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31. Ambra R, Rimbach G, de Pascual Teresa S, Fuchs D, Wenzel U, Daniel H, Virgili F: Genistein affects the expression of genes involved in blood pressure regulation and angiogenesis in primary human endothelial cells. Nutr Metab Cardiovasc Dis; 2006 Jan;16(1):35-43
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  • BACKGROUND: Several lines of evidence suggest that the dietary isoflavone genistein (Gen) has beneficial effects with regard to cardiovascular disease and in particular on aspects related to blood pressure and angiogenesis.
  • Gen significantly affected the expression of genes encoding for proteins centrally involved in the vascular tone such as endothelin-converting enzyme-1, endothelin-2, estrogen related receptor alpha and atrial natriuretic peptide receptor A precursor.
  • [MeSH-minor] Base Sequence. Blotting, Northern. Cells, Cultured. Enzyme Inhibitors / pharmacology. Humans. Lipoproteins, LDL / drug effects. Lipoproteins, LDL / metabolism. Oligonucleotide Array Sequence Analysis. Oxidation-Reduction. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16399490.001).
  • [ISSN] 0939-4753
  • [Journal-full-title] Nutrition, metabolism, and cardiovascular diseases : NMCD
  • [ISO-abbreviation] Nutr Metab Cardiovasc Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Lipoproteins, LDL; 0 / oxidized low density lipoprotein; DH2M523P0H / Genistein
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32. Omatsu T, Bak EJ, Ishii Y, Kyuwa S, Tohya Y, Akashi H, Yoshikawa Y: Induction and sequencing of Rousette bat interferon alpha and beta genes. Vet Immunol Immunopathol; 2008 Jul 15;124(1-2):169-76
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  • [Title] Induction and sequencing of Rousette bat interferon alpha and beta genes.
  • Bats are considered to be natural reservoirs for several viruses of clinical importance, including rabies virus, Nipah virus, and Hendra virus.
  • Type I interferons (IFNs) is an important part of the immune system in the defense against viral infection.
  • To investigate the function of type I IFNs upon viral infection in bats, the nucleic acid, and amino acid sequences of Egyptian Rousette (Rousettus aegyptiacus) IFN-alpha and -beta were characterized.
  • Sequence data indicated that bat IFN-alpha consists of 562-bp encoded 187-aa, and IFN-beta consisted of 558-bp encoded 186-aa.
  • Stimulation of bat primary kidney cells (BPKCs) and bat lung cell lines, Tb-1 Lu, with polyinosinic-polycytidylic acid (poly(I:C)) or exogenous bat type I IFNs resulted in increased type I IFNs mRNA expression in BPKCs, but not in Tb-1 Lu.
  • Characterization of the bat IFN-alpha and -beta genes allows understanding of the immune responses upon stimulation in different tissues, thus providing practical strategies for control and treatment of clinically important diseases.
  • These results are important especially for the virus infection, and suggest that future molecular studies on virus infection experiment of bats in vitro will require careful consideration of the differences of type I IFN expression patterns in different cell types.
  • [MeSH-major] Chiroptera / genetics. Chiroptera / immunology. Interferon-alpha / genetics. Interferon-beta / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line. Cloning, Molecular. DNA / chemistry. DNA / genetics. Molecular Sequence Data. Open Reading Frames. Phylogeny. Poly I-C / immunology. Polymerase Chain Reaction / veterinary

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  • (PMID = 18436311.001).
  • [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 / Interferon-alpha; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta; 9007-49-2 / DNA
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33. Liu L, Ning X, Sun L, Shi Y, Han S, Guo C, Chen Y, Sun S, Yin F, Wu K, Fan D: Involvement of MGr1-Ag/37LRP in the vincristine-induced HIF-1 expression in gastric cancer cells. Mol Cell Biochem; 2007 Sep;303(1-2):151-60
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  • [MeSH-major] Antigens, Neoplasm / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Stomach Neoplasms / metabolism. Vincristine / pharmacology
  • [MeSH-minor] Blotting, Western. Caspase 3 / metabolism. Cell Hypoxia. Focal Adhesion Kinase 1 / genetics. Focal Adhesion Kinase 1 / metabolism. Humans. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription, Genetic. Tumor Cells, Cultured

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  • (PMID = 17476462.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents, Phytogenic; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / MGr1-antigen, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3
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3
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4. Tilkeridis C, Bei T, Garantziotis S, Stratakis CA: Association of a COL1A1 polymorphism with lumbar disc disease in young military recruits. J Med Genet; 2005 Jul;42(7):e44
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  • [Title] Association of a COL1A1 polymorphism with lumbar disc disease in young military recruits.
  • BACKGROUND: Lumbar disc disease (LDD), one of the most common conditions for which patients seek medical care, has been associated with sequence changes of the COL genes.
  • All patients had radiological confirmation of their disease; a control group was also studied.
  • CONCLUSIONS: A previously studied sequence change of the regulatory region of the COL1A1 gene, the same as has previously been associated with low BMD in many populations and LDD in older adults, showed a strong association with LDD in young male soldiers who were recently diagnosed with this disease.
  • [MeSH-major] Collagen Type I / genetics. Intervertebral Disc / pathology. Military Personnel. Polymorphism, Genetic. Spinal Diseases / genetics
  • [MeSH-minor] Adult. Alleles. Bone Density. DNA Mutational Analysis. Genetic Predisposition to Disease. Greece. Heterozygote. Homozygote. Humans. Low Back Pain / etiology. Lumbosacral Region. Magnetic Resonance Imaging. Male

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  • (PMID = 15994869.001).
  • [ISSN] 1468-6244
  • [Journal-full-title] Journal of medical genetics
  • [ISO-abbreviation] J. Med. Genet.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain
  • [Other-IDs] NLM/ PMC1736100
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35. Hercus TR, Thomas D, Guthridge MA, Ekert PG, King-Scott J, Parker MW, Lopez AF: The granulocyte-macrophage colony-stimulating factor receptor: linking its structure to cell signaling and its role in disease. Blood; 2009 Aug 13;114(7):1289-98
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  • [Title] The granulocyte-macrophage colony-stimulating factor receptor: linking its structure to cell signaling and its role in disease.
  • Already 20 years have passed since the cloning of the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor alpha-chain, the first member of the GM-CSF/interleukin (IL)-3/IL-5 family of hemopoietic cytokine receptors to be molecularly characterized.
  • Unlike other hemopoietin receptors, the GM-CSF receptor has a significant nonredundant role in myeloid hematologic malignancies, macrophage-mediated acute and chronic inflammation, pulmonary homeostasis, and allergic disease.
  • The new insights in GM-CSF receptor activation have clinical significance as the structural and signaling nuances can be harnessed for the development of new treatments for malignant and inflammatory diseases.

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  • (PMID = 19436055.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI050744; United States / NIAID NIH HHS / AI / R01-AI50744-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 144
  • [Other-IDs] NLM/ PMC2727416
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36. Schuh RA, Matthews CC, Fishman PS: Interaction of mitochondrial respiratory inhibitors and excitotoxins potentiates cell death in hippocampal slice cultures. J Neurosci Res; 2008 Nov 15;86(15):3306-13
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  • The broad-spectrum insecticide rotenone, an inhibitor of complex I of the mitochondrial electron transport chain (ETC), gives rise to oxidative stress and bioenergetic failure.
  • Pesticides including rotenone have been implicated in human neurodegenerative diseases, including Parkinson's disease.
  • Another intensively investigated hypothesis of neurodegenerative disease involves the toxic action of the excitatory neurotransmitter glutamate.
  • In the present study, we determined whether concomitant exposure of rotenone plus tetraethylammonium chloride (TEA) or the specific glutamate receptor agonists N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) would cause greater cell death in organotypic hippocampal slice cultures than when given separately.

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  • (PMID = 18615648.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Excitatory Amino Acid Agonists; 0 / Neurotoxins; 0 / Potassium Channel Blockers; 0 / Uncoupling Agents; 03L9OT429T / Rotenone; 6384-92-5 / N-Methylaspartate; 66-40-0 / Tetraethylammonium
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37. Liu YH, Zhang ZS, Zhong D, Xiao B, Liu J, Wu JB, He JD, Yang YJ, Guo WY: [Screening and preliminary analysis of colorectal carcinoma-associated antigen genes]. Nan Fang Yi Ke Da Xue Xue Bao; 2006 Feb;26(2):166-8, 173
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  • Among the 11 obtained positive clones, 3 were the same cDNA having homology with interferon-induced transmembrance protein-1 and possessing anti-proliferation effect; another 6 represented different genes, namely human BAC clone RP11-453E17 whose function have not been cleared, human cartilage-hair hypoplasia region gene responsible for cartilage-hair hypoplasia, human chromosome 5 clone CTD-2030B15 with insertion mutation, human gene similar to anti tumor necrosis factor-alpha antibody light-chain Fab fragment associated with tumor growth, mRNA of human beta-2-microglobulin in relation to tumor cell proliferation, and human aldolase A gene promoting tumor cell proliferation.

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  • (PMID = 16503520.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Peptide Library; 0 / TRAPPC10 protein, human; 0 / Vesicular Transport Proteins
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38. Salter-Cid LM, Wang E, O'Rourke AM, Miller A, Gao H, Huang L, Garcia A, Linnik MD: Anti-inflammatory effects of inhibiting the amine oxidase activity of semicarbazide-sensitive amine oxidase. J Pharmacol Exp Ther; 2005 Nov;315(2):553-62
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  • LJP 1207 also reduced serum levels of tumor necrosis factor-alpha and interleukin 6 in lipopolysaccharide (LPS)-challenged mice and prolonged survival post-LPS-induced endotoxemia.
  • Overall, the data suggest that small molecule SSAO/VAP-1 inhibitors may provide clinical benefit in the treatment of acute and chronic inflammatory diseases.
  • [MeSH-minor] Animals. Carrageenan. Cell Adhesion / drug effects. Cloning, Molecular. Colitis / chemically induced. Colitis / drug therapy. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Edema / chemically induced. Edema / drug therapy. Endothelial Cells / drug effects. Endotoxemia / chemically induced. Endotoxemia / drug therapy. Female. Inflammation / drug therapy. Inflammation / pathology. Male. Mice. Mice, Inbred Strains. Oxazolone. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16081681.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Hydrazines; 0 / Monoamine Oxidase Inhibitors; 0 / N'-(2-phenylallyl)hydrazine; 15646-46-5 / Oxazolone; 9000-07-1 / Carrageenan; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.4.3.21 / Amine Oxidase (Copper-Containing)
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39. Shaikh M, Mohanty J, Bhasikuttan AC, Pal H: Tuning dual emission behavior of p-dialkylaminobenzonitriles by supramolecular interactions with cyclodextrin hosts. Photochem Photobiol Sci; 2008 Aug;7(8):979-85
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  • Ground state absorption and steady-state and time-resolved fluorescence measurements have been carried out to understand the host-guest interactions of p-diethylaminobenzonitrile (DEABN) and p-dimethylaminobenzonitrile (DMABN) dyes with alpha-cyclodextrin (alpha-CD) and beta-cyclodextrin (beta-CD) hosts.
  • DEABN and DMABN dyes show both locally excited (LE) state and intramolecular charge transfer (ICT) state emissions in solution.
  • The LE and ICT emissions of the dyes are seen to get modulated in the presence of alpha-CD and beta-CD hosts.
  • The results indicate that the dyes form 1 : 1 inclusion complexes with both the hosts.
  • Comparing the binding constants and the fluorescence characteristics of different dye x CD systems it is inferred that DEABN adopts a completely different orientation on complexation with alpha-CD than in the other cases of dye.CD systems.
  • It is indicated that while in all other cases of dye x CD systems the N,N-dialkyl group of the dyes enters the host cavity leaving the C[triple bond, length as m-dash]N group projected out into the water phase, the DEABN dye enters the alpha-CD cavity (smallest CD) with its C[triple bond, length as m-dash]N group entering the host cavity.
  • The differences in the orientation of the dye in the host cavities is understood to be determined by the requirement of maximum van der Waals contact of the encapsulated dye with the host cavity for maximum stability of the complex and the relative sizes of the substituents of the dye compared to the host cavities.

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  • (PMID = 18688506.001).
  • [ISSN] 1474-905X
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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40. Sierra S, Lara-Villoslada F, Comalada M, Olivares M, Xaus J: Dietary fish oil n-3 fatty acids increase regulatory cytokine production and exert anti-inflammatory effects in two murine models of inflammation. Lipids; 2006 Dec;41(12):1115-25
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  • The higher incidence of inflammatory diseases in Western countries might be related, in part, to a high consumption of saturated fatty acids and n-6 polyunsaturated fatty acids (PUFA) and an insufficient intake of n-3 fatty acids.
  • Balb/C mice were fed for 3 wk either n-6 or n-3 PUFA-fortified diets.
  • Reduction in weight, edema, thickness, leukocyte infiltration, and enhancement of antioxidant defenses in the inflamed ears of mice from both models along with the prevention of delayed-type hypersensitivity induced in atopic dermatitis proved n-3 PUFA efficacy.
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / administration & dosage. Anti-Inflammatory Agents / pharmacology. Cell Proliferation / drug effects. Cells, Cultured. Dermatitis / prevention & control. Eicosanoids / metabolism. Enzyme-Linked Immunosorbent Assay. Gene Expression / drug effects. Lipids / blood. Lymphocytes / cytology. Lymphocytes / drug effects. Lymphocytes / metabolism. Macrophages / drug effects. Macrophages / metabolism. Male. Mice. Mice, Inbred BALB C. PPAR alpha / genetics. PPAR gamma / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17269557.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Eicosanoids; 0 / Fatty Acids, Omega-3; 0 / Fish Oils; 0 / Lipids; 0 / PPAR alpha; 0 / PPAR gamma; 0 / RNA, Messenger
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41. Collado-Romero M, Arce C, Ramírez-Boo M, Carvajal A, Garrido JJ: Quantitative analysis of the immune response upon Salmonella typhimurium infection along the porcine intestinal gut. Vet Res; 2010 Mar-Apr;41(2):23
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  • [Title] Quantitative analysis of the immune response upon Salmonella typhimurium infection along the porcine intestinal gut.
  • Salmonella enterica serovar Typhimurium causes enteric disease and compromises food safety.
  • In pigs, the molecular response of the intestine to S. typhimurium has been traditionally characterized by in vitro models that do not reflect the actual immunological competence of the intestinal mucosa.
  • In this work, we performed an oral S. typhimurium infection study to obtain insight into the in vitro response in three different sections (jejunum, ileum and colon) of the porcine intestine.
  • For this, samples from one-month-old infected piglets were collected during a time course comprising 1, 2, and 6 days post inoculation to evaluate the intestinal response by quantifying the mRNA expression of gene coding for 28 innate immune system molecules using quantitative real-time PCR assays.
  • In addition, samples from non-infected control animals were also employed to establish differences in the steady state gene expression between intestinal sections.
  • Changes in gene expression occurred in the three different parts of the intestine and during the course of the S. typhimurium infection.
  • Moreover, the high variation observed in expression patterns of genes coding for inflammatory mediators could indicate that each intestinal section responds differently to the infection.
  • In conclusion, our results reveal regional differences in gene expression profiles along the porcine intestinal gut as well as regional differences in the inflammatory response to S. typhimurium infection.
  • Taken together, these data should provide a basis for a complete understanding of the porcine intestinal response to bacterial infection.
  • [MeSH-major] Intestinal Mucosa / immunology. Salmonella Infections, Animal / immunology. Salmonella typhimurium / immunology. Swine Diseases / immunology
  • [MeSH-minor] Animals. Caspase 1 / genetics. Caspase 1 / metabolism. Female. Gene Expression Profiling. Gene Expression Regulation. Interleukin-8 / blood. Interleukin-8 / metabolism. Male. Myeloid Differentiation Factor 88 / genetics. Myeloid Differentiation Factor 88 / metabolism. NF-kappa B / genetics. NF-kappa B / metabolism. Polymerase Chain Reaction / veterinary. RNA, Messenger / genetics. RNA, Messenger / metabolism. Swine. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] INRA, EDP Sciences, 2010
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  • (PMID = 19941811.001).
  • [ISSN] 0928-4249
  • [Journal-full-title] Veterinary research
  • [ISO-abbreviation] Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Myeloid Differentiation Factor 88; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.36 / Caspase 1
  • [Other-IDs] NLM/ PMC2820228
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42. Zimman A, Chen SS, Komisopoulou E, Titz B, Martínez-Pinna R, Kafi A, Berliner JA, Graeber TG: Activation of aortic endothelial cells by oxidized phospholipids: a phosphoproteomic analysis. J Proteome Res; 2010 Jun 4;9(6):2812-24
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  • Previous studies have shown that oxidized products of the phospholipid PAPC (Ox-PAPC) are strong activators of aortic endothelial cells and play an important role in atherosclerosis and other inflammatory diseases.

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  • (PMID = 20307106.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / K22 HG002807-05; United States / NHGRI NIH HHS / HG / HG002807; United States / NHLBI NIH HHS / HL / HL030568; United States / NHGRI NIH HHS / HG / K22 HG002807; United States / NHLBI NIH HHS / HL / HL030568-150006; United States / NCI NIH HHS / CA / T32 CA009056; None / None / / K22 HG002807-05; United States / NHLBI NIH HHS / HL / P01 HL030568; United States / NHLBI NIH HHS / HL / P01 HL030568-150006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myosin Light Chains; 0 / Peptide Fragments; 0 / Phosphatidylcholines; 0 / Phosphoproteins; 0 / Proteome; 0 / myosin light chain 2; 0 / oxidized-L-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine; EC 2.7.10.1 / Receptor, TIE-1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.1.- / Cardiac Myosins
  • [Other-IDs] NLM/ NIHMS193036; NLM/ PMC2922471
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43. Ergang P, Leden P, Bryndová J, Zbánková S, Miksík I, Kment M, Pácha J: Glucocorticoid availability in colonic inflammation of rat. Dig Dis Sci; 2008 Aug;53(8):2160-7
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  • Recent in vitro studies have shown the involvement of pro-inflammatory cytokines in the regulation of the local metabolism of glucocorticoids via 11beta-hydroxysteroid dehydrogenase type 1 and type 2 (11HSD1 and 11HSD2).
  • We have therefore examined the changes in the local metabolism of glucocorticoids during colonic inflammation induced by TNBS and the consequences of corticosterone metabolism inhibition by carbenoxolone on 11HSD1, 11HSD2, cyclooxygenase 2 (COX-2), mucin 2 (MUC-2), tumor necrosis factor alpha (TNF-alpha), and interleukin 1beta (IL-1beta).
  • The metabolism of glucocorticoids was measured in tissue slices in vitro and their 11HSD1, 11HSD2, COX-2, MUC-2, TNF-alpha, and IL-1beta mRNA abundances by quantitative reverse transcription-polymerase chain reaction.
  • In contrast to the local metabolism of glucocorticoids, carbenoxolone neither potentiates nor diminishes gene expression for COX-2, TNF-alpha, and IL-1beta, despite the fact that budesonide down-regulated all of them.
  • However, these changes in the local metabolism of glucocorticoids do not modulate the expression of COX-2, TNF-alpha, and IL-1beta in inflamed tissue.
  • [MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics. 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism. 11-beta-Hydroxysteroid Dehydrogenase Type 2 / genetics. 11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism. Animals. Budesonide / pharmacology. Carbenoxolone / pharmacology. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Disease Models, Animal. Hormone Antagonists / pharmacology. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. Male. Mifepristone / pharmacology. Mucin-2. Mucins / genetics. Mucins / metabolism. Peroxidase / metabolism. RNA, Messenger / metabolism. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Trinitrobenzenesulfonic Acid. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18095161.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Interleukin-1beta; 0 / Muc2 protein, rat; 0 / Mucin-2; 0 / Mucins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 320T6RNW1F / Mifepristone; 51333-22-3 / Budesonide; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 1; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2; EC 1.11.1.7 / Peroxidase; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat; MM6384NG73 / Carbenoxolone; W980KJ009P / Corticosterone
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44. Zhu ZX, Xu YJ, Zou H, Zhang ZX, Ni W, Chen SX: [Pulmonary vascular remodeling and protein kinase C-alpha expression in chronic smoke exposure and/or hypoxia rats]. Zhonghua Jie He He Hu Xi Za Zhi; 2005 Dec;28(12):825-9
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  • [Title] [Pulmonary vascular remodeling and protein kinase C-alpha expression in chronic smoke exposure and/or hypoxia rats].
  • OBJECTIVE: To investigate pulmonary vascular remodeling and protein kinase C-alpha (PKC-alpha) expression in chronic smoke exposure and/or hypoxia rats.
  • To evaluate vascular remodeling, alpha-smooth muscle actin (alpha-SM-actin) staining and count of the percentage of muscularized small pulmonary arteries which was determined by morphometric analysis of histological sections were used.
  • Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence staining and Western blot analysis were used for the detection of PKC-alpha mRNA and protein expression in pulmonary arteries.
  • In S(4W), S(8W), H(4W), H(8W), SH(4W) and SH(8W) group, RVHI (0.258 +/- 0.024, 0.394 +/- 0.021, 0.374 +/- 0.020, 0.414 +/- 0.019, 0.434 +/- 0.023, 0.442 +/- 0.020, respectively), the percentage of muscularized arteries [(33.5 +/- 6.8)%, (41.1 +/- 9.8)%, (35.9 +/- 6.6)%, (46.0 +/- 6.3)%, (42.9 +/- 6.5)%, (50.2 +/- 9.9)%, respectively] and alpha-SM-actin expression (53 +/- 15, 75 +/- 14, 56 +/- 11, 82 +/- 17, 83 +/- 17, 98 +/- 16, respectively) were increased significantly (all P < 0.01).
  • The expressions of PKC-alpha mRNA and protein were higher than those of C group (all P < 0.01).
  • [MeSH-major] Anoxia. Environmental Exposure. Muscle, Smooth, Vascular / metabolism. Protein Kinase C-alpha / metabolism. Smoke / adverse effects

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  • (PMID = 16409783.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Smoke; EC 2.7.11.13 / Protein Kinase C-alpha
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45. Gomes MA, Rodrigues FH, Afonso-Cardoso SR, Buso AM, Silva AG, Favoreto S Jr, Souza MA: Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease. J Periodontal Res; 2006 Jun;41(3):177-83
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  • [Title] Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease.
  • BACKGROUND: Diabetes mellitus and periodontal disease have high incidence in the general population and are associated with various degrees of dysfunction in the immune system.
  • It has been shown that diabetic patients with severe periodontal disease have more complications of diabetes and less effective metabolic control compared with diabetic patients with healthy gingiva.
  • Patients with diabetes and severe periodontal disease present higher levels of serous immunoglobulin A (IgA).
  • OBJECTIVE: In this study we tested the hypothesis that type 2 diabetic patients with chronic moderate periodontal disease have differences in salivary IgA1 titers and cytokine expression when compared with the chronic severe periodontal disease cases.
  • METHODS: We utilized a jacalin-IgA capture assay to determine the IgA1 titers in total saliva and reverse transcriptase-polymerase chain reaction to detect mRNA for interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in total saliva samples of 13 patients with chronic moderate periodontal disease and 10 with chronic severe periodontal disease.
  • RESULTS AND CONCLUSIONS: We observed a predominance of IgA1 titers of 64 (45.5%) in saliva samples from chronic severe periodontal disease patients and titers averaging 512 (30.8%) in chronic moderate periodontal disease patients.
  • We detected mRNA for IFN-gamma in six out of 10 chronic severe periodontal disease subjects and in two out of 13 chronic moderate periodontal disease patients.
  • TNF-alpha expression was similar in both groups.
  • Our data suggest that higher levels of IgA1 may exert partial protection of the periodontal tissue in chronic moderate periodontal disease diabetic patients when compared to severe periodontal disease.
  • Despite the small number of patients, IFN-gamma expression had a trend association with severity of periodontitis and TNF-alpha gene expression did not correlate with severity of periodontal disease.
  • [MeSH-major] Diabetes Mellitus, Type 2 / immunology. Immunoglobulin A / analysis. Interferon-gamma / analysis. Periodontal Diseases / immunology. RNA, Messenger / analysis. Saliva / immunology. Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Artocarpus. Chronic Disease. Female. Humans. Male. Middle Aged. Plant Lectins. Reverse Transcriptase Polymerase Chain Reaction. Salivary Proteins and Peptides / analysis

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  • (PMID = 16677285.001).
  • [ISSN] 0022-3484
  • [Journal-full-title] Journal of periodontal research
  • [ISO-abbreviation] J. Periodont. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Plant Lectins; 0 / RNA, Messenger; 0 / Salivary Proteins and Peptides; 0 / Tumor Necrosis Factor-alpha; 0 / jacalin; 82115-62-6 / Interferon-gamma
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46. Xiaomin L, Fenglin C, Jianmin H, Yuzhi S, Binsheng G, Yingmei Z: Correlation between genetic polymorphism of cytokine genes, plasma protein levels and bronchial asthma in the Han people in northern China. J Asthma; 2008 Sep;45(7):583-9
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  • The polymorphism-based genotypes were identified by the sequence-specific primer-polymerase chain reaction.
  • In this network, IL-6 and TNF-alpha, were found with a high degree (D = 343 and 235, respectively) and IL-1beta with a moderate degree of connection (D = 155).
  • During the analysis of correlation between genetic polymorphism and a complex disease, the effects of environmental factors should be taken into account.
  • The information at the protein level should be fully developed and the bioinformatics techniques can be used for the comprehensive analysis, to have a deep understanding of molecular mechanisms of incidence and development of diseases.
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. China / epidemiology. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression. Genetic Predisposition to Disease. Humans. Incidence. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 18773331.001).
  • [ISSN] 1532-4303
  • [Journal-full-title] The Journal of asthma : official journal of the Association for the Care of Asthma
  • [ISO-abbreviation] J Asthma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / Cytokines
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47. Murakami M, Ohta T, Ito S: Interleukin-1beta enhances the action of bradykinin in rat myenteric neurons through up-regulation of glial B1 receptor expression. Neuroscience; 2008 Jan 2;151(1):222-31
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  • Interleukin (IL)-1beta and tumor necrosis factor alpha (TNFalpha) are released under pathological conditions in the gastrointestinal tract such as inflammatory bowel diseases (IBD).
  • In both cell types, the [Ca(2+)]i responses to BK were abolished by D-Arg(0)[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-BK (HOE140), a B2R antagonist, but not affected by des-Arg(9)-HOE140, a B1R antagonist.
  • Only in glial cells did the B1R agonists des-Arg(9)-BK and BK fragment 1-8 evoke a [Ca(2+)]i rise in a dose-dependent manner.
  • The alteration of phenotypes of glial cells may be the cause of the changes in neural function in the enteric nervous system in IBD.
  • [MeSH-minor] Animals. Calcium / metabolism. Calcium / physiology. Cells, Cultured. Cytokines / biosynthesis. Dinoprostone / metabolism. Dinoprostone / physiology. Enteric Nervous System / drug effects. Female. Immunohistochemistry. Male. Neuroglia / drug effects. Neuroglia / metabolism. Rats. Rats, Wistar. Receptor Cross-Talk / drug effects. Receptor, Bradykinin B1 / biosynthesis. Receptor, Bradykinin B1 / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects

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  • (PMID = 18053651.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Receptor, Bradykinin B1; 0 / Tumor Necrosis Factor-alpha; K7Q1JQR04M / Dinoprostone; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
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48. Gary-Bobo M, Elachouri G, Gallas JF, Janiak P, Marini P, Ravinet-Trillou C, Chabbert M, Cruccioli N, Pfersdorff C, Roque C, Arnone M, Croci T, Soubrié P, Oury-Donat F, Maffrand JP, Scatton B, Lacheretz F, Le Fur G, Herbert JM, Bensaid M: Rimonabant reduces obesity-associated hepatic steatosis and features of metabolic syndrome in obese Zucker fa/fa rats. Hepatology; 2007 Jul;46(1):122-9
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  • This study investigated the effects of rimonabant (SR141716), an antagonist of the cannabinoid receptor type 1 (CB1), on obesity-associated hepatic steatosis and related features of metabolic syndrome: inflammation (elevated plasma levels of tumor necrosis factor alpha [TNFalpha]), dyslipidemia, and reduced plasma levels of adiponectin.
  • These results demonstrate that rimonabant plays a hepatoprotective role and suggest that this CB1 receptor antagonist potentially has clinical applications in the treatment of obesity-associated liver diseases and related features of metabolic syndrome.
  • [MeSH-minor] Animals. Cannabinoid Receptor Antagonists. Inflammation / prevention & control. Liver / drug effects. Liver / pathology. Male. RNA / genetics. RNA / isolation & purification. Rats. Rats, Zucker. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / blood


49. Zhang W, Sharma R, Ju ST, He XS, Tao Y, Tsuneyama K, Tian Z, Lian ZX, Fu SM, Gershwin ME: Deficiency in regulatory T cells results in development of antimitochondrial antibodies and autoimmune cholangitis. Hepatology; 2009 Feb;49(2):545-52
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  • There have been several descriptions of mouse models that manifest select immunological and clinical features of autoimmune cholangitis with similarities to primary biliary cirrhosis in humans.
  • Some of these models require immunization with complete Freund's adjuvant, whereas others suggest that a decreased frequency of T regulatory cells (Tregs) facilitates spontaneous disease.
  • Furthermore, mice have moderate to severe lymphocytic infiltrates surrounding portal areas with evidence of biliary duct damage, and dramatic elevation of cytokines in serum and messenger RNAs encoding cytokines in liver tissue, including tumor necrosis factor alpha, interferon-gamma, interleukin (IL)-6, IL-12, and IL-23.

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  • (PMID = 19065675.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P50 AR045222; United States / NIDDK NIH HHS / DK / DK074768; United States / NIAMS NIH HHS / AR / AR051203; United States / NIDDK NIH HHS / DK / DK039588-21; United States / NIDDK NIH HHS / DK / R21 DK077961; United States / NIAMS NIH HHS / AR / AR047988; United States / NIDDK NIH HHS / DK / R01 DK074768; United States / NIDDK NIH HHS / DK / DK39588; United States / NIAMS NIH HHS / AR / R01 AR051203; United States / NIDDK NIH HHS / DK / R37 DK039588-21; United States / NIDCR NIH HHS / DE / DE017579; United States / NIAMS NIH HHS / AR / AR049449; United States / NIAMS NIH HHS / AR / R01 AR049449; United States / NIDDK NIH HHS / DK / R37 DK039588; United States / NIAMS NIH HHS / AR / R01 AR047988; United States / NIDDK NIH HHS / DK / R01 DK039588; United States / NIAMS NIH HHS / AR / AR045222; United States / NIDDK NIH HHS / DK / DK077961
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
  • [Other-IDs] NLM/ NIHMS77273; NLM/ PMC2635418
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50. Sakamoto A, Chen M, Nakamura T, Xie T, Karsenty G, Weinstein LS: Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical bone. J Biol Chem; 2005 Jun 3;280(22):21369-75
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  • [Title] Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical bone.
  • The G-protein alpha-subunit G(s)alpha is required for the intracellular cAMP responses to hormones and other agonists.
  • G(s)alpha is known to mediate the cAMP response to parathyroid hormone and other hormones and cytokines in bone and cartilage.
  • To analyze the in vivo role of G(s)alpha signaling in osteoblasts, we developed mice with osteoblast/osteocyte-specific G(s)alpha deficiency (BGsKO) by mating G(s)alpha-floxed mice with collagen Ialpha1 promoter-Cre recombinase transgenic mice.
  • Overall, our findings have similarities to parathyroid hormone null mice and confirm that the differential effects of parathyroid hormone on trabecular and cortical bone are primarily mediated via G(s)alpha in osteoblasts.
  • Osteoblast-specific G(s)alpha deficiency leads to reduced bone turnover.
  • [MeSH-major] Bone and Bones / metabolism. GTP-Binding Protein alpha Subunits, Gs / chemistry. Osteoblasts / metabolism
  • [MeSH-minor] Acid Phosphatase / pharmacology. Alkaline Phosphatase / metabolism. Animals. Bone Marrow Cells / metabolism. Carrier Proteins / metabolism. Cartilage / metabolism. Cell Differentiation. Chondrocytes / metabolism. Collagen Type I / metabolism. Cyclic AMP / metabolism. Cytokines / metabolism. DNA Primers / chemistry. Gene Expression Regulation. Isoenzymes / pharmacology. Membrane Glycoproteins / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Models, Biological. Models, Genetic. Osteocalcin / metabolism. Osteopontin. Phenotype. Polymerase Chain Reaction. Promoter Regions, Genetic. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Reverse Transcriptase Polymerase Chain Reaction. Sialoglycoproteins / metabolism. Signal Transduction. Skull / metabolism. Time Factors


51. Ramasawmy R, Cunha-Neto E, Faé KC, Müller NG, Cavalcanti VL, Drigo SA, Ianni B, Mady C, Kalil J, Goldberg AC: BAT1, a putative anti-inflammatory gene, is associated with chronic Chagas cardiomyopathy. J Infect Dis; 2006 May 15;193(10):1394-9
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  • Heart-infiltrating lymphocytes from patients with CCC also express proinflammatory cytokines (tumor necrosis factor- alpha and interferon- gamma ) that are detectable in biopsy samples and surgical heart-tissue samples.
  • METHODS: We assessed, by polymerase chain reaction restriction fragment-length polymorphism analysis, BAT1 variants in the promoter region at positions -22C/G and -348C/T in 154 patients with CCC and in 76 T. cruzi-infected but asymptomatic (ASY) patients.
  • [MeSH-major] Chagas Cardiomyopathy / genetics. Genetic Predisposition to Disease. RNA Helicases / genetics
  • [MeSH-minor] Brazil. Chronic Disease. DEAD-box RNA Helicases. DNA / analysis. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Genetic. Polymorphism, Restriction Fragment Length. Promoter Regions, Genetic / genetics

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  • (PMID = 16619187.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA; EC 3.6.1.- / DDX39B protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases; EC 3.6.4.13 / RNA Helicases
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52. Giamarellos-Bourboulis EJ, Mouktaroudi M, Bodar E, van der Ven J, Kullberg BJ, Netea MG, van der Meer JW: Crystals of monosodium urate monohydrate enhance lipopolysaccharide-induced release of interleukin 1 beta by mononuclear cells through a caspase 1-mediated process. Ann Rheum Dis; 2009 Feb;68(2):273-8
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  • Production of tumour necrosis factor alpha (TNFalpha), interleukin (IL)1 beta and IL6, as well as the intracellular concentrations of proIL1 beta were measured by ELISA. mRNA transcripts of TNFalpha and IL1 beta were assessed by real-time PCR.
  • [MeSH-minor] Adult. Carrier Proteins / genetics. Cells, Cultured. Crystallization. Cytokines / biosynthesis. Dose-Response Relationship, Immunologic. Female. Gene Expression Regulation / immunology. Humans. Inflammation Mediators / metabolism. Male. Mutation. Polymerase Chain Reaction / methods. RNA, Messenger / genetics. Young Adult

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  • (PMID = 18390571.001).
  • [ISSN] 1468-2060
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytokines; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / NLRP3 protein, human; 0 / RNA, Messenger; 268B43MJ25 / Uric Acid; EC 3.4.22.36 / Caspase 1
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53. Tripputi P, Bianchi S, Fedele L: A possible mechanism for non-replication of allelic association between a single nucleotide polymorphism of the human beta T-cell receptor and autoimmune diseases. Int J Immunogenet; 2008 Apr;35(2):141-4
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  • [Title] A possible mechanism for non-replication of allelic association between a single nucleotide polymorphism of the human beta T-cell receptor and autoimmune diseases.
  • Gene polymorphisms, in particular single nucleotide polymorphisms (SNPs), have been associated to multifactorial diseases such as cancer, inflammation and autoimmunity.
  • Indeed for some autoimmune diseases, it has been possible to identify critical residues that play a major role in susceptibility to diseases.
  • The association of a common T/C polymorphism in the promoter region of the beta 2 constant chain of the T-cell receptor with autoimmune diseases, such as insulin-dependent diabetes, autoimmune hepatitis, IgA nephropathy, membranous nephropathy, Graves' disease and Hashimoto's thyroiditis, was described in the 1990 s.
  • This finding led us to make an allele frequency study of this single nucleotide polymorphism between sexes in a new series of patients.
  • If the higher frequency of CC homozygous genotype (that is associated with an increased risk of autoimmune diseases) in females would be confirmed in normal population, this could be an explanation of the controversial results obtained by association studies made between this SNP and autoimmune diseases.
  • [MeSH-major] Alleles. Autoimmune Diseases / genetics. Gene Frequency / genetics. Polymorphism, Single Nucleotide. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • (PMID = 18279372.001).
  • [ISSN] 1744-313X
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
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54. Pettersson-Kastberg J, Aits S, Gustafsson L, Mossberg A, Storm P, Trulsson M, Persson F, Mok KH, Svanborg C: Can misfolded proteins be beneficial? The HAMLET case. Ann Med; 2009;41(3):162-76
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  • Amyloid-forming proteins are one example, in which conformational change may lead to fibril formation and, in many cases, neurodegenerative disease.
  • We have proposed that partial unfolding provides a mechanism to generate new and useful functional variants from a given polypeptide chain.
  • Here we present HAMLET (Human Alpha-lactalbumin Made LEthal to Tumor cells) as an example where partial unfolding and the incorporation of cofactor create a complex with new, beneficial properties.
  • Native alpha-lactalbumin functions as a substrate specifier in lactose synthesis, but when partially unfolded the protein binds oleic acid and forms the tumoricidal HAMLET complex.
  • [MeSH-minor] Amyloid / chemistry. Amyloid / metabolism. Animals. Antimicrobial Cationic Peptides / chemistry. Antimicrobial Cationic Peptides / metabolism. Antineoplastic Agents / chemistry. Antineoplastic Agents / therapeutic use. Calcium / metabolism. Cell Death / drug effects. Humans. Models, Molecular. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / pathology. Neurodegenerative Diseases / metabolism. Neurodegenerative Diseases / pathology. Prions / chemistry. Prions / metabolism. Protein Binding. Protein Conformation

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  • (PMID = 18985467.001).
  • [ISSN] 1365-2060
  • [Journal-full-title] Annals of medicine
  • [ISO-abbreviation] Ann. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Amyloid; 0 / Antimicrobial Cationic Peptides; 0 / Antineoplastic Agents; 0 / HAMLET complex, human; 0 / Oleic Acids; 0 / Prions; 9013-90-5 / Lactalbumin; SY7Q814VUP / Calcium
  • [Number-of-references] 106
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55. Nishida H, Ichikawa H, Konishi T: Shengmai-san enhances antioxidant potential in C2C12 myoblasts through the induction of intracellular glutathione peroxidase. J Pharmacol Sci; 2007 Dec;105(4):342-52
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  • Because of its antioxidative property, SMS might be useful not only for the oxidative damage associated diseases but also for the transplantation of myoblasts into muscular dystrophy patients.
  • [MeSH-minor] Acetylcysteine / pharmacology. Animals. Apoptosis / drug effects. Cell Line. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Combinations. Drug Synergism. Enzyme-Linked Immunosorbent Assay. Glutathione / metabolism. Hydrogen Peroxide / pharmacology. Immunoblotting. Immunohistochemistry. In Situ Nick-End Labeling. Intracellular Fluid / drug effects. Intracellular Fluid / enzymology. Protein Carbonylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. alpha-Tocopherol / pharmacology

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  • (PMID = 18057775.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 0 / RNA, Messenger; 0 / fructus schizandrae, radix ginseng, radix ophiopogonis drug combination; BBX060AN9V / Hydrogen Peroxide; EC 1.11.1.9 / Glutathione Peroxidase; GAN16C9B8O / Glutathione; H4N855PNZ1 / alpha-Tocopherol; WYQ7N0BPYC / Acetylcysteine
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56. Hu XD, Yang Y, Zhong XG, Zhang XH, Zhang YN, Zheng ZP, Zhou Y, Tang W, Yang YF, Hu LH, Zuo JP: Anti-inflammatory effects of Z23 on LPS-induced inflammatory responses in RAW264.7 macrophages. J Ethnopharmacol; 2008 Dec 8;120(3):447-51
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  • RESULTS: Z23 significantly decreased the production of PGE2, NO, tumour necrosis factor alpha (TNFalpha) and IL6 production.
  • ) Merr and indicated that Z23 has the potential for treatment of various inflammatory diseases where the overproduction of NO, PGE2 and inflammatory cytokines has been shown to play a role, e.g. rheumatoid arthritis.
  • [MeSH-major] Amides / pharmacology. Annonaceae / chemistry. Anti-Inflammatory Agents / pharmacology. Interleukin-6 / metabolism. Nitric Oxide / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Dinoprostone / metabolism. Gene Expression. Herbal Medicine. Lipopolysaccharides. Macrophages / drug effects. Macrophages / metabolism. Medicine, Chinese Traditional. Mice. Nitric Oxide Synthase / genetics. Nitric Oxide Synthase / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18952160.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 7'-(3',4'-dihydroxyphenyl)-N-((4-methoxyphenyl)ethyl)propenamide; 0 / Amides; 0 / Anti-Inflammatory Agents; 0 / Cytokines; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
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57. Lau AC, Duong TT, Ito S, Yeung RS: Intravenous immunoglobulin and salicylate differentially modulate pathogenic processes leading to vascular damage in a model of Kawasaki disease. Arthritis Rheum; 2009 Jul;60(7):2131-41
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  • [Title] Intravenous immunoglobulin and salicylate differentially modulate pathogenic processes leading to vascular damage in a model of Kawasaki disease.
  • OBJECTIVE: Kawasaki disease (KD) is a multisystem vasculitis affecting children and is characterized by immune activation in the acute stage of disease.
  • KD is the leading cause of acquired heart disease among children in North America.
  • The aim of this study was to examine the effect of IVIG and salicylate at each stage of disease development.
  • METHODS: Using a murine model of KD, we established and validated several in vitro techniques to reflect 3 key steps involved in disease pathogenesis, as follows: thymidine incorporation to evaluate T cell activation, enzyme-linked immunosorbent assay to measure tumor necrosis factor alpha (TNFalpha) production, and real-time polymerase chain reaction to examine TNFalpha-mediated expression of matrix metalloproteinase 9 (MMP-9).
  • [MeSH-major] Immunoglobulins, Intravenous / therapeutic use. Immunologic Factors / therapeutic use. Mucocutaneous Lymph Node Syndrome / complications. Mucocutaneous Lymph Node Syndrome / drug therapy. Salicylates / therapeutic use. Vascular Diseases / etiology
  • [MeSH-minor] Animals. Cell Proliferation. Cells, Cultured. Disease Models, Animal. Dose-Response Relationship, Drug. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. NF-kappa B / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19565485.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulins, Intravenous; 0 / Immunologic Factors; 0 / NF-kappa B; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Salicylates; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.35 / Matrix Metalloproteinase 9
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58. Momeni P, Cairns NJ, Perry RH, Bigio EH, Gearing M, Singleton AB, Hardy J: Mutation analysis of patients with neuronal intermediate filament inclusion disease (NIFID). Neurobiol Aging; 2006 May;27(5):778.e1-778.e6
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  • [Title] Mutation analysis of patients with neuronal intermediate filament inclusion disease (NIFID).
  • Abnormal neuronal aggregates of alpha-internexin and the three neurofilament (NF) subunits, NFL, NFM, and NFH have recently been identified as the signature lesions of neuronal intermediate filament (IF) inclusion disease (NIFID), a novel neurological disease of early onset with a variable clinical phenotype including frontotemporal dementia, pyramidal and extrapyramidal signs.
  • In other neurodegenerative diseases in which protein aggregates contribute to disease pathogenesis, mutations in the encoding protein cause the hereditary variant of the disease.
  • To determine the molecular genetic contribution to this disease we performed a mutation analysis of all type IV neuronal IF, SOD1 and NUDEL genes in cases of NIFID and unaffected control cases.
  • [MeSH-major] Inclusion Bodies / genetics. Neurodegenerative Diseases / genetics. Neurofilament Proteins / genetics
  • [MeSH-minor] Adult. Amino Acid Substitution. Case-Control Studies. Cloning, Molecular. DNA / biosynthesis. DNA / genetics. DNA Primers. Exons / genetics. Female. Gene Deletion. Gene Frequency. Great Britain / epidemiology. Humans. Intermediate Filament Proteins / genetics. Male. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction. Risk. Superoxide Dismutase / genetics. United States / epidemiology

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  • (PMID = 16005115.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intermediate Filament Proteins; 0 / Neurofilament Proteins; 0 / alpha-internexin; 9007-49-2 / DNA; EC 1.15.1.- / superoxide dismutase 1; EC 1.15.1.1 / Superoxide Dismutase
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59. Bhavsar MD, Amiji MM: Oral IL-10 gene delivery in a microsphere-based formulation for local transfection and therapeutic efficacy in inflammatory bowel disease. Gene Ther; 2008 Sep;15(17):1200-9
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  • [Title] Oral IL-10 gene delivery in a microsphere-based formulation for local transfection and therapeutic efficacy in inflammatory bowel disease.
  • The objective of this study was to examine the potential of oral interleukin-10 (IL-10) gene therapy for the treatment of inflammatory bowel disease (IBD).
  • Nanoparticles-in-microsphere oral system (NiMOS) was formulated with murine IL-10-expressing plasmid DNA in type-B gelatin nanoparticles, which were further encapsulated in poly(epsilon-caprolactone) microsphere matrix.
  • Upon oral administration in an acute colitis model, IL-10 expression in the large intestine was measured by quantitative real-time PCR and ELISA.
  • The locally expressed IL-10 was able to suppress the levels of proinflammatory cytokines, such as IFN-gamma, TNF-alpha, IL-1alpha, IL-1beta and IL-12, as well as certain chemokines.
  • The therapeutic benefits of transfected IL-10 were further demonstrated by an increase in body weight, favorable clinical activity score, restoration in colon length and weight, and suppression of inflammatory response as assessed by tissue histological analysis and myeloperoxidase activity.
  • [MeSH-major] Genetic Therapy / methods. Inflammatory Bowel Diseases / therapy. Interleukin-10 / genetics. Transfection / methods
  • [MeSH-minor] Administration, Oral. Animals. Biomarkers / analysis. Chemistry, Pharmaceutical. Colon / immunology. Colon / pathology. Enzyme-Linked Immunosorbent Assay. Female. Gelatin. Gene Expression. Intestinal Mucosa / immunology. Intestinal Mucosa / pathology. Mice. Mice, Inbred BALB C. Microscopy, Electron, Scanning. Microspheres. Models, Animal. Nanoparticles. Peroxidase / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transgenes. Trinitrobenzenesulfonic Acid

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  • (PMID = 18418416.001).
  • [ISSN] 1476-5462
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 130068-27-8 / Interleukin-10; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid; 9000-70-8 / Gelatin; EC 1.11.1.7 / Peroxidase
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60. di Meglio P, Ianaro A, Ghosh S: Amelioration of acute inflammation by systemic administration of a cell-permeable peptide inhibitor of NF-kappaB activation. Arthritis Rheum; 2005 Mar;52(3):951-8
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  • The expression levels of NF-kappaB-regulated cyclooxygenase 2 (COX-2) protein and tumor necrosis factor alpha (TNFalpha) messenger RNA (mRNA) were evaluated by immunoblot analysis and polymerase chain reaction amplification of reverse-transcribed mRNA, respectively.
  • CONCLUSION: These studies further establish NF-kappaB as a target for antiinflammatory therapy and provide support for the use of the NBD peptide as a possible therapeutic agent for inflammatory diseases.

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  • (PMID = 15751079.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R37 AI033443; United States / NHLBI NIH HHS / HV / N01-HV-28186; United States / NIAID NIH HHS / AI / R37-AI-33443
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / NBD peptide, mouse; 0 / NF-kappa B; 0 / Peptides; 0 / Polysaccharides; 0 / Tumor Necrosis Factor-alpha; 9000-07-1 / Carrageenan; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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61. Nunes JS, Lawhon SD, Rossetti CA, Khare S, Figueiredo JF, Gull T, Burghardt RC, Bäumler AJ, Tsolis RM, Andrews-Polymenis HL, Adams LG: Morphologic and cytokine profile characterization of Salmonella enterica serovar typhimurium infection in calves with bovine leukocyte adhesion deficiency. Vet Pathol; 2010 Mar;47(2):322-33
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  • [Title] Morphologic and cytokine profile characterization of Salmonella enterica serovar typhimurium infection in calves with bovine leukocyte adhesion deficiency.
  • Morphologic studies revealed that infection of CD18- calves with S Typhimurium resulted in no significant tissue infiltration by neutrophils, less tissue damage, reduced luminal fluid accumulation, and increased bacterial invasion, when compared with CD18+ calves.
  • Study of cytokine gene expression by quantitative real-time polymerase chain reaction revealed that early stages of acute infection (4-8 hours postinfection) were associated with increased interleukin 8 gene expression in the absence of tissue influx of neutrophils in CD18- calves, whereas later stages of infection (12 hours postinfection) were associated with increased expression of growth-related oncogene alpha in the presence of neutrophil influx in CD18+ calves.
  • In contrast, the proinflammatory cytokines interleukin 1beta and tumor necrosis factor alpha were poorly correlated with the presence or absence of tissue neutrophils.

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  • (PMID = 20118318.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI044170-01A1; United States / NIAID NIH HHS / AI / R01 AI076246; United States / NIAID NIH HHS / AI / R01 AI044170; United States / NIAID NIH HHS / AI / AI044170-01A1; United States / PHS HHS / / 1 RO1 A144170-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD18; 0 / CXCL1 protein, Bos taurus; 0 / Chemokine CXCL1; 0 / Interleukin-1beta; 0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA
  • [Other-IDs] NLM/ NIHMS165622; NLM/ PMC2848297
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62. Okabayashi K, Kano R, Watanabe T, Hasegawa A: Serotypes and mating types of clinical isolates from feline cryptococcosis in Japan. J Vet Med Sci; 2006 Jan;68(1):91-4
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  • [Title] Serotypes and mating types of clinical isolates from feline cryptococcosis in Japan.
  • Most isolates of Cryptococcus neoformans (teleomorph: Filobasidiella neoformans) from human patients and from environmental materials in Japan have been identified as serotype A mating type a by the seroagglutination test and mating experiments.
  • A PCR method using the mating type alpha allele-specific primer of the STE12 gene and the serotype- and mating type-specific primers of the STE20 gene for identification of C. neoformans has been developed.
  • Using the PCR method, conserved strains and clinical isolates from feline cryptococcosis were examined for serotype and the mating type.
  • The results showed that all clinical isolates examined were identified as serotype A, MATalpha, indicating that feline cryptococcsis cases in Japan are caused by C. neoformans serotype A, MATalpha, as is the case in humans.

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  • (PMID = 16462126.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers
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63. Ferrarezi MC, Cardoso TC, Dutra IS: Genotyping of Clostridium perfringens isolated from calves with neonatal diarrhea. Anaerobe; 2008 Dec;14(6):328-31
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  • Clostridium perfringens is a widespread enteropathogen, and is responsible for many animal diseases such as bovine neonatal diarrhea.
  • Multiple isolates from primary isolation plates were subjected to simultaneous genotyping by multiplex PCR, with primers amplifying fragments of alpha (cpa), beta (cpb), epsilon (etx), iota (itxA), enterotoxin (cpe) and beta2 (cpb2) toxin-encoding genes.
  • Fourteen isolate mixtures from animals with diarrhea had only cpa (type A), one had cpa and cpb2 (type A beta2 positive), one with cpa, itxA, and cpb2 (type E, beta2 positive), and one with cpa, etx, itxA, and cpb2 toxin producing strains.
  • Among 17 isolate mixtures from healthy calves, 10 were exclusively type A, one was type A cpb2 positive, two were type E, three were type E cpb2 positive, and one was types D and E cpb2 positive.
  • There was no correlation between isolation of a given toxin type and the presence of diarrhea.
  • [MeSH-major] Cattle Diseases / microbiology. Clostridium perfringens / classification. Clostridium perfringens / genetics. Diarrhea / veterinary
  • [MeSH-minor] Animals. Animals, Newborn. Bacterial Toxins / genetics. Cattle. DNA, Bacterial / genetics. Female. Genotype. Male. Polymerase Chain Reaction / methods

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  • (PMID = 19114113.001).
  • [ISSN] 1095-8274
  • [Journal-full-title] Anaerobe
  • [ISO-abbreviation] Anaerobe
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / DNA, Bacterial
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64. Ko H, Das A, Carter RL, Fricks IP, Zhou Y, Ivanov AA, Melman A, Joshi BV, Kovác P, Hajduch J, Kirk KL, Harden TK, Jacobson KA: Molecular recognition in the P2Y(14) receptor: Probing the structurally permissive terminal sugar moiety of uridine-5'-diphosphoglucose. Bioorg Med Chem; 2009 Jul 15;17(14):5298-311
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  • For example, the carboxylate group of uridine-5'-diphosphoglucuronic acid proved to be suitable for flexible substitution by chain extension through an amide linkage.
  • Functionalized congeners containing terminal 2-acylaminoethylamides prepared by this strategy retained P2Y(14) activity, and molecular modeling predicted close proximity of this chain to the second extracellular loop of the receptor.
  • The beta-glucoside was twofold less potent than the native alpha-isomer, but methylene replacement of the 1''-oxygen abolished activity.

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  • (PMID = 19502066.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM038213; United States / Intramural NIH HHS / / Z01 DK031116-20; United States / Intramural NIH HHS / / Z99 DK999999; United States / NIGMS NIH HHS / GM / GM38213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P2Y14 receptor, human; 0 / Purinergic P2 Receptor Agonists; 0 / Receptors, Purinergic P2; 0 / Uracil Nucleotides; EC 3.1.4.- / Type C Phospholipases; V50K1D7P4Y / Uridine Diphosphate Glucose
  • [Other-IDs] NLM/ NIHMS130149; NLM/ PMC2760346
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65. Shen CL, Chen WH, Zou SX: In vitro and in vivo effects of hydrolysates from conglycinin on intestinal microbial community of mice after Escherichia coli infection. J Appl Microbiol; 2007 Jan;102(1):283-9
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  • [Title] In vitro and in vivo effects of hydrolysates from conglycinin on intestinal microbial community of mice after Escherichia coli infection.
  • AIMS: To detect the effect of pepsin-hydrolysate conglycinin (PTC) on the growth of Escherichia coli O(138)in vitro, and investigate the effect of PTC on intestinal microbial community of mice after E. coli infection.
  • The mice activities were monitored and polymerase chain reaction-denaturing gradient gel electrophoresis was used to analyse the microbial community in mice faeces.
  • There was high similarity of intestinal microbial community in mice between PTC and normal groups.
  • SIGNIFICANCE AND IMPACT OF THE STUDY: This study demonstrated the antibacterial activity of PTC against E. coli and its ability to maintain healthy intestinal microbial community in mice even after they were infected with E. coli.
  • This observation is significant in the application of PTC to prevent gastrointestinal diseases caused by E. coli and unbalanced intestinal microflora.
  • [MeSH-minor] Animals. Antigens, Plant. Electrophoresis, Polyacrylamide Gel / methods. Feces / microbiology. Hydrolysis. Intestines / microbiology. Male. Mice. Pepsin A / metabolism. Polymerase Chain Reaction / methods. Seed Storage Proteins. Soybeans / chemistry

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  • (PMID = 17184345.001).
  • [ISSN] 1364-5072
  • [Journal-full-title] Journal of applied microbiology
  • [ISO-abbreviation] J. Appl. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antigens, Plant; 0 / Globulins; 0 / Seed Storage Proteins; 0 / Soybean Proteins; 0 / alpha-conglycinin, Glycine max; 0 / beta-conglycinin protein, Glycine max; EC 3.4.23.1 / Pepsin A
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66. Gloerich J, Ijlst L, Wanders RJ, Ferdinandusse S: Bezafibrate induces FALDH in human fibroblasts; implications for Sjögren-Larsson syndrome. Mol Genet Metab; 2006 Sep-Oct;89(1-2):111-5
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  • In animal studies, the expression of the murine ortholog of FALDH, has been shown to be under the control of peroxisome proliferator-activated receptor alpha (PPARalpha).

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  • (PMID = 16837225.001).
  • [ISSN] 1096-7192
  • [Journal-full-title] Molecular genetics and metabolism
  • [ISO-abbreviation] Mol. Genet. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypolipidemic Agents; 0 / Peroxisome Proliferator-Activated Receptors; EC 1.2.- / Aldehyde Oxidoreductases; EC 1.2.1.48 / long-chain-aldehyde dehydrogenase; Y9449Q51XH / Bezafibrate
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67. Malik ZA, Hailpern SM, Burk RD: Predictors of seropositivity to human papillomavirus type 53: one of the most prevalent high risk-related cervical human papillomaviruses. Viral Immunol; 2008 Sep;21(3):371-7
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  • [Title] Predictors of seropositivity to human papillomavirus type 53: one of the most prevalent high risk-related cervical human papillomaviruses.
  • HPV53, part of the alpha 6 species group along with HPV types 30, 56, and 66, is one of the most prevalent high risk-related HPV types, yet little is known about the molecular basis of its benign behavior.
  • In conclusion, host serological responses to HPV53 VLPs are strongly type-specific, and subjects' risk for HPV53 seropositivity is independently associated with sexual behavior and OCP use.
  • [MeSH-minor] Adolescent. Adult. Contraception. Female. Humans. Immunoglobulin G / blood. Polymerase Chain Reaction. Prevalence. Risk Factors. Sexual Behavior. Sexual Partners. United States / epidemiology. Vaginal Smears

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  • (PMID = 18681800.001).
  • [ISSN] 1557-8976
  • [Journal-full-title] Viral immunology
  • [ISO-abbreviation] Viral Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI031055
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Immunoglobulin G
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68. Andersson D, Kotarsky K, Wu J, Agace W, Duan RD: Expression of alkaline sphingomyelinase in yeast cells and anti-inflammatory effects of the expressed enzyme in a rat colitis model. Dig Dis Sci; 2009 Jul;54(7):1440-8
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  • Alkaline sphingomyelinase (Alk-SMase) is a key enzyme in the intestinal tract for digestion of dietary sphingomyelin (SM), which generates lipid messengers with cell-cycle regulating effects.
  • We found a tendency for decreased tumor necrosis factor (TNF)-alpha expression in the Alk-SMase-treated group.
  • This study, for the first time, provides a method to produce the enzyme and shows the potential applicability of the enzyme in the treatment of inflammatory bowel diseases.
  • [MeSH-minor] Administration, Rectal. Animals. Colon / pathology. Dextran Sulfate / adverse effects. Disease Models, Animal. Female. Inflammation / prevention & control. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Pichia / cytology. Pilot Projects. Polymerase Chain Reaction. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18989780.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 9042-14-2 / Dextran Sulfate; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase; EC 3.1.4.12 / intestinal alkaline sphingomyelinase, human
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69. Tuin A, Huizinga-Van der Vlag A, van Loenen-Weemaes AM, Meijer DK, Poelstra K: On the role and fate of LPS-dephosphorylating activity in the rat liver. Am J Physiol Gastrointest Liver Physiol; 2006 Feb;290(2):G377-85
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  • Gut-derived lipopolysaccharide (LPS) plays a role in the pathogenesis of liver diseases like fibrosis.
  • The enzyme alkaline phosphatase (AP) is present in, among others, the intestinal wall and liver and has been previously shown to dephosphorylate LPS.
  • Furthermore, in vitro and in vivo studies showed that exogenous intestinal AP quickly bound to the asialoglycoprotein receptor on hepatocytes.
  • This intestinal isoform significantly attenuated LPS-induced hepatic tumor necrosis factor-alpha and nitric oxide (nitrite and nitrate) responses in vitro.
  • This study shows that LPS enhances AP expression in hepatocytes and that intestinal AP is rapidly taken up by these same cells, leading to an attenuation of LPS-induced responses in vivo.
  • [MeSH-minor] Animals. Antigens, CD14 / metabolism. Collagen Type III / metabolism. Enterocytes / enzymology. Gluconeogenesis / drug effects. Hepatocytes / enzymology. Hepatocytes / metabolism. Hepatocytes / ultrastructure. Immunohistochemistry. In Vitro Techniques. Kidney / enzymology. Kidney / metabolism. Kidney / ultrastructure. Liver Cirrhosis / metabolism. Liver Cirrhosis / pathology. Male. Nitric Oxide / metabolism. Phosphorylation. RNA / biosynthesis. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16223948.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Collagen Type III; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 63231-63-0 / RNA; EC 3.1.3.1 / Alkaline Phosphatase
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70. Attanasio F, Cataldo S, Fisichella S, Nicoletti S, Nicoletti VG, Pignataro B, Savarino A, Rizzarelli E: Protective effects of L- and D-carnosine on alpha-crystallin amyloid fibril formation: implications for cataract disease. Biochemistry; 2009 Jul 14;48(27):6522-31
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  • [Title] Protective effects of L- and D-carnosine on alpha-crystallin amyloid fibril formation: implications for cataract disease.
  • Mildly denaturing conditions induce bovine alpha-crystallin, the major structural lens protein, to self-assemble into fibrillar structures in vitro.
  • The natural dipeptide l-carnosine has been shown to have potential protective and therapeutic significance in many diseases.
  • Here we report the inhibitory effect induced by the peptide (l- and d-enantiomeric form) on alpha-crystallin fibrillation and the almost complete restoration of the chaperone activity lost after denaturant and/or heat stress.
  • Scanning force microscopy (SFM), thioflavin T, and a turbidimetry assay have been used to determine the morphology of alpha-crystallin aggregates in the presence and absence of carnosine.
  • DSC and a near-UV CD assay evidenced that the structural precursors of amyloid fibrils are polypeptide chain segments that lack stable structural elements.
  • Moreover, we have found a disassembling effect of carnosine on alpha-crystallin amyloid fibrils.
  • [MeSH-major] Amyloid / chemistry. Carnosine / chemistry. Cataract / metabolism. alpha-Crystallins / chemistry

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  • (PMID = 19441807.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Molecular Chaperones; 0 / alpha-Crystallins; 8HO6PVN24W / Carnosine
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71. Javor J, Bucova M, Ferencik S, Grosse-Wilde H, Buc M: Single nucleotide polymorphisms of cytokine genes in the healthy Slovak population. Int J Immunogenet; 2007 Aug;34(4):273-80
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  • Several cytokine gene polymorphisms have been identified to play a role in susceptibility to various diseases, including autoimmune, infectious, allergic or cardiovascular diseases.
  • A polymerase chain reaction with sequence-specific primers was used to genotype polymorphisms within genes encoding IL-1alpha, IL-1beta, IL-1R, IL-1RA, IL-4Ralpha, IL-12, IFN-gamma, TGF-beta, TNF-alpha, IL-2, IL-4, IL-6 and IL-10 in a sample of 140 unrelated Slovak subjects.
  • The obtained data represent a basis for further studies on association of cytokine gene polymorphisms with some diseases.

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  • (PMID = 17627763.001).
  • [ISSN] 1744-3121
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
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72. Kim N, Cho SI, Yim JY, Kim JM, Lee DH, Park JH, Kim JS, Jung HC, Song IS: The effects of genetic polymorphisms of IL-1 and TNF-A on Helicobacter pylori-induced gastroduodenal diseases in Korea. Helicobacter; 2006 Apr;11(2):105-12
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  • [Title] The effects of genetic polymorphisms of IL-1 and TNF-A on Helicobacter pylori-induced gastroduodenal diseases in Korea.
  • OBJECTIVE: To evaluate whether or not genetic polymorphism of IL-1B, IL-1RN, and TNF-Alpha is an important factor in the different expression of gastroduodenal diseases after Helicobacter pylori infection.
  • METHODS: This study consisted of 1360 subjects: control, gastric cancer (GC, intestinal type, and diffuse type), benign gastric ulcer (BGU), duodenal ulcer, and first-degree gastric cancer relative (GCR).
  • IL-1Beta-511 and TNF-A-308 biallelic polymorphism were genotyped by 5' nuclease polymerase chain reaction (PCR) assays, and PCR-restriction fragment length polymorphism (PCR-RFLP).
  • There was no significance in the polymorphism of TNF-Alpha-308 regardless of H. pylori-induced gastroduodenal diseases.
  • CONCLUSIONS: The IL-1Beta-511 T-carrier polymorphism has a negative effect on the development of H. pylori-positive BGU, and high frequency of IL-1RN 2/2 was found in the H. pylori-positive relatives of GC patients, which suggest that this genetic polymorphism could play some role in the H. pylori-induced gastroduodenal diseases in Korea.
  • [MeSH-major] Gastrointestinal Diseases / genetics. Helicobacter Infections / complications. Interleukin-1 / genetics. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Aged. Duodenal Ulcer / genetics. Duodenal Ulcer / microbiology. Female. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Korea. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Stomach Neoplasms / genetics. Stomach Neoplasms / microbiology. Stomach Ulcer / genetics. Stomach Ulcer / microbiology

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  • [ErratumIn] Helicobacter. 2006 Jun;11(3):215
  • (PMID = 16579840.001).
  • [ISSN] 1083-4389
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha
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73. Zhao YP, Wang H, Fang M, Ji Q, Yang ZX, Gao CF: Study of the association between polymorphisms of the COL1A1 gene and HBV-related liver cirrhosis in Chinese patients. Dig Dis Sci; 2009 Feb;54(2):369-76
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  • Polymorphisms -1997T>G, -1663 ins/del T and -1363C>G of the COL1A1 gene were detected by direct sequencing.
  • No polymorphism at -1663 ins/del T was observed in any subject.
  • [MeSH-major] Collagen Type I / genetics. Hepatitis B, Chronic / complications. Liver Cirrhosis / genetics

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  • (PMID = 18536987.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain; 82115-62-6 / Interferon-gamma
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74. Wex T, Kuester D, Vieth M, Treiber G, Krieg A, Roessner A, Malfertheiner P: Helicobacter pylori infection and short-term intake of low-dose aspirin have different effects on alpha-1 antitrypsin/alpha-1 peptidase inhibitor (alpha1-PI) levels in antral mucosa and peripheral blood. Scand J Gastroenterol; 2008;43(10):1194-201
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  • [Title] Helicobacter pylori infection and short-term intake of low-dose aspirin have different effects on alpha-1 antitrypsin/alpha-1 peptidase inhibitor (alpha1-PI) levels in antral mucosa and peripheral blood.
  • OBJECTIVE: Alpha-1 protease inhibitor (alpha1-PI) is the major circulating serine protease inhibitor.
  • The purpose of the study was to investigate alpha1-PI expression in gastroduodenal mucosa and blood with respect to two major etiological risk factors for gastroduodenal diseases, Helicobacter pylori infection and intake of low-dose aspirin.
  • Blood and tissue samples were obtained on days 0, 1, 3 and 7; alpha1-PI levels were determined by enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and analyzed for histopathological findings.
  • Alpha-1-PI transcript levels were similarly induced in H. pylori-infected subjects (0.13+/-0.15 versus 0.027+/-0.043 a.u. (arbitrary units), p=0.018).
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Aspirin / administration & dosage. Gene Expression Regulation, Enzymologic / drug effects. Helicobacter Infections / metabolism. alpha 1-Antitrypsin / metabolism
  • [MeSH-minor] Adult. Enzyme-Linked Immunosorbent Assay. Female. Gastric Mucosa / chemistry. Gastric Mucosa / metabolism. Gastric Mucosa / microbiology. Gene Expression / drug effects. Helicobacter pylori. Humans. Male. Pyloric Antrum / chemistry. Reverse Transcriptase Polymerase Chain Reaction. Time Factors


75. Ramasawmy R, Fae KC, Cunha-Neto E, Müller NG, Cavalcanti VL, Ferreira RC, Drigo SA, Ianni B, Mady C, Goldberg AC, Kalil J: Polymorphisms in the gene for lymphotoxin-alpha predispose to chronic Chagas cardiomyopathy. J Infect Dis; 2007 Dec 15;196(12):1836-43
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  • [Title] Polymorphisms in the gene for lymphotoxin-alpha predispose to chronic Chagas cardiomyopathy.
  • BACKGROUND: Chagas disease, caused by Trypanosoma cruzi infection, displays clinical heterogeneity and may be attributable to differential genetic susceptibility.
  • Chronic Chagas cardiomyopathy (CCC) develops only in a subset of T. cruzi-infected individuals and may lead to heart failure that has a worse clinical course and that leads to reduced life expectancy, compared with heart failure of other etiologies.
  • Clinical, genetic, and epidemiological studies have linked lymphotoxin-alpha (LTA), a proinflammatory cytokine, to coronary artery disease and myocardial infarction.
  • METHODS: We used polymerase chain reaction to genotype the LTA +80A-->C and LTA +252A-->G variants in 169 patients with CCC and in 76 T. cruzi-infected asymptomatic (ASY) patients.
  • Furthermore, homozygosity for the LTA +80A allele correlated with the lowest levels of plasmatic tumor-necrosis factor-alpha.
  • CONCLUSIONS: Our results suggest that the study of genetic variations in patients with Chagas disease may help in the identification of individuals at increased risk of progressing to CCC and, by providing early treatment, reduce the morbidity and mortality associated with this disease.
  • [MeSH-major] Chagas Cardiomyopathy / genetics. Lymphotoxin-alpha / genetics. Trypanosoma cruzi / growth & development
  • [MeSH-minor] Animals. Female. Gene Frequency / genetics. Genetic Predisposition to Disease. Genotype. Haplotypes / genetics. Humans. Male. Middle Aged. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / blood. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18190265.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha
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76. Ota T, Taketani S, Iwai S, Miyagawa S, Furuta M, Hara M, Uchimura E, Okita Y, Sawa Y: Novel method of decellularization of porcine valves using polyethylene glycol and gamma irradiation. Ann Thorac Surg; 2007 Apr;83(4):1501-7
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  • BACKGROUND: Recent tissue-engineered valves are in need of a breakthrough to overcome several limitations against clinical applications.
  • These were evaluated by histologic, biochemical (DNA, solubilized protein and collagen content), mechanical (strength test, transmission electron microscopy) and immunologic (porcine endogenous retrovirus and the alpha-1.3 galactosyl epitope) analyses.
  • The DNA sequence of a porcine endogenous retrovirus and the alpha-1.3 galactosyl epitope were eliminated after the decellularizing process.
  • [MeSH-major] Bioprosthesis. Gamma Rays. Heart Valve Diseases / surgery. Heart Valve Prosthesis Implantation / methods. Polyethylene Glycols / pharmacology. Tissue Engineering / methods
  • [MeSH-minor] Animals. Aortic Valve / cytology. Aortic Valve / radiation effects. Cell Movement / drug effects. Disease Models, Animal. Dogs. Microscopy, Electron, Transmission. Polymerase Chain Reaction. Prosthesis Design. Rats. Sensitivity and Specificity. Swine

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  • [CommentIn] Ann Thorac Surg. 2008 Jun;85(6):2163; author reply 2163-4 [18498860.001]
  • (PMID = 17383366.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 30IQX730WE / Polyethylene Glycols
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77. Boyer JF, Balard P, Authier H, Faucon B, Bernad J, Mazières B, Davignon JL, Cantagrel A, Pipy B, Constantin A: Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes. Arthritis Res Ther; 2007;9(2):R22
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  • [Title] Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes.
  • In chronic inflammatory diseases, such as rheumatoid arthritis, inflammation acts as an independent cardiovascular risk factor and the use of anti-inflammatory drugs, such as anti-tumor necrosis factor alpha (anti-TNFalpha), may decrease this risk.
  • Further studies are needed to investigate the clinical implications of these results in accelerated atherosclerosis observed in rheumatoid arthritis.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antibodies, Monoclonal / pharmacology. Antigens, CD36 / drug effects. Monocytes / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Adalimumab. Antibodies, Monoclonal, Humanized. Arthritis, Rheumatoid / complications. Arthritis, Rheumatoid / metabolism. Arthritis, Rheumatoid / physiopathology. Atherosclerosis / etiology. Atherosclerosis / metabolism. Atherosclerosis / physiopathology. Cells, Cultured. Electrophoretic Mobility Shift Assay. Flow Cytometry. Gene Expression / drug effects. Humans. Immunoglobulin Fab Fragments / pharmacology. PPAR gamma / metabolism. RNA, Messenger / drug effects. Reactive Oxygen Species / analysis. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17335569.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD36; 0 / Immunoglobulin Fab Fragments; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; FYS6T7F842 / Adalimumab
  • [Other-IDs] NLM/ PMC1906797
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78. Arrigo AP, Simon S, Gibert B, Kretz-Remy C, Nivon M, Czekalla A, Guillet D, Moulin M, Diaz-Latoud C, Vicart P: Hsp27 (HspB1) and alphaB-crystallin (HspB5) as therapeutic targets. FEBS Lett; 2007 Jul 31;581(19):3665-74
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  • This review summarizes the current knowledge about Hsp27 and alphaB-crystallin and the implications, either positive or deleterious, of these proteins in pathologies such as neurodegenerative diseases, myopathies, asthma, cataracts and cancers.
  • [MeSH-major] Heat-Shock Proteins / metabolism. Inflammation / drug therapy. Molecular Chaperones / metabolism. Neoplasm Proteins / metabolism. Neoplasms / drug therapy. alpha-Crystallin B Chain / metabolism

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  • (PMID = 17467701.001).
  • [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; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CRYAB protein, human; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / Neoplasm Proteins; 0 / alpha-Crystallin B Chain
  • [Number-of-references] 104
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79. Chen A, Liao WP, Lu Q, Wong WS, Wong PT: Upregulation of dihydropyrimidinase-related protein 2, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1 and tropomodulin 2 after focal cerebral ischemia in rats--a proteomics approach. Neurochem Int; 2007 Jun;50(7-8):1078-86
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  • [Title] Upregulation of dihydropyrimidinase-related protein 2, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1 and tropomodulin 2 after focal cerebral ischemia in rats--a proteomics approach.
  • In recent years, there are an increasing number of proteomics studies that investigated the alterations in the protein expression relevant to human diseases but none for stroke.
  • Two spots were identified as spectrin alpha II chain (rat fragment, also known as alpha-fodrin or non-erythroid alpha chain, SPNA-2); and one spot each for heat shock cognate protein 70 pseudogene 1 (HSC70-ps1, also known as heat shock protein 8 pseudogene 1), and tropomodulin 2 (Tmod2).
  • [MeSH-minor] Animals. Disease Models, Animal. Gene Expression Regulation, Enzymologic. Male. Pseudogenes. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17196711.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / collapsin response mediator protein-2; 12634-43-4 / Spectrin
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80. Stamatiou R, Paraskeva E, Boukas K, Gourgoulianis KI, Molyvdas PA, Hatziefthimiou AA: Azithromycin has an antiproliferative and autophagic effect on airway smooth muscle cells. Eur Respir J; 2009 Sep;34(3):721-30
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  • Azithromycin is used in long-term, low-dose treatment of airway diseases where airway wall remodelling is present.
  • Since it improves total score symptom and respiratory function of such patients, we hypothesise that azithromycin's additional clinical benefits are due to an inhibition of airway smooth muscle cell (SMC) proliferation.
  • Induction of autophagy was studied by indirect immmunofluorescence and/or Western blotting with antibodies against human smooth muscle alpha-actin, beclin 1, light chain 3 and caspase 3.

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  • (PMID = 19386688.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 83905-01-5 / Azithromycin
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81. Amaral AU, Leipnitz G, Fernandes CG, Seminotti B, Schuck PF, Wajner M: Alpha-ketoisocaproic acid and leucine provoke mitochondrial bioenergetic dysfunction in rat brain. Brain Res; 2010 Apr 9;1324:75-84
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  • [Title] Alpha-ketoisocaproic acid and leucine provoke mitochondrial bioenergetic dysfunction in rat brain.
  • Patients affected by maple syrup urine disease (MSUD) present severe neurological symptoms and brain abnormalities, whose pathophysiology is poorly known.
  • In the present study we investigated the in vitro effects of leucine (Leu), alpha-ketoisocaproic acid (KIC) and alpha-hydroxyisovaleric acid (HIV), respectively, the branched-chain amino, keto and hydroxy acids that most accumulate in MSUD, on brain bioenergetic homeostasis, evaluating respiratory parameters obtained by oxygen consumption, membrane potential (Psim), NAD(P)H content, swelling and citric acid cycle enzyme activities in mitochondrial preparations from rat forebrain using glutamate plus malate, succinate or alpha-ketoglutarate as respiratory substrates.
  • Furthermore, KIC and Leu, but not HIV, decreased state 3 using alpha-ketoglutarate.
  • A KIC-induced selective inhibition of alpha-ketoglutarate dehydrogenase activity was also verified, with no alteration of the other citric acid cycle activities.
  • The ADP/O ratio and the mitochondrial NAD(P)H levels were also reduced by KIC using glutamate/malate and alpha-ketoglutarate.
  • In addition, KIC caused a reduction in the Psim when alpha-ketoglutarate was the substrate.
  • The present data indicate that KIC acts as an uncoupler of oxidative phosphorylation and as a metabolic inhibitor possibly through its inhibitory effect on alpha-ketoglutarate dehydrogenase activity, while Leu acts as a metabolic inhibitor.
  • It is suggested that impairment of mitochondrial homeostasis caused by the major metabolites accumulating in MSUD may be involved in the neuropathology of this disease.
  • [MeSH-major] Brain / drug effects. Central Nervous System Agents / toxicity. Keto Acids / toxicity. Leucine / toxicity. Mitochondrial Diseases / chemically induced
  • [MeSH-minor] Animals. Electron Transport / drug effects. Homeostasis / drug effects. Ketoglutarate Dehydrogenase Complex / metabolism. Maple Syrup Urine Disease. Membrane Potential, Mitochondrial / drug effects. Mitochondrial Swelling / drug effects. NADP / metabolism. Oxygen Consumption / drug effects. Prosencephalon / drug effects. Prosencephalon / physiopathology. Rats. Rats, Wistar. Valerates / toxicity

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  • [Copyright] Copyright (c) 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20153737.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Central Nervous System Agents; 0 / Keto Acids; 0 / Valerates; 4026-18-0 / 2-hydroxyisovaleric acid; 53-59-8 / NADP; 816-66-0 / alpha-ketoisocaproic acid; EC 1.2.4.2 / Ketoglutarate Dehydrogenase Complex; GMW67QNF9C / Leucine
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82. Sardinha LR, Mosca T, Elias RM, do Nascimento RS, Gonçalves LA, Bucci DZ, Marinho CR, Penha-Gonçalves C, Lima MR, Alvarez JM: The liver plays a major role in clearance and destruction of blood trypomastigotes in Trypanosoma cruzi chronically infected mice. PLoS Negl Trop Dis; 2010;4(1):e578
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  • Intravenous challenge with Trypanosoma cruzi can be used to investigate the process and consequences of blood parasite clearance in experimental Chagas disease.
  • Following clearance, the number of infiltrating cells in the hepatic tissue notably increased: initially (at 24 h) as diffuse infiltrates affecting the whole parenchyma, and at 48 h, in the form of large focal infiltrates in both the parenchyma and perivascular spaces.
  • [MeSH-major] Chagas Disease / immunology. Chagas Disease / parasitology. Liver / immunology. Liver / parasitology. Trypanosoma cruzi / immunology
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Female. Immunohistochemistry. Interferon-gamma / metabolism. Interleukin-2 Receptor alpha Subunit / metabolism. Interleukin-2 Receptor beta Subunit / metabolism. Killer Cells, Natural / immunology. Mice. Mice, Inbred C57BL. Polymerase Chain Reaction

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  • (PMID = 20052269.001).
  • [ISSN] 1935-2735
  • [Journal-full-title] PLoS neglected tropical diseases
  • [ISO-abbreviation] PLoS Negl Trop Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2 Receptor alpha Subunit; 0 / Interleukin-2 Receptor beta Subunit; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2793026
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83. Villaverde J, Maqueda C, Undabeytia T, Morillo E: Effect of various cyclodextrins on photodegradation of a hydrophobic herbicide in aqueous suspensions of different soil colloidal components. Chemosphere; 2007 Sep;69(4):575-84
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  • The irradiation of NFL aqueous solutions in the presence of CDs showed that the higher the formation constant of NFL-CD complexes (Kc) and their solubility, the higher their photocatalytic effects, following the CDs in the order: RAMEB>HPBCD>beta-CD>alpha-CD>gamma-CD.

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  • (PMID = 17462707.001).
  • [ISSN] 0045-6535
  • [Journal-full-title] Chemosphere
  • [ISO-abbreviation] Chemosphere
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Colloids; 0 / Cyclodextrins; 0 / Environmental Pollutants; 0 / Herbicides; 0 / Pyridazines; 0 / Soil; 0 / Solutions; KES1HB07E4 / norflurazone
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84. Herndler-Brandstetter D, Veel E, Laschober GT, Pfister G, Brunner S, Walcher S, Parson W, Lepperdinger G, Grubeck-Loebenstein B: Non-regulatory CD8+CD45RO+CD25+ T-lymphocytes may compensate for the loss of antigen-inexperienced CD8+CD45RA+ T-cells in old age. Biol Chem; 2008 May;389(5):561-8
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  • The age-related decline in immune system functions is responsible for the increased prevalence of infectious diseases and the low efficacy of vaccination in elderly individuals.
  • [MeSH-major] Aged / physiology. Aging / immunology. Antigens, CD45 / immunology. CD8-Positive T-Lymphocytes / immunology. Interleukin-2 Receptor alpha Subunit / immunology
  • [MeSH-minor] Adult. Cell Differentiation / immunology. Cell Separation. Cells, Cultured. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Flow Cytometry. Gene Expression Regulation / immunology. Gene Expression Regulation / physiology. Genes, T-Cell Receptor / immunology. Humans. In Situ Hybridization. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Stimulation, Chemical. Telomere / ultrastructure

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  • (PMID = 18953723.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Interleukin-2 Receptor alpha Subunit; EC 3.1.3.48 / Antigens, CD45
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85. Watanabe N: [Tumor necrosis factor alpha (TNFalpha)]. Nihon Rinsho; 2005 Aug;63 Suppl 8:83-5
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  • [Title] [Tumor necrosis factor alpha (TNFalpha)].
  • [MeSH-major] Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Animals. Biomarkers / blood. Enzyme-Linked Immunosorbent Assay. Humans. Inflammation / diagnosis. Inflammation / etiology. Parasitic Diseases / diagnosis. Polymerase Chain Reaction / methods. Shock, Septic / diagnosis

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  • (PMID = 16149458.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 15
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86. Hao F, Pei XY, Zhang XL, Zhang SB, Lai XH, Wang HH: [Molecular cloning, expression, purification and properties of isocitrate lyase gene from Mycobacterium tuberculosis H37Rv]. Zhonghua Jie He He Hu Xi Za Zhi; 2005 Dec;28(12):845-8
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  • METHODS: The icl gene was amplified by polymerase chain reaction (PCR) from Mycobacterium tuberculosis H(37)Rv strain genomic DNA and cloned into pET28-a(+) vector.
  • The CD spectrum showed that the percentages for alpha- helix, beta- sheet, beta- turn, and random coil were 43.8%, 31.9%, 3.4%, and 20.9%, respectively.

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  • (PMID = 16409788.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Bacterial Proteins; EC 4.1.3.1 / Isocitrate Lyase
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87. Zaima N, Sugawara T, Goto D, Hirata T: Trans geometric isomers of EPA decrease LXRalpha-induced cellular triacylglycerol via suppression of SREBP-1c and PGC-1beta. J Lipid Res; 2006 Dec;47(12):2712-7
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  • Dietary mono- or di-trans fatty acids with chain lengths of 18-22 increase the risk of cardiovascular diseases because they increase LDL cholesterol and decrease HDL cholesterol in the plasma.
  • Dietary PUFAs, especially eicosapentaenoic acid (EPA) in marine oils, improve serum lipid profiles by suppressing liver X receptor alpha (LXRalpha) activity in the liver.

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  • (PMID = 17005995.001).
  • [ISSN] 0022-2275
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Orphan Nuclear Receptors; 0 / PPARGC1B protein, human; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Sterol Regulatory Element Binding Protein 1; 0 / Triglycerides; 0 / liver X receptor; AAN7QOV9EA / Eicosapentaenoic Acid
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88. Kokot A, Sindrilaru A, Schiller M, Sunderkötter C, Kerkhoff C, Eckes B, Scharffetter-Kochanek K, Luger TA, Böhm M: alpha-melanocyte-stimulating hormone suppresses bleomycin-induced collagen synthesis and reduces tissue fibrosis in a mouse model of scleroderma: melanocortin peptides as a novel treatment strategy for scleroderma? Arthritis Rheum; 2009 Feb;60(2):592-603
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  • [Title] alpha-melanocyte-stimulating hormone suppresses bleomycin-induced collagen synthesis and reduces tissue fibrosis in a mouse model of scleroderma: melanocortin peptides as a novel treatment strategy for scleroderma?
  • OBJECTIVE: Recently, we found that human dermal fibroblasts (HDFs) express melanocortin 1 receptors (MC-1R) that bind alpha-melanocyte-stimulating hormone (alpha-MSH).
  • In search of novel therapies for scleroderma (systemic sclerosis [SSc]), we used the bleomycin (BLM) model to investigate the effects of alpha-MSH on collagen synthesis and fibrosis.
  • METHODS: Collagen expression in HDFs was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses.
  • The effect of alpha-MSH in the BLM mouse model of scleroderma was assessed by histologic, immunohistochemical, real-time RT-PCR, and protein analyses.
  • RESULTS: Treatment with alpha-MSH (and related peptides) suppressed BLM-induced expression of type I and type III collagen in HDFs, and this effect was cAMP-dependent.
  • Neither BLM nor alpha-MSH altered Smad signaling, but antioxidants inhibited BLM-induced collagen expression in vitro.
  • In addition, alpha-MSH suppressed BLM-induced oxidative stress and enhanced the expression of superoxide dismutase 2 (SOD2) and heme oxygenase 1 (HO-1).
  • In the BLM mouse model, alpha-MSH reduced skin fibrosis and collagen content and increased tissue levels of SOD2 and HO-1.
  • CONCLUSION: Alpha-melanocyte-stimulating hormone and related peptides that exert their effects via MC-1R may provide a novel antifibrogenic therapeutic tool for the treatment of fibrotic diseases such as scleroderma.
  • [MeSH-major] Collagen / drug effects. Fibrosis / drug therapy. Hormones / pharmacology. Receptors, Melanocortin / drug effects. Scleroderma, Systemic / drug therapy. alpha-MSH / pharmacology
  • [MeSH-minor] Adult. Aged. Animals. Antibiotics, Antineoplastic / toxicity. Antioxidants / pharmacology. Bleomycin / toxicity. Dermis / drug effects. Dermis / metabolism. Dermis / pathology. Disease Models, Animal. Drug Antagonism. Fibroblasts / drug effects. Fibroblasts / metabolism. Gene Expression / drug effects. Heme Oxygenase-1 / genetics. Heme Oxygenase-1 / metabolism. Humans. Infant, Newborn. Male. Mice. Middle Aged. Oxidative Stress / drug effects. Pro-Opiomelanocortin / genetics. Pro-Opiomelanocortin / metabolism. RNA, Messenger / metabolism. Signal Transduction / drug effects. Superoxide Dismutase / genetics. Superoxide Dismutase / metabolism. Young Adult

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  • (PMID = 19180474.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antioxidants; 0 / Hormones; 0 / RNA, Messenger; 0 / Receptors, Melanocortin; 11056-06-7 / Bleomycin; 581-05-5 / alpha-MSH; 66796-54-1 / Pro-Opiomelanocortin; 9007-34-5 / Collagen; EC 1.14.99.3 / Heme Oxygenase-1; EC 1.15.1.1 / Superoxide Dismutase
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89. Díez-Marqués ML, Ruiz-Torres MP, Griera M, López-Ongil S, Saura M, Rodríguez-Puyol D, Rodríguez-Puyol M: Arg-Gly-Asp (RGD)-containing peptides increase soluble guanylate cyclase in contractile cells. Cardiovasc Res; 2006 Feb 1;69(2):359-69
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  • RGDS effects on sGC regulation were due to the specific interaction with alpha(5)beta(1) integrin.
  • Elucidation of this novel mechanism provides a rationale for future pharmacotherapy in certain vascular diseases.
  • [MeSH-minor] Aorta. Cells, Cultured. Enzyme Activation. Gene Expression. Humans. Mesangial Cells. Mitogen-Activated Protein Kinase 8 / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Cardiovasc Res. 2006 Feb 1;69(2):302-3 [16412404.001]
  • (PMID = 16360131.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Oligopeptides; 99896-85-2 / arginyl-glycyl-aspartic acid; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 8; EC 4.6.1.2 / Guanylate Cyclase
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90. Sun YY, Wang CY, Hsu MF, Juan SH, Chang CY, Chou CM, Yang LY, Hung KS, Xu J, Lee YH, Hsu CY: Glucocorticoid protection of oligodendrocytes against excitotoxin involving hypoxia-inducible factor-1alpha in a cell-type-specific manner. J Neurosci; 2010 Jul 14;30(28):9621-30
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  • [Title] Glucocorticoid protection of oligodendrocytes against excitotoxin involving hypoxia-inducible factor-1alpha in a cell-type-specific manner.
  • Glucocorticoids are commonly used in treating diseases with white matter lesions, including demyelinating diseases and spinal cord injury (SCI).
  • We report here a novel mechanism of methylprednisolone (MP), a synthetic glucocorticoid widely used for treating multiple sclerosis and SCI, in protecting oligodendrocytes (OLGs) against AMPA-induced excitotoxicity, which has been implicated in the white matter injuries and diseases.
  • MP transactivation of Epo expression involves dual transcription factors: glucocorticoid receptor (GR) and hypoxia-inducible factor-1alpha (HIF-1alpha).
  • Coimmunoprecipitation, chromatin immunoprecipitation analysis, yeast two-hybrid analysis, and structure modeling of three-dimensional protein-protein interactions confirm that MP induces interaction between GR DNA binding domain and HIF-1alpha PAS domain, with subsequent recruitment of HIF-1beta to transactivate Epo expression in OLGs.
  • In contrast, MP activates GR but does not induce GR-HIF-1alpha interaction, HIF-1alpha binding to Epo enhancer/promoter, or Epo expression in cultured cortical neurons.
  • The OLG-specific GR-HIF-1alpha transactivation of Epo provides novel insights into the development of more effective therapies for diseases affecting the white matter.
  • [MeSH-major] Cell Death / drug effects. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Methylprednisolone / pharmacology. Oligodendroglia / drug effects. alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / toxicity
  • [MeSH-minor] Analysis of Variance. Animals. Cells, Cultured. Chromatin Immunoprecipitation. Computer Simulation. Erythropoietin / genetics. Erythropoietin / metabolism. Immunoprecipitation. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20631191.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 11096-26-7 / Erythropoietin; 77521-29-0 / alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; X4W7ZR7023 / Methylprednisolone
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91. Qian J, Cuerrier D, Davies PL, Li Z, Powers JC, Campbell RL: Cocrystal structures of primed side-extending alpha-ketoamide inhibitors reveal novel calpain-inhibitor aromatic interactions. J Med Chem; 2008 Sep 11;51(17):5264-70
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  • [Title] Cocrystal structures of primed side-extending alpha-ketoamide inhibitors reveal novel calpain-inhibitor aromatic interactions.
  • When Ca(2+) homeostasis is disrupted, calpain overactivation causes unregulated proteolysis, which can contribute to diseases such as postischemic injury and cataract formation.
  • Here, we present crystal structures of rat calpain 1 protease core (muI-II) bound to two alpha-ketoamide-based calpain inhibitors containing adenyl and piperazyl primed-side extensions.
  • An unexpected aromatic-stacking interaction is observed between the primed-side adenine moiety and the Trp298 side chain.

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  • (PMID = 18702462.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS053801-02; United States / NINDS NIH HHS / NS / R21 NS053801; United States / NINDS NIH HHS / NS / R21 NS053801-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Aromatic; 0 / Carbamates; 0 / Dipeptides; 0 / Glycoproteins; 0 / calpain inhibitors; EC 3.4.22.- / Calpain
  • [Other-IDs] NLM/ NIHMS86262; NLM/ PMC2631982
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92. Bauman DR, Steckelbroeck S, Williams MV, Peehl DM, Penning TM: Identification of the major oxidative 3alpha-hydroxysteroid dehydrogenase in human prostate that converts 5alpha-androstane-3alpha,17beta-diol to 5alpha-dihydrotestosterone: a potential therapeutic target for androgen-dependent disease. Mol Endocrinol; 2006 Feb;20(2):444-58
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  • [Title] Identification of the major oxidative 3alpha-hydroxysteroid dehydrogenase in human prostate that converts 5alpha-androstane-3alpha,17beta-diol to 5alpha-dihydrotestosterone: a potential therapeutic target for androgen-dependent disease.
  • Androgen-dependent prostate diseases initially require 5alpha-dihydrotestosterone (DHT) for growth.
  • Candidate enzymes that posses 3alpha-HSD activity are type 3 3alpha-HSD (AKR1C2), 11-cis retinol dehydrogenase (RODH 5), L-3-hydroxyacyl coenzyme A dehydrogenase , RODH like 3alpha-HSD (RL-HSD), novel type of human microsomal 3alpha-HSD, and retinol dehydrogenase 4 (RODH 4).
  • The data show that the major oxidative 3alpha-HSD in normal human prostate is RL-HSD and may be a new therapeutic target for treating prostate diseases.
  • [MeSH-major] 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) / metabolism. Androgens / metabolism. Androstane-3,17-diol / metabolism. Dihydrotestosterone / metabolism. Prostate / enzymology. Prostatic Diseases / enzymology

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  • (PMID = 16179381.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R25-CA-10187-D1; United States / NCI NIH HHS / CA / R01 CA-90744
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone; 25126-76-5 / Androstane-3,17-diol; EC 1.1.1.50 / 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific); EC 1.3.1.- / short chain trans-2-enoyl-CoA reductase; EC 1.6.- / NADH, NADPH Oxidoreductases; EC 2.3.1.85 / Fatty Acid Synthases
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93. Wilkins T, Malcolm JK, Raina D, Schade RR: Hepatitis C: diagnosis and treatment. Am Fam Physician; 2010 Jun 1;81(11):1351-7
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  • [Title] Hepatitis C: diagnosis and treatment.
  • Testing for hepatitis C is recommended for at-risk populations, and confirmatory testing includes quantification of virus by polymerase chain reaction. The U.S.
  • The American Association for the Study of Liver Diseases recommends ultrasound surveillance for hepatocellular carcinoma in persons with chronic hepatitis C virus infection and cirrhosis.
  • [MeSH-major] Hepatitis C / diagnosis
  • [MeSH-minor] Adult. Antiviral Agents / adverse effects. Antiviral Agents / therapeutic use. Female. Hepacivirus / drug effects. Hepacivirus / genetics. Humans. Interferon-alpha / adverse effects. Interferon-alpha / therapeutic use. Male. Middle Aged. Polyethylene Glycols / adverse effects. Polyethylene Glycols / therapeutic use. Recombinant Proteins. Ribavirin / adverse effects. Ribavirin / therapeutic use. Viral Load

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  • [CommentIn] Am Fam Physician. 2011 Mar 15;83(6):647; author reply 648 [21404974.001]
  • [CommentIn] Am Fam Physician. 2010 Jun 1;81(11):1359-60 [20527364.001]
  • (PMID = 20521755.001).
  • [ISSN] 1532-0650
  • [Journal-full-title] American family physician
  • [ISO-abbreviation] Am Fam Physician
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2a; 30IQX730WE / Polyethylene Glycols; 49717AWG6K / Ribavirin; 76543-88-9 / interferon alfa-2a
  • [Number-of-references] 45
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94. Schaefermeier PK, Cabeza N, Besser JC, Lohse P, Daebritz SH, Schmitz C, Reichart B, Sodian R: Potential cell sources for tissue engineering of heart valves in comparison with human pulmonary valve cells. ASAIO J; 2009 Jan-Feb;55(1):86-92
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  • We assessed the extent to which the endothelial cells from the inspected sources in vitro resemble endothelial cells of human pulmonary heart valves, and we found that myofibroblast cells, respective of their source, in vitro differ from the interstitial cells from human pulmonary heart valves regarding collagen and smooth muscle alpha-actin.
  • [MeSH-minor] Biomarkers / analysis. Gene Expression. Heart Valve Diseases / therapy. Humans. Immunohistochemistry. Immunophenotyping. Reverse Transcriptase Polymerase Chain Reaction. Saphenous Vein / cytology. Umbilical Veins / cytology

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  • (PMID = 19092668.001).
  • [ISSN] 1538-943X
  • [Journal-full-title] ASAIO journal (American Society for Artificial Internal Organs : 1992)
  • [ISO-abbreviation] ASAIO J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
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95. Siciliano G, Volpi L, Piazza S, Ricci G, Mancuso M, Murri L: Functional diagnostics in mitochondrial diseases. Biosci Rep; 2007 Jun;27(1-3):53-67
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  • [Title] Functional diagnostics in mitochondrial diseases.
  • Mitochondrial diseases (MD) with respiratory chain defects are caused by genetic mutations that determine an impairment of the electron transport chain functioning.
  • Diagnosis often requires a complex approach with measurements of serum lactate, magnetic resonance spectroscopy (MRS), muscle histology and ultrastructure, enzymology, genetic analysis, and exercise testing.
  • Exercise intolerance is a common symptom of MD, due to increased dependence of skeletal muscle on anaerobic metabolism, with an excess lactate generation, phosphocreatine depletion, enhanced free radical production, reduced oxygen extraction and electron flux through the respiratory chain.
  • MD treatment has included antioxidants (vitamin E, alpha lipoic acid), coenzyme Q10, riboflavin, creatine monohydrate, dichloroacetate and exercise training.
  • Exercise is a particularly important tool in diagnosis as well as in the management of these diseases.
  • [MeSH-major] DNA, Mitochondrial / genetics. Mitochondrial Diseases / diagnosis
  • [MeSH-minor] DNA Mutational Analysis / methods. Exercise Test. Humans. Mitochondrial Myopathies / diagnosis. Mitochondrial Myopathies / genetics. Mitochondrial Myopathies / physiopathology. Muscle Fatigue / physiology. Mutation

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  • (PMID = 17492503.001).
  • [ISSN] 0144-8463
  • [Journal-full-title] Bioscience reports
  • [ISO-abbreviation] Biosci. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Mitochondrial
  • [Number-of-references] 92
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96. Chung H, Nettleton JA, Lemaitre RN, Barr RG, Tsai MY, Tracy RP, Siscovick DS: Frequency and type of seafood consumed influence plasma (n-3) fatty acid concentrations. J Nutr; 2008 Dec;138(12):2422-7
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  • [Title] Frequency and type of seafood consumed influence plasma (n-3) fatty acid concentrations.
  • Few studies have adequately considered the type of seafood and background dietary factors when evaluating diet-biomarker and diet-disease associations.
  • The objective of this paper is to evaluate the relationship between different seafood meals and long-chain (n-3) fatty acids [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] biomarkers in the Multi-Ethnic Study of Atherosclerosis (MESA) with white, Chinese-American, black, and Hispanic participants.
  • The magnitude of this correlation was attenuated by up to 67% when type of seafood was not taken into account.
  • The association of nonfried fish consumption was not modified by intake of (n-6) PUFA or alpha-linolenic acid.
  • This study highlights the importance of cooking methods (nonfried vs. fried fish), types of seafood (fish vs. shellfish), and the overall seafood consumption when assessing health effects of long-chain (n-3) fatty acids of seafood consumption.

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  • (PMID = 19022967.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HC / N01 HC095159; United States / NHLBI NIH HHS / HC / N01-HC-95159; United States / NHLBI NIH HHS / HC / N01-HC-95165; United States / NHLBI NIH HHS / HC / N01-HC-95169
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Omega-3
  • [Other-IDs] NLM/ PMC3970314
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97. Zhou Z, Kang X, Jiang Y, Song Z, Feng W, McClain CJ, Kang YJ: Preservation of hepatocyte nuclear factor-4alpha is associated with zinc protection against TNF-alpha hepatotoxicity in mice. Exp Biol Med (Maywood); 2007 May;232(5):622-8
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  • [Title] Preservation of hepatocyte nuclear factor-4alpha is associated with zinc protection against TNF-alpha hepatotoxicity in mice.
  • The present study was undertaken to determine the role of HNF-4alpha in zinc protection against tumor necrosis factor-alpha (TNF-alpha) hepatotoxicity.
  • Mice were treated with murine TNF-alpha via intravenous injection at 20 mug/kg body wt 30 mins after d-galactosamine (d-Gal) sensitization (800 mg/kg body wt).
  • Two doses of zinc sulfate (5 mg elemental zinc/kg body wt) were administered at 36 and 12 hrs before TNF-alpha treatment via subcutaneous injection.
  • TNF-alpha treatment after sensitization induced liver injury as detected by plasma alanine aminotransferase activity and apoptotic cell death in the liver.
  • Zinc pretreatment attenuated TNF-alpha-induced liver injury.
  • Furthermore, TNF-alpha-induced activations of caspase 3 and caspase 8 in the liver were significantly inhibited by zinc pretreatment.
  • The mRNA and protein levels of HNF-4alpha in the liver were remarkably decreased by TNF-alpha treatment, which was suppressed by zinc.
  • To determine if HNF-4alpha depletion is involved in d-Gal sensitization to TNF-alpha toxicity, mice were administered either d-Gal or TNF-alpha.
  • Immunohistochemistry demonstrated that HNF-4alpha depletion in the liver is associated with d-Gal sensitization but not TNF-alpha treatment.
  • To define the link between HNF-4alpha depletion and TNF-alpha-induced cell death, the effect of silencing the HNF-4alpha gene by siRNA transfection on TNF-alpha cytotoxicity was determined in HepG2 cells.
  • A lactate dehydrogenase cytotoxicity assay showed that neither TNF-alpha nor HNF-4alpha siRNA transfection had a toxic effect, but TNF-alpha treatment after HNF-4alpha siRNA transfection caused HepG2 cell death.
  • These results suggest that zinc protects against TNF-alpha hepatotoxicity, at least partially, through preservation of the zinc finger protein HNF-4alpha.
  • [MeSH-major] Hepatocyte Nuclear Factor 4 / metabolism. Liver / drug effects. Tumor Necrosis Factor-alpha / toxicity. Zinc / pharmacology
  • [MeSH-minor] Alanine Transaminase / metabolism. Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3 / metabolism. Caspase 8 / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Drug-Induced Liver Injury. Humans. Immunohistochemistry. Injections, Intravenous. Injections, Subcutaneous. Liver Diseases / prevention & control. Mice. Mice, Inbred Strains. Protective Agents / pharmacology. RNA Interference. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Zinc Sulfate / administration & dosage. Zinc Sulfate / pharmacology

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  • (PMID = 17463158.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 4; 0 / Protective Agents; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 7733-02-0 / Zinc Sulfate; EC 2.6.1.2 / Alanine Transaminase; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; J41CSQ7QDS / Zinc
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98. Clément N, Glorian M, Raymondjean M, Andréani M, Limon I: PGE2 amplifies the effects of IL-1beta on vascular smooth muscle cell de-differentiation: a consequence of the versatility of PGE2 receptors 3 due to the emerging expression of adenylyl cyclase 8. J Cell Physiol; 2006 Sep;208(3):495-505
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PGE2 amplifies the effects of IL-1beta on vascular smooth muscle cell de-differentiation: a consequence of the versatility of PGE2 receptors 3 due to the emerging expression of adenylyl cyclase 8.
  • In most inflammatory diseases, cell activation induced by these compounds leads to a massive production of type E2 prostaglandin (PGE2) which often takes over and even potentiates the pro-inflammatory cytokine-related effects.
  • To address this issue, we took advantage of vascular smooth muscle cells in primary culture and tracked two markers: PLA2 secretion and alpha-actin filament disorganization.
  • Whereas on contractile cells, stimulated subtypes 3 inhibit type 4-dependent PLA2 secretion, this negative regulation is switched to positive on IL-1beta-treated cells.
  • Using real time PCR, pharmacological tools and small interfering RNA (siRNA), we demonstrated that the different integration of PGE2 signals depends on the upregulation of calcium/calmodulin stimulable adenylyl cyclase 8.
  • [MeSH-minor] Animals. Aorta, Thoracic. Cells, Cultured. Cyclic AMP / metabolism. Drug Synergism. Gene Expression Regulation, Enzymologic / drug effects. Male. Phospholipases A2. RNA, Small Interfering / genetics. Rats. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / drug effects. Vasoconstriction / drug effects

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 16741924.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / RNA, Small Interfering; 0 / Receptors, Prostaglandin E; E0399OZS9N / Cyclic AMP; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Phospholipases A2; EC 4.6.1.1 / Adenylyl Cyclases; EC 4.6.1.1 / adenylyl cyclase 8; K7Q1JQR04M / Dinoprostone
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99. Hosaka Y, Kirisawa R, Ueda H, Yamaguchi M, Takehana K: Differences in tumor necrosis factor (TNF)alpha and TNF receptor-1-mediated intracellular signaling factors in normal, inflamed and scar-formed horse tendons. J Vet Med Sci; 2005 Oct;67(10):985-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in tumor necrosis factor (TNF)alpha and TNF receptor-1-mediated intracellular signaling factors in normal, inflamed and scar-formed horse tendons.
  • To detect these signaling factors, samples were subjected to immunohistochemistry and Western blot analysis, and some samples were also subjected to reverse transcription-polymerase chain reaction (RT-PCR), PCR-Southern blot analysis and in situ hybridization to detect the expression of TNFalpha mRNA.
  • In the normal tendon, large amounts of TRAF2 were found in tendinocytes, but the amounts of TNF-R1 were small.

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  • (PMID = 16276053.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / TNF Receptor-Associated Factor 2; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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100. Carmans S, Hendriks JJ, Thewissen K, Van den Eynden J, Stinissen P, Rigo JM, Hellings N: The inhibitory neurotransmitter glycine modulates macrophage activity by activation of neutral amino acid transporters. J Neurosci Res; 2010 Aug 15;88(11):2420-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We demonstrate that glycine does not affect the production of reactive oxygen species but stimulates myelin phagocytosis and the production of the proinflammatory mediators nitric oxide (NO) and tumor necrosis factor (TNF)-alpha by rat macrophages.
  • In contrast, 2-aminoisobutyric acid, a substrate of neutral amino acid transporters (NAATs), inhibits the glycine-mediated enhancement of myelin phagocytosis as well as of NO and TNF-alpha production.
  • Glycine may thereby influence immunological processes in inflammatory diseases involving macrophage activation and demyelination, including MS and related conditions associated with altered glycine levels.
  • [MeSH-minor] Animals. Biotransformation / drug effects. Cell Proliferation / drug effects. Cell Survival. Dose-Response Relationship, Drug. Fluorescent Antibody Technique. Glycine Agents / pharmacology. Inflammation / pathology. Male. Multiple Sclerosis / metabolism. Myelin Sheath / physiology. Nitric Oxide / biosynthesis. Phagocytosis / drug effects. Rats. Rats, Wistar. Reactive Oxygen Species / metabolism. Receptors, Glycine / biosynthesis. Receptors, Glycine / genetics. Reverse Transcriptase Polymerase Chain Reaction. Strychnine / pharmacology. Tumor Necrosis Factor-alpha / biosynthesis

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20623529.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acid Transport Systems, Neutral; 0 / Glycine Agents; 0 / Neurotransmitter Agents; 0 / Reactive Oxygen Species; 0 / Receptors, Glycine; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; H9Y79VD43J / Strychnine; TE7660XO1C / Glycine
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