001
]
[Cites]
Chem Biol. 1999 Mar;6(3):153-65
[
10074469.001
]
[Cites]
Science. 1992 Nov 20;258(5086):1355-8
[
1455230.001
]
[Cites]
Biochemistry. 2000 Oct 24;39(42):12939-52
[
11041859.001
]
[Cites]
Biochemistry. 1996 Feb 6;35(5):1560-70
[
8634287.001
]
[Cites]
Structure. 1996 Dec 15;4(12):1491-508
[
8994974.001
]
[Cites]
Biochemistry. 1991 May 21;30(20):4844-54
[
2036355.001
]
[Cites]
Biochemistry. 1994 May 3;33(17):5291-7
[
8172903.001
]
[Cites]
Biochemistry. 2002 Feb 26;41(8):2516-25
[
11851398.001
]
[Cites]
J Mol Biol. 2000 Sep 15;302(2):339-58
[
10970738.001
]
[Cites]
J Mol Biol. 1990 Dec 5;216(3):585-610
[
2258934.001
]
[Cites]
EMBO J. 1998 Dec 1;17(23):7091-104
[
9843513.001
]
[Cites]
RNA. 2001 Aug;7(8):1115-25
[
11497430.001
]
[Cites]
Nature. 1993 Jan 7;361(6407):85-8
[
8421499.001
]
[Cites]
Biochemistry. 1993 Aug 17;32(32):8312-21
[
7688573.001
]
[Cites]
RNA. 2000 Feb;6(2):199-205
[
10688359.001
]
[Cites]
Nat Struct Biol. 1997 Jul;4(7):553-8
[
9228948.001
]
[Cites]
Nucleic Acids Res. 2001 Sep 15;29(18):3705-27
[
11557805.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6498-502
[
8341661.001
]
[Cites]
Biochemistry. 1999 Oct 26;38(43):14192-204
[
10571993.001
]
[Cites]
Chem Rev. 1996 Nov 7;96(7):2435-2458
[
11848832.001
]
[Cites]
Science. 1992 May 15;256(5059):992-7
[
1589782.001
]
[Cites]
Biochemistry. 1994 Nov 22;33(46):13864-79
[
7947795.001
]
[Cites]
Nucleic Acids Res. 1999 Jan 15;27(2):479-84
[
9862968.001
]
[Cites]
Biochemistry. 1988 Dec 13;27(25):8924-31
[
3069131.001
]
[Cites]
Nucleic Acids Res. 1991 Mar 25;19(6):1183-8
[
1709484.001
]
[Cites]
Biochemistry. 1990 Nov 6;29(44):10159-71
[
2271645.001
]
[Cites]
EMBO J. 2002 May 1;21(9):2253-62
[
11980722.001
]
[Cites]
Nat Struct Mol Biol. 2005 Jan;12(1):82-9
[
15580277.001
]
[Cites]
Nature. 1997 Aug 21;388(6644):801-5
[
9285595.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12299-304
[
10535916.001
]
[Cites]
Nature. 2000 Dec 14;408(6814):881-4
[
11130730.001
]
[Cites]
Biochemistry. 1993 May 4;32(17):4475-80
[
7683490.001
]
[Cites]
Chem Rev. 1996 Nov 7;96(7):2909-2926
[
11848845.001
]
[Cites]
Nature. 1997 Aug 21;388(6644):805-8
[
9285596.001
]
[Cites]
Biochemistry. 2004 May 18;43(19):5707-15
[
15134445.001
]
[Cites]
RNA. 2000 Aug;6(8):1091-105
[
10943889.001
]
[Cites]
Biochemistry. 2002 Nov 26;41(47):13851-60
[
12437341.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2300-5
[
12591943.001
]
[Cites]
Genes Dev. 1999 Jul 1;13(13):1729-41
[
10398685.001
]
[Cites]
RNA. 2000 Apr;6(4):511-9
[
10786842.001
]
[Cites]
Biochemistry. 2001 May 1;40(17):5161-71
[
11318638.001
]
[Cites]
Chem Biol. 2000 Feb;7(2):85-96
[
10662698.001
]
[Cites]
RNA. 1998 May;4(5):498-519
[
9582093.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8362-6
[
8378306.001
]
[Cites]
RNA. 1995 Apr;1(2):210-8
[
7585250.001
]
[Cites]
Nat Struct Biol. 2001 Oct;8(10):893-8
[
11573097.001
]
[Cites]
Nucleic Acids Res. 1997 Feb 1;25(3):648-53
[
9016608.001
]
[Cites]
J Mol Biol. 1999 Aug 13;291(2):295-311
[
10438622.001
]
[Cites]
Biochemistry. 2002 Sep 17;41(37):11171-83
[
12220182.001
]
[Cites]
Nature. 2004 Jul 1;430(6995):45-50
[
15175762.001
]
(PMID = 16092891.001).
[ISSN]
1545-7885
[Journal-full-title]
PLoS biology
[ISO-abbreviation]
PLoS Biol.
[Language]
eng
[Databank-accession-numbers]
PDB/ 1U6B/ 1X8W/ 1Y0Q
[Grant]
United States / NIGMS NIH HHS / GM / GM49243; United States / NIGMS NIH HHS / GM / R37 GM049243; United States / NIGMS NIH HHS / GM / T32 GM008720; United States / NIGMS NIH HHS / GM / R01 GM049243; United States / NIGMS NIH HHS / GM / 2 T32 GM008720-06
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cations, Divalent; 0 / Metals; 0 / RNA, Catalytic
[Other-IDs]
NLM/ PMC1184590
31.
Loukas M, Tubbs RS, Tongson JM, Polepalli S, Curry B, Jordan R, Wagner T:
The clinical anatomy of the crista terminalis, pectinate muscles and the teniae sagittalis.
Ann Anat
; 2008;190(1):81-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
We were able to classify the course of the PM, including the most prominent PM called the tenia sagittalis (
TS
), into 6 different patterns with 3 different
TS
types.
In Type A (15%), the
TS
was absent.
Type B (65%) demonstrated a single
TS
and Type C (20%) was characterized by the presence of
multiple TS
.
The exact morphology of PM and
TS
may be clinically important in right atrial catheterization procedures, as well as in the development of arrhythmias but further investigations are now necessary to prove this theory.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18342146.001).
[ISSN]
0940-9602
[Journal-full-title]
Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft
[ISO-abbreviation]
Ann. Anat.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
32.
Mednikova YS, Pasikova NV:
The temperature sensitivity of the cholinergic responses of cortical neurons in the guinea pig brain.
Neurosci Behav Physiol
; 2005 Jul;35(6):615-21
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The
temperature sensitivity
of the cholinergic responses of cortical neurons in the guinea pig
brain
.
Studies on slices of the parietal cortex of the guinea-pig
brain
showed that a change in
temperature
from 20 degrees C to 36 degrees C led to increases in responses to microintophoretic application of acetylcholine to individual nerve
cells
.
The greatest changes occurred over two
temperature
ranges: 27-29 degrees C and 34-36 degrees C.
[MeSH-major]
Acetylcholine / administration & dosage. Action Potentials / physiology. Biological Clocks / physiology. Parietal Lobe / physiology.
Temperature
[MeSH-minor]
Animals.
Cells
, Cultured. Guinea Pigs
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Physiol. 1986 Jun;375:169-94
[
2879035.001
]
[Cites]
Fed Proc. 1979 Jun;38(7):2084-94
[
221268.001
]
[Cites]
Fiziol Zh Im I M Sechenova. 1993 Jan;79(1):119-22
[
8518842.001
]
[Cites]
Zh Vyssh Nerv Deiat Im I P Pavlova. 1996 Sep-Oct;46(5):893-903
[
9054141.001
]
[Cites]
Usp Fiziol Nauk. 1996 Jul-Sep;27(3):84-105
[
8975507.001
]
[Cites]
J Comp Neurol. 1985 Apr 1;234(1):17-34
[
3980786.001
]
[Cites]
Cell Mol Neurobiol. 1983 Jun;3(2):163-81
[
6140079.001
]
[Cites]
J Physiol. 1971 May;215(1):199-222
[
5579652.001
]
[Cites]
Usp Fiziol Nauk. 1992 Jan-Feb;23(1):40-57
[
1316690.001
]
[Cites]
Exp Brain Res. 1981;43(2):159-72
[
6265265.001
]
[Cites]
Physiol Rev. 1992 Oct;72(4 Suppl):S159-86
[
1438585.001
]
[Cites]
Ross Fiziol Zh Im I M Sechenova. 2002 Nov;88(11):1492-500
[
12587278.001
]
[Cites]
Brain Res. 2001 Mar 2;893(1-2):36-45
[
11222990.001
]
[Cites]
Biophys J. 1968 Mar;8(3):305-18
[
5759917.001
]
[Cites]
Physiol Rev. 1997 Jan;77(1):217-55
[
9016303.001
]
[Cites]
Zh Vyssh Nerv Deiat Im I P Pavlova. 2002 Jul-Aug;52(4):479-88
[
12391874.001
]
[Cites]
J Physiol. 1971 May;215(1):247-68
[
5579661.001
]
(PMID = 16342618.001).
[ISSN]
0097-0549
[Journal-full-title]
Neuroscience and behavioral physiology
[ISO-abbreviation]
Neurosci. Behav. Physiol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
N9YNS0M02X / Acetylcholine
33.
Grichnik JM:
Melanoma, nevogenesis, and stem cell biology.
J Invest Dermatol
; 2008 Oct;128(10):2365-80
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Melanoma, nevogenesis, and
stem cell
biology.
It is now well established that a subpopulation of tumor
stem cells
(
TSCs
) are present within cancer tissues.
This suggests that tumors evolve from
stem cells
; however, the exact
cell
of tumor origin, the potential role of dedifferentiation, and the role of plasticity in tumor development are largely unknown.
The developmental biology of melanocytes is relatively well understood, the
cells
pigment as they differentiate making them easy to identify, and benign and malignant tumors develop on the skin
surface
allowing direct observation of growth features, early detection, and removal.
This ready access to early-stage tumors will facilitate study of the early oncologic processes and the role of
tissue stem cells
.
Melanomas, like other cancers, include a subpopulation of
TSCs
.
These
TSCs
have access to embryologic developmental programs, including the capacity to differentiate along
multiple cell
lineages.
For example, melanomas can activate germ-
cell
pathways with major implications for
TSC
self-renewal through the activation of telomerase and genomic instability through the collision of meiotic and mitotic pathways (meiomitosis).
The
TSC
model is still evolving, but the existence of
TSCs
has significant ramifications for tumor development,
diagnosis
, prognosis, and treatment of melanoma and other cancers.
[MeSH-major]
Melanoma / etiology. Melanoma / pathology. Nevus / etiology. Nevus / pathology. Skin Neoplasms / etiology. Skin Neoplasms / pathology.
Stem Cells
/ pathology
[MeSH-minor]
Animals.
Cell
Differentiation.
Cell
Lineage.
Cell
Proliferation. Genomic Instability. Humans. Meiosis. Melanocytes / pathology
MedlinePlus Health Information.
consumer health - Birthmarks
.
MedlinePlus Health Information.
consumer health - Melanoma
.
MedlinePlus Health Information.
consumer health - Moles
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
MedlinePlus Health Information.
consumer health - Stem Cells
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18787546.001).
[ISSN]
1523-1747
[Journal-full-title]
The Journal of investigative dermatology
[ISO-abbreviation]
J. Invest. Dermatol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
91
34.
Jiang X, Yeung RS:
Regulation of microtubule-dependent protein transport by the TSC2/mammalian target of rapamycin pathway.
Cancer Res
; 2006 May 15;66(10):5258-69
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Protein transport plays a critical role in the interaction of the
cell
with its environment.
Recent studies have identified TSC1 and TSC2, two tumor suppressor genes involved in
tuberous sclerosis complex
, as regulators of the mammalian target of rapamycin (mTOR) pathway.
Cells
deficient in TSC1 or TSC2 possess high levels of Rheb-GTP resulting in constitutive mTOR activation.
We have shown previously that the TSC1/TSC2
complex
is involved in post-Golgi transport of VSVG and caveolin-1 in mammalian
cells
.
Tsc1- and Tsc2-null
cells
exhibit abnormal caveolin-1 localization that is accompanied by disorganized microtubules in the subcortical region.
Analyses of green fluorescent protein-EB1 and tubulin in live mutant
cells
suggest a failure of the plus-ends to sense cortical signals and to halt microtubule growth.
Down-regulation of CLIP-170, a putative mTOR substrate with microtubule-binding properties, rescued the abnormal microtubule arrangement and caveolin-1 localization in Tsc2-/-
cells
.
[MeSH-minor]
Animals. Caveolin 1 / metabolism.
Cells
, Cultured. Down-Regulation. Mice. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Protein Transport / drug effects. Protein Transport / physiology. Rats. Signal Transduction. TOR Serine-Threonine Kinases. Transfection
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16707451.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA77882
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Caveolin 1; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Proteins; 148349-95-5 / cytoplasmic linker protein 170; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse
35.
Ferguson N, Sharpe TD, Johnson CM, Fersht AR:
The transition state for folding of a peripheral subunit-binding domain contains robust and ionic-strength dependent characteristics.
J Mol Biol
; 2006 Mar 10;356(5):1237-47
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The
transition state
for folding of a peripheral subunit-binding domain contains robust and ionic-strength dependent characteristics.
The denaturant dependencies of the folding and unfolding kinetics were used to characterize the
structure
of the
transition state
for folding of E3BD, a peripheral subunit-binding domain.
The
structure
of the
transition state
for folding was grossly conserved at 298 K and 325 K, with residues in Helix I playing a lesser role in folding than those located in the 3(10) helix, disordered loop and Helix II.
However, the energetic contributions of a cluster of basic residues close to the N-terminus and Helix I, which are an integral part of the ligand-binding site, were susceptible to ionic strength effects because of electrostatic strain in native and
transition states
of E3BD at
low
ionic strength.
We found no evidence of the downhill folding previously proposed for E3BD, even though the conditions employed in this study significantly increased the energetic bias towards the native
state
.
[MeSH-minor]
Osmolar
Concentration
. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Static Electricity. Thermodynamics
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16406408.001).
[ISSN]
0022-2836
[Journal-full-title]
Journal of molecular biology
[ISO-abbreviation]
J. Mol. Biol.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / MC/ U105484373
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Bacterial Proteins; 0 / Protein Subunits; 0 / Recombinant Proteins
36.
Grünwald M, Dellago C:
Transition state analysis of solid-solid transformations in nanocrystals.
J Chem Phys
; 2009 Oct 28;131(16):164116
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Transition state
analysis of solid-solid transformations in nanocrystals.
The atomistic mechanisms of nucleation and growth in a structural transformation of pressurized CdSe nanocrystals are identified using
transition
path sampling computer simulation.
A committor-based
transition state
analysis is applied to extract activation enthalpies and activation volumes from transformation pathways at experimental conditions.
The qualitative dependence of activation enthalpies on nanocrystal size is in good agreement with experimental data and supports the observed nucleation mechanism, which is characterized by a critical nucleus of elongated shape located on the crystal
surface
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19894936.001).
[ISSN]
1089-7690
[Journal-full-title]
The Journal of chemical physics
[ISO-abbreviation]
J Chem Phys
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
37.
da Silva G, Bozzelli JW:
Variational analysis of the phenyl + O2 and phenoxy + O reactions.
J Phys Chem A
; 2008 Apr 24;112(16):3566-75
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Variational
transition state
analysis was performed on the barrierless phenyl + O2 and phenoxy + O association reactions.
Frequency calculations were performed for all reactants and products and at points along the potential energy surfaces, allowing us to evaluate thermochemical properties as a function of
temperature
according to the principles of statistical mechanics and the rigid rotor harmonic oscillator (RRHO) approximation.
The
low
-frequency vibrational modes corresponding to R-OO internal rotation were omitted from the RRHO analysis and replaced with a hindered internal rotor analysis using O3LYP/6-31G(d) rotor potentials.
Rate constants were calculated as a function of
temperature
(300-2000 K) and position from activation entropies and enthalpies, according to canonical
transition state
theory; these rate constants were minimized with respect to position to obtain variational rate constants as a function of
temperature
.
For the phenyl + O2 reaction, we identified the
transition state
to be located at a C-OO bond length of between 2.56 and 2.16 A (300-2000 K), while for the phenoxy + O reaction, the
transition state
was located at a CO-O bond length of 2.00-1.90 A.
Variational rate constants were fit
to a
three-parameter form of the Arrhenius equation, and for the phenyl + O2 association reaction, we found k(T) = 1.860 x 1013T-0.217 exp(0.358/T) (with k in cm3 mol-1 s-1 and T in K); this rate equation provides good agreement with
low
-
temperature
experimental measurements of the phenyl + O2 rate constant.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18348555.001).
[ISSN]
1520-5215
[Journal-full-title]
The journal of physical chemistry. A
[ISO-abbreviation]
J Phys Chem A
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
38.
Uchida K, Danenberg PV, Danenberg KD, Grem JL:
Thymidylate synthase, dihydropyrimidine dehydrogenase, ERCC1, and thymidine phosphorylase gene expression in primary and metastatic gastrointestinal adenocarcinoma tissue in patients treated on a phase I trial of oxaliplatin and capecitabine.
BMC Cancer
; 2008 Dec 23;8:386
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Thymidylate synthase, dihydropyrimidine dehydrogenase, ERCC1, and thymidine phosphorylase gene expression in primary and metastatic gastrointestinal adenocarcinoma
tissue
in patients treated on a phase I trial of oxaliplatin and capecitabine.
BACKGROUND: Over-expression of thymidylate synthase (
TS
) and dihydropyrimidine dehydrogenase (DPD) in tumor
tissue
is associated with insensitivity to 5-fluorouracil (5-FU).
Over-expression of ERCC1 correlates with insensitivity to oxaliplatin (OX) therapy, while high thymidine phosphorylase (TP) levels predict for increased
sensitivity to
capecitabine (Xel).
Micro-dissected metastatic and primary tumors were analyzed for relative gene expression by real-
time
quantitative polymerase chain reaction.
Endpoints for the molecular analyses were correlation of median, first and third quartiles for relative gene expression of each target with response,
time to
treatment failure (TTF), and survival.
In paired samples, median mRNA levels were significantly higher in metastatic versus primary tumor (-fold):
TS
(1.9), DPD (3.8), ERCC1 (2.1) and TP (1.6).
A strong positive correlation was noted between DPD and TP mRNA levels in both primary (r = 0.693, p < 0.0005) and metastatic
tissue
(r = 0.697, p < 0.00001).
There was an association between
TS
gene expression and responsive and stable
disease
: patients whose intratumoral
TS
mRNA levels were above the median value had significantly greater risk of early
disease
progression (43% vs 17%), but this did not translate into a significant difference in TTF.
Patients whose
TS
mRNA levels in metastatic tumor
tissue
were below the median had a longer overall survival (median 417 vs 294 days, p = 0.042).
CONCLUSION: Target gene expression in primary tumor was significantly lower than that in paired metastatic
tissue
.
Lower expression of
TS
mRNA correlated with a lower chance of early PD with XelOX therapy and improved overall survival.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CAPECITABINE
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Clin Oncol. 1999 Jun;17(6):1760-70
[
10561213.001
]
[Cites]
CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66
[
17237035.001
]
[Cites]
Clin Cancer Res. 2000 Apr;6(4):1322-7
[
10778957.001
]
[Cites]
Int J Oncol. 2000 Jul;17(1):33-8
[
10853015.001
]
[Cites]
Int J Cancer. 2001 May 1;92(3):451-6
[
11291085.001
]
[Cites]
Oncol Rep. 2001 Jul-Aug;8(4):753-8
[
11410777.001
]
[Cites]
Kurume Med J. 2001;48(2):93-8
[
11501504.001
]
[Cites]
J Clin Oncol. 2001 Dec 1;19(23):4298-304
[
11731512.001
]
[Cites]
Eur J Cancer. 2002 Mar;38(4):527-34
[
11872345.001
]
[Cites]
Lancet Oncol. 2001 Aug;2(8):483-90
[
11905724.001
]
[Cites]
Oncol Rep. 2002 May-Jun;9(3):479-82
[
11956613.001
]
[Cites]
J Clin Oncol. 2002 Jun 15;20(12):2832-43
[
12065560.001
]
[Cites]
J Clin Oncol. 2003 Feb 1;21(3):406-12
[
12560427.001
]
[Cites]
Clin Cancer Res. 2003 Feb;9(2):792-801
[
12576452.001
]
[Cites]
Cancer Lett. 2004 Feb 10;204(1):97-104
[
14744539.001
]
[Cites]
Anticancer Res. 2004 Jan-Feb;24(1):273-9
[
15015608.001
]
[Cites]
Cancer Chemother Pharmacol. 2004 May;53(5):391-6
[
15060742.001
]
[Cites]
Int J Cancer. 2004 Aug 20;111(2):252-8
[
15197779.001
]
[Cites]
Br J Cancer. 2004 Oct 4;91(7):1245-50
[
15354215.001
]
[Cites]
J Clin Oncol. 1997 Oct;15(10):3223-9
[
9336359.001
]
[Cites]
Science. 1997 Nov 21;278(5342):1481,1483
[
9411767.001
]
[Cites]
Cancer Res. 1998 Feb 15;58(4):685-90
[
9485021.001
]
[Cites]
Biochem J. 1998 Aug 15;334 ( Pt 1):1-8
[
9693094.001
]
[Cites]
Clin Cancer Res. 1998 Oct;4(10):2371-6
[
9796967.001
]
[Cites]
Cancer Treat Rev. 1998 Oct;24(5):331-44
[
9861196.001
]
[Cites]
Clin Cancer Res. 1999 Feb;5(2):325-8
[
10037181.001
]
[Cites]
Genes Dev. 1999 Apr 1;13(7):768-85
[
10197977.001
]
[Cites]
Mol Carcinog. 1999 Jun;25(2):86-91
[
10365909.001
]
[Cites]
Clin Cancer Res. 1999 Aug;5(8):1996-9
[
10473077.001
]
[Cites]
Int J Cancer. 2006 Aug 1;119(3):522-6
[
16572420.001
]
[Cites]
J Clin Oncol. 2006 Sep 1;24(25):4069-77
[
16943524.001
]
[Cites]
J Gastrointest Surg. 2000 Mar-Apr;4(2):135-42
[
10675236.001
]
(PMID = 19105824.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
ENG
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
England
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Organoplatinum Compounds; 0 / RNA, Messenger; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.4 / Thymidine Phosphorylase; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases; U3P01618RT / Fluorouracil
[Other-IDs]
NLM/ PMC2637882
39.
Vekilov PG, Galkin O, Pettitt BM, Choudhury N, Nagel RL:
Determination of the transition-state entropy for aggregation suggests how the growth of sickle cell hemoglobin polymers can be slowed.
J Mol Biol
; 2008 Mar 28;377(3):882-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Determination of the
transition
-
state
entropy for aggregation suggests how the growth of sickle
cell
hemoglobin polymers can be slowed.
Sickle
cell
anemia is associated with the mutant hemoglobin HbS, which forms polymers in red blood
cells
of patients.
The entropy of the
transition state
for incorporation into a fiber is 95 J mol(-1) K(-1), very close to the known entropy of polymerization.
This agrees with a recent theoretical estimate for the hydrophobic interaction and suggests that the gain of entropy in the
transition state
is due to the release of the last layer of water molecules structured around contact sites on the
surface
of the HbS molecules.
This
finding
suggests that fiber growth can be slowed by components of the red
cell
cytosol, native or intentionally introduced, which restructure the hydration layer around the HbS molecules and thus lower the
transition state
entropy for incorporation of an incoming molecule into the growing fiber.
MedlinePlus Health Information.
consumer health - Sickle Cell Anemia
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Methods Mol Biol. 2001;168:17-36
[
11357625.001
]
[Cites]
Chem Rev. 2004 Apr;104(4):2099-123
[
15080722.001
]
[Cites]
Q Rev Biophys. 2001 May;34(2):105-267
[
11771120.001
]
[Cites]
Nature. 2002 May 30;417(6888):491
[
12037545.001
]
[Cites]
Acta Crystallogr D Biol Crystallogr. 2002 Oct;58(Pt 10 Pt 1):1611-6
[
12351872.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):792-6
[
12552115.001
]
[Cites]
Microcirculation. 2004 Mar;11(2):101-13
[
15280086.001
]
[Cites]
Lancet. 2004 Oct 9-15;364(9442):1343-60
[
15474138.001
]
[Cites]
Proc Natl Acad Sci U S A. 1974 Dec;71(12):4864-8
[
4531026.001
]
[Cites]
J Mol Biol. 1975 Oct 15;98(1):179-94
[
1195378.001
]
[Cites]
J Biol Chem. 1976 Aug 25;251(16):4968-72
[
956170.001
]
[Cites]
J Mol Biol. 1979 Jun 5;130(4):451-72
[
480359.001
]
[Cites]
J Clin Invest. 1984 Aug;74(2):652-6
[
6205021.001
]
[Cites]
J Mol Biol. 1985 Jun 25;183(4):591-610
[
4020872.001
]
[Cites]
J Mol Biol. 1985 Jun 25;183(4):611-31
[
4020873.001
]
[Cites]
J Mol Biol. 1988 Jan 20;199(2):315-31
[
3351926.001
]
[Cites]
Adv Protein Chem. 1990;40:63-279
[
2195851.001
]
[Cites]
Blood. 1993 Dec 1;82(11):3474-81
[
8241514.001
]
[Cites]
Proteins. 1994 Feb;18(2):133-47
[
8159663.001
]
[Cites]
Biophys J. 1994 Mar;66(3 Pt 1):601-14
[
8011893.001
]
[Cites]
Biochemistry. 1994 Jul 26;33(29):8629-40
[
8038152.001
]
[Cites]
J Mol Biol. 1995 Feb 3;245(5):710-23
[
7844835.001
]
[Cites]
Blood. 1996 Dec 15;88(12):4701-10
[
8977264.001
]
[Cites]
Lancet. 1997 Sep 6;350(9079):725-30
[
9291916.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2267-72
[
9482874.001
]
[Cites]
Curr Opin Struct Biol. 1998 Apr;8(2):218-21
[
9631296.001
]
[Cites]
Biopolymers. 1999 Oct 15;50(5):459-71
[
10479730.001
]
[Cites]
Methods Mol Biol. 2005;300:15-52
[
15657478.001
]
[Cites]
J Am Chem Soc. 2005 Mar 16;127(10):3556-67
[
15755177.001
]
[Cites]
Nature. 2005 Sep 29;437(7059):640-7
[
16193038.001
]
[Cites]
Acta Crystallogr D Biol Crystallogr. 2006 Jan;62(Pt 1):116-24
[
16369101.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1681-6
[
16446456.001
]
[Cites]
J Phys Chem B. 2006 Apr 27;110(16):8459-63
[
16623532.001
]
[Cites]
J Phys Chem B. 2005 Apr 7;109(13):6422-9
[
16851715.001
]
[Cites]
J Mol Biol. 2007 Jan 12;365(2):425-39
[
17069853.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Dec 19;103(51):19237-42
[
17158220.001
]
[Cites]
Biophys J. 2007 Aug 1;93(3):902-13
[
17449671.001
]
[Cites]
Faraday Discuss. 2003;123:221-36; discussion 303-22, 419-21
[
12638863.001
]
[Cites]
Biophys Chem. 2003;100(1-3):109-16
[
12646356.001
]
[Cites]
Nature. 2003 May 1;423(6935):25-6
[
12721610.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5142-7
[
12702764.001
]
[Cites]
J Am Chem Soc. 2003 Sep 24;125(38):11684-93
[
13129373.001
]
[Cites]
Biophys J. 2003 Dec;85(6):3935-42
[
14645082.001
]
[Cites]
Methods Enzymol. 2003;368:84-105
[
14674270.001
]
[Cites]
J Mol Biol. 2004 Feb 6;336(1):43-59
[
14741202.001
]
[Cites]
Blood Cells Mol Dis. 2001 Jan-Feb;27(1):71-80
[
11358364.001
]
(PMID = 18280499.001).
[ISSN]
1089-8638
[Journal-full-title]
Journal of molecular biology
[ISO-abbreviation]
J. Mol. Biol.
[Language]
ENG
[Grant]
United States / PHS HHS / / G091474; United States / NIGMS NIH HHS / GM / GM037657-17; United States / NIGMS NIH HHS / GM / R01 GM037657; United States / NIGMS NIH HHS / GM / GM37657; United States / NIGMS NIH HHS / GM / R01 GM037657-17
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biopolymers; 0 / Hemoglobin, Sickle
[Other-IDs]
NLM/ NIHMS80409; NLM/ PMC2596688
40.
Gloster TM, Davies GJ:
Glycosidase inhibition: assessing mimicry of the transition state.
Org Biomol Chem
; 2010 Jan 21;8(2):305-20
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Glycosidase inhibition: assessing mimicry of the
transition state
.
Glycoside hydrolases, the enzymes responsible for hydrolysis of the glycosidic bond in
di
-, oligo- and polysaccharides, and glycoconjugates, are ubiquitous in Nature and fundamental to existence.
Such rate enhancements mean that enzymes bind the substrate at the
transition state
with extraordinary affinity; the dissociation constant for the
transition state
is predicted to be 10(-22) M.
If inhibitors are designed to mimic the
transition state
, it should be possible to harness some of the
transition state
affinity, resulting in highly potent and specific drugs.
A number of criteria have been proposed to ascertain which of these inhibitors are true
transition state
mimics, but these features have only be critically investigated in a very few cases.
[MeSH-minor]
Carbohydrate Metabolism. Humans. Hydrogen-Ion
Concentration
. Thermodynamics
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Chem Biol. 1995 Nov;2(11):709-12
[
9383477.001
]
[Cites]
Biochim Biophys Acta. 1989 Dec 21;999(3):227-32
[
2532549.001
]
[Cites]
Phytochemistry. 2001 Feb;56(3):265-95
[
11243453.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9127-32
[
12093900.001
]
[Cites]
Curr Opin Chem Biol. 2002 Oct;6(5):619-29
[
12413546.001
]
[Cites]
J Am Chem Soc. 2001 May 30;123(21):5116-7
[
11457350.001
]
[Cites]
J Am Chem Soc. 2003 Jun 25;125(25):7532-3
[
12812490.001
]
[Cites]
Hoppe Seylers Z Physiol Chem. 1969 Sep;350(9):1088-92
[
5349377.001
]
[Cites]
Adv Enzymol Relat Areas Mol Biol. 1988;61:201-301
[
3281418.001
]
[Cites]
J Am Chem Soc. 2007 Apr 18;129(15):4530-1
[
17385869.001
]
[Cites]
Nat Prod Rep. 2004 Apr;21(2):211-23
[
15042146.001
]
[Cites]
Biochem J. 1993 Apr 1;291 ( Pt 1):15-7
[
8471034.001
]
[Cites]
J Biol Chem. 1981 Apr 25;256(8):3703-11
[
6452453.001
]
[Cites]
Angew Chem Int Ed Engl. 2007;46(22):4115-9
[
17455176.001
]
[Cites]
J Biol Chem. 1972 Dec 25;247(24):8195-7
[
4640942.001
]
[Cites]
J Antibiot (Tokyo). 1966 Nov;19(6):288-92
[
6013242.001
]
[Cites]
Tetrahedron. 1968 Mar;24(5):2125-44
[
5636917.001
]
[Cites]
J Biol Chem. 2009 Jun 26;284(26):17404-10
[
19411257.001
]
[Cites]
Clin Cancer Res. 1995 Sep;1(9):935-44
[
9816064.001
]
[Cites]
Biochemistry. 2000 Aug 15;39(32):9746-53
[
10933791.001
]
[Cites]
Biochim Biophys Acta. 1996 Nov 14;1298(1):78-86
[
8948491.001
]
[Cites]
CRC Crit Rev Biochem. 1976 Nov;4(2):165-73
[
12913.001
]
[Cites]
J Am Chem Soc. 2007 Jan 24;129(3):635-44
[
17227027.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4593-8
[
11287638.001
]
[Cites]
Biochemistry. 2002 Oct 15;41(41):12320-8
[
12369820.001
]
[Cites]
Drugs. 2005;65(3):385-411
[
15669880.001
]
[Cites]
Protein Eng. 1994 Mar;7(3):291-9
[
8177877.001
]
[Cites]
J Biol Chem. 2008 Dec 12;283(50):34687-95
[
18842583.001
]
[Cites]
J Org Chem. 2000 Apr 21;65(8):2599-602
[
10789483.001
]
[Cites]
J Biol Chem. 2009 Apr 24;284(17):11676-89
[
19181667.001
]
[Cites]
Chembiochem. 2008 Nov 3;9(16):2612-8
[
18833549.001
]
[Cites]
Biochemistry. 2008 Mar 18;47(11):3507-12
[
18284211.001
]
[Cites]
Biochemistry. 1983 Sep 27;22(20):4618-24
[
6626519.001
]
[Cites]
J Biol Chem. 1994 Mar 18;269(11):8362-5
[
8132559.001
]
[Cites]
Org Biomol Chem. 2003 Jan 21;1(2):282-7
[
12929423.001
]
[Cites]
Biochemistry. 1998 Dec 8;37(49):17192-8
[
9860832.001
]
[Cites]
J Am Chem Soc. 2007 Feb 28;129(8):2345-54
[
17279749.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):8949-54
[
10430876.001
]
[Cites]
J Virol. 2005 Jul;79(14):8698-706
[
15994763.001
]
[Cites]
Biochemistry. 1995 Dec 5;34(48):15619-23
[
7495789.001
]
[Cites]
Biochemistry. 2001 Dec 11;40(49):14781-94
[
11732897.001
]
[Cites]
J Am Chem Soc. 2004 Sep 29;126(38):11870-6
[
15382922.001
]
[Cites]
Arzneimittelforschung. 1980;30(12):2182-5
[
7194082.001
]
[Cites]
J Biol Chem. 2005 Jul 8;280(27):25313-22
[
15795231.001
]
[Cites]
Biochem Soc Trans. 2003 Jun;31(Pt 3):523-7
[
12773149.001
]
[Cites]
J Biol Chem. 2005 Aug 26;280(34):30320-8
[
15961383.001
]
[Cites]
Mol Pharmacol. 2002 Jan;61(1):186-93
[
11752220.001
]
[Cites]
J Biol Chem. 2004 Aug 20;279(34):36022-8
[
15166216.001
]
[Cites]
Naturwissenschaften. 1979 Nov;66(11):584-5
[
390406.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15428-33
[
12434014.001
]
[Cites]
J Org Chem. 2001 Apr 6;66(7):2312-7
[
11281771.001
]
[Cites]
Nat Struct Mol Biol. 2005 Jan;12(1):90-6
[
15608653.001
]
[Cites]
Curr Opin Struct Biol. 2005 Dec;15(6):637-45
[
16263268.001
]
[Cites]
Acc Chem Res. 2001 Dec;34(12):938-45
[
11747411.001
]
[Cites]
J Am Chem Soc. 2001 Jul 4;123(26):6268-71
[
11427050.001
]
[Cites]
Biochemistry. 1995 Aug 15;34(32):10153-61
[
7640269.001
]
[Cites]
Ann Neurol. 2007 Dec;62(6):671-5
[
17994547.001
]
[Cites]
Curr Opin Chem Biol. 1999 Oct;3(5):557-63
[
10508661.001
]
[Cites]
Biochemistry. 1973 Jan 2;12(1):47-51
[
4734224.001
]
[Cites]
Chem Commun (Camb). 2006 Nov 13;(42):4372-4
[
17057847.001
]
[Cites]
Adv Carbohydr Chem Biochem. 1990;48:319-84
[
2077872.001
]
[Cites]
J Biol Chem. 2000 Dec 15;275(50):39385-93
[
10978344.001
]
[Cites]
Biochem Cell Biol. 2008 Apr;86(2):169-77
[
18443630.001
]
[Cites]
Carbohydr Res. 2007 Sep 3;342(12-13):1551-80
[
17559821.001
]
[Cites]
Nat Chem Biol. 2008 Aug;4(8):483-90
[
18587388.001
]
[Cites]
Nat Biotechnol. 2007 Apr;25(4):454-64
[
17401360.001
]
[Cites]
Biochemistry. 1996 Aug 6;35(31):9958-66
[
8756457.001
]
[Cites]
Biochim Biophys Acta. 1977 May 12;482(1):109-24
[
861229.001
]
[Cites]
J Bacteriol. 1988 Mar;170(3):1153-61
[
2981046.001
]
[Cites]
N Engl J Med. 1999 Oct 28;341(18):1336-43
[
10536125.001
]
[Cites]
J Biosci. 2002 Mar;27(2):121-6
[
11937682.001
]
[Cites]
Proc Natl Acad Sci U S A. 1981 Dec;78(12):7393-7
[
6801650.001
]
[Cites]
Glycobiology. 1994 Dec;4(6):759-67
[
7734838.001
]
[Cites]
J Am Chem Soc. 2006 Dec 27;128(51):16484-5
[
17177381.001
]
[Cites]
Glycobiology. 2008 Aug;18(8):570-86
[
18499865.001
]
[Cites]
J Biol Chem. 1990 Sep 15;265(26):15599-605
[
2144287.001
]
[Cites]
Chem Biol. 2008 Oct 20;15(10):1058-67
[
18848471.001
]
[Cites]
Curr Opin Chem Biol. 2008 Oct;12(5):539-55
[
18558099.001
]
[Cites]
J Am Chem Soc. 2003 Jun 25;125(25):7496-7
[
12812472.001
]
[Cites]
Annu Rev Biochem. 1998;67:693-720
[
9759501.001
]
[Cites]
Biochemistry. 1989 Jul 25;28(15):6294-305
[
2790000.001
]
[Cites]
Handb Exp Pharmacol. 2009;(189):111-54
[
19048199.001
]
[Cites]
Nat Struct Biol. 1996 Jul;3(7):638-48
[
8673609.001
]
[Cites]
J Biol Chem. 2008 Feb 22;283(8):4469-79
[
18096701.001
]
[Cites]
Biochemistry. 1995 Oct 3;34(39):12729-37
[
7548026.001
]
[Cites]
Carbohydr Res. 2009 Sep 8;344(13):1753-7
[
19595298.001
]
[Cites]
Biochemistry. 2005 Dec 20;44(50):16529-39
[
16342944.001
]
[Cites]
J Biol Chem. 2004 Aug 20;279(34):36029-37
[
15181003.001
]
[Cites]
Arch Biochem Biophys. 2005 Jan 1;433(1):13-26
[
15581562.001
]
[Cites]
Chem Rev. 2002 Feb;102(2):515-53
[
11841253.001
]
[Cites]
Biochem Biophys Res Commun. 1968 Sep 30;32(6):1025-30
[
5750221.001
]
[Cites]
Nat Chem Biol. 2008 May;4(5):306-12
[
18408714.001
]
[Cites]
Methods Cell Biol. 2008;84:79-113
[
17964929.001
]
[Cites]
Am J Physiol Cell Physiol. 2006 Apr;290(4):C1076-82
[
16531566.001
]
[Cites]
Curr Opin Chem Biol. 2000 Oct;4(5):573-80
[
11006547.001
]
[Cites]
Chem Rev. 1997 Aug 5;97(5):1281-1302
[
11851452.001
]
[Cites]
Biophys Chem. 2001 Nov 28;93(2-3):215-30
[
11804727.001
]
[Cites]
Biochemistry. 1985 Jul 2;24(14):3530-9
[
3929833.001
]
[Cites]
Chemistry. 2000 Jan;6(2):278-87
[
11931107.001
]
[Cites]
J Biol Chem. 2005 May 6;280(18):18265-73
[
15749708.001
]
[Cites]
Protein Sci. 2001 Mar;10(3):661-7
[
11344335.001
]
[Cites]
J Am Chem Soc. 2004 Feb 25;126(7):1971-9
[
14971930.001
]
[Cites]
J Am Chem Soc. 1997 Jan 29;119(4):681-90
[
16526129.001
]
[Cites]
Blood. 2006 Oct 1;108(7):2392-8
[
16778146.001
]
[Cites]
Biochemistry. 1990 Sep 11;29(36):8358-64
[
2252896.001
]
[Cites]
Carbohydr Res. 1996 Oct 4;292:103-15
[
8870240.001
]
[Cites]
Chem Commun (Camb). 2004 Aug 21;(16):1794-5
[
15306887.001
]
[Cites]
J Org Chem. 2003 Mar 21;68(6):2115-22
[
12636369.001
]
[Cites]
Eur J Biochem. 1991 May 8;197(3):815-8
[
2029909.001
]
[Cites]
Org Biomol Chem. 2009 Jul 7;7(13):2738-47
[
19532990.001
]
[Cites]
Biochemistry. 2009 Jun 16;48(23):5226-38
[
19425594.001
]
[Cites]
Chembiochem. 2001 May 4;2(5):311-8
[
11828459.001
]
[Cites]
Biochem J. 2000 Jul 1;349(Pt 1):211-5
[
10861230.001
]
[Cites]
Nat Med. 1999 Jan;5(1):112-5
[
9883849.001
]
[Cites]
J Biol Chem. 2004 Feb 6;279(6):4970-80
[
14597633.001
]
[Cites]
Nature. 1993 Jun 3;363(6428):418-23
[
8502295.001
]
[Cites]
Nucleic Acids Res. 2009 Jan;37(Database issue):D233-8
[
18838391.001
]
[Cites]
Biochemistry. 2006 Oct 3;45(39):11879-84
[
17002288.001
]
[Cites]
Chem Commun (Camb). 2003 Apr 21;(8):944-5
[
12744311.001
]
[Cites]
Curr Opin Struct Biol. 1997 Oct;7(5):637-44
[
9345621.001
]
[Cites]
FEBS Lett. 1998 Jun 23;430(1-2):17-22
[
9678587.001
]
[Cites]
Cell Mol Life Sci. 2009 May;66(9):1479-92
[
19132292.001
]
[Cites]
J Am Chem Soc. 2004 Jul 14;126(27):8354-5
[
15237973.001
]
[Cites]
Biochemistry. 1996 Jun 25;35(25):8319-28
[
8679589.001
]
[Cites]
J Nat Prod. 1997 Mar;60(3):312-4
[
9157194.001
]
[Cites]
J Org Chem. 2006 Feb 3;71(3):1262-4
[
16438551.001
]
[Cites]
J Biol Chem. 2007 Sep 28;282(39):28297-300
[
17690091.001
]
[Cites]
Biochemistry. 1995 Oct 24;34(42):13961-6
[
7577992.001
]
[Cites]
Nature. 1948 May 8;161(4097):707-9
[
18860270.001
]
[Cites]
Structure. 2000 Oct 15;8(10):1025-35
[
11080624.001
]
[Cites]
Biochim Biophys Acta. 2001 Feb 9;1545(1-2):207-15
[
11342046.001
]
[Cites]
Biochemistry. 1992 Feb 4;31(4):959-63
[
1734971.001
]
[Cites]
J Biol Chem. 2005 May 6;280(18):18274-82
[
15746096.001
]
[Cites]
Biochem J. 1990 Feb 15;266(1):245-9
[
2310375.001
]
[Cites]
Chemistry. 2001 Sep 3;7(17):3744-7
[
11575775.001
]
[Cites]
Diabetes Metab Rev. 1998 Sep;14 Suppl 1:S31-8
[
9816485.001
]
[Cites]
J Antibiot (Tokyo). 1987 Apr;40(4):563-5
[
3294776.001
]
[Cites]
J Biol Chem. 2008 Dec 26;283(52):36328-37
[
18981178.001
]
[Cites]
Biochem J. 1997 Jan 15;321 ( Pt 2):557-9
[
9020895.001
]
[Cites]
Philos Trans R Soc Lond B Biol Sci. 2003 May 29;358(1433):961-6
[
12803930.001
]
[Cites]
Glycobiology. 2003 Oct;13(10):93R-104R
[
12851286.001
]
[Cites]
Arzneimittelforschung. 1986 Jul;36(7):1136-8
[
3533089.001
]
[Cites]
Chem Rev. 2003 May;103(5):1955-77
[
12744697.001
]
[Cites]
Chembiochem. 2006 May;7(5):738-42
[
16628756.001
]
[Cites]
Nat Rev Drug Discov. 2007 Dec;6(12):967-74
[
18049471.001
]
[Cites]
JAMA. 1996 Jan 24-31;275(4):295-9
[
8544269.001
]
[Cites]
EMBO J. 2006 Apr 5;25(7):1569-78
[
16541109.001
]
[Cites]
J Biol Chem. 1982 Nov 25;257(22):13650-62
[
6815178.001
]
(PMID = 20066263.001).
[ISSN]
1477-0539
[Journal-full-title]
Organic & biomolecular chemistry
[ISO-abbreviation]
Org. Biomol. Chem.
[Language]
eng
[Grant]
United Kingdom / Wellcome Trust / / 082572
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Enzyme Inhibitors; EC 3.2.1.- / Glycoside Hydrolases
[Number-of-references]
223
[Other-IDs]
NLM/ PMC2822703; NLM/ UKMS28709
41.
Gainer JL, Stennett AK, Murray RJ:
The effect of trans sodium crocetinate (TSC) in a rat oleic acid model of acute lung injury.
Pulm Pharmacol Ther
; 2005;18(3):213-6
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The effect of trans
sodium
crocetinate (
TSC
) in a rat oleic acid model of acute lung injury.
Trans
sodium
crocetinate is a novel drug, which has been shown previously to increase whole-body oxygen consumption during hemorrhagic shock.
TSC
has been suggested to work by increasing the diffusion rate of oxygen through plasma rather than on a specific symptom of hemorrhagic shock and has been suggested as a general treatment for hypoxemia.
This study employed an oleic acid model of acute lung injury to determine if
TSC
could increase arterial PO2 in that model.
[MeSH-major]
Antioxidants / therapeutic use. Carotenoids / therapeutic use. Respiratory Distress
Syndrome
, Adult / drug therapy
MedlinePlus Health Information.
consumer health - Antioxidants
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
OLEIC ACID
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15707856.001).
[ISSN]
1094-5539
[Journal-full-title]
Pulmonary pharmacology & therapeutics
[ISO-abbreviation]
Pulm Pharmacol Ther
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antioxidants; 20TC155L9C / crocetin; 2UMI9U37CP / Oleic Acid; 36-88-4 / Carotenoids
42.
Zhu Y, Liu PZ, Leung KM, Su LY, Wu DX, Zhou M:
P300 differences exist between Tourette's syndrome with and without attention deficiency and hyperactivity disorder in children.
World J Biol Psychiatry
; 2006;7(2):91-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
P300 differences exist between Tourette's
syndrome
with and without attention deficiency and hyperactivity
disorder
in children.
OBJECTIVE: To study the characteristics of P300 in Tourette's
syndrome
(
TS
) with and without attention deficiency and hyperactivity
disorder
(ADHD).
METHOD: Auditory evoked P300 were recorded in 19
TS
only (
TS
-ADHD) children, 15
TS
with ADHD (
TS
+ ADHD) children and 20 unaffected control subjects, and their waveforms, amplitudes, latencies and topographies were compared at Fz, Cz, C3, C4 and Pz.
RESULTS: The
TS
+ ADHD group showed shorter latencies than control subjects at all electrode sites (P<0.05 or 0.01), and the
TS
-ADHD group at CZ and PZ (P<0.05); however, there was no significant difference between control subjects and the
TS
-ADHD group.
The
TS
-ADHD group showed smaller amplitudes than the control group at all electrode sites (P<0.05), and the
TS
+ ADHD group at Cz (P<0.05); however, there were no significant differences between control subjects and the
TS
+ ADHD group.
There was no significant difference in the prevalence of abnormal waveforms between the control,
TS
,
TS
-ADHD and
TS
+ ADHD groups, but there were significant differences in the variability of localization of P300 between the control and the
TS
group (P=0.003), control and
TS
+ ADHD groups (P=0.000), and the
TS
-ADHD and
TS
+ ADHD groups (P=0.039).
P300 in the
TS
+ ADHD group tended to spread out to the left and that of the
TS
-ADHD group tended to spread out to the right.
CONCLUSIONS: P300 differences exist between
TS
-ADHD and
TS
+ ADHD in children.
These suggested that establishment different development defects or delay of communications between different
structures
rather than a delay in maturation of the
structures
themselves may be involved in
TS
+ ADHD and
TS
-ADHD children and ADHD symptoms in
TS
patients are likely a trait rather than adventitious or acquired within the
TS
syndrome
.
[MeSH-major]
Attention Deficit
Disorder
with Hyperactivity / physiopathology. Evoked Potentials, Auditory. Tourette
Syndrome
/ physiopathology
[MeSH-minor]
Acoustic
Stimulation
. Adolescent. Child. Female. Humans.
Intelligence
Tests. Male. Reaction
Time
. Retrospective Studies
MedlinePlus Health Information.
consumer health - Attention Deficit Hyperactivity Disorder
.
MedlinePlus Health Information.
consumer health - Tourette Syndrome
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16684681.001).
[ISSN]
1562-2975
[Journal-full-title]
The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry
[ISO-abbreviation]
World J. Biol. Psychiatry
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Scotland
43.
Weichhart T, Costantino G, Poglitsch M, Rosner M, Zeyda M, Stuhlmeier KM, Kolbe T, Stulnig TM, Hörl WH, Hengstschläger M, Müller M, Säemann MD:
The TSC-mTOR signaling pathway regulates the innate inflammatory response.
Immunity
; 2008 Oct 17;29(4):565-77
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The
TSC
-mTOR signaling pathway regulates the innate inflammatory response.
Here, we showed that the
tuberous sclerosis complex
-mammalian target of rapamycin (
TSC
-mTOR) pathway regulated inflammatory responses after bacterial
stimulation
in monocytes, macrophages, and primary dendritic
cells
.
Rapamycin-hyperactivated monocytes displayed a strong T helper 1 (Th1)
cell
- and Th17
cell
-polarizing potency.
These data identify the TSC2-mTOR pathway as a key regulator of innate immune homeostasis with broad clinical implications for infectious and autoimmune
diseases
, vaccination, cancer, and transplantation.
[MeSH-minor]
Animals. Anti-Bacterial Agents / pharmacology. Female. Humans. Inflammation / immunology. Inflammation / metabolism. Lipopolysaccharides / immunology. Listeria monocytogenes / immunology. Mice. Mice, Inbred BALB C. Mice, Knockout. NF-kappa B / metabolism. STAT3 Transcription Factor / metabolism. Signal Transduction. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Th1
Cells
/ immunology. Th1
Cells
/ metabolism.
Tuberous Sclerosis
MedlinePlus Health Information.
consumer health - Listeria Infections
.
Hazardous Substances Data Bank.
SIROLIMUS
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18848473.001).
[ISSN]
1097-4180
[Journal-full-title]
Immunity
[ISO-abbreviation]
Immunity
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE6002
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Bacterial Agents; 0 / Cytokines; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / STAT3 Transcription Factor; 0 / Tumor Suppressor Proteins; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
44.
Chierchia GB, Capulzini L, de Asmundis C, Sarkozy A, Roos M, Paparella G, Boussy T, Van Camp G, Kerkhove D, Brugada P:
First experience with real-time three-dimensional transoesophageal echocardiography-guided transseptal in patients undergoing atrial fibrillation ablation.
Europace
; 2008 Nov;10(11):1325-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
First experience with real-
time
three-dimensional transoesophageal echocardiography-guided transseptal in patients undergoing atrial fibrillation ablation.
AIMS: Transseptal (
TS
) puncture during atrial fibrillation (AF) ablation is a relatively safe procedure in experienced hands.
Real-
time
three-dimensional transeosophageal echocardiography (RT 3D TEE) is a novel imaging technology that permits direct visualization of the fossa ovalis in a 3D perspective, thereby sensibly lowering the likelihood of potential adverse effects during
TS
.
In our study, we describe the technique and assess the feasibility, advantages, and safety of this novel imaging method in guiding
TS
puncture in a series of consecutive patients undergoing AF ablation.
METHODS AND RESULTS: We performed
TS
puncture guided by RT 3D TEE under general anaesthesia in 24 consecutive patients (16 male, 55.4 +/- 8.1 years) undergoing ablation for drug refractory AF.
The fossa ovalis could clearly be seen and easily be distinguished from surrounding anatomical
structures
in all 24 patients.
Total fluoroscopic
time
was 120.6 +/- 34 s.
CONCLUSION: Real-
time
three-dimensional transeosophageal is a very useful tool in guiding
TS
puncture in patients undergoing AF ablation with the invaluable advantage of the 3D direct visualization of the fossa ovalis.
MedlinePlus Health Information.
consumer health - Atrial Fibrillation
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18835940.001).
[ISSN]
1532-2092
[Journal-full-title]
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
[ISO-abbreviation]
Europace
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
England
45.
Albracht K, Arampatzis A, Baltzopoulos V:
Assessment of muscle volume and physiological cross-sectional area of the human triceps surae muscle in vivo.
J Biomech
; 2008 Jul 19;41(10):2211-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The purpose of the present study was to investigate whether it is possible to predict the individual muscle volumes within the triceps surae (
TS
) muscle group by means of easily measurable parameters based on a theoretical consideration.
A further objective was to verify the use of the available literature data to assess the contribution of each muscle of the group to the entire
TS
volume or physiological cross-sectional-area (PCSA).
Therefore, magnetic resonance images of the right calf of 13 male subjects were acquired and each muscle of the
TS
was reconstructed.
The size of the fraction depends on muscle shape and its coefficient of variance among the examined population was considerable
low
(soleus 6%, gastrocnemius 4% and gastrocnemius lateralis 7%) in the present study.
Further, the soleus, gastrocnemius medialis and gastrocnemius lateralis accounted on average for about 52+/-3%, 32+/-2% and 16+/-2% of the total
TS
volume and 62+/-5%, 26+/-3% and 12+/-2% of the entire
TS
PCSA, respectively.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18555257.001).
[ISSN]
0021-9290
[Journal-full-title]
Journal of biomechanics
[ISO-abbreviation]
J Biomech
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
46.
Vernieuw CR, Stephenson LA, Kolka MA:
Thermal comfort and sensation in men wearing a cooling system controlled by skin temperature.
Hum Factors
; 2007 Dec;49(6):1033-44
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Thermal comfort and sensation in men wearing a cooling
system
controlled by skin
temperature
.
OBJECTIVE: The study was done to determine whether thermal comfort (TC), thermal sensation (
TS
), and subjective factors gauging environmental stress were negatively affected with different cooling methods in men exercising in chemical protective clothing.
The circulating fluid in the cooling garment was provided during exercise to the head (6% body
surface
area [BSA]), torso (22% BSA), and thighs (44% BSA) and manipulated under three methods: (a) CC, (b) pulsed cooling (PC), and (c) PC activated by mean skin
temperature
(T(sk)) control (PC(skin)).
TC and
TS
ratings were recorded every 20 min during the 80-min
test
.
RESULTS: TC and
TS
ratings were not different for PC(skin) and CC; thus the participants perceived PC(skin) as being similar to CC.
TS
was significantly warmer with PC than with PC(skin) and CC (p < .001).
In PC(skin), T(sk) was significantly higher than in PC and CC (p < .001), and PC(skin) was rated as being not as warm as PC according
to TS
.
[MeSH-major]
Body
Temperature
Regulation. Heat Exhaustion / prevention & control. Protective Clothing. Skin
Temperature
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18074702.001).
[ISSN]
0018-7208
[Journal-full-title]
Human factors
[ISO-abbreviation]
Hum Factors
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Hazardous Substances
47.
Mollard P, Woorons X, Letournel M, Cornolo J, Lamberto C, Beaudry M, Richalet JP:
Role of maximal heart rate and arterial O2 saturation on the decrement of VO2max in moderate acute hypoxia in trained and untrained men.
Int J Sports Med
; 2007 Mar;28(3):186-92
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Seventeen healthy males, nine trained endurance athletes (
TS
) and eight untrained individuals (US) were studied.
The decrement in HR (max) (DeltaHR (max)) was significant from 1000 m for
TS
and 2500 m for US and more important in
TS
than US (at 1500 m and 3500 m).
At maximal exercise,
TS
had a greater reduction in SaO (2) (DeltaSaO (2)) at each altitude.
DeltaHR (max) observed in
TS
was correlated with DeltaSaO (2).
However,
a multiple
regression analysis demonstrated that DeltaSaO (2) alone may account for DeltaV.O (2max).
Furthermore, in spite of a greater reduction in SaO (2) and HR (max) in
TS
, no difference was evidenced in relative DeltaV.O (2max) between groups.
MedlinePlus Health Information.
consumer health - Exercise and Physical Fitness
.
Hazardous Substances Data Bank.
OXYGEN
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17024632.001).
[ISSN]
0172-4622
[Journal-full-title]
International journal of sports medicine
[ISO-abbreviation]
Int J Sports Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
S88TT14065 / Oxygen
48.
Weiner HL, Carlson C, Ridgway EB, Zaroff CM, Miles D, LaJoie J, Devinsky O:
Epilepsy surgery in young children with tuberous sclerosis: results of a novel approach.
Pediatrics
; 2006 May;117(5):1494-502
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Epilepsy
surgery in young children with
tuberous sclerosis
: results of a novel approach.
OBJECTIVE:
Tuberous sclerosis complex
(
TSC
) is associated with medically refractory
epilepsy
and developmental delay in children and usually results from cortical tubers.
Previous reports have shown modest benefit from surgical resection of single tubers/seizure foci in older children; however, many children with
TSC
develop uncontrolled seizures before age 1.
METHODS: Of 110 consecutive children who underwent
epilepsy
surgery by a single surgeon in the past 6 years, 25 patients (9 boys and 16 girls) had
TSC
.
At the
time
of their first surgery at our institution, they were a median age of 4.0 years.
A total of 31 separate admissions for
epilepsy
surgery in these 25 patients were identified.
CONCLUSIONS: This approach can help to identify both primary and secondary epileptogenic zones in young
TSC
patients with
multiple
tubers.
Multiple
or bilateral seizure foci are not necessarily a contraindication to surgery.
[MeSH-major]
Epilepsies, Partial / surgery.
Tuberous Sclerosis
/ complications
[MeSH-minor]
Adolescent.
Brain
Mapping. Child. Child, Preschool. Electrodes, Implanted. Female. Humans. Male. Monitoring, Physiologic. Neurosurgical Procedures / methods
Genetic Alliance.
consumer health - Epilepsy
.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16651302.001).
[ISSN]
1098-4275
[Journal-full-title]
Pediatrics
[ISO-abbreviation]
Pediatrics
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
49.
Ben-Aroya S, Pan X, Boeke JD, Hieter P:
Making temperature-sensitive mutants.
Methods Enzymol
; 2010;470:181-204
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Making
temperature
-
sensitive
mutants.
The study of
temperature
-
sensitive
(
Ts
) mutant phenotypes is fundamental to gene identification and for dissecting essential gene function.
In this chapter, we describe two "shuffling" methods for producing
Ts
mutants using a combination of PCR, in vivo recombination, and transformation of diploid strains heterozygous for a knockout of the desired mutation.
In the "plasmid" version, the product is a knockout mutant carrying a centromeric plasmid carrying the
Ts
mutant.
In the "chromosomal" version, The
Ts
alleles are integrated directly into the endogenous locus, albeit not in an entirely native configuration.
COS Scholar Universe.
author profiles
.
Saccharomyces Genome Database.
Saccharomyces Genome Database
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
[Cites]
Genetics. 1989 May;122(1):19-27
[
2659436.001
]
[Cites]
Gene. 1988 Dec 30;74(2):527-34
[
3073106.001
]
[Cites]
Yeast. 1995 Apr 15;11(4):355-60
[
7785336.001
]
[Cites]
Yeast. 1998 Jan 30;14(2):115-32
[
9483801.001
]
[Cites]
Genetics. 1964 Apr;49:649-62
[
14156925.001
]
[Cites]
Mol Cell. 2004 Nov 5;16(3):487-96
[
15525520.001
]
[Cites]
Adv Genet. 1950;3:33-71
[
15425388.001
]
[Cites]
Cell. 2005 Nov 4;123(3):507-19
[
16269340.001
]
[Cites]
Cell. 2006 Mar 10;124(5):1069-81
[
16487579.001
]
[Cites]
Nat Methods. 2007 Mar;4(3):251-6
[
17293868.001
]
[Cites]
Nat Methods. 2008 Feb;5(2):167-9
[
18193055.001
]
[Cites]
Mol Cell. 2008 Apr 25;30(2):248-58
[
18439903.001
]
[Cites]
Genes Dev. 2008 Aug 1;22(15):2062-74
[
18676811.001
]
[Cites]
Science. 2001 Feb 9;291(5506):1001-4
[
11232561.001
]
[Cites]
Nature. 2001 May 3;411(6833):41-2
[
11333967.001
]
[Cites]
Funct Integr Genomics. 2002 Sep;2(4-5):199-211
[
12192593.001
]
[Cites]
Yeast. 2003 Aug;20(11):985-93
[
12898713.001
]
[Cites]
Cell. 2004 Jul 9;118(1):31-44
[
15242642.001
]
[Cites]
J Bacteriol. 1967 May;93(5):1662-70
[
5337848.001
]
[Cites]
Gene. 1990 Nov 30;96(1):23-8
[
2265755.001
]
(PMID = 20946811.001).
[ISSN]
1557-7988
[Journal-full-title]
Methods in enzymology
[ISO-abbreviation]
Meth. Enzymol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA016519-34; United States / NCI NIH HHS / CA / P01 CA016519; United States / NCI NIH HHS / CA / P01 CA016519-34
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS191056; NLM/ PMC2957654
50.
Sanz-Ortega J, Olivier C, Pérez Segura P, Galante Romo I, San José Mansó L, Saez M:
[Hereditary renal cancer].
Actas Urol Esp
; 2009 Feb;33(2):127-33
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[
Hereditary
renal cancer].
[Transliterated title]
Cáncer
de
riñón hereditario.
People with Von Hippel-Lindau
syndrome
have about a 40% risk of developing
multiple
bilateral clear
cell
kidney cancers.
They can also develop retinal and
brain
hemangioblastoma, kidneys or pancreas cysts, pheochromocytoma and endolymphatic sac tumor.
Hereditary
papillary renal
cell
carcinoma
syndrome
has type 1 papillary renal
cell
carcinomas associated with protooncogene c-MET germline mutations.
Birt-Hogg-Dubé
syndrome
has FLCN gene mutations associated with fibrofolliculomas, lung cysts with a high risk for spontaneous pneumothorax, and a 15% to 30% risk of kidney cancer (most classified as chromophobe carcinoma, oncocytoma or oncocytic hybrid, but clear
cell
and papillary kidney cancers have also been reported).
Histopathological findings such as oncocytosis and oncocytic hybrids are very unusual outside the
syndrome
.
Hereditary
leiomyomatosis and renal
cell
cancer
syndrome
shows mutations of Fumarate hydratase gene and cutaneous leiomyomata in 76% of affected individuals, uterine leiomyomata in 100% of females, and unilateral, solitary, and aggressive papillary renal cancer in 10 to 16% of patients.
Tuberous sclerosis complex
is one of the most prevalent (1/5.800)
hereditary
syndromes where renal
disease
is the second leading cause of death, associated with angiomyolipomas (70%), renal cysts, oncocytomas or clear
cell
cancer.
[MeSH-minor]
Cysts / genetics. Hair Follicle. Humans. Lung
Diseases
/ genetics. Skin Neoplasms / genetics.
Syndrome
. von Hippel-Lindau
Disease
/
diagnosis
. von Hippel-Lindau
Disease
/ genetics
Genetic Alliance.
consumer health - Hereditary Cancer
.
Genetic Alliance.
consumer health - Kidney cancer
.
MedlinePlus Health Information.
consumer health - Kidney Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19418834.001).
[ISSN]
0210-4806
[Journal-full-title]
Actas urologicas españolas
[ISO-abbreviation]
Actas Urol Esp
[Language]
spa
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Spain
[Number-of-references]
45
51.
Laín A, García-Casillas MA, Matute JA, Cañizo A, Parente A, Fanjul M, Carrera N, Vázquez J:
[Tracheal stenosis: outcome analysis of the last 14 years].
Cir Pediatr
; 2008 Jul;21(3):138-42
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Transliterated title]
Estenosis traqueal: análisis
de
los resultados obtenidos en los últimos 14 años.
Tracheal stenosis (
TS
) is an unusual and sometimes lethal condition.
AIM: Analyze the outcome of patients with
TS
diagnosed and treated in our institution realted to the applied surgical technique during the study period.
MATERIAL AND METHODS: The clinical records of patients with
TS
(period 1991 to 2006) were reviewed analyzing the following variables: age, gender, associated malformations, intubation
time
, medium hospital stay and outcome.
In the tracheoplasty-group there were 2 exitus (1 due
to a
neurological lesion after a prolonged preoperative cardiorrespiratory arrest, one due
to a
surgical treatment delay with previous inadequate management).
No statistically significant differences were found in the medium intubation
time
, medium hospital stay and medium follow-up
time
.
Short segmental
TS
should be corrected with RTA, long
TS
with tracheoplasties (slide), remaining the TAIC technique obsolete.
[MeSH-minor]
Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male. Retrospective Studies.
Time
Factors
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18756866.001).
[ISSN]
0214-1221
[Journal-full-title]
Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
[ISO-abbreviation]
Cir Pediatr
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Spain
52.
Miyake M, Tateishi U, Maeda T, Kusumoto M, Satake M, Arai Y, Sugimura K:
Pulmonary lymphangioleiomyomatosis in a male patient with tuberous sclerosis complex.
Radiat Med
; 2005 Nov;23(7):525-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Pulmonary lymphangioleiomyomatosis in a male patient with
tuberous sclerosis complex
.
Pulmonary lymphangioleiomyomatosis (LAM) is a rare
disease
of unknown etiology that occurs almost exclusively in women of reproductive age.
The correct
diagnosis
may be delayed by several years after the onset of symptoms because of the rarity of the
disease
and the need for chest CT scans to identify the lung involvement.
We describe a case of pulmonary LAM in a male patient associated with
tuberous sclerosis complex
(
TSC
), in whom the early stage of
disease
could be depicted by chest HRCT scans.
[MeSH-major]
Lung Neoplasms / radiography. Lymphangioleiomyomatosis / radiography. Tomography, X-Ray Computed.
Tuberous Sclerosis
/ radiography
[MeSH-minor]
Adolescent.
Diagnosis
, Differential. Humans. Male. Thoracic Surgery, Video-Assisted
Genetic Alliance.
consumer health - Lymphangioleiomyomatosis
.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - CT Scans
.
MedlinePlus Health Information.
consumer health - Lung Cancer
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16485546.001).
[ISSN]
0288-2043
[Journal-full-title]
Radiation medicine
[ISO-abbreviation]
Radiat Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
53.
Park CM, Lee WY, Chun HK, Cho YB, Yun HR, Heo JS, Yun SH, Kim HC:
Relationship of polymorphism of the tandem repeat sequence in the thymidylate synthase gene and the survival of stage III colorectal cancer patients receiving adjuvant 5-flurouracil-based chemotherapy.
J Surg Oncol
; 2010 Jan 1;101(1):22-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
BACKGROUND: The aim of this study was to determine whether the different polymorphisms in the thymidylate synthase (
TS
) gene, novel G>C single nucleotide polymorphism (SNP) and variable number of tandem repeat (VNTR), may be related with
disease
-free survival (DFS) in patients with stage III colorectal cancer receiving adjuvant chemotherapy.
DNA was extracted from fresh tumor
tissue
and sequenced.
Patients with
TS
genotypes of 2R3G, 3C3G, or 3G3G were assigned
to a
high expression group, and those with 2R2R, 2R3C, or 3C3C,
to a low
expression group.
RESULTS: Frequencies of the
TS
tandem repeat polymorphisms among the tumor genotypes were 6.0% in 2R2R, 25.4% in 2R3R, and 68.7% in 3R3R.
The
low
expression group included 52 patients (25.9%), and the high expression group included 149 patients (74.1%).
Groups classified according to possession of VNTR, SNP, and
low
- or high-expression genotypes did not differ significantly in DFS.
CONCLUSIONS:
TS
polymorphisms do not predict clinical outcome of colorectal cancer patients treated with adjuvant 5-FU-based chemotherapy.
[MeSH-minor]
Adult. Aged.
Disease
-Free Survival. Female. Fluorouracil / administration & dosage. Genotype. Humans. Male. Middle Aged. Neoplasm Staging
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19798689.001).
[ISSN]
1096-9098
[Journal-full-title]
Journal of surgical oncology
[ISO-abbreviation]
J Surg Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 2.1.1.45 / Thymidylate Synthase; U3P01618RT / Fluorouracil
54.
Kano Y, Ohta M, Nagai Y, Spector I, Budman C:
Rage attacks and aggressive symptoms in Japanese adolescents with tourette syndrome.
CNS Spectr
; 2008 Apr;13(4):325-32
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Rage attacks and aggressive symptoms in Japanese adolescents with tourette
syndrome
.
OBJECTIVE: This study was conducted to explore possible causes of rage attacks as well as clinically significant aggressive symptoms in Japanese adolescents with Tourette
syndrome
(
TS
).
Eighteen subjects (62.1%) were diagnosed with
TS
only, 11 (37.9%) with
TS
and comorbidities, including attention-deficit/hyperactivity
disorder
and obsessive-compulsive
disorder
.
Child Behavior Checklist ratings to compare 11 aggressive and 12 non-aggressive subjects <16 years of age revealed elevated t-
test
scores on the anxious/depressed, thought problems, aggressive, internalizing, externalizing subscales, and total scale in the aggressive group versus the non-aggressive group.
CONCLUSION: Rage attacks and clinically significant aggressive symptoms are common problems in Japanese
TS
youth.
[MeSH-major]
Aggression / psychology. Rage. Tourette
Syndrome
/
diagnosis
[MeSH-minor]
Adolescent. Child. Comorbidity. Cross-Sectional Studies. Female. Humans. Japan. Male. Mental Disorders /
diagnosis
. Mental Disorders / epidemiology. Mental Disorders / psychology. Personality Assessment
Genetic Alliance.
consumer health - Tourette Syndrome
.
MedlinePlus Health Information.
consumer health - Tourette Syndrome
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18408652.001).
[ISSN]
1092-8529
[Journal-full-title]
CNS spectrums
[ISO-abbreviation]
CNS Spectr
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
55.
Baldin AD, Armani MC, Morcillo AM, Lemos-Marini SH, Baptista MT, Maciel-Guerra AT, Guerra Júnior G:
[Body proportions in a group of Brazilian patients with Turner Syndrome].
Arq Bras Endocrinol Metabol
; 2005 Aug;49(4):529-35
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Body proportions in a group of Brazilian patients with Turner
Syndrome
].
[Transliterated title]
Proporções corporais em um grupo
de
pacientes brasileiras com síndrome
de
Turner.
OBJECTIVE: The first Brazilian study aimed to evaluate body proportions in patients with Turner
Syndrome
(
TS
) with no growth hormone treatment.
METHODS: A cross-sectional study with 50
TS
patients (5 to 43 years) evaluating age, karyotype, pubertal development, height, sitting height, arm span, weight, BMI, head circumference, length of hand, foot and leg, waist to hip ratio, biacromial and biiliac diameters.
A descriptive analysis was done and Mann-Whitney
test
and analysis of variance was applied.
CONCLUSION: The retardation of growth in
TS
occurs mainly on the longitudinal axis, and the results showed in this study are similar to the Danish report.
[MeSH-major]
Anthropometry / methods. Body Weights and Measures / methods. Turner
Syndrome
/ pathology
Genetic Alliance.
consumer health - Turner syndrome
.
MedlinePlus Health Information.
consumer health - Turner Syndrome
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16358081.001).
[ISSN]
0004-2730
[Journal-full-title]
Arquivos brasileiros de endocrinologia e metabologia
[ISO-abbreviation]
Arq Bras Endocrinol Metabol
[Language]
por
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Brazil
56.
Huang C, Liu D, Masuya D, Nakashima T, Kameyama K, Ishikawa S, Ueno M, Haba R, Yokomise H:
Clinical application of biological markers for treatments of resectable non-small-cell lung cancers.
Br J Cancer
; 2005 Apr 11;92(7):1231-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Clinical application of biological markers for treatments of resectable non-small-
cell
lung cancers.
We performed a clinical study to identify biological markers useful for the treatment of resectable non-small-
cell
lung cancers (NSCLCs).
By immunohistochemistry, we evaluated the Ki-67 proliferation index, tumour vascularity, thymidylate synthase (
TS
), vascular endothelial growth factor (VEGF)-A, VEGF-C, and E (epithelial)-cadherin.
The Ki-67 proliferation index (P=0.02) and
TS
status (P<0.01) were significant prognostic factors in patients with stage II-III NSCLCs.
In patients with stage II-III NSCLCs, furthermore, the survival of UFT (a combination of tegafur and uracil)-treated patients with
TS
-negative tumours was significantly better than those of any other patients.
In contrast, tumour proliferation rate and
TS
status are useful markers for identifying less aggressive tumours in locally advanced NSCLCs.
[MeSH-major]
Biomarkers, Tumor / analysis. Carcinoma, Non-Small-
Cell
Lung / immunology. Carcinoma, Non-Small-
Cell
Lung / pathology. Lung Neoplasms / immunology. Lung Neoplasms / pathology. Neoplasm Staging / methods
[MeSH-minor]
Adult. Aged. Antineoplastic Agents / therapeutic use.
Cell
Proliferation. Female. Growth Substances / analysis. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Middle Aged. Neovascularization, Pathologic. Patient Care Planning. Predictive Value of Tests. Prognosis. Retrospective Studies.
Sensitivity
and Specificity. Thymidylate Synthase / analysis
MedlinePlus Health Information.
consumer health - Lung Cancer
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer. 1998 May 1;82(9):1626-31
[
9576280.001
]
[Cites]
Cell Struct Funct. 1995 Jun;20(3):191-7
[
7586009.001
]
[Cites]
J Thorac Cardiovasc Surg. 1998 May;115(5):1007-14
[
9605068.001
]
[Cites]
Mol Cell Biol. 1999 Feb;19(2):1582-94
[
9891091.001
]
[Cites]
Clin Cancer Res. 1999 Aug;5(8):2048-58
[
10473085.001
]
[Cites]
Nat Med. 1995 Jan;1(1):27-31
[
7584949.001
]
[Cites]
Int J Oncol. 2000 Jul;17(1):47-54
[
10853017.001
]
[Cites]
Hepatogastroenterology. 2000 May-Jun;47(33):742-5
[
10919023.001
]
[Cites]
Nat Med. 2001 Feb;7(2):192-8
[
11175850.001
]
[Cites]
Ann Thorac Surg. 2001 Mar;71(3):949-54; discussion 954-5
[
11269479.001
]
[Cites]
Br J Cancer. 2001 Jul 20;85(2):255-60
[
11461086.001
]
[Cites]
Cancer. 2001 Nov 15;92(10):2628-38
[
11745198.001
]
[Cites]
Am J Health Syst Pharm. 2002 Apr 1;59(7):611-42
[
11944603.001
]
[Cites]
J Clin Oncol. 1996 Apr;14(4):1048-54
[
8648356.001
]
[Cites]
Cancer Res. 1996 Sep 1;56(17):4063-70
[
8752180.001
]
[Cites]
Chest. 1997 Jun;111(6):1710-7
[
9187198.001
]
[Cites]
Int J Oncol. 1998 Mar;12(3):553-63
[
9472092.001
]
[Cites]
J Clin Oncol. 1998 Apr;16(4):1397-406
[
9552043.001
]
[Cites]
Am J Respir Crit Care Med. 1998 Apr;157(4 Pt 1):1319-23
[
9563756.001
]
[Cites]
J Clin Oncol. 2002 Apr 15;20(8):1989-95
[
11956257.001
]
[Cites]
J Biol Chem. 2002 Nov 15;277(46):44376-84
[
12221087.001
]
[Cites]
Cancer. 2003 Jan 15;97(2):457-64
[
12518370.001
]
[Cites]
J Clin Oncol. 2003 Jul 15;21(14):2787-99
[
12860957.001
]
[Cites]
Lung Cancer. 2003 Aug;41 Suppl 1:S97-102
[
12867068.001
]
[Cites]
Lung Cancer. 2003 Aug;41 Suppl 1:S115-21
[
12867070.001
]
[Cites]
N Engl J Med. 2004 Jan 22;350(4):351-60
[
14736927.001
]
[Cites]
J Thorac Cardiovasc Surg. 2004 Jan;127(1):108-13
[
14752420.001
]
[Cites]
Cancer Cell. 2004 Apr;5(4):341-51
[
15093541.001
]
[Cites]
N Engl J Med. 2004 Apr 22;350(17):1713-21
[
15102997.001
]
[Cites]
Med Sci Monit. 2004 Jun;10(6):BR157-65
[
15173661.001
]
[Cites]
J Biol Chem. 1980 Aug 10;255(15):7386-90
[
7391086.001
]
[Cites]
J Immunol. 1984 Oct;133(4):1710-5
[
6206131.001
]
[Cites]
Cancer Res. 1986 Aug;46(8 Suppl):4244s-4248s
[
3524805.001
]
[Cites]
Eur J Cancer. 1993;29A(3):363-5
[
8398336.001
]
[Cites]
Eur J Cancer. 1994;30A(10):1517-22
[
7833111.001
]
[Cites]
Cancer Res. 1995 Apr 1;55(7):1407-12
[
7882343.001
]
[Cites]
Am J Pathol. 1995 May;146(5):1029-39
[
7538264.001
]
[Cites]
Mol Cell Biol. 1995 Aug;15(8):4215-24
[
7623816.001
]
[Cites]
Ann Thorac Surg. 1998 May;65(5):1405-9
[
9594875.001
]
(PMID = 15785747.001).
[ISSN]
0007-0920
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Growth Substances; 0 / Ki-67 Antigen; EC 2.1.1.45 / Thymidylate Synthase
[Other-IDs]
NLM/ PMC2361974
57.
Tanabe K, Yoshida K, Hamai Y, Ukon K, Hihara J, Toge T:
[A case of remnant gastric cancer with multiple bone metastasis and peritoneal dissemination; efficacy of combination therapy of docetaxel and TS-1].
Gan To Kagaku Ryoho
; 2005 Jul;32(7):1037-40
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[A case of remnant gastric cancer with
multiple
bone metastasis and peritoneal dissemination; efficacy of combination therapy of docetaxel and
TS
-1].
She was diagnosed as remnant gastric cancer with
multiple
bone metastasis and peritoneal dissemination.
Treatment with docetaxel and
TS
-1 was started with the following regimen: daily oral administration of 100 mg/body
TS
-1 for 14 days, followed by a 7 day rest and infusion of 40 mg/m2 docetaxel on day 1.
Two months after the initial administration of docetaxel/
TS
-1, the sites of the remnant gastric cancer and bone metastasis were reduced in size, and the ALP returned to almost the normal level.
Currently (nine months after
diagnosis
), she is undergoing therapy with
TS
-1.
The combination of docetaxel and
TS
-1 can be a new tool for the management of gastric cancer with bone metastasis.
Genetic Alliance.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Bone Cancer
.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
DOCETAXEL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16044969.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Drug Combinations; 0 / Pyridines; 0 / Taxoids; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 15H5577CQD / docetaxel; 5VT6420TIG / Oxonic Acid
58.
Singh V, Evans GB, Lenz DH, Mason JM, Clinch K, Mee S, Painter GF, Tyler PC, Furneaux RH, Lee JE, Howell PL, Schramm VL:
Femtomolar transition state analogue inhibitors of 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase from Escherichia coli.
J Biol Chem
; 2005 May 6;280(18):18265-73
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Femtomolar
transition state
analogue inhibitors of 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase from Escherichia coli.
Hydrolysis of MTA by E. coli MTAN involves a highly dissociative
transition state
with ribooxacarbenium ion character.
Iminoribitol mimics of MTA at the
transition state
of MTAN were synthesized and tested as inhibitors.
DADMe-Immucillins are better inhibitors of E. coli MTAN, since they are more closely related to the highly dissociative nature of the
transition state
.
Replacing the 5'-methyl group with other hydrophobic groups gave 17
transition state
analogue inhibitors with dissociation constants from 10(-12) to 10(-14) m.
The inhibitory potential of these
transition state
analogue inhibitors supports
a transition state structure
closely resembling a fully dissociated ribooxacarbenium ion.
The accompanying article reports crystal
structures
of MTAN with these analogues.
COS Scholar Universe.
author profiles
.
BioCyc.
gene/protein/disease-specific - mtn
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 15749708.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Escherichia coli Proteins; 0 / Thionucleosides; 634Z2VK3UQ / 5'-methylthioadenosine; EC 3.2.2.- / N-Glycosyl Hydrolases; EC 3.2.2.9 / adenosylhomocysteine nucleosidase
59.
Inoki K, Ouyang H, Li Y, Guan KL:
Signaling by target of rapamycin proteins in cell growth control.
Microbiol Mol Biol Rev
; 2005 Mar;69(1):79-100
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Signaling by target of rapamycin proteins in
cell
growth control.
TOR proteins integrate signals from growth factors, nutrients, stress, and cellular energy levels to control
cell
growth.
The ribosomal S6 kinase 1 (S6K) and eukaryotic initiation factor 4E binding protein 1(4EBP1) are two cellular targets of TOR kinase activity and are known to mediate TOR function in translational control in mammalian
cells
.
One of the recent breakthrough studies in TOR signaling resulted in the identification of the
tuberous sclerosis complex
gene products, TSC1 and TSC2, as negative regulators for TOR signaling.
Here we review the
current
understanding of the regulation of TOR signaling and discuss its function as a signaling nexus to control
cell
growth during normal development and tumorigenesis.
[MeSH-major]
Cell
Division / physiology
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
Saccharomyces Genome Database.
Saccharomyces Genome Database
.
antibodies-online.
View related products from antibodies-online.com
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Mol Cell. 2003 Apr;11(4):895-904
[
12718876.001
]
[Cites]
Curr Biol. 2003 May 13;13(10):797-806
[
12747827.001
]
[Cites]
Methods. 1997 Apr;11(4):343-52
[
9126549.001
]
[Cites]
Curr Opin Genet Dev. 1997 Apr;7(2):170-5
[
9115420.001
]
[Cites]
Nat Genet. 1997 May;16(1):64-7
[
9140396.001
]
[Cites]
Mol Cell Biol. 1997 Jun;17(6):3254-60
[
9154824.001
]
[Cites]
Science. 1997 Jul 4;277(5322):99-101
[
9204908.001
]
[Cites]
Gene. 1997 Jun 19;192(2):245-50
[
9224897.001
]
[Cites]
Nat Genet. 1997 Aug;16(4):333-4
[
9241266.001
]
[Cites]
Science. 1997 Aug 8;277(5327):805-8
[
9242607.001
]
[Cites]
J Biol Chem. 1997 Aug 29;272(35):21661-4
[
9268289.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10624-9
[
9380685.001
]
[Cites]
Cell. 2002 Jul 26;110(2):177-89
[
12150926.001
]
[Cites]
J Cell Biol. 2002 Jul 8;158(1):165-74
[
12105188.001
]
[Cites]
Genetics. 2002 Jul;161(3):1053-63
[
12136010.001
]
[Cites]
J Biol Chem. 2002 Aug 2;277(31):27975-81
[
12032158.001
]
[Cites]
Cell. 2002 Jul 26;110(2):163-75
[
12150925.001
]
[Cites]
Nature. 2004 Sep 9;431(7005):200-5
[
15306821.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Sep 14;101(37):13489-94
[
15342917.001
]
[Cites]
Curr Biol. 2004 Sep 21;14(18):1650-6
[
15380067.001
]
[Cites]
Genes Dev. 2004 Oct 15;18(20):2479-84
[
15466161.001
]
[Cites]
Eur J Biochem. 1983 Jun 1;133(1):135-9
[
6343083.001
]
[Cites]
Eur J Biochem. 1983 Jun 1;133(1):141-4
[
6343084.001
]
[Cites]
Proc Natl Acad Sci U S A. 1984 Oct;81(20):6442-6
[
6387704.001
]
[Cites]
Annu Rev Biochem. 1986;55:801-30
[
3527052.001
]
[Cites]
Eur J Biochem. 1987 May 4;164(3):607-12
[
3552673.001
]
[Cites]
Mol Cell Biol. 1987 Apr;7(4):1338-45
[
3299046.001
]
[Cites]
J Biol Chem. 2002 Sep 20;277(38):35364-70
[
12167664.001
]
[Cites]
Biochem Pharmacol. 2002 Oct 1;64(7):1071-7
[
12234610.001
]
[Cites]
Mol Cell Biol. 2002 Oct;22(20):7004-14
[
12242281.001
]
[Cites]
Curr Opin Cardiol. 2002 Sep;17(5):518-25
[
12357129.001
]
[Cites]
EMBO Rep. 2002 Oct;3(10):988-94
[
12231510.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13571-6
[
12271141.001
]
[Cites]
Cancer Res. 2002 Oct 15;62(20):5645-50
[
12384518.001
]
[Cites]
Mol Cell. 2002 Sep;10(3):457-68
[
12408816.001
]
[Cites]
Biol Res. 2002;35(2):305-13
[
12415748.001
]
[Cites]
Mol Cell Biol. 2002 Dec;22(23):8101-13
[
12417714.001
]
[Cites]
Eur J Biochem. 2002 Nov;269(22):5338-49
[
12423332.001
]
[Cites]
Microbiol Mol Biol Rev. 2002 Dec;66(4):579-91, table of contents
[
12456783.001
]
[Cites]
J Biol Chem. 2002 Dec 27;277(52):51017-24
[
12397075.001
]
[Cites]
Trends Cell Biol. 2003 Feb;13(2):79-85
[
12559758.001
]
[Cites]
Mol Cell Biol. 1997 Feb;17(2):921-33
[
9001246.001
]
[Cites]
Cell. 1997 Feb 21;88(4):531-42
[
9038344.001
]
[Cites]
J Biol Chem. 1997 Apr 11;272(15):10240-7
[
9092573.001
]
[Cites]
J Biol Chem. 1997 Apr 18;272(16):10608-15
[
9099708.001
]
[Cites]
J Biol Chem. 2001 Nov 23;276(47):43939-48
[
11500493.001
]
[Cites]
Mol Cell Biol. 2001 Dec;21(24):8671-83
[
11713299.001
]
[Cites]
Nat Cell Biol. 2001 Nov;3(11):1014-9
[
11715023.001
]
[Cites]
Science. 2001 Nov 30;294(5548):1942-5
[
11729323.001
]
[Cites]
Mol Biol Cell. 2001 Dec;12(12):4103-13
[
11739804.001
]
[Cites]
Bioessays. 2001 Dec;23(12):1112-9
[
11746230.001
]
[Cites]
Yeast. 2001 Dec;18(16):1479-91
[
11748725.001
]
[Cites]
Hum Mol Genet. 2001 Dec 1;10(25):2889-98
[
11741832.001
]
[Cites]
Mol Cell. 2001 Nov;8(5):1017-26
[
11741537.001
]
[Cites]
Bioessays. 2002 Jan;24(1):65-71
[
11782951.001
]
[Cites]
J Biol Chem. 1998 Feb 13;273(7):3963-6
[
9461583.001
]
[Cites]
Am J Hum Genet. 1998 Feb;62(2):286-94
[
9463313.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1432-7
[
9465032.001
]
[Cites]
Genes Dev. 1998 Feb 15;12(4):502-13
[
9472019.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4264-9
[
9539725.001
]
[Cites]
Hum Mol Genet. 1998 Jun;7(6):1053-7
[
9580671.001
]
[Cites]
J Biol Chem. 1998 Jun 5;273(23):14424-9
[
9603954.001
]
[Cites]
J Biol Chem. 1998 Jun 5;273(23):14484-94
[
9603962.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7772-7
[
9636226.001
]
[Cites]
Blood. 1998 Jul 15;92(2):539-46
[
9657754.001
]
[Cites]
Mol Cell Biol. 1998 Aug;18(8):4463-70
[
9671456.001
]
[Cites]
Biochem J. 1998 Aug 15;334 ( Pt 1):261-7
[
9693128.001
]
[Cites]
Annu Rev Biochem. 1998;67:821-55
[
9759505.001
]
[Cites]
J Biol Chem. 1998 Oct 23;273(43):28178-84
[
9774438.001
]
[Cites]
Mol Cell. 2002 Jul;10(1):151-62
[
12150915.001
]
[Cites]
Eur J Biochem. 2002 Aug;269(15):3751-9
[
12153572.001
]
[Cites]
J Biol Chem. 2002 Aug 23;277(34):30958-67
[
12045200.001
]
[Cites]
Curr Biol. 2002 Aug 20;12(16):1419-23
[
12194824.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):648-57
[
12172553.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):658-65
[
12172554.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):699-704
[
12172555.001
]
[Cites]
Oncogene. 2002 Sep 12;21(41):6356-65
[
12214276.001
]
[Cites]
Curr Biol. 2002 Sep 3;12(17):1448-61
[
12225660.001
]
[Cites]
Development. 1999 Apr;126(8):1601-9
[
10079223.001
]
[Cites]
Mol Biol Cell. 1999 Apr;10(4):987-1000
[
10198052.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4240-5
[
10200246.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4438-42
[
10200280.001
]
[Cites]
Biochem J. 1999 May 15;340 ( Pt 1):135-41
[
10229668.001
]
[Cites]
EMBO J. 1999 May 17;18(10):2782-92
[
10329624.001
]
[Cites]
Mol Cell Biol. 1999 Jun;19(6):4101-12
[
10330150.001
]
[Cites]
Science. 1999 May 14;284(5417):1161-4
[
10325225.001
]
[Cites]
Oncogene. 1999 May 13;18(19):2988-96
[
10378694.001
]
[Cites]
EMBO J. 1999 Aug 2;18(15):4210-21
[
10428959.001
]
[Cites]
Trends Biochem Sci. 1999 Aug;24(8):306-11
[
10431174.001
]
[Cites]
Cancer Res. 1999 Aug 1;59(15):3581-7
[
10446965.001
]
[Cites]
J Cell Biol. 1999 Sep 20;146(6):1227-38
[
10491387.001
]
[Cites]
J Clin Invest. 1999 Sep;104(6):687-95
[
10491404.001
]
[Cites]
Science. 1999 Sep 24;285(5436):2126-9
[
10497130.001
]
[Cites]
Eur J Biochem. 1999 Oct;265(2):754-62
[
10504407.001
]
[Cites]
Nat Cell Biol. 2004 Nov;6(11):1122-8
[
15467718.001
]
[Cites]
Mol Biol Cell. 2002 Mar;13(3):795-804
[
11907262.001
]
[Cites]
Curr Biol. 2002 Apr 16;12(8):632-9
[
11967149.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):6422-7
[
11983923.001
]
[Cites]
J Biol Chem. 2002 May 17;277(20):17657-62
[
11884412.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 May 14;99(10):6784-9
[
11997479.001
]
[Cites]
J Biol Chem. 2002 May 31;277(22):20104-12
[
11914378.001
]
[Cites]
Genes Dev. 2002 Jun 15;16(12):1472-87
[
12080086.001
]
[Cites]
J Biol Chem. 2002 Jul 5;277(27):23977-80
[
11997383.001
]
[Cites]
Genes Dev. 2002 Jul 1;16(13):1587-609
[
12101119.001
]
[Cites]
Mol Cell Biol. 2002 Aug;22(15):5575-84
[
12101249.001
]
[Cites]
J Biol Chem. 2004 Mar 26;279(13):12220-31
[
14709557.001
]
[Cites]
J Biol Chem. 2004 Mar 26;279(13):12706-13
[
14718525.001
]
[Cites]
Mol Cell Biol. 2004 Apr;24(8):3112-24
[
15060135.001
]
[Cites]
J Biol Chem. 2004 Apr 9;279(15):14752-62
[
14736892.001
]
[Cites]
Oncogene. 2004 Apr 19;23(18):3151-71
[
15094765.001
]
[Cites]
Nature. 2004 May 13;429(6988):197-201
[
15141215.001
]
[Cites]
Nat Genet. 2004 Jun;36(6):585-95
[
15146184.001
]
[Cites]
Genes Dev. 2004 Jul 1;18(13):1533-8
[
15231735.001
]
[Cites]
Mol Cell Biol. 2004 Aug;24(15):6710-8
[
15254238.001
]
[Cites]
J Biol. 2003;2(4):28
[
14511394.001
]
[Cites]
Cancer Cell. 2004 Jul;6(1):91-9
[
15261145.001
]
[Cites]
J Cell Biol. 2004 Jul 19;166(2):213-23
[
15249583.001
]
[Cites]
Curr Biol. 2004 Jul 27;14(14):1296-302
[
15268862.001
]
[Cites]
Mol Cell Biol. 2004 Sep;24(18):7965-75
[
15340059.001
]
[Cites]
Gastroenterology. 1988 Jan;94(1):182-8
[
3335289.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 Jun;86(12):4579-83
[
2660141.001
]
[Cites]
Genes Dev. 1990 Mar;4(3):313-23
[
2186966.001
]
[Cites]
Mol Cell Biol. 1991 Apr;11(4):2133-48
[
1848673.001
]
[Cites]
Ann N Y Acad Sci. 1991;615:1-7
[
2039135.001
]
[Cites]
Science. 1991 Aug 23;253(5022):905-9
[
1715094.001
]
[Cites]
Curr Opin Cell Biol. 1991 Dec;3(6):1019-24
[
1839953.001
]
[Cites]
Cell. 1992 Jun 26;69(7):1227-36
[
1377606.001
]
[Cites]
Science. 1992 Aug 14;257(5072):973-7
[
1380182.001
]
[Cites]
Mol Cell Biol. 1992 Nov;12(11):4946-59
[
1328868.001
]
[Cites]
Cell. 1993 May 7;73(3):585-96
[
8387896.001
]
[Cites]
Cell. 1993 Dec 31;75(7):1305-15
[
8269512.001
]
[Cites]
FASEB J. 1994 Jan;8(1):13-9
[
8299885.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 May 10;91(10):4441-5
[
8183928.001
]
[Cites]
Curr Biol. 2002 Mar 5;12(5):389-95
[
11882290.001
]
[Cites]
Genes Cells. 2003 Jan;8(1):65-79
[
12558800.001
]
[Cites]
Nat Rev Mol Cell Biol. 2003 Feb;4(2):117-26
[
12563289.001
]
[Cites]
Mol Cell Biol. 2003 Mar;23(5):1546-57
[
12588975.001
]
[Cites]
Mol Biol Cell. 2003 Mar;14(3):1204-20
[
12631735.001
]
[Cites]
Genes Dev. 2003 Apr 1;17(7):859-72
[
12654728.001
]
[Cites]
J Biol Chem. 2003 Apr 18;278(16):13663-71
[
12582162.001
]
[Cites]
J Biol Chem. 2003 May 2;278(18):15461-4
[
12604610.001
]
[Cites]
J Cell Biol. 2003 Apr 28;161(2):333-47
[
12719473.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12574-8
[
7809080.001
]
[Cites]
Biochem J. 1995 Jan 1;305 ( Pt 1):25-8
[
7826337.001
]
[Cites]
J Biol Chem. 1995 Feb 3;270(5):2320-6
[
7836465.001
]
[Cites]
Mol Cell Biol. 1995 May;15(5):2333-40
[
7739516.001
]
[Cites]
Cell. 1995 Jul 28;82(2):241-50
[
7543024.001
]
[Cites]
J Biol Chem. 1995 Aug 4;270(31):18531-8
[
7629182.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Aug 1;92(16):7222-6
[
7638171.001
]
[Cites]
J Biol Chem. 1995 Sep 8;270(36):21396-403
[
7545671.001
]
[Cites]
Biochem J. 1995 Oct 1;311 ( Pt 1):17-29
[
7575450.001
]
[Cites]
Nature. 1995 Oct 5;377(6548):441-6
[
7566123.001
]
[Cites]
EMBO J. 1995 Nov 1;14(21):5279-87
[
7489717.001
]
[Cites]
EMBO J. 1995 Nov 15;14(22):5701-9
[
8521827.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11696-700
[
8524831.001
]
[Cites]
FEBS Lett. 1995 Dec 18;377(2):221-6
[
8543055.001
]
[Cites]
EMBO J. 1996 Feb 1;15(3):658-64
[
8599949.001
]
[Cites]
EMBO J. 1996 May 1;15(9):2291-7
[
8641294.001
]
[Cites]
J Biol Chem. 1996 Mar 1;271(9):5033-9
[
8617780.001
]
[Cites]
Mol Cell Biol. 1996 Jun;16(6):2744-55
[
8649382.001
]
[Cites]
Annu Rev Immunol. 1996;14:483-510
[
8717522.001
]
[Cites]
Genes Dev. 1996 Aug 1;10(15):1904-16
[
8756348.001
]
[Cites]
Mol Biol Cell. 1996 Jan;7(1):25-42
[
8741837.001
]
[Cites]
Annu Rev Biochem. 1996;65:241-69
[
8811180.001
]
[Cites]
Cell Growth Differ. 1996 Sep;7(9):1199-209
[
8877101.001
]
[Cites]
Cancer Surv. 1996;27:271-92
[
8909805.001
]
[Cites]
J Biol Chem. 1996 Dec 6;271(49):31166-71
[
8940115.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13780-5
[
8943012.001
]
[Cites]
Mol Cell Biol. 1996 Dec;16(12):6744-51
[
8943329.001
]
[Cites]
Curr Biol. 2000 Dec 14-28;10(24):1574-81
[
11137008.001
]
[Cites]
Physiol Rev. 2001 Jan;81(1):153-208
[
11152757.001
]
[Cites]
Biochem Biophys Res Commun. 2001 Jan 26;280(3):776-81
[
11162588.001
]
[Cites]
Oncogene. 2000 Dec 14;19(54):6306-16
[
11175345.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3373-81
[
11309295.001
]
[Cites]
Cell. 2001 May 4;105(3):345-55
[
11348591.001
]
[Cites]
Cell. 2001 May 4;105(3):357-68
[
11348592.001
]
[Cites]
Curr Opin Genet Dev. 2001 Jun;11(3):279-86
[
11377964.001
]
[Cites]
Genes Dev. 2001 Jun 1;15(11):1383-92
[
11390358.001
]
[Cites]
Methods Enzymol. 2001;333:217-31
[
11400338.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7283-8
[
11416207.001
]
[Cites]
Mol Cell Biol. 2001 Aug;21(15):5050-62
[
11438661.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8762-7
[
11438694.001
]
[Cites]
Biochem J. 2001 Sep 1;358(Pt 2):497-503
[
11513750.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10320-5
[
11504907.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10314-9
[
11504908.001
]
[Cites]
Microbiol Mol Biol Rev. 2001 Sep;65(3):463-79, table of contents
[
11528006.001
]
[Cites]
Endocr Relat Cancer. 2001 Sep;8(3):249-58
[
11566616.001
]
[Cites]
Prog Mol Subcell Biol. 2001;26:115-54
[
11575164.001
]
[Cites]
Mol Microbiol. 2001 Sep;41(6):1339-47
[
11580838.001
]
[Cites]
Genes Dev. 2001 Nov 1;15(21):2852-64
[
11691836.001
]
[Cites]
Science. 2001 Nov 2;294(5544):1102-5
[
11691993.001
]
[Cites]
Mol Biol Cell. 2001 Nov;12(11):3428-38
[
11694578.001
]
[Cites]
Trends Biochem Sci. 2001 Nov;26(11):657-64
[
11701324.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):1047-52
[
11792863.001
]
[Cites]
Mol Cell Biol. 2002 Mar;22(6):1674-83
[
11865047.001
]
[Cites]
Hum Mol Genet. 2002 Mar 1;11(5):525-34
[
11875047.001
]
[Cites]
J Biol Chem. 2003 May 30;278(22):19667-73
[
12665511.001
]
[Cites]
Biochem Biophys Res Commun. 1998 Oct 20;251(2):520-6
[
9792806.001
]
[Cites]
Mol Pharmacol. 1998 Nov;54(5):815-24
[
9804616.001
]
[Cites]
Cancer Res. 1998 Nov 1;58(21):4766-70
[
9809973.001
]
[Cites]
Biochem J. 1998 Nov 15;336 ( Pt 1):39-48
[
9806882.001
]
[Cites]
EMBO J. 1998 Nov 16;17(22):6649-59
[
9822608.001
]
[Cites]
EMBO J. 1998 Dec 1;17(23):6924-31
[
9843498.001
]
[Cites]
J Biol Chem. 1999 Jan 8;274(2):1058-65
[
9873051.001
]
[Cites]
Annu Rev Cell Dev Biol. 1998;14:305-38
[
9891786.001
]
[Cites]
Biochem Pharmacol. 1999 Feb 15;57(4):321-8
[
9933020.001
]
[Cites]
J Biol Chem. 2003 Aug 8;278(32):29655-60
[
12777372.001
]
[Cites]
Curr Opin Pharmacol. 2003 Aug;3(4):371-7
[
12901945.001
]
[Cites]
Curr Biol. 2003 Aug 5;13(15):1259-68
[
12906785.001
]
[Cites]
J Biol Chem. 2003 Aug 29;278(35):32493-6
[
12842888.001
]
[Cites]
Cancer Cell. 2003 Aug;4(2):147-58
[
12957289.001
]
[Cites]
Cancer Res. 2003 Sep 1;63(17):5173-7
[
14500340.001
]
[Cites]
J Biol Chem. 2003 Sep 26;278(39):37288-96
[
12867426.001
]
[Cites]
EMBO J. 2003 Oct 1;22(19):5102-14
[
14517248.001
]
[Cites]
J Biol Chem. 2003 Oct 10;278(41):39921-30
[
12869548.001
]
[Cites]
Mol Cell. 2003 Aug;12(2):271-80
[
14536067.001
]
[Cites]
J Biol Chem. 2003 Oct 17;278(42):40717-22
[
12912989.001
]
[Cites]
Curr Top Microbiol Immunol. 2004;279:299-319
[
14560965.001
]
[Cites]
Trends Biochem Sci. 2003 Nov;28(11):573-6
[
14607085.001
]
[Cites]
EMBO J. 2003 Nov 17;22(22):6045-56
[
14609951.001
]
[Cites]
Mol Cell Biol. 2003 Dec;23(23):8862-77
[
14612424.001
]
[Cites]
Curr Biol. 2003 Nov 11;13(22):2004-8
[
14614828.001
]
[Cites]
Science. 2003 Nov 14;302(5648):1208-12
[
14615539.001
]
[Cites]
Cell. 2003 Nov 26;115(5):577-90
[
14651849.001
]
[Cites]
Cancer Cell. 2003 Nov;4(5):343-8
[
14667501.001
]
[Cites]
J Biol Chem. 2003 Dec 19;278(51):51372-9
[
14551205.001
]
[Cites]
J Biol Chem. 2004 Jan 2;279(1):772-8
[
14578359.001
]
[Cites]
J Biol Chem. 2004 Jan 23;279(4):2737-46
[
14576155.001
]
[Cites]
Trends Biochem Sci. 2004 Jan;29(1):18-24
[
14729328.001
]
[Cites]
Trends Biochem Sci. 2004 Jan;29(1):32-8
[
14729330.001
]
[Cites]
EMBO J. 2004 Feb 25;23(4):833-43
[
14976552.001
]
[Cites]
Genes Dev. 2004 Feb 15;18(4):423-34
[
15004009.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3329-35
[
14985505.001
]
[Cites]
Mol Biol Cell. 1994 Jan;5(1):105-18
[
8186460.001
]
[Cites]
J Biol Chem. 1994 Jun 10;269(23):16333-9
[
8206940.001
]
[Cites]
Nature. 1994 Jun 30;369(6483):756-8
[
8008069.001
]
[Cites]
Cell. 1994 Jul 15;78(1):35-43
[
7518356.001
]
[Cites]
Nature. 1994 Oct 27;371(6500):762-7
[
7935836.001
]
[Cites]
Science. 1994 Oct 28;266(5185):653-6
[
7939721.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11477-81
[
7972087.001
]
[Cites]
Nature. 1994 Dec 8;372(6506):570-3
[
7990932.001
]
[Cites]
Int J Immunopharmacol. 1994 Sep;16(9):711-21
[
7528736.001
]
[Cites]
Trends Biochem Sci. 1999 Nov;24(11):437-40
[
10542411.001
]
[Cites]
Biochem J. 1999 Dec 1;344 Pt 2:427-31
[
10567225.001
]
[Cites]
J Biol Chem. 1999 Nov 26;274(48):34493-8
[
10567431.001
]
[Cites]
J Biol Chem. 1999 Dec 3;274(49):34758-64
[
10574945.001
]
[Cites]
Nature. 1999 Dec 9;402(6762):689-92
[
10604478.001
]
[Cites]
Annu Rev Cell Dev Biol. 1999;15:1-32
[
10611955.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14866-70
[
10611304.001
]
[Cites]
Genes Dev. 1999 Dec 15;13(24):3271-9
[
10617575.001
]
[Cites]
Curr Biol. 2000 Jan 13;10(1):47-50
[
10660304.001
]
[Cites]
Genetics. 2000 Feb;154(2):787-801
[
10655230.001
]
[Cites]
J Biol Chem. 2000 Mar 10;275(10):7416-23
[
10702316.001
]
[Cites]
J Biol Chem. 2000 Apr 14;275(15):11198-206
[
10753927.001
]
[Cites]
Mol Cell Biol. 2000 May;20(10):3558-67
[
10779345.001
]
[Cites]
Genetics. 2000 Jun;155(2):611-22
[
10835385.001
]
[Cites]
Mol Endocrinol. 2000 Jun;14(6):783-94
[
10847581.001
]
[Cites]
Mol Cell Biol. 2000 Jul;20(13):4604-13
[
10848587.001
]
[Cites]
Annu Rev Biochem. 1999;68:913-63
[
10872469.001
]
[Cites]
Curr Biol. 2000 Jul 13;10(14):861-4
[
10899009.001
]
[Cites]
Cancer Res. 2000 Jul 1;60(13):3504-13
[
10910062.001
]
[Cites]
Biochem Biophys Res Commun. 2000 Aug 18;275(1):115-20
[
10944451.001
]
[Cites]
J Cell Biol. 2000 Sep 18;150(6):1507-13
[
10995454.001
]
[Cites]
Eur J Biochem. 2000 Nov;267(21):6321-30
[
11029573.001
]
[Cites]
Cell. 2000 Oct 13;103(2):253-62
[
11057898.001
]
[Cites]
Genes Dev. 2000 Nov 1;14(21):2689-94
[
11069885.001
]
[Cites]
Genes Dev. 2000 Nov 1;14(21):2712-24
[
11069888.001
]
[Cites]
J Cell Biol. 2000 Nov 13;151(4):863-78
[
11076970.001
]
[Cites]
Am J Hum Genet. 2001 Jan;68(1):64-80
[
11112665.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):559-65
[
12766775.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):566-71
[
12766776.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):578-81
[
12771962.001
]
[Cites]
Am J Physiol Gastrointest Liver Physiol. 2003 Jul;285(1):G115-27
[
12646420.001
]
[Cites]
EMBO J. 2003 Jun 16;22(12):3062-72
[
12805220.001
]
[Cites]
Mol Cell. 2003 Jun;11(6):1457-66
[
12820960.001
]
[Cites]
Mol Cell. 2003 Jun;11(6):1467-78
[
12820961.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8839-43
[
12847291.001
]
[Cites]
Genes Dev. 2003 Aug 1;17(15):1829-34
[
12869586.001
]
(PMID = 15755954.001).
[ISSN]
1092-2172
[Journal-full-title]
Microbiology and molecular biology reviews : MMBR
[ISO-abbreviation]
Microbiol. Mol. Biol. Rev.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
[Number-of-references]
279
[Other-IDs]
NLM/ PMC1082789
60.
Dubbeldam D, Beerdsen E, Calero S, Smit B:
Dynamically corrected transition state theory calculations of self-diffusion in anisotropic nanoporous materials.
J Phys Chem B
; 2006 Feb 23;110(7):3164-72
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Dynamically corrected
transition state
theory calculations of self-diffusion in anisotropic nanoporous materials.
We apply the dynamically corrected
transition state
theory to confinements with
complex structures
.
This method is able to compute self-diffusion coefficients for adsorbate-adsorbent systems far beyond the
time
scales accessible to molecular dynamics.
The anisotropic behavior of ERI-type cages reverses with loading, i.e., at
low
loading the diffusion in the z direction is two times faster than in the xy direction, while for higher loadings this changes
to a
z diffusivity that is more than two times slower.
At
low
loading the diffusion is impeded by the eight-ring windows, i.e., the exits out of the cage to the next, but at higher loadings the barrier is formed by the center of the cages.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16494324.001).
[ISSN]
1520-6106
[Journal-full-title]
The journal of physical chemistry. B
[ISO-abbreviation]
J Phys Chem B
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
61.
Di Nardo A, Kramvis I, Cho N, Sadowski A, Meikle L, Kwiatkowski DJ, Sahin M:
Tuberous sclerosis complex activity is required to control neuronal stress responses in an mTOR-dependent manner.
J Neurosci
; 2009 May 6;29(18):5926-37
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Tuberous sclerosis complex
activity is required to control neuronal stress responses in an mTOR-dependent manner.
Tuberous sclerosis complex
(
TSC
) is a neurogenetic
disorder
caused by loss-of-function mutations in either the TSC1 or TSC2 genes and frequently results in prominent CNS manifestations, including
epilepsy
, mental retardation, and autism spectrum
disorder
.
The TSC1/TSC2 protein
complex
plays a major role in controlling the Ser/Thr kinase mammalian target of rapamycin (mTOR), which is a master regulator of protein synthesis and
cell
growth.
In this study, we show that endoplasmic reticulum (ER) stress regulates TSC1/TSC2
complex to
limit mTOR activity.
In addition, Tsc2-deficient rat hippocampal neurons and
brain
lysates from a Tsc1-deficient mouse model demonstrate both elevated ER and oxidative stress.
Neurons lacking a functional TSC1/TSC2
complex
have increased vulnerability to ER stress-induced
cell
death via the activation of the mitochondrial death pathway.
These observations indicate that ER stress modulates mTOR activity through the
TSC
protein
complex
and that ER stress is elevated in
cells
lacking this
complex
.
They also suggest that some of the neuronal dysfunction and neurocognitive deficits seen in
TSC
patients may be attributable to ER and oxidative stress and therefore potentially responsive to agents moderating these pathways.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
L-SERINE
.
Hazardous Substances Data Bank.
L-Threonine
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
antibodies-online.
View related products from antibodies-online.com
(subscription/membership/fee required).
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Biochim Biophys Acta. 2008 Apr;1783(4):549-56
[
18191641.001
]
[Cites]
Science. 2000 Jan 28;287(5453):664-6
[
10650002.001
]
[Cites]
Cell. 2000 May 26;101(5):451-4
[
10850487.001
]
[Cites]
Nat Cell Biol. 2000 Jun;2(6):326-32
[
10854322.001
]
[Cites]
Mol Cell Biol. 2000 Jul;20(14):5096-106
[
10866666.001
]
[Cites]
J Biol Chem. 2000 Aug 11;275(32):24881-5
[
10835430.001
]
[Cites]
Mol Cell Biol. 2001 Feb;21(4):1249-59
[
11158311.001
]
[Cites]
Free Radic Biol Med. 2000 Jan 15;28(2):289-309
[
11281297.001
]
[Cites]
J Biol Chem. 2001 Sep 7;276(36):33869-74
[
11448953.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):10996-1002
[
11572959.001
]
[Cites]
Nat Cell Biol. 2001 Nov;3(11):E255-63
[
11715037.001
]
[Cites]
Mol Cell. 2000 Nov;6(5):1099-108
[
11106749.001
]
[Cites]
Genes Dev. 2002 Feb 15;16(4):452-66
[
11850408.001
]
[Cites]
J Mol Biol. 2002 May 17;318(5):1351-65
[
12083523.001
]
[Cites]
Epilepsia. 2002;43 Suppl 5:217-9
[
12121324.001
]
[Cites]
Eur J Pharmacol. 2002 Jul 5;447(2-3):141-54
[
12151006.001
]
[Cites]
Mol Cell. 2002 Jul;10(1):151-62
[
12150915.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):648-57
[
12172553.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):658-65
[
12172554.001
]
[Cites]
Free Radic Biol Med. 2002 Sep 1;33(5):715-23
[
12208358.001
]
[Cites]
J Clin Invest. 2002 Nov;110(10):1389-98
[
12438434.001
]
[Cites]
Free Radic Res. 2002 Nov;36(11):1139-46
[
12592665.001
]
[Cites]
Mol Cell. 2003 Mar;11(3):619-33
[
12667446.001
]
[Cites]
J Biol Chem. 2003 May 16;278(20):17680-7
[
12637535.001
]
[Cites]
Trends Cell Biol. 2004 Jan;14(1):20-8
[
14729177.001
]
[Cites]
Cell Death Differ. 2004 Apr;11(4):381-9
[
14685163.001
]
[Cites]
Ann N Y Acad Sci. 2004 Mar;1012:84-93
[
15105257.001
]
[Cites]
Ann Neurol. 2008 Apr;63(4):444-53
[
18389497.001
]
[Cites]
J Neurosci. 2008 May 21;28(21):5422-32
[
18495876.001
]
[Cites]
Nat Med. 2008 Aug;14(8):843-8
[
18568033.001
]
[Cites]
Genes Dev. 2008 Sep 15;22(18):2485-95
[
18794346.001
]
[Cites]
Science. 2008 Nov 7;322(5903):963-6
[
18988856.001
]
[Cites]
Curr Med Chem. 2004 Jun;11(12):1545-61
[
15180563.001
]
[Cites]
Mol Cell. 2004 Sep 10;15(5):767-76
[
15350220.001
]
[Cites]
Ann Neurol. 2004 Oct;56(4):478-87
[
15455405.001
]
[Cites]
EMBO J. 1992 Apr;11(4):1563-71
[
1373378.001
]
[Cites]
Science. 1993 Jun 25;260(5116):1946-50
[
8100368.001
]
[Cites]
Nature. 1993 Jul 8;364(6433):147-9
[
8321285.001
]
[Cites]
Neuron. 1996 Feb;16(2):345-55
[
8789949.001
]
[Cites]
EMBO J. 1998 Jul 1;17(13):3619-30
[
9649432.001
]
[Cites]
Biochim Biophys Acta. 1998 Aug 10;1366(1-2):211-23
[
9714810.001
]
[Cites]
Biochem J. 1999 Apr 1;339 ( Pt 1):135-41
[
10085237.001
]
[Cites]
J Biol Chem. 2004 Nov 19;279(47):49420-9
[
15339911.001
]
[Cites]
Free Radic Biol Med. 2004 Dec 15;37(12):1995-2011
[
15544918.001
]
[Cites]
Genes Dev. 2004 Dec 15;18(24):3066-77
[
15601821.001
]
[Cites]
Neuron. 2005 Apr 21;46(2):191-204
[
15848799.001
]
[Cites]
Mol Ther. 2005 Jun;11(6):932-40
[
15922964.001
]
[Cites]
Hum Mol Genet. 2005 Oct 15;14 Spec No. 2:R251-8
[
16244323.001
]
[Cites]
Nat Neurosci. 2005 Dec;8(12):1727-34
[
16286931.001
]
[Cites]
Cancer Res. 2005 Dec 1;65(23):10881-90
[
16322235.001
]
[Cites]
Neurology. 2006 Jan 24;66(2 Suppl 1):S102-9
[
16432136.001
]
[Cites]
Curr Mol Med. 2006 Feb;6(1):55-69
[
16472113.001
]
[Cites]
Science. 2006 Feb 17;311(5763):1008-12
[
16484497.001
]
[Cites]
J Neuropathol Exp Neurol. 2006 Mar;65(3):217-25
[
16651883.001
]
[Cites]
Epilepsy Res. 2006 Aug;70 Suppl 1:S206-17
[
16860540.001
]
[Cites]
N Engl J Med. 2006 Sep 28;355(13):1345-56
[
17005952.001
]
[Cites]
Mol Cell. 2006 Oct 20;24(2):185-97
[
17052453.001
]
[Cites]
J Neurosci. 2007 Jan 24;27(4):901-8
[
17251432.001
]
[Cites]
Neuroscience. 2007 Apr 14;145(4):1233-48
[
17303344.001
]
[Cites]
J Neurosci. 2007 May 23;27(21):5546-58
[
17522300.001
]
[Cites]
Brain Res. 2007 Jun 4;1152:27-31
[
17434462.001
]
[Cites]
Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29
[
17565364.001
]
[Cites]
Int Rev Neurobiol. 2007;82:297-325
[
17678968.001
]
[Cites]
J Biol Chem. 2008 Feb 15;283(7):4252-60
[
18086661.001
]
[Cites]
Mol Cell. 2008 Mar 14;29(5):541-51
[
18342602.001
]
(PMID = 19420259.001).
[ISSN]
1529-2401
[Journal-full-title]
The Journal of neuroscience : the official journal of the Society for Neuroscience
[ISO-abbreviation]
J. Neurosci.
[Language]
ENG
[Grant]
United States / NICHD NIH HHS / HD / P30 HD018655; United States / NINDS NIH HHS / NS / R01 NS058956-02; United States / NINDS NIH HHS / NS / P01 NS024279; United States / NINDS NIH HHS / NS / R01 NS058956; United States / NINDS NIH HHS / NS / NS058956-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Carrier Proteins; 0 / Ddit3 protein, mouse; 0 / Lactones; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / Sesquiterpenes; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; 11089-65-9 / Tunicamycin; 147336-12-7 / Transcription Factor CHOP; 2ZD004190S / Threonine; 452VLY9402 / Serine; 4JG2LF96VF / tuberous sclerosis complex 2 protein; 67526-94-7 / thapsigargicin; EC 1.14.99.3 / Heme Oxygenase-1; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.1.1 / mTOR protein, rat
[Other-IDs]
NLM/ NIHMS115539; NLM/ PMC2691854
62.
Ess DH, Nielsen RJ, Goddard WA 3rd, Periana RA:
Transition-state charge transfer reveals electrophilic, ambiphilic, and nucleophilic carbon-hydrogen bond activation.
J Am Chem Soc
; 2009 Aug 26;131(33):11686-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Transition
-
state
charge transfer reveals electrophilic, ambiphilic, and nucleophilic carbon-hydrogen bond activation.
Absolutely localized molecular orbital energy decomposition analysis of C-H activation
transition states
(TSs), including Pt, Au, Ir, Ru, W, Sc, and Re metal centers, shows an electrophilic, ambiphilic, and nucleophilic charge transfer (CT) continuum irrespective of the bonding paradigm (oxidative addition, sigma-bond metathesis, oxidative hydrogen migration, 1,2-substitution).
In this ambiphilic activation regime, an increase in one direction of CT typically leads
to a
decrease in the reverse direction.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19653684.001).
[ISSN]
1520-5126
[Journal-full-title]
Journal of the American Chemical Society
[ISO-abbreviation]
J. Am. Chem. Soc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
63.
Cohen E, Sade M, Benarroch F, Pollak Y, Gross-Tsur V:
Locus of control, perceived parenting style, and symptoms of anxiety and depression in children with Tourette's syndrome.
Eur Child Adolesc Psychiatry
; 2008 Aug;17(5):299-305
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Locus of control, perceived parenting style, and symptoms of anxiety and depression in children with Tourette's
syndrome
.
AIM: This study explored the contribution of two psychosocial factors, locus of control (LOC) and perceived parenting style, to symptoms of internalizing disorders in children with Tourette
syndrome
(
TS
).
This contribution was further evaluated in relation
to TS
severity.
METHODS: Sixty-five children (53 boys, 12 girls) ages 9.0-16.9 years, of normal
intelligence
, completed questionnaires evaluating their depression and anxiety symptoms, LOC, and maternal parenting style.
Their mothers rated
TS
severity, determined by tic severity, symptoms of attention-deficit hyperactivity
disorder
(ADHD) and obsessive compulsive symptoms (OCS).
CONCLUSIONS: Rates of symptoms of anxiety and depression in children with
TS
are markedly influenced by psychosocial factors, extending beyond the influence of ADHD and OCD, both common comorbid disorders in
TS
.
[MeSH-major]
Anxiety Disorders / psychology. Conduct
Disorder
/ psychology. Depressive
Disorder
/ psychology. Internal-External Control. Parenting / psychology. Tourette
Syndrome
/ psychology
[MeSH-minor]
Adolescent. Attention Deficit
Disorder
with Hyperactivity /
diagnosis
. Attention Deficit
Disorder
with Hyperactivity / psychology. Child. Comorbidity. Female. Humans. Israel. Male. Obsessive-Compulsive
Disorder
/
diagnosis
. Obsessive-Compulsive
Disorder
/ psychology. Personality Assessment. Personality Inventory. Risk Factors
Genetic Alliance.
consumer health - Depression
.
Genetic Alliance.
consumer health - Anxiety
.
MedlinePlus Health Information.
consumer health - Anxiety
.
MedlinePlus Health Information.
consumer health - Parenting
.
MedlinePlus Health Information.
consumer health - Tourette Syndrome
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Br J Psychiatry. 1994 Feb;164(2):215-21
[
8173824.001
]
[Cites]
Psychol Bull. 1998 Sep;124(2):197-229
[
9747186.001
]
[Cites]
J Abnorm Child Psychol. 1978 Jun;6(2):221-36
[
670589.001
]
[Cites]
J Child Psychol Psychiatry. 2007 Feb;48(2):157-66
[
17300554.001
]
[Cites]
Am J Psychiatry. 2006 Jun;163(6):1066-73
[
16741208.001
]
[Cites]
Eur Child Adolesc Psychiatry. 2002 Dec;11(6):261-5
[
12541004.001
]
[Cites]
Soc Sci Med. 2002 May;54(9):1453-61
[
12058860.001
]
[Cites]
Arch Gen Psychiatry. 1989 Nov;46(11):1006-11
[
2684084.001
]
[Cites]
Am J Psychiatry. 1997 Feb;154(2):274-6
[
9016283.001
]
[Cites]
J Child Psychol Psychiatry. 2003 Jan;44(1):134-51
[
12553416.001
]
[Cites]
J Am Acad Child Adolesc Psychiatry. 2002 Oct;41(10):1150-81
[
12364838.001
]
[Cites]
Annu Rev Psychol. 1998;49:377-412
[
9496627.001
]
[Cites]
J Am Acad Child Adolesc Psychiatry. 2003 Jan;42(1):98-105
[
12500082.001
]
[Cites]
J Child Psychol Psychiatry. 2000 Feb;41(2):215-23
[
10750547.001
]
[Cites]
J Consult Clin Psychol. 2006 Feb;74(1):89-98
[
16551146.001
]
[Cites]
Epilepsia. 1999 Feb;40(2):216-24
[
9952270.001
]
[Cites]
J Am Acad Child Adolesc Psychiatry. 2006 Nov;45(11):1354-62
[
17075358.001
]
[Cites]
J Behav Med. 1996 Jun;19(3):289-305
[
8740470.001
]
[Cites]
Lancet Neurol. 2005 Mar;4(3):149-59
[
15721825.001
]
[Cites]
Child Dev. 1965 Jun;36:413-24
[
14300862.001
]
[Cites]
J Pediatr. 2007 Jul;151(1):56-60, 60.e1
[
17586191.001
]
[Cites]
J Am Acad Child Adolesc Psychiatry. 1989 Jul;28(4):566-73
[
2768151.001
]
[Cites]
J Am Acad Child Adolesc Psychiatry. 2000 May;39(5):562-8
[
10802973.001
]
[Cites]
J Am Acad Child Adolesc Psychiatry. 2003 Sep;42(9):1015-37
[
12960702.001
]
[Cites]
J Abnorm Child Psychol. 1978 Jun;6(2):271-80
[
670592.001
]
[Cites]
Psychol Bull. 1998 Jul;124(1):3-21
[
9670819.001
]
(PMID = 18301938.001).
[ISSN]
1018-8827
[Journal-full-title]
European child & adolescent psychiatry
[ISO-abbreviation]
Eur Child Adolesc Psychiatry
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
64.
Elsässer B, Valiev M, Weare JH:
A dianionic phosphorane intermediate and transition states in an associative A(N)+D(N) mechanism for the ribonucleaseA hydrolysis reaction.
J Am Chem Soc
; 2009 Mar 25;131(11):3869-71
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A dianionic phosphorane intermediate and
transition states
in an associative A(N)+D(N) mechanism for the ribonucleaseA hydrolysis reaction.
Most of this debate centers around the roles of the conserved residues,
structures
of the
transition state
or
states
, the possibility of a stable intermediate, and the charge and
structure
of this intermediate.
In the
transition state
in the path from the reactant to the intermediate
state
(with barrier of 3.96 kcal/mol and intermediate stability of 2.21 kcal/mol) a proton from the attacking water is partially transferred to the His119 residue and the PO bond only partially formed from the remaining nucleophilic OH(-) species (bond order (BO) 0.11).
In passing from the intermediate to the product
state
(barrier 13.22 kcal/mol) the PO bond on the cyclic phosphorane intermediate is nearly broken (BO 0.28) and the transfer of the proton from the Lys41 is almost complete (Lys41-H BO 0.87).
In the product
state a
proton has been transferred from Lys41 to the O2' position of the sugar.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19245210.001).
[ISSN]
1520-5126
[Journal-full-title]
Journal of the American Chemical Society
[ISO-abbreviation]
J. Am. Chem. Soc.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Phosphoranes; EC 3.1.27.5 / Ribonuclease, Pancreatic
65.
Swaroop Mr, Nischal Kc, Rajesh Gowda Cm, Umashankar Nu, Basavaraj Hb, Sathyanarayana Bd:
Radiofrequency ablation of adenoma sebaceum.
J Cutan Aesthet Surg
; 2008 Jul;1(2):89-91
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Radiofrequency ablation of
adenoma sebaceum
.
Adenoma sebaceum
is one of the diagnostic features of
tuberous sclerosis
.
Laser treatment is expensive and any form of treatment for
adenoma sebaceum
is not a one-
time
procedure but is a recurring process as the condition is genetic in aetiology.
We hereby report a case of
tuberous sclerosis
in whom we ablated the lesions by radiofrequency technique with acceptable results.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Dermatol. 2004 Jan;31(1):42-6
[
14739503.001
]
[Cites]
Ann Plast Surg. 1992 Apr;28(4):377-80
[
1317695.001
]
[Cites]
Ann Plast Surg. 2001 Mar;46(3):332-5
[
11293529.001
]
[Cites]
Br J Plast Surg. 2005 Dec;58(8):1143-7
[
16061214.001
]
[Cites]
Actas Dermosifiliogr. 2005 Oct;96(8):498-503
[
16476284.001
]
[Cites]
Ann Plast Surg. 2006 Oct;57(4):415-7
[
16998334.001
]
[Cites]
Arch Dermatol. 1997 Jul;133(7):853-7
[
9236523.001
]
[Cites]
HNO. 2007 Dec;55(13):1009-11
[
17909732.001
]
[Cites]
Cutis. 2007 Oct;80(4):284-8
[
18038689.001
]
[Cites]
J Cutan Aesthet Surg. 2008 Jan;1(1):29-30
[
20300339.001
]
[Cites]
J Dermatol Surg Oncol. 1990 Apr;16(4):317-20
[
2157741.001
]
[Cites]
Ann Plast Surg. 1988 May;20(5):426-33
[
2837129.001
]
[Cites]
Ann Plast Surg. 1980 Feb;4(2):158-60
[
6245615.001
]
[Cites]
Indian J Dermatol Venereol Leprol. 2001 Nov-Dec;67(6):326-8
[
17664790.001
]
(PMID = 20300351.001).
[ISSN]
0974-5157
[Journal-full-title]
Journal of cutaneous and aesthetic surgery
[ISO-abbreviation]
J Cutan Aesthet Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC2840910
[Keywords]
NOTNLM ; Adenoma sebaceum / disfigurement / radiofrequency / tuberous sclerosis
66.
Fariña-Sarasqueta A, Gosens MJ, Moerland E, van Lijnschoten I, Lemmens VE, Slooter GD, Rutten HJ, van den Brule AJ:
TS gene polymorphisms are not good markers of response to 5-FU therapy in stage III colon cancer patients.
Anal Cell Pathol (Amst)
; 2010;33(1):1-11
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
TS
gene polymorphisms are not good markers of response to 5-FU therapy in stage III colon cancer patients.
AIM: Although the predictive and prognostic value of thymidylate synthase (
TS
) expression and gene polymorphism in colon cancer has been widely studied, the results are inconclusive probably because of methodological differences.
With this study, we aimed to elucidate the role of
TS
gene polymorphisms genotyping in therapy response in stage III colon carcinoma patients treated with 5-FU adjuvant chemotherapy.
The variable number of tandem repeats (VNTR) and the single nucleotide polymorphism (SNP) in the 5'-untranslated region of the
TS
gene were genotyped.
CONCLUSION: We conclude that the
TS
VNTR and SNP do not predict response to 5-FU therapy in patients with stage III colon carcinoma.
However, age appears to modify the effects of
TS
polymorphisms on survival.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
Cell Oncol (Dordr). 2011 Aug;34(4):407-8
(PMID = 20966539.001).
[ISSN]
2210-7185
[Journal-full-title]
Analytical cellular pathology (Amsterdam)
[ISO-abbreviation]
Anal Cell Pathol (Amst)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; EC 2.1.1.45 / Thymidylate Synthase; U3P01618RT / Fluorouracil
[Other-IDs]
NLM/ PMC4605551
67.
Mink JW, Walkup J, Frey KA, Como P, Cath D, Delong MR, Erenberg G, Jankovic J, Juncos J, Leckman JF, Swerdlow N, Visser-Vandewalle V, Vitek JL, Tourette Syndrome Association, Inc:
Patient selection and assessment recommendations for deep brain stimulation in Tourette syndrome.
Mov Disord
; 2006 Nov;21(11):1831-8
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Patient selection and assessment recommendations for deep
brain stimulation
in Tourette
syndrome
.
In response to recent publicity regarding the potential use of deep
brain stimulation
(DBS) for reducing tic severity in Tourette's
syndrome
(
TS
), the Tourette
Syndrome
Association convened a group of
TS
and DBS experts to develop recommendations to guide the early use and potential clinical trials of DBS for
TS
and other tic disorders.
[MeSH-major]
Deep
Brain Stimulation
/ methods. Health Planning Guidelines. Patient Selection. Tourette
Syndrome
/ therapy
Genetic Alliance.
consumer health - Tourette Syndrome
.
MedlinePlus Health Information.
consumer health - Tourette Syndrome
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[CommentIn]
Mov Disord. 2007 Jul 15;22(9):1366; author reply 1367-8
[
17516487.001
]
[CommentIn]
Mov Disord. 2007 Jul 15;22(9):1366-7; author reply 1367-8
[
17469199.001
]
(PMID = 16991144.001).
[ISSN]
0885-3185
[Journal-full-title]
Movement disorders : official journal of the Movement Disorder Society
[ISO-abbreviation]
Mov. Disord.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
68.
Tang R, Yu B, Zhang K, Chen D:
Effects of supplementing two levels of magnesium aspartate and transportation stress on pork quality and gene expression of micro-calpain and calpastatin of finishing pigs.
Arch Anim Nutr
; 2008 Oct;62(5):415-25
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Then six pigs from each dietary treatment were subjected either to no transportation stress (NTS) or 2 h of transportation stress (
TS
).
Transportation stress resulted in higher
concentrations
(p < 0.01) of serum calcium, glucose and cortisol, lower pH (p < 0.01), higher Warner-Bratzler shear force (WBSF) (p < 0.05) and higher calpastatin mRNA abundance (p = 0.05) of longissimus muscle (LM) compared with NTS treatments.
Supplementation of MgAsp in
TS
treatments increased serum Mg
concentration
(p < 0.05) at 2000 mg of Mg/kg, reduced drip loss (p < 0.05) and improved pork quality colour (p < 0.05) at 2000 mg of Mg/kg, and decreased 1-day and 3-day WBSF (p < 0.05) at 1000 mg of Mg/kg compared with
TS
treatments fed the control diet.
[MeSH-minor]
Animal Feed. Animal Nutritional Physiological Phenomena / physiology. Animals. Dietary Supplements. Dose-Response Relationship, Drug. Male. Muscle, Skeletal / chemistry. Muscle, Skeletal / drug effects. RNA, Messenger / metabolism. Random Allocation.
Time
Factors. Transportation
MedlinePlus Health Information.
consumer health - Stress
.
Hazardous Substances Data Bank.
(L)-ASPARTIC ACID
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 18942588.001).
[ISSN]
1745-039X
[Journal-full-title]
Archives of animal nutrition
[ISO-abbreviation]
Arch Anim Nutr
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Calcium-Binding Proteins; 0 / RNA, Messenger; 30KYC7MIAI / Aspartic Acid; 79079-11-1 / calpastatin; EC 3.4.22.- / Calpain
69.
Waters T, O'Hair RA:
Endocyclic versus exocyclic mechanisms for methyl migration in protonated N,N'-dimethylpropane-1,3-diamine.
Eur J Mass Spectrom (Chichester)
; 2009;15(2):105-12
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
A recent paper has suggested that an endocyclic methyl transfer pathway occurs in competition with methylamine loss for protonated N,N'-dimethylpropane-1,3-diamine under conditions of
low
-energy collision induced dissociation [X. Zhang, S. Yao and Y.
Therefore, in order to gain additional insights into the competition between methylamine loss and methyl transfer in this
system
, DFT calculations were performed at the B3LYP/6-311+G(d,p) level of theory for a number of competing mechanisms.
Three mechanisms were considered for loss of methylamine: (i) a 1,2-elimination reaction to give N-methylallylamine (
TS
= 276.7 kJ mol(-1));.
(ii) a neighbouring group reaction to give N-methylazitidine (
TS
= 146.4 kJ mol(-1)); and (iii) a 1,3-hydride shift to give N-methyl-1-propylimine (
TS
= 248.5 kJ mol(-1)).
Accordingly, the neighbouring group pathway is expected to be kinetically favoured and dominate under conditions of
low
-energy collision-induced dissociation.
Similarly, three different mechanisms were considered for intramolecular methyl transfer: (i) the previously proposed endocyclic reaction involving backside attack with inversion of configuration (
TS
= 252.3 kJ mol(-1));.
(ii) the previously proposed endocyclic reaction involving frontside attack with retention of configuration (
TS
= 272.4 kJ mol(-1));.
(iii) a multi-step mechanism which combines the neighbouring group pathway for methylamine loss and combinations of S(N)2 and proton transfer reactions within a series of ion-molecule complexes (highest
TS
= 201.7 kJ mol(-1)).
These results suggest that the alternative pathway proposed here for methyl transfer should be preferred under conditions of
low
energy collision- induced dissociation.
Hazardous Substances Data Bank.
METHANE
.
Hazardous Substances Data Bank.
METHYLAMINE
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19423897.001).
[ISSN]
1469-0667
[Journal-full-title]
European journal of mass spectrometry (Chichester, England)
[ISO-abbreviation]
Eur J Mass Spectrom (Chichester)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Diamines; 0 / Ions; 0 / Methylamines; 0 / N,N'-dimethylpropane-1,3-diamine; 0 / Protons; 2229-07-4 / methyl radical; BSF23SJ79E / methylamine; OP0UW79H66 / Methane
70.
Lesma E, Sirchia SM, Ancona S, Carelli S, Bosari S, Ghelma F, Montanari E, Di Giulio AM, Gorio A:
The methylation of the TSC2 promoter underlies the abnormal growth of TSC2 angiomyolipoma-derived smooth muscle cells.
Am J Pathol
; 2009 Jun;174(6):2150-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
The methylation of the TSC2 promoter underlies the abnormal growth of TSC2 angiomyolipoma-derived smooth muscle
cells
.
Tuberous sclerosis complex
(
TSC
) is an autosomal-dominant
disease
that is caused by mutations in either the TSC1 or TSC2 gene.
Smooth muscle-like
cells
(ASMs) were isolated from an angiomyolipoma of a patient with
TSC
.
These
cells
lacked tuberin, were labeled by both HMB45 and CD44v6 antibodies, and had constitutive S6 phosphorylation.
The
cells
bear a germline TSC2 intron 8-exon 9 junction mutation, but DNA analysis and polymerase chain reaction amplification failed to demonstrate loss of heterozygosity.
These
cells
were named TSC2(-/meth) ASMs.
In addition, rapamycin effectively blocked the proliferation of these
cells
.
Our data show for the first
time
that methylation of the TSC2 promoter might cause a complete loss of tuberin in TSC2
cells
, and that the pathogenesis of angiomyolipomas might also originate from epigenetic defects in smooth muscle
cells
.
Additionally, the effect of chromatin-remodeling agents in these
cells
suggests a further avenue for the treatment of
TSC
as well as lymphangioleiomyomatosis.
[MeSH-minor]
Adult. Antibiotics, Antineoplastic / pharmacology. Antigens, Neoplasm. Apoptosis / drug effects. Blotting, Western.
Cell
Proliferation / drug effects. DNA Mutational Analysis. Germ-Line Mutation. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Kidney Neoplasms / genetics. Kidney Neoplasms / metabolism. Kidney Neoplasms / pathology. Male. Melanoma-Specific Antigens. Microscopy, Fluorescence. Neoplasm Proteins. Promoter Regions, Genetic / genetics. Sirolimus / pharmacology.
Tuberous Sclerosis
/ complications.
Tuberous Sclerosis
/ genetics.
Tuberous Sclerosis
/ pathology
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
SIROLIMUS
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
PLoS One. 2008;3(10):e3558
[
18958173.001
]
[Cites]
BMC Cancer. 2008;8:163
[
18538015.001
]
[Cites]
Am J Hum Genet. 1999 Dec;65(6):1790-5
[
10577937.001
]
[Cites]
Hum Mol Genet. 2000 Feb 12;9(3):447-52
[
10655555.001
]
[Cites]
Oncogene. 2000 Mar 16;19(12):1556-63
[
10734315.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 May 23;97(11):6085-90
[
10823953.001
]
[Cites]
Hum Genet. 2000 Jun;106(6):663-8
[
10942116.001
]
[Cites]
Hum Genet. 2000 Aug;107(2):97-114
[
11030407.001
]
[Cites]
Oncogene. 2000 Dec 14;19(54):6306-16
[
11175345.001
]
[Cites]
Cell. 2001 May 4;105(3):345-55
[
11348591.001
]
[Cites]
Mutat Res. 2001 Jul;488(3):233-9
[
11397651.001
]
[Cites]
Am J Hum Genet. 2001 Sep;69(3):493-503
[
11468687.001
]
[Cites]
Am J Pathol. 2001 Aug;159(2):483-91
[
11485907.001
]
[Cites]
Cancer Res. 2002 May 1;62(9):2455-61
[
11980632.001
]
[Cites]
Mol Cell. 2003 Jun;11(6):1457-66
[
12820960.001
]
[Cites]
Genes Dev. 2003 Aug 1;17(15):1829-34
[
12869586.001
]
[Cites]
Clin Cancer Res. 2003 Aug 1;9(8):3034-41
[
12912953.001
]
[Cites]
Science. 1975 Jan 24;187(4173):226-32
[
1111098.001
]
[Cites]
Cell. 1993 Dec 31;75(7):1305-15
[
8269512.001
]
[Cites]
Nat Med. 1995 Jul;1(7):686-92
[
7585152.001
]
[Cites]
Am J Hum Genet. 1996 Aug;59(2):400-6
[
8755927.001
]
[Cites]
Science. 1997 Aug 8;277(5327):805-8
[
9242607.001
]
[Cites]
Adv Cancer Res. 1998;72:141-96
[
9338076.001
]
[Cites]
Am J Pathol. 1997 Dec;151(6):1639-47
[
9403714.001
]
[Cites]
EMBO J. 1998 Sep 1;17(17):4905-8
[
9724627.001
]
[Cites]
Mol Med Today. 1998 Jul;4(7):313-9
[
9743993.001
]
[Cites]
Semin Pediatr Neurol. 1998 Dec;5(4):269-75
[
9874854.001
]
[Cites]
Nat Genet. 1999 Feb;21(2):163-7
[
9988266.001
]
[Cites]
Curr Opin Genet Dev. 1999 Apr;9(2):158-63
[
10322130.001
]
[Cites]
Nat Genet. 2005 Jan;37(1):19-24
[
15624019.001
]
[Cites]
J Neuropathol Exp Neurol. 2004 Dec;63(12):1236-42
[
15624760.001
]
[Cites]
Genes Chromosomes Cancer. 2005 Mar;42(3):213-27
[
15578690.001
]
[Cites]
Cancer Res. 2005 Mar 15;65(6):2139-46
[
15781624.001
]
[Cites]
Cancer Res. 2005 Mar 15;65(6):2474-81
[
15781664.001
]
[Cites]
Eur J Cancer. 2005 Jul;41(11):1628-36
[
15951164.001
]
[Cites]
Am J Pathol. 2005 Oct;167(4):1093-103
[
16192644.001
]
[Cites]
Oncology (Williston Park). 2006 Apr;20(5 Suppl 2):15-25
[
16736979.001
]
[Cites]
Cell Mol Immunol. 2006 Aug;3(4):285-90
[
16978537.001
]
[Cites]
Nat Biotechnol. 2007 Jan;25(1):84-90
[
17211407.001
]
[Cites]
Mol Med. 2007 Mar-Apr;13(3-4):166-77
[
17592551.001
]
[Cites]
Cancer Res. 2007 Nov 1;67(21):10573-81
[
17975002.001
]
[Cites]
N Engl J Med. 2008 Jan 10;358(2):140-51
[
18184959.001
]
[Cites]
J Neurosci. 2008 May 21;28(21):5422-32
[
18495876.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):13825-30
[
10570157.001
]
(PMID = 19443708.001).
[ISSN]
1525-2191
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / Antigens, Neoplasm; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Proteins; 4JG2LF96VF / tuberous sclerosis complex 2 protein; W36ZG6FT64 / Sirolimus
[Other-IDs]
NLM/ PMC2684180
71.
Roca M, Andrés J, Moliner V, Tuñón I, Bertrán J:
On the nature of the transition state in catechol O-methyltransferase. A complementary study based on molecular dynamics and potential energy surface explorations.
J Am Chem Soc
; 2005 Aug 3;127(30):10648-55
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
On the nature of the
transition state
in catechol O-methyltransferase. A complementary study based on molecular dynamics and potential energy
surface
explorations.
From QM/MM optimizations, we will first analyze the participation of the environment on the
transition
vector.
The study of molecular dynamics trajectories will allow us to estimate the transmission coefficient from a previously localized
transition state
as the maximum in the potential of mean force profile.
The analysis of the reactive and nonreactive trajectories in the enzyme environment and in solution will also allow studying the geometrical and electronic changes, with special attention to the chemical
system
movements and the coupling with the environment.
The main result, coming from both analyses, is the approximation of the magnesium cation to the nucleophilic and the hydroxyl group of the catecholate as a result of a general movement of the protein, stabilizing in this way the
transition state
.
[MeSH-minor]
Catechols / chemistry. Catechols / metabolism. Models, Molecular. Quantum Theory.
Surface
Properties. Thermodynamics
Hazardous Substances Data Bank.
CATECHOL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16045352.001).
[ISSN]
0002-7863
[Journal-full-title]
Journal of the American Chemical Society
[ISO-abbreviation]
J. Am. Chem. Soc.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Catechols; EC 2.1.1.6 / Catechol O-Methyltransferase; LF3AJ089DQ / catechol
72.
Xu L, Doubleday CE, Houk KN:
Dynamics of 1,3-dipolar cycloaddition reactions of diazonium betaines to acetylene and ethylene: bending vibrations facilitate reaction.
Angew Chem Int Ed Engl
; 2009;48(15):2746-8
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Getting the bends: The dynamics of 1,3-dipolar cycloaddition reactions have been explored by decomposing
transition
vector, quasi-classical trajectories, and single trajectories.
Dipole bending (see picture) makes the largest contribution to the
TS
distortion energy and constitutes the major part of
transition
-
state
distortion energy in the favored concerted pathway.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19235191.001).
[ISSN]
1521-3773
[Journal-full-title]
Angewandte Chemie (International ed. in English)
[ISO-abbreviation]
Angew. Chem. Int. Ed. Engl.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
73.
Schmotzer CL, Brown AE, Roth S, Johnson J, Ines-Castillejo M, Reisner A, Hillyer CD, Josephson CD:
Procedure-specific preoperative red blood cell preparation and utilization management in pediatric surgical patients.
Transfusion
; 2010 Apr;50(4):861-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Procedure-specific preoperative red blood
cell
preparation and utilization management in pediatric surgical patients.
BACKGROUND: Data-driven practices in preoperative red blood
cell
(RBC) preparation for pediatric surgical procedures are not well established.
Resulting P:
Ts
were compared
to a
target P:T of 2:1.
Vp-max values were applied to the study data set to predict the impact on P:
Ts
and Vp.
CONCLUSIONS: P:
Ts
for pediatric surgical procedures at this institution indicate potentially excessive preoperative RBC preparations.
[MeSH-minor]
Blood Loss, Surgical / prevention & control. Blood Volume.
Brain
Neoplasms / surgery. Child. Craniotomy. Hospitals, Pediatric / statistics & numerical data. Humans. Medicine. Postoperative Hemorrhage / therapy. Retrospective Studies. Seizures / surgery. Skull / surgery
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 20003058.001).
[ISSN]
1537-2995
[Journal-full-title]
Transfusion
[ISO-abbreviation]
Transfusion
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
74.
Koizumi W, Tanabe S, Azuma M, Ishido K, Nishimura K, Sasaki T, Nakatani K, Higuchi K, Nakayama N, Katada C:
Impacts of fluorouracil-metabolizing enzymes on the outcomes of patients treated with S-1 alone or S-1 plus cisplatin for first-line treatment of advanced gastric cancer.
Int J Cancer
; 2010 Jan 1;126(1):162-70
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
In the present retrospective biomarker study, we aimed to develop a methodology to identify the patients with advanced gastric cancer who would respond better
to S
-1 alone than SP.
We studied 120 patients who received S-1 alone or SP for first-line chemotherapy for advanced gastric cancer, and quantitatively evaluated mRNA levels of thymidylate synthase (
TS
), thymidine phosphorylase (TP), orotate phosphoribosyltransferase (OPRT), dihydropyrimidine dehydrogenase, vascular endothelial growth factor-A, and epidermal growth factor receptor in paraffin-embedded specimens of primary tumors.
Multivariate survival analysis in patients who received S-1 monotherapy (66 patients) demonstrated that
low
TP expression (hazard ratio: 2.55 (95% CI: (1.33 to 4.89)),
low TS
(2.71 (1.36 to 5.37)), and high OPRT (0.33 (0.13 to 0.86)) were significant predictors of long overall survival.
In patients with lower expression of both TP and
TS
(n = 23) than their cutoff values, the S-1 alone group (n = 15) had longer overall survival than the SP group (n = 8; median overall survival, 18.2 months vs. 9.4 months), whereas the frequency of overall adverse events in the S-1 alone group tended to be lower than that in SP group.
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19588501.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase III; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Enzymes; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
75.
Nordmann JP, Mesbah M, Berdeaux G:
Scoring of visual field measured through Humphrey perimetry: principal component varimax rotation followed by validated cluster analysis.
Invest Ophthalmol Vis Sci
; 2005 Sep;46(9):3169-76
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The number and content of constituent variable scores were identified by principal components analysis followed by Varimax Rotation and simple clustering, taking spatial distribution homogeneity and visual
system
anatomy into account.
Six scores were identified: four peripheral scores (nasal superior, NS; nasal inferior, NI; temporal superior,
TS
; and temporal inferior, TI) and two paracentral scores (PCSs; superior, PCSS; and inferior, PCSI).
Scores of AC were lower in NS, NI, and
TS
; PCSS was less in PCS; BSE scores were less in
TS
and TI; NaS scores were less in NS and NI.
[MeSH-major]
Glaucoma /
diagnosis
. Vision Disorders /
diagnosis
. Visual Field Tests / methods. Visual Fields
MedlinePlus Health Information.
consumer health - Glaucoma
.
MedlinePlus Health Information.
consumer health - Vision Impairment and Blindness
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16123416.001).
[ISSN]
0146-0404
[Journal-full-title]
Investigative ophthalmology & visual science
[ISO-abbreviation]
Invest. Ophthalmol. Vis. Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
United States
76.
Zhang X, Bruice TC:
The proficiency of a thermophilic chorismate mutase enzyme is solely through an entropic advantage in the enzyme reaction.
Proc Natl Acad Sci U S A
; 2005 Dec 20;102(51):18356-60
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
The
transition state
(
TS
)
structures
and partial atom charges are much the same in the enzymatic and water reactions.
The difference in the electrostatic interactions of Arg-89 with O13 in the enzyme-substrate
complex
and enzyme-
TS complex
provides the latter with but 0.55 kcal/mol of 1.92 kcal/mol total
TS
stabilization.
Differences in electrostatic interactions between components at the active site in the enzyme-substrate
complex
and enzyme-
TS complex
are barely significant, such that
TS
stabilization is of minor importance and the enzymatic catalysis is through an entropic advantage.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Biochemistry. 2005 Aug 9;44(31):10443-8
[
16060652.001
]
[Cites]
Biochemistry. 2005 May 31;44(21):7805-17
[
15909995.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9032-7
[
11481470.001
]
[Cites]
Acc Chem Res. 2002 Mar;35(3):139-48
[
11900517.001
]
[Cites]
J Am Chem Soc. 2002 Mar 27;124(12):3093-124
[
11902900.001
]
[Cites]
J Am Chem Soc. 2003 Mar 19;125(11):3206-7
[
12630863.001
]
[Cites]
Angew Chem Int Ed Engl. 2003 Apr 4;42(13):1508-11
[
12698486.001
]
[Cites]
J Am Chem Soc. 2003 May 14;125(19):5964-72
[
12733937.001
]
[Cites]
J Am Chem Soc. 2003 Jun 4;125(22):6663-72
[
12769575.001
]
[Cites]
J Am Chem Soc. 2003 Jun 11;125(23):6892-9
[
12783541.001
]
[Cites]
J Am Chem Soc. 2003 Aug 27;125(34):10228-37
[
12926945.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12015-20
[
14523243.001
]
[Cites]
Arch Microbiol. 2004 Mar;181(3):195-203
[
14727008.001
]
[Cites]
J Mol Biol. 2004 Apr 9;337(5):1149-60
[
15046984.001
]
[Cites]
J Mol Biol. 1976 May 15;103(2):227-49
[
985660.001
]
[Cites]
Annu Rev Biophys Biophys Chem. 1989;18:431-92
[
2660832.001
]
[Cites]
J Mol Biol. 1989 Jul 5;208(1):159-81
[
2769750.001
]
[Cites]
Eur J Biochem. 1999 Apr;261(1):25-32
[
10103029.001
]
[Cites]
J Am Chem Soc. 2005 Sep 21;127(37):12957-64
[
16159290.001
]
(PMID = 16344484.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / 5R37DK9174-41
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
EC 5.4.99.5 / Chorismate Mutase; GI1BLY82Y1 / Chorismic Acid
[Other-IDs]
NLM/ PMC1317962
77.
Mulakala C, Nerinckx W, Reilly PJ:
Docking studies on glycoside hydrolase Family 47 endoplasmic reticulum alpha-(1-->2)-mannosidase I to elucidate the pathway to the substrate transition state.
Carbohydr Res
; 2006 Sep 25;341(13):2233-45
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Docking studies on glycoside hydrolase Family 47 endoplasmic reticulum alpha-(1-->2)-mannosidase I to elucidate the pathway to the substrate
transition state
.
Catalytic-domain crystal
structures
of yeast and human ERMan1s have been determined, the former with a hydrolytic product and the latter without ligands, with the inhibitors 1-deoxymannojirimycin and kifunensine, and with a thiodisaccharide substrate analog.
In the
current
study, AutoDock was used to dock alpha-D-mannopyranosyl-(1-->2)-alpha-D-mannopyranose with its glycon in chair (1C4,4C1), half-chair (3H2,3H4,4H3), skew-boat (OS2,3S1,5S1), boat (2,5B,3,OB,B1,4,B2,5), and envelope (3E,4E,E3,E4) conformations into the yeast ERManI active site.
Both docked energies and forces on docked ligand atoms were calculated to determine how the ligand distorts to the
transition state
.
(3) the
transition state
is likely to be close
to a
3E conformation.
[MeSH-minor]
Binding Sites. Carbohydrate Conformation. Computational Biology. Computer Simulation. Glycoside Hydrolases / chemistry. Humans. Models, Molecular. Protein Binding. Protein Conformation.
Structure
-Activity Relationship. Substrate Specificity
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
Saccharomyces Genome Database.
Saccharomyces Genome Database
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 16806128.001).
[ISSN]
0008-6215
[Journal-full-title]
Carbohydrate research
[ISO-abbreviation]
Carbohydr. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 3.2.1.- / Glycoside Hydrolases; EC 3.2.1.- / Mannosidases; EC 3.2.1.113 / mannosyl-oligosaccharide 1,2-alpha-mannosidase
78.
Fu T, Zhao H, Zeng J, Zhong M, Shi C:
Two-color optical charge-coupled-device-based pyrometer using a two-peak filter.
Rev Sci Instrum
; 2010 Dec;81(12):124903
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Two-color optical charge-coupled-device-based pyrometer using a two-
peak
filter.
The effective and simple method adjusts the fixed spectrum response characteristics of a color CCD to allow improved
temperature
measurements.
This pyrometer
system
not only has the advantage of traditional two-color (two-wavelength) pyrometry, but also overcomes the restrictions of color CCDs that can only be applied in waveband measurements.
The measurement performance of the
system
using a two-
peak
filter (λ(1)=643 nm, λ(2)=564 nm) was evaluated by blackbody experiments.
The results show that the
low temperature
detection limit is increased about 200 K with an increase in the
sensitivity
of the measured signals compared with the original
system
without two-
peak
filter [Fu, et al., Opt.
And the effective
temperature
range is also increased when T > 1233 K.
The measured ratio C(R)/C(G) is monotonically relative to the
temperature
, which simplifies the measurements.
The
temperature sensitivity
of 2.49 is larger and more uniform than the
temperature sensitivity
of 1.36 in the previous original
system
.
Thus, the measurement performance of the new
system
is greatly improved.
Finally, as an application, the
surface temperature
distribution of stainless steel sample in hot environments was determined by this new CCD-based pyrometer.
The results agree well with the spectrometer-based results and further verify the applicability of the new
system
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21198043.001).
[ISSN]
1089-7623
[Journal-full-title]
The Review of scientific instruments
[ISO-abbreviation]
Rev Sci Instrum
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
79.
Christen M, Kunz AP, van Gunsteren WF:
Sampling of rare events using hidden restraints.
J Phys Chem B
; 2006 Apr 27;110(16):8488-98
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
It makes use of distance or dihedral-angle restraints to overcome an energy barrier separating two metastable
states
or to stabilize
a transition state
between the two metastable
states
.
In order not to perturb these metastable end
states
themselves, a prefactor is introduced into the restraining energy function, which smoothly increases the weight of this function from zero to one at the
transition state
or on top of the separating energy barrier and then decreases the weight again to zero at the final
state
.
As first example the free energy difference of a cyclic alpha-aminoxy-hexapeptide-ion
complex
upon changing the ion from Cl- to Na+ was calculated.
Stabilizing the
transition state
by (hidden) restraints facilitates that.
In unrestrained simulations the change from the 4C1 into the 1C4 conformation was never observed because of the high energy barrier separating the two
states
.
Using (hidden) restraints, the
transition
from the 4C1 into the 1C4
state
and back could be enforced without perturbing the end
states
.
COS Scholar Universe.
author profiles
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[ErratumIn]
J Phys Chem B. 2008 Sep 11;112(36):11446
(PMID = 16623536.001).
[ISSN]
1520-6106
[Journal-full-title]
The journal of physical chemistry. B
[ISO-abbreviation]
J Phys Chem B
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
80.
Assefa G, Alemie B:
Tuberous sclerosis complex (TSC) and Klippel-Trenaunay-Weber (KTW) syndromes association of two complete phakomatoses in a single individual.
Ethiop Med J
; 2010 Oct;48(4):315-20
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Tuberous sclerosis complex
(
TSC
) and Klippel-Trenaunay-Weber (KTW) syndromes association of two complete phakomatoses in a single individual.
Tuberous sclerosis
or
tuberous sclerosis complex
(
TSC
) and Klippel-Trenaunay-Weber (KTW) syndromes are phakomatoses which are believed to be inherited separately were associated in a 21 years old female, with no family history of similar illness presented with facial rash of reddish spots or bumps, facial angiofibroma (
adenoma
cebaceum), which appeared on the nose and cheeks in a butterfly distribution, and sub ependymal calcific nodules on
brain
CT, and
multiple
liver, pancreas hamartomas and
multiple
angiomyolipomas and cysts of both kidney on ultrasound, which is consistent with a sporadic
TSC
, in addition, the diagnostic triad of KTW involved the left upper limb : cutaneous naevi a vascular anomaly, soft
tissue
and osteohypertrophy.
This is the second reported association of the fully developed symptomatology of
TSC
and KTW in one person in Ethiopian setting.
[MeSH-major]
Klippel-Trenaunay-Weber
Syndrome
/ complications.
Tuberous Sclerosis
/ complications
[MeSH-minor]
Brain
/ radiography. Female. Humans. Tomography, X-Ray Computed. Ultrasonography. Young Adult
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 21280434.001).
[ISSN]
0014-1755
[Journal-full-title]
Ethiopian medical journal
[ISO-abbreviation]
Ethiop. Med. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Ethiopia
81.
Liu H, Radisky DC, Nelson CM, Zhang H, Fata JE, Roth RA, Bissell MJ:
Mechanism of Akt1 inhibition of breast cancer cell invasion reveals a protumorigenic role for TSC2.
Proc Natl Acad Sci U S A
; 2006 Mar 14;103(11):4134-9
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Mechanism of Akt1 inhibition of breast cancer
cell
invasion reveals a protumorigenic role for TSC2.
Akt1 is frequently up-regulated in human tumors and has been shown to accelerate
cell
proliferation and to suppress programmed
cell
death; consequently, inhibition of the activity of Akt1 has been seen as an attractive target for therapeutic intervention.
Here we show that overexpression of activated myr-Akt1 in human breast cancer
cells
phosphorylates and thereby targets the tumor suppressor
tuberous sclerosis complex
2 (TSC2) for degradation, leading to reduced Rho-GTPase activity, decreased actin stress fibers and focal adhesions, and reduced motility and invasion.
Overexpression of TSC2 rescues the migration phenotype of myr-Akt1-expressing tumor
cells
, and high levels of TSC2 in breast cancer patients correlate with increased metastasis and reduced survival.
These data indicate that the functional properties of genes designated as oncogenes or tumor suppressor genes depend on the context of the
cell
type and the tissues studied, and suggest the need for caution in designing therapies targeting the function of individual genes in epithelial tissues.
[MeSH-minor]
Animals.
Cell
Line, Tumor.
Cell
Movement. Female. Focal Adhesions. Humans. Mice. Mice, Nude. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Neoplasm Invasiveness / physiopathology. Neoplasm Transplantation. Oncogenes. Transplantation, Heterologous. rho GTP-Binding Proteins / antagonists & inhibitors
Genetic Alliance.
consumer health - Breast Cancer
.
MedlinePlus Health Information.
consumer health - Breast Cancer
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
Cancer Invest. 2004;22(4):588-603
[
15565817.001
]
[Cites]
J Cell Biol. 2004 Dec 20;167(6):1171-82
[
15611338.001
]
[Cites]
Mol Biol Cell. 2005 Jan;16(1):84-96
[
15525681.001
]
[Cites]
Nat Genet. 2005 Jan;37(1):19-24
[
15624019.001
]
[Cites]
J Cell Biol. 2005 Jul 4;170(1):91-101
[
15998801.001
]
[Cites]
Cancer Sci. 2005 Jul;96(7):379-86
[
16053508.001
]
[Cites]
Adv Cancer Res. 2005;94:29-86
[
16095999.001
]
[Cites]
Dev Cell. 2005 Sep;9(3):389-402
[
16139227.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):658-65
[
12172554.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):E214-6
[
12205484.001
]
[Cites]
J Biol Chem. 2002 Sep 20;277(38):35364-70
[
12167664.001
]
[Cites]
J Biol Chem. 2002 Oct 18;277(42):39417-24
[
12176984.001
]
[Cites]
J Biol Chem. 2002 Nov 22;277(47):44593-6
[
12364343.001
]
[Cites]
J Cell Biol. 2005 Dec 19;171(6):1023-34
[
16365168.001
]
[Cites]
Nat Cell Biol. 2005 Nov;7(11):1074-82
[
16244670.001
]
[Cites]
Cold Spring Harb Symp Quant Biol. 2005;70:343-56
[
16869771.001
]
[Cites]
Science. 1999 Nov 5;286(5442):1102-3
[
10610524.001
]
[Cites]
J Cell Biol. 1999 Dec 27;147(7):1561-8
[
10613912.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1560-5
[
10677499.001
]
[Cites]
Biochem Biophys Res Commun. 2000 Mar 24;269(3):652-9
[
10720471.001
]
[Cites]
J Neurooncol. 1999;45(2):111-6
[
10778726.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6475-80
[
12438239.001
]
[Cites]
Oncogene. 2002 Dec 5;21(55):8470-6
[
12466966.001
]
[Cites]
N Engl J Med. 2002 Dec 19;347(25):1999-2009
[
12490681.001
]
[Cites]
Cancer Res. 2003 Jan 1;63(1):196-206
[
12517798.001
]
[Cites]
Cell. 2003 Feb 21;112(4):453-65
[
12600310.001
]
[Cites]
J Biol Chem. 2003 Apr 18;278(16):13663-71
[
12582162.001
]
[Cites]
Annu Rev Cell Dev Biol. 2005;21:247-69
[
16212495.001
]
[Cites]
Oncogene. 2005 Nov 14;24(50):7455-64
[
16288292.001
]
[Cites]
Oncogene. 2005 Nov 14;24(50):7482-92
[
16288295.001
]
[Cites]
Mol Cell. 2005 Nov 23;20(4):539-50
[
16307918.001
]
[Cites]
Nat Cell Biol. 2000 May;2(5):281-7
[
10806479.001
]
[Cites]
Nature. 2000 Aug 3;406(6795):532-5
[
10952316.001
]
[Cites]
Cancer Res. 2001 Jan 15;61(2):589-93
[
11212254.001
]
[Cites]
Nature. 2001 May 17;411(6835):355-65
[
11357143.001
]
[Cites]
Cancer Res. 2001 Jun 15;61(12):4885-91
[
11406567.001
]
[Cites]
FASEB J. 2001 Sep;15(11):1953-62
[
11532975.001
]
[Cites]
Laryngoscope. 2001 Jul;111(7):1285-9
[
11568556.001
]
[Cites]
Nat Rev Mol Cell Biol. 2001 Oct;2(10):760-8
[
11584303.001
]
[Cites]
Pancreas. 2002 Jan;24(1):34-41
[
11741180.001
]
[Cites]
Annu Rev Biochem. 2001;70:535-602
[
11395417.001
]
[Cites]
Cancer Res. 2002 Feb 15;62(4):982-5
[
11861368.001
]
[Cites]
J Biol Chem. 2002 Apr 5;277(14):12479-85
[
11805108.001
]
[Cites]
Nat Rev Cancer. 2002 Jul;2(7):489-501
[
12094235.001
]
[Cites]
Nat Rev Cancer. 2002 Aug;2(8):563-72
[
12154349.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):648-57
[
12172553.001
]
[Cites]
Nat Rev Cancer. 2003 May;3(5):362-74
[
12724734.001
]
[Cites]
Cancer Res. 2003 May 1;63(9):2172-8
[
12727836.001
]
[Cites]
Cell Signal. 2003 Aug;15(8):729-39
[
12781866.001
]
[Cites]
Science. 2003 Dec 5;302(5651):1704-9
[
14657486.001
]
[Cites]
Trends Biochem Sci. 2004 Jan;29(1):32-8
[
14729330.001
]
[Cites]
J Cell Biol. 2004 Feb 16;164(4):603-12
[
14769856.001
]
[Cites]
Breast Cancer Res Treat. 2004 Mar;84(1):13-9
[
14999150.001
]
[Cites]
Cancer Res. 2004 May 1;64(9):3171-8
[
15126356.001
]
[Cites]
Microvasc Res. 1977 Jul;14(1):53-65
[
895546.001
]
[Cites]
Nature. 1984 Jun 7-13;309(5968):552-6
[
6203040.001
]
[Cites]
Science. 1990 Jun 29;248(4963):1656-60
[
2163544.001
]
[Cites]
Symp Soc Exp Biol. 1993;47:183-95
[
7513090.001
]
[Cites]
Cancer Res. 1996 May 1;56(9):2039-44
[
8616848.001
]
[Cites]
Int J Cancer. 1996 Jul 17;67(2):275-82
[
8760599.001
]
[Cites]
Trends Neurosci. 1997 Jan;20(1):23-31
[
9004416.001
]
[Cites]
Science. 1997 Apr 4;276(5309):75-81
[
9082989.001
]
[Cites]
J Cell Biol. 1997 Apr 7;137(1):231-45
[
9105051.001
]
[Cites]
Endocrinology. 1997 Aug;138(8):3559-62
[
9231812.001
]
[Cites]
Science. 1998 Jan 23;279(5350):509-14
[
9438836.001
]
[Cites]
Mol Carcinog. 1998 Feb;21(2):81-6
[
9496907.001
]
[Cites]
Oncogene. 1998 Sep 17;17(11 Reviews):1343-52
[
9779982.001
]
[Cites]
Dev Dyn. 1998 Oct;213(2):228-35
[
9786423.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14821-6
[
9843973.001
]
[Cites]
Int J Cancer. 1999 May 31;81(5):682-7
[
10328216.001
]
[Cites]
Cell Motil Cytoskeleton. 1999;43(4):269-87
[
10423269.001
]
[Cites]
Carcinogenesis. 2004 Nov;25(11):2053-9
[
15240509.001
]
(PMID = 16537497.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Proteins; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / rho GTP-Binding Proteins
[Other-IDs]
NLM/ PMC1390746
82.
Davis CH, Deerfield D 2nd, Wymore T, Stafford DW, Pedersen LG:
A quantum chemical study of the mechanism of action of Vitamin K carboxylase (VKC) III. Intermediates and transition states.
J Mol Graph Model
; 2007 Sep;26(2):409-14
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
A quantum chemical study of the mechanism of action of Vitamin K carboxylase (VKC) III. Intermediates and
transition states
.
A reaction path including
transition states
is generated for the Dowd mechanism [P. Dowd, R.
The geometries of the proposed model intermediates and
transition states
in the mechanism are energy optimized.
[MeSH-minor]
Hydroquinones / chemistry. Hydroquinones / metabolism. Models, Chemical. Models, Molecular. Molecular
Structure
. Vitamin K / chemistry. Vitamin K / metabolism
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17182265.001).
[ISSN]
1093-3263
[Journal-full-title]
Journal of molecular graphics & modelling
[ISO-abbreviation]
J. Mol. Graph. Model.
[Language]
eng
[Grant]
United States / NHLBI NIH HHS / HL / HL-06350; United States / NHLBI NIH HHS / HL / HL-48318; United States / NCRR NIH HHS / RR / RR06009
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Hydroquinones; 12001-79-5 / Vitamin K; EC 6.4.- / Carbon-Carbon Ligases
83.
Jing H, Liu H, Pointing SB:
Identification and characterization of thermophilic Synechococcus spp. isolates from Asian geothermal springs.
Can J Microbiol
; 2007 Apr;53(4):480-7
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Two thermophilic cyanobacterial strains,
Ts
and Bs, collected from Asian geothermal springs were identified morphologically and phylogenetically as Synechococcus in the order Chroococcales and were isolated into axenic cultures.
Strain
Ts
had elevated levels of photoprotective pigments such as carotenoid and scytonemin even after prolonged culture under identical laboratory conditions, whereas strain Bs produced more chlorophyll a per unit
cell
volume, perhaps resulting from UV adaptation in the natural habitats.
In addition, strain
Ts
had more content than strain Bs in terms of the total fatty acids and the proportion of unsaturated fatty acids.
COS Scholar Universe.
author profiles
.
SILVA.
SILVA SSU Database
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17612602.001).
[ISSN]
0008-4166
[Journal-full-title]
Canadian journal of microbiology
[ISO-abbreviation]
Can. J. Microbiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Canada
[Chemical-registry-number]
0 / Bacterial Proteins; 0 / Fatty Acids; 0 / RNA, Bacterial; 0 / RNA, Ribosomal, 16S
84.
Okumura K, Mekata E, Shiomi H, Naitoh H, Abe H, Endo Y, Kurumi Y, Tani T:
Expression level of thymidylate synthase mRNA reflects 5-fluorouracil sensitivity with low dose and long duration in primary colorectal cancer.
Cancer Chemother Pharmacol
; 2008 Apr;61(4):587-94
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Expression level of thymidylate synthase mRNA reflects 5-fluorouracil
sensitivity
with
low
dose and long duration in primary colorectal cancer.
METHODS: Primary colorectal cancer
tissue
from 24 patients was investigated to evaluate the relationship between the mRNA expression level of several 5-fluorouracil (5-FU)-related metabolic enzymes (thymidylate synthase,
TS
; dihydropyrimidine dehydrogenase, DPD; and thymidine phosphorylase, TP) and chemosensitivity to two different 5-FU doses and duration (1: 5-FU
concentration
1.0 microg/mL (7.68 microM), 24 h exposure and 2: 5-FU
concentration
0.3 microg/mL (2.30 microM), 144 h exposure).
Chemosensitivity and mRNA expression levels were measured using collagen gel droplet embedded culture drug
sensitivity
tests and real-
time
quantitative reverse transcription-polymerase chain reaction.
RESULTS: The
TS
mRNA expression level was significantly higher in the 5-FU resistant group (T/C > 60%) compared with the 5-FU
sensitive
group (T/C < 60%) in both 5-FU regimens (1: 5.03 +/- 0.92 vs. 1.58 +/- 0.76, p < 0.01, 2: 4.88 +/- 0.91 vs. 0.96 +/- 0.20, p < 0.001).
The group with the higher
TS
mRNA expression level (>3.83, the average) were more resistant to both 5-FU regimens than those with lower
TS
mRNA (<3.83) (1: T/C = 80 vs. 66%, p = 0.11, 2: T/C = 89 vs. 64%, p < 0.005).
The
TS
mRNA expression level inversely correlated with the
sensitivity to
the latter 5-FU regimen (R = 0.577, p < 0.01).
CONCLUSIONS: The
TS
mRNA expression level might be a good marker of chemosensitivity to 5-FU in primary colorectal cancer, especially the
sensitivity to low
dose 5-FU with a long duration.
Genetic Alliance.
consumer health - Colorectal Cancer
.
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 17520254.001).
[ISSN]
0344-5704
[Journal-full-title]
Cancer chemotherapy and pharmacology
[ISO-abbreviation]
Cancer Chemother. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antimetabolites; 0 / Genetic Markers; 0 / RNA, Messenger; 9007-34-5 / Collagen; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.4 / Thymidine Phosphorylase; U3P01618RT / Fluorouracil
85.
Bongiorni L, Arroyo HA, Lubienicki F:
[Subependymal nodules-sudependymal giant cell astrocytoma complex in children with tuberous sclerosis].
Medicina (B Aires)
; 2009;69(1 Pt 1):8-14
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
[Subependymal nodules-sudependymal giant
cell
astrocytoma
complex
in children with
tuberous sclerosis
].
[Transliterated title]
Complejo nódulo subependimario-astrocitoma subependimario gigantocelular en niños con
esclerosis tuberosa
.
The object of this paper is to describe the imaging and clinical characteristics of subependymal nodule (SN) - subependymal giant
cell
astrocytoma (SGCA)
complex
in
tuberous sclerosis
and analyze its evolution in order to attempt early detection and the prevention of intracranial hypertension.
We evaluated 22 patients with the pathological
diagnosis
of SGCA.
The
diagnosis
was made at a median of 10.1 years old.
We were able to observe the evolution of SN to ASGC: these SN were localized adjacent to the foramen of Monro and with
time
they underwent an important development with intense contrast enhancement and hydrocephalus.
Prospective studies could determine whether the SN-SGCA
complex
corresponds to the same entity in distinct evolution stages or to two lesions with different growth potential.
[MeSH-major]
Astrocytoma / pathology.
Brain
Neoplasms / pathology.
Cerebral
Ventricles / pathology.
Tuberous Sclerosis
/ pathology
[MeSH-minor]
Adolescent.
Cerebral
Ventricle Neoplasms / pathology.
Cerebral
Ventricle Neoplasms / radiography.
Cerebral
Ventricle Neoplasms / surgery. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Hydrocephalus / etiology. Infant. Intellectual Disability / etiology. Intracranial Hypertension / prevention & control. Male
Genetic Alliance.
consumer health - Subependymal giant cell astrocytoma
.
Genetic Alliance.
consumer health - Tuberous sclerosis
.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
MedlinePlus Health Information.
consumer health - Childhood Brain Tumors
.
MedlinePlus Health Information.
consumer health - Tuberous Sclerosis
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
(PMID = 19239998.001).
[ISSN]
0025-7680
[Journal-full-title]
Medicina
[ISO-abbreviation]
Medicina (B Aires)
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Argentina
86.
Scheidenhelm DK, Cresswell J, Haipek CA, Fleming TP, Mercer RW, Gutmann DH:
Akt-dependent cell size regulation by the adhesion molecule on glia occurs independently of phosphatidylinositol 3-kinase and Rheb signaling.
Mol Cell Biol
; 2005 Apr;25(8):3151-62
[Fulltext service]
Download
fulltext PDF
of
this article and others
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Akt-dependent
cell
size regulation by the adhesion molecule on glia occurs independently of phosphatidylinositol 3-kinase and Rheb signaling.
The role of
cell
adhesion molecules in mediating interactions with neighboring
cells
and the extracellular matrix has long been appreciated.
More recently, these molecules have been shown to modulate intracellular signal transduction cascades critical for
cell
growth and proliferation.
Expression of adhesion molecule on glia (AMOG) is downregulated in human and mouse gliomas, suggesting that AMOG may be important for growth regulation in the
brain
.
In this report, we examined the role of AMOG expression on
cell
growth and intracellular signal transduction.
We show that AMOG does not negatively regulate
cell
growth in vitro or in vivo.
Instead, expression of AMOG in AMOG-deficient
cells
results in a dramatic increase in
cell
size associated with protein kinase B/Akt hyperactivation, which occurs independent of phosphatidylinositol 3-kinase activation.
AMOG-mediated Akt phosphorylation specifically activates the mTOR/p70S6 kinase pathway previously implicated in
cell
size regulation, but it does not depend on
tuberous sclerosis complex
/Ras homolog enriched in
brain
(Rheb) signaling.
These data support a novel role for a glial adhesion molecule in
cell
size regulation through selective activation of the Akt/mTOR/S6K signal transduction pathway.
MedlinePlus Health Information.
consumer health - Brain Tumors
.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
[Email]
Email this result item
Email the results to the following email address:
[X] Close
[Cites]
J Biol Chem. 2004 Apr 16;279(16):16441-51
[
14761976.001
]
[Cites]
Trends Biochem Sci. 2004 May;29(5):233-42
[
15130559.001
]
[Cites]
Ann N Y Acad Sci. 2004 Apr;1014:58-66
[
15153420.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):559-65
[
12766775.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):566-71
[
12766776.001
]
[Cites]
Nat Cell Biol. 2003 Jun;5(6):578-81
[
12771962.001
]
[Cites]
Mol Cell. 2003 Jun;11(6):1457-66
[
12820960.001
]
[Cites]
Neuropathol Appl Neurobiol. 2003 Aug;29(4):370-7
[
12887597.001
]
[Cites]
Genes Dev. 2003 Aug 1;17(15):1829-34
[
12869586.001
]
[Cites]
J Mol Cell Cardiol. 1997 Nov;29(11):3157-67
[
9405189.001
]
[Cites]
Science. 1998 Jan 30;279(5351):707-10
[
9445476.001
]
[Cites]
Gene. 1998 Feb 27;208(2):221-7
[
9524271.001
]
[Cites]
Cancer Res. 1998 May 1;58(9):2020-8
[
9581848.001
]
[Cites]
Glia. 2004 Aug 1;47(2):180-8
[
15185396.001
]
[Cites]
J Biol Chem. 2004 Jul 30;279(31):33024-34
[
15166238.001
]
[Cites]
Mol Cell Biol. 2004 Sep;24(18):7965-75
[
15340059.001
]
[Cites]
Genes Dev. 2004 Oct 15;18(20):2479-84
[
15466161.001
]
[Cites]
J Cell Biol. 1987 Jun;104(6):1587-95
[
2438288.001
]
[Cites]
J Neurosci. 1988 Aug;8(8):2961-6
[
2457661.001
]
[Cites]
Am J Physiol. 1989 Nov;257(5 Pt 1):C851-8
[
2556932.001
]
[Cites]
J Cell Biol. 1990 Jan;110(1):165-74
[
1688561.001
]
[Cites]
J Biol Chem. 1993 Dec 15;268(35):26260-7
[
7504672.001
]
[Cites]
J Cell Biol. 1994 Nov;127(3):835-45
[
7525597.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Jan 17;92(2):542-6
[
7831326.001
]
[Cites]
Nature. 1996 Feb 8;379(6565):560-4
[
8596638.001
]
[Cites]
Endocrinology. 1996 Mar;137(3):846-56
[
8603594.001
]
[Cites]
Cancer Res. 1996 Mar 15;56(6):1440-4
[
8640837.001
]
[Cites]
J Biol Chem. 1996 Apr 26;271(17):10372-8
[
8626609.001
]
[Cites]
Cell. 1996 May 31;85(5):707-20
[
8646779.001
]
[Cites]
Cell. 1996 May 31;85(5):721-32
[
8646780.001
]
[Cites]
Cell. 1996 May 31;85(5):733-44
[
8646781.001
]
[Cites]
Brain Res Bull. 1996;40(3):167-74
[
8736577.001
]
[Cites]
EMBO J. 1996 Dec 2;15(23):6584-94
[
8978685.001
]
[Cites]
J Cell Sci. 1997 Feb;110 ( Pt 3):345-56
[
9057087.001
]
[Cites]
J Biol Chem. 1997 Apr 18;272(16):10608-15
[
9099708.001
]
[Cites]
Curr Biol. 1997 Oct 1;7(10):776-89
[
9368760.001
]
[Cites]
Nat Cell Biol. 1999 Dec;1(8):500-6
[
10587646.001
]
[Cites]
J Biol Chem. 1999 Dec 24;274(52):37307-14
[
10601297.001
]
[Cites]
Genes Dev. 1999 Dec 15;13(24):3244-58
[
10617573.001
]
[Cites]
Biochem J. 2000 Mar 15;346 Pt 3:561-76
[
10698680.001
]
[Cites]
Mol Cell Neurosci. 2000 Mar;15(3):288-302
[
10736205.001
]
[Cites]
J Biol Chem. 2000 Sep 8;275(36):27832-7
[
10874030.001
]
[Cites]
J Biol Chem. 2000 Sep 8;275(36):27838-44
[
10874029.001
]
[Cites]
Cell. 2000 Dec 8;103(6):919-30
[
11136977.001
]
[Cites]
Endocrinology. 2001 Jan;142(1):498-501
[
11145615.001
]
[Cites]
Differentiation. 2000 Dec;66(4-5):165-72
[
11269942.001
]
[Cites]
Cell. 2001 May 4;105(3):345-55
[
11348591.001
]
[Cites]
Cell. 2001 May 4;105(3):357-68
[
11348592.001
]
[Cites]
Methods Enzymol. 2001;333:217-31
[
11400338.001
]
[Cites]
Mol Microbiol. 2001 Sep;41(6):1339-47
[
11580838.001
]
[Cites]
Nat Genet. 2001 Dec;29(4):396-403
[
11726926.001
]
[Cites]
Annu Rev Pharmacol Toxicol. 2002;42:283-323
[
11807174.001
]
[Cites]
Immunity. 2002 Jan;16(1):51-65
[
11825565.001
]
[Cites]
Ann Neurol. 2002 Mar;51(3):393-405
[
11891838.001
]
[Cites]
Glia. 2002 Apr 15;38(2):146-54
[
11948808.001
]
[Cites]
J Biol Chem. 2002 May 24;277(21):18694-702
[
11907028.001
]
[Cites]
Oncogene. 2002 Jun 6;21(25):4050-9
[
12037687.001
]
[Cites]
Mol Biol Cell. 2002 Jul;13(7):2276-88
[
12134068.001
]
[Cites]
Hepatology. 2002 Sep;36(3):582-91
[
12198650.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):648-57
[
12172553.001
]
[Cites]
Nat Cell Biol. 2002 Sep;4(9):658-65
[
12172554.001
]
[Cites]
J Biol Chem. 2002 Sep 20;277(38):35364-70
[
12167664.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13571-6
[
12271141.001
]
[Cites]
Mol Cell Biol. 2003 Jan;23(2):566-78
[
12509455.001
]
[Cites]
Ann N Y Acad Sci. 2003 Apr;986:497-503
[
12763870.001
]
[Cites]
J Biol Chem. 1998 Jun 12;273(24):15249-56
[
9614140.001
]
[Cites]
J Neurobiol. 1999 Mar;38(4):542-58
[
10084688.001
]
[Cites]
J Biol Chem. 1999 Jul 2;274(27):19323-8
[
10383443.001
]
[Cites]
Cell. 1999 Jun 25;97(7):865-75
[
10399915.001
]
[Cites]
Curr Biol. 1999 Sep 23;9(18):1019-29
[
10508611.001
]
[Cites]
Curr Biol. 2003 Aug 5;13(15):1259-68
[
12906785.001
]
[Cites]
J Biol Chem. 2003 Aug 29;278(35):32493-6
[
12842888.001
]
[Cites]
J Biol Chem. 2003 Sep 26;278(39):37288-96
[
12867426.001
]
[Cites]
Oncogene. 2003 Oct 9;22(44):6891-9
[
14534536.001
]
[Cites]
Nat Neurosci. 2003 Nov;6(11):1153-61
[
14528310.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12923-8
[
14534328.001
]
[Cites]
Nat Rev Cancer. 2003 Dec;3(12):945-51
[
14737124.001
]
(PMID = 15798201.001).
[ISSN]
0270-7306
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / R01 NS041097; United States / NIGMS NIH HHS / GM / T32 GM007200; United States / NIGMS NIH HHS / GM / 5 T32 GM07200; United States / NINDS NIH HHS / NS / NS41097
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / ATP1B2 protein, human; 0 / Atp1b2 protein, mouse; 0 / Cation Transport Proteins; 0 / Cell Adhesion Molecules, Neuronal; 0 / Neuropeptides; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Rheb protein, mouse; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; EC 3.6.5.2 / Monomeric GTP-Binding Proteins
[Other-IDs]
NLM/ PMC1069598
87.
Jeremiah ZA, Koate BB:
Reference percentiles of hematological and biochemical iron values of blood donors in Port Harcourt, Nigeria.
Hematology
; 2009 Dec;14(6):366-70
[Fulltext service]
Get downloadable
fulltext PDFs
of
articles closely matching to this article
, as many as you want.
[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Four biochemical parameters: serum ferritin (SF), serum iron (SI), total iron binding capacity (TIBC) and transferrin saturation (
TS
) and four hematological parameters: hemoglobin (Hb), packed
cell
volume (PCV), total white blood
cell
count (WBC) and erythrocyte sedimentation rate (ESR), were assessed.
The median and percentile ranges (10-90% percentile) of the biochemical and hematological parameters were as follows: SF 46.8 ng/ml (0.0-173.1), SI 85.9 microg/dl (19.7-338.0), TIBC 224.7 microg/dl (60.9-541.4),
TS
41.2% (15.3-90.6), Hb 12.9 g/dl (7.74-15.6), PCV 38.0% (22.9-47.0), WBC 4.5 x 10(9)/l (3.0-8.0) and ESR 8.0 mm/h (1.0-24.6).
At a cut-off value of Hb 12.0 g/dl, SF 15.0 ng/ml and
TS
16, 10.4 and 6.0% had iron deficiency and iron deficiency anemia respectively in this study population.
MedlinePlus Health Information.
consumer health - Blood Transfusion and Donation
.<