[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
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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



5. Ackermans L, Temel Y, Visser-Vandewalle V: Deep brain stimulation in Tourette's Syndrome. Neurotherapeutics; 2008 Apr;5(2):339-44
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



7. Kamen BA: The 3 ts of therapy: typing, tailoring, and targeting. J Pediatr Hematol Oncol; 2008 Nov;30(11):789-90
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



10. Piedimonte LR, Wailes IK, Weiner HL: Tuberous sclerosis complex: molecular pathogenesis and animal models. Neurosurg Focus; 2006;20(1):E4
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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.



23. Klingenberg M: Ligand-protein interaction in biomembrane carriers. The induced transition fit of transport catalysis. Biochemistry; 2005 Jun 21;44(24):8563-70
PDF icon [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
  •  go-up   go-down



24. Debes NM, Skov L, Hjalgrim H: [Tourette syndrome. Genetics, neuroanatomy and neurotransmitters]. Ugeskr Laeger; 2008 Aug 25;170(35):2695-700
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



33. Grichnik JM: Melanoma, nevogenesis, and stem cell biology. J Invest Dermatol; 2008 Oct;128(10):2365-80
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



36. Grünwald M, Dellago C: Transition state analysis of solid-solid transformations in nanocrystals. J Chem Phys; 2009 Oct 28;131(16):164116
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



40. Gloster TM, Davies GJ: Glycosidase inhibition: assessing mimicry of the transition state. Org Biomol Chem; 2010 Jan 21;8(2):305-20
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



49. Ben-Aroya S, Pan X, Boeke JD, Hieter P: Making temperature-sensitive mutants. Methods Enzymol; 2010;470:181-204
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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.



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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.



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



77. Mulakala C, Nerinckx W, Reilly PJ: Docking studies on glycoside hydrolase Family 47 endoplasmic reticulum alpha-(1--&gt;2)-mannosidase I to elucidate the pathway to the substrate transition state. Carbohydr Res; 2006 Sep 25;341(13):2233-45
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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



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
PDF icon [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
  •  go-up   go-down



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
PDF icon [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.