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1. George TI, Wrede JE, Bangs CD, Cherry AM, Warnke RA, Arber DA: Low-grade B-Cell lymphomas with plasmacytic differentiation lack PAX5 gene rearrangements. J Mol Diagn; 2005 Aug;7(3):346-51
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  • [Title] Low-grade B-Cell lymphomas with plasmacytic differentiation lack PAX5 gene rearrangements.
  • The chromosomal translocation t(9;14)(p13;q32) has been reported in association with lymphoplasmacytic lymphoma (LPL).
  • Although this translocation involving the paired homeobox-5 (PAX5) gene at chromosome band 9p13 and the immunoglobulin heavy chain (IgH) gene at 14q32 has been described in approximately 50% of LPL cases, the actual number of cases studied is quite small.
  • Many of the initial cases associated with t(9;14)(p13;q32) were actually low-grade B-cell lymphomas with plasmacytic differentiation other than LPL.
  • Thus, we analyzed a series of low-grade B-cell lymphomas for PAX5 gene rearrangements.
  • We searched records from the Department of Pathology, Stanford University Medical Center for low-grade B-cell lymphomas, with an emphasis on plasmacytic differentiation, that had available paraffin blocks or frozen tissue.
  • We identified 37 cases, including 13 LPL, 18 marginal zone lymphomas (nodal, extranodal, splenic, and alpha-heavy chain disease), and 6 small lymphocytic lymphomas.
  • All cases failed to demonstrate a PAX5 translocation, indicating that t(9;14)(p13;q32) and other PAX5 translocations are uncommon events in low-grade B-cell lymphomas with plasmacytic differentiation.

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  • (PMID = 16049306.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / DNA Probes; 0 / DNA-Binding Proteins; 0 / PAX5 protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1867539
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2. Jiang X, Ren YP, Lv ZR: Ouabain induces cardiac remodeling in rats independent of blood pressure. Acta Pharmacol Sin; 2007 Mar;28(3):344-52
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  • After 4 and 6 weeks, echocardiography were performed, hemodynamic parameters were measured by invasive cardiac catheterization, changes in cardiac ultrastructure were analyzed using transmission electron microscopy, the collagen fraction of the left ventricle was assessed with Picrosirius red stain, and RT-PCR was applied to evaluate the mRNA level of myosin heavy chain-alpha and -beta in the left ventricle.
  • Moreover, the cardiac MHC-beta mRNA was upregulated by ouabain treatment, whereas MHC-alpha mRNA was downregulated.
  • [MeSH-minor] Animals. Echocardiography. Glyceraldehyde-3-Phosphate Dehydrogenases / biosynthesis. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Male. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17302996.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 5ACL011P69 / Ouabain; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.4.1 / Myosin Heavy Chains
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3. Sekine H, Shimizu T, Yang J, Kobayashi E, Okano T: Pulsatile myocardial tubes fabricated with cell sheet engineering. Circulation; 2006 Jul 4;114(1 Suppl):I87-93
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  • METHODS AND RESULTS: Neonatal rat cardiomyocyte sheets were sequentially wrapped around a resected adult rat thoracic aorta and transplanted in place of the abdominal aorta of athymic rats (n=17).
  • Finally, when myocardial tubes used for aortic replacement were compared with grafts implanted in the abdominal cavity (n=7), we observed significantly increased tissue thickness, as well as expression of brain natriuretic peptide, myosin heavy chain-alpha, and myosin heavy chain-beta.
  • [MeSH-major] Aorta, Abdominal / surgery. Myocardial Contraction. Myocardium / cytology. Myocytes, Cardiac / transplantation. Tissue Engineering / methods
  • [MeSH-minor] Animals. Animals, Newborn. Aorta, Thoracic / transplantation. Cell Culture Techniques / instrumentation. Cells, Cultured / transplantation. Electrocardiography. Gene Expression Profiling. Microsurgery. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Natriuretic Peptide, Brain / biosynthesis. Natriuretic Peptide, Brain / genetics. Organ Culture Techniques. Rats. Rats, Nude. Rats, Wistar. Temperature

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  • (PMID = 16820651.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bmyo protein, rat; 0 / natriuretic peptide precursor type B, rat; 114471-18-0 / Natriuretic Peptide, Brain; EC 3.6.4.1 / Myosin Heavy Chains
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4. Zheng H, Li M, Ren W, Zeng L, Liu HD, Hu D, Deng X, Tang M, Shi Y, Gong J, Cao Y: Expression and secretion of immunoglobulin alpha heavy chain with diverse VDJ recombinations by human epithelial cancer cells. Mol Immunol; 2007 Mar;44(9):2221-7
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  • [Title] Expression and secretion of immunoglobulin alpha heavy chain with diverse VDJ recombinations by human epithelial cancer cells.
  • Recently, we found the expression of Ig alpha heavy chain in human epithelial cancer cells unexpectedly.
  • Further, the configuration of the Ig heavy chain genomic locus was analyzed in human cancer cells.
  • These provide further proofs for Ig alpha expression.
  • In addition, we found that human cancer cells not only express the protein of Ig alpha chain, but also secrete the protein in secretory IgA (SIgA) pattern.
  • Since IgA is the key immunoglobulin which contributes to local immunity of mucous membrane, the aberrant expression of Ig alpha heavy chain might increase our further comprehension to development and immunity of cancers.
  • [MeSH-major] Epithelial Cells / immunology. Epithelial Cells / pathology. Immunoglobulin A, Secretory / genetics. Immunoglobulin alpha-Chains / genetics. Neoplasms / immunology. Recombination, Genetic. VDJ Exons / genetics

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  • (PMID = 17174398.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Immunoglobulin A, Secretory; 0 / Immunoglobulin alpha-Chains; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RAG2 protein, human; 0 / RNA, Messenger; 128559-51-3 / RAG-1 protein; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
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5. Lin YS, Zhou H, Forrest RH, Frampton CM, Hickford JG: Association between variation in faecal egg count for a mixed field-challenge of nematode parasites and IGHA gene polymorphism. Vet Immunol Immunopathol; 2009 Apr 15;128(4):389-94
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  • Research has shown that variation in ovine immunoglobulin A (IgA) levels are associated with reduced faecal egg counts (FECs) in sheep hosting gastro-intestinal (GI) parasites.
  • Variation in the constant region of the ovine IgA heavy alpha chain gene (IGHA) may result in structurally and functionally different IgA molecules and may consequently lead to variation in the IgA response to parasitisation.
  • However, when the data was split into predominant challenge type groups, associations were detected.
  • [MeSH-major] Gastrointestinal Diseases / veterinary. Immunoglobulin A / genetics. Nematoda / growth & development. Nematode Infections / veterinary. Sheep Diseases / immunology. Sheep Diseases / parasitology
  • [MeSH-minor] Alleles. Animals. DNA, Helminth / chemistry. DNA, Helminth / genetics. Feces / parasitology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Heavy Chains / immunology. Male. Parasite Egg Count / veterinary. Polymerase Chain Reaction / veterinary. Polymorphism, Single-Stranded Conformational. Sheep

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  • (PMID = 19150137.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Helminth; 0 / Immunoglobulin A; 0 / Immunoglobulin Heavy Chains
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6. Hara T, Tsurumi H, Kato T, Imao Y, Kojima Y, Kojima K, Kitagawa J, Katsumura N, Araki H, Takami T, Moriwaki H: Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression. Intern Med; 2008;47(4):299-303
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  • [Title] Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression.
  • A 52-year-old man was admitted to our hospital in October 2001 with abdominal pain.
  • Abdominal X-ray indicated a diagnosis of ileus.
  • Histopathological and immunological examination resulted in a diagnosis of immunoproliferative small intestinal disease (IPSID).
  • He was diagnosed with relapsed IPSID and salvage chemotherapy was started.
  • Immunohistochemical staining revealed T-cell lymphoma.
  • [MeSH-major] Duodenal Neoplasms / etiology. Immunoproliferative Small Intestinal Disease / complications. Lymphoma, T-Cell / etiology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Proteins / metabolism

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  • (PMID = 18277034.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proteins
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7. Vaiphei K, Kumari N, Sinha SK, Dutta U, Nagi B, Joshi K, Singh K: Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease. World J Gastroenterol; 2006 Jun 14;12(22):3602-8
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  • [Title] Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease.
  • AIM: To evaluate roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease (IPSID) and to study profiles of kappa (kappa) and lambda (lambda) light chains and IgA heavy chain.
  • METHODS: The study consisted of 11 cases of IPSID and similar number of controls which included 11 of normal intestinal mucosa and 11 of high grade B cell lymphoma of ileum.
  • The parameters analyzed included clinical profiles, biochemical and other laboratory investigations, radiologic and histological findings including immunohistochemistry.
  • RESULTS: All IPSID cases had demonstrable serum IgA heavy chain and heavy mucosal plasma cell infiltration.
  • According to Galian's histological staging, there were 4 patients with stage A and 7 with stage B. kappa and lambda light chains were over-expressed in 7 patients; 1 stage A patient had H pylori-positive active gastritis and eradication of H pylori led to disease remission.
  • Syndecan-1, kappa and lambda light chains and IgA heavy chain showed inverse relationship with bcl6 and p53.
  • CHOP regime was added in 5 patients who developed frank lymphoma.
  • Three died of the disease due to extensive organ infiltration.
  • CONCLUSION: Certain immunomarkers like syndecan-1, kappa and lambda light chains and IgA heavy chain could be of much help in identifying early stage IPSID.
  • Stage B IPSID showed higher expression for bcl6 and p53 than stage A IPSID. bcl6 and p53 expressions correlated with a more advanced disease stage and aggressive tumour behavior.
  • [MeSH-major] DNA-Binding Proteins / genetics. Immunoproliferative Small Intestinal Disease / diagnosis. Immunoproliferative Small Intestinal Disease / genetics. Membrane Glycoproteins / genetics. Proteoglycans / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Case-Control Studies. Disease Progression. Doxycycline / therapeutic use. Endoscopy, Gastrointestinal. Female. Gene Expression Regulation. Helicobacter pylori. Humans. Immunoglobulin alpha-Chains / blood. Immunoglobulin alpha-Chains / genetics. Immunoglobulin kappa-Chains / analysis. Immunoglobulin kappa-Chains / genetics. Immunoglobulin lambda-Chains / analysis. Immunoglobulin lambda-Chains / genetics. Immunohistochemistry. Intestinal Mucosa / chemistry. Intestinal Mucosa / microbiology. Intestinal Mucosa / pathology. Intestine, Small / chemistry. Intestine, Small / microbiology. Intestine, Small / pathology. Male. Middle Aged. Prognosis. Syndecan-1. Syndecans

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  • (PMID = 16773719.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Immunoglobulin alpha-Chains; 0 / Immunoglobulin kappa-Chains; 0 / Immunoglobulin lambda-Chains; 0 / Membrane Glycoproteins; 0 / Proteoglycans; 0 / SDC1 protein, human; 0 / Syndecan-1; 0 / Syndecans; 0 / Tumor Suppressor Protein p53; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ PMC4087578
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8. Dillmann W: Cardiac hypertrophy and thyroid hormone signaling. Heart Fail Rev; 2010 Mar;15(2):125-32
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  • These multiple thyroid hormone effects are largely mediated by the action of nuclear based thyroid hormone receptors (TR) the thyroid hormone receptor alpha and beta.
  • Related to myofibrillar proteins, myosin heavy chain alpha is increased by T3 and MHC beta is decreased.
  • [MeSH-minor] Animals. Humans. Myosin Heavy Chains / metabolism. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism

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  • (PMID = 19125327.001).
  • [ISSN] 1573-7322
  • [Journal-full-title] Heart failure reviews
  • [ISO-abbreviation] Heart Fail Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Thyroid Hormone; 0 / Thyroid Hormones; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
  • [Number-of-references] 60
  • [Other-IDs] NLM/ PMC2820695
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9. Huang YC, Khait L, Birla RK: Modulating the functional performance of bioengineered heart muscle using growth factor stimulation. Ann Biomed Eng; 2008 Aug;36(8):1372-82
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  • Also, at 25 ng/mL, myosin heavy chain alpha and SERCA2 expression increased by 1.3 +/- 0.188 and 1.1 +/- 0.04 fold, respectively.

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  • (PMID = 18500554.001).
  • [ISSN] 1573-9686
  • [Journal-full-title] Annals of biomedical engineering
  • [ISO-abbreviation] Ann Biomed Eng
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins
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10. Dutta U, Udawat H, Noor MT, Sidhu GS, Kochhar R, Vaiphei K, Singh K: Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori. J Gastrointest Cancer; 2010 Sep;41(3):212-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori.
  • A 20-year-old male presented with low-grade fever, abdominal pain, anorexia, and weight loss of 4-month duration.
  • Contrast-enhanced computed tomography of the abdomen revealed extensive proximal small-bowel thickening with mesenteric lymphadenopathy.
  • Upper gastrointestinal endoscopy and enteroscopy revealed thickening of folds with multiple small superficial ulceration involving antrum, duodenum, and jejunum.
  • The duodenal and jejunal biopsy was suggestive of immunoproliferative small intestinal disease, stage 0 (Salem) or stage A (Galian).
  • He underwent H. pylori eradication following which he had significant clinical improvement; repeat evaluation at 6 months showed dramatic improvement in his clinical, radiological, and histological parameters.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Helicobacter Infections / complications. Immunoproliferative Small Intestinal Disease / drug therapy. Immunoproliferative Small Intestinal Disease / microbiology

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  • (PMID = 20300878.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Organometallic Compounds; 033KF7V46H / Tinidazole; 0K5C5T2QPG / Lansoprazole; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; HS813P8QPX / bismuth tripotassium dicitrate; KG60484QX9 / Omeprazole; N12000U13O / Doxycycline
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11. Zhou H, Hickford JG, Fang Q: Identification of allelic polymorphism in the caprine IGHA gene. Dev Comp Immunol; 2006;30(9):741-5
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  • Variation in the immunoglobulin heavy alpha chain (IGHA) constant region has been reported in a number of species.
  • The variation reported here may affect the structure of the hinge and hence the function of IgA.
  • [MeSH-major] Goats / genetics. Goats / immunology. Immunoglobulin alpha-Chains / genetics
  • [MeSH-minor] Alleles. Amino Acid Sequence. Animals. Base Sequence. DNA / chemistry. DNA / genetics. Hinge Exons. Molecular Sequence Data. Polymerase Chain Reaction / veterinary. Polymorphism, Single-Stranded Conformational. Sequence Alignment

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  • (PMID = 16343618.001).
  • [ISSN] 0145-305X
  • [Journal-full-title] Developmental and comparative immunology
  • [ISO-abbreviation] Dev. Comp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin alpha-Chains; 9007-49-2 / DNA
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12. Ben Ammar A, Cheikh I, Jouini M, Belkahla N, Fadhel SF, Hager O, Maamouri N, Chaabouni H, Ben Safta Z, Haouet S: [Alpha heavy chain disease. A Tunisian case]. Tunis Med; 2006 Sep;84(9):581-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Alpha heavy chain disease. A Tunisian case].
  • [Transliterated title] Maladie des chaines lourdes alpha. A propos d'un cas tunisien.
  • Alpha heavy chain disease is a rare affection in the West and reported mainly in developing countries with the improvement of hygienic conditions, the disease become rare in Tunisia, the last case was reported in 1991.
  • The aim of the study is to report a new Tunisian case and to describe clinical, endoscopical and histological characteristics of the disease.
  • The diagnosis of alpha heavy chain disease was confirmed by histological examination of the resected intestine after surgery for intestinal obstruction.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis
  • [MeSH-minor] Adult. Humans. Intestinal Obstruction / etiology. Intestinal Obstruction / surgery. Male

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  • (PMID = 17263208.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
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13. Parfenov AI, Krums LM, Sivash ES, Tsaregorodtseva TM, Poleva NI, Ruchkina IN, Sabel'nikova EA, Chikunova BZ: [Algorithm for diagnosis of small intestinal diseases]. Ter Arkh; 2008;80(4):46-51

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  • [Title] [Algorithm for diagnosis of small intestinal diseases].
  • AIM: To review diagnostic approaches in chronic diseases of the small intestine.
  • MATERIAL AND METHODS: A total of 1096 patients with chronic diseases of the small intestine were admitted to the clinic of the Central Research Institute of Gastroenterological Diseases in 1987-2006.
  • RESULTS: Most of the patients (90.5%) had celiac disease, hypolactasia and other types of disaccharidase deficiency, yersiniosis ileitis, Krohn's disease, postresection syndrome of a short small intestine, mesenterial ischemia and endocrine enteropathy.
  • Rare diseases (general variable hypogammaglobulinemia, lymphoma, Wipple's disease and diverticulosis of the small intestine) were diagnosed in 5.8% cases.
  • Primary amyloidosis of the small intestine, eosinophilic gastroenteritis, arteriomesenterial obstruction, primary intestinal pseudoobstruction, hypogammaglobulinemic spru, primary intestinal lymphangiectasia, tuberculosis, total polyposis, Peutz-Eggers and Cronkhite-Canada syndromes, collagenic sprue, erosive-ulcerative jejunoileitis, adenocarcinoma and heavy alpha-chain disease were detected in 3.7% examinees.
  • These diseases were encountered in one to 5 cases for the latest 20 years.
  • CONCLUSION: Clinical diagnosis of small intestinal diseases is based on the syndromes of chronic diarrhea, defective absorption, enteral protein loss, small intestinal obstruction and intestinal hemorrhage.
  • Differential diagnosis of the nosological entities employs x-ray, endoscopic, histological, immunological and other methods.
  • Most of the small intestinal diseases including rare can be diagnosed in any gastroentorological department.
  • [MeSH-major] Algorithms. Endoscopy, Gastrointestinal / methods. Immunologic Tests / methods. Intestinal Diseases / diagnosis. Intestine, Small. Radiography, Abdominal / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18491580.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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14. Pai RK, Snider WK, Starkey CR, Viswanatha D, Foucar MK, Wilson CS: Nonsecretory variant of immunoproliferative small intestinal disease: a case report with pathologic, immunophenotypic, and molecular findings. Arch Pathol Lab Med; 2005 Nov;129(11):1487-90
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  • [Title] Nonsecretory variant of immunoproliferative small intestinal disease: a case report with pathologic, immunophenotypic, and molecular findings.
  • We report a case of the nonsecretory variant of immunoproliferative small intestinal disease involving the distal small bowel and the mesenteric and retroperitoneal lymph nodes in a 19-year-old woman from Mexico.
  • This variant extranodal marginal zone B-cell lymphoma appeared similar in the different sites of involvement, with more interspersed large cells and greater plasmacytic differentiation present in intestinal specimens.
  • Characteristic lymphoepithelial lesions and follicular colonization were seen in intestinal and lymph node sections, respectively.
  • The neoplastic B cells were cytoplasmic immunoglobulin (Ig) A heavy-chain restricted and lacked surface and cytoplasmic light-chain expression by flow cytometric analysis.
  • Molecular studies showed absence of immunoglobulin heavy-chain (IgH) gene rearrangement, with a nonfunctional clonotypic rearrangement of the kappa light-chain gene.
  • This case highlights the role for kappa light-chain gene evaluation in immunoproliferative small intestinal disease, because IgH gene rearrangement analysis is often negative.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / pathology. Lymph Nodes / pathology. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Adult. Amoxicillin / therapeutic use. Anti-Bacterial Agents / therapeutic use. Benzimidazoles / therapeutic use. Drug Therapy, Combination. Female. Gene Rearrangement, B-Lymphocyte, Light Chain / genetics. Humans. Immunophenotyping. Intestine, Small / pathology. Mesentery. Metronidazole / therapeutic use. Omeprazole / analogs & derivatives. Omeprazole / therapeutic use. Retroperitoneal Space. Sulfoxides / therapeutic use

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  • (PMID = 16253033.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Benzimidazoles; 0 / Sulfoxides; 140QMO216E / Metronidazole; 804826J2HU / Amoxicillin; D8TST4O562 / pantoprazole; KG60484QX9 / Omeprazole
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15. Liu Z, Takazaki H, Nakazawa Y, Sakato M, Yagi T, Yasunaga T, King SM, Kamiya R: Partially functional outer-arm dynein in a novel Chlamydomonas mutant expressing a truncated gamma heavy chain. Eukaryot Cell; 2008 Jul;7(7):1136-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Partially functional outer-arm dynein in a novel Chlamydomonas mutant expressing a truncated gamma heavy chain.
  • The outer dynein arm of Chlamydomonas flagella contains three heavy chains (alpha, beta, and gamma), each of which exhibits motor activity.
  • Here we report the isolation of a novel mutant, oda2-t, whose gamma heavy chain is truncated at about 30% of the sequence.
  • While the previously isolated gamma chain mutant oda2 lacks the entire outer arm, oda2-t retains outer arms that contain alpha and beta heavy chains, suggesting that the N-terminal sequence (corresponding to the tail region) is necessary and sufficient for stable outer-arm assembly.
  • Thin-section electron microscopy and image analysis localize the gamma heavy chain to a basal region of the outer-arm image in the axonemal cross section.
  • The motility of oda2-t is lower than that of the wild type and oda11 (lacking the alpha heavy chain) but higher than that of oda2 and oda4-s7 (lacking the motor domain of the beta heavy chain).
  • Thus, the outer-arm dynein lacking the gamma heavy-chain motor domain is partially functional.
  • The availability of mutants lacking individual heavy chains should greatly facilitate studies on the structure and function of the outer-arm dynein.

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  • (PMID = 18487347.001).
  • [ISSN] 1535-9786
  • [Journal-full-title] Eukaryotic cell
  • [ISO-abbreviation] Eukaryotic Cell
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM051293; United States / NIGMS NIH HHS / GM / GM51293
  • [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 / Protein Subunits; 0 / Protozoan Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.4.2 / Dyneins
  • [Other-IDs] NLM/ PMC2446680
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16. Ishikawa T, Sakakibara H, Oiwa K: The architecture of outer dynein arms in situ. J Mol Biol; 2007 May 18;368(5):1249-58

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Outer dynein arms, the force generators for axonemal motion, form arrays on microtubule doublets in situ, although they are bouquet-like complexes with separated heads of multiple heavy chains when isolated in vitro.
  • To understand how the three heavy chains are folded in the array, we reconstructed the detailed 3D structure of outer dynein arms of Chlamydomonas flagella in situ by electron cryo-tomography and single-particle averaging.
  • The three AAA rings of heavy chains, seen as stacked plates, are connected in a striking manner on microtubule doublets.
  • The tail of the alpha-heavy chain, identified by analyzing the oda11 mutant, which lacks alpha-heavy chain, extends from the AAA ring tilted toward the tip of the axoneme and towards the inside of the axoneme at 50 degrees , suggesting a three-dimensional power stroke.
  • The neighboring outer dynein arms are connected through two filamentous structures: one at the exterior of the axoneme and the other through the alpha-tail.
  • Although the beta-tail seems to merge with the alpha-tail at the internal side of the axoneme, the gamma-tail is likely to extend at the exterior of the axoneme and join the AAA ring.
  • This suggests that the fold and function of gamma-heavy chain are different from those of alpha and beta-chains.

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  • (PMID = 17391698.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.6.4.2 / Dyneins
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17. Zhou H, Hickford JG, Fang Q: Polymorphism of the IGHA gene in sheep. Immunogenetics; 2005 Jul;57(6):453-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, variation in the immunoglobulin heavy alpha chain constant gene (IGHA) of sheep was investigated by amplification of a fragment that included the hinge coding sequence, followed by single-strand conformational polymorphism (SSCP) analysis and DNA sequencing.
  • [MeSH-major] Immunoglobulin alpha-Chains / genetics. Polymorphism, Single-Stranded Conformational. Sheep / immunology

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  • (PMID = 16025324.001).
  • [ISSN] 0093-7711
  • [Journal-full-title] Immunogenetics
  • [ISO-abbreviation] Immunogenetics
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY956424/ AY956425/ AY956426
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Immunoglobulin alpha-Chains
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18. Furuta A, Yagi T, Yanagisawa HA, Higuchi H, Kamiya R: Systematic comparison of in vitro motile properties between Chlamydomonas wild-type and mutant outer arm dyneins each lacking one of the three heavy chains. J Biol Chem; 2009 Feb 27;284(9):5927-35

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic comparison of in vitro motile properties between Chlamydomonas wild-type and mutant outer arm dyneins each lacking one of the three heavy chains.
  • Outer arm dynein (OAD) of cilia and flagella contains two or three distinct heavy chains, each having a motor function.
  • To elucidate their functional difference, we compared the in vitro motile properties of Chlamydomonas wild-type OAD containing the alpha, beta, and gamma heavy chains and three kinds of mutant OADs, each lacking one of the three heavy chains.
  • Wild-type OAD displayed microtubule gliding in the presence of ATP and ADP, with a maximal velocity of 5.0 mum/s, which is approximately 1/4 of the microtubule sliding velocity in the axoneme.
  • The absence of the beta heavy chain lowered both the gliding velocity and ATPase activity, whereas the absence of the gamma heavy chain increased both activities.
  • Strikingly, the absence of the alpha heavy chain lowered the gliding velocity but increased the ATPase activity.
  • Thus, the three heavy chains are likely to play distinct roles and regulate each other to achieve coordinated force production.

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  • (PMID = 19124458.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Subunits; EC 3.6.4.2 / Dyneins
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19. Quinn BA, Hayes MA, Waelchli RO, Kennedy MW, Betteridge KJ: Changes in major proteins in the embryonic capsule during immobilization (fixation) of the conceptus in the third week of pregnancy in the mare. Reproduction; 2007 Jul;134(1):161-70
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  • During fixation, beta2M in the capsule underwent limited proteolysis to an approximately 8 kDa form lacking nine amino acids from the N terminus, and was subsequently degraded.
  • During this period, beta2M in the capsule was evidently not part of a complex with major histocompatibility complex class 1 heavy alpha chain bands because these were undetectable in the capsule and uterine lavage.
  • These studies indicate that intact beta2M is a major protein associated with the embryonic capsule before fixation, after which it undergoes limited proteolysis to a truncated approximately 8 kDa form that remains in the capsule after the conceptus is immobilized.
  • [MeSH-minor] Animals. Electrophoresis, Polyacrylamide Gel. Female. Gene Expression. Gestational Age. Histocompatibility Antigens Class I / genetics. Histocompatibility Antigens Class I / metabolism. Immunoblotting. Pregnancy. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Uteroglobin / analysis. Uteroglobin / metabolism. Uterus / chemistry. Uterus / metabolism. Yolk Sac / chemistry. Yolk Sac / metabolism. beta 2-Microglobulin / analysis. beta 2-Microglobulin / metabolism

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  • (PMID = 17641098.001).
  • [ISSN] 1470-1626
  • [Journal-full-title] Reproduction (Cambridge, England)
  • [ISO-abbreviation] Reproduction
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Histocompatibility Antigens Class I; 0 / MHC class I-related chain A; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 9060-09-7 / Uteroglobin
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20. Mielcarek-Kuchta D, Olofsson J, Golusinski W: Laminin expression in advanced laryngeal squamous cell carcinoma does not correlate to neck metastases. Eur Arch Otorhinolaryngol; 2008 Oct;265(10):1257-61
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  • Laminins are a family of glycoproteins that consist of one heavy alpha chain and two light beta and gamma chains.
  • The study was carried out on 70 patients with squamous cell carcinoma of the larynx treated at the ENT Department University of Medical Sciences in Poznań.
  • The clinical data consisted of sex, age, stage of the tumor, and histological and immunohistochemical studies.
  • The patients with advanced clinical disease dominated in our material.

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  • (PMID = 18516614.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
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21. Economidou I, Manousos ON, Triantafillidis JK, Vaslamatzis MM, Zafiropoulou R, Papadakis T: Immunoproliferative small intestinal disease in Greece: presentation of 13 cases including two from Albania. Eur J Gastroenterol Hepatol; 2006 Sep;18(9):1029-38
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  • [Title] Immunoproliferative small intestinal disease in Greece: presentation of 13 cases including two from Albania.
  • OBJECTIVES: Immunoproliferative small intestinal disease (IPSID) represents a spectrum of clinicopathological entities including alpha-chain disease and other types of lymphoplasmacytic proliferations of the lamina propria of the small intestine, presenting with severe malabsorption.
  • IPSID has been described mainly in the Mediterranean, Middle East, and African countries.
  • METHODS: Current immunological and immunohistochemical methods for the detection of alpha heavy chains and the presence of clonality have been used to study 13 cases of IPSID diagnosed in Greece, two of whom were Albanian residents.
  • RESULTS: The patients were categorized in three subgroups of IPSID: alpha-chain disease (n=8), non-alpha chain disease with other monoclonal immunoglobulins (n=3), and polyclonal 'non-malignant' IPSID (n=2).
  • In several patients the disease had unusual features, and this in some cases delayed the diagnosis.
  • Patients with stage C disease had a short survival, whereas two patients with stage A alpha-chain disease responded to treatment with cyclophosphamide, vincristine and prednisolone, and cyclophosphamide, doxorubicine, vincristine and prednisolone, respectively, have a disease-free long survival of 35 and 12 years, and appear to be cured.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis

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  • (PMID = 16894320.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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22. Lampton PW, Goldstein CY, Warner CM: The role of tapasin in MHC class I protein trafficking in embryos and T cells. J Reprod Immunol; 2008 Jun;78(1):28-39
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  • Similar in structure to MHC class Ia proteins, Qa-2 protein is a trimer of the alpha (heavy) chain, beta(2) microglobulin and a bound peptide.

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  • (PMID = 18061684.001).
  • [ISSN] 0165-0378
  • [Journal-full-title] Journal of reproductive immunology
  • [ISO-abbreviation] J. Reprod. Immunol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD039215-05; United States / NICHD NIH HHS / HD / R01 HD039215; United States / NICHD NIH HHS / HD / HD39215; United States / NICHD NIH HHS / HD / R01 HD039215-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Molecular Chaperones; 0 / Peptides; 0 / Q surface antigens; 0 / Tap1 protein, mouse; 0 / beta 2-Microglobulin
  • [Other-IDs] NLM/ NIHMS51787; NLM/ PMC2459227
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23. Wahner-Roedler DL, Kyle RA: Heavy chain diseases. Best Pract Res Clin Haematol; 2005;18(4):729-46
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  • [Title] Heavy chain diseases.
  • Heavy chain diseases (HCDs) are rare B-cell lymphoplasma-cell proliferative disorders characterized by production of truncated monoclonal immunoglobulin heavy chains without associated light chains.
  • HCDs involving the three main immunoglobulin classes have been described; alpha-HCD is the most common and has the most uniform presentation, gamma- and mu-HCDs have variable clinical presentations and histopathologic features.
  • HCDs can be thought of as variant types of non-Hodgkin lymphoma: alpha-HCD presents as an extranodal marginal-zone lymphoma of mucosa-associated lymph-node tissue, gamma-HCD as lymphoplasmacytoid non-Hodgkin lymphoma, and mu-HCD as small lymphocytic non-Hodgkin lymphoma or chronic lymphocytic leukemia.
  • Diagnosis of HCD requires documentation of a deleted immunoglobulin heavy chain without a bound light chain in the serum or urine.
  • Prognosis is variable, and no standardized effective treatment programs are available except for alpha-HCD, which in its early stage may respond to antibiotics.
  • [MeSH-major] Heavy Chain Disease / diagnosis
  • [MeSH-minor] Clinical Laboratory Techniques. Humans. Immunoglobulin Heavy Chains / genetics. Lymphoproliferative Disorders / etiology. Prognosis

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  • (PMID = 16026747.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 38
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24. Salem PA, Estephan FF: Immunoproliferative small intestinal disease: current concepts. Cancer J; 2005 Sep-Oct;11(5):374-82
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  • [Title] Immunoproliferative small intestinal disease: current concepts.
  • Immunoproliferative small intestinal disease is a distinctive lymphoproliferative disorder.
  • Among these disorders, it is the only disease associated with a specific and characteristic abnormal protein, and also an identifiable, at least in some patients, early phase with a benign-looking histo-pathologic expression.
  • Whether the disease at this stage is malignant or not is not known.
  • This observation is significant and raises the question of chemoprevention in lymphomas.
  • In contrast to primary nonimmunoproliferative small intestinal lymphomas, in which the pathology in the intestine is usually focal and involving specific segments of the intestine and leaving the segments between the involved areas free of disease, the pathology in immunoproliferative small intestinal disease is diffuse, with a mucosal cellular infiltrate involving large segments of the intestine and sometimes the entire length of the intestine, thus producing malabsorption.
  • Preliminary recent epidemiological data have shown a decrease in the incidence of this disease in endemic areas, and therefore environmental factors are suspected to play a major role in its pathogenesis.
  • Additional research is indicated not only to understand this specific lymphoproliferative disorder but also to understand lymphomas in general.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease

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  • (PMID = 16259867.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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25. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
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  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

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  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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26. Hendriksen SW, van Leengoed LA, Roest HI, van Nes A: [Neonatal diarrhoea in pigs: alpha- and beta2-toxin produced by Clostridium perfringens]. Tijdschr Diergeneeskd; 2006 Dec 15;131(24):910-3
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  • [Title] [Neonatal diarrhoea in pigs: alpha- and beta2-toxin produced by Clostridium perfringens].
  • [Transliterated title] Neonatale diarree bij biggen: alpha- en beta2-toxine producerende Clostridium perfringens.
  • Toxin typing by polymerase chain reaction led to the detection of genes encoding a-toxin (cpa) and beta2-toxin (cpb2).
  • Surprisingly, alpha- and beta2-toxin-producing C. perfringens was isolated from all tested herds with piglets with neonatal diarrhoea.
  • [MeSH-major] Bacterial Toxins / biosynthesis. Clostridium Infections / veterinary. Clostridium perfringens / metabolism. Diarrhea / veterinary. Swine Diseases / microbiology
  • [MeSH-minor] Animals. Animals, Newborn / microbiology. Calcium-Binding Proteins / genetics. Calcium-Binding Proteins / isolation & purification. Disease Outbreaks / veterinary. Netherlands / epidemiology. Polymerase Chain Reaction. Swine. Type C Phospholipases / genetics. Type C Phospholipases / isolation & purification. Vaccination / veterinary

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  • (PMID = 17278609.001).
  • [ISSN] 0040-7453
  • [Journal-full-title] Tijdschrift voor diergeneeskunde
  • [ISO-abbreviation] Tijdschr Diergeneeskd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Calcium-Binding Proteins; 0 / cpb2 protein, Clostridium perfringens; EC 3.1.4.- / Type C Phospholipases; EC 3.1.4.3 / alpha toxin, Clostridium perfringens
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27. Seremak-Mrozikiewicz A, Drews K, Bartkowiak-Wieczorek J, Kurzawińska G, Pieńkowski W, Spaczyński M, Mrozikiewicz PM: [PvuII genetic polymorphism of estrogen receptor alpha in the group of postmenopausal women with osteopenia and osteoporosis]. Ginekol Pol; 2005 Sep;76(9):679-86
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  • [Title] [PvuII genetic polymorphism of estrogen receptor alpha in the group of postmenopausal women with osteopenia and osteoporosis].
  • [Transliterated title] Znaczenie polimorfizmu Pvuii genu receptora estrogenowego alpha w grupie kobiet po menopauzie z osteopenia oraz osteoporoza.
  • PvuII restriction polymorphism in the intron 1 of the gene coding estrogen receptor alpha (ER-alpha) is indicated to play a significant role in osteopenia and osteoporosis development.
  • The goal of our study was to determine the frequency and the significance of PvuII polymorphism of the ER-alpha gene in the group of postmenopausal women with osteopenia and osteoporosis.
  • MATERIALS AND METHODS: 93 postmenopausal women with osteopenia and osteoporosis (t-score lower than (-1), and 141 healthy postmenopausal women have been investigated for PvuII polymorphism of the ER-a gene using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) assays.
  • [MeSH-major] Deoxyribonucleases, Type II Site-Specific / genetics. Estrogen Receptor alpha / genetics. Osteoporosis, Postmenopausal / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adult. Aged. Analysis of Variance. Bone Density / genetics. Bone Diseases, Metabolic / genetics. Female. Humans. Middle Aged. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length

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  • (PMID = 16417078.001).
  • [ISSN] 0017-0011
  • [Journal-full-title] Ginekologia polska
  • [ISO-abbreviation] Ginekol. Pol.
  • [Language] pol
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; EC 3.1.21.4 / Deoxyribonucleases, Type II Site-Specific
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28. Du MQ: MALT lymphoma : recent advances in aetiology and molecular genetics. J Clin Exp Hematop; 2007 Nov;47(2):31-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MALT lymphoma : recent advances in aetiology and molecular genetics.
  • Mucosa-associated lymphoid tissue (MALT) lymphoma is a common low grade B-cell lymphoma arising from a background of chronic inflammatory disease at a number of mucosal sites.
  • Those originating in the stomach are causatively linked to Helicobacter pylori infection and eradication of the bacterium with antibiotics leads to long-term complete regression of the lymphoma in aproximately 70% of cases.
  • Now, there is further evidence of linking Campylobacter jejuni, Borrelia burgdorferi and Chlamydia psittaci infection with immunoproliferative small intestine disease, MALT lymphoma of the skin and ocular adnexa respectively. t(11;18)/API2-MALT1, t(1;14)/IGH-BCL10, t(14;18)/IGH-MALT1 and t(3;14)/IGH-FOXP1 occur at considerably variable incidences in MALT lymphomas of different sites.
  • The first three chromosome translocations are specifically associated with the MALT lymphoma entity and the oncogenic products of these translocations have been shown to target a common molecular pathway, i.e. the nuclear factor-kappaB pathway.
  • Here, I review the recent advances in our understanding of the association of microbial pathogens with MALT lymphoma of various sites and the molecular genetics underlying the lymphoma development.
  • [MeSH-major] Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / microbiology

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  • (PMID = 18040143.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 99
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29. Kelkitli E, Bilgici B, Tokgöz B, Dilek M, Bedir A, Akpolat I, Utas C, Akpolat T: SAA1 alpha/alpha alleles in amyloidosis. J Nephrol; 2006 Mar-Apr;19(2):189-91
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  • [Title] SAA1 alpha/alpha alleles in amyloidosis.
  • BACKGROUND: Amyloidosis, mainly AA type, is one of the common diseases in nephrology clinics in Turkey.
  • AA type amyloidosis is a complication of various chronic infections or inflammatory diseases such as familial Mediterranean fever (FMF), rheumatoid arthritis (RA), tuberculosis and bronchiectasis.
  • A controversy exists in the literature regarding the relationship between SAA1 genotypes and AA type amyloidosis.
  • SAA1 genotypes were studied by the polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP) method.
  • RESULTS: The homozygous alpha/alpha genotype is the most common SAA1 genotype among patient groups with amyloidosis, and the alpha/alpha genotype frequency is significantly higher than in healthy controls (68 vs. 38%, p<0.05).
  • CONCLUSIONS: The SAA1 alpha/alpha genotype is a risk factor for AA type amyloidosis in Caucasoid populations and more studies are needed to investigate why the gamma/gamma genotype is associated with AA type amyloidosis in Japan.
  • [MeSH-minor] Adult. Asian Continental Ancestry Group. European Continental Ancestry Group. Familial Mediterranean Fever / ethnology. Familial Mediterranean Fever / genetics. Familial Mediterranean Fever / pathology. Female. Genotype. Humans. Japan. Male. Turkey

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  • (PMID = 16736418.001).
  • [ISSN] 1121-8428
  • [Journal-full-title] Journal of nephrology
  • [ISO-abbreviation] J. Nephrol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Serum Amyloid A Protein
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30. Mutanabbi M, Noor MK, Helal MA, Rahman MH: Coeliac disease. Mymensingh Med J; 2009 Jan;18(1 Suppl):S136-139
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coeliac disease.
  • Coeliac disease is an autoimmune disorder of the small bowel that occurs in genetically predisposed people of all ages from middle infancy.
  • Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat.
  • Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein and the immune system cross reacts with the bowel tissue, causing an inflammatory reaction that leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrient's.
  • He had loose mucoid stool, abdominal distension, bloating and history of loss of weight for two years.
  • Along with the routine examinations foecal fat estimation, MT, USG of whole abdomen, Barium follow through, endoscopic biopsy and tissue transglutaminage IgA autoantibody was done.
  • Histopathological report was in favour of immunoproliferative small intestinal disease.
  • Tissue transglutaminage IgA autoantibody was in higher level though done in a gluten free state.
  • Symptoms of diarrhoea, abdominal distention and bloatedness gradually decreased.
  • For patients presenting with alteration of bowel habit, abdominal distension, bloating and history of weight loss for long time, the importance of considering coeliac diseases as a differential diagnosis cannot be overemphasized.

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  • (PMID = 19377424.001).
  • [ISSN] 1022-4742
  • [Journal-full-title] Mymensingh medical journal : MMJ
  • [ISO-abbreviation] Mymensingh Med J
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Bangladesh
  • [Chemical-registry-number] 0 / Immunoglobulin A; 9007-90-3 / Gliadin; EC 2.3.2.13 / Transglutaminases
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31. Stratigos P, Kouskos E, Kouroglou M, Chrisafis I, Fois L, Mavrogiorgis A, Axiotis E, Zamtrakis S: Emergency pancreatoduodenectomy (whipple procedure) for massive upper gastrointestinal bleeding caused by a diffuse B-cell lymphoma of the duodenum: report of a case. Surg Today; 2007;37(8):680-4
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  • [Title] Emergency pancreatoduodenectomy (whipple procedure) for massive upper gastrointestinal bleeding caused by a diffuse B-cell lymphoma of the duodenum: report of a case.
  • We herein report a rare case of a massive upper gastrointestinal (GI) bleeding, caused by high-grade diffuse B-cell lymphoma of the duodenum, secondary to immunoproliferative small intestinal disease (IPSID) and treated with an emergency partial pancreatoduodenectomy.
  • An urgent abdominal ultrasound raised the suspicion of a large, possibly bleeding, neoplasm of the duodenum, which was finally confirmed by abdominal computed tomography.
  • Histologically, the tumor was a high-grade B-cell lymphoma of the duodenum.
  • The nearby small intestinal mucosa was suggestive of IPSID.
  • A massive upper GI hemorrhage from a high-grade B-cell non-Hodgkin lymphoma of the duodenum, which develops secondary to IPSID, is a very rare clinical demonstration of this disease.
  • [MeSH-major] Duodenal Neoplasms / complications. Emergency Treatment. Gastrointestinal Hemorrhage / surgery. Lymphoma, B-Cell / complications. Pancreaticoduodenectomy / methods. Upper Gastrointestinal Tract / surgery
  • [MeSH-minor] Humans. Immunoproliferative Small Intestinal Disease

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32. Emadi S, Barkhordarian H, Wang MS, Schulz P, Sierks MR: Isolation of a human single chain antibody fragment against oligomeric alpha-synuclein that inhibits aggregation and prevents alpha-synuclein-induced toxicity. J Mol Biol; 2007 May 11;368(4):1132-44
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  • [Title] Isolation of a human single chain antibody fragment against oligomeric alpha-synuclein that inhibits aggregation and prevents alpha-synuclein-induced toxicity.
  • Protein misfolding and aggregation are pathological aspects of numerous neurodegenerative diseases.
  • Aggregates of alpha-synuclein are major components of the Lewy bodies and Lewy neurites associated with Parkinson's Disease (PD).
  • A natively unfolded protein, alpha-synuclein can adopt different aggregated morphologies, including oligomers, protofibrils and fibrils.
  • The small oligomeric aggregates have been shown to be particularly toxic.
  • Antibodies that neutralize the neurotoxic aggregates without interfering with beneficial functions of monomeric alpha-synuclein can be useful therapeutics.
  • We were able to isolate single chain antibody fragments (scFvs) from a phage displayed antibody library against the target antigen morphology using a novel biopanning technique that utilizes atomic force microscopy (AFM) to image and immobilize specific morphologies of alpha-synuclein.
  • The scFv described here binds only to an oligomeric form of alpha-synuclein and inhibits both aggregation and toxicity of alpha-synuclein in vitro.
  • This scFv can have potential therapeutic value in controlling misfolding and aggregation of alpha-synuclein in vivo when expressed intracellularly in dopaminergic neurons as an intrabody.

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  • (PMID = 17391701.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG017984; United States / NIA NIH HHS / AG / R01 AG017984-01; United States / NIA NIH HHS / AG / R01 AG017984-02; United States / NIA NIH HHS / AG / R01 AG017984-04; United States / NIA NIH HHS / AG / R01 AG017984-03; United States / NIA NIH HHS / AG / AG17984
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / Peptide Library; 0 / alpha-Synuclein
  • [Other-IDs] NLM/ NIHMS22525; NLM/ PMC2235820
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33. Vasseur-Godbillon C, Marden MC, Giordano P, Wajcman H, Baudin-Creuza V: Impaired binding of AHSP to alpha chain variants: Hb Groene Hart illustrates a mechanism leading to unstable hemoglobins with alpha thalassemic like syndrome. Blood Cells Mol Dis; 2006 Nov-Dec;37(3):173-9
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  • [Title] Impaired binding of AHSP to alpha chain variants: Hb Groene Hart illustrates a mechanism leading to unstable hemoglobins with alpha thalassemic like syndrome.
  • Alpha hemoglobin stabilizing protein (AHSP) is a small protein of 102 residues induced by GATA-1, Oct-1- and EKLF.
  • It is synthesized at a high level in the red blood cell precursors and acts as a chaperone protecting the alpha hemoglobin (alpha-Hb) chains against precipitation.
  • AHSP and alpha-Hb form a heterodimer complex.
  • In the absence of AHSP, alpha-Hb oxidizes and precipitates within the erythrocyte precursors of the bone marrow leading to apoptosis and defective erythropoiesis.
  • In vitro the binding of AHSP to ferrous alpha-Hb accelerates oxidation of the heme iron in alpha-Hb, but the complex is more resistant to protein unfolding.
  • Some alpha-Hb variants with structural abnormality located in the contact area between alpha-Hb and AHSP exhibit an instability and a thalassemic like syndrome.
  • We suggest that this could result from a disturbed interaction between alpha-Hb variants and AHSP.
  • To study this interaction, we constructed the pGEX-alpha-AHSP vector that co-expressed human alpha-Hb and AHSP.
  • Results obtained with recombinant Groene Hart alpha-Hb and Diamant alpha-Hb, in which proline 119 is replaced by a serine and a leucine, respectively, showed clearly an impaired interaction with AHSP.
  • In contrast, the alpha mutants at the sites 42 and 104 exhibit a normal interaction with AHSP.
  • The CO rebinding kinetics of the AHSP/alpha-Hb(42mutant) complexes were similar to those previously obtained with the AHSP/alpha-Hb(WT) complex, which shows a modified rate that is intermediate to the classical Hb allosteric states.

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  • (PMID = 17052927.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AHSP protein, human; 0 / Blood Proteins; 0 / Hemoglobins, Abnormal; 0 / Molecular Chaperones; 0 / Recombinant Proteins; 0 / hemoglobin Groene Hart
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34. Soriano A, Lozano F, Oliva H, García F, Nomdedéu M, De Lazzari E, Rodríguez C, Barrasa A, Lorenzo JI, Del Romero J, Plana M, Miró JM, Gatell JM, Vives J, Gallart T: Polymorphisms in the interleukin-4 receptor alpha chain gene influence susceptibility to HIV-1 infection and its progression to AIDS. Immunogenetics; 2005 Oct;57(9):644-54
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  • [Title] Polymorphisms in the interleukin-4 receptor alpha chain gene influence susceptibility to HIV-1 infection and its progression to AIDS.
  • Our objective is to investigate whether single-nucleotide polymorphisms (SNPs) in the IL-4 receptor alpha chain gene (IL4RA) affect HIV infection and its progression to AIDS.
  • The I50V SNP in exon 5 and the haplotypes of six SNPs in exon 12 (E375A, C406R, S411L, S478P, Q551R, and V554I) were studied by polymerase chain reaction and sequencing in 30 HIV+ long-term nonprogressors (LTNP), 36 HIV+ typical progressors (TP), 55 highly exposed but uninfected individuals (EU), 25 EU-sexuals (EU-Sex; mostly women) and 30 EU-hemophiliacs (EU-Hem; hepatitis C virus+), and 97 healthy controls (HC), all Caucasians and lacking CCR5Delta32 homozygosity.
  • [MeSH-major] Genetic Predisposition to Disease. HIV Infections / genetics. Polymorphism, Single Nucleotide. Receptors, Cell Surface / genetics
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / genetics. Exons. Female. Gene Frequency. Genotype. Haplotypes. Homozygote. Humans. Interleukin-4 Receptor alpha Subunit. Male. Protein Subunits / genetics


35. Mak JC, Ko FW, Chu CM, Leung HC, Chan HW, Cheung AH, Ip MS, Chan-Yeung M: Polymorphisms in the IL-4, IL-4 receptor alpha chain, TNF-alpha, and lymphotoxin-alpha genes and risk of asthma in Hong Kong Chinese adults. Int Arch Allergy Immunol; 2007;144(2):114-22
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  • [Title] Polymorphisms in the IL-4, IL-4 receptor alpha chain, TNF-alpha, and lymphotoxin-alpha genes and risk of asthma in Hong Kong Chinese adults.
  • BACKGROUND: Susceptibility to the development of asthma and other atopic diseases is known to be associated with genetic components.
  • However, association studies with interleukin-4 (IL-4), IL-4 receptor alpha subunit (IL-4R alpha), tumor necrosis factor-alpha (TNF-alpha) and lymphotoxin-alpha (LT-alpha) genes were inconclusive, as both positive and negative results were obtained in several populations studied.
  • We aimed to investigate the association of the polymorphisms for IL-4 (C-589T), IL-4R alpha (Gln576Arg), TNF-alpha (G-308A) and LT-alpha (A252G) genes as candidates and asthma in adult Hong Kong Chinese population.
  • METHODS: The association study was conducted in an age- and smoking status-matched case-control design in asthma patients (n = 292) and healthy controls (n = 292) using polymerase chain reaction and restriction fragment length polymorphism.
  • After stratification by atopic status, the heterozygous AG genotype of LT-alpha (A252G) was found to increase risk of asthma in atopic population [odds ratio (OR) = 2.00, 95% CI 1.09-3.67, p = 0.024].
  • When stratified by smoking status, we found increased risk of asthma with subjects carrying the heterozygous AG and homozygous GG genotypes of LT-alpha in ever-smokers (OR = 2.73, 95% CI 1.11-6.69, p = 0.028 for heterozygotes; OR = 3.34, 95% CI 1.16-9.62, p = 0.026 for homozygotes).
  • CONCLUSION: Our results suggest that the variability of LT-alpha genotypes may have potential implications for individual susceptibility to asthma in atopic or in ever-smoking Chinese adults in Hong Kong.
  • [MeSH-major] Asthma / genetics. Genetic Predisposition to Disease. Lymphotoxin-alpha / genetics
  • [MeSH-minor] Adult. Asian Continental Ancestry Group / genetics. Female. Hong Kong / ethnology. Humans. Interleukin-4 / genetics. Interleukin-4 Receptor alpha Subunit / genetics. Male. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / genetics

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17536219.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interleukin-4 Receptor alpha Subunit; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4
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36. Geng S, Chang H, Qin W, Li Y, Feng J, Shen B: Overexpression, effective renaturation, and bioactivity of novel single-chain antibodies against TNF-alpha. Prep Biochem Biotechnol; 2008;38(1):74-86
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  • [Title] Overexpression, effective renaturation, and bioactivity of novel single-chain antibodies against TNF-alpha.
  • Neutralization of tumor necrosis factor-alpha (TNF-alpha) has become an effective therapeutic strategy for TNF-related autoimmune diseases.
  • Due to the limitations of the large molecular inhibitors in the therapy, development of novel TNF-alpha inhibitors is very attractive and useful.
  • In this study, based on the previously designed domain antibody, two novel human anti-TNF single-chain antibodies were constructed using modular consensus frameworks of human antibody as scaffold to display the antagonistic peptides.
  • The single-chain antibodies were always overexpressed in E.coli BL21(DE3) host as inclusion bodies.
  • Under the optimized refolding conditions, the inclusion bodies were renatured successfully and the refolded single-chain antibodies could bind with TNF-alpha and block TNF-induced cytotoxicity on L929 cells.
  • The bioactivity of the single-chain antibodies was significantly increased over the domain antibody.
  • [MeSH-major] Antibodies / immunology. Autoimmune Diseases / therapy. Cytotoxicity, Immunologic / drug effects. Gene Expression Regulation / drug effects. Protein Renaturation / drug effects. Tumor Necrosis Factor-alpha

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  • (PMID = 18080912.001).
  • [ISSN] 1082-6068
  • [Journal-full-title] Preparative biochemistry & biotechnology
  • [ISO-abbreviation] Prep. Biochem. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Tumor Necrosis Factor-alpha
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37. Gawlik KI, Li JY, Petersén A, Durbeej M: Laminin alpha1 chain improves laminin alpha2 chain deficient peripheral neuropathy. Hum Mol Genet; 2006 Sep 15;15(18):2690-700
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laminin alpha1 chain improves laminin alpha2 chain deficient peripheral neuropathy.
  • Absence of laminin alpha2 chain leads to a severe form of congenital muscular dystrophy (MDC1A) associated with peripheral neuropathy.
  • Pre-clinical studies in animal models have mainly focused on ameliorating the muscle phenotype.
  • Here we show that transgenic expression of laminin alpha1 chain in muscles and the peripheral nervous system of laminin alpha2 chain deficient mice reduced muscular dystrophy and largely corrected the peripheral nerve defects.
  • The presence of laminin alpha1 chain in the peripheral nervous system resulted in near-normal myelination, restored Schwann cell basement membranes and improved rotarod performance.
  • In summary, we postulate that laminin alpha1 chain is an excellent substitute for laminin alpha2 chain in multiple tissues and suggest that treatment with laminin alpha1 chain may be beneficial for MDC1A in humans.
  • [MeSH-major] Laminin / deficiency. Laminin / physiology. Peripheral Nervous System Diseases / physiopathology

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  • (PMID = 16893907.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Laminin; 0 / laminin alpha 2; 151186-83-3 / laminin A
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38. Hu ZW, Luo HB, Xu YM, Guo JW, Deng XL, Tong YW, Tang X: Tumor necrosis factor--alpha gene promoter polymorphisms in Chinese patients with nonalcoholic fatty liver diseases. Acta Gastroenterol Belg; 2009 Apr-Jun;72(2):215-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor--alpha gene promoter polymorphisms in Chinese patients with nonalcoholic fatty liver diseases.
  • BACKGROUND: Nonalcoholic Fatty Liver Disease (NAFLD) encompasses a histopathological spectrum of clinical conditions such as simple fatty liver (steatosis), nonalcoholic steatohepatitis (NASH), and a variant that has degrees of fibrosis.
  • Tumor Necrosis Factor-alpha (TNF-alphalpha) is considered essential for NAFLD.
  • PATIENTS AND METHODS: The TNF-alpha gene polymorphisms at position -238 and -308 were analyzed in 189 Chinese patients with NAFLD and 138 healthy controls by using polymerase chain reaction and restriction fragment length polymorphism assay.
  • The serum levels of TNF-alpha in both patient and control groups were measured by ELISA.
  • The associations of TNF-alpha polymorphism and serum TNF-alpha, and/or insulin resistance, and/or clinical features were analyzed.
  • RESULTS: The carrier frequencies of TNF-alpha gene polymorphism with G/A mutation at -238 were significantly higher in the patients with NAFLD than those in the control subjects (p < 0.05).
  • In addition, the serum level of TNF-alpha was markedly higher in the patients with NAFLD than in the control subjects (p < 0.05).
  • There were significant associations between TNF-alpha gene polymorphism in the -238 A allele and increased serum TNF-alpha, insulin resistance, as well as increased body mass index in the NAFLD patients.
  • CONCLUSIONS: The results indicate that the TNF-alpha gene polymorphism at position -238 is associated with susceptibility of nonalcoholic Fatty Liver Disease in a Chinese population.
  • [MeSH-major] Fatty Liver / genetics. Promoter Regions, Genetic. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 19637776.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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39. Kawamura T, Andoh A, Nishida A, Shioya M, Yagi Y, Nishimura T, Hashimoto T, Tsujikawa T, Yasui H, Fujiyama Y: Inhibitory effects of short-chain fatty acids on matrix metalloproteinase secretion from human colonic subepithelial myofibroblasts. Dig Dis Sci; 2009 Feb;54(2):238-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effects of short-chain fatty acids on matrix metalloproteinase secretion from human colonic subepithelial myofibroblasts.
  • BACKGROUND AND AIMS: Short-chain fatty acids (SCFAs), such as acetate, propionate and butyrate, are the major by-product of bacterial fermentation of dietary fiber in the colon.
  • MATERIALS AND METHODS: SEMFs were identified by expression of alpha-smooth muscle actin and vimentin.
  • Propionate and butyrate significantly attenuated IL-1 beta- and TNF-alpha-induced MMP-1 and MMP-3 secretion.
  • Propionate and butyrate did not modulate IL-1 beta- and TNF-alpha-induced activation of mitogen-activated protein kinases (MAPKs), which play a crucial role in MMP induction.
  • Trichostatin A, a histone-deacetylase inhibitor, reduced IL-1 beta-induced MMP-1 and MMP-3 mRNA expression, and suppressed TNF-alpha-induced MMP-3 mRNA expression.
  • [MeSH-minor] Cells, Cultured. Enzyme Activation. Female. Humans. Hydroxamic Acids. Interleukin-1beta / physiology. Male. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. RNA, Messenger / metabolism. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 18629644.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Volatile; 0 / Hydroxamic Acids; 0 / Interleukin-1beta; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 3X2S926L3Z / trichostatin A; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.7 / Matrix Metalloproteinase 1
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40. Kadam JS, Gonzalez SA, Ahmed F, Menezes A, Jacobson IM: Prognostic significance of hepatitis C virus RNA detection by transcription-mediated amplification with negative polymerase chain reaction during therapy with peginterferon alpha and ribavirin. Dig Dis Sci; 2007 Oct;52(10):2525-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of hepatitis C virus RNA detection by transcription-mediated amplification with negative polymerase chain reaction during therapy with peginterferon alpha and ribavirin.
  • The lower limit of detection of most polymerase chain reaction (PCR) assays for hepatitis C virus (HCV) RNA is 50 IU/ml, compared to 5 IU/ml for the transcription-mediated amplification (TMA) method.
  • [MeSH-major] Antiviral Agents / therapeutic use. Hepacivirus / genetics. Hepatitis C, Chronic / drug therapy. Interferon-alpha / therapeutic use. Nucleic Acid Amplification Techniques / methods. Polyethylene Glycols / therapeutic use. RNA, Viral / analysis. Ribavirin / therapeutic use
  • [MeSH-minor] Drug Carriers. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Predictive Value of Tests. Prognosis. Recombinant Proteins. Retrospective Studies. Transcription, Genetic. Viremia / drug therapy. Viremia / virology

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  • (PMID = 17406826.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Drug Carriers; 0 / Interferon-alpha; 0 / RNA, Viral; 0 / Recombinant Proteins; 0 / peginterferon alfa-2a; 30IQX730WE / Polyethylene Glycols; 49717AWG6K / Ribavirin; 76543-88-9 / interferon alfa-2a
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41. Malfait F, Symoens S, De Backer J, Hermanns-Lê T, Sakalihasan N, Lapière CM, Coucke P, De Paepe A: Three arginine to cysteine substitutions in the pro-alpha (I)-collagen chain cause Ehlers-Danlos syndrome with a propensity to arterial rupture in early adulthood. Hum Mutat; 2007 Apr;28(4):387-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Three arginine to cysteine substitutions in the pro-alpha (I)-collagen chain cause Ehlers-Danlos syndrome with a propensity to arterial rupture in early adulthood.
  • Mutations in the COL1A1 and COL1A2 genes, encoding the proalpha1 and 2 chains of type I collagen, cause osteogenesis imperfecta (OI) or Ehlers-Danlos syndrome (EDS) arthrochalasis type.
  • Although the majority of missense mutations in the collagen type I triple helix affect glycine residues in the Gly-Xaa-Yaa repeat, few nonglycine substitutions have been reported.
  • Two arginine-to-cysteine substitutions in the alpha1(I)-collagen chain are associated with classic EDS [R134C (p.R312C)] or autosomal dominant Caffey disease with mild EDS features [R836C (p.R1014C)].
  • Dermal fibroblasts from the patients produced disulfide-bonded alpha1(I)-dimers in approximately 20% of type I collagen, which were efficiently secreted into the medium in case of the R396C and R915C substitution.
  • Theoretical stability calculations of the collagen type I heterotrimer and thermal denaturation curves of monomeric mutant alpha1(I)-collagen chains showed minor destabilization of the collagen helix.
  • Our findings demonstrate that R-to-C substitutions in the alpha1(I) chain may result in a phenotype with propensity to arterial rupture in early adulthood.
  • This broadens the phenotypic range of nonglycine substitutions in collagen type I and has important implications for genetic counseling and follow-up of patients carrying this type of mutation.
  • [MeSH-major] Collagen Type I / genetics. Ehlers-Danlos Syndrome / complications. Ehlers-Danlos Syndrome / genetics. Rupture, Spontaneous / genetics
  • [MeSH-minor] Adolescent. Adult. Amino Acid Substitution. Arginine / genetics. Arginine / metabolism. Base Sequence. Bone Diseases, Metabolic / complications. Bone Diseases, Metabolic / genetics. Bone Diseases, Metabolic / metabolism. Collagen / genetics. Collagen Type III / genetics. Cysteine / genetics. Cysteine / metabolism. Female. Femoral Artery. Humans. Iliac Artery. Male. Molecular Sequence Data. Mutation, Missense. Protein Structure, Secondary. RNA, Messenger / genetics


42. Liu JZ, Wang LR, Huang LJ, Xiao B, Zhou Y: [Study on genetic diagnosis and prenatal diagnosis of alpha-thalassemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 Feb;26(2):103-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study on genetic diagnosis and prenatal diagnosis of alpha-thalassemia].
  • OBJECTIVE: To develop a single-tube multiplex polymerase chain reaction (mPCR) technique to detect three common deletional alpha-thalassemias (alpha-Thal) in Chinese, and to perform genetic diagnosis and prenatal diagnosis for an alpha-Thal family from Hebei province, China.
  • METHODS: Fourty-two blood samples including samples from one alpha-Thal family from Hebei province were assayed.
  • The mPCR containing 7 primers, gel electrophoresis and DNA sequencing were used for the genetic diagnosis and prenatal diagnosis.
  • A HbH child and a fetus of the alpha-Thal family were diagnosed as--(SEA)/alpha(cs)alpha and alpha alpha/alpha alpha respectively by using the mPCR and DNA sequencing.
  • The result of postnatal analysis of the cord blood was consistent with the prenatal result (alpha alpha/alpha alpha).
  • CONCLUSION: The developed mPCR technique can be used for genetic diagnosis and prenatal diagnosis of the 3 deletional alpha-Thal in Chinese.
  • [MeSH-major] Genetic Testing. Prenatal Diagnosis. alpha-Thalassemia / diagnosis
  • [MeSH-minor] Adult. Child, Preschool. Family Health. Female. Fetal Diseases / diagnosis. Fetal Diseases / genetics. Gene Deletion. Humans. Male. Molecular Diagnostic Techniques / methods. Point Mutation. Polymerase Chain Reaction / methods. Pregnancy. Sequence Analysis, DNA

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  • (PMID = 15921628.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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43. Mitchell BL, Yasui Y, Lampe JW, Gafken PR, Lampe PD: Evaluation of matrix-assisted laser desorption/ionization-time of flight mass spectrometry proteomic profiling: identification of alpha 2-HS glycoprotein B-chain as a biomarker of diet. Proteomics; 2005 May;5(8):2238-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of matrix-assisted laser desorption/ionization-time of flight mass spectrometry proteomic profiling: identification of alpha 2-HS glycoprotein B-chain as a biomarker of diet.
  • Biomarkers have the potential to impact a wide range of public health concerns, including early detection of diseases, drug discovery, and improved accuracy of monitoring effects of interventions.
  • However, before applying this approach to screening of complex diseases, we evaluated the approach in a controlled dietary intervention study.
  • The 2740 m/z peak was identified as the B-chain of alpha 2-HS glycoprotein, a serum protein previously found to vary with diet and be involved in insulin resistance and immune function.

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  • (PMID = 15841498.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA108339; United States / NCI NIH HHS / CA / CA108339; United States / NCI NIH HHS / CA / CA80416-05; United States / NCI NIH HHS / CA / R01 CA070913
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / AHSG protein, human; 0 / Biomarkers; 0 / Blood Proteins; 0 / alpha-2-HS-Glycoprotein
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44. Yao XS, Diao Y, Sun WB, Luo JM, Qin M, Tang XY: Analysis of the CDR3 length repertoire and the diversity of TCR alpha chain in human peripheral blood T lymphocytes. Cell Mol Immunol; 2007 Jun;4(3):215-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of the CDR3 length repertoire and the diversity of TCR alpha chain in human peripheral blood T lymphocytes.
  • Analysis of complementarity determining region 3 (CDR3) length of T lymphocyte receptors (TCRs) by immunoscope spectratyping technique has been used successfully to investigate the diversity of TCR in autoimmune diseases and infection diseases.
  • These results may be helpful to further study the recombination mechanism of human TCR genes, the TCR CDR3 gene repertoire, and the repertoire drift in health people and disease state.
  • [MeSH-major] Complementarity Determining Regions / chemistry. Complementarity Determining Regions / genetics. Genetic Variation. Receptors, Antigen, T-Cell, alpha-beta / chemistry. Receptors, Antigen, T-Cell, alpha-beta / genetics. T-Lymphocyte Subsets / immunology

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  • (PMID = 17601376.001).
  • [ISSN] 1672-7681
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / Receptors, Antigen, T-Cell, alpha-beta
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45. Buargub M, El Huni S, Tagdi M: Tolerance and efficacy of interferon-alpha in hemodialysis patients in Tripoli. Saudi J Kidney Dis Transpl; 2006 Sep;17(3):338-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tolerance and efficacy of interferon-alpha in hemodialysis patients in Tripoli.
  • A prospective non-randomized study was conducted at the Department of Infectious Diseases at Tripoli Medical Center.
  • We evaluated the tolerance and efficacy of interferon-alpha (IFN) monotherapy in our hemodialysis (HD) patients with chronic hepatitis C virus (HCV) infection.
  • Patients with evidence of active viral infection i.e. positive polymerase chain reaction (PCR) results and who were potential transplant candidates were included in the study.
  • They received three million units of IFN-alpha, administered subcutaneously, three times a week for 12 months.
  • Our study suggests that the efficacy of IFN-alpha in our patients was less than anticipated and the tolerance to the drug was poor.
  • [MeSH-major] Antiviral Agents / therapeutic use. Drug Tolerance. Hepatitis C, Chronic / drug therapy. Interferon-alpha / therapeutic use. Renal Dialysis
  • [MeSH-minor] Adolescent. Adult. Female. Follow-Up Studies. Hepacivirus / genetics. Humans. Injections, Subcutaneous. Kidney Failure, Chronic / complications. Kidney Failure, Chronic / therapy. Male. Middle Aged. Polymerase Chain Reaction. Prospective Studies. RNA, Viral / genetics. Treatment Outcome

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  • (PMID = 16970253.001).
  • [ISSN] 1319-2442
  • [Journal-full-title] Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia
  • [ISO-abbreviation] Saudi J Kidney Dis Transpl
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / RNA, Viral
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46. SanGiovanni JP, Chew EY: The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina. Prog Retin Eye Res; 2005 Jan;24(1):87-138
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina.
  • In this work we advance the hypothesis that omega-3 (omega-3) long-chain polyunsaturated fatty acids (LCPUFAs) exhibit cytoprotective and cytotherapeutic actions contributing to a number of anti-angiogenic and neuroprotective mechanisms within the retina. omega-3 LCPUFAs may modulate metabolic processes and attenuate effects of environmental exposures that activate molecules implicated in pathogenesis of vasoproliferative and neurodegenerative retinal diseases.
  • We discuss the relationship of LCPUFAs with these bioactivators and bioactive compounds in the context of three blinding retinal diseases of public health significance that exhibit both vascular and neural pathology.
  • What evidence exists to suggest that LCPUFAs modulate factors and processes implicated in diseases of the vascular and neural retina?
  • DHA activates a number of nuclear hormone receptors that operate as transcription factors for molecules that modulate reduction-oxidation-sensitive and proinflammatory genes; these include the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and the retinoid X receptor.
  • In the case of PPAR-alpha, this action is thought to prevent endothelial cell dysfunction and vascular remodeling through inhibition of: vascular smooth muscle cell proliferation, inducible nitric oxide synthase production, interleukin-1 induced cyclooxygenase (COX)-2 production, and thrombin-induced endothelin 1 production.
  • [MeSH-major] Fatty Acids, Omega-3 / physiology. Retina / metabolism. Retinal Diseases / metabolism

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  • (PMID = 15555528.001).
  • [ISSN] 1350-9462
  • [Journal-full-title] Progress in retinal and eye research
  • [ISO-abbreviation] Prog Retin Eye Res
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 EY999999
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3
  • [Number-of-references] 454
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47. Kobayashi M, Jasinski J, Liu E, Li M, Miao D, Zhang L, Yu L, Nakayama M, Eisenbarth GS: Conserved T cell receptor alpha-chain induces insulin autoantibodies. Proc Natl Acad Sci U S A; 2008 Jul 22;105(29):10090-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conserved T cell receptor alpha-chain induces insulin autoantibodies.
  • A fundamental question is what are the molecular determinants that lead to spontaneous preferential targeting of specific autoantigens in autoimmune diseases, such as the insulin B:9-23 peptide sequence in type 1 diabetes.
  • Anti-insulin B:9-23 T cell clones isolated from prediabetic NOD islets have a conserved Valpha-segment/Jalpha-segment, but no conservation of the alpha-chain N region and no conservation of the Vbeta-chain.
  • Here, we show that the conserved T cell receptor alpha-chain generates insulin autoantibodies when transgenically or retrogenically introduced into mice without its corresponding Vbeta.
  • We suggest that a major part of the mystery as to why islet autoimmunity develops relates to recognition of a primary insulin peptide by a conserved alpha chain T cell receptor.

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  • (PMID = 18626021.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK057516; United States / NIDDK NIH HHS / DK / R01DK55969-08; United States / NIDDK NIH HHS / DK / K99 DK080885; United States / NIDDK NIH HHS / DK / R01 DK055969; United States / NIDDK NIH HHS / DK / P30 DK57516; United States / NIAID NIH HHS / AI / U19 AI050864; United States / NIAID NIH HHS / AI / 2U19 AI050864-07; United States / NIDDK NIH HHS / DK / K99 DK080885-01
  • [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 / Autoantibodies; 0 / DNA Primers; 0 / Insulin; 0 / Insulin Antibodies; 0 / Receptors, Antigen, T-Cell, alpha-beta; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2464615
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48. Peters IR, Helps CR, Calvert EL, Hall EJ, Day MJ: Measurement of messenger RNA encoding the alpha-chain, polymeric immunoglobulin receptor, and J-chain in duodenal mucosa from dogs with and without chronic diarrhea by use of quantitative real-time reverse transcription-polymerase chain reaction assays. Am J Vet Res; 2005 Jan;66(1):11-6
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  • [Title] Measurement of messenger RNA encoding the alpha-chain, polymeric immunoglobulin receptor, and J-chain in duodenal mucosa from dogs with and without chronic diarrhea by use of quantitative real-time reverse transcription-polymerase chain reaction assays.
  • OBJECTIVE: To examine the difference in expression of messenger RNA (mRNA) transcripts for polymeric immunoglobulin receptor (plgR), alpha-chain, and J-chain determined by use of quantitative real-time reverse transcription-polymerase chain reaction (QRT-PCR) assays in duodenal biopsy specimens obtained from dogs with and without chronic diarrhea.
  • SAMPLE POPULATION: Biopsy specimens of the proximal portion of the duodenum were obtained endoscopically from 39 dogs evaluated because of chronic diarrhea (12 German Shepherd Dogs and 27 non-German Shepherd Dog breeds); specimens were also obtained from a control group of 7 dogs evaluated because of other gastrointestinal tract diseases and 2 dogs that were euthanatized as a result of nongastrointestinal tract disease.
  • One-step QRT-PCR was used to quantify the level of expression of transcripts for the housekeeper gene glyceraldehyde-3-phosphate dehydrogenase, plgR, alpha-chain, and J-chain in duodenal mucosal tissue.
  • Conclusions and Clinical Relevance-Results indicated that the susceptibility of German Shepherd Dogs to chronic diarrhea is not a result of simple failure of transcription of the key genes that encode molecules involved in mucosal IgA secretion.
  • [MeSH-major] Diarrhea / veterinary. Dog Diseases / immunology. Immunoglobulin A, Secretory / biosynthesis. Immunoglobulin J-Chains / biosynthesis. Immunoglobulin alpha-Chains / biosynthesis. Receptors, Polymeric Immunoglobulin / biosynthesis
  • [MeSH-minor] Animals. Chronic Disease. Dogs. Duodenum / immunology. Female. Gene Expression. Intestinal Mucosa / immunology. Male. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / veterinary

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  • (PMID = 15691029.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A, Secretory; 0 / Immunoglobulin J-Chains; 0 / Immunoglobulin alpha-Chains; 0 / RNA, Messenger; 0 / Receptors, Polymeric Immunoglobulin
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49. Abkowitz JL, Sabo KM, Yang Z, Vite CH, Shields LE, Haskins ME: In utero transplantation of monocytic cells in cats with alpha-mannosidosis. Transplantation; 2009 Aug 15;88(3):323-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In utero transplantation of monocytic cells in cats with alpha-mannosidosis.
  • BACKGROUND: Lysosomal storage diseases are devastating illnesses, in large part because of their neurologic consequences.
  • METHODS: We studied the feasibility and efficacy of IU injections of monocytic cells (derived from normal marrow) in feline alpha-mannosidosis.
  • Heterozygous cats were interbred to produce affected (homozygous) and control (heterozygous and wild-type) offspring.
  • After birth, affected kittens were evaluated clinically and pathologically, tissue alpha-mannosidase levels were assayed, and in many studies, the numbers of alpha-mannosidase-containing cells were enumerated.
  • When male donor cells were transplanted into female recipients, engraftment was also quantified using polymerase chain reaction to amplify a Y chromosome-specific sequence.
  • We show that the donor monocytic cells engraft and persist (for up to 125 days) in the brain, liver, and spleen, albeit at levels below those needed to alter the clinical or pathological progression of the alpha-mannosidosis.
  • CONCLUSIONS: This is the first study of monocyte transplantation in a large animal model of a lysosomal storage disorder and demonstrates its feasibility, safety, and promise.

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  • (PMID = 19667933.001).
  • [ISSN] 1534-6080
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK049652-07; United States / NIDDK NIH HHS / DK / R01 DK049652; United States / NCRR NIH HHS / RR / P40 RR002512; United States / NIDDK NIH HHS / DK / R01 DK049652-08; United States / NIDDK NIH HHS / DK / R01 DK 49652; United States / NIDDK NIH HHS / DK / DK049652-06; United States / NIDDK NIH HHS / DK / R01 DK049652-06; United States / NIDDK NIH HHS / DK / DK049652-05; United States / NIDDK NIH HHS / DK / DK049652-08; United States / NIDDK NIH HHS / DK / R01 DK049652-07; United States / NCRR NIH HHS / RR / P40 RR 02512; United States / NIDDK NIH HHS / DK / R01 DK049652-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.1.24 / alpha-Mannosidase
  • [Other-IDs] NLM/ NIHMS131484; NLM/ PMC2742773
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50. Probert CS, Saubermann LJ, Balk S, Blumberg RS: Repertoire of the alpha beta T-cell receptor in the intestine. Immunol Rev; 2007 Feb;215:215-25
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  • [Title] Repertoire of the alpha beta T-cell receptor in the intestine.
  • The majority of T cells in the human and mouse intestine express the T-cell receptor (TCR) as an alphabeta heterodimer on their cell surface.
  • As the major recognition element of antigens in the context of major histocompatibility complex-derived proteins, an examination of the structure of the alpha beta TCR in intestines has provided significant insights into the potential function of these cells and the major determinants that drive their selection.
  • Studies in the human intestine have shown that the repertoires of intraepithelial lymphocytes (IELs), and likely lamina propria lymphocytes, are polyclonal before and shortly after birth, with the repertoire becoming oligoclonal in adults.
  • Studies in human inflammatory bowel disease (IBD) indicate that inflammation further skews the TCR repertoire.
  • [MeSH-major] Immunity, Mucosal. Intestinal Mucosa / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Animals. Epithelial Cells / immunology. Gene Rearrangement, beta-Chain T-Cell Antigen Receptor. Humans. Inflammatory Bowel Diseases / immunology. Phenotype

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  • (PMID = 17291291.001).
  • [ISSN] 0105-2896
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK44319; United States / NIDDK NIH HHS / DK / DK51362; United States / NIDDK NIH HHS / DK / DK53056
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
  • [Number-of-references] 69
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51. Nannenga BL, Zameer A, Sierks MR: Anti-oligomeric single chain variable domain antibody differentially affects huntingtin and alpha-synuclein aggregates. FEBS Lett; 2008 Feb 20;582(4):517-22
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  • [Title] Anti-oligomeric single chain variable domain antibody differentially affects huntingtin and alpha-synuclein aggregates.
  • Huntington's and Parkinson's diseases are both neurodegenerative disorders caused at least in part by misfolding and aggregation of huntingtin (htt) and alpha-synuclein, respectively.
  • Here we use a single chain antibody fragment (scFv) isolated against oligomeric alpha-synuclein to probe similarities and differences between the aggregation and toxic mechanisms of htt and alpha-synuclein.
  • Previous studies with monomeric alpha-synuclein showed the scFv prevented fibrillar aggregation, but blocked toxicity of oligomeric aggregates.
  • [MeSH-major] Biopolymers / immunology. Immunoglobulin Fragments / immunology. Nerve Tissue Proteins / immunology. Nuclear Proteins / immunology. alpha-Synuclein / immunology

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  • (PMID = 18230361.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biopolymers; 0 / HTT protein, human; 0 / Immunoglobulin Fragments; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / alpha-Synuclein
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52. Surguchev A, Surguchov A: Conformational diseases: looking into the eyes. Brain Res Bull; 2010 Jan 15;81(1):12-24
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  • [Title] Conformational diseases: looking into the eyes.
  • Conformational diseases, a general term comprising more than 40 disorders are caused by the accumulation of unfolded or misfolded proteins.
  • The gradual accumulation of protein aggregates and the acceleration of their formation by stress explain the characteristic late or episodic onset of the diseases.
  • The best studied in this group are neurodegenerative diseases and amyloidosis accompanied by the deposition of a specific aggregation-prone proteins or protein fragments and formation of insoluble fibrils.
  • Amyloidogenic protein accumulation often occurs in the brain tissues, e.g. in Alzheimer's disease with the deposition of amyloid-beta and Tau, in scrapie and bovine spongiform encephalopathy with the accumulation of prion protein, in Parkinson's disease with the deposition of alpha-synuclein.
  • Other examples of amyloid proteins are transthyretin, immunoglobulin light chain, gelsolin, etc.
  • The best studied ocular conformational diseases are cataract in the lens and retinitis pigmentosa in the retina, but accumulation of misfolded proteins also occurs in other parts of the eye causing various disorders.
  • Here we present the data regarding naturally unfolded and misfolded proteins in eye tissues, their structure-function relationships, and molecular mechanisms underlying their involvement in diseases.
  • We also summarize the etiology of ocular conformational diseases and discuss approaches to their treatment.
  • [MeSH-major] Eye Diseases / physiopathology. Proteostasis Deficiencies / physiopathology

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  • (PMID = 19808079.001).
  • [ISSN] 1873-2747
  • [Journal-full-title] Brain research bulletin
  • [ISO-abbreviation] Brain Res. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 159
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53. Ulmanen I, Halonen M, Ilmarinen T, Peltonen L: Monogenic autoimmune diseases - lessons of self-tolerance. Curr Opin Immunol; 2005 Dec;17(6):609-15
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  • [Title] Monogenic autoimmune diseases - lessons of self-tolerance.
  • The molecular defects recently identified in the rare monogenic autoimmune diseases (AIDs) have pinpointed critical steps in the pathways that contribute to the development of normal immune responses and self-tolerance.
  • Recent studies of autoimmune polyendocrinopathy syndrome type 1, autoimmune lymphoproliferative syndrome, immunodysregulation, polyendocrinopathy and enteropathy, X-linked, IL-2 receptor alpha-chain deficiency, and, in particular, their corresponding mouse models, have revealed the details of the molecular mechanisms of normal immune tolerance, and exposed how defects in these mechanisms result in human autoimmunity.
  • [MeSH-major] Autoimmune Diseases / genetics. Autoimmune Diseases / immunology. Self Tolerance
  • [MeSH-minor] Animals. Genetic Diseases, X-Linked / genetics. Genetic Diseases, X-Linked / immunology. Interleukin-2 Receptor alpha Subunit. Lymphoproliferative Disorders / genetics. Mice. Polyendocrinopathies, Autoimmune / genetics. Polyendocrinopathies, Autoimmune / immunology. Receptors, Interleukin / deficiency. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 16226439.001).
  • [ISSN] 0952-7915
  • [Journal-full-title] Current opinion in immunology
  • [ISO-abbreviation] Curr. Opin. Immunol.
  • [Language] eng
  • [Databank-accession-numbers] OMIM/ 240300/ 606367
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IL2RA protein, human; 0 / Il2ra protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin
  • [Number-of-references] 68
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54. Kanamaru Y, Pfirsch S, Aloulou M, Vrtovsnik F, Essig M, Loirat C, Deschênes G, Guérin-Marchand C, Blank U, Monteiro RC: Inhibitory ITAM signaling by Fc alpha RI-FcR gamma chain controls multiple activating responses and prevents renal inflammation. J Immunol; 2008 Feb 15;180(4):2669-78
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  • [Title] Inhibitory ITAM signaling by Fc alpha RI-FcR gamma chain controls multiple activating responses and prevents renal inflammation.
  • Monovalent targeting of the IgA Fc receptor (FcalphaRI or CD89) by anti-FcalphaRI Fab triggers potent inhibitory ITAM (ITAM(i)) signaling through the associated FcRgamma chain (FcalphaRI-FcRgamma ITAM(i)) that prevents IgG phagocytosis and IgE-mediated asthma.
  • This treatment also prevented ex vivo LPS activation of monocytes from patients with lupus nephritis or vasculitis, as well as receptor activation through serum IgA complexes from IgA nephropathy patients.
  • They also identify anti-FcalphaRI Fab as a new potential therapeutic tool for preventing progression of renal inflammatory diseases.
  • [MeSH-major] Cell Migration Inhibition / immunology. Cell Movement / immunology. Glomerulonephritis, IGA / pathology. Glomerulonephritis, IGA / prevention & control. Receptors, Immunologic / physiology. Signal Transduction / immunology

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  • (PMID = 18250479.001).
  • [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 / Antigens, CD; 0 / Fc(alpha) receptor; 0 / Receptors, Fc; 0 / Receptors, IgG; 0 / Receptors, Immunologic
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55. Potaczek DP, Sanak M, Mastalerz L, Setkowicz M, Kaczor M, Nizankowska E, Szczeklik A: The alpha-chain of high-affinity receptor for IgE (FcepsilonRIalpha) gene polymorphisms and serum IgE levels. Allergy; 2006 Oct;61(10):1230-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The alpha-chain of high-affinity receptor for IgE (FcepsilonRIalpha) gene polymorphisms and serum IgE levels.
  • BACKGROUND: The high-affinity receptor for immunoglobulin-E (IgE) (FcepsilonRI) plays a major role in the pathogenesis of allergy, but there are only two published studies on its alpha subunit (FcepsilonRIalpha) genetic variability in allergic diseases.

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  • (PMID = 16942574.001).
  • [ISSN] 0105-4538
  • [Journal-full-title] Allergy
  • [ISO-abbreviation] Allergy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Receptors, IgE; 37341-29-0 / Immunoglobulin E
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56. Joshi MA, Jeoung NH, Obayashi M, Hattab EM, Brocken EG, Liechty EA, Kubek MJ, Vattem KM, Wek RC, Harris RA: Impaired growth and neurological abnormalities in branched-chain alpha-keto acid dehydrogenase kinase-deficient mice. Biochem J; 2006 Nov 15;400(1):153-62
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  • [Title] Impaired growth and neurological abnormalities in branched-chain alpha-keto acid dehydrogenase kinase-deficient mice.
  • The BCKDH (branched-chain alpha-keto acid dehydrogenase complex) catalyses the rate-limiting step in the oxidation of BCAAs (branched-chain amino acids).
  • At 12 weeks of age, BDK-/- mice were 15% smaller than wild-type mice and their fur lacked normal lustre.

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  • (PMID = 16875466.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK R01 19259; United States / NIDDK NIH HHS / DK / DK R01 47844
  • [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, Branched-Chain; EC 1.2.4.4 / 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide); EC 2.7.- / Protein Kinases; EC 2.7.11.4 / (3-methyl-2-oxobutanoate dehydrogenase (lipoamide)) kinase; HG18B9YRS7 / Valine
  • [Other-IDs] NLM/ PMC1635446
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57. Carneiro FS, Zemse S, Giachini FR, Carneiro ZN, Lima VV, Webb RC, Tostes RC: TNF-alpha infusion impairs corpora cavernosa reactivity. J Sex Med; 2009 Mar;6 Suppl 3:311-9
MedlinePlus Health Information. consumer health - Erectile Dysfunction.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TNF-alpha infusion impairs corpora cavernosa reactivity.
  • INTRODUCTION: Erectile dysfunction (ED), as well as cardiovascular diseases (CVDs), is associated with endothelial dysfunction and increased levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha).
  • AIM: We hypothesized that increased TNF-alpha levels impair cavernosal function.
  • METHODS: In vitro organ bath studies were used to measure cavernosal reactivity in mice infused with vehicle or TNF-alpha (220 ng/kg/min) for 14 days.
  • Gene expression of nitric oxide synthase isoforms was evaluated by real-time polymerase chain reaction.
  • MAIN OUTCOME MEASURES: Corpora cavernosa from TNF-alpha-infused mice exhibited decreased nitric oxide (NO)-dependent relaxation, which was associated with decreased endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) cavernosal expression.
  • RESULTS: Cavernosal strips from the TNF-alpha-infused mice displayed decreased nonadrenergic-noncholinergic (NANC)-induced relaxation (59.4 +/- 6.2 vs. control: 76.2 +/- 4.7; 16 Hz) compared with the control animals.
  • Sympathetic-mediated, as well as phenylephrine (PE)-induced, contractile responses (PE-induced contraction; 1.32 +/- 0.06 vs. control: 0.9 +/- 0.09, mN) were increased in cavernosal strips from TNF-alpha-infused mice.
  • Additionally, infusion of TNF-alpha increased cavernosal responses to endothelin-1 and endothelin receptor A subtype (ET(A)) receptor expression (P < 0.05) and slightly decreased tumor necrosis factor-alpha receptor 1 (TNFR1) expression (P = 0.063).
  • CONCLUSION: Corpora cavernosa from TNF-alpha-infused mice display increased contractile responses and decreased NANC nerve-mediated relaxation associated with decreased eNOS and nNOS gene expression.
  • These changes may trigger ED and indicate that TNF-alpha plays a detrimental role in erectile function.
  • Blockade of TNF-alpha actions may represent an alternative therapeutic approach for ED, especially in pathologic conditions associated with increased levels of this cytokine.

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  • (PMID = 19267854.001).
  • [ISSN] 1743-6109
  • [Journal-full-title] The journal of sexual medicine
  • [ISO-abbreviation] J Sex Med
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL74167; United States / NHLBI NIH HHS / HL / P01 HL074167; United States / NHLBI NIH HHS / HL / HL71138; United States / NHLBI NIH HHS / HL / R01 HL071138-06; None / None / / R01 HL071138-06; United States / NHLBI NIH HHS / HL / R01 HL071138
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; EC 1.14.13.39 / Nitric Oxide Synthase
  • [Other-IDs] NLM/ NIHMS115461; NLM/ PMC2701672
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58. Lai MI, Garner C, Jiang J, Silver N, Best S, Menzel S, Thein SL: A twins heritability study on alpha hemoglobin stabilizing protein (AHSP) expression variability. Twin Res Hum Genet; 2010 Dec;13(6):567-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A twins heritability study on alpha hemoglobin stabilizing protein (AHSP) expression variability.
  • Alpha hemoglobin stabilizing protein (AHSP) was found to bind only to free α-globin monomers creating a stable and inert complex which remains soluble in the cytoplasm thus preventing harmful precipitations.
  • Alpha hemoglobin stabilizing protein was shown to bind nascent α-globin monomers with transient strength before transferring α-globin to β-globin to form hemoglobin tetramer.
  • A classical twin study would be beneficial to investigate the role of genetics and environment in the variation of alpha hemoglobin stabilizing protein expression as this knowledge will enable us to determine further investigations with regards to therapeutic interventions if alpha hemoglobin stabilizing protein is to be a therapeutic agent for β-thalassemia.
  • This study investigates the heritability influence of alpha hemoglobin stabilizing protein expression and factors that may contribute to this.
  • Results indicated that a major proportion of alpha hemoglobin stabilizing protein expression was influenced by genetic heritability (46%) with cis-acting factors accounting for 19% and trans-acting factors at 27%.
  • [MeSH-major] Blood Proteins / genetics. Diseases in Twins / genetics. Gene Expression Regulation. Genetic Predisposition to Disease / genetics. Molecular Chaperones / genetics. beta-Thalassemia / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. RNA, Messenger / genetics. Regulatory Elements, Transcriptional / genetics. Reverse Transcriptase Polymerase Chain Reaction. Twins, Dizygotic / genetics. Twins, Monozygotic / genetics. Young Adult

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  • (PMID = 21142933.001).
  • [ISSN] 1832-4274
  • [Journal-full-title] Twin research and human genetics : the official journal of the International Society for Twin Studies
  • [ISO-abbreviation] Twin Res Hum Genet
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0000111; United Kingdom / Medical Research Council / / ID51640
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Twin Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AHSP protein, human; 0 / Blood Proteins; 0 / Molecular Chaperones; 0 / RNA, Messenger
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59. Phylipsen M, Vogelaar IP, Schaap RA, Arkesteijn SG, Boxma GL, van Helden WC, Wildschut IC, de Bruin-Roest AC, Giordano PC, Harteveld CL: A new alpha(0)-thalassemia deletion found in a Dutch family (--(AW)). Blood Cells Mol Dis; 2010 Aug 15;45(2):133-5
Genetic Alliance. consumer health - Thalassemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new alpha(0)-thalassemia deletion found in a Dutch family (--(AW)).
  • Alpha-thalassemia is an inherited hemoglobin disorder characterized by a microcytic hypochromic anemia caused by a quantitative reduction of the alpha-globin chain.
  • The majority of the alpha-thalassemias is caused by deletions in the alpha-globin gene cluster.
  • A deletion in the alpha-globin gene cluster, which was found in a Dutch family, was characterized by MLPA, long-range PCR and direct sequencing.
  • We describe the molecular characterization of a novel 8.2kb deletion (--(AW)), involving both alpha-globin genes in cis.
  • This deletion is the third example of a non-homologous recombination event involving an Alu and an L1 repeat, and the first described in the human alpha-globin gene cluster.
  • Because of a 25% risk of Hb Bart's with hydrops foetalis in the offspring when in combination with another alpha(0)-thalassemia allele, it is important to diagnose this deletion.
  • [MeSH-major] Sequence Deletion / genetics. alpha-Globins / deficiency. alpha-Globins / genetics. alpha-Thalassemia / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682466.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha-Globins
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60. Fallah MS, Mahdian R, Aleyasin SA, Jamali S, Hayat-Nosaeid M, Karimipour M, Raeisi M, Zeinali S: Development of a quantitative real-time PCR assay for detection of unknown alpha-globin gene deletions. Blood Cells Mol Dis; 2010 Jun 15;45(1):58-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a quantitative real-time PCR assay for detection of unknown alpha-globin gene deletions.
  • BACKGROUND: Alpha-Thalassemia is the most common inherited disorder of hemoglobin (Hb) synthesis in the world.
  • Unlike beta-thalassemia, in which non-deletional mutations predominate, most of recognized alpha-thalassemia mutations include deletion of one or both alpha-globin genes.
  • The importance of alpha-thalassemia detection is mainly due to its shared blood parameters with beta-thalassemia and its impact on discrimination between unknown alpha-thalassemia and normal HbA2 beta-thalassemia during thalassemia prevention program.
  • Common alpha-globin deletional mutations including alpha(3.7)kb, alpha(4.2)kb, alpha(20.5)kb, and alpha(MED) and point mutation including 5 nt, Constant Spring (CS), and C19 were checked using either GAP-PCR or ARMS-PCR.
  • For this, five pairs of primers were used spanning from theta-globin gene up to the 3' upstream of alpha(2) gene.
  • RESULTS: After validation of primers specificity and performing serial dilution analysis in order to calculate PCR efficiency, the assay was performed on normal samples and cases with known alpha-globin gene deletions as positive and negative controls, respectively.
  • CONCLUSION: Gene dosage study by quantitative real-time PCR can be suggested as a rapid and reliable assay to screen probable carrier of alpha-thalassemia for unknown alpha-globin gene deletions.
  • [MeSH-major] Gene Deletion. Polymerase Chain Reaction / methods. alpha-Globins / genetics. alpha-Thalassemia / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20363165.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha-Globins
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61. Motohashi S, Nakayama T: Natural killer T cell-mediated immunotherapy for malignant diseases. Front Biosci (Schol Ed); 2009;1:108-16

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural killer T cell-mediated immunotherapy for malignant diseases.
  • Human invariant Valpha24 Natural Killer T (NKT) cells are unique lymphocyte subsets, characterized by an invariant T-cell receptor Valpha24 chain paired with Vbeta11.
  • Valpha24 NKT cells are activated by a specific glycolipid ligand, alpha-Galactosylceramide and rapidly produce high levels of cytokines upon stimulation, thereby modulating other immune cells such as NK cells antigen-specific CD4+ and CD8+ T cells and dendritic cells.
  • Abnormalities in the numbers and functions of Valpha24 NKT cells have been observed in patients with various malignant diseases.
  • The quantitative alteration and functional impairment of circulating Valpha24 NKT cells are herein reviewed in various cancer-bearing patients and the progress to date in the clinical applications of NKT cell-based tumor immunotherapy is summarized.

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  • (PMID = 19482686.001).
  • [ISSN] 1945-0524
  • [Journal-full-title] Frontiers in bioscience (Scholar edition)
  • [ISO-abbreviation] Front Biosci (Schol Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 41
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62. Schnizler MK, Schnizler K, Zha XM, Hall DD, Wemmie JA, Hell JW, Welsh MJ: The cytoskeletal protein alpha-actinin regulates acid-sensing ion channel 1a through a C-terminal interaction. J Biol Chem; 2009 Jan 30;284(5):2697-705
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cytoskeletal protein alpha-actinin regulates acid-sensing ion channel 1a through a C-terminal interaction.
  • ASIC1a confers pH-dependent modulation on postsynaptic dendritic spines and has critical effects in neurological diseases associated with a reduced pH.
  • Here, we show that alpha-actinin, which links membrane proteins to the actin cytoskeleton, associates with ASIC1a in brain and in cultured cells.
  • The interaction depended on an alpha-actinin-binding site in the ASIC1a C terminus that was specific for ASIC1a versus other ASICs and for alpha-actinin-1 and -4.
  • Co-expressing alpha-actinin-4 altered ASIC1a current density, pH sensitivity, desensitization rate, and recovery from desensitization.
  • Moreover, reducing alpha-actinin expression altered acid-activated currents in hippocampal neurons.
  • These findings suggest that alpha-actinins may link ASIC1a to a macromolecular complex in the postsynaptic membrane where it regulates ASIC1a activity.

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  • (PMID = 19028690.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG017502; United States / NHLBI NIH HHS / HL / HL61234; United States / NIDDK NIH HHS / DK / DK54759; United States / NINDS NIH HHS / NS / R01 NS035563; United States / NHLBI NIH HHS / HL / P50 HL061234; United States / Howard Hughes Medical Institute / / ; United States / NHLBI NIH HHS / HL / HL515670; United States / NIDDK NIH HHS / DK / P30 DK054759
  • [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 / Accn2 protein, mouse; 0 / Acid Sensing Ion Channels; 0 / DNA Primers; 0 / Nerve Tissue Proteins; 0 / Sodium Channels; 11003-00-2 / Actinin
  • [Other-IDs] NLM/ PMC2631967
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63. Depetris M, Casalis P, Kratje R, Etcheverrigaray M, Oggero M: A scFv antibody fragment as a therapeutic candidate to neutralize a broad diversity of human IFN-alpha subtypes. J Immunol Methods; 2008 May 20;334(1-2):104-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A scFv antibody fragment as a therapeutic candidate to neutralize a broad diversity of human IFN-alpha subtypes.
  • In this way, the increased expression of human interferon alpha (hIFN-alpha) is associated with acute viral infections, inflammatory disorders and several autoimmune illnesses, where the cytokine may be a factor in either initiating or maintaining the disease.
  • Currently, there are several mAbs marketed for a variety of indications and many more in clinical trials, in which IFN-alpha represents a potential target for antibody-based therapy.
  • A panel of 11 murine mAbs was prepared using recombinant hIFN-alpha2b as immunogen, all of which bound to the native form of the cytokine with affinity constants ranging from 1.7x10(7) M(-1) to 1.4x10(10) M(-1).
  • Taking into account the characterization of the antibodies and their ability to inhibit the IFN-alpha biological activity, four mAbs were selected to produce scFv fragments.
  • One of these fragments (CA5E6) was able to neutralize a wide spectrum of subtypes of the IFN-alpha family, including the recombinant cytokines hIFN-alpha2a and hIFN-alpha2b and a heterogeneous collection of IFN-alpha produced by activated leukocytes and Namalwa cells.
  • By using this strategy, it was possible to generate a new fragment (EP18) with increased affinity and ability to neutralize a broad diversity of IFN-alpha subtypes.
  • Consequently, the scFv EP18 represents a potential therapeutic agent for those immune and inflammatory diseases which are associated with an increased IFN-alpha expression.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Immunoglobulin Fragments / immunology. Immunoglobulin Variable Region / immunology. Interferon Type I / immunology. Interferon-alpha / immunology
  • [MeSH-minor] Animals. Antibody Affinity. Cloning, Molecular. Epitope Mapping. Female. Humans. Mice. Mice, Inbred BALB C. Neutralization Tests. Polymerase Chain Reaction. Recombinant Proteins

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  • (PMID = 18394641.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Interferon Type I; 0 / Interferon-alpha; 0 / Recombinant Proteins
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64. Hu S, Ciancio MJ, Lahav M, Fujiya M, Lichtenstein L, Anant S, Musch MW, Chang EB: Translational inhibition of colonic epithelial heat shock proteins by IFN-gamma and TNF-alpha in intestinal inflammation. Gastroenterology; 2007 Dec;133(6):1893-904
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  • [Title] Translational inhibition of colonic epithelial heat shock proteins by IFN-gamma and TNF-alpha in intestinal inflammation.
  • BACKGROUND & AIMS: Inducible heat shock proteins (iHsp), Hsp25/27 and Hsp70, play essential roles in protecting cells against stress and, in intestinal mucosal inflammation, potentially lessening the extent and severity of injury.
  • We examined the expression and regulation of iHsp in human and experimental inflammatory bowel diseases (IBD) and in vitro.
  • METHODS: iHsp expression and regulation were assessed in normal and IBD colonic biopsy specimens, IL-10(-/-) mice, and young adult mouse colonic epithelial cells by immunohistochemistry, Western blot, and real-time polymerase chain reaction (PCR).
  • Wild-type mice treated in vivo with interferon (IFN)-gamma + tumor necrosis factor (TNF)-alpha also demonstrated reduced colonic Hsp25/27 and Hsp70.
  • In young adult mouse colonic epithelial cells, IFN-gamma+TNF-alpha inhibited heat induction of Hsp25/27 and Hsp70, an effect not associated with changes in iHsp messenger RNA or protein half-lives but caused by suppressed de novo iHsp synthesis.
  • IFN-gamma+TNF-alpha cotreatment activated PKR, resulting in phosphorylation and inactivation of eIF-2alpha, an essential factor in protein translation.

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  • [Cites] Chin J Dig Dis. 2004;5(2):45-50 [15612656.001]
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  • (PMID = 18054561.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK-47722-11S1; United States / NIDDK NIH HHS / DK / P30 DK042086; United States / NIDDK NIH HHS / DK / DK047722-12; United States / NIDDK NIH HHS / DK / R01 DK038510-22; United States / NIDDK NIH HHS / DK / R01 DK038510; United States / NIDDK NIH HHS / DK / P30 DK042086-16; United States / NIDDK NIH HHS / DK / DK-42086; United States / NIDDK NIH HHS / DK / DK-38510; United States / NIDDK NIH HHS / DK / R01 DK047722-12; United States / NIDDK NIH HHS / DK / R37 DK047722; United States / NIDDK NIH HHS / DK / DK-62265; United States / NIDDK NIH HHS / DK / DK042086-17; United States / NIDDK NIH HHS / DK / DK042086-16; United States / NIDDK NIH HHS / DK / DK038510-22; United States / NIDDK NIH HHS / DK / DK-47722; United States / NIDDK NIH HHS / DK / P30 DK042086-17; United States / NIDDK NIH HHS / DK / R01 DK047722
  • [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 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hspb1 protein, mouse; 0 / Neoplasm Proteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ NIHMS35725; NLM/ PMC2180161
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65. Takenaka A, Kita A, Ikeya M, Arai H, Igarashi K: Galactosamine-induced acute liver injury in rats reduces hepatic alpha-tocopherol transfer protein production. J Nutr Sci Vitaminol (Tokyo); 2007 Aug;53(4):366-71
Hazardous Substances Data Bank. VITAMIN E .

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  • [Title] Galactosamine-induced acute liver injury in rats reduces hepatic alpha-tocopherol transfer protein production.
  • The liver plays the main role in the secretion of food-derived alpha-tocopherol into the circulation through the functioning of alpha-tocopherol transfer protein (alpha-TTP).
  • However, the effect of liver disease on alpha-TTP level and alpha-tocopherol metabolism has not been clarified.
  • We examined the amount of liver alpha-TTP and its effect on serum alpha-tocopherol concentration in liver injury.
  • Male Wistar rats were injected intraperitoneally with D-galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, alpha-tocopherol concentrations, and hepatic alpha-TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection.
  • The hepatic alpha-TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the alpha-TTP protein level had begun to decrease.
  • Lipid and alpha-tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h.
  • Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver alpha-tocopherol concentration was unchanged.
  • These results show that galactosamine-induced liver injury decreases hepatic alpha-TTP synthesis in rats.
  • Serum alpha-tocopherol concentration was not directly affected by the acute change in hepatic alpha-TTP level, suggesting that the chronic changes in alpha-TTP activity would be necessary to regulate serum alpha-tocopherol concentration.
  • [MeSH-major] Carrier Proteins / biosynthesis. Liver Diseases / metabolism
  • [MeSH-minor] Alanine Transaminase / blood. Animals. Aspartate Aminotransferases / blood. Blotting, Western. Cholesterol / blood. Disease Models, Animal. Drug-Induced Liver Injury. Galactosamine. L-Lactate Dehydrogenase / blood. Male. Phospholipids / blood. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Random Allocation. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Triglycerides / blood. alpha-Tocopherol / blood. alpha-Tocopherol / metabolism

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  • (PMID = 17934244.001).
  • [ISSN] 0301-4800
  • [Journal-full-title] Journal of nutritional science and vitaminology
  • [ISO-abbreviation] J. Nutr. Sci. Vitaminol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Phospholipids; 0 / RNA, Messenger; 0 / Triglycerides; 0 / alpha-tocopherol transfer protein; 7535-00-4 / Galactosamine; 97C5T2UQ7J / Cholesterol; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; H4N855PNZ1 / alpha-Tocopherol
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66. Trebec DP, Chandra D, Gramoun A, Li K, Heersche JN, Manolson MF: Increased expression of activating factors in large osteoclasts could explain their excessive activity in osteolytic diseases. J Cell Biochem; 2007 May 1;101(1):205-20
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  • [Title] Increased expression of activating factors in large osteoclasts could explain their excessive activity in osteolytic diseases.
  • We hypothesized this was related to increased resorptive activity of large osteoclasts and have demonstrated previously that larger osteoclasts are 8-fold more likely to be resorbing than small osteoclasts (2-5 nuclei).
  • We found 2- to 4.5-fold increases in the expression of the integrins alpha(v) and beta(3), the proteases proMMP9, matMMP9 and pro-cathepsinK, and in activating receptors RANK, IL-1R1, and TNFR1 in large osteoclasts.
  • In contrast, small osteoclasts had higher expression of the fusion protein SIRPalpha1 and the decoy receptor IL-1R2.
  • This increased responsiveness of large osteoclasts to IL-1 may, in part, explain the pathological bone loss noted in inflammatory diseases.
  • [MeSH-minor] Acid Phosphatase / analysis. Animals. Cell Line. Enzyme Precursors / metabolism. Immunoblotting. Integrin alpha1beta1 / metabolism. Interleukin 1 Receptor Antagonist Protein / analysis. Interleukin 1 Receptor Antagonist Protein / metabolism. Interleukin-1beta / metabolism. Isoenzymes / analysis. Macrophage Colony-Stimulating Factor / analysis. Macrophage Colony-Stimulating Factor / metabolism. Matrix Metalloproteinase 9 / metabolism. Mice. RANK Ligand / analysis. RANK Ligand / metabolism. Rabbits. Receptor Activator of Nuclear Factor-kappa B / metabolism. Receptor, Macrophage Colony-Stimulating Factor / analysis. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Receptors, Immunologic / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / analysis. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17216600.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Enzyme Precursors; 0 / Integrin alpha1beta1; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1beta; 0 / Isoenzymes; 0 / Ptpns1 protein, mouse; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Immunologic; 0 / Tumor Necrosis Factor-alpha; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase; EC 3.4.24.- / pro-matrix metalloproteinase 9; EC 3.4.24.35 / Matrix Metalloproteinase 9
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67. Liu TX, Becker MW, Jelinek J, Wu WS, Deng M, Mikhalkevich N, Hsu K, Bloomfield CD, Stone RM, DeAngelo DJ, Galinsky IA, Issa JP, Clarke MF, Look AT: Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation. Nat Med; 2007 Jan;13(1):78-83
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  • [Title] Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation.
  • Interstitial loss of all or part of the long arm of chromosome 5, or del(5q), is a frequent clonal chromosomal abnormality in human myelodysplastic syndrome (MDS, a preleukemic disorder) and acute myeloid leukemia (AML), and is thought to contribute to the pathogenesis of these diseases by deleting one or more tumor-suppressor genes.
  • Here we show that the gene encoding alpha-catenin (CTNNA1) is expressed at a much lower level in leukemia-initiating stem cells from individuals with AML or MDS with a 5q deletion than in individuals with MDS or AML lacking a 5q deletion or in normal hematopoietic stem cells.
  • Thus, loss of expression of the alpha-catenin tumor suppressor in hematopoietic stem cells may provide a growth advantage that contributes to human MDS or AML with del(5q).
  • [MeSH-major] Cell Transformation, Neoplastic. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Myeloid Progenitor Cells / pathology. alpha Catenin / genetics
  • [MeSH-minor] Acute Disease. Blotting, Western. Cell Line. Cell Line, Tumor. DNA Methylation / drug effects. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HL-60 Cells. Humans. Hydroxamic Acids / pharmacology. In Situ Hybridization, Fluorescence / methods. K562 Cells. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Mutation. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells

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  • (PMID = 17159988.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA104987; United States / NCI NIH HHS / CA / CA108631
  • [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 / CTNNA1 protein, human; 0 / Hydroxamic Acids; 0 / alpha Catenin; 147336-22-9 / Green Fluorescent Proteins; 3X2S926L3Z / trichostatin A
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68. Li X, Kimura H, Hirota K, Kasuno K, Torii K, Okada T, Kurooka H, Yokota Y, Yoshida H: Synergistic effect of hypoxia and TNF-alpha on production of PAI-1 in human proximal renal tubular cells. Kidney Int; 2005 Aug;68(2):569-83
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  • [Title] Synergistic effect of hypoxia and TNF-alpha on production of PAI-1 in human proximal renal tubular cells.
  • BACKGROUND: Chronic hypoxia has been newly proposed as a common mechanism of tubulointerstitial fibrosis in the progression of various chronic inflammatory renal diseases, where plasminogen activator inhibitor-1 (PAI-1) plays an important role in the accumulation of extracellular matrix (ECM) through inhibition of plasmin-dependent ECM degradation.
  • We also closely examined the effects of hypoxia and tumor necrosis factor-alpha (TNF-alpha) on PAI-1 expression in cultured human proximal renal tubular cells (HPTECs).
  • METHODS: Confluent cells growth-arrested in Dulbecco's modified Eagle's medium (DMEM) for 24 hours were exposed to hypoxia (1% O(2)) and/or TNF-alpha at 10 ng/mL for up to 48 hours.
  • Amounts of PAI-1 protein and mRNA after stimulation were measured by enzyme-linked immunosorbent assay (ELISA) and TaqMan quantitative polymerase chain reaction (PCR) or cDNA array analysis, respectively, and compared to those in cells incubated under control conditions (18% O(2) without TNF-alpha).
  • Treatment of 24 hours with hypoxia, TNF-alpha, and their combination induced a 2.8-fold, a 1.8-fold, and a 4.6-fold increase in PAI-1 protein secretion, and produced a 3.6-fold, a 3.3-fold, and a 12.1-fold increase at the PAI-1 mRNA level, respectively.
  • Immunoblot analysis and immunocytochemistry revealed that hypoxia-inducible factor-1alpha (HIF-1alpha) was markedly accumulated in the cell lysates and exclusively translocated to nuclei after 16 hours' exposure of HPTECs to hypoxia but not to TNF-alpha.
  • Luciferase reporter gene assay showed that hypoxia, TNF-alpha, and their combination increased PAI-1 transcription activity by 1.8-fold, 1.4-fold, and 2.2-fold, respectively.
  • A dominant-negative form of HIF-1alpha significantly suppressed PAI-1 transcription activity induced by hypoxia.
  • TNF-alpha can synergistically enhance this hypoxia-induced PAI-1 expression.
  • [MeSH-major] Anoxia / metabolism. Kidney Tubules, Proximal / metabolism. Oxygen / pharmacology. Plasminogen Activator Inhibitor 1 / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Nucleus / metabolism. Cell Survival / drug effects. Cells, Cultured. Drug Synergism. Gene Expression Regulation. Genistein / pharmacology. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. NF-kappa B / antagonists & inhibitors. Proline / analogs & derivatives. Proline / pharmacology. Promoter Regions, Genetic / physiology. Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects. Thiocarbamates / pharmacology. Transcription Factors / metabolism

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  • (PMID = 16014034.001).
  • [ISSN] 0085-2538
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / NF-kappa B; 0 / Plasminogen Activator Inhibitor 1; 0 / Thiocarbamates; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 135467-92-4 / prolinedithiocarbamate; 9DLQ4CIU6V / Proline; DH2M523P0H / Genistein; EC 2.7.10.1 / Protein-Tyrosine Kinases; S88TT14065 / Oxygen
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69. Tachdjian R, Al Khatib S, Schwinglshackl A, Kim HS, Chen A, Blasioli J, Mathias C, Kim HY, Umetsu DT, Oettgen HC, Chatila TA: In vivo regulation of the allergic response by the IL-4 receptor alpha chain immunoreceptor tyrosine-based inhibitory motif. J Allergy Clin Immunol; 2010 May;125(5):1128-1136.e8
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  • [Title] In vivo regulation of the allergic response by the IL-4 receptor alpha chain immunoreceptor tyrosine-based inhibitory motif.
  • BACKGROUND: Signaling by IL-4 and IL-13 through the IL-4 receptor alpha chain (IL-4Ralpha) plays a critical role in the pathology of allergic diseases.

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  • [Copyright] Copyright 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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  • (PMID = 20392476.001).
  • [ISSN] 1097-6825
  • [Journal-full-title] The Journal of allergy and clinical immunology
  • [ISO-abbreviation] J. Allergy Clin. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI065617-06A3; United States / NIAID NIH HHS / AI / AI065617-07; United States / NIAID NIH HHS / AI / R01 AI054471; United States / NIAID NIH HHS / AI / R01 AI065617-09; United States / NIAID NIH HHS / AI / R01 AI065617-07; United States / NIAID NIH HHS / AI / AI065617-06A3; United States / NIAID NIH HHS / AI / U19AI070453; United States / NIAID NIH HHS / AI / R01 AI026322; United States / NIAID NIH HHS / AI / R01 AI065617-09S1; United States / NIAID NIH HHS / AI / R21 AI080002; United States / NIAID NIH HHS / AI / AI080002-02; United States / NICHD NIH HHS / HD / T32 HD007512; United States / NIAID NIH HHS / AI / AI087627-01; United States / NIAID NIH HHS / AI / R21 AI080002-01; United States / NIAID NIH HHS / AI / R21 AI087627-01; United States / NIAID NIH HHS / AI / R01 AI065617; United States / Howard Hughes Medical Institute / / ; United States / NIAID NIH HHS / AI / 2R01AI065617; United States / NIAID NIH HHS / AI / AI065617-10; United States / NIAID NIH HHS / AI / R01AI054471; United States / NIAID NIH HHS / AI / AI065617-09; United States / NIAID NIH HHS / AI / R01 AI065617-10; United States / NIAID NIH HHS / AI / AI080002-01; United States / NIAID NIH HHS / AI / R21 AI080002-02; United States / NIAID NIH HHS / AI / R01 AI065617-08; United States / NIAID NIH HHS / AI / AI065617-09S1; United States / NIAID NIH HHS / AI / AI065617-08; United States / NIAID NIH HHS / AI / R21 AI087627
  • [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 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 0 / STAT6 Transcription Factor; 207137-56-2 / Interleukin-4; 42HK56048U / Tyrosine
  • [Other-IDs] NLM/ NIHMS177848; NLM/ PMC2889905
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70. Ottiger M, Thiel MA, Feige U, Lichtlen P, Urech DM: Efficient intraocular penetration of topical anti-TNF-alpha single-chain antibody (ESBA105) to anterior and posterior segment without penetration enhancer. Invest Ophthalmol Vis Sci; 2009 Feb;50(2):779-86
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  • [Title] Efficient intraocular penetration of topical anti-TNF-alpha single-chain antibody (ESBA105) to anterior and posterior segment without penetration enhancer.
  • PURPOSE: This study was designed to characterize ocular penetration pathways of ESBA105, a topically administered single-chain antibody (scFv) against tumor necrosis factor (TNF)-alpha, to the anterior and posterior segment of the eye.
  • Drug penetration and ocular biodistribution patterns of ESBA105 applied as eye drops appear highly attractive for clinical use to treat TNF-alpha dependant diseases of the eye.
  • [MeSH-major] Anterior Eye Segment / metabolism. Antibodies, Monoclonal / pharmacokinetics. Retina / metabolism. Tumor Necrosis Factor-alpha / immunology. Vitreous Body / metabolism

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  • (PMID = 18757511.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Ophthalmic Solutions; 0 / Tumor Necrosis Factor-alpha; 0 / immunoglobulin Fv
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71. Ko CW, Cuthbert RJ, Orsi NM, Brooke DA, Perry SL, Markham AF, Coletta PL, Hull MA: Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice. J Pathol; 2008 Apr;214(5):603-9
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  • [Title] Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice.
  • Interleukin (IL)-4 receptor (IL-4R) alpha chain-dependent signalling by IL-4 and IL-13 promotes tumour growth and metastasis in mouse models of colorectal cancer.
  • However, the role of IL-4R alpha-dependent signalling during the early, pre-malignant stages of colorectal carcinogenesis has not been investigated.
  • Therefore, we investigated the effect of deletion of the IL-4R alpha gene on azoxymethane-induced colorectal aberrant crypt focus (ACF) multiplicity and size in Balb/c mice.
  • IL-4R alpha(-/-) mice developed significantly more ACFs [median 8, inter-quartile range (IQR) 4-11.5; n = 9] than wild-type (WT) animals (median 4, IQR 1-6; n = 9; p = 0.04, Mann-Whitney U-test).
  • There were significantly higher levels of IL-4 in serum from azoxymethane- and sham-treated IL-4R alpha(-/-) mice than WT animals, but no difference in serum IL-13 levels.
  • In the absence of functional IL-4Rs, IL-13 can also signal via the IL-13R alpha2 receptor, leading to induction of transforming growth factor (TGF) beta, which has pro-tumourigenic activity at early stages of intestinal tumourigenesis.
  • We found that mucosal TGFbeta mRNA levels and intestinal epithelial cell TGFbeta immunoreactivity were significantly higher in IL-4R alpha(-/-) mice than in WT animals.
  • In summary, IL-4R alpha-dependent signalling has a protective, anti-neoplastic role during the post-initiation phase of azoxymethane-induced colorectal carcinogenesis in Balb/c mice.
  • Our data should prompt thorough investigation of the role of IL-4R alpha-dependent signalling during human colorectal carcinogenesis, particularly as antagonism of IL-4R signalling represents a therapeutic strategy for asthma and other allergic diseases.
  • [MeSH-minor] Animals. Azoxymethane. Carcinogens. Cell Transformation, Neoplastic / immunology. Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Female. Interleukin-13 / blood. Interleukin-4 / blood. Intestinal Mucosa / immunology. Intestinal Mucosa / pathology. Mice. Mice, Inbred BALB C. Mice, Knockout. Signal Transduction / immunology. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / blood

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  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland
  • (PMID = 18220315.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/146; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; MO0N1J0SEN / Azoxymethane
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72. North KN, Laing NG: Skeletal muscle alpha-actin diseases. Adv Exp Med Biol; 2008;642:15-27
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  • [Title] Skeletal muscle alpha-actin diseases.
  • Skeletal muscle alpha-actin is the principal protein component of the adult skeletal muscle thin filament.
  • The interaction between skeletal muscle alpha-actin and the various myosin heavy chain proteins in the different muscle fibre types generates the force of muscle contraction.
  • Skeletal muscle alpha-alpha actin is thus of fundamental importance to normal muscle contraction.
  • To date over 140 different disease-causing mutations have been identified in the skeletal muscle alpha-actin gene ACTA1.
  • These mutations are associated with histologically distinct congenital myopathies, including nemaline myopathy, actin myopathy, intranuclear rod myopathy, congenital fibre type disproportion and myopathy with cores.
  • Mutations in ACTA1 are associated with a wide range of clinical severity although the majority of patients tend to have severe congenital-onset disease.
  • Most of the patients have de novo dominant mutations not present in either parent.
  • However mild ACTA1 disease may be dominantly inherited and there are also recessive mutations.
  • Information from the clinic suggests that exercise and L-tyrosine may benefit some patients and that in the future decreasing the proportion of mutant actin may ameliorate the disease in some patients.
  • [MeSH-major] Actins / metabolism. Muscular Diseases / metabolism

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  • (PMID = 19181090.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins
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73. Cui G, Olsen T, Christiansen I, Vonen B, Florholmen J, Goll R: Improvement of real-time polymerase chain reaction for quantifying TNF-alpha mRNA expression in inflamed colorectal mucosa: an approach to optimize procedures for clinical use. Scand J Clin Lab Invest; 2006;66(3):249-59
The Lens. Cited by Patents in .

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  • [Title] Improvement of real-time polymerase chain reaction for quantifying TNF-alpha mRNA expression in inflamed colorectal mucosa: an approach to optimize procedures for clinical use.
  • OBJECTIVE: The precise measurement of local tumor necrosis factor alpha (TNF-alpha) expression in tissue is important in understanding the pathogenesis of inflammatory bowel diseases (IBD).
  • Real-time polymerase chain reaction (PCR) is a sensitive, versatile method and is becoming a commonly used tool for the quantification of gene expression.
  • The aim of this study was to optimize the laboratory procedure for biopsy sampling, storage and calibration of result for TNF-alpha mRNA quantification with real-time PCR of colorectal biopsies.
  • MATERIAL AND METHODS: Endoscopic biopsies from the colorectum were obtained from 18 patients with ulcerative colitis (UC), 11 patients with Crohn's disease (CD) and 18 normal controls.
  • The observed interassay variations were 7.4 % coefficient of variation (CV) and 7.2 % CV in low and high TNF-alpha mRNA expression biopsies, respectively.
  • TNF-alpha mRNA levels in colorectal biopsies from patients with either CD or moderate to severe UC were markedly increased, and 8 approximately 9-fold higher than those in healthy controls.
  • CONCLUSIONS: This optimization improves the clinical use of real-time PCR for quantification of TNF-alpha gene expression in colorectal biopsies and provides a sensitive reproducible assay.
  • [MeSH-major] Inflammatory Bowel Diseases / genetics. Polymerase Chain Reaction / methods. RNA, Messenger / analysis. RNA, Messenger / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Base Sequence. Case-Control Studies. Colitis, Ulcerative / genetics. Crohn Disease / genetics. DNA Primers / genetics. Female. Gene Expression. Humans. Intestinal Mucosa / chemistry. Male. Middle Aged

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  • (PMID = 16714253.001).
  • [ISSN] 0036-5513
  • [Journal-full-title] Scandinavian journal of clinical and laboratory investigation
  • [ISO-abbreviation] Scand. J. Clin. Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
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74. Adam-Vizi V: Production of reactive oxygen species in brain mitochondria: contribution by electron transport chain and non-electron transport chain sources. Antioxid Redox Signal; 2005 Sep-Oct;7(9-10):1140-9
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  • [Title] Production of reactive oxygen species in brain mitochondria: contribution by electron transport chain and non-electron transport chain sources.
  • Overwhelming evidence has accumulated indicating that oxidative stress is a crucial factor in the pathogenesis of neurodegenerative diseases.
  • The major site of production of superoxide, the primary reactive oxygen species (ROS), is considered to be the respiratory chain in the mitochondria, but the exact mechanism and the precise location of the physiologically relevant ROS generation within the respiratory chain have not been disclosed as yet.
  • In contrast, complex I inhibition to a small degree is sufficient to enhance ROS generation, indicating that inhibition of complex I by approximately 25-30% observed in postmortem samples of substantia nigra from patients suffering from Parkinson's disease could be important in inducing oxidative stress.
  • Recently, it has been described that a key Krebs cycle enzyme, alpha-ketoglutarate dehydrogenase (alpha-KGDH), is also able to produce ROS.
  • ROS formation by alpha-KGDH is regulated by the NADH/NAD+ ratio, suggesting that this enzyme could substantially contribute to generation of oxidative stress due to inhibition of complex I.
  • As alpha-KGDH is not only a generator but also a target of ROS, it is proposed that alpha-KGDH is a key factor in a vicious cycle by which oxidative stress is induced and promoted in nerve terminals.
  • [MeSH-major] Brain / pathology. Electron Transport Chain Complex Proteins / metabolism. Gene Expression Regulation, Enzymologic. Mitochondria / pathology. Reactive Oxygen Species

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  • (PMID = 16115017.001).
  • [ISSN] 1523-0864
  • [Journal-full-title] Antioxidants & redox signaling
  • [ISO-abbreviation] Antioxid. Redox Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Electron Transport Chain Complex Proteins; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 6384-92-5 / N-Methylaspartate; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / Superoxide Dismutase; EC 1.2.4.2 / Ketoglutarate Dehydrogenase Complex
  • [Number-of-references] 111
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75. Nannicini F, Sofi F, Avanzi G, Abbate R, Gensini GF: Alpha-linolenic acid and cardiovascular diseases omega-3 fatty acids beyond eicosapentaenoic acid and docosahexaenoic acid. Minerva Cardioangiol; 2006 Aug;54(4):431-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-linolenic acid and cardiovascular diseases omega-3 fatty acids beyond eicosapentaenoic acid and docosahexaenoic acid.
  • Over the last decades, an increasing body of evidence has been accumulated on the beneficial effect of polyunsaturated fatty acids both in primary and secondary prevention of cardiovascular diseases.
  • However, the vast majority of the studies has been performed on long-chain polyunsaturated fatty acids, such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) and not on their biochemical precursor, alpha-linolenic acid (ALA).
  • [MeSH-major] Cardiovascular Diseases / prevention & control. alpha-Linolenic Acid / therapeutic use
  • [MeSH-minor] Clinical Trials as Topic. Docosahexaenoic Acids / therapeutic use. Eicosapentaenoic Acid / therapeutic use. Humans

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  • (PMID = 17016414.001).
  • [ISSN] 0026-4725
  • [Journal-full-title] Minerva cardioangiologica
  • [ISO-abbreviation] Minerva Cardioangiol
  • [Language] eng; ita
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0RBV727H71 / alpha-Linolenic Acid; 25167-62-8 / Docosahexaenoic Acids; AAN7QOV9EA / Eicosapentaenoic Acid
  • [Number-of-references] 36
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76. Chang HW, Wu VC, Wu KD, Huang HY, Hsieh BS, Chen YM: In rat renal fibroblasts, mycophenolic acid inhibits proliferation and production of the chemokine CCL2, stimulated by tumour necrosis factor-alpha. Br J Pharmacol; 2010 Aug;160(7):1611-20
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  • [Title] In rat renal fibroblasts, mycophenolic acid inhibits proliferation and production of the chemokine CCL2, stimulated by tumour necrosis factor-alpha.
  • BACKGROUND AND PURPOSE: Renal fibroblasts play a pivotal role in the development of tubulointerstitial fibrosis, a condition highly predictive of progression towards end-stage renal disease.
  • Furthermore, MPA attenuated tumour necrosis factor-alpha-induced CCL2 expression through down-regulation of p38 MAPK, but not that of ERK1/2 or JNK.
  • This dual effect of MPA may form the rationale for animal or clinical trials for the treatment of fibrotic renal diseases.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cell Proliferation / drug effects. Chemokine CCL2 / antagonists & inhibitors. Fibroblasts / drug effects. Kidney / drug effects. Mycophenolic Acid / pharmacology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3 / metabolism. Cell Culture Techniques. Cell Line. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Rats. Reverse Transcriptase Polymerase Chain Reaction. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors

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  • (PMID = 20649565.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3; HU9DX48N0T / Mycophenolic Acid
  • [Other-IDs] NLM/ PMC2936834
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77. An Y, Cai L, Wang Y, Zhu D, Guan Y, Zheng J: Local expression of insulin-like growth factor-I, insulin-like growth factor-I receptor, and estrogen receptor alpha in ovarian cancer. Onkologie; 2009 Nov;32(11):638-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Local expression of insulin-like growth factor-I, insulin-like growth factor-I receptor, and estrogen receptor alpha in ovarian cancer.
  • Estrogen receptor alpha (ERalpha), which plays a role in the etiology of ovarian cancer, both regulates and is influenced by the IGF family.
  • Fresh specimens were collected from ovarian cancer patients and matched controls who underwent surgery for benign diseases.
  • IGF-I, IGF-IR, and ERalphaexpression was analyzed using quantitative real-time polymerase chain reaction.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Insulin-Like Growth Factor I / metabolism. Neoplasm Proteins / metabolism. Ovarian Neoplasms / metabolism. Receptor, IGF Type 1 / metabolism

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  • [CommentIn] Onkologie. 2009 Nov;32(11):623-4 [19887864.001]
  • (PMID = 19887867.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Neoplasm Proteins; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1
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78. Schachner T, Golderer G, Sarg B, Lindner HH, Bonaros N, Mikuz G, Laufer G, Werner ER: The amounts of alpha 1 antitrypsin protein are reduced in the vascular wall of the acutely dissected human ascending aorta. Eur J Cardiothorac Surg; 2010 Mar;37(3):684-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The amounts of alpha 1 antitrypsin protein are reduced in the vascular wall of the acutely dissected human ascending aorta.
  • The anti-protease alpha 1 antitrypsin plays an important role in the tissue protease - anti-protease equilibrium.
  • We aim to investigate the molecular pathology of these diseases by differential proteomics and mass-spectrometric analysis.
  • RESULTS: Among the most significant differentially expressed protein spots in the DIGE analysis, the most notable protein identified by nanospray mass spectrometry was alpha 1 antitrypsin.
  • Western blot analysis confirmed the reduced amounts of alpha 1 antitrypsin in aortic dissections (p=0.008 vs controls) but not for aneurysms (p=0.258).
  • By quantitative reverse transcription polymerase chain reaction (RT-PCR), mRNA level of alpha 1 antitrypsin was found to be increased in aortic dissections (p=0.035 vs controls), whereas in aneurysms a non-significant reduction of alpha 1 antitrypsin mRNA was present (p=0.123 vs controls).
  • CONCLUSION: In the vascular wall of ascending aortic dissections, alpha 1 antitrypsin protein amounts are reduced compared with healthy aortas.
  • Local alpha 1 antitrypsin deficiency in the human ascending aorta might lead to proteolytic damage easing aortic dissection.
  • [MeSH-major] Aneurysm, Dissecting / etiology. Aortic Aneurysm / etiology. alpha 1-Antitrypsin / metabolism. alpha 1-Antitrypsin Deficiency / complications

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  • [Copyright] Copyright (c) 2009 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
  • (PMID = 19709897.001).
  • [ISSN] 1873-734X
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / alpha 1-Antitrypsin
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79. Vudattu NK, Kuhlmann-Berenzon S, Khademi M, Seyfert V, Olsson T, Maeurer MJ: Increased numbers of IL-7 receptor molecules on CD4+CD25-CD107a+ T-cells in patients with autoimmune diseases affecting the central nervous system. PLoS One; 2009;4(8):e6534
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  • [Title] Increased numbers of IL-7 receptor molecules on CD4+CD25-CD107a+ T-cells in patients with autoimmune diseases affecting the central nervous system.
  • BACKGROUND: High content immune profiling in peripheral blood may reflect immune aberrations associated with inflammation in multiple sclerosis (MS) and other autoimmune diseases affecting the central nervous system.
  • METHODS AND FINDINGS: Peripheral blood mononuclear cells from 46 patients with multiple sclerosis (MS), 9 patients diagnosed with relapsing remitting MS (RRMS), 13 with secondary progressive multiple sclerosis (SPMS), 9 with other neurological diseases (OND) and well as 15 healthy donors (HD) were analyzed by 12 color flow cytometry (TCRalphabeta, TCRgammadelta, CD4, CD8alpha, CD8beta, CD45RA, CCR7, CD27, CD28, CD107a, CD127, CD14) in a cross-sectional study to identify variables significantly different between controls (HD) and patients (OND, RRMS, SPMS).
  • We analyzed 187 individual immune cell subsets (percentages) and the density of the IL-7 receptor alpha chain (CD127) on 59 individual immune phenotypes using a monoclonal anti-IL-7R antibody (clone R34.34) coupled to a single APC molecule in combination with an APC-bead array.
  • CONCLUSION: These data show that immunophenotyping represents a powerful tool to differentiate healthy individuals from individuals suffering from neurological diseases and that the number of IL-7 receptor molecules on differentiated TCRalphabeta+CD4+CD25-CD107a+ T-cells, but not the percentage of IL-7R-positive cells, segregates healthy individuals from patients with neurological disorders.
  • [MeSH-major] Antigens, CD4 / analysis. Autoimmune Diseases / metabolism. Central Nervous System Diseases / metabolism. Interleukin-2 Receptor alpha Subunit / analysis. Lysosomal-Associated Membrane Protein 1 / analysis. Receptors, Interleukin-7 / metabolism. T-Lymphocytes / metabolism

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  • (PMID = 19657390.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [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 / Antigens, CD4; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Lysosomal-Associated Membrane Protein 1; 0 / Receptors, Interleukin-7
  • [Other-IDs] NLM/ PMC2717329
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80. Semnani RT, Venugopal PG, Mahapatra L, Skinner JA, Meylan F, Chien D, Dorward DW, Chaussabel D, Siegel RM, Nutman TB: Induction of TRAIL- and TNF-alpha-dependent apoptosis in human monocyte-derived dendritic cells by microfilariae of Brugia malayi. J Immunol; 2008 Nov 15;181(10):7081-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Induction of TRAIL- and TNF-alpha-dependent apoptosis in human monocyte-derived dendritic cells by microfilariae of Brugia malayi.
  • Interestingly, 48-h exposure of DC to mf induced mRNA expression of the proapoptotic gene TRAIL and both mRNA and protein expression of TNF-alpha. mAb to TRAIL-R2, TNF-R1, or TNF-alpha partially reversed mf-induced cell death in DC, as did knocking down the receptor for TRAIL-R2 using small interfering RNA.
  • Our data suggest that mf induce DC apoptosis in a TRAIL- and TNF-alpha-dependent fashion.
  • [MeSH-minor] Animals. BH3 Interacting Domain Death Agonist Protein / biosynthesis. Brugia malayi / immunology. Cytochromes c / biosynthesis. Flow Cytometry. Gene Expression. Gene Expression Regulation. Humans. Immunoblotting. Macrophages / immunology. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 18981128.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AR041133-06; United States / Intramural NIH HHS / / ZIA AI000197-33
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tumor Necrosis Factor-alpha; 9007-43-6 / Cytochromes c
  • [Other-IDs] NLM/ NIHMS461893; NLM/ PMC3662363
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81. Fujino H, Kitaoka Y, Hayashi Y, Munemasa Y, Takeda H, Kumai T, Kobayashi S, Ueno S: Axonal protection by brain-derived neurotrophic factor associated with CREB phosphorylation in tumor necrosis factor-alpha-induced optic nerve degeneration. Acta Neuropathol; 2009 Jan;117(1):75-84
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Axonal protection by brain-derived neurotrophic factor associated with CREB phosphorylation in tumor necrosis factor-alpha-induced optic nerve degeneration.
  • In this study, we show that intravitreal injection of tumor necrosis factor (TNF)-alpha induces transient increases in phosphorylated-CREB (p-CREB) and BDNF expression in the optic nerve.
  • Administration of exogenous BDNF further increased the p-CREB and endogenous BDNF level and exerted a neuroprotective effect against TNF-alpha-induced axonal loss.
  • The increases in BDNF mRNA and protein induced by TNF-alpha were inhibited significantly by a CRE decoy oligonucleotide.
  • [MeSH-major] Axons / drug effects. Brain-Derived Neurotrophic Factor / pharmacology. CREB-Binding Protein / metabolism. Optic Nerve / drug effects. Tumor Necrosis Factor-alpha / toxicity
  • [MeSH-minor] Analysis of Variance. Animals. Blotting, Western. Immunohistochemistry. Male. Nerve Degeneration / metabolism. Nerve Degeneration / pathology. Nerve Degeneration / prevention & control. Optic Nerve Diseases / metabolism. Optic Nerve Diseases / pathology. Optic Nerve Diseases / prevention & control. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18830614.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 2.3.1.48 / CREB-Binding Protein
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82. Zhao Y, Xu J, Gong J, Qian L: L-type calcium channel current up-regulation by chronic stress is associated with increased alpha(1c) subunit expression in rat ventricular myocytes. Cell Stress Chaperones; 2009 Jan;14(1):33-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] L-type calcium channel current up-regulation by chronic stress is associated with increased alpha(1c) subunit expression in rat ventricular myocytes.
  • The L-type calcium channel plays a pivotal role in the regulation of a wide range of cellular processes, including membrane excitability, Ca(2+) homeostasis, protein phosphorylation, and gene regulation.
  • Alterations in the density or function of the L-type calcium channel have been implicated in a variety of cardiovascular diseases.
  • Our previous study found that acute restraint stress could cause an enhancement of the L-type calcium current (I (Ca-L))(,) which correlated with an up-regulation of activation characters of the calcium channel.
  • The results showed that chronic restraint stress could also enhance I (Ca-L), but increased I (Ca-L) was not accompanied by an alteration of the characteristics of activation and inactivation of the L-type calcium channel.
  • Furthermore, results from reverse-transcription polymerase chain reaction and Northern blot showed that the abundance of alpha(1c) subunit messenger RNA of the L-type calcium channel in the ventricle was increased significantly after chronic stress, and Western blot analysis revealed the amount of alpha(1c) subunit protein also was elevated.
  • These results suggest that the L-type calcium channel is involved in stress-induced cardiomyocyte injury, and the up-regulated expression of the L-type calcium channel alpha(1c) subunit might contribute to the I (Ca-L) change under chronic stress, which is different from the regulation mechanism of acute restraint stress that mostly relates to an alteration in protein kinase A-dependent channel activation.
  • [MeSH-major] Calcium Channels, L-Type / genetics. Heart Ventricles / cytology. Ion Channel Gating. Myocytes, Cardiac / metabolism. Protein Subunits / genetics. Stress, Physiological. Up-Regulation / genetics

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  • (PMID = 18566917.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Calcium Channels, L-Type; 0 / L-type calcium channel alpha(1C); 0 / Protein Subunits
  • [Other-IDs] NLM/ PMC2673898
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83. Hsieh MH, Chong IW, Hwang JJ, Lee CH, Ho CK, Yu ML, Huang CT, Lee CY, Wu MT, Christiani DC: Lack of associations between several polymorphisms in cytokine genes and the risk of chronic obstructive pulmonary diseases in Taiwan. Kaohsiung J Med Sci; 2008 Mar;24(3):126-37
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Lack of associations between several polymorphisms in cytokine genes and the risk of chronic obstructive pulmonary diseases in Taiwan.
  • Cytokine-induced inflammation is the predominant underlying mechanism in chronic obstructive pulmonary disease (COPD).
  • Genetic factors may play a pivotal role in the development of this disease.
  • The genetic polymorphisms examined in this study were tumor necrosis factor (TNF)-alpha(-308), TNF-alpha(+489), interleukin(IL)-1beta(-31), interleukin-1 receptor antagonist (IL-1 RN), and IL-6(-174).
  • DNA was collected from these subjects and analyzed by polymerase chain reaction with sequence-specific primers and restriction enzyme fragment length polymorphism analysis.
  • The frequencies of cytokine genotypes in COPD cases and controls, respectively, were as follows: for G/G in TNF-alpha(-308), 76.7% and 83.5%; for G/G in TNF-alpha(+489), 76.7% and 68.7%; for C/T in IL-1beta(-31), 60.0% and 55.7%; for 4R/4R in IL-1 RN, 80.0% and 86.1%; and for G/G in IL-6(-174), 100.1% and 98.3%.
  • [MeSH-major] Interleukin 1 Receptor Antagonist Protein / genetics. Interleukin-1beta / genetics. Interleukin-6 / genetics. Polymorphism, Genetic. Pulmonary Disease, Chronic Obstructive / genetics. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 18364273.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
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84. Kanematsu A, Ramachandran A, Adam RM: GATA-6 mediates human bladder smooth muscle differentiation: involvement of a novel enhancer element in regulating alpha-smooth muscle actin gene expression. Am J Physiol Cell Physiol; 2007 Sep;293(3):C1093-102
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GATA-6 mediates human bladder smooth muscle differentiation: involvement of a novel enhancer element in regulating alpha-smooth muscle actin gene expression.
  • Knockdown of endogenous GATA-6 in primary human bladder smooth muscle cells (pBSMC) led to decreased mRNA levels of the differentiation markers alpha-smooth muscle actin (alpha-SMA), calponin, and smooth muscle myosin heavy chain.
  • Forskolin treatment of pBSMC abolished recruitment of GATA-6 to the alpha-SMA promoter in vivo and reduced activity of human alpha-SMA promoter-directed gene expression by >60%.
  • This inhibitory effect was rescued by enforced expression of wild-type GATA-6 but not by a zinc-finger-deleted mutant, GATA-6-DeltaZF, which lacks DNA-binding ability.
  • In silico analysis of a region of the human alpha-SMA promoter, described previously as a transcriptional enhancer, identified a putative GATA-binding site at position -919/-913.
  • In addition, these findings demonstrate that GATA-6 regulates human alpha-SMA expression via a novel regulatory cis element in the alpha-SMA promoter-enhancer.

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  • (PMID = 17626241.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / GATA6 Transcription Factor; 0 / RNA, Messenger; E0399OZS9N / Cyclic AMP
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85. Kallen J, Lattmann R, Beerli R, Blechschmidt A, Blommers MJ, Geiser M, Ottl J, Schlaeppi JM, Strauss A, Fournier B: Crystal structure of human estrogen-related receptor alpha in complex with a synthetic inverse agonist reveals its novel molecular mechanism. J Biol Chem; 2007 Aug 10;282(32):23231-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Crystal structure of human estrogen-related receptor alpha in complex with a synthetic inverse agonist reveals its novel molecular mechanism.
  • Inverse agonists of the constitutively active human estrogen-related receptor alpha (ERRalpha, NR3B1) are of potential interest for several disease indications (e.g. breast cancer, metabolic diseases, or osteoporosis).
  • As a consequence of the new side chain conformation of Phe(328) (on helix H3), Phe(510)(H12) has to move away, and thus the activation helix H12 is displaced from its agonist position.
  • This is a novel mechanism of H12 inactivation, different from ERRgamma, estrogen receptor (ER) alpha, and ERbeta.
  • Despite a practically filled LBP, the finding that a suitable ligand can induce an opening of the cavity also has broad implications for other orphan nuclear hormone receptors (e.g. the NGFI-B subfamily).
  • [MeSH-minor] Crystallography, X-Ray. Drug Design. Estrogen Receptor alpha / chemistry. Humans. Kinetics. Ligands. Magnetic Resonance Spectroscopy. Models, Chemical. Models, Molecular. Molecular Conformation. Nitrogen / chemistry. Protein Binding. Protein Conformation. Protein Structure, Tertiary

  • Guide to Pharmacology. gene/protein/disease-specific - Estrogen-related receptor-alpha / NR3B1 - data and references .
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  • (PMID = 17556356.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2PJL
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ERRalpha estrogen-related receptor; 0 / Estrogen Receptor alpha; 0 / Ligands; 0 / Receptors, Estrogen; N762921K75 / Nitrogen
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86. Di Renzo L, Bigioni M, Del Gobbo V, Premrov MG, Barbini U, Di Lorenzo N, De Lorenzo A: Interleukin-1 (IL-1) receptor antagonist gene polymorphism in normal weight obese syndrome: relationship to body composition and IL-1 alpha and beta plasma levels. Pharmacol Res; 2007 Feb;55(2):131-8
MedlinePlus Health Information. consumer health - Obesity.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-1 (IL-1) receptor antagonist gene polymorphism in normal weight obese syndrome: relationship to body composition and IL-1 alpha and beta plasma levels.
  • Interleukin-1 receptor antagonist concentration is upregulated in the plasma of patients with obese related disease, and its synthesis is under genetic control.
  • In normal weight obese women, plasma concentrations of interleukin-1 alpha and interleukin-1 beta were significantly higher than in non-obese.
  • Our findings suggest that the allele 2 might be an important high-risk genetic marker for normal weight obese syndrome and obesity related diseases.
  • [MeSH-minor] Absorptiometry, Photon. Adult. Body Mass Index. Body Weight. DNA / analysis. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 17174563.001).
  • [ISSN] 1043-6618
  • [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 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1alpha; 0 / Interleukin-1beta; 9007-49-2 / DNA
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87. Sato T, Suzuki H, Shibata M, Kusuyama T, Omori Y, Soda T, Shoji M, Iso Y, Koba S, Geshi E, Katagiri T, Shioda S, Sekikawa K: Tumor-necrosis-factor-alpha-gene-deficient mice have improved cardiac function through reduction of intercellular adhesion molecule-1 in myocardial infarction. Circ J; 2006 Dec;70(12):1635-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-necrosis-factor-alpha-gene-deficient mice have improved cardiac function through reduction of intercellular adhesion molecule-1 in myocardial infarction.
  • BACKGROUND: Tumor necrosis factor (TNF)-alpha is linked to the pathogenesis of cardiovascular diseases, but how it affects myocardial infarction (MI), so the present study examined the effects of TNF-alpha and the involvement of intercellular adhesion molecule (ICAM)-1 on MI.
  • METHODS AND RESULTS: Left coronary arteries of C57BL/6 wild type (WT) and TNF-alpha knockout (KO) mice were ligated and the mice were killed 1, 3, and 7 days later.
  • CONCLUSION: In a permanent occlusion model of MI TNF-alpha decreased cardiac function and ameliorated myocardial remodeling through the induction of ICAM-1.
  • [MeSH-major] Heart / physiology. Intercellular Adhesion Molecule-1 / metabolism. Myocardial Infarction / physiopathology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Echocardiography. Immunohistochemistry. Macrophages / physiology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Myocardium / immunology. Myocardium / metabolism. Myocardium / pathology. Neutrophils / physiology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17127813.001).
  • [ISSN] 1346-9843
  • [Journal-full-title] Circulation journal : official journal of the Japanese Circulation Society
  • [ISO-abbreviation] Circ. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1
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88. Tahrani A, Bowler L, Singh P, Coates P: Resolution of diabetes in type 2 diabetic patient treated with IFN-alpha and ribavirin for hepatitis C. Eur J Gastroenterol Hepatol; 2006 Mar;18(3):291-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resolution of diabetes in type 2 diabetic patient treated with IFN-alpha and ribavirin for hepatitis C.
  • We report on a patient whose type 2 diabetes mellitus resolved during IFN-alpha therapy for hepatitis C virus (HCV).
  • A 40-year-old man was diagnosed with type II diabetes in year 2000.
  • In September 2003 he was started on IFN-alpha and ribavirin.
  • After 24 weeks of treatment his HCV polymerase chain reaction remained positive and treatment was stopped as per guidelines.
  • Most of the earlier literature describes diabetes developing in the course of IFN-alpha therapy for a variety of diseases.
  • Responders to IFN-alpha treatment manifest an improvement in insulin sensitivity compared with non-responders after the completion of IFN-alpha therapy.
  • Our case shows the resolution of pre-existing diabetes in a patient with chronic HCV infection, which did not respond to IFN-alpha therapy.
  • Whether this occurred as a direct result of IFN-alpha on insulin sensitivity or indirectly as a result of weight loss because the therapy for HCV precipitated additional lifestyle changes in the patient is as yet unclear.
  • [MeSH-major] Antiviral Agents / therapeutic use. Diabetes Mellitus, Type 2 / therapy. Hepatitis C, Chronic / drug therapy. Interferon-alpha / therapeutic use. Ribavirin / therapeutic use

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  • (PMID = 16462544.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Hemoglobin A, Glycosylated; 0 / Interferon-alpha; 49717AWG6K / Ribavirin
  • [Number-of-references] 16
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89. Murata K, Toba T, Nakanishi K, Takahashi B, Yamamura T, Miyake S, Annoura H: Total synthesis of an immunosuppressive glycolipid, (2S,3S,4R)-1-O- (alpha-d-galactosyl)-2- tetracosanoylamino-1,3,4-nonanetriol. J Org Chem; 2005 Mar 18;70(6):2398-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Total synthesis of an immunosuppressive glycolipid, (2S,3S,4R)-1-O- (alpha-d-galactosyl)-2- tetracosanoylamino-1,3,4-nonanetriol.
  • [reaction: see text] A practical and efficient total synthesis of (2S,3S,4R)-1-O-(alpha-d-galactosyl)-2-tetracosanoylamino-1,3,4-nonanetriol, OCH 1b, a potential therapeutic candidate for Th1-mediated autoimmune diseases, is described.
  • The synthesis incorporates direct alkylation onto epoxide 5 and stereospecific halide ion catalyzed alpha-glycosidation reaction.
  • This method will enable the synthesis of a variety of phytosphingolipids, especially that with the shorter sphingosine side chain than 1a, in a highly stereoselective manner.

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  • (PMID = 15760242.001).
  • [ISSN] 0022-3263
  • [Journal-full-title] The Journal of organic chemistry
  • [ISO-abbreviation] J. Org. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycosphingolipids; 0 / Immunosuppressive Agents
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90. Liu M, Wang X, Yin C, Zhang Z, Lin Q, Zhen Y, Huang H: A novel bivalent single-chain variable fragment (scFV) inhibits the action of tumour necrosis factor alpha. Biotechnol Appl Biochem; 2008 Aug;50(Pt 4):173-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel bivalent single-chain variable fragment (scFV) inhibits the action of tumour necrosis factor alpha.
  • Suppression of TNFalpha (tumour necrosis factor alpha) activity is widely considered to be among the most efficient treatments available for chronic inflammatory diseases.
  • Here, a bivalent scFv (single-chain variable fragment) fragment, named TNF-BAb, was engineered by fusing two anti-TNFalpha scFV fragments in tandem via a long and flexible linking peptide derived from human serum albumin and produced in functional form from Escherichia coli inclusion bodies.
  • [MeSH-major] Immunoglobulin Fragments / immunology. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 18047471.001).
  • [ISSN] 1470-8744
  • [Journal-full-title] Biotechnology and applied biochemistry
  • [ISO-abbreviation] Biotechnol. Appl. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin Fragments; 0 / Tumor Necrosis Factor-alpha
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91. Stangou AJ, Banner NR, Hendry BM, Rela M, Portmann B, Wendon J, Monaghan M, Maccarthy P, Buxton-Thomas M, Mathias CJ, Liepnieks JJ, O'Grady J, Heaton ND, Benson MD: Hereditary fibrinogen A alpha-chain amyloidosis: phenotypic characterization of a systemic disease and the role of liver transplantation. Blood; 2010 Apr 15;115(15):2998-3007
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hereditary fibrinogen A alpha-chain amyloidosis: phenotypic characterization of a systemic disease and the role of liver transplantation.
  • Variants of fibrinogen A alpha-chain (AFib) cause the most common type of hereditary renal amyloidosis in Europe and, possibly, the United States as well.
  • We assessed 22 AFib patients for combined liver and kidney transplantation (LKT) and report the clinical features and outcome.
  • Fibrinogen amyloidosis is a systemic amyloid disease with visceral, vascular, cardiac, and neurologic involvement.
  • [MeSH-minor] Adult. Cardiomyopathy, Dilated / complications. Cardiomyopathy, Dilated / pathology. Cardiomyopathy, Dilated / ultrasonography. Cardiovascular System / pathology. Female. Humans. Kidney Transplantation / radionuclide imaging. Male. Middle Aged. Mutation / genetics. Nervous System Diseases / complications. Nervous System Diseases / pathology. Patient Selection. Phenotype. Technetium Tc 99m Dimercaptosuccinic Acid. Treatment Outcome


92. Beyer K, Domingo-Sábat M, Lao JI, Carrato C, Ferrer I, Ariza A: Identification and characterization of a new alpha-synuclein isoform and its role in Lewy body diseases. Neurogenetics; 2008 Feb;9(1):15-23
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  • [Title] Identification and characterization of a new alpha-synuclein isoform and its role in Lewy body diseases.
  • Three transcript variants of alpha-synuclein, a neuronal protein mainly involved in synapses, have been described so far.
  • Whereas alpha-synuclein 140 is the whole and main transcript, alpha-synuclein 112 and 126 are short proteins that result from in-frame deletions of exons 3 and 5, respectively.
  • Because the aforesaid alpha-synuclein isoforms show differential expression changes in Lewy body diseases (LBDs), in the present work, we searched for a fourth alpha-synuclein isoform and studied its expression levels in LBD brains.
  • By using isoform-specific primers, isoform co-amplification and direct sequencing, we identified alpha-synuclein 98, which lacks exons 3 and 5. mRNA expression analyses in non-neuronal tissue revealed that alpha-synuclein 98 is a brain-specific splice variant with varying expression levels in different areas of fetal and adult brain.
  • Additionally, we studied alpha-synuclein 98 expression levels by real-time semi-quantitative RT-PCR in the frontal cortices of LBD patients and compared them with those of Alzheimer disease (AD) patients and control subjects.
  • Overexpression of alpha-synuclein 98 in LBD and AD brains would indicate its specific involvement in the pathogenesis of these neurodegenerative disorders.
  • [MeSH-major] Brain / metabolism. Lewy Body Disease / genetics. Lewy Body Disease / metabolism. alpha-Synuclein / genetics. alpha-Synuclein / metabolism
  • [MeSH-minor] Adult. Alternative Splicing. Alzheimer Disease / etiology. Alzheimer Disease / genetics. Alzheimer Disease / metabolism. Amino Acid Sequence. Base Sequence. Case-Control Studies. DNA Primers / genetics. Exons. Fetus / metabolism. Frontal Lobe / metabolism. Gene Expression. Humans. Molecular Sequence Data. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sequence Homology, Amino Acid

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  • (PMID = 17955272.001).
  • [ISSN] 1364-6753
  • [Journal-full-title] Neurogenetics
  • [ISO-abbreviation] Neurogenetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / SNCA protein, human; 0 / alpha-Synuclein
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93. Skapenko A, Kalden JR, Lipsky PE, Schulze-Koops H: The IL-4 receptor alpha-chain-binding cytokines, IL-4 and IL-13, induce forkhead box P3-expressing CD25+CD4+ regulatory T cells from CD25-CD4+ precursors. J Immunol; 2005 Nov 1;175(9):6107-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The IL-4 receptor alpha-chain-binding cytokines, IL-4 and IL-13, induce forkhead box P3-expressing CD25+CD4+ regulatory T cells from CD25-CD4+ precursors.
  • In this study the IL-4R alpha-chain-binding cytokines, IL-4 and IL-13, were identified as inducers of CD25+ Tregs from peripheral CD25-CD4 naive T cells.
  • Moreover, our findings might provide the basis for the design of novel therapeutic approaches for targeted immunotherapy with Tregs to known Ags in autoimmune diseases or graft-vs-host reactions.


94. Hutson SM: The case for regulating indispensable amino acid metabolism: the branched-chain alpha-keto acid dehydrogenase kinase-knockout mouse. Biochem J; 2006 Nov 15;400(1):e1-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The case for regulating indispensable amino acid metabolism: the branched-chain alpha-keto acid dehydrogenase kinase-knockout mouse.
  • BCAAs (branched-chain amino acids) are indispensable (essential) amino acids that are required for body protein synthesis.
  • It is well known from inborn errors of BCAA metabolism that dysregulation of the BCAA catabolic pathways that leads to excess BCAAs and their alpha-keto acid metabolites results in neural dysfunction.
  • In this issue of Biochemical Journal, Joshi and colleagues have disrupted the murine BDK (branched-chain alpha-keto acid dehydrogenase kinase) gene.
  • [MeSH-major] Amino Acids, Branched-Chain / metabolism. Protein Kinases / metabolism
  • [MeSH-minor] 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) / metabolism. Animals. Growth Disorders / enzymology. Growth Disorders / genetics. Growth Disorders / metabolism. Mice. Mice, Knockout. Nervous System Diseases / enzymology. Nervous System Diseases / genetics. Nervous System Diseases / metabolism

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  • (PMID = 17061958.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids, Branched-Chain; EC 1.2.4.4 / 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide); EC 2.7.- / Protein Kinases; EC 2.7.11.4 / (3-methyl-2-oxobutanoate dehydrogenase (lipoamide)) kinase
  • [Other-IDs] NLM/ PMC1635442
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95. Tatineni S, Sagaram US, Gowda S, Robertson CJ, Dawson WO, Iwanami T, Wang N: In planta distribution of 'Candidatus Liberibacter asiaticus' as revealed by polymerase chain reaction (PCR) and real-time PCR. Phytopathology; 2008 May;98(5):592-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In planta distribution of 'Candidatus Liberibacter asiaticus' as revealed by polymerase chain reaction (PCR) and real-time PCR.
  • Huanglongbing (HLB) is one of the most devastating diseases of citrus worldwide, and is caused by a phloem-limited fastidious prokaryotic alpha-proteobacterium that is yet to be cultured.
  • In this study, a combination of traditional polymerase chain reaction (PCR) and real-time PCR targeting the putative DNA polymerase and 16S rDNA sequence of 'Candidatus Liberibacter asiaticus,' respectively, were used to examine the distribution and movement of the HLB pathogen in the infected citrus tree.
  • [MeSH-major] Citrus / microbiology. DNA, Bacterial / genetics. Plant Diseases / microbiology. Polymerase Chain Reaction / methods. Rhizobiaceae / genetics

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  • (PMID = 18943228.001).
  • [ISSN] 0031-949X
  • [Journal-full-title] Phytopathology
  • [ISO-abbreviation] Phytopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / DNA, Bacterial; 0 / RNA, Ribosomal, 16S; EC 2.7.7.7 / DNA-Directed DNA Polymerase
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96. Muskiet FA, van Goor SA, Kuipers RS, Velzing-Aarts FV, Smit EN, Bouwstra H, Dijck-Brouwer DA, Boersma ER, Hadders-Algra M: Long-chain polyunsaturated fatty acids in maternal and infant nutrition. Prostaglandins Leukot Essent Fatty Acids; 2006 Sep;75(3):135-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-chain polyunsaturated fatty acids in maternal and infant nutrition.
  • Homo sapiens has evolved on a diet rich in alpha-linolenic acid and long chain polyunsaturated fatty acids (LCP).
  • The many dietary changes, including lower intake of omega3-fatty acids, are related to 'typically Western' diseases.
  • This flux may in the fetus augment de novo synthesis of fatty acids, which not only dilutes transplacentally transported EFA/LCP, but also causes competition of de novo synthesized oleic acid with linoleic acid for delta-6 desaturation.

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  • (PMID = 16876396.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Fatty Acids, Essential; 0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Unsaturated
  • [Number-of-references] 81
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97. Harrington NP, Surujballi OP, Prescott JF: Cervine (Cervus elaphus) cytokine mRNA quantification by real-time polymerase chain reaction. J Wildl Dis; 2006 Apr;42(2):219-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cervine (Cervus elaphus) cytokine mRNA quantification by real-time polymerase chain reaction.
  • Recently, simple and rapid assays for quantifying mRNA expression by real-time reverse transcription-polymerase chain reaction (RT-PCR) have been used for analysis of cytokine profiles in humans and other mammalian species.
  • This report describes the development and application of real time RT-PCR to measure the expression of several important elk (Cervus elaphus) cytokine mRNAs, including interleukin (IL)-2, IL-4, IL-10, IL-12p40, interferon-gamma, tumor necrosis factor (TNF)-alpha, and the enzyme-inducible nitric oxide synthase, all of which are involved in immune responses and regulation.
  • Whereas PPD-bovis optimally induced IL-2 mRNA after 8 hr of in vitro stimulation, longer in vitro stimulation times were necessary for the optimal induction of IL-4 and TNF-alpha mRNA (up to 48 hr).
  • [MeSH-major] Cytokines / biosynthesis. Deer / immunology. Leukocytes, Mononuclear / immunology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / veterinary

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  • (PMID = 16870845.001).
  • [ISSN] 0090-3558
  • [Journal-full-title] Journal of wildlife diseases
  • [ISO-abbreviation] J. Wildl. Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Cytokines; 0 / Mitogens; 0 / RNA, Messenger
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98. Fujii Y, Matsutani T, Kitaura K, Suzuki S, Itoh T, Takasaki T, Suzuki R, Kurane I: Comprehensive analysis and characterization of the TCR alpha chain sequences in the common marmoset. Immunogenetics; 2010 Jun;62(6):383-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comprehensive analysis and characterization of the TCR alpha chain sequences in the common marmoset.
  • The common marmoset (Callithrix jacchus) is useful as a nonhuman primate model of human diseases.
  • Although the marmoset model has great potential for studying autoimmune diseases and immune responses against pathogens, little information is available regarding the genes involved in adaptive immunity.
  • Here, we identified one TCR alpha constant (TRAC), 46 TRAJ (joining), and 35 TRAV (variable) segments from marmoset cDNA.
  • The amino acid sequences were less conserved in TRAC than in TCRbeta chain constant (TRBC).
  • [MeSH-major] Callithrix / immunology. Receptors, Antigen, T-Cell, alpha-beta / chemistry

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  • (PMID = 20405119.001).
  • [ISSN] 1432-1211
  • [Journal-full-title] Immunogenetics
  • [ISO-abbreviation] Immunogenetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
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99. Guerranti R, Bertocci E, Fioravanti A, Papakostas P, Montella A, Guidelli GM, Cortelazzo A, Nuti R, Giordano N: Serum proteome of patients with systemic sclerosis: molecular analysis of expression and prevalence of haptoglobin alpha chain isoforms. Int J Immunopathol Pharmacol; 2010 Jul-Sep;23(3):901-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum proteome of patients with systemic sclerosis: molecular analysis of expression and prevalence of haptoglobin alpha chain isoforms.
  • The Hpt 2-2 phenotype is associated with increased prevalence of various systemic diseases, including autoimmune disorders.
  • On this basis, we performed serum proteomic analysis of patients with Systemic Sclerosis (SSc), a connective tissue disorder associated with Th2-type immune response and characterized by interstitial and perivascular fibrosis due to different factors (including genetic, environmental, immunological and microchimeric factors).
  • Serum depleted of HAP was analyzed by 2-DE, and Hpt chain spots were identified by WB.
  • The expression frequency of each Hpt α chain in SSc patients and controls was compared and quantitative analysis of spot expression (percent Vol) was performed.
  • Above all,, our study amplifies the limited data in the literature on proteomic analysis in SSc, also confirming previous data that revealed a significant increase of haptoglobin type 2-2 and a concomitant decrease of the 1-1 phenotype in SSc patients.
  • According to our results, the c and e spots can be considered markers for SSc and thus be of use for the early diagnosis of connective tissue disorders and in establishing appropriate treatment.

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  • (PMID = 20943062.001).
  • [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 / Biomarkers; 0 / HP protein, human; 0 / Haptoglobins; 0 / Immunoglobulin G; 0 / Serum Albumin
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100. Simsek I, de Mazancourt P, Horellou MH, Erdem H, Pay S, Dinc A, Samama MM: Afibrinogenemia resulting from homozygous nonsense mutation in A alpha chain gene associated with multiple thrombotic episodes. Blood Coagul Fibrinolysis; 2008 Apr;19(3):247-53
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  • [Title] Afibrinogenemia resulting from homozygous nonsense mutation in A alpha chain gene associated with multiple thrombotic episodes.
  • Congenital afibrinogenemia is a rare disorder characterized by the absence in circulating fibrinogen, a hexamer composed of two sets of three polypeptides (Aalpha, Bbeta and gamma).
  • Purified DNAs of the propositus was used for amplification by polymerase chain reaction of all the exons of the A subunit gene with primers allowing the analysis of the intron-exon boundaries.
  • Analysis of the genes coding for the three fibrinogen chains of the propositus found a homozygous G to A transition in the exon 5 of the A alpha chain gene (g.g4277a; access number gi458553).
  • The TGG to TGA codon change predicts a homozygous W315X in the A alpha chain (p.W334X when referring to the translation initiation codon).
  • Our patient was free of known risk factors as well as diseases associated with thrombosis including atherosclerosis, vasculitis, Buerger's disease, and it seems therefore probable that afibrinogenemia itself might have contributed to both arterial and venous thrombosis.

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  • (PMID = 18388508.001).
  • [ISSN] 0957-5235
  • [Journal-full-title] Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
  • [ISO-abbreviation] Blood Coagul. Fibrinolysis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / fibrinogen Aalpha; 9001-32-5 / Fibrinogen
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