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1. Lindhagen-Persson M, Vestling M, Reixach N, Olofsson A: Formation of cytotoxic transthyretin is not dependent on inter-molecular disulphide bridges commonly found within the amyloid form. Amyloid; 2008 Dec;15(4):240-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Formation of cytotoxic transthyretin is not dependent on inter-molecular disulphide bridges commonly found within the amyloid form.
  • Familial amyloidotic polyneuropathy (FAP) is linked to destabilising point mutations in the human plasma protein transthyretin (TTR).
  • Moreover, substitution of Cys10 in a mouse model for TTR-amyloidosis abolishes TTR deposits, indicating an important role of Cys10 in FAP pathogenesis.
  • However, the role of disulphide bridges in TTR cytotoxicity has not been elucidated.
  • By probing Cys10Ser TTR variants to the human neuroblastoma SH-SY5Y cell line, we have addressed this question, and our results clearly show that formation of an inter-molecular disulphide bridge is not a pre-requisite for TTR cytotoxicity.
  • This finding suggests that prevention of inter-molecular TTR disulphide bridges as a therapeutic intervention will not impair the cytotoxic potential of TTR.
  • [MeSH-minor] Amino Acid Substitution. Amyloid Neuropathies, Familial / etiology. Amyloid Neuropathies, Familial / genetics. Amyloid Neuropathies, Familial / metabolism. Cell Line. Cell Survival / drug effects. Cysteine / chemistry. Disulfides / chemistry. Humans. Multiprotein Complexes / chemistry. Multiprotein Complexes / genetics. Multiprotein Complexes / toxicity. Mutagenesis, Site-Directed. Protein Structure, Quaternary. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / toxicity

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  • (PMID = 19065295.001).
  • [ISSN] 1744-2818
  • [Journal-full-title] Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
  • [ISO-abbreviation] Amyloid
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Disulfides; 0 / Multiprotein Complexes; 0 / Prealbumin; 0 / Recombinant Proteins; K848JZ4886 / Cysteine
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2. Gadish T, Tulchinsky H, Deutsch AA, Rabau M: Pinealoblastoma in a patient with familial adenomatous polyposis: variant of Turcot syndrome type 2? Report of a case and review of the literature. Dis Colon Rectum; 2005 Dec;48(12):2343-6
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  • [Title] Pinealoblastoma in a patient with familial adenomatous polyposis: variant of Turcot syndrome type 2? Report of a case and review of the literature.
  • We report a case of a 23-year-old Turcot female patient who was first diagnosed as having a pinealoblastoma.
  • Thyroid papillary carcinoma was diagnosed a few months later, and multiple colonic polyps were detected three years after that.
  • A genetic workup revealed an APC gene mutation in her family.
  • Restorative proctocolectomy may itself cause major morbidity but is currently the only way to prevent colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Brain Neoplasms / genetics. Pineal Gland. Pinealoma / genetics
  • [MeSH-minor] Adult. Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. DNA Mutational Analysis. Female. Genes, APC. Humans. Syndrome. Thyroid Neoplasms / genetics. Thyroid Neoplasms / pathology


3. Park IJ, Kim HC, Yu CS, Koo HL, Kim JS, Kim JC: A giant colonic hamartoma and multiple colonic hamartomatous polyps in a middle-aged man. Yonsei Med J; 2006 Oct 31;47(5):755-8
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  • [Title] A giant colonic hamartoma and multiple colonic hamartomatous polyps in a middle-aged man.
  • We report an unusual case of multiple colonic hamartomatous polyps, including a giant hamartoma, unrelated to hereditary or familial polyposis syndromes, in a 48-year-old man.
  • The diameter of the largest polyp was 9.5 cm, and endoscopy revealed that the lesion caused colonic obstruction.
  • [MeSH-major] Colonic Diseases / pathology. Colonic Polyps / pathology. Hamartoma / pathology. Intestinal Obstruction / pathology

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  • (PMID = 17066524.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2687766
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4. Albert M, Song JS, Schultz D, Cormack RA, Tempany CM, Haker S, Devlin PM, Beard C, Hurwitz MD, Suh WW, Jolesz F, D'Amico AV: Defining the rectal dose constraint for permanent radioactive seed implantation of the prostate. Urol Oncol; 2008 Mar-Apr;26(2):147-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: This study was performed to define the rectal dose constraint that would predict late rectal bleeding requiring argon plasma coagulation (APC) following prostate brachy mono-therapy.
  • For those patients requiring APC, the date on which a patient reported rectal bleeding was recorded.
  • Comparisons of estimates of rectal bleeding requiring APC were made using a 2-sided log rank test.
  • RESULTS: There was a significant association (hazard ratio = 5.6 [95% confidence interval: 1.3, 23.8]; P = 0.002) between the rectal volume exceeding 100 Gy and rectal bleeding requiring APC.
  • After a median follow-up of 4.25 (1-6) years, no patient with less than a median value of 8 cc of rectum exceeding 100 Gy required APC, whereas 20% (P = 0.004) were estimated to require APC within 3 years following treatment.
  • CONCLUSIONS: Keeping the rectal volume receiving more than 100 Gy below 8 cc will minimize the risk of rectal bleeding requiring APC following I(125) permanent prostate brachy mono-therapy.


5. Castellsagué E, González S, Guinó E, Stevens KN, Borràs E, Raymond VM, Lázaro C, Blanco I, Gruber SB, Capellá G: Allele-specific expression of APC in adenomatous polyposis families. Gastroenterology; 2010 Aug;139(2):439-47, 447.e1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allele-specific expression of APC in adenomatous polyposis families.
  • BACKGROUND & AIMS: Germline mutations in the APC gene cause of most cases of familial adenomatous polyposis (FAP) and a lesser proportion of attenuated FAP (AFAP).
  • Systematic analysis of APC at the RNA level could provide insight into the pathogenicity of identified mutations and the molecular basis of FAP/AFAP in families without identifiable mutations.
  • Here, we analyzed the prevalence of imbalances in the allelic expression of APC in polyposis families with germline mutations in the gene and without detectable mutations in APC and/or MUTYH.
  • In total, 52 APC-mutation-positive (36 families) and 24 APC/MUTYH-mutation-negative (23 families) informative patients were analyzed.
  • RESULTS: Of the APC-mutation-positive families, most of those in whom the mutation was located before the last exon of the gene (12 of 14) had ASE imbalance, which is consistent with a mechanism of nonsense-mediated decay.
  • Of the APC/MUTYH-mutation-negative families, 2 (9%) had ASE imbalance, which might cause the disease.
  • CONCLUSIONS: ASE analysis might be used to determine the pathogenesis of some cases of FAP and AFAP in which APC mutations are not found.
  • ASE also might be used to prioritize the order in which different areas of APC are tested.
  • RNA-level studies are important for the molecular diagnosis of FAP.

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  • [Copyright] Copyright (c) 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20434453.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / P30 CA46592; United States / NCI NIH HHS / CA / R01 CA081488-01; United States / NCI NIH HHS / CA / R01 CA081488; United States / NCI NIH HHS / CA / R01 CA81488
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
  • [Other-IDs] NLM/ NIHMS200922; NLM/ PMC2910837
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6. Farinella E, Soobrah R, Phillips RK, Clark SK: Familial adenomatous polyposis (FAP) and gender. Does gender influence the genetic transmission of FAP? Fam Cancer; 2010 Sep;9(3):405-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Familial adenomatous polyposis (FAP) and gender. Does gender influence the genetic transmission of FAP?
  • Familial adenomatous polyposis (FAP) is an autosomal dominant syndrome with a penetrance close to 100% at the age of 40 years.
  • The incidence is thought to be equal among both sexes, but we noticed an excess of males undergoing primary surgery for FAP at our institution.
  • The aim of the study is to investigate the hypothesis that FAP patients produce an excess of affected male offspring.
  • We identified all families with known APC mutation in the polyposis registry at St Mark's from its foundation until October 2009.
  • The overall ratio of affected/unaffected and male/female offspring did not differ from the expected 50%.
  • Further sub-analysis by gender of parents did not show any statistically significant difference in gender and mutation status of offspring.
  • In addition the mean number of children per affected parent did not depend on gender (males 2.34; females 2.30).
  • This study shows that gender does not influence the genetic transmission of FAP.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics


7. Preston SL, Leedham SJ, Oukrif D, Deheregoda M, Goodlad RA, Poulsom R, Alison MR, Wright NA, Novelli M: The development of duodenal microadenomas in FAP patients: the human correlate of the Min mouse. J Pathol; 2008 Feb;214(3):294-301
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The development of duodenal microadenomas in FAP patients: the human correlate of the Min mouse.
  • The morphological changes associated with the adenoma-carcinoma sequence are well documented in the colorectum.
  • Small intestinal carcinogenesis is thought to progress through a similar adenoma-to-carcinoma pathway, but there is a relative dearth of studies examining the associated morphological changes.
  • The best-known mouse model of intestinal neoplasia, the multiple intestinal neoplasia (Min) mouse, has been criticized as a genetic model of intestinal neoplasia, as the majority of its tumours occur in the small intestine.
  • We examined pancreatico-duodenal resection specimens from seven familial adenomatous polyposis (FAP) patients.
  • Individual dysplastic crypts were isolated and mutations in the FAP (APC) gene compared between the top and bottom of the crypt.
  • We found that: (a) duodenal microadenomas are extremely common in FAP patients;.
  • (d) migrating adenomatous cells lose their dysplastic phenotype as they migrate up the crypt villous axis; and (e) Paneth cells lose positional information.
  • IN CONCLUSION: (a) the morphological similarity of adenomas in the Min mouse and human suggest the Min mouse is a good model of FAP;.
  • (b) duodenal adenomas in FAP originate in monocryptal adenomas and follow the 'bottom-up' rather than the 'top-down' model of morphogenesis;.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyposis Coli / pathology. Duodenal Neoplasms / pathology
  • [MeSH-minor] Animals. Antigens, CD44 / analysis. Cell Differentiation. Cell Movement. Gene Expression. Genes, APC. Humans. Immunohistochemistry. Mice. Mice, Mutant Strains. Models, Animal. Mutation. Paneth Cells / pathology. Polymerase Chain Reaction. Precancerous Conditions / pathology. Staining and Labeling. beta Catenin / analysis


8. Wen Y, Wang CT, Ma TT, Li ZY, Zhou LN, Mu B, Leng F, Shi HS, Li YO, Wei YQ: Immunotherapy targeting fibroblast activation protein inhibits tumor growth and increases survival in a murine colon cancer model. Cancer Sci; 2010 Nov;101(11):2325-32
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  • [Title] Immunotherapy targeting fibroblast activation protein inhibits tumor growth and increases survival in a murine colon cancer model.
  • Murine studies have shown that immunological targeting of fibroblast activation protein (FAP) can elicit protective immunity in the absence of significant pathology.
  • Fibroblast activation protein is a product overexpressed by tumor-associated fibroblasts (TAF) and is the predominant component of the stoma in most types of cancer.
  • Tumor-associated fibroblasts differ from normal adult tissue fibroblasts, and instead resemble transient fetal and wound healing-associated fibroblasts.
  • Tumor-associated fibroblasts are critical regulators of tumorigenesis, but differ from tumor cells by being more genetically stable.
  • To specifically target TAF, we constructed a DNA vaccine directed against FAP.
  • This vaccine significantly suppressed primary tumor and pulmonary metastases primarily through CD8(+) T-cell-mediated killing in tumor-bearing mice.
  • Most importantly, tumor-bearing mice vaccinated against FAP exhibited a 1.5-fold increase in lifespan and no significant pathology.
  • These results suggest that FAP, a product preferentially expressed by TAF, could function as an effective tumor rejection antigen.
  • [MeSH-major] Colonic Neoplasms / therapy. Gelatinases / immunology. Immunotherapy / methods. Membrane Proteins / immunology. Serine Endopeptidases / immunology. Vaccines, DNA / immunology
  • [MeSH-minor] Animals. CD8-Positive T-Lymphocytes / immunology. Cancer Vaccines / genetics. Cancer Vaccines / immunology. Cell Line, Tumor. Disease Models, Animal. Female. Fibroblasts / immunology. Fibroblasts / metabolism. Fibroblasts / pathology. Humans. Immunization / methods. Immunohistochemistry. Lung Neoplasms / immunology. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Survival Analysis. Tumor Burden / immunology

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  • [Copyright] © 2010 Japanese Cancer Association.
  • (PMID = 20804499.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Membrane Proteins; 0 / Vaccines, DNA; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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9. Kim JC, Ka IH, Lee YM, Koo KH, Kim HC, Yu CS, Jang SJ, Kim YS, Lee HI, Lee KH: MYH, OGG1, MTH1, and APC alterations involved in the colorectal tumorigenesis of Korean patients with multiple adenomas. Virchows Arch; 2007 Mar;450(3):311-9
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  • [Title] MYH, OGG1, MTH1, and APC alterations involved in the colorectal tumorigenesis of Korean patients with multiple adenomas.
  • This study was done to characterize base excision repair (BER) genes and adenomatous polyposis coli (APC) alterations in the tumorigenesis of multiple colorectal adenomas in Korean patients.
  • The heterozygous genotype of OGG1 c.1-18G>T was closely associated with multiple adenoma families (P < 0.001), while MYH A359V mutation exhibited a tendency (P = 0.053).
  • MYH R170G mutation was exclusively identified in one patient.
  • The G:C>T:A transversion or attenuated familial adenomatous polyposis (AFAP) mutations of APC was identified in the specific genotypes of BER variants.
  • Tubular adenomas or adenomas with none-to-mild dysplasia were significantly associated with polymorphic genotypes of OGG1 IVS4-15 and S326C.
  • In addition, large and pedunculated adenomas were more frequent in patients with G:C>T:A transversion and AFAP mutations of APC, respectively.
  • However, BER variants were not associated with mismatch repair or altered p53 protein expression.
  • Conclusively, two novel mutations of MYH and a novel OGG1 polymorphism seemed to be associated with multiple colorectal adenomas in Korean families, differing from those in other ethnic groups.
  • Some BER variants involved in specific APC mutations are associated with characteristics of histogenesis other than altered mismatch repair or p53 pathway.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Mutation. Neoplasms, Multiple Primary / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Adult. Aged. Aged, 80 and over. DNA Glycosylases / genetics. DNA Glycosylases / metabolism. DNA Mismatch Repair. DNA Mutational Analysis. DNA Repair Enzymes / genetics. DNA Repair Enzymes / metabolism. DNA-(Apurinic or Apyrimidinic Site) Lyase / genetics. DNA-(Apurinic or Apyrimidinic Site) Lyase / metabolism. Female. Humans. Male. Middle Aged. Mitochondrial Proteins / genetics. Mitochondrial Proteins / metabolism. N-Glycosyl Hydrolases / genetics. N-Glycosyl Hydrolases / metabolism. Neoplasm Staging. Phosphoric Monoester Hydrolases / genetics. Phosphoric Monoester Hydrolases / metabolism. Polymorphism, Single Nucleotide. Prospective Studies

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  • (PMID = 17252231.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mitochondrial Proteins; EC 3.1.3.2 / Phosphoric Monoester Hydrolases; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / N-Glycosyl Hydrolases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.2.2.- / oxoguanine glycosylase 1, human; EC 3.6.1.55 / 8-oxodGTPase; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase; EC 6.5.1.- / DNA Repair Enzymes
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10. Amiot A, Dokmak S, Sauvanet A, Vilgrain V, Bringuier PP, Scoazec JY, Sastre X, Ruszniewski P, Bedossa P, Couvelard A: Sporadic desmoid tumor. An exceptional cause of cystic pancreatic lesion. JOP; 2008;9(3):339-45
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  • Intra-abdominal forms involve the mesentery and retroperitoneum and usually occur associated with familial adenomatous polyposis or Gardner's syndrome.
  • Although desmoid tumors do not metastasize, their evolution can be life-threatening due to aggressive local invasion, such as mesentery involvement.
  • The diagnosis of mucinous cystadenocarcinoma was suspected preoperatively and the patient underwent a splenopancreatectomy with en-bloc resection of the left colonic flexure, duodenojejunal junction and part of the posterior gastric wall.
  • The diagnosis was confirmed by immunocytochemical analysis and the assessment of the beta-catenin gene mutation.
  • After a 1-year follow-up, no recurrence was observed.
  • CONCLUSION: Desmoid tumors are very rare in the pancreas and their diagnosis can be difficult, such as in our case where it presented as a cystic lesion.
  • In contrast to intra-abdominal forms, sporadic pancreatic desmoid tumors are more frequent than those associated with familial adenomatous polyposis.
  • [MeSH-minor] Abdominal Pain / diagnosis. Abdominal Pain / etiology. Female. Humans. Middle Aged

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  • (PMID = 18469451.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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11. Richard MJ, Tornetta P 3rd: Emergent management of APC-2 pelvic ring injuries with an anteriorly placed C-clamp. J Orthop Trauma; 2009 May-Jun;23(5):322-6
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  • [Title] Emergent management of APC-2 pelvic ring injuries with an anteriorly placed C-clamp.
  • OBJECTIVE: Can anteriorly placed pelvic C-clamps be used successfully in the emergent management of APC-2 pelvic fractures?
  • PATIENTS: A single-surgeon series of 24 patients with an anteroposterior compression type 2 pelvic fracture.
  • RESULTS: Twenty-four patients with a mean age of 29 years (14-58 years) had an APC-2 pelvic fracture diagnosed by an anteroposterior radiograph of the pelvis on presentation.
  • Eleven patients presented with hypotension (systolic blood pressure <90 mm Hg) and had an average elevation of their blood pressure of 23 mm Hg (10-44 mm Hg).
  • Complications included 1 misdiagnosis of an APC-3 injury and 2 cases in which the clamp became dislodged when the patients were rolled in the intensive care unit.
  • Thirteen patients required laparotomy or angiography for further management after the C-clamp was applied.
  • The C-clamp was easily draped out of the field for both procedures.
  • CONCLUSIONS: The pelvic C-clamp can be placed anteriorly as a part of the early management of APC-2 pelvic fractures with a short application time in a variety of patient care areas.

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  • (PMID = 19390358.001).
  • [ISSN] 1531-2291
  • [Journal-full-title] Journal of orthopaedic trauma
  • [ISO-abbreviation] J Orthop Trauma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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12. Heald B, Moran R, Milas M, Burke C, Eng C: Familial adenomatous polyposis in a patient with unexplained mental retardation. Nat Clin Pract Neurol; 2007 Dec;3(12):694-700
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  • [Title] Familial adenomatous polyposis in a patient with unexplained mental retardation.
  • BACKGROUND: A 22-year-old woman was referred to a genomic medicine clinic for evaluation of suspected Prader-Willi syndrome (PWS) after normal DNA methylation studies on chromosome 15 were obtained.
  • DIAGNOSIS: Familial adenomatous polyposis with mental retardation, caused by an interstitial deletion of the long arm of chromosome 5 encompassing the APC (adenomatous polyposis coli) tumor suppressor locus.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Intellectual Disability / complications


13. Andersson HM, Arantes MJ, Crawley JT, Luken BM, Tran S, Dahlbäck B, Lane DA, Rezende SM: Activated protein C cofactor function of protein S: a critical role for Asp95 in the EGF1-like domain. Blood; 2010 Jun 10;115(23):4878-85
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  • [Title] Activated protein C cofactor function of protein S: a critical role for Asp95 in the EGF1-like domain.
  • Protein S has an established role in the protein C anticoagulant pathway, where it enhances the factor Va (FVa) and factor VIIIa (FVIIIa) inactivating property of activated protein C (APC).
  • Despite its physiological role and clinical importance, the molecular basis of its action is not fully understood.
  • To clarify the mechanism of the protein S interaction with APC, we have constructed and expressed a library of composite or point variants of human protein S, with residue substitutions introduced into the Gla, thrombin-sensitive region (TSR), epidermal growth factor 1 (EGF1), and EGF2 domains.
  • Cofactor activity for APC was evaluated by calibrated automated thrombography (CAT) using protein S-deficient plasma.
  • Of 27 variants tested initially, only one, protein S D95A (within the EGF1 domain), was largely devoid of functional APC cofactor activity.
  • Protein S D95A was, however, gamma-carboxylated and bound phospholipids with an apparent dissociation constant (Kd(app)) similar to that of wild-type (WT) protein S.
  • In a purified assay using FVa R506Q/R679Q, purified protein S D95A was shown to have greatly reduced ability to enhance APC-induced cleavage of FVa Arg306.
  • It is concluded that residue Asp95 within EGF1 is critical for APC cofactor function of protein S and could define a principal functional interaction site for APC.
  • [MeSH-major] Amino Acid Substitution. Aspartic Acid. Mutation, Missense. Protein C / chemistry. Protein S / chemistry
  • [MeSH-minor] Factor VIIIa / chemistry. Factor VIIIa / genetics. Factor VIIIa / metabolism. Factor Va / chemistry. Factor Va / genetics. Factor Va / metabolism. Humans. Protein Structure, Tertiary

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  • (PMID = 20308596.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 075160; United Kingdom / British Heart Foundation / / PG/09/105/28138; United Kingdom / British Heart Foundation / / PG/07/005; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein C; 0 / Protein S; 30KYC7MIAI / Aspartic Acid; 65522-14-7 / Factor Va; 72175-66-7 / Factor VIIIa
  • [Other-IDs] NLM/ PMC2884152; NLM/ UKMS29809
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14. Sarangi PP, Lee HW, Kim M: Activated protein C action in inflammation. Br J Haematol; 2010 Mar;148(6):817-33
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  • [Title] Activated protein C action in inflammation.
  • Activated protein C (APC) is a natural anticoagulant that plays an important role in coagulation homeostasis by inactivating the procoagulation factor Va and VIIIa.
  • In addition to its anticoagulation functions, APC also has cytoprotective effects such as anti-inflammatory, anti-apoptotic, and endothelial barrier protection.
  • Recently, a recombinant form of human APC (rhAPC or drotrecogin alfa activated; known commercially as 'Xigris') was approved by the US Federal Drug Administration for treatment of severe sepsis associated with a high risk of mortality.
  • Sepsis, also known as systemic inflammatory response syndrome (SIRS) resulting from infection, is a serious medical condition in critical care patients.
  • In sepsis, hyperactive and dysregulated inflammatory responses lead to secretion of pro- and anti-inflammatory cytokines, activation and migration of leucocytes, activation of coagulation, inhibition of fibrinolysis, and increased apoptosis.
  • Although initial hypotheses focused on antithrombotic and profibrinolytic functions of APC in sepsis, other agents with more potent anticoagulation functions were not effective in treating severe sepsis.
  • Furthermore, APC therapy is also associated with the risk of severe bleeding in treated patients.
  • Therefore, the cytoprotective effects, rather than the anticoagulant effect of APC are postulated to be responsible for the therapeutic benefit of APC in the treatment of severe sepsis.

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  • (PMID = 19995397.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R21 HL094797-01A1; United States / NHLBI NIH HHS / HL / HL18208; United States / NHLBI NIH HHS / HL / P01 HL018208; United States / NHLBI NIH HHS / HL / HL094797; United States / NHLBI NIH HHS / HL / HL094797-01A1; United States / NHLBI NIH HHS / HL / R01 HL087088; None / None / / P01 HL018208-33; United States / NHLBI NIH HHS / HL / R21 HL094797; United States / NHLBI NIH HHS / HL / P01 HL018208-33
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein C
  • [Number-of-references] 130
  • [Other-IDs] NLM/ NIHMS188551; NLM/ PMC2868910
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15. Reichling T, Goss KH, Carson DJ, Holdcraft RW, Ley-Ebert C, Witte D, Aronow BJ, Groden J: Transcriptional profiles of intestinal tumors in Apc(Min) mice are unique from those of embryonic intestine and identify novel gene targets dysregulated in human colorectal tumors. Cancer Res; 2005 Jan 1;65(1):166-76
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  • [Title] Transcriptional profiles of intestinal tumors in Apc(Min) mice are unique from those of embryonic intestine and identify novel gene targets dysregulated in human colorectal tumors.
  • The adenomatous polyposis coli (APC) tumor suppressor is a major regulator of the Wnt signaling pathway in normal intestinal epithelium.
  • APC, in conjunction with AXIN and GSK-3beta, forms a complex necessary for the degradation of beta-catenin, thereby preventing beta-catenin/T-cell factor interaction and alteration of growth-controlling genes such as c-MYC and cyclin D1.
  • Inappropriate activation of the Wnt pathway, via Apc/APC mutation, leads to gastrointestinal tumor formation in both the mouse and human.
  • In order to discover novel genes that may contribute to tumor progression in the gastrointestinal tract, we used cDNA microarrays to identify 114 genes with altered levels of expression in Apc(Min) mouse adenomas from the duodenum, jejunum, and colon.
  • Changes in the expression of 24 of these 114 genes were not observed during mouse development at embryonic day 16.5, postnatal day 1, or postnatal day 14 (relative to normal adult intestine).
  • These 24 genes are not previously known Wnt targets.
  • [MeSH-major] Colorectal Neoplasms / genetics. Gene Deletion. Genes, APC. Intestines / embryology. Transcription, Genetic
  • [MeSH-minor] Adenoma / genetics. Animals. Colonic Neoplasms / genetics. DNA, Complementary / genetics. Duodenal Neoplasms / genetics. Gastrointestinal Neoplasms / genetics. Genetic Markers. Humans. Jejunal Neoplasms / genetics. Mice. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction


16. Jeter JM, Kohlmann W, Gruber SB: Genetics of colorectal cancer. Oncology (Williston Park); 2006 Mar;20(3):269-76; discussion 285-6, 288-9
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  • Familial adenomatous polyposis is an autosomal dominant syndrome classically presenting with hundreds to thousands of adenomatous colorectal polyps that are caused by mutations in the APC gene.
  • A low-penetrance susceptibility allele that is common in Jews from Eastern Europe, APC 11307K, confers a two-fold increased risk of colorectal cancer without the full expression of familial adenomatous polyposis.
  • Biallelic mutations in the MYH gene are associated with an attenuated familial adenomatous polyposis phenotype.
  • Lynch syndrome (hereditary nonpolyposis colorectal cancer) is an autosomal dominant disorder characterized by early onset of colorectal cancer with microsatellite instability.
  • Mutations in mismatch repair genes lead to a lifetime colon cancer risk of 85% in these patients; carcinomas of the endometrium, ovary, and other organs also occur with increased frequency.
  • Although adenomas are not characteristic of the hamartomatous polyp syndromes such as juvenile polyposis and Peutz-Jeghers syndrome, individuals with these diseases have a markedly increased risk of colorectal cancer relative to the general population.
  • In this review, we will describe the phenotypes, genotypes, diagnosis, and management of hereditary colon cancer syndromes.
  • [MeSH-minor] Alleles. Disease Susceptibility. Humans. Mutation. Risk Assessment. Risk Factors

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  • (PMID = 16629258.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5T32CA09357
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 60
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17. Song M, Tao D, Liu Z, Li X, Zhou M: Image ratio features for facial expression recognition application. IEEE Trans Syst Man Cybern B Cybern; 2010 Jun;40(3):779-88
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  • In addition, to further improve facial expression recognition accuracy based on image ratio features, we combine image ratio features with facial animation parameters (FAPs), which describe the geometric motions of facial feature points.
  • Experimental results show that the proposed image ratio feature is more robust to albedo and lighting variations, and the combination of image ratio features and FAPs outperforms each feature alone.

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  • (PMID = 19884092.001).
  • [ISSN] 1941-0492
  • [Journal-full-title] IEEE transactions on systems, man, and cybernetics. Part B, Cybernetics : a publication of the IEEE Systems, Man, and Cybernetics Society
  • [ISO-abbreviation] IEEE Trans Syst Man Cybern B Cybern
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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18. Zhang Z, Roe SM, Diogon M, Kong E, El Alaoui H, Barford D: Molecular structure of the N-terminal domain of the APC/C subunit Cdc27 reveals a homo-dimeric tetratricopeptide repeat architecture. J Mol Biol; 2010 Apr 16;397(5):1316-28
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  • [Title] Molecular structure of the N-terminal domain of the APC/C subunit Cdc27 reveals a homo-dimeric tetratricopeptide repeat architecture.
  • The anaphase promoting complex/cyclosome (APC/C) is a large multi-subunit E3 ubiquitin ligase that targets specific cell cycle regulatory proteins for ubiquitin-dependent degradation, thereby controlling cell cycle events such as the metaphase to anaphase transition and the exit from mitosis.
  • Biochemical and genetic studies are consistent with the notion that subunits of APC/C are organised into two distinct sub-complexes; a catalytic sub-complex including the cullin domain and RING finger subunits Apc2 and Apc11, respectively, and a tetratricopeptide repeat (TPR) sub-complex composed of the TPR subunits Cdc16, Cdc23 and Cdc27 (Apc3).
  • Mutation of the Cdc27(Nterm) dimer interface destabilises the protein, disrupts dimerisation in solution, and abolishes the capacity of E. cuniculi Cdc27 to complement Saccharomyces cerevisiae Cdc27 in vivo.
  • These results establish the existence of functional APC/C genes in E. cuniculi, the evolutionarily conserved dimeric properties of Cdc27, and provide a framework for understanding the architecture of full-length Cdc27.
  • [MeSH-major] Encephalitozoon cuniculi / enzymology. Repetitive Sequences, Amino Acid. Ubiquitin-Protein Ligase Complexes / chemistry. Ubiquitin-Protein Ligases / chemistry
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Apc2 Subunit, Anaphase-Promoting Complex-Cyclosome. Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome. Apc8 Subunit, Anaphase-Promoting Complex-Cyclosome. Crystallography, X-Ray. Molecular Structure. Protein Multimerization. Protein Structure, Tertiary. Saccharomyces cerevisiae Proteins / chemistry

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20206185.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 3KAE
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome; 0 / Apc8 Subunit, Anaphase-Promoting Complex-Cyclosome; 0 / CDC23 protein, S cerevisiae; 0 / Saccharomyces cerevisiae Proteins; EC 6.3.2.19 / APC2 protein, S cerevisiae; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Apc2 Subunit, Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / CDC27 protein, S cerevisiae; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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19. Ghafir Y, Daube G: Comparison of swabbing and destructive methods for microbiological pig carcass sampling. Lett Appl Microbiol; 2008 Oct;47(4):322-6
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  • AIMS: To compare the Belgian swabbing sampling method for pig carcasses with the reference destructive method with regard to Escherichia coli and aerobic plate counts, Salmonella and Campylobacter prevalence and their relationship.
  • METHODS AND RESULTS: Recovery was significantly lower for the swabbing method and corresponded to a recovery of 36% for E. coli counts and 81% for aerobic plate counts in comparison with the destructive method.
  • A higher median for E. coli counts was detected for samples where Salmonella or Campylobacter were detected.
  • [MeSH-minor] Animals. Campylobacter / isolation & purification. Colony Count, Microbial / methods. Escherichia coli / isolation & purification. Food Handling / methods. Food Microbiology. Salmonella / isolation & purification

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  • (PMID = 19241527.001).
  • [ISSN] 0266-8254
  • [Journal-full-title] Letters in applied microbiology
  • [ISO-abbreviation] Lett. Appl. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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21. Suciu-Foca N, Manavalan JS, Scotto L, Kim-Schulze S, Galluzzo S, Naiyer AJ, Fan J, Vlad G, Cortesini R: Molecular characterization of allospecific T suppressor and tolerogenic dendritic cells: review. Int Immunopharmacol; 2005 Jan;5(1):7-11
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  • These CD8(+)CD28(-) T(S) cells can be generated in vitro after multiple rounds of stimulation of human peripheral blood mononuclear cells (PBMCs) with either allogenic- or xenogeneic-donor APCs.
  • CD8(+)CD28(-) T(S) cells are FOXP3+, MHC class I-restricted and tolerize both professional antigen presenting cells, such as dendritic cells (DC) and nonprofessional APC such as endothelial cells (EC) by up-regulating the cell surface expression of inhibitory receptors immunoglobulin-like transcript (ILT)-3 and ILT4 and down-regulating the expression of costimulatory molecules such as CD58 and CD86.
  • Tolerized ILT3(high), ILT4(high) APC anergize CD4(+) T(H) cells and can induce the generation of antigen-specific CD4(+)CD25(+) T regulatory cells (T(R)) cells and CD8(+)CD28(-) T(S) cells.
  • In this review, we present our recent studies on the molecular characterization of these antigen specific T suppressor cells and tolerogenic APC.

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  • (PMID = 15589454.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI25210-18; United States / NIAID NIH HHS / AI / AI55234-02
  • [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.; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 22
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22. Boks MA, Zwaginga JJ, van Ham SM, ten Brinke A: An optimized CFSE-based T-cell suppression assay to evaluate the suppressive capacity of regulatory T-cells induced by human tolerogenic dendritic cells. Scand J Immunol; 2010 Aug;72(2):158-68
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  • In autoimmune diseases or transplant graft rejection, a therapy that will prevent or reduce the present immune activation is highly desired.
  • Ex vivo generated tolerogenic dendritic cells (DC) are considered to have a strong potential as cellular therapy for these diseases.
  • Our results show that the suppressive capacity of IL-10 DC-induced Treg measured in the suppression assay increases with the iTreg dose and decreases with higher numbers of antigen-presenting cells (APC) as T-cell stimulation.
  • In conclusion, we recommend titrations of both APC and iTreg in the suppression assay and to include a negative control condition with T-cells primed by mDC, to distinguish specific and functional suppression by iTreg from possible generalized suppressive activity.
  • [MeSH-minor] Antigen-Presenting Cells / cytology. Antigen-Presenting Cells / immunology. Cell Communication / immunology. Cell Growth Processes / immunology. Cytokines / biosynthesis. Dose-Response Relationship, Immunologic. Humans. Interleukin-10 / immunology. Interleukin-10 / pharmacology. Lymphocyte Activation / drug effects. Lymphocyte Activation / immunology

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  • (PMID = 20618775.001).
  • [ISSN] 1365-3083
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5-(6)-carboxyfluorescein diacetate succinimidyl ester; 0 / Cytokines; 0 / Fluoresceins; 0 / Succinimides; 130068-27-8 / Interleukin-10
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23. Han YY, Dinse GE, Umbach DM, Davis DL, Weissfeld JL: Age-period-cohort analysis of cancers not related to tobacco, screening, or HIV: sex and race differences. Cancer Causes Control; 2010 Aug;21(8):1227-36
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  • [Title] Age-period-cohort analysis of cancers not related to tobacco, screening, or HIV: sex and race differences.
  • OBJECTIVE: To identify trends in a residual category of cancers not typically associated with tobacco, screening, or human immunodeficiency virus (HIV) infection.
  • METHODS: For persons aged 20-84, we used sex- and race-specific age-period-cohort (APC) models to describe temporal patterns of incidence (1975-2004) and mortality (1970-2004) in the U.S. for a residual cancer category that excluded non-Hodgkin lymphoma, Kaposi sarcoma, and cancer of the oral cavity and pharynx, esophagus, pancreas, larynx, lung and bronchus, urinary bladder, kidney and renal pelvis, colon and rectum, prostate, female breast, and cervix uteri.
  • Extrapolations of APC models predicted higher age-adjusted incidence rates in white women (11%), black women (5%), and white men (4%) in 2005-2009, relative to 2000-2004, and lower rates in black men (-3%), accompanied by lower age-adjusted mortality rates in every sex-race group (-8% in black men, -3% in black women, -1% in white men, and -1% in white women).

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  • (PMID = 20373012.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA ES102265-03
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ NIHMS202679; NLM/ PMC2904415
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24. Buslje CM, Santos J, Delfino JM, Nielsen M: Correction for phylogeny, small number of observations and data redundancy improves the identification of coevolving amino acid pairs using mutual information. Bioinformatics; 2009 May 1;25(9):1125-31
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  • MOTIVATION: Mutual information (MI) theory is often applied to predict positional correlations in a multiple sequence alignment (MSA) to make possible the analysis of those positions structurally or functionally important in a given fold or protein family.
  • Accurate identification of coevolving positions in protein sequences is difficult due to the high background signal imposed by phylogeny and noise.
  • Several methods have been proposed using MI to identify coevolving amino acids in protein families.
  • The evaluation is made on large sets of both in silico-generated alignments as well as on biological sequence data.
  • The methods included in the analysis are the APC (average product correction) and RCW (row-column weighting) methods.
  • The best performing method was APC including sequence-weighting and low-count corrections.
  • The use of sequence-permutations to calculate a MI rescaling is shown to significantly improve the prediction accuracy and allows for direct comparison of information values across protein families.
  • With our contribution, we achieve a noteworthy improvement on the current procedures to determine coevolution and residue contacts, and we believe that this will have potential impacts on the understanding of protein structure, function and folding.

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  • (PMID = 19276150.001).
  • [ISSN] 1367-4811
  • [Journal-full-title] Bioinformatics (Oxford, England)
  • [ISO-abbreviation] Bioinformatics
  • [Language] ENG
  • [Grant] United States / PHS HHS / / HHSN266200400025C
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Proteins
  • [Other-IDs] NLM/ PMC2672635
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25. Yamamuro T, Kano K, Naito K: Functions of FZR1 and CDC20, activators of the anaphase-promoting complex, during meiotic maturation of swine oocytes. Biol Reprod; 2008 Dec;79(6):1202-9
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  • Cell division cycle 20 (CDC20) and fizzy/cell division cycle 20 related 1 (FZR1) are activators of the anaphase-promoting complex (APC), which ubiquitinates M-phase regulating proteins, such as cyclin B and securin, and induces their degradation.
  • The inhibition of CDC20 expression by the injection of CDC20 antisense RNA induced the meiotic arrest at the first meiotic metaphase (M1) and the accumulation of a large amount of cyclin B.
  • On the other hand, the inhibition of FZR1 expression accelerated cyclin B accumulation and the start of germinal vesicle breakdown (GVBD), but did not affect the exit from M1.
  • Surprisingly, the injection of CDC20 mRNA into the immature oocytes could not increase CDC20 expression, but increased cyclin B accumulation and accelerated the meiotic progression.
  • As CDC20 is a substrate of APC (FZR1), CDC20 might have competed with cyclin B and inhibited the FZR1 function.
  • [MeSH-major] Anaphase / physiology. Cell Cycle Proteins / genetics. Meiosis / physiology. Oocytes / physiology. Ubiquitin-Protein Ligase Complexes / physiology

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  • (PMID = 18753608.001).
  • [ISSN] 0006-3363
  • [Journal-full-title] Biology of reproduction
  • [ISO-abbreviation] Biol. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin B; 0 / Cyclin B1; 0 / DNA, Complementary; 0 / RNA, Antisense; 0 / RNA, Messenger; EC 2.7.11.22 / Maturation-Promoting Factor; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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26. Graf B, Bushnell T, Miller J: LFA-1-mediated T cell costimulation through increased localization of TCR/class II complexes to the central supramolecular activation cluster and exclusion of CD45 from the immunological synapse. J Immunol; 2007 Aug 1;179(3):1616-24
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  • [Title] LFA-1-mediated T cell costimulation through increased localization of TCR/class II complexes to the central supramolecular activation cluster and exclusion of CD45 from the immunological synapse.
  • T cell activation is associated with a dramatic reorganization of cell surface proteins and associated signaling components into discrete subdomains within the immunological synapse in T cell:APC conjugates.
  • However, the signals that direct the localization of these proteins and the functional significance of this organization have not been established.
  • In this study, we have used wild-type and LFA-1-deficient, DO11.10 TCR transgenic T cells to examine the role of LFA-1 in the formation of the immunological synapse.
  • We found that coengagement of LFA-1 is not required for the formation of the central supramolecular activation cluster (cSMAC) region, but does increase the accumulation of TCR/class II complexes within the cSMAC.
  • In addition, LFA-1 is required for the recruitment and localization of talin into the peripheral supramolecular activation cluster region and exclusion of CD45 from the synapse.
  • These data support the idea that in addition to its important role on regulating T cell:APC adhesion, coengagement of LFA-1 can enhance T cell signaling, and suggest that this may be accomplished in part through the organization of proteins within the immunological synapse.

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  • (PMID = 17641028.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI048237; United States / NIAID NIH HHS / AI / R01 AI048237-01; United States / NIAID NIH HHS / AI / R01-AI48237
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Histocompatibility Antigens Class II; 0 / Lymphocyte Function-Associated Antigen-1; 0 / Receptors, Antigen, T-Cell; 0 / Talin; EC 3.1.3.48 / Antigens, CD45
  • [Other-IDs] NLM/ NIHMS336669; NLM/ PMC3993012
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27. Roberts LE, Fini MA, Derkash N, Wright RM: PD98059 enhanced insulin, cytokine, and growth factor activation of xanthine oxidoreductase in epithelial cells involves STAT3 and the glucocorticoid receptor. J Cell Biochem; 2007 Aug 15;101(6):1567-87
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  • [Title] PD98059 enhanced insulin, cytokine, and growth factor activation of xanthine oxidoreductase in epithelial cells involves STAT3 and the glucocorticoid receptor.
  • PD98059 and U0126 are organic compound inhibitors frequently used to block the activity of the MEK-1/2 protein kinase.
  • In the present work, promoter activation analyses of xanthine oxidoreductase (XOR) in epithelial cells uncovered the unexpected opposite effect of these inhibitors on activation of XOR.
  • Activation of an XOR-luciferase fusion gene was studied in stably transfected epithelial cells.
  • The XOR reporter gene was activated by the epidermal growth factors (EGF), prolactin, and dexamethasone and by the acute phase cytokines (APC) IL-1, IL-6, and TNFalpha as previously reported for its native gene, and insulin further stimulated activation induced with acute phase cytokines or growth factors.
  • Activation of the proximal promoter was blocked by inhibitors of the glucocorticoid receptor (GR), p38 MAP kinase, and U0126.
  • Unexpectedly, PD98059 activated the promoter and significantly enhanced expression induced by insulin, APC, or growth factors.
  • Analysis of the XOR upstream DNA and proximal promoter revealed primary roles for the GR and STAT3 in mediating the effects of PD98059 on XOR activation and protein complex formation with the promoter.
  • XOR activation by PD98059, dexamethasone, or insulin was superinduced by a constitutively active derivative of STAT3, while a dominant negative derivative of STAT3 blocked the enhancing effect of PD98059 on XOR activation.
  • These data demonstrate a previously unrecognized effect of PD98059 on STAT3 and the GR that could have unanticipated consequences when used to infer the involvement of the MEK-1/2 protein kinase.
  • [MeSH-minor] Animals. Cell Line. Dexamethasone / metabolism. Enzyme Activation. Genes, Reporter. Glucocorticoids / metabolism. Hormone Antagonists / metabolism. Humans. MAP Kinase Kinase Kinases / antagonists & inhibitors. MAP Kinase Kinase Kinases / metabolism. Mice. Mifepristone / metabolism. Promoter Regions, Genetic. Rats. Rats, Sprague-Dawley

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  • (PMID = 17370312.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL45582; United States / NHLBI NIH HHS / HL / HL52509
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Insulin; 0 / Receptors, Glucocorticoid; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, rat; 320T6RNW1F / Mifepristone; 7S5I7G3JQL / Dexamethasone; EC 1.17.1.4 / Xanthine Dehydrogenase; EC 2.7.11.25 / MAP Kinase Kinase Kinases
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28. Yang J, Zhang W, Evans PM, Chen X, He X, Liu C: Adenomatous polyposis coli (APC) differentially regulates beta-catenin phosphorylation and ubiquitination in colon cancer cells. J Biol Chem; 2006 Jun 30;281(26):17751-7
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  • [Title] Adenomatous polyposis coli (APC) differentially regulates beta-catenin phosphorylation and ubiquitination in colon cancer cells.
  • Most colorectal cancers have mutations of the adenomatous polyposis coli (APC) gene or the beta-catenin gene that stabilize beta-catenin and activate beta-catenin target genes, leading ultimately to cancer.
  • The molecular mechanisms of APC function in beta-catenin degradation are not completely known.
  • APC binds beta-catenin and is involved in the Axin complex, suggesting that APC regulates beta-catenin phosphorylation.
  • Some evidence also suggests that APC regulates beta-catenin nuclear export.
  • Here, we examine the effects of APC mutations on beta-catenin phosphorylation, ubiquitination, and degradation in the colon cancer cell lines SW480, DLD-1, and HT29, each of which contains a different APC truncation.
  • Although the current models suggest that beta-catenin phosphorylation should be inhibited by APC mutations, we detected significant beta-catenin phosphorylation in these cells.
  • However, beta-catenin ubiquitination and degradation were inhibited in SW480 but not in DLD-1 and HT29 cells.
  • The ubiquitination ofbeta-catenin in SW480 cells can be rescued by exogenous expression of APC.
  • The APC domains required for beta-catenin ubiquitination were analyzed.
  • Our results suggest that APC regulates beta-catenin phosphorylation and ubiquitination by distinct domains and by separate molecular mechanisms.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / metabolism. Colonic Neoplasms / metabolism. Ubiquitin / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Dinucleotide Repeats. HT29 Cells. Humans. Mutation. Phosphorylation. Protein Structure, Tertiary

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  • (PMID = 16798748.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 112007
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Ubiquitin; 0 / beta Catenin
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29. Conlin A, Smith G, Carey FA, Wolf CR, Steele RJ: The prognostic significance of K-ras, p53, and APC mutations in colorectal carcinoma. Gut; 2005 Sep;54(9):1283-6
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  • [Title] The prognostic significance of K-ras, p53, and APC mutations in colorectal carcinoma.
  • BACKGROUND: Accumulation of molecular alterations, including mutations in Kirsten-ras (K-ras), p53, and adenomatous polyposis coli (APC), contribute to colorectal carcinogenesis.
  • AIMS: To correlate the presence or absence of mutations in K-ras, p53, and APC with survival in a cohort of colorectal cancer patients.
  • METHODS: Colorectal tumours were characterised for mutations in K-ras, p53, and APC.
  • Kaplan-Meier survival curves were constructed using overall survival and disease specific survival as the primary end points.
  • K-ras mutations were also significantly associated with poorer disease specific survival.
  • The presence of APC and p53 mutations did not affect survival in this cohort of patients (p = 0.9034 and p = 0.8290, respectively).
  • [MeSH-minor] Aged, 80 and over. DNA Mutational Analysis. Female. Genes, APC. Genes, p16. Genes, p53. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Proportional Hazards Models. Scotland. Survival Analysis

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  • (PMID = 15843421.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1774675
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30. Laurent-Puig P, Zucman-Rossi J: Genetics of hepatocellular tumors. Oncogene; 2006 Jun 26;25(27):3778-86
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  • It includes integration of hepatitis B virus (HBV) DNA, R249S TP53 (tumor protein p53) mutation in aflatoxin B1-exposed patients, KRAS mutations related to vinyl chloride exposure, hepatocyte nuclear factor 1alpha (HNF1alpha) mutations associated to hepatocellular adenomas and adenomatosis polyposis coli (APC) germline mutations predisposing to hepatoblastomas.
  • The second set of genetic alterations are etiological nonspecific, it includes recurrent gains and losses of chromosomes, alteration of TP53 gene, activation of WNT/beta-catenin pathway through CTNNB1/beta-catenin and AXIN (axis inhibition protein) mutations, inactivation of retinoblastoma and IGF2R (insulin-like growth factor 2 receptor) pathways through inactivation of RB1 (retinoblastoma 1), P16 and IGF2R.
  • Hepatitis B virus and poorly differentiated tumors are related to chromosome instable tumors associated with frequent TP53 mutations, whereas non-HBV and well-differentiated tumors are related to chromosomal stable samples that are frequently beta-catenin activated.


31. Nguyen HG, Chinnappan D, Urano T, Ravid K: Mechanism of Aurora-B degradation and its dependency on intact KEN and A-boxes: identification of an aneuploidy-promoting property. Mol Cell Biol; 2005 Jun;25(12):4977-92
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  • [Title] Mechanism of Aurora-B degradation and its dependency on intact KEN and A-boxes: identification of an aneuploidy-promoting property.
  • During the cell cycle, the level of this protein is tightly controlled, and its deregulated abundance is suspected to contribute to aneuploidy.
  • Here, we provide evidence that Aurora-B is a short-lived protein degraded by the proteasome via the anaphase-promoting cyclosome complex (APC/c) pathway.
  • Aurora-B interacts with the APC/c through the Cdc27 subunit, Aurora-B is ubiquitinated, and its level is increased upon treatment with inhibitors of the proteasome.
  • Aurora-B binds in vivo to the degradation-targeting proteins Cdh1 and Cdc20, the overexpression of which accelerates Aurora-B degradation.
  • Using deletions or point mutations of the five putative degradation signals in Aurora-B, we show that degradation of this protein does not depend on its D-boxes (RXXL), but it does require intact KEN boxes and A-boxes (QRVL) located within the first 65 amino acids.
  • Cells transfected with wild-type or A-box-mutated or KEN box-mutated Aurora-B fused to green fluorescent protein display the protein localized to the chromosomes and then to the midzone during mitosis, but the mutated forms are detected at greater intensities.
  • Intriguingly, overexpression of a stable form of Aurora-B alone induces aneuploidy and anchorage-independent growth.

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  • (PMID = 15923616.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007035; United States / PHS HHS / / 58537; United States / NHLBI NIH HHS / HL / T32 HL07035
  • [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 / Antineoplastic Agents; 0 / Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome; 0 / CDC27 protein, human; 0 / Cdc20 Proteins; 0 / Cell Cycle Proteins; 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 0 / Proteasome Inhibitors; 0 / Recombinant Fusion Proteins; 0 / Ubiquitin; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 156288-95-8 / CDC20 protein, human; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; SH1WY3R615 / Nocodazole
  • [Other-IDs] NLM/ PMC1140599
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32. Munar-Qués M, Masjuan J, Coelho T, Moreira P, Viader-Farré C, Saraiva MJ: Familial amyloid polyneuropathy associated with TTRSer50Arg mutation in two Iberian families presenting a novel single base change in the mutant gene. Amyloid; 2007 Jun;14(2):147-52
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  • [Title] Familial amyloid polyneuropathy associated with TTRSer50Arg mutation in two Iberian families presenting a novel single base change in the mutant gene.
  • We present two families, from Spain and Portugal, with familial amyloid polyneuropathy (FAP) associated with the mutation TTRSer50Arg.
  • This mutation was first described in two Japanese patients from independent families and later in a French-Italian patient and a Vietnamese family.
  • In the patients of both families, FAP was very aggressive as they rapidly developed multiple symptoms with progressive deterioration; we emphasize the presence of severe orthostatic hypotension in the Spanish proband which confined him to a wheelchair.
  • The mutation was detected in four patients and one disease-free relative by DNA sequencing of exon 3 and induced mutation restriction analysis.
  • To our knowledge only six FAP mutations with more than one single nucleotide mutation for the same codon have been reported to date.
  • [MeSH-major] Amyloid Neuropathies, Familial / genetics. Point Mutation. Prealbumin / genetics

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  • (PMID = 17577688.001).
  • [ISSN] 1350-6129
  • [Journal-full-title] Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
  • [ISO-abbreviation] Amyloid
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Prealbumin; 9007-49-2 / DNA
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33. Wada Y, Ando Y, Kai N, Takahashi W, Kikukawa H, Nakanishi J, Honda J, Jinnouchi Y, Ueda S: Lower urinary tract dysfunction in type 1 familial amyloidotic polyneuropathy in Kumamoto, Japan. Int J Urol; 2006 Dec;13(12):1475-8
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  • [Title] Lower urinary tract dysfunction in type 1 familial amyloidotic polyneuropathy in Kumamoto, Japan.
  • OBJECTIVE: To evaluate lower urinary tract dysfunction of type 1 familial amyloidotic polyneuropathy (FAP) patients in Kumamoto, Japan.
  • METHODS: Lower urinary tract symptoms were evaluated in FAP patients.
  • Urodynamic studies were evaluated in FAP patients as compared to those in control subjects.
  • First desire to void (FDV), strong desire to void (SDV) and post-voided residual urine (PVR) were increased in FAP patients as compared to those in control subjects.
  • In the urethral pressure profilometry, 71%, 10% and 19% patients showed incompetent, normal functional and overactive urethral closure mechanism, respectively.
  • Maximum urethral pressure (MUP), maximum urethral closure pressure (MUCP) and functional profile length (FPL) were decreased in FAP patients compared to those in control subjects.
  • CONCLUSION: Autonomic, somatic nerve systems and bladder detrusor musculature might be impaired in lower urinary tract of type 1 FAP patients in Kumamoto, Japan.
  • [MeSH-major] Amyloid Neuropathies, Familial / complications. Urban Population. Urinary Bladder, Overactive / complications. Urinary Incontinence / complications. Urinary Retention / complications

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  • (PMID = 17118020.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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34. Abstracts of the 1st Conference of InSiGHT, the International Society for Gastrointestinal Hereditary Tumors, Newcastle upon Tyne, United Kingdom, 14-17 June 2005. Fam Cancer; 2005;4 Suppl 1:25-140
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  • [Title] Abstracts of the 1st Conference of InSiGHT, the International Society for Gastrointestinal Hereditary Tumors, Newcastle upon Tyne, United Kingdom, 14-17 June 2005.
  • [MeSH-major] Adenomatous Polyposis Coli. Colorectal Neoplasms, Hereditary Nonpolyposis

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  • (PMID = 15889224.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] Netherlands
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35. Fernandez U, Vodovotz Y, Courtney P, Pascall MA: Extended shelf life of soy bread using modified atmosphere packaging. J Food Prot; 2006 Mar;69(3):693-8
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  • This study investigated the use of modified atmosphere packaging (MAP) to extend the shelf life of soy bread with and without calcium propionate as a chemical preservative.
  • The shelf life was determined by monitoring mold and yeast (M+Y) and aerobic plate counts (APC) in soy bread samples stored at 21 degrees C +/- 3 degrees C and 38% +/- 2% relative humidity.
  • At 0, 2, 4, 6, 8, 10, and 12 days of storage, soy bread samples were removed, and the M+Y and APC were determined.
  • The preservative, the films, and the headspace gases had significant effects on both the M+Y counts and the APC of soy bread samples.
  • The combination of film 2 in the 50% CO2-50% N2 or 20% CO2-80% N2 headspace gases without calcium propionate as the preservative inhibited the M+Y growth by 6 days and the APC by 4 days.
  • It was thus concluded that MAP using film 2 with either the 50% CO2-50% N2 or 20% CO2-80% N2 was the best combination for shelf-life extension of the soy bread without the need for a chemical preservative.
  • These MAP treatments extended the shelf life by at least 200%.

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  • (PMID = 16541708.001).
  • [ISSN] 0362-028X
  • [Journal-full-title] Journal of food protection
  • [ISO-abbreviation] J. Food Prot.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Food Preservatives; 0 / Propionates; 0 / calcium propionate; 142M471B3J / Carbon Dioxide; 79-09-4 / propionic acid; N762921K75 / Nitrogen
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36. Roether JA, Daniel DJ, Rani DA, Deegan DE, Cheeseman CR, Boccaccini AR: Properties of sintered glass-ceramics prepared from plasma vitrified air pollution control residues. J Hazard Mater; 2010 Jan 15;173(1-3):563-9
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  • Air pollution control (APC) residues, obtained from a major UK energy from waste (EfW) plant, processing municipal solid waste, have been blended with silica and alumina and melted using DC plasma arc technology.
  • The research demonstrates that glass-ceramics can be readily formed from DC plasma treated APC residues and that these have comparable properties to marble and porcelain.
  • This novel approach represents a technically and commercially viable treatment option for APC residues that allow the beneficial reuse of this problematic waste.

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  • (PMID = 19773123.001).
  • [ISSN] 1873-3336
  • [Journal-full-title] Journal of hazardous materials
  • [ISO-abbreviation] J. Hazard. Mater.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Air Pollutants, Occupational; 85422-94-2 / Glass ceramics
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37. Pan SY, Xie EF, Shu YQ, Gao L, Zhang LX, Chen D, Chen JB, Zhao WJ, Mu Y, Zhang JN: [Methylation quantification of adenomatous polyposis coli (APC) gene promoter in plasma of lung cancer patients]. Ai Zheng; 2009 Apr;28(4):384-9
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  • [Title] [Methylation quantification of adenomatous polyposis coli (APC) gene promoter in plasma of lung cancer patients].
  • BACKGROUND AND OBJECTIVE: The protein encoded by adenomatous polyposis coli (APC) gene participates in the signaling transduction pathway.
  • Substantial studies have revealed that hypermethylation of APC gene promoter is closely related to the pathogenesis and development of cancer.
  • This study was to develop a real-time quantitative methylation specific PCR (real-time QMSP) method, and detect the methylation of APC gene promoter in plasma of lung cancer patients.
  • METHODS: Genomic DNA with methylated APC gene promoter was extracted from the lung cancer cell line NCI-H460 using phenol-chloroform and quantified by spectrophotometric measurements.
  • The concentration of cell-free methylated APC gene promoter in the plasma samples was quantified by the external reference method with the standard curve constructed using simulated plasma.
  • Of 78 lung cancer patients, positive methylation of the APC gene promoter was detected in tumor tissues of 40 cases.
  • Among the 40 lung cancer patients, positive methylation of the APC gene promoter was found in the plasma of 19 patients (47.5%).
  • The concentrations of methylated APC promoter in the 19 lung cancer patients ranged from 1.67x10(2) to 6.78x10(3) copies/mL, with a median concentration of 1.67x10(3) copies/mL.
  • No positive methylation of the APC gene promoter was detected in the plasma of 38 lung cancer patients without APC gene methylation in tissues, 31 benign lung diseases and 23 healthy controls.
  • CONCLUSIONS: The newly developed real-time QMSP method allows the quantitative measurement of APC gene promoter methylation in plasma.
  • Hypermethylation of the APC gene promoter in plasma is a potential diagnostic marker for lung cancer diagnosis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Genes, APC. Lung Neoplasms / genetics. Promoter Regions, Genetic

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  • (PMID = 19622298.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / DNA, Neoplasm
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38. Azevedo GD, Franco RF, Baggio MS, Maranhão TM, Sá MF: Procoagulant state after raloxifene therapy in postmenopausal women. Fertil Steril; 2005 Dec;84(6):1680-4
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  • MAIN OUTCOME MEASURE(S): Plasma activities of coagulation factors (II, V, VII, VIII, IX, X, XI, XII, and fibrinogen), prothrombin-derived fragment 1+2, and activated protein C (APC) sensitivity ratio were measured at baseline and after 1, 3, and 6 months of treatment.
  • A significant reduction of APC sensitivity ratio also was observed after 6 months of treatment.
  • CONCLUSION(S): A procoagulant state characterized by increased factor VIII, XI, and XII plasma levels and by reduced APC sensitivity was observed after raloxifene therapy in post-menopausal women.
  • [MeSH-minor] Blood Coagulation Factors / metabolism. Female. Fibrinogen / metabolism. Humans. Longitudinal Studies. Middle Aged. Peptide Fragments / metabolism. Prospective Studies. Protein C / metabolism. Protein Precursors / metabolism. Prothrombin / metabolism. Thrombosis / chemically induced

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  • (PMID = 16359964.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Coagulation Factors; 0 / Peptide Fragments; 0 / Protein C; 0 / Protein Precursors; 0 / Selective Estrogen Receptor Modulators; 4F86W47BR6 / Raloxifene Hydrochloride; 72270-84-9 / prothrombin fragment 1; 78768-79-3 / prothrombin fragment 2; 9001-26-7 / Prothrombin; 9001-32-5 / Fibrinogen
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39. Alferez D, Wilkinson RW, Watkins J, Poulsom R, Mandir N, Wedge SR, Pyrah IT, Smith NR, Jackson L, Ryan AJ, Goodlad RA: Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice. Mol Cancer Ther; 2008 Mar;7(3):590-8
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  • [Title] Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice.
  • Both the epidermal growth factor (EGF) and the vascular endothelial growth factor (VEGF) pathways are associated with intestinal cancer, and therapeutic approaches targeting either EGF receptor (EGFR) or VEGF receptor (VEGFR) signaling have recently been approved for patients with advanced colorectal cancer.
  • The Apc(Min/+) mouse is a well-characterized in vivo model of intestinal tumorigenesis, and animals with this genetic mutation develop macroscopically detectable adenomas from approximately 6 weeks of age.
  • Previous work in the Apc(Min/+) mouse has shown that therapeutic approaches targeting either VEGFR or EGFR signaling affect predominantly the size or number of adenomas, respectively.
  • To assess the effects of ZD6474 on early- and later-stage disease, treatment was initiated in 6- and 10-week-old Apc(Min/+) mice for 28 days.
  • ZD6474 markedly reduced both the number and the size of polyps when administered at either an early or a later stage of polyp development.
  • This reduction in both adenoma number and size resulted in a total reduction in tumor burden in the small intestine of nearly 75% in both studies (P < 0.01).
  • The current data build on the concept that EGFR-dependent tumor cell proliferation and VEGF/VEGFR2-dependent angiogenesis and survival are distinct key mechanisms in polyp development.
  • Pharmacologic inhibition of both signaling pathways has significant antitumor effects at both early and late stages of polyp development.
  • Therefore, targeting both VEGFR- and EGFR-dependent signaling may be a beneficial strategy in early intestinal cancer.
  • [MeSH-major] Adenoma / pathology. Genes, APC. Intestinal Neoplasms / pathology. Receptor, Epidermal Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Signal Transduction

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  • (PMID = 18347145.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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40. Berdah SV, Mardion RB, Grimaud JC, Barthet M, Orsoni P, Moutardier V, Brunet C: Mid-term functional outcome of laparoscopic restorative proctocolectomy: a prospective study of 40 consecutive cases. J Laparoendosc Adv Surg Tech A; 2009 Aug;19(4):485-8
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  • MATERIALS AND METHODS: From May 1999 to May 2008, 68 consecutive two-stage laparoscopic total proctocolectomies with ileal pouch-anal anastomosis were performed (ulcerative colitis: n = 61; familial adenomatous polyposis: n = 7).
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Colitis, Ulcerative / surgery. Colonic Pouches. Laparoscopy. Proctocolectomy, Restorative

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  • (PMID = 19489673.001).
  • [ISSN] 1092-6429
  • [Journal-full-title] Journal of laparoendoscopic & advanced surgical techniques. Part A
  • [ISO-abbreviation] J Laparoendosc Adv Surg Tech A
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Eglezos S: The bacteriological quality of retail-level peanut, almond, cashew, hazelnut, brazil, and mixed nut kernels produced in two Australian nut-processing facilities over a period of 3 years. Foodborne Pathog Dis; 2010 Jul;7(7):863-6
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  • A total of 564 ready-to-eat retail packs were analyzed for aerobic plate count (APC), Salmonella, coagulase-positive staphylococci, Listeria monocytogenes, and Escherichia coli.
  • There was no Salmonella, E. coli, or coagulase-positive staphylococci detected in any sample. L. monocytogenes was detected in two of the mixed packs after enrichment, but was not detected from samples by an alternate enumeration method (detection limit = 10/g).
  • The APC percentages of positive samples with counts above the detection level of the plating method used (100 CFU/g) for peanuts, almonds, cashews, hazelnuts, brazil nuts, and mixed nuts were 48%, 36%, 62%, 36%, 56%, and 44%, respectively.
  • The maximum APC was 3.9 log CFU/g.
  • The bacteriological quality of roasted peanut, almond, cashew, hazelnut, brazil, and mixed nut kernels processed in Australian facilities does not appear to suggest a public health concern.

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  • (PMID = 20184453.001).
  • [ISSN] 1556-7125
  • [Journal-full-title] Foodborne pathogens and disease
  • [ISO-abbreviation] Foodborne Pathog. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Igarashi H, Ito T, Kawabe K, Hisano T, Arita Y, Kaku T, Takayanagi R: Chemoradiotherapy with twice-weekly administration of low-dose gemcitabine for locally advanced pancreatic cancer. World J Gastroenterol; 2008 Sep 14;14(34):5311-5
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  • After that, maintenance systemic chemotherapy with gemcitabine, at a dose of 1000 mg/m(2), was administered weekly for 3 wk with 1-wk rest until disease progression or unacceptable toxicity developed.
  • Three of those patients could not continue with the therapy; one patient had interstitial pneumonia during radiation therapy and two other patients showed liver metastasis or peritoneal metastasis during an early stage of the therapy.
  • The subgroup which showed the reduction of tumor development, more than 50% showed a tendency for a better prognosis; however, other parameters including age, gender and performance status did not correlate with survival.
  • [MeSH-minor] Aged. Combined Modality Therapy. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Kaplan-Meier Estimate. Liver Neoplasms / secondary. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18785284.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Radiation-Sensitizing Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ PMC2744062
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43. McCartney BM, Price MH, Webb RL, Hayden MA, Holot LM, Zhou M, Bejsovec A, Peifer M: Testing hypotheses for the functions of APC family proteins using null and truncation alleles in Drosophila. Development; 2006 Jun;133(12):2407-18
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  • [Title] Testing hypotheses for the functions of APC family proteins using null and truncation alleles in Drosophila.
  • Adenomatous polyposis coli (APC) is mutated in colon cancers.
  • During normal development, APC proteins are essential negative regulators of Wnt signaling and have cytoskeletal functions.
  • Many functions have been proposed for APC proteins, but these have often rested on dominant-negative or partial loss-of-function approaches.
  • Thus, despite intense interest in APC, significant questions remain about its full range of cellular functions and about how mutations in the gene affect these.
  • Two resemble the truncation alleles found in human tumors and one is a protein null.
  • We generated ovaries and embryos null for both APC2 and APC1, and assessed the consequences of total loss of APC function, allowing us to test several previous hypotheses.
  • Surprisingly, although complete loss of APC1 and APC2 resulted in strong activation of Wingless signaling, it did not substantially alter cell viability, cadherin-based adhesion, spindle morphology, orientation or selection of division plane, as predicted from previous studies.
  • We also tested the hypothesis that truncated APC proteins found in tumors are dominant negative.
  • Two mutant proteins have dominant effects on cytoskeletal regulation, affecting Wnt-independent nuclear retention in syncytial embryos.
  • However, they do not have dominant-negative effects on Wnt signaling.
  • [MeSH-major] Alleles. Cytoskeletal Proteins. Drosophila Proteins. Drosophila melanogaster / genetics. Protein Isoforms. Tumor Suppressor Proteins
  • [MeSH-minor] Animals. Armadillo Domain Proteins / genetics. Armadillo Domain Proteins / metabolism. Cell Adhesion / physiology. Cell Nucleus / metabolism. Cell Nucleus / ultrastructure. Embryo, Nonmammalian / cytology. Embryo, Nonmammalian / physiology. Female. Humans. Male. Mutation. Ovary / anatomy & histology. Ovary / metabolism. Phenotype. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Signal Transduction / physiology. Spindle Apparatus / metabolism. Spindle Apparatus / ultrastructure. Transcription Factors / genetics. Transcription Factors / metabolism. Wnt Proteins / genetics. Wnt Proteins / metabolism. Wnt1 Protein

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  • (PMID = 16720878.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / 5T32GM07092; United States / NIGMS NIH HHS / GM / R01GM59068; United States / NIGMS NIH HHS / GM / R01GM67236
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APC protein, Drosophila; 0 / APC2 protein, Drosophila; 0 / Armadillo Domain Proteins; 0 / Cytoskeletal Proteins; 0 / Drosophila Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Wnt Proteins; 0 / Wnt1 Protein; 0 / armadillo protein, Drosophila; 0 / wg protein, Drosophila
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44. Kuriyama N, Isaji S, Hamada T, Kishiwada M, Ohsawa I, Usui M, Sakurai H, Tabata M, Suzuki K, Uemoto S: Activated protein C prevents hepatic ischaemia-reperfusion injury in rats. Liver Int; 2009 Feb;29(2):299-307
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  • [Title] Activated protein C prevents hepatic ischaemia-reperfusion injury in rats.
  • Activated protein C (APC), a potent anticoagulant serine protease, has been shown to have cell-protective properties by virtue of its anti-inflammatory and anti-apoptotic activities.
  • METHODS: The present study was designed to examine the cytoprotective effects of APC in a 60-min warm-IRI rat model.
  • RESULTS: Following a single intravenous injection of APC before reperfusion, APC exerted cytoprotective effects 4 h after reperfusion, as evidenced by: (i) decreased levels of transaminase and improved histological findings of IRI, (ii) reduced infiltration and activation of neutrophils, macrophages and T cells, (iii) reduced expression of tumour necrosis factor-alpha, (iv) reduced expression of P-selectin and intracellular adhesion molecule-1, (v) inhibited coagulation and attenuated sinusoidal endothelial cell injury, (vi) improved hepatic microcirculation and (vii) decreased transferase-mediated dUTP nick end-labelling-positive cells.
  • These effects of APC were observed 4 h but not 24 h after reperfusion.
  • However, multiple injections of APC after reperfusion significantly decreased the levels of transaminase and the activity of myeloperoxidase, and improved histological findings of IRI 24 h after reperfusion.
  • CONCLUSION: These results suggest that APC is a promising therapeutic option for hepatic warm-IRI; however, multiple injections of APC are necessary to maintain its cell-protective action over the long term.
  • [MeSH-major] Liver / blood supply. Protein C / therapeutic use. Reperfusion Injury / prevention & control

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  • (PMID = 18507760.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Selectin; 0 / Protein C; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase; EC 2.6.1.- / Transaminases; EC 3.4.22.- / Caspase 3
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45. Singh H, Demers AA, Xue L, Turner D, Bernstein CN: Time trends in colon cancer incidence and distribution and lower gastrointestinal endoscopy utilization in Manitoba. Am J Gastroenterol; 2008 May;103(5):1249-56
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  • [Title] Time trends in colon cancer incidence and distribution and lower gastrointestinal endoscopy utilization in Manitoba.
  • OBJECTIVES: There are limited data on recent trends in subsite-specific colon cancer incidence and utilization of lower gastrointestinal endoscopy from Canada.
  • The aim of our study was to determine the concomitant trends in right-sided colon cancer incidence and utilization of colonoscopy and flexible sigmoidoscopy (FS) in Manitoba.
  • METHODS: Cases of colon cancer diagnosed from 1964 to 2004 were identified from the Manitoba Cancer Registry.
  • RESULTS: Rates of right-sided colon cancer showed a monotonic increase in both sexes (annual percent change [APC] in both sexes 1.04%, P < 0.001).
  • While rates of colonoscopies without polypectomies quadrupled between 1985 (257 per 100,000) and 2003 (1,083 per 100,000, APC 8.89%, P < 0.001), rates of colonoscopies with polypectomies quadrupled from 35 per 100,000 in 1985 to 140 per 100,000 in 2000, and then increased more rapidly in the subsequent 4 yr (233 per 100,000 in 2003, APC 20%, P < 0.001).
  • Rates of FS declined between 1999 (342 per 100,000) and 2003 (257 per 100,000, APC -6.68%, P= 0.01).
  • CONCLUSIONS: The rates of right-sided colon cancer are continuing to increase in Manitoba, with the most rapid increase occurring in older individuals.
  • Reasons for the increasing incidence of right-sided colon cancer despite increasing rates of colonoscopy need to be further explored, and may reflect increased detection of asymptomatic cancers or a real increase in right-sided colon cancer incidence.
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / epidemiology. Adult. Age Factors. Aged. Biopsy / utilization. Colonic Polyps / epidemiology. Colonic Polyps / surgery. Cross-Sectional Studies. Female. Humans. Incidence. Male. Manitoba. Mass Screening / utilization. Middle Aged. Registries. Sex Factors. Survival Rate. Utilization Review

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  • (PMID = 18190650.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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46. Pai S, O'Sullivan B, Abdul-Jabbar I, Peng J, Connoly G, Khanna R, Thomas R: Nasopharyngeal carcinoma-associated Epstein-Barr virus-encoded oncogene latent membrane protein 1 potentiates regulatory T-cell function. Immunol Cell Biol; 2007 Jul;85(5):370-7
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  • [Title] Nasopharyngeal carcinoma-associated Epstein-Barr virus-encoded oncogene latent membrane protein 1 potentiates regulatory T-cell function.
  • Sequence variation in the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) oncogene structure may affect antigen-presenting cell (APC) function of infected B cells and immune escape by EBV-specific T cells and thus contribute to the development of malignancy.
  • Normal B cell-associated LMP1 (B-LMP1) upregulates B cell APC function through activation of the necrosis factor (NF)-kappaB subunit, RelB.
  • We examined the ability of B-LMP1 and a nasopharyngeal carcinoma-associated LMP1 (NPC-LMP1) to modulate B cell APC function and T-cell responses.
  • Thus, after primary EBV infection, T cells may escape activation by NPC-LMP1.
  • These observations have important implications for the establishment of EBV-associated malignancy in the context of infection with tumour-associated EBV LMP1 variants.
  • [MeSH-major] Nasopharyngeal Neoplasms / immunology. T-Lymphocytes, Regulatory / immunology. Viral Matrix Proteins / immunology
  • [MeSH-minor] Antigen-Presenting Cells / drug effects. Antigens, CD4 / metabolism. B-Lymphocytes / drug effects. Cell Line. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Humans. Interleukin-10 / pharmacology. Interleukin-2 Receptor alpha Subunit / metabolism. Mutation / genetics. NF-kappa B / metabolism. Protein Transport / drug effects. Transfection

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  • (PMID = 17372611.001).
  • [ISSN] 0818-9641
  • [Journal-full-title] Immunology and cell biology
  • [ISO-abbreviation] Immunol. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / EBV-associated membrane antigen, Epstein-Barr virus; 0 / Interleukin-2 Receptor alpha Subunit; 0 / NF-kappa B; 0 / Viral Matrix Proteins; 130068-27-8 / Interleukin-10
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47. Beckjord EB, Glinder J, Langrock A, Compas BE: Measuring multiple dimensions of perceived control in women with newly diagnosed breast cancer. Psychol Health; 2009 Apr;24(4):423-38
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  • [Title] Measuring multiple dimensions of perceived control in women with newly diagnosed breast cancer.
  • A multidimensional approach to the study of focus of perceived control (FPC) can provide a more specific understanding of associations between FPC and adjustment to cancer.
  • We developed and tested a measure to capture multiple dimensions of FPC and examined FPC dimensions in relation to positive expectancies and three indices of psychosocial adjustment in 219 women with breast cancer.
  • Confirmatory factor analysis supported a 6-factor model of FPC (chi(2)(284 df) = 433.67, p < 0.001; CFI = 0.94; RMSEA = 0.049, 90% C.I.
  • Specific associations between FPC and adjustment were observed: more emotional PC was associated with less emotional distress, more physical PC was associated with better physical quality of life (QOL), and more medical PC was associated with better medical QOL.
  • Positive expectancies were also associated with better outcomes.
  • These results indicate dimensions of FPC as differentially associated with indices of adjustment, suggesting multiple targets of interventions aimed at benefiting breast cancer survivors.
  • [MeSH-major] Breast Neoplasms / diagnosis. Breast Neoplasms / psychology. Internal-External Control


48. Gagné M, Robitaille Y, Hamel D, St-Laurent D: Firearms regulation and declining rates of male suicide in Quebec. Inj Prev; 2010 Aug;16(4):247-53
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  • Since 1996, the pace of decline was twice as great in men aged 15-34 years (annual percentage change (APC) -11.1%) compared with men aged 35-64 years (APC -5.6%).

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  • (PMID = 20587817.001).
  • [ISSN] 1475-5785
  • [Journal-full-title] Injury prevention : journal of the International Society for Child and Adolescent Injury Prevention
  • [ISO-abbreviation] Inj. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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49. Kurzik-Dumke U, Hörner M, Czaja J, Nicotra MR, Simiantonaki N, Koslowski M, Natali PG: Progression of colorectal cancers correlates with overexpression and loss of polarization of expression of the htid-1 tumor suppressor. Int J Mol Med; 2008 Jan;21(1):19-31
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  • Recently, we identified htid-1, the human counterpart of the Drosophila tumor suppressor gene lethal(2)tumorous imaginal discs [l(2)tid], as a direct molecular ligand of the adenomatous polyposis coli (APC) tumor suppressor.
  • The gene encodes three cytosolic (Tid50, Tid48 and Tid46) and three mitochondrial (Tid43, Tid40 and Tid38) proteins.
  • In the colorectal epithelium the cytosolic forms hTid50/hTid48 interact under physiological conditions with the N-terminal region of APC.
  • This complex which associates with additional proteins such as Hsp70, Hsc70, Actin, Dvl and Axin defines a novel physiological state of APC unrelated to beta-catenin degradation.
  • Here we show that the expression of the genes htid-1 and APC was altered in colorectal tumors.
  • These changes concerned both the localization and the expression level of all three htid-1 splice variants and of APC.
  • Furthermore, we showed that the protein products of the two tumor suppressors co-localized in the basal and apical region of normal colon epithelia and that loss of differentiation capacity of colorectal cancers correlated with a shift in their expression patterns from compartmentalized to diffuse cytoplasmic.
  • These findings support our hypothesis that the building of the multi-component complex mentioned above is associated with the maintenance of the polarity of cells and tissues.
  • In addition, we provide evidence that colon cancer progression correlates with up-regulation of htid-1 and its ligand Hsp70.
  • Since the Tid proteins are members of the DnaJ-like protein family, an essential component of the Hsp70/Hsc70 chaperone machinery, our findings describe a novel, causal link between the function of chaperone machines, APC-mediated Wg/Wnt signaling and tumor development.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Gene Expression Regulation, Neoplastic. HSP40 Heat-Shock Proteins / genetics. HSP40 Heat-Shock Proteins / metabolism. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Antibodies, Neoplasm. Cell Differentiation. DNA Primers. Disease Progression. HSP70 Heat-Shock Proteins / metabolism. Humans. Intestinal Mucosa / pathology. RNA Splicing. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism

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  • (PMID = 18097612.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antibodies, Neoplasm; 0 / DNA Primers; 0 / DNAJA3 protein, human; 0 / HSP40 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / RNA, Neoplasm; 0 / Tumor Suppressor Proteins
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50. Ellinger J, Bastian PJ, Jurgan T, Biermann K, Kahl P, Heukamp LC, Wernert N, Müller SC, von Ruecker A: CpG island hypermethylation at multiple gene sites in diagnosis and prognosis of prostate cancer. Urology; 2008 Jan;71(1):161-7
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  • [Title] CpG island hypermethylation at multiple gene sites in diagnosis and prognosis of prostate cancer.
  • We investigated its role at multiple gene sites during prostate carcinogenesis.
  • METHODS: A quantitative, methylation-specific polymerase chain reaction was used to analyze the hypermethylation patterns at nine gene loci (Annexin2, APC, EDNRB, GSTP1, PTGS2, MDR1, RARbeta, Reprimo, and TIG1) in 80 patients with prostate cancer (PCa) and 26 patients with benign prostatic hyperplasia (BPH).
  • RESULTS: Hypermethylation was more frequent in PCa than in BPH tissues (EDNRB, 100% versus 88%; TIG1, 96% versus 12%; RARbeta, 95% versus 35%; GSTP1, 93% versus 15%; APC, 80% versus 50%; MDR1, 80% versus 31%; PTGS2, 68% versus 15%; Reprimo, 59% versus 19%; and Annexin2, 4% versus 0%).
  • Hypermethylation at a single gene locus did not correlate with any clinicopathologic variables.
  • In contrast, hypermethylation at two genes (eg, APC and TIG1, APC and GSTP1, APC and PTGS2, APC or MDR, GSTP1 or PTGS2) correlated significantly with the pathologic stage and/or Gleason score (P = 0.033 to 0.045).
  • Hypermethylation at APC and Reprimo, as well as DNA hypermethylation at more than five genes, correlated significantly with the rate of prostate-specific antigen recurrence after radical prostatectomy (P = 0.0078 and P = 0.0074, respectively).
  • CONCLUSIONS: Our results have confirmed that the hypermethylation patterns are helpful in the diagnosis and prognosis of PCa.
  • Increases in CpG island hypermethylation at multiple gene sites occur during PCa progression and indicate early biochemical recurrence after radical prostatectomy.
  • [MeSH-major] CpG Islands / physiology. DNA Methylation. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / mortality
  • [MeSH-minor] Aged. Annexin A2 / metabolism. Cell Cycle Proteins / metabolism. Cyclooxygenase 2 / metabolism. Gene Silencing / physiology. Glutathione S-Transferase pi / metabolism. Glycoproteins / metabolism. Humans. Lymphatic Metastasis. Male. Membrane Proteins / metabolism. Middle Aged. Neoplasm Invasiveness. P-Glycoprotein / metabolism. Polymerase Chain Reaction / methods. Prognosis. Prostatic Hyperplasia / diagnosis. Prostatic Hyperplasia / genetics. Prostatic Hyperplasia / metabolism. Seminal Vesicles / metabolism. Sensitivity and Specificity

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  • (PMID = 18242387.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Cell Cycle Proteins; 0 / Glycoproteins; 0 / Membrane Proteins; 0 / P-Glycoprotein; 0 / RARRES1 protein, human; 0 / RPRM protein, human; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi
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51. Fu JF, Hsu HC, Shih LY: MLL is fused to EB1 (MAPRE1), which encodes a microtubule-associated protein, in a patient with acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2005 Jun;43(2):206-10
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  • [Title] MLL is fused to EB1 (MAPRE1), which encodes a microtubule-associated protein, in a patient with acute lymphoblastic leukemia.
  • Southern blot analysis indicated that a rearrangement of the MLL gene was involved in the chromosomal abnormality. cDNA panhandle polymerase chain reaction (PCR) identified the fusion transcript, in which MLL exon 6 was fused in-frame with EB1 exon 5.
  • Sequencing of the break junctions revealed that multiple DNA breaks had occurred and that the DNA fragments flanked by these breaks had been duplicated, deleted, or inverted.
  • EB1 is a microtubule-associated protein that interacts with the colorectal adenomatous polyposis coli tumor-suppressor protein and plays important roles in regulating microtubule dynamics, cell polarity, and chromosome stability.
  • Immunofluorescence staining demonstrated that the MLL-EB1 fusion proteins were localized in the nuclei.
  • [MeSH-major] DNA-Binding Proteins / genetics. Microtubule-Associated Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. Molecular Sequence Data. Myeloid-Lymphoid Leukemia Protein

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15751040.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY752858/ AY752859/ AY752860/ AY752861
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MAPRE1 protein, human; 0 / MLL protein, human; 0 / Microtubule-Associated Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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52. Quina MJ, Bordado JC, Quinta-Ferreira RM: Chemical stabilization of air pollution control residues from municipal solid waste incineration. J Hazard Mater; 2010 Jul 15;179(1-3):382-92
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  • The by-products of the municipal solid waste incineration (MSWI) generally contain hazardous pollutants, with particular relevance to air pollution control (APC) residues.
  • In our work, the chemical stabilization of APC residues by using NaHS x xH(2)O, H(3)PO(4), Na(2)CO(3), C(5)H(10)NNaS(2) x 3 H(2)O, Na(2)O x SiO(2) was investigated, and it was possible to conclude that all these additives lead to an improvement of the stabilization process of the most problematic heavy metals.
  • The effect of the additives tested on the elements associated with soluble salts (K, Na, Cl(-)) is almost negligible, and therefore, the soluble fraction is hardly reduced without further treatment, such as pre-washing.

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  • [Copyright] 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20359820.001).
  • [ISSN] 1873-3336
  • [Journal-full-title] Journal of hazardous materials
  • [ISO-abbreviation] J. Hazard. Mater.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Air Pollutants; 0 / Indicators and Reagents; 0 / Metals, Heavy; 0 / Phosphates; 0 / Silicates
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53. Ansorge S, Bank U, Heimburg A, Helmuth M, Koch G, Tadje J, Lendeckel U, Wolke C, Neubert K, Faust J, Fuchs P, Reinhold D, Thielitz A, Täger M: Recent insights into the role of dipeptidyl aminopeptidase IV (DPIV) and aminopeptidase N (APN) families in immune functions. Clin Chem Lab Med; 2009;47(3):253-61
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  • With the identification of new peptidases of the DPIV family (DASH) with the same or similar substrate specificity [fibroblast activation protein (FAP), DP8/9], the question arose whether and to what extent the inhibition of intracellularly localized enzymes, DP8 and DP9, contribute to the observed immunosuppression.
  • Hence, the concept of a combined targeting of both families of peptidases for treatment of inflammatory diseases is a promising strategy.
  • RESULTS/CONCLUSIONS: Summarizing data obtained from the usage of different non-selective and selective inhibitors of DPIV, DP8/9, FAP, and DPII, this review provides evidence that in addition to DPIV, DP8/9 also regulate the immune response via modulation of cell cycle progression and cytokine production.
  • Consequently, the concomitant inhibition of both APN and DPIV enzyme families by means of two separate inhibitors or by binary inhibitors with specificity for both enzyme families (PETIR, peptidase targeted immunoregulation) synergistically affects immune cells on the level of cell cycle regulation, suppression of TH1, TH2, and TH17 cytokines as well as the activation of regulatory T-cells.
  • This strongly suggests a broad potential of the multiple anti-inflammatory effects of PETIR in treatment of chronic inflammatory diseases, such as autoimmune diseases, allergies, and transplant rejections, as well as of inflammatory skin diseases, such as acne, psoriasis, rosacea or atopic dermatitis.

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  • (PMID = 19327105.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dipeptidyl-Peptidase IV Inhibitors; 0 / Protease Inhibitors; EC 3.4.11.2 / Antigens, CD13; EC 3.4.14.5 / Dipeptidyl Peptidase 4
  • [Number-of-references] 42
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54. Narra K, Mullins SR, Lee HO, Strzemkowski-Brun B, Magalong K, Christiansen VJ, McKee PA, Egleston B, Cohen SJ, Weiner LM, Meropol NJ, Cheng JD: Phase II trial of single agent Val-boroPro (Talabostat) inhibiting Fibroblast Activation Protein in patients with metastatic colorectal cancer. Cancer Biol Ther; 2007 Nov;6(11):1691-9
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  • [Title] Phase II trial of single agent Val-boroPro (Talabostat) inhibiting Fibroblast Activation Protein in patients with metastatic colorectal cancer.
  • PURPOSE: Fibroblast Activation Protein (FAP) is a tumor fibroblast protease that has been shown to potentiate colorectal cancer growth.
  • The clinical impact of FAP inhibition was tested using Val-boroPro (Talabostat), the first clinical inhibitor of FAP enzymatic activity, in a phase II study of patients with metastatic colorectal cancer.
  • Eligibility included measurable disease, performance status of 0 to 2, and adequate organ function.
  • Laboratory correlates evaluated the pharmacodynamic effects of Val-boroPro on FAP enzymatic function in the peripheral blood.
  • Six of 28 (21%) patients had stable disease for a median of 25 weeks (range 11-38 weeks).
  • Laboratory analysis demonstrated significant, although incomplete inhibition of FAP enzymatic activity in the peripheral blood.
  • However it provides the initial proof-of-concept that physiologic inhibition of FAP activity can be accomplished in patients with colorectal cancer, and lays the groundwork for future studies targeting the tumor stroma.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, Neoplasm / blood. Female. Gelatinases. Humans. Immunohistochemistry. Male. Membrane Proteins. Middle Aged. Neoplasm Metastasis. Serine Endopeptidases / blood. alpha-2-Antiplasmin / analysis

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  • (PMID = 18032930.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA006927; United States / NCI NIH HHS / CA / CA090468; United States / NCI NIH HHS / CA / CA122301; United States / NHLBI NIH HHS / HL / HL072995-01
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / Dipeptides; 0 / Membrane Proteins; 0 / alpha-2-Antiplasmin; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases; KZ1O2SH88Z / talabostat
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55. Bursch LS, Rich BE, Hogquist KA: Langerhans cells are not required for the CD8 T cell response to epidermal self-antigens. J Immunol; 2009 Apr 15;182(8):4657-64
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  • [Title] Langerhans cells are not required for the CD8 T cell response to epidermal self-antigens.
  • Langerhans cells (LC) are APC that reside at the barrier surfaces.
  • Earlier results suggested that LC were the predominant APC, inducing a robust T cell response and autoimmunity.
  • In this study, we used a whole protein model system, the K14-mOVA mouse, in which a transmembrane form of OVA was expressed in keratinocytes.
  • In contrast to K14-OVAp mice, T cells in K14-mOVA mice were activated, but did not expand and instead died by apoptosis.
  • Furthermore, in double-transgenic mice expressing both mOVA and OVAp, robust OT-I expansion occurred, indicating that tolerance to this Ag is not dominant and was due to lack of activating signals.
  • We sought to identify the relevant APC in K14 mice using bone marrow chimeras and found that radioresistant cells (presumably LC) were able to cross-present the OVA Ag from keratinocytes to naive T cells in the lymph node.
  • However, use of LC-deficient mice indicated that LC were not required for the expansion of OT-I in K14-OVAp or the deletion of OT-I in K14-mOVA mice.

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  • (PMID = 19342641.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / U01 AI070380; United States / NIAID NIH HHS / AI / AI35296; United States / NIAID NIH HHS / AI / P01 AI035296; United States / NIAID NIH HHS / AI / AI070380-03; United States / NIAID NIH HHS / AI / U01 AI070380-03; United States / NIAID NIH HHS / AI / AI70380
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 9006-59-1 / Ovalbumin
  • [Other-IDs] NLM/ NIHMS132434; NLM/ PMC2722807
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56. Koike E, Takano H, Inoue KI, Yanagisawa R, Sakurai M, Aoyagi H, Shinohara R, Kobayashi T: Pulmonary exposure to carbon black nanoparticles increases the number of antigen-presenting cells in murine lung. Int J Immunopathol Pharmacol; 2008 Jan-Mar;21(1):35-42
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  • [Title] Pulmonary exposure to carbon black nanoparticles increases the number of antigen-presenting cells in murine lung.
  • The present study was designed to determine the effects of different sizes of nanoparticles on the antigen-presenting cells (APC) in the lung.
  • 14 nm nanoparticles, but not 56 nm nanoparticles, increased the number of the total lung cells.
  • The expression of MHC class II and/or costimulatory molecules and the number of APC in the lung were increased by 14 nm nanoparticles in the presence or absence of OVA.
  • 56 nm nanoparticles did not show any significant effects.
  • 14 nm CB nanoparticles can increase the expression of MHC class II and costimulatory molecules and the number of APC in the lung, especially in the presence of antigen, which can result in subsequent antigen-related airway inflammation and immunoglobulin production.

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  • (PMID = 18336729.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Histocompatibility Antigens Class II; 0 / Soot; 9006-59-1 / Ovalbumin
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57. Fogelson AL, Tania N: Coagulation under flow: the influence of flow-mediated transport on the initiation and inhibition of coagulation. Pathophysiol Haemost Thromb; 2005;34(2-3):91-108
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  • A mathematical model of intravascular coagulation is presented; it encompasses the biochemistry of the tissue factor pathway, platelet activation and deposition on the subendothelium, and flow- and diffusion-mediated transport of coagulation proteins and platelets.
  • Simulation experiments carried out with the model indicate the predominant role played by the physical processes of platelet deposition and flow-mediated removal of enzymes in inhibiting coagulation in the vicinity of vascular injury.
  • Chemical inhibitors are seen to play almost no (TFPI) or little (AT-III and APC) role in determining whether substantial thrombin production will occur.
  • The role of APC is limited by the necessity for diffusion of thrombin from the site of injury to nearby endothelial cells to form the thrombomodulin-thrombin complex and for diffusion in the reverse direction of the APC made by this complex.
  • TFPI plays an insignificant part in inhibiting the TF:VIIa complex under the conditions studied whether its action involves sequential binding of TFPI to Xa and then TFPI:Xa to TF:VIIa, or direct binding of TFPI to Xa already bound to the TF:VIIa complex.

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  • [Copyright] Copyright 2005 S. Karger AG, Basel.
  • (PMID = 16432311.001).
  • [ISSN] 1424-8832
  • [Journal-full-title] Pathophysiology of haemostasis and thrombosis
  • [ISO-abbreviation] Pathophysiol. Haemost. Thromb.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Blood Coagulation Factors; 9035-58-9 / Thromboplastin; EC 3.4.21.5 / Thrombin
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58. Moran AE, Carothers AM, Weyant MJ, Redston M, Bertagnolli MM: Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse. Cancer Res; 2005 Feb 1;65(3):1097-104
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  • [Title] Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse.
  • Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%.
  • Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes.
  • Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate.
  • Moreover, treatment of WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue.
  • Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin.
  • Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
  • [MeSH-major] Adenoma / prevention & control. Colonic Neoplasms / prevention & control. Cytoskeletal Proteins / metabolism. Diterpenes, Abietane / pharmacology. Phenanthrenes / pharmacology. Trans-Activators / metabolism
  • [MeSH-minor] Animals. Cadherins / metabolism. Cell Adhesion / drug effects. Cell Membrane / drug effects. Cell Membrane / metabolism. Enterocytes / drug effects. Enterocytes / metabolism. Female. Intestine, Small / cytology. Intestine, Small / drug effects. Intestine, Small / metabolism. Mice. Mice, Inbred C57BL. Phosphorylation / drug effects. Rosmarinus / chemistry. Tyrosine / metabolism. Vanadates / antagonists & inhibitors. Vanadates / pharmacology. beta Catenin

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  • (PMID = 15705912.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R29 CA 74162; United States / NCI NIH HHS / CA / T32 CA 68971
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Diterpenes, Abietane; 0 / Phenanthrenes; 0 / Trans-Activators; 0 / beta Catenin; 0 / pervanadate; 3WHH0066W5 / Vanadates; 42HK56048U / Tyrosine; 5957-80-2 / carnosol
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59. Gierek T, Jura-Szołtys E: [Argon plasma coagulation (APC) for interior turbinates reduction]. Otolaryngol Pol; 2005;59(1):37-41
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  • [Title] [Argon plasma coagulation (APC) for interior turbinates reduction].
  • [Transliterated title] Konchoplastyka z uzyciem plazmy argonowej (APC).
  • Authors analyze results of argon plasma coagulation (APC) for interior turbinates reduction in patients with chronic nasal obstruction treated ineffectively with nasal drops.
  • The obtained results confirmed high effectiveness of APC for interior turbinates reduction.
  • [MeSH-major] Argon / therapeutic use. Electrocoagulation / methods. Nasal Obstruction / surgery. Otorhinolaryngologic Surgical Procedures / methods. Turbinates / surgery
  • [MeSH-minor] Adult. Case-Control Studies. Chronic Disease. Female. Humans. Male. Middle Aged. Nasal Mucosa / pathology. Nasal Mucosa / surgery. Time Factors. Treatment Outcome

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  • (PMID = 15915917.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 67XQY1V3KH / Argon
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60. Dopeso H, Mateo-Lozano S, Mazzolini R, Rodrigues P, Lagares-Tena L, Ceron J, Romero J, Esteves M, Landolfi S, Hernández-Losa J, Castaño J, Wilson AJ, Ramon y Cajal S, Mariadason JM, Schwartz S Jr, Arango D: The receptor tyrosine kinase EPHB4 has tumor suppressor activities in intestinal tumorigenesis. Cancer Res; 2009 Sep 15;69(18):7430-8
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  • [Title] The receptor tyrosine kinase EPHB4 has tumor suppressor activities in intestinal tumorigenesis.
  • Colorectal cancer is the second cause of cancer-related death in the western world, and although the genetic and molecular mechanisms involved in the initiation and progression of these tumors are among the best characterized, there are significant gaps in our understanding of this disease.
  • Here, we use animal models to investigate the role of EphB4 in intestinal tumorigenesis.
  • Modulation of EPHB4 levels in colon cancer cell lines resulted in significant differences in tumor growth in a xenograft model, with low levels of EPHB4 associated with faster growth.
  • In addition, using a genetic model of intestinal tumorigenesis where adenomatous polyposis coli (Apc) mutations lead to initiation of the tumorigenic process (Apc(min) mice), we show that inactivation of a single allele of EphB4 results in higher proliferation in both the normal epithelium and intestinal tumors, significantly larger tumors in the small intestine, and a 10-fold increase in the number of tumors in the large intestine.
  • This was associated with a 25% reduction in the lifespan of Apc(min) mice (P < 0.0001).
  • Gene expression analysis showed that EphB4 mutations result in a profound transcriptional reprogramming, affecting genes involved in cell proliferation, remodeling of the extracellular matrix, and cell attachment to the basement membrane among other functional groups of genes.
  • Importantly, in agreement with the expression profiling experiments, using an in vitro assay, we show that loss of EPHB4 in colon cancer cells results in a significantly increased potential to invade through a complex extracellular matrix.
  • Collectively, these results indicate that EphB4 has tumor suppressor activities and that regulation of cell proliferation, extracellular matrix remodeling, and invasive potential are important mechanisms of tumor suppression.


61. Ritchie KJ, Walsh S, Sansom OJ, Henderson CJ, Wolf CR: Markedly enhanced colon tumorigenesis in Apc(Min) mice lacking glutathione S-transferase Pi. Proc Natl Acad Sci U S A; 2009 Dec 8;106(49):20859-64
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  • [Title] Markedly enhanced colon tumorigenesis in Apc(Min) mice lacking glutathione S-transferase Pi.
  • Glutathione transferases are a multigene family of proteins that catalyze the conjugation of toxic electrophiles and carcinogens to glutathione.
  • To investigate the unique functions of this enzyme, we have crossed Gstp null mice with an initiated model of colon cancer, the Apc(Min) mouse.
  • In contrast to the Apc(Min/+) Gstp1/p2(+/+) (Gstp-wt Apc(Min)) mice, which rarely develop colonic tumours, Apc(Min/+)Gstp1/p2(-/-) (Gstp-null Apc(Min)) mice had a 6-fold increase in colon adenoma incidence, and a 50-fold increase in colorectal adenoma multiplicity, relative to Gstp-wt Apc(Min).
  • This increase was associated with early tumor onset and decreased survival.
  • Analysis of the biochemical changes in the colon tissue of Gstp-null Apc(Min) mice demonstrated a marked induction of many inflammatory genes, including IL-6, IL-4, IFN-gamma, and inducible nitric oxide synthase.
  • Gstp therefore appears to play a role in controlling inflammatory responses in the colon, which would explain the change in tumor incidence observed.
  • These data also suggest that individual variation in GSTP levels may be a factor in colon cancer susceptibility.


62. Chen HJ, Lin CM, Lin CS, Perez-Olle R, Leung CL, Liem RK: The role of microtubule actin cross-linking factor 1 (MACF1) in the Wnt signaling pathway. Genes Dev; 2006 Jul 15;20(14):1933-45
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  • MACF1 (microtubule actin cross-linking factor 1) is a multidomain protein that can associate with microfilaments and microtubules.
  • In the absence of Wnt, MACF1 associated with a complex that contained Axin, beta-catenin, GSK3beta, and APC.
  • Reduction of MACF1 with small interfering RNA decreased the amount of beta-catenin in the nucleus, and led to an inhibition of Wnt-induced TCF/beta-catenin-dependent transcriptional activation.
  • [MeSH-major] Microfilament Proteins / metabolism. Signal Transduction. Wnt Proteins / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Animals. Axin Protein. Base Sequence. Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Membrane / metabolism. Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. Gene Expression Regulation, Developmental. Glycogen Synthase Kinase 3 / metabolism. Mesoderm / pathology. Mice. Mice, Knockout. Molecular Sequence Data. Multiprotein Complexes. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Protein Structure, Tertiary. Protein Transport. Repressor Proteins / metabolism. beta Catenin / metabolism


63. Bocharova NA, Sokolov SS, Knorre DA, Skulachev VP, Severin FF: Unexpected link between anaphase promoting complex and the toxicity of expanded polyglutamines expressed in yeast. Cell Cycle; 2008 Dec 15;7(24):3943-6
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  • Protein aggregation is intimately linked to a number of neurodegenerative diseases.
  • Expansion of the huntingtin polyglutamine-rich domain causes protein aggregation and neuronal degeneration.
  • Ase1 is a substrate of the Cdh1 form of anaphase promoting complex, APC/Cdh1.
  • We tested Cdh1 overexpression and the deletion of CLB2 (mitotic cyclin, substrate of APC/Cdh1) and found that both mutations had a rescuing effect on the expanded polyglutamine toxicity.
  • Our data suggest that the toxic effect of aggregated proteins is partly indirect.
  • We speculate that cellular attempt to degrade the aggregates overloads the proteasome, and this leads to pathological accumulation of APC substrates.
  • [MeSH-major] DNA Repeat Expansion. Peptides / genetics. Saccharomyces cerevisiae / genetics. Ubiquitin-Protein Ligase Complexes / metabolism
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Apoptosis Regulatory Proteins / metabolism. Caspases / metabolism. Cdh1 Proteins. Cyclin B / metabolism. Microtubule-Associated Proteins / metabolism. Neurons / metabolism. Saccharomyces cerevisiae Proteins / metabolism

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  • (PMID = 19066445.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Ase1 protein, S cerevisiae; 0 / CDH1 protein, S cerevisiae; 0 / CLB2 protein, S cerevisiae; 0 / Cdh1 Proteins; 0 / Cyclin B; 0 / Microtubule-Associated Proteins; 0 / Peptides; 0 / Saccharomyces cerevisiae Proteins; 26700-71-0 / polyglutamine; EC 3.4.22.- / Caspases; EC 3.4.22.- / MCA1 protein, S cerevisiae; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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64. Nowak B, Heise A, Tarnowski N, Von Mueffling T: Microbiological and color aspects of cooked sausages made from a standardized porcine blood cell concentrate. J Food Prot; 2007 May;70(5):1181-6
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  • [Title] Microbiological and color aspects of cooked sausages made from a standardized porcine blood cell concentrate.
  • The objective of this study was to determine the potential for blood cell concentrates (BCCs) from pigs as an ingredient in food.
  • Sausages were made for this study according to a basic recipe for a type of blood sausage that is common in Germany.
  • First, sausages were produced with rind and kettle broth only, and different amounts (2.5 to 31%) of standardized blood cell concentrate (s-BCC) were added (15% table salt [NaCl] and 25% protein content).
  • These sausages were investigated microbiologically and compared to customary commercial blood sausage products (with whole blood) in terms of aerobic plate count (APC), Enterobacteriaceae, sulfite-reducing anaerobic bacteria, coagulase-positive staphylococci, and spore-forming bacilli.
  • The microbial counts of both the blood (APC, 4.4 log CFU/g) and the natural spices (APC, 6.6 log CFU/g) were relatively high.
  • The bacterial loads of the sausages produced with 12% s-BCC and spice extracts were significantly lower (APC and bacilli, 2.0 log CFU/g) than those of the other blood sausages (APC, -4.4 log CFU/g; bacilli, 3.2 to 4.0 log CFU/g).

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  • (PMID = 17536677.001).
  • [ISSN] 0362-028X
  • [Journal-full-title] Journal of food protection
  • [ISO-abbreviation] J. Food Prot.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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65. Stephens WZ, Senecal M, Nguyen M, Piotrowski T: Loss of adenomatous polyposis coli (apc) results in an expanded ciliary marginal zone in the zebrafish eye. Dev Dyn; 2010 Jul;239(7):2066-77
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  • [Title] Loss of adenomatous polyposis coli (apc) results in an expanded ciliary marginal zone in the zebrafish eye.
  • We provide a detailed gene expression analysis of the eyes of apc mutant zebrafish where the Wnt/beta-catenin pathway is constitutively active.
  • Retinal identity genes rx1 and vsx2, as well as meis1 and pax6a act upstream of Wnt/beta-catenin pathway activation.
  • Our results introduce the zebrafish apc mutation as a new model to study signaling pathways regulating the CMZ.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Eye / embryology. Eye / metabolism
  • [MeSH-minor] Animals. Immunohistochemistry. In Situ Hybridization. In Situ Nick-End Labeling. Signal Transduction. Wnt Proteins / metabolism. Zebrafish / embryology. Zebrafish / metabolism. beta Catenin / metabolism

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20549742.001).
  • [ISSN] 1097-0177
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Wnt Proteins; 0 / beta Catenin
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66. López-Arce G, Téllez-Avila FI, García-Osogobio S, Chavez-Tapia NC, Barahona-Garrido J, Barreto-Zúñiga R, Valdovinos-Andraca F: Endoscopic treatment with argon plasma coagulation in postradiation proctopathy. Int J Colorectal Dis; 2010 Jul;25(7):895-8
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  • Argon plasma coagulation (APC) had been shown to be successful with low complications.
  • The aim was to describe our experience with APC in the management of PP.
  • METHODS: We conducted a retrospective analysis of electronic- and paper-based records of patients with PP managed with APC.
  • The most frequent cause of radiotherapy for cancer was cervicouterine and prostate ENDOSCOPIC FINDINGS: Moderate disease was observed in nine patients; mild and severe diseases were observed in five patients each.
  • Median of APC sessions was two (one to seven).
  • Mean dose of APC was 30 W (30-40 W) and 1.7 l (1.5-2.0 l).
  • No complications were related to the APC treatment.
  • CONCLUSIONS: According to our data, APC is successful in treatment of PP, with few sessions and low morbidity and null mortality.

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  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
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67. Ramburan A, Oladiran F, Smith C, Hadley GP, Govender D: Microsatellite analysis of the adenomatous polyposis coli (APC) gene and immunoexpression of beta catenin in nephroblastoma: a study including 83 cases treated with preoperative chemotherapy. J Clin Pathol; 2005 Jan;58(1):44-50
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  • [Title] Microsatellite analysis of the adenomatous polyposis coli (APC) gene and immunoexpression of beta catenin in nephroblastoma: a study including 83 cases treated with preoperative chemotherapy.
  • AIMS: To determine whether microsatellite mutations of the adenomatous polyposis coli (APC) gene have pathological or prognostic significance in nephroblastomas and to correlate APC alterations with beta catenin immunoexpression.
  • Polymerase chain reaction using four APC microsatellite markers-D5S210, D5S299, D5S82, and D5S346-was performed and the products analysed.
  • Although there was a significant correlation between the results for individual markers and the clinicopathological data, the overall results do not support a prognostic role for APC in nephroblastoma.
  • CONCLUSION: Microsatellite analysis of APC and immunoexpression of beta catenin did not provide significant pathological or prognostic information in this cohort of nephroblastomas.
  • [MeSH-major] Cytoskeletal Proteins / metabolism. Genes, APC. Kidney Neoplasms / genetics. Microsatellite Repeats / genetics. Trans-Activators / metabolism. Wilms Tumor / genetics

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  • (PMID = 15623481.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC1770552
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68. Husøy T, Knutsen HK, Cruciani V, Olstørn HB, Mikalsen SO, Løberg EM, Alexander J: Connexin43 is overexpressed in Apc(Min/+)-mice adenomas and colocalises with COX-2 in myofibroblasts. Int J Cancer; 2005 Sep 1;116(3):351-8
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  • [Title] Connexin43 is overexpressed in Apc(Min/+)-mice adenomas and colocalises with COX-2 in myofibroblasts.
  • The expression of gap junction proteins, connexins, in the intestine and their role in tumorigenesis are poorly characterised.
  • Truncating mutations in the tumour suppressor gene adenomatous polyposis coli (APC) are early and important events, both in inheritable (familial adenomatous polyposis, FAP) and spontaneous forms of intestinal cancer.
  • Multiple intestinal neoplasia (Min) mice, a FAP model with inherited heterozygous mutation in Apc, spontaneously develop numerous intestinal adenomas.
  • We further examine the expression of connexin43 (Cx43) and other connexins as a function of heterozygous and homozygous Apc mutation in normal intestinal tissues and adenomas of Min-mice.
  • Qualitative analysis of connexin mRNA in intestine revealed a similar expression pattern in Min- and wild-type (wt) mice.
  • Connexin26 and connexin40 proteins were found in equal amounts in Min and wt epithelia of large and small intestine, respectively.
  • However, the COX-2-specific inhibitor, celecoxib, did not reduce Cx43 expression.
  • Although both Cx43 and COX-2 are target genes for beta-catenin, they were overexpressed in stromal cells but not in epithelial tumour cells.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Connexin 43 / biosynthesis. Genes, APC. Prostaglandin-Endoperoxide Synthases / physiology

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  • (PMID = 15800939.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Connexin 43; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib
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69. Moseley JB, Bartolini F, Okada K, Wen Y, Gundersen GG, Goode BL: Regulated binding of adenomatous polyposis coli protein to actin. J Biol Chem; 2007 Apr 27;282(17):12661-8
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  • [Title] Regulated binding of adenomatous polyposis coli protein to actin.
  • Adenomatous polyposis coli (APC) protein is a large tumor suppressor that is truncated in most colorectal cancers.
  • The carboxyl-terminal third of APC protein mediates direct interactions with microtubules and the microtubule plus-end tracking protein EB1.
  • In addition, APC has been localized to actin-rich regions of cells, but the mechanism and functional significance of this localization have remained unclear.
  • Here we show that purified carboxyl-terminal basic domain of human APC protein (APC-basic) bound directly to and bundled actin filaments and associated with actin stress fibers in microinjected cells.
  • Actin filaments and microtubules competed for binding to APC-basic, but APC-basic also could cross-link actin filaments and microtubules at specific concentrations, suggesting a possible role in cytoskeletal cross-talk.
  • APC interactions with actin in vitro were inhibited by its ligand EB1, and co-microinjection of EB1 prevented APC association with stress fibers.
  • Point mutations in EB1 that disrupted APC binding relieved the inhibition in vitro and restored APC localization to stress fibers in vivo, demonstrating that EB1-APC regulation is direct.
  • Because tumor formation and metastasis involve coordinated changes in the actin and microtubule cytoskeletons, this novel function for APC and its regulation by EB1 may have direct implications for understanding the molecular basis of tumor suppression.
  • [MeSH-major] Actin Cytoskeleton / chemistry. Adenomatous Polyposis Coli Protein / chemistry. Stress Fibers / chemistry
  • [MeSH-minor] Animals. Humans. Mice. NIH 3T3 Cells. Neoplasms / metabolism. Point Mutation. Protein Binding / genetics. Protein Structure, Tertiary / genetics

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  • (PMID = 17293347.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] Italy / Telethon / / GFP03006; United States / NIGMS NIH HHS / GM / R01 GM062939; United States / NIGMS NIH HHS / GM / GM062939; United States / NIGMS NIH HHS / GM / GM63691
  • [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 / Adenomatous Polyposis Coli Protein
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70. Weijenberg MP, Lüchtenborg M, de Goeij AF, Brink M, van Muijen GN, de Bruïne AP, Goldbohm RA, van den Brandt PA: Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes. Cancer Causes Control; 2007 Oct;18(8):865-79
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  • [Title] Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes.
  • OBJECTIVE: To investigate baseline fat intake and the risk of colon and rectal tumors lacking MLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2) repair gene expression and harboring mutations in the APC (adenomatous polyposis coli) tumor suppressor gene and in the KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) oncogene.
  • METHODS: After 7.3 years of follow-up of the Netherlands Cohort Study (n = 120,852), adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were computed, based on 401 colon and 130 rectal cancer patients.
  • RESULTS: Total, saturated and monounsaturated fat were not associated with the risk of colon or rectal cancer, or different molecular subgroups.
  • Linoleic acid, the most abundant polyunsaturated fatty acid in the diet, was associated with increased risk of colon tumors with only a KRAS mutation and no additional truncating APC mutation or lack of MLH1 expression (RR = 1.41, 95% CI 1.18-1.69 for one standard deviation (i.e., 7.5 g/day) increase in intake, p-trend over the quartiles of intake <0.001).
  • Linoleic acid intake was not associated with risk of colon tumors without any of the gene defects, or with tumors harboring aberrations in either MLH1 or APC.
  • CONCLUSION: Linoleic acid intake is associated with colon tumors with an aberrant KRAS gene, but an intact APC gene and MLH1 expression, suggesting a unique etiology of tumors with specific genetic aberrations.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Adenomatous Polyposis Coli Protein / genetics. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. Dietary Fats / administration & dosage. Genes, ras / genetics. Mutation / genetics. Nuclear Proteins / genetics

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  • (PMID = 17636402.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Dietary Fats; 0 / MLH1 protein, human; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2039842
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71. Mathieu-Rivet E, Gévaudant F, Sicard A, Salar S, Do PT, Mouras A, Fernie AR, Gibon Y, Rothan C, Chevalier C, Hernould M: Functional analysis of the anaphase promoting complex activator CCS52A highlights the crucial role of endo-reduplication for fruit growth in tomato. Plant J; 2010 Jun 1;62(5):727-41
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  • Endo-reduplication is an impairment of mitosis that originates from the selective degradation of M phase-specific cyclins via the ubiquitin-mediated proteolytic pathway, requiring the E3 ubiquitin ligase anaphase promoting complex/cyclosome (APC/C).
  • Two types of APC/C activators, namely CCS52 and CDC20 proteins, exist in plants.
  • We report here the molecular characterization of such APC/C activators during fruit development, and provide an in planta functional analysis of SlCCS52A, a gene that is specifically associated with endo-reduplication in tomato.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Fruit / growth & development. Lycopersicon esculentum / genetics. Plant Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / metabolism
  • [MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Cell Cycle. DNA, Plant / metabolism. Gene Expression Regulation, Developmental. Gene Expression Regulation, Plant. Protein Interaction Mapping. Transformation, Genetic

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  • (PMID = 20230486.001).
  • [ISSN] 1365-313X
  • [Journal-full-title] The Plant journal : for cell and molecular biology
  • [ISO-abbreviation] Plant J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA, Plant; 0 / Plant Proteins; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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72. Li G, Braunstein LA, Buldyrev SV, Havlin S, Stanley HE: Transport and percolation theory in weighted networks. Phys Rev E Stat Nonlin Soft Matter Phys; 2007 Apr;75(4 Pt 2):045103
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  • Each link has conductance g triple bond e-ax, where x is a random number taken from a uniform distribution between 0 and 1 and the parameter a represents the strength of the disorder.
  • We find, both analytically and numerically, that P(sigma) for ER networks exhibits two regimes: (i) A low conductance regime for sigma<e-apc, where pc=1/(k) is the critical percolation threshold of the network and k is the average degree of the network.
  • In this regime P(sigma) is independent of N and follows the power law P(sigma) approximately sigma-alpha, where alpha=1-(ka)/a. (ii) A high conductance regime for sigma>e-apc in which we find that P(sigma) has strong N dependence and scales as P(sigma) approximately f(sigma,apc/N1/3) .

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  • (PMID = 17500947.001).
  • [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
  • [Publication-country] United States
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73. Jahnsen FL, Strickland DH, Thomas JA, Tobagus IT, Napoli S, Zosky GR, Turner DJ, Sly PD, Stumbles PA, Holt PG: Accelerated antigen sampling and transport by airway mucosal dendritic cells following inhalation of a bacterial stimulus. J Immunol; 2006 Nov 1;177(9):5861-7
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  • [Title] Accelerated antigen sampling and transport by airway mucosal dendritic cells following inhalation of a bacterial stimulus.
  • An increase in the tempo of local dendritic cell (DC)-mediated immune surveillance is a recognized feature of the response to acute inflammation at airway mucosal surfaces, and transient up-regulation of the APC functions of these DC preceding their emigration to regional lymph nodes has recently been identified as an important trigger for T cell-mediated airway tissue damage in diseases such as asthma.
  • Notably, Ag-bearing AMDC expressing full APC activity reach regional lymph nodes within 30 min of cessation of microbial exposure, and in contrast to recall responses to nonpathogenic Ags, there is no evidence of local expression of APC activity within the airway mucosa preceding DC emigration.
  • [MeSH-minor] Administration, Inhalation. Aerosols. Animals. Antigen-Presenting Cells / immunology. Antigens, Bacterial / metabolism. Cell Movement. Coculture Techniques. Lymph Nodes / immunology. Protein Transport. Rats. Rats, Inbred Strains

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  • (PMID = 17056510.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aerosols; 0 / Antigens, Bacterial
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74. Pu RT, Laitala LE, Clark DP: Methylation profiling of urothelial carcinoma in bladder biopsy and urine. Acta Cytol; 2006 Sep-Oct;50(5):499-506
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  • STUDY DESIGN: Thirty-three bladder specimens were analyzed for the DNA p16INK4a, RASSF1, APC, GSTP, E-Cad and CyclinD2 genes to determine if there is a difference in gene methylation between benign and malignant cases.
  • We analyzed methylation profiles in 37 cytologically atypical urine samples with malignant or benign diagnosis on surgical follow-up andfound that only APC (55% in malignant vs. 0% in benign, p=0.025) and CyclinD2 were differentially methylated (35% in malignant vs. 0% in benign, p=0.2) while p14ARF, p16INK4a, RASSF1, GSTP and E-Cad had similar methylation profiles.
  • CONCLUSION: These results suggest that methylation of p14ARF, p16INK4a, RASSF1, GSTP and E-Cad genes may not accurately identify carcinoma, but methylated APC and CyclinD2 might be useful biomarkers for urothelial carcinoma in urine.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / genetics. DNA Fingerprinting / methods. DNA Methylation. Urinary Bladder Neoplasms / diagnosis. Urinary Bladder Neoplasms / genetics. Urothelium / pathology
  • [MeSH-minor] Aged. Anaphase-Promoting Complex-Cyclosome. Cadherins / genetics. Cadherins / metabolism. Cyclin D2. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Cyclins / genetics. Cyclins / metabolism. DNA / genetics. DNA / urine. Diagnostic Errors / prevention & control. False Negative Reactions. Feasibility Studies. Genetic Markers / genetics. Humans. Middle Aged. Predictive Value of Tests. Reproducibility of Results. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Protein p14ARF / metabolism. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / genetics. Ubiquitin-Protein Ligase Complexes / metabolism

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  • (PMID = 17017434.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cadherins; 0 / Cyclin D2; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclins; 0 / Genetic Markers; 0 / RASSF1 protein, human; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Proteins; 9007-49-2 / DNA; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
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75. Macedo B, Magalhães J, Batista AR, Saraiva MJ: Carvedilol treatment reduces transthyretin deposition in a familial amyloidotic polyneuropathy mouse model. Pharmacol Res; 2010 Dec;62(6):514-22
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  • [Title] Carvedilol treatment reduces transthyretin deposition in a familial amyloidotic polyneuropathy mouse model.
  • Carvedilol is a β-antagonist with strong anti-oxidant effect in lipids, proteins and superoxide production protecting biological membranes from oxidative stress.
  • We hypothesised a possible therapeutical application of carvedilol in familial amyloidotic polyneuropathy (FAP), a neurodegenerative disease caused by deposition of transthyretin (TTR) amyloid fibrils.
  • Oxidative stress, apoptosis and inflammation related to aggregation of non-fibrillar and fibrillar TTR have been detected both in pre-symptomatic and symptomatic stages of the disease, respectively.
  • In this study we show by semi-quantitative immunohistochemistry and western blot analysis that administration of carvedilol to a transgenic mouse model of FAP influences the expression of oxidative and apoptotic biomarkers usually associated with TTR deposition, namely oxidation products such as HNE and 8-OHdG, and markers of ER stress.
  • We also observed that carvedilol rescues a mice neuroblastoma cell line from death induced by TTR oligomers, by decreasing activation of BiP and other ER stress biomarkers.
  • Since carvedilol has no effect on TTR aggregation "in vitro", this finding points for the "in vivo" modulation of TTR aggregation by oxidative stress and apoptosis and prompts for the use of this safe drug in prophylactic and therapeutical measures in the FAP population.
  • [MeSH-major] Adrenergic beta-Antagonists / therapeutic use. Amyloid Neuropathies, Familial / drug therapy. Antioxidants / therapeutic use. Carbazoles / therapeutic use. Polyneuropathies / drug therapy. Prealbumin / metabolism. Propanolamines / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Humans. Mice. Mice, Transgenic. Oxidation-Reduction / drug effects. Oxidative Stress / drug effects. Protein Multimerization / drug effects

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20692343.001).
  • [ISSN] 1096-1186
  • [Journal-full-title] Pharmacological research
  • [ISO-abbreviation] Pharmacol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic beta-Antagonists; 0 / Antioxidants; 0 / Carbazoles; 0 / Prealbumin; 0 / Propanolamines; 0K47UL67F2 / carvedilol
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76. Ksiaa F, Ziadi S, Amara K, Korbi S, Trimeche M: Biological significance of promoter hypermethylation of tumor-related genes in patients with gastric carcinoma. Clin Chim Acta; 2009 Jun 27;404(2):128-33
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  • BACKGROUND: DNA promoter hypermethylation is a potential means of inactivating tumor-related genes in several types of cancers.
  • RESULTS: In gastric carcinoma tissues, hypermethylation frequencies of the investigated genes were 61.8% for RASSFIA, 52.9% for APC, 36.8% for MGMT, 30.9% for DAPK, 29.4% for P16, 26.5% for P14, 25% for SHP1, 23.5% for RAR-beta2, 20.6% for GSTP1, 13.2% for TIMP3, and 8.8% for hMLH1.
  • Hypermethylation of P16 correlates with intestinal subtype and cardiac location (P = 0.044 and P = 0.004, respectively), whereas methylation of GSTP1 correlates with diffuse subtype (P = 0.050).
  • Methylation of SHP1 was associated with EBV infection (P = 0.014).
  • Methylation of APC and RAR-beta2 genes were significantly associated with improved patient's outcome (P = 0.007 and P = 0.042, respectively).
  • CONCLUSIONS: Our data suggest that methylation of multiple genes may be involved in the pathogenesis and correlated with the prognosis of gastric carcinomas.


77. Constantinescu CS, Tani M, Ransohoff RM, Wysocka M, Hilliard B, Fujioka T, Murphy S, Tighe PJ, Das Sarma J, Trinchieri G, Rostami A: Astrocytes as antigen-presenting cells: expression of IL-12/IL-23. J Neurochem; 2005 Oct;95(2):331-40
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  • Interleukin-12 (IL-12, p70) a heterodimeric cytokine of p40 and p35 subunits, important for Th1-type immune responses, has been attributed a prominent role in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).
  • Recently, the related heterodimeric cytokine, IL-23, composed of the same p40 subunit as IL-12 and a unique p19 subunit, was shown to be involved in Th1 responses and EAE.
  • We investigated whether astrocytes and microglia, CNS cells with antigen-presenting cell (APC) function can present antigen to myelin basic protein (MBP)-reactive T cells, and whether this presentation is blocked with antibodies against IL-12/IL-23p40.
  • Interferon (IFN)-gamma-treated APC induced proliferation of MBP-reactive T cells.
  • [MeSH-minor] Animals. Animals, Newborn / physiology. Cell Proliferation. Cell Separation. Cells, Cultured. Interleukin-23. Interleukin-23 Subunit p19. Mice. Myelin Basic Protein / metabolism. Neuroglia / immunology. Neuroglia / physiology. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / immunology. T-Lymphocytes / physiology

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  • (PMID = 16086689.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / K11 HD-01049; United States / NINDS NIH HHS / NS / NS 29226; United States / NINDS NIH HHS / NS / NS32151
  • [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] England
  • [Chemical-registry-number] 0 / Il23a protein, mouse; 0 / Interleukin-23; 0 / Interleukin-23 Subunit p19; 0 / Interleukins; 0 / Myelin Basic Protein; 187348-17-0 / Interleukin-12
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78. Casal A, Sumen C, Reddy TE, Alber MS, Lee PP: Agent-based modeling of the context dependency in T cell recognition. J Theor Biol; 2005 Oct 21;236(4):376-91
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  • In the physiological setting, a typical APC presents tens of thousands of diverse endogenous self-derived peptides complexed to MHC (pMHC complexes).
  • In this paper, we present a computational model to test how complex, varied peptide populations on an APC could potentially modulate a T cell's ability to detect the presence of small numbers of agonist peptides among a diverse population.
  • We use the model to investigate the notion that under physiological conditions, T cell recognition of foreign peptides is context dependent, that is, T cells process signals gathered from all pMHC interactions, not just from a few agonist peptides while ignoring all others.
  • [MeSH-minor] Animals. Antigens / immunology. Lymphocyte Activation. Major Histocompatibility Complex. Peptides / immunology. Self Tolerance

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  • [ErratumIn] J Theor Biol. 2012 Jun 21;303:152-3 [22783551.001]
  • (PMID = 15899504.001).
  • [ISSN] 0022-5193
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 090809
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Peptides
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79. Fisher GW, Adler SA, Fuhrman MH, Waggoner AS, Bruchez MP, Jarvik JW: Detection and quantification of beta2AR internalization in living cells using FAP-based biosensor technology. J Biomol Screen; 2010 Jul;15(6):703-9
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  • [Title] Detection and quantification of beta2AR internalization in living cells using FAP-based biosensor technology.
  • In this article, the authors describe a new kind of live-cell biosensor of receptor internalization that takes advantage of fluorogen-activating protein (FAP) technology.
  • Recombinant genes that express the human beta2 adrenergic receptor (beta2AR) with FAP domains at their extracellular N-termini were transduced into mammalian cells.
  • The approach described here is generalizable to other receptors and cell surface proteins and is adaptable to a variety of fluorescence-based high-throughput screening platforms.

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  • (PMID = 20488980.001).
  • [ISSN] 1552-454X
  • [Journal-full-title] Journal of biomolecular screening
  • [ISO-abbreviation] J Biomol Screen
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / U54 RR022241; United States / NCRR NIH HHS / RR / U54 RR022241
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-2 Receptor Agonists; 0 / Adrenergic beta-2 Receptor Antagonists; 0 / Fluorescent Dyes; 0 / Receptors, Adrenergic, beta-2; 9Y8NXQ24VQ / Propranolol; L628TT009W / Isoproterenol
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80. Knapik JJ, Darakjy S, Hauret KG, Canada S, Scott S, Rieger W, Marin R, Jones BH: Increasing the physical fitness of low-fit recruits before basic combat training: an evaluation of fitness, injuries, and training outcomes. Mil Med; 2006 Jan;171(1):45-54
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  • If they failed the test, then they entered the Fitness Assessment Program (FAP), where they physically trained until they passed the test and subsequently entered BCT.
  • The effectiveness of the FAP was evaluated by examining fitness, injury, and training outcomes.
  • Recruits who failed the test, trained in the FAP, and entered BCT after passing the test were designated the preconditioning (PC) group (64 men and 94 women).
  • Recruits who failed the test but were allowed to enter BCT without going into the FAP were called the no preconditioning (NPC) group (32 men and 73 women).
  • Compared with NNPC men, injury risk was 1.5 (95% confidence interval, 1.0-2.2) and 1.7 (95% confidence interval, 1.0-3.1) times higher for PC and NPC men, respectively.
  • Compared with NNPC women, injury risk was 1.2 (95% confidence interval, 0.9-1.6) and 1.5 (95% confidence interval, 1.1-2.1) times higher for PC and NPC women, respectively.
  • This program evaluation showed that low-fit recruits who preconditioned before BCT had reduced attrition and tended to have lower injury risk, compared with recruits of similar low fitness who did not precondition.


81. Bonfill X: [Establishment and evaluation of screening programs for familial adenomatous polyposis]. Med Clin (Barc); 2007 Jun 9;129(2):53-4
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  • [Title] [Establishment and evaluation of screening programs for familial adenomatous polyposis].
  • [Transliterated title] Implantación y evaluación del cribado poblacional de la poliposis adenomatosa familiar.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis


82. Lopez-Kostner F, Alvarez K, de la Fuente M, Wielandt AM, Orellana P, Hurtado C: Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli. Hum Genet; 2010 Apr;127(4):481
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  • [Title] Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC

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  • (PMID = 21488302.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Codon
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83. Jeon CH, Lee HI, Shin IH, Park JW: Genetic alterations of APC, K-ras, p53, MSI, and MAGE in Korean colorectal cancer patients. Int J Colorectal Dis; 2008 Jan;23(1):29-35
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  • [Title] Genetic alterations of APC, K-ras, p53, MSI, and MAGE in Korean colorectal cancer patients.
  • We investigated the presence of adenomatous polyposis coli gene (APC), Kirsten-ras (K-ras), p53, microsatellite instability (MSI), and melanoma antigen gene (MAGE) alterations in CRC and correlated the results obtained with clinical data.
  • Genetic analyses were performed on APC, K-ras, p53, and MSI (BAT 25 and BAT 26), and in addition, MAGE expression was tested by reverse transcription polymerase chain reaction.
  • RESULT: The positive rates for alterations of APC, K-ras, p53, MSI, and MAGE in 78 tissue samples were 33.3, 29.5, 34.6, 9.0, and 68.4%, respectively.
  • Mutations were frequently detected in codons 1291 and 1450 of APC, in codon 12 of K-ras and in codons 248, 282, and 176 of p53.
  • APC mutations were frequently noted in early-stage cancer, whereas MSI was observed in right-sided and multiple cancers.
  • No associations were found between the presence of alterations in APC, K-ras, p53, MSI, and MAGE.
  • INTERPRETATION: In Koreans, positive rates of alterations in APC and p53 were slightly lower than those of APC and p53 in Caucasians, and the genetic alterations including MAGE expression are involved in 92.1% of CRCs.
  • The lack of multiple mutations and of a relation between mutation rates and clinical stage suggest that genetic alterations might have independent influences on CRC development in Koreans.
  • [MeSH-major] Antigens, Neoplasm / genetics. Asian Continental Ancestry Group / genetics. Colorectal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, APC. Genes, ras. Microsatellite Instability. Neoplasm Proteins / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Aged. Base Sequence. DNA Mutational Analysis. Female. Genetic Predisposition to Disease. Humans. Korea. Male. Melanoma-Specific Antigens. Middle Aged. Molecular Sequence Data. Mutation

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  • (PMID = 17704924.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MAGEA1 protein, human; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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84. Sancho R, Jandke A, Davis H, Diefenbacher ME, Tomlinson I, Behrens A: F-box and WD repeat domain-containing 7 regulates intestinal cell lineage commitment and is a haploinsufficient tumor suppressor. Gastroenterology; 2010 Sep;139(3):929-41
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  • [Title] F-box and WD repeat domain-containing 7 regulates intestinal cell lineage commitment and is a haploinsufficient tumor suppressor.
  • BACKGROUND & AIMS: The E3 ubiquitin ligase F-box and WD repeat domain-containing 7 (Fbw7) degrades several proto-oncogenes including c-Myc, cyclinE, Notch1, and c-Jun.
  • Fbw7 is the fourth most frequently mutated gene in human colorectal carcinomas and has recently been described as a poor prognosis marker in human colorectal carcinoma; however, the molecular mechanism underlying fbw7 mutations in intestinal tumor suppression is unclear.
  • METHODS: To address the role of fbw7 in intestinal homeostasis and tumorigenesis, we generated conditional knock-out mice lacking fbw7 in the intestine and evaluated the effect of fbw7 absence in normal intestinal homeostasis and in adenomatous polyposis coli-mediated tumorigenesis.
  • Fbw7 exhibited haploinsufficiency for intestinal tumor suppression.
  • Biallelic fbw7 inactivation increased cellular proliferation in physiologic and pathologic conditions in a c-Jun-dependent manner.
  • CONCLUSIONS: Fbw7 regulates intestinal biology and tumorigenesis by controlling the abundance of different substrates in a dose-dependent fashion, providing a molecular explanation for the heterozygous mutations of fbw7 observed in human colorectal carcinoma.

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  • [Copyright] Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20638938.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / Proto-Oncogene Proteins c-jun; 0 / Receptors, Notch; 0 / Tumor Suppressor Proteins; 0 / Wnt Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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85. Muzaffarova TA, Pospekhova NI, Sachkov IY, Kuz'minov AM, Ginter EK, Karpukhin AV: New mutations in the APC gene in familial adenomatous polyposis: detection, characterization, and analysis. Bull Exp Biol Med; 2005 Mar;139(3):352-4
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  • [Title] New mutations in the APC gene in familial adenomatous polyposis: detection, characterization, and analysis.
  • The spectrum of mutations in the APC gene in familial adenomatous polyposis was detected in a sampling from the Russian population.
  • Deletions associated with the loss of only 1 or 2 nucleotides (89% cases) prevailed among new (unique) mutations, while all known deletions were caused by the loss of 4 or 5 nucleotides.
  • The detected differences in the deletion characteristics between unique and repeated mutations in the APC gene were typical of samples of patients from a number of populations.
  • The incidence of 1-2-nucleotide deletions among unique and repeated deletions in the APC gene in patient samplings from different countries were in negative correlation.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Mutation

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  • (PMID = 16027851.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng; rus
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Terminator
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86. Chen CS, Phillips KD, Grist S, Bennet G, Craig JE, Muecke JS, Suthers GK: Congenital hypertrophy of the retinal pigment epithelium (CHRPE) in familial colorectal cancer. Fam Cancer; 2006;5(4):397-404
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  • [Title] Congenital hypertrophy of the retinal pigment epithelium (CHRPE) in familial colorectal cancer.
  • BACKGROUND AND AIM: Congenital hypertrophy of the retinal pigment epithelium (CHRPE) is a pigmented fundus lesion associated with familial adenomatous polyposis (FAP).
  • CHRPE prevalence has been reported to be increased in subjects with familial or sporadic non-polyposis colorectal cancer (CRC), suggesting that some individuals with non-polyposis CRC have an attenuated form of FAP.
  • Other studies have not confirmed these clinical observations and have failed to identify mutations in the gene responsible for FAP, but the reason for the discrepancy in relation to CHRPE prevalence has not been resolved.
  • We determined the prevalence of CHRPE in subjects without CRC (negative control cohort), subjects with FAP (positive control cohort), and subjects with familial non-polyposis CRC (test cohort).
  • METHOD: A cohort study consisting of 37 negative control subjects, 9 positive control subjects with documented APC gene mutations, and 36 test subjects with familial non-polyposis CRC but no identified pathogenic APC gene mutation.
  • The diagnosis of hereditary non-polyposis colon cancer was excluded in the test cohort by testing for microsatellite instability in tumour tissue.
  • Five of nine (56%) patients with FAP had multiple CHRPE lesions.
  • CONCLUSIONS: Ophthalmoscopy may contribute to risk assessment in families with FAP but not in familial non-polyposis CRC.
  • Care must be exercised when interpreting pigmented fundus lesions because 8-13% of subjects in each of the cohorts had pigmented retinal lesions that were not CHRPE.
  • Bilateral lesions and lesions with a depigmented halo were the hallmarks of CHRPE associated with FAP.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Pigment Epithelium of Eye / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Genes, APC. Humans. Hypertrophy. Male. Middle Aged. Mutation

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  • (PMID = 16944273.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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87. Charames GS, Ramyar L, Mitri A, Berk T, Cheng H, Jung J, Bocangel P, Chodirker B, Greenberg C, Spriggs E, Bapat B: A large novel deletion in the APC promoter region causes gene silencing and leads to classical familial adenomatous polyposis in a Manitoba Mennonite kindred. Hum Genet; 2008 Dec;124(5):535-41
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  • [Title] A large novel deletion in the APC promoter region causes gene silencing and leads to classical familial adenomatous polyposis in a Manitoba Mennonite kindred.
  • Familial adenomatous polyposis (FAP) is an autosomal dominant syndrome caused by the inheritance of germline mutations in the APC tumour suppressor gene.
  • The vast majority of these are nonsense and frameshift mutations resulting in a truncated protein product and abnormal function.
  • While APC promoter hypermethylation has been previously documented, promoter-specific deletion mutations have not been reported.
  • In a large Canadian Mennonite polyposis kindred, we identified a large novel germline deletion in the APC promoter region by linkage analysis and MLPA.
  • By RT-PCR and sequence analysis, this mutation was found to result in transcriptional silencing of the APC allele.
  • A few genetic disorders have been characterized as over-represented in the Manitoba Mennonite population, however, the incidence of cancer has not been recognized as increased in this population as compared to other Manitoba ethnic groups.
  • This study strengthens the likelihood that this novel APC promoter mutation is linked to this unique population as a founder mutation.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Ethnic Groups / genetics. Genes, APC. Germ-Line Mutation


88. Milandri C, Calzolari F, Passardi A, Tison C, Giampalma E, Cecconetto L, Golfieri R: Intra-arterial chemotherapy of advanced pancreatic cancer: a single center experience. Hepatogastroenterology; 2007 Dec;54(80):2373-7
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  • RESULTS: There were 16 patients evaluable for response, of whom 4 (25%) had a partial response, 7 (44%) showed stable disease, and 5 (31%) progressed.
  • No grade 4 toxicity or severe complications relating to the angiographic procedure were observed.
  • [MeSH-minor] Adult. Aged. Carboplatin / therapeutic use. Disease Progression. Epirubicin / therapeutic use. Female. Fluorouracil / therapeutic use. Humans. Leucovorin / therapeutic use. Liver Neoplasms / secondary. Male. Middle Aged. Treatment Outcome

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  • (PMID = 18265668.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; BG3F62OND5 / Carboplatin; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; FLEC protocol
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89. Pagenstecher C, Gadzicki D, Stienen D, Uhlhaas S, Mangold E, Rahner N, Arslan-Kirchner M, Propping P, Friedl W, Aretz S: A complex rearrangement in the APC gene uncovered by multiplex ligation-dependent probe amplification. J Mol Diagn; 2007 Feb;9(1):122-6
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  • [Title] A complex rearrangement in the APC gene uncovered by multiplex ligation-dependent probe amplification.
  • Germline mutations in the tumor suppressor gene APC are the underlying cause of familial adenomatous polyposis, an autosomal-dominant cancer predisposition syndrome of the colorectum.
  • Here, we describe a complex pathogenic rearrangement in the APC gene that was detected during deletion screening and transmitted throughout at least three generations.
  • The rearrangement consists of a deletion of 604 bp in intron 4 that impairs the binding site of the reverse primer for exon 4 and of an insertion of 119 bp in exon 4 that interferes with the binding site of the multiplex ligation-dependent probe amplification (MLPA) probes for exon 4.
  • The rearrangement would not have been identified had it occurred outside the MLPA hybridization site.
  • Moreover, MLPA and RNA analysis alone would have led to an incorrect interpretation of a genomic deletion of exon 4.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. DNA Probes / genetics. Gene Rearrangement / genetics. Genes, APC. Molecular Diagnostic Techniques / methods. Nucleic Acid Amplification Techniques / methods. Polymerase Chain Reaction / methods

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  • (PMID = 17251345.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA Probes
  • [Other-IDs] NLM/ PMC1867434
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90. Schilling GD, Shelley JT, Barnes JH 4th, Sperline RP, Denton MB, Barinaga CJ, Koppenaal DW, Hieftje GM: Detection of positive and negative ions from a flowing atmospheric pressure afterglow using a Mattauch-Herzog mass spectrograph equipped with a Faraday-strip array detector. J Am Soc Mass Spectrom; 2010 Jan;21(1):97-103
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  • [Title] Detection of positive and negative ions from a flowing atmospheric pressure afterglow using a Mattauch-Herzog mass spectrograph equipped with a Faraday-strip array detector.
  • An ambient desorption/ionization (ADI) source, known as the flowing atmospheric pressure afterglow (FAPA), has been coupled to a Mattauch-Herzog mass spectrograph (MHMS) equipped with a focal plane camera (FPC) array detector.
  • Use of the FAPA source with the MHMS allows the FPC detector to be characterized for the determination of molecular species, whereas previously only atomic mass spectrometry (MS) has been demonstrated.
  • Furthermore, the FPC is shown to be sensitive to negative ions without the need to change any detector parameters.

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  • [Copyright] 2010 American Society for Mass Spectrometry. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 19889553.001).
  • [ISSN] 1879-1123
  • [Journal-full-title] Journal of the American Society for Mass Spectrometry
  • [ISO-abbreviation] J. Am. Soc. Mass Spectrom.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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91. Verschuren EW, Ban KH, Masek MA, Lehman NL, Jackson PK: Loss of Emi1-dependent anaphase-promoting complex/cyclosome inhibition deregulates E2F target expression and elicits DNA damage-induced senescence. Mol Cell Biol; 2007 Nov;27(22):7955-65
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  • Expression of the anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 is required for the accumulation of APC/C substrates crucial for DNA synthesis and mitotic entry.
  • Emi1 depletion leads to strong decreases in E2F target mRNA and APC/C substrate protein abundances.
  • However, cyclin E mRNA and cyclin E protein levels and associated kinase activities are increased.
  • Cells lacking Emi1 undergo DNA damage, likely explained by replication stress upon deregulated cyclin E- and A-associated kinase activities.
  • Our data suggest that maintenance of a protein stabilization/mRNA expression positive-feedback circuit fueled by Emi1 is required for accurate cell cycle progression, maintenance of DNA integrity, and prevention of cellular senescence.

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  • (PMID = 17875940.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS045077; United States / NIGMS NIH HHS / GM / R01 GM054811; United States / NIGMS NIH HHS / GM / R01 GM063023; United States / NINDS NIH HHS / NS / K08 NS45077
  • [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 / Cyclin E; 0 / E2F Transcription Factors; 0 / Emi1 protein, mouse; 0 / Evi5 protein, mouse; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
  • [Other-IDs] NLM/ PMC2169152
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92. Wheway J, Herzog H, Mackay F: The Y1 receptor for NPY: a key modulator of the adaptive immune system. Peptides; 2007 Feb;28(2):453-8
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  • Y(1) expression on antigen-presenting cells (APC) is essential for their function as T cell priming elements.
  • The opposite role of Y(1) on APC and T cells has reconciled previous disparities by showing that signaling via Y(1) protects against inflammation by inhibiting T cell responses, whereas Y(1)(-/-) mice are protected in the same inflammatory models due to defective APCs.