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1. Anwari K, Poggio S, Perry A, Gatsos X, Ramarathinam SH, Williamson NA, Noinaj N, Buchanan S, Gabriel K, Purcell AW, Jacobs-Wagner C, Lithgow T: A modular BAM complex in the outer membrane of the alpha-proteobacterium Caulobacter crescentus. PLoS One; 2010 Jan 08;5(1):e8619
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  • [Title] A modular BAM complex in the outer membrane of the alpha-proteobacterium Caulobacter crescentus.
  • Mitochondria are organelles derived from an intracellular alpha-proteobacterium.
  • Caulobacter crescentus is an alpha-proteobacterium, and the BAM (beta-barrel assembly machinery) complex was purified and characterized from this model organism.

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  • (PMID = 20062535.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM076698; United States / NIGMS NIH HHS / GM / GM065835; United States / Intramural NIH HHS / / ; United States / NIGMS NIH HHS / GM / R01 GM065835; United States / NIGMS NIH HHS / GM / GM076698
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Outer Membrane Proteins; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2797634
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2. Alves C, Toralles MB, Carvalho GC: HLA class II polymorphism in patients with type 1 diabetes mellitus from a Brazilian racially admixtured population. Ethn Dis; 2009;19(4):420-4
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  • [Title] HLA class II polymorphism in patients with type 1 diabetes mellitus from a Brazilian racially admixtured population.
  • BACKGROUND: Several studies have demonstrated a fundamental role for the histocompatibility antigens (ie, human leukocyte antigens or HLA) in the susceptibility of, or protection to, type 1 diabetes mellitus (T1DM).
  • The HLA genotyping was performed by a polymerase chain reaction hybridization assay.
  • The T1DM's susceptibility was associated with an increased frequency of the HLA of risk (-DRB1*0401, -DRB1*0402, DQA1*03, -DQA1*05, -DQB1*02 e -DQB1*0302); and a small frequency of protective alleles (-DRB1*0404, -DRB1*0407, -DQA1*0201, -DQB1*0602, -DQB*0603 e -DQB1*0604) in all subjects.
  • [MeSH-major] Diabetes Mellitus, Type 1 / ethnology. Diabetes Mellitus, Type 1 / genetics. Genetic Predisposition to Disease / ethnology. Genetic Predisposition to Disease / genetics. HLA-D Antigens / genetics
  • [MeSH-minor] Adolescent. Adult. Brazil / epidemiology. Child. Child, Preschool. Cross-Sectional Studies. Female. Genotype. HLA-DQ Antigens / genetics. HLA-DQ alpha-Chains. HLA-DQ beta-Chains. HLA-DR Antigens / genetics. HLA-DRB1 Chains. Humans. Infant. Male. Young Adult

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  • (PMID = 20073143.001).
  • [ISSN] 1049-510X
  • [Journal-full-title] Ethnicity & disease
  • [ISO-abbreviation] Ethn Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-D Antigens; 0 / HLA-DQ Antigens; 0 / HLA-DQ alpha-Chains; 0 / HLA-DQ beta-Chains; 0 / HLA-DQA1 antigen; 0 / HLA-DQB1 antigen; 0 / HLA-DR Antigens; 0 / HLA-DRB1 Chains; 0 / HLA-DRB1*04:01 antigen; 0 / HLA-DRB1*04:02 antigen
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3. Franceschi DS, Mazini PS, Rudnick CC, Sell AM, Tsuneto LT, Ribas ML, Peixoto PR, Visentainer JE: Influence of TNF and IL10 gene polymorphisms in the immunopathogenesis of leprosy in the south of Brazil. Int J Infect Dis; 2009 Jul;13(4):493-8
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  • METHODS: Genotyping using polymerase chain reaction with sequence-specific primers (PCR-SSP) was performed for: TNF(-308/-238), IL2(-330/+166), IL6(-174), IFNG(+874), TGFB1(+869/+915), and IL10(-592/-819/-1082) in 240 healthy controls and 167 patients with leprosy.
  • [MeSH-major] Interleukin-10 / genetics. Leprosy / genetics. Polymorphism, Genetic. Polymorphism, Single Nucleotide. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Brazil / epidemiology. Ethnic Groups. Female. Gene Frequency. Genotype. Humans. Male. Polymerase Chain Reaction. Reference Values

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  • (PMID = 19058987.001).
  • [ISSN] 1878-3511
  • [Journal-full-title] International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
  • [ISO-abbreviation] Int. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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4. Lee JM, Libermann TA, Cho JY: The synergistic regulatory effect of Runx2 and MEF transcription factors on osteoblast differentiation markers. J Periodontal Implant Sci; 2010 Feb;40(1):39-44
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  • PURPOSE: Bone tissues for clinical application can be improved by studies on osteoblast differentiation.
  • Reverse-transcription polymerase chain reaction was also done to check the mRNA levels of Opn after Runx2 and MEF transfection into rat osteoblast (ROS) cells.

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  • (PMID = 20498758.001).
  • [ISSN] 2093-2286
  • [Journal-full-title] Journal of periodontal & implant science
  • [ISO-abbreviation] J Periodontal Implant Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2872803
  • [Keywords] NOTNLM ; Cell differentiation / Core binding factor alpha 1 subunit / Osteoblasts
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5. Gan W, Zhao G, Xu H, Wu W, Du W, Huang J, Yu X, Hu X: Reverse vaccinology approach identify an Echinococcus granulosus tegumental membrane protein enolase as vaccine candidate. Parasitol Res; 2010 Mar;106(4):873-82
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  • Primers are designed according to the 5' end and 3'end of the putative encoding sequence to amplify the genomic DNA of E. granulosus strain isolated from sheep in Qinghai province of China by polymerase chain reaction (PCR).
  • SWISS-MODEL modulated its 3D structure as a barrel which constitutes of alternatively arranged alpha helix-beta sheet, with the key sites such as substrate binding region, active sites, Mg(2+)-binding sites closely located at the center.

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  • (PMID = 20127115.001).
  • [ISSN] 1432-1955
  • [Journal-full-title] Parasitology research
  • [ISO-abbreviation] Parasitol. Res.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ GU080332
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Helminth; 0 / DNA, Helminth; 0 / Epitopes, B-Lymphocyte; 0 / Epitopes, T-Lymphocyte; 0 / Helminth Proteins; 0 / Membrane Proteins; 0 / Nuclear Localization Signals; EC 4.2.1.11 / Phosphopyruvate Hydratase
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6. Xu D, Jiang HR, Kewin P, Li Y, Mu R, Fraser AR, Pitman N, Kurowska-Stolarska M, McKenzie AN, McInnes IB, Liew FY: IL-33 exacerbates antigen-induced arthritis by activating mast cells. Proc Natl Acad Sci U S A; 2008 Aug 05;105(31):10913-8
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  • IL-33, a cytokine of the IL-1 family, is closely associated with type II T cell responses.
  • Mice lacking ST2, the IL-33 receptor alpha-chain, developed attenuated collagen-induced arthritis (CIA) and reduced ex vivo collagen-specific induction of proinflammatory cytokines (IL-17, TNFalpha, and IFNgamma), and antibody production.
  • Conversely, treatment of wild-type (WT) but not ST2(-/-) mice with IL-33 exacerbated CIA and elevated production of both proinflammatory cytokines and anti-collagen antibodies.
  • Disease exacerbation was accompanied by elevated expression levels of proinflammatory cytokines.
  • Our results demonstrate that IL-33 is a critical proinflammatory cytokine for inflammatory joint disease that integrates fibroblast activation with downstream immune activation mainly via an IL-33-driven, mast-cell-dependent pathway.

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  • (PMID = 18667700.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G9818261; United Kingdom / Medical Research Council / / G84/6704; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MC/ U105178805; United Kingdom / Medical Research Council / / G0801198; United Kingdom / Wellcome Trust / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Il1rl1 protein, mouse; 0 / Il33 protein, mouse; 0 / Interleukin-1 Receptor-Like 1 Protein; 0 / Interleukin-33; 0 / Interleukins; 0 / Membrane Proteins; 0 / Receptors, Interleukin
  • [Other-IDs] NLM/ PMC2491487
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7. Hernández-Pascacio J, Garza C, Banquy X, Díaz-Vergara N, Amigo A, Ramos S, Castillo R, Costas M, Piñeiro A: Cyclodextrin-based self-assembled nanotubes at the water/air interface. J Phys Chem B; 2007 Nov 8;111(44):12625-30
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  • Native alpha-cyclodextrin (alpha-CD) is found to spontaneously form films at aqueous solution/air interfaces.
  • By using isothermal titration calorimetry (ITC), Brewster angle microscopy (BAM), atomic force microscopy (AFM), and molecular dynamics (MD) simulations, it is shown that the films consist of self-assembled nanotubes whose building blocks are cyclodextrin dimers (alpha-CD2) and alpha-CD2-SDS1 complexes.

  • Hazardous Substances Data Bank. SODIUM LAURYL SULFATE .
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  • (PMID = 17941668.001).
  • [ISSN] 1520-6106
  • [Journal-full-title] The journal of physical chemistry. B
  • [ISO-abbreviation] J Phys Chem B
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Solutions; 059QF0KO0R / Water; 368GB5141J / Sodium Dodecyl Sulfate
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8. Bryan DL, Hart P, Forsyth K, Gibson R: Modulation of respiratory syncytial virus-induced prostaglandin E2 production by n-3 long-chain polyunsaturated fatty acids in human respiratory epithelium. Lipids; 2005 Oct;40(10):1007-11
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  • [Title] Modulation of respiratory syncytial virus-induced prostaglandin E2 production by n-3 long-chain polyunsaturated fatty acids in human respiratory epithelium.
  • We investigated the production of inflammatory mediators [prostaglandin E2 (PGE2), interleukin (IL)-1beta, tumor necrosis factor alpha] and chemokines [IL-8, RANTES (regulation on activation, normal T cell expressed and secreted)] by alveolar epithelial cells in response to RSV infection.
  • By altering cell membrane FA through incorporation of the long-chain PUFA (LCPUFA) arachidonic acid, EPA, and DHA, we were subsequently able to significantly modulate PGE2 production by the infected epithelium.
  • Because of the dynamic nature of the effects of PGE2 on lung function, regulation of this prostaglandin during RSV infection by n-3 LCPUFA has the potential to significantly alter the disease process.

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  • (PMID = 16382572.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chemokine CCL5; 0 / Fatty Acids, Omega-3; 0 / Interleukin-8; 0 / Phospholipids; 25167-62-8 / Docosahexaenoic Acids; 27YG812J1I / Arachidonic Acid; AAN7QOV9EA / Eicosapentaenoic Acid; K7Q1JQR04M / Dinoprostone
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9. Gonçales FL Jr, Moma CA, Vigani AG, Angerami AF, Gonçales ES, Tozzo R, Pavan MH, Gonçales NS: Retreatment of hepatitis C patients with pegylated interferon combined with ribavirin in non-responders to interferon plus ribavirin. Is it different in real life? BMC Infect Dis; 2010;10:212
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  • The aim of this study was to evaluate the efficacy of retreatment with Peg-Interferon alpha-2b (PEG-IFN alpha-2b) plus RBV, in patients with HCV, genotypes 1 or 3, who were non-responders to the previous standard treatment with IFN/RBV.
  • Of these 130 agreed to be retreated with PEG-IFN alpha-2b and participated in this evaluation (90 with genotype 1 HCV and 40 with genotype 3 HCV).
  • They received subcutaneous PEG-IFN alpha-2b, 1.5 microg, once weekly, associated with RBV, through the oral route, with doses determined according to weight (1,000 mg if weight <or= 75 kg and 1,250 mg if > 75 kg).
  • HCV-RNA was tested by polymerase chain reaction (PCR) at baseline, at week 12, at the end of the treatment, and 6 months thereafter.
  • CONCLUSIONS: PEG-IFN alpha-2b plus weight-based ribavirin is effective in re-treating previous interferon-alpha plus RBV failure; 22.2% of the patients with genotype 1 HCV and 40% of patients with genotype 3 HCV achieved SVR.
  • [MeSH-major] Antiviral Agents / administration & dosage. Hepatitis C, Chronic / drug therapy. Interferon-alpha / administration & dosage. Interferons / administration & dosage. Polyethylene Glycols / administration & dosage. Ribavirin / administration & dosage

  • Genetic Alliance. consumer health - Hepatitis.
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  • (PMID = 20646277.001).
  • [ISSN] 1471-2334
  • [Journal-full-title] BMC infectious diseases
  • [ISO-abbreviation] BMC Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / RNA, Viral; 0 / Recombinant Proteins; 0 / peginterferon alfa-2b; 30IQX730WE / Polyethylene Glycols; 49717AWG6K / Ribavirin; 9008-11-1 / Interferons; 99210-65-8 / interferon alfa-2b
  • [Other-IDs] NLM/ PMC2912909
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10. Watanabe T, Tsuge H, Imagawa T, Kise D, Hirano K, Beppu M, Takahashi A, Yamaguchi K, Fujiki H, Suganuma M: Nucleolin as cell surface receptor for tumor necrosis factor-alpha inducing protein: a carcinogenic factor of Helicobacter pylori. J Cancer Res Clin Oncol; 2010 Jun;136(6):911-21
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  • [Title] Nucleolin as cell surface receptor for tumor necrosis factor-alpha inducing protein: a carcinogenic factor of Helicobacter pylori.
  • PURPOSE: Tumor necrosis factor-alpha inducing protein (Tipalpha) is a unique carcinogenic factor released from Helicobacter pylori (H. pylori).
  • Tipalpha specifically binds to cells and is incorporated into cytosol and nucleus, where it strongly induces expression of TNF-alpha and chemokine genes mediated through NF-kappaB activation, resulting in tumor development.
  • Incorporation of Tipalpha into the cells was determined by Western blotting and expression of TNF-alpha gene was quantified by RT-PCR.
  • RESULTS: Nucleolin was co-precipitated with Tipalpha-FLAG, but not with del-Tipalpha-FLAG (an inactive mutant).
  • In addition, pretreatment with tunicamycin, an inhibitor of N-glycosylation, decreased the amounts of cell surface nucleolin and inhibited both internalization of Tipalpha and expression of TNF-alpha gene.
  • [MeSH-major] Bacterial Proteins / metabolism. Carcinogens / metabolism. Phosphoproteins / metabolism. RNA-Binding Proteins / metabolism. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Blotting, Western. Chromatography, Liquid. Down-Regulation. Epithelial Cells / metabolism. Epithelial Cells / pathology. Flow Cytometry. Gene Expression Regulation, Neoplastic. Immunoprecipitation. Mass Spectrometry. Mice. Molecular Sequence Data. NF-kappa B / metabolism. Receptors, Cell Surface / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20049476.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Carcinogens; 0 / NF-kappa B; 0 / Phosphoproteins; 0 / RNA-Binding Proteins; 0 / Receptors, Cell Surface; 0 / Tipalpha protein, Helicobacter pylori; 0 / Tumor Necrosis Factor-alpha; 0 / nucleolin
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11. Hosokawa Y, Hosokawa I, Ozaki K, Nakae H, Murakami K, Miyake Y, Matsuo T: CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease. Clin Exp Immunol; 2005 Sep;141(3):467-74
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  • [Title] CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease.
  • However, the expression and roles of CXCL12 in periodontal disease are uncertain.
  • Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)).
  • Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS.
  • [MeSH-major] Chemokines, CXC / metabolism. Fibroblasts / metabolism. Gingiva / metabolism. Periodontal Diseases / metabolism. Receptors, CXCR4 / metabolism
  • [MeSH-minor] Cells, Cultured. Chemokine CCL20. Chemokine CCL5 / pharmacology. Chemokine CXCL12. Chemokines, CC / pharmacology. Flow Cytometry. Humans. Immunohistochemistry / methods. Interferon-gamma / pharmacology. Lipopolysaccharides / pharmacology. Macrophage Inflammatory Proteins / pharmacology. Porphyromonas gingivalis / metabolism. Porphyromonas gingivalis / pathogenicity. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / pharmacology. Tumor Necrosis Factor-alpha / pharmacology. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16045736.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCL20 protein, human; 0 / CXCL12 protein, human; 0 / Chemokine CCL20; 0 / Chemokine CCL5; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / Lipopolysaccharides; 0 / Macrophage Inflammatory Proteins; 0 / RNA, Messenger; 0 / Receptors, CXCR4; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1809465
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12. Emadi S, Barkhordarian H, Wang MS, Schulz P, Sierks MR: Isolation of a human single chain antibody fragment against oligomeric alpha-synuclein that inhibits aggregation and prevents alpha-synuclein-induced toxicity. J Mol Biol; 2007 May 11;368(4):1132-44
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  • [Title] Isolation of a human single chain antibody fragment against oligomeric alpha-synuclein that inhibits aggregation and prevents alpha-synuclein-induced toxicity.
  • Protein misfolding and aggregation are pathological aspects of numerous neurodegenerative diseases.
  • Aggregates of alpha-synuclein are major components of the Lewy bodies and Lewy neurites associated with Parkinson's Disease (PD).
  • A natively unfolded protein, alpha-synuclein can adopt different aggregated morphologies, including oligomers, protofibrils and fibrils.
  • The small oligomeric aggregates have been shown to be particularly toxic.
  • Antibodies that neutralize the neurotoxic aggregates without interfering with beneficial functions of monomeric alpha-synuclein can be useful therapeutics.
  • We were able to isolate single chain antibody fragments (scFvs) from a phage displayed antibody library against the target antigen morphology using a novel biopanning technique that utilizes atomic force microscopy (AFM) to image and immobilize specific morphologies of alpha-synuclein.
  • The scFv described here binds only to an oligomeric form of alpha-synuclein and inhibits both aggregation and toxicity of alpha-synuclein in vitro.
  • This scFv can have potential therapeutic value in controlling misfolding and aggregation of alpha-synuclein in vivo when expressed intracellularly in dopaminergic neurons as an intrabody.

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  • (PMID = 17391701.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG017984; United States / NIA NIH HHS / AG / R01 AG017984-01; United States / NIA NIH HHS / AG / R01 AG017984-02; United States / NIA NIH HHS / AG / R01 AG017984-04; United States / NIA NIH HHS / AG / R01 AG017984-03; United States / NIA NIH HHS / AG / AG17984
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / Peptide Library; 0 / alpha-Synuclein
  • [Other-IDs] NLM/ NIHMS22525; NLM/ PMC2235820
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13. Lammers I, Buijs J, Ariese F, Gooijer C: Sensitized enantioselective laser-induced phosphorescence detection in chiral capillary electrophoresis. Anal Chem; 2010 Nov 15;82(22):9410-7
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  • Excitation was performed at 266 nm with a pulsed, small-sized, quadrupled Nd:YAG laser.

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  • (PMID = 20964317.001).
  • [ISSN] 1520-6882
  • [Journal-full-title] Analytical chemistry
  • [ISO-abbreviation] Anal. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Resins, Synthetic; 76-22-2 / Camphor; RAL3591W33 / camphorquinone
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14. Okumura AJ, Peterson LF, Okumura F, Boyapati A, Zhang DE: t(8;21)(q22;q22) Fusion proteins preferentially bind to duplicated AML1/RUNX1 DNA-binding sequences to differentially regulate gene expression. Blood; 2008 Aug 15;112(4):1392-401
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  • Here, using a 25-bp random double-stranded oligonucleotide library and a polymerase chain reaction (PCR)-based DNA-binding site screen, we show that compared with native AML1, AML1-ETO fusion proteins preferentially bind to DNA sequences with duplicated AML1 consensus sites.
  • This finding is further confirmed by both in vitro and in vivo DNA-protein interaction assays.

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  • (PMID = 18511808.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104509; United States / NCI NIH HHS / CA / CA104509
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oligonucleotides; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
  • [Other-IDs] NLM/ PMC2515118
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15. Cheinquer N, Cheinquer H, Wolff FH, Coelho-Borges S: Effect of sustained virologic response on the incidence of hepatocellular carcinoma in patients with HCV cirrhosis. Braz J Infect Dis; 2010 Sep-Oct;14(5):457-61
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  • Sustained virological response was defined as negative polymerase chain reaction assay 24 weeks after the end of treatment.
  • Patients were followed every 6 months with ultrasound and alpha-fetoprotein.
  • Hepatocellular carcinoma was diagnosed by the finding of a focal liver lesion greater than 2 cm with arterial hypervascularization on two imaging techniques and/or by liver biopsy.

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  • [CommentIn] Braz J Infect Dis. 2011 Jul-Aug;15(4):410 [21861021.001]
  • (PMID = 21221473.001).
  • [ISSN] 1678-4391
  • [Journal-full-title] The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
  • [ISO-abbreviation] Braz J Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antiviral Agents; 0 / RNA, Viral; 49717AWG6K / Ribavirin; 9008-11-1 / Interferons
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16. Rock MT, Yoder SM, Talbot TR, Edwards KM, Crowe JE Jr: Cellular immune responses to diluted and undiluted aventis pasteur smallpox vaccine. J Infect Dis; 2006 Aug 15;194(4):435-43
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  • Furthermore, expression of the interleukin-7 receptor alpha chain, which has been proposed to distinguish antigen-specific T cells that differentiate into long-lived memory T cells, did not differ among groups, suggesting that dilution of the vaccine does not affect the quantity of VV-specific memory T cells.

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  • (PMID = 16845626.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21-AI-59365; United States / NIAID NIH HHS / AI / R21 AI059365-02; United States / NCRR NIH HHS / RR / RR000095; United States / NIAID NIH HHS / AI / AI059365-02; United States / NIAID NIH HHS / AI / N01-AI-25462; United States / NIAID NIH HHS / AI / R01-AI-57661
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Smallpox Vaccine; 82115-62-6 / Interferon-gamma
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17. Liu XM, Xu J, Wang ZF: Pathogenesis of acute lung injury in rats with severe acute pancreatitis. Hepatobiliary Pancreat Dis Int; 2005 Nov;4(4):614-7
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  • The elucidation of the mechanism of ALI contributes to the diagnosis and treatment of the illness.
  • The gene expressions of tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) in the pancreas and lung tissues were detected by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • Gene expressions of TNF-alpha and ICAM-1 in the pancreas rose at 1 hour and peaked at 7 hours.
  • [MeSH-minor] Acute Disease. Animals. Disease Models, Animal. Intercellular Adhesion Molecule-1 / genetics. Pancreas / pathology. Rats. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16286275.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1
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18. Jiang X, Ren YP, Lv ZR: Ouabain induces cardiac remodeling in rats independent of blood pressure. Acta Pharmacol Sin; 2007 Mar;28(3):344-52
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  • After 4 and 6 weeks, echocardiography were performed, hemodynamic parameters were measured by invasive cardiac catheterization, changes in cardiac ultrastructure were analyzed using transmission electron microscopy, the collagen fraction of the left ventricle was assessed with Picrosirius red stain, and RT-PCR was applied to evaluate the mRNA level of myosin heavy chain-alpha and -beta in the left ventricle.
  • Moreover, the cardiac MHC-beta mRNA was upregulated by ouabain treatment, whereas MHC-alpha mRNA was downregulated.
  • [MeSH-minor] Animals. Echocardiography. Glyceraldehyde-3-Phosphate Dehydrogenases / biosynthesis. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Male. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17302996.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 5ACL011P69 / Ouabain; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.4.1 / Myosin Heavy Chains
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19. Walker CA, Hinderhofer M, Witte DJ, Boos W, Möller HM: Solution structure of the soluble domain of the NfeD protein YuaF from Bacillus subtilis. J Biomol NMR; 2008 Sep;42(1):69-76
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  • Full backbone and side chain assignments of sYuaF were obtained from triple-resonance spectra.
  • The structure was determined from distance restraints derived from 3D NOESY spectra collected at 600 MHz and 800 MHz, together with phi, psi, and chi(1) torsion angle restraints based on the analysis of (1)H(N), (15)N, (1)H(alpha), (13)C(alpha), (13)CO, and (13)C(beta) chemical shifts, and HNHA, HNHB and HACAHB-COSY spectra.
  • Structures were calculated using CYANA 2.0 and refined in AMBER 8. sYuaF is composed of an extended N-terminal alpha-helix and a beta-barrel formed by five beta-strands.

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  • (PMID = 18696230.001).
  • [ISSN] 0925-2738
  • [Journal-full-title] Journal of biomolecular NMR
  • [ISO-abbreviation] J. Biomol. NMR
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bacterial Proteins
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20. Vos JB, Datson NA, van Kampen AH, Luyf AC, Verhoosel RM, Zeeuwen PL, Olthuis D, Rabe KF, Schalkwijk J, Hiemstra PS: A molecular signature of epithelial host defense: comparative gene expression analysis of cultured bronchial epithelial cells and keratinocytes. BMC Genomics; 2006;7:9
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  • Using an in silico approach, an epithelial-specific molecular signature of gene expression was identified in bronchial epithelial cells and keratinocytes comprising of family members of keratins, small proline-rich proteins and proteinase inhibitors.
  • Using polymerase chain reaction, presence of expression of selected tissue-specific genes was validated.
  • We show that bronchial epithelial cells, similar to keratinocytes, express components that are able to form a cross-linked protein envelope that may contribute to an effective barrier against noxious stimuli and pathogens.
  • [MeSH-minor] Algorithms. Base Sequence. Cells, Cultured. DNA Primers / genetics. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Expressed Sequence Tags. Genomics. Humans. Interleukin-1beta / pharmacology. Models, Genetic. Multigene Family. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tissue Distribution. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16420688.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Interleukin-1beta; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1382211
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21. Healy M, Reece K, Walton D, Huong J, Frye S, Raad II, Kontoyiannis DP: Use of the Diversi Lab System for species and strain differentiation of Fusarium species isolates. J Clin Microbiol; 2005 Oct;43(10):5278-80
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  • The system utilizes automated repetitive sequence-based PCR (rep-PCR) and web-based data analyses. rep-PCR dendrogram cluster analysis showed agreement with species sequence identification (elongation factor 1 alpha gene).
  • [MeSH-minor] DNA Fingerprinting. Humans. Mycoses / microbiology. Polymerase Chain Reaction / methods. Reagent Kits, Diagnostic. Species Specificity

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  • (PMID = 16207996.001).
  • [ISSN] 0095-1137
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
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  • [Chemical-registry-number] 0 / Reagent Kits, Diagnostic
  • [Other-IDs] NLM/ PMC1248465
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22. Baumgart DC, Thomas S, Przesdzing I, Metzke D, Bielecki C, Lehmann SM, Lehnardt S, Dörffel Y, Sturm A, Scheffold A, Schmitz J, Radbruch A: Exaggerated inflammatory response of primary human myeloid dendritic cells to lipopolysaccharide in patients with inflammatory bowel disease. Clin Exp Immunol; 2009 Sep;157(3):423-36
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  • [Title] Exaggerated inflammatory response of primary human myeloid dendritic cells to lipopolysaccharide in patients with inflammatory bowel disease.
  • Inflammatory bowel disease (IBD) results from a breakdown of tolerance towards the indigenous flora in genetically susceptible hosts.
  • Primary (conventional, non-monocyte generated) CD1c(+)CD11c(+)CD14(-)CD16(-)CD19(-) myeloid blood or mucosal dendritic cells (mDC) from 76 patients with Crohn's disease (CD) or ulcerative colitis (UC) in remission, during flare-ups (FU) and 76 healthy or non-IBD controls were analysed by fluorescence activated cell sorter (FACS) flow cytometry and real-time polymerase chain reaction.
  • Stimulated circulating mDC from IBD patients secrete significantly more tumour necrosis factor (TNF)-alpha and interleukin (IL)-8.
  • Our data suggest an aberrant LPS response of mDC in IBD patients, resulting in an inflammatory phenotype and possibly intestinal homing in acute flares.
  • [MeSH-major] Dendritic Cells / immunology. Inflammatory Bowel Diseases / immunology. Intestinal Mucosa / immunology
  • [MeSH-minor] Acute Disease. Adult. Antigen Presentation. Antigens, CD40 / analysis. Case-Control Studies. Cells, Cultured. Colitis, Ulcerative / immunology. Crohn Disease / immunology. Female. Flow Cytometry. Humans. Immunization. Immunophenotyping. Inflammation. Lipopolysaccharides. Lymphocyte Activation. Male. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Toll-Like Receptor 2 / genetics. Toll-Like Receptor 4 / genetics. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 19664152.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / TLR2 protein, human; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2745038
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23. Pan-Montojo F, Anichtchik O, Dening Y, Knels L, Pursche S, Jung R, Jackson S, Gille G, Spillantini MG, Reichmann H, Funk RH: Progression of Parkinson's disease pathology is reproduced by intragastric administration of rotenone in mice. PLoS One; 2010 Jan 19;5(1):e8762
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  • [Title] Progression of Parkinson's disease pathology is reproduced by intragastric administration of rotenone in mice.
  • In patients with Parkinson's disease (PD), the associated pathology follows a characteristic pattern involving inter alia the enteric nervous system (ENS), the dorsal motor nucleus of the vagus (DMV), the intermediolateral nucleus of the spinal cord and the substantia nigra, providing the basis for the neuropathological staging of the disease.
  • Here we report that intragastrically administered rotenone, a commonly used pesticide that inhibits Complex I of the mitochondrial respiratory chain, is able to reproduce PD pathological staging as found in patients.
  • Our results show that low doses of chronically and intragastrically administered rotenone induce alpha-synuclein accumulation in all the above-mentioned nervous system structures of wild-type mice.
  • Moreover, we also observed inflammation and alpha-synuclein phosphorylation in the ENS and DMV.
  • [MeSH-major] Disease Models, Animal. Parkinson Disease / pathology. Rotenone / administration & dosage
  • [MeSH-minor] Animals. Chromatography, High Pressure Liquid. Enteric Nervous System / drug effects. Mice. Mice, Inbred BALB C. Stomach

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  • (PMID = 20098733.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United Kingdom / Parkinson's UK / / G-0701
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 03L9OT429T / Rotenone
  • [Other-IDs] NLM/ PMC2808242
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24. Hegazy SK, El-Bedewy MM: Effect of probiotics on pro-inflammatory cytokines and NF-kappaB activation in ulcerative colitis. World J Gastroenterol; 2010 Sep 7;16(33):4145-51
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  • Colonic activity of myeloperoxidase (MPO) was assayed with UV spectrophotometry, the colonic content of interleukin (IL)-6 was determined by enzyme-linked immunosorbent assay (ELISA), fecal calprotectin was determined by ELISA, and expression of NF-kappaB p65 and tumor necrosis factor (TNF)-alpha proteins in colonic tissue was identified by immunohistochemistry and reverse transcription polymerase chain reaction, respectively.
  • RESULTS: At the start of the study, colonic mucosal injury and inflammation were demonstrated in UC patients by hematoxylin and eosin staining, and an increase in colonic MPO activity, fecal calprotectin, and expression of colonic TNF-alpha and NF-kappaB p65 proteins.
  • The use of probiotic for 8 wk significantly ameliorated the inflammation by decreasing the colonic concentration of IL-6, expression of TNF-alpha and NF-kappaB p65, leukocyte recruitment, as demonstrated by a decrease in colonic MPO activity, and the level of fecal calprotectin compared to sulfasalazine group and the control group (P < 0.05).
  • [MeSH-major] Colitis, Ulcerative / metabolism. Interleukin-6 / metabolism. NF-kappa B / metabolism. Probiotics / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Feces. Female. Humans. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Lactobacillus delbrueckii / physiology. Lactobacillus fermentum / physiology. Leukocyte L1 Antigen Complex / metabolism. Male. Middle Aged. Peroxidase / metabolism. Sulfasalazine / therapeutic use. Treatment Outcome

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  • (PMID = 20806430.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Interleukin-6; 0 / Leukocyte L1 Antigen Complex; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 3XC8GUZ6CB / Sulfasalazine; EC 1.11.1.7 / Peroxidase
  • [Other-IDs] NLM/ PMC2932917
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25. Kelly P, Bajaj-Elliott M, Katubulushi M, Zulu I, Poulsom R, Feldman RA, Bevins CL, Dhaliwal W: Reduced gene expression of intestinal alpha-defensins predicts diarrhea in a cohort of African adults. J Infect Dis; 2006 May 15;193(10):1464-70
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  • [Title] Reduced gene expression of intestinal alpha-defensins predicts diarrhea in a cohort of African adults.
  • BACKGROUND: Human defensin (HD) 5 and HD6, both Paneth cell alpha-defensins, contribute to the antimicrobial barrier against intestinal infection.
  • The aim of the present study was to determine, during 2 years of follow-up, whether alpha-defensin expression in Zambian adults is related to susceptibility to diarrhea.
  • METHODS: We analyzed intestinal biopsy samples from a longitudinal cohort study conducted in 83 Zambian adults by quantitative reverse-transcription polymerase chain reaction, Western blotting, immunohistochemistry, and in situ hybridization, and we measured the incidence of diarrhea.
  • CONCLUSIONS: These data indicate that intestinal alpha-defensin expression is dynamic and seasonal and suggest that susceptibility to intestinal infection is related to alpha-defensin expression.
  • [MeSH-major] Diarrhea / epidemiology. Diarrhea / genetics. Genetic Predisposition to Disease. Intestine, Small / metabolism. alpha-Defensins / genetics
  • [MeSH-minor] Adult. African Continental Ancestry Group / genetics. Cohort Studies. Enterocolitis, Pseudomembranous / epidemiology. Enterocolitis, Pseudomembranous / genetics. European Continental Ancestry Group / genetics. Female. Gene Expression Regulation. Genetics, Population. Humans. Incidence. Longitudinal Studies. Male. Middle Aged. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Zambia / epidemiology

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  • (PMID = 16619196.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 067948; United Kingdom / Wellcome Trust / / 056481; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / alpha-Defensins
  • [Other-IDs] NLM/ PMC2629849; NLM/ UKMS3500
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26. Meijer MJ, Mieremet-Ooms MA, van Duijn W, van der Zon AM, Hanemaaijer R, Verheijen JH, van Hogezand RA, Lamers CB, Verspaget HW: Effect of the anti-tumor necrosis factor-alpha antibody infliximab on the ex vivo mucosal matrix metalloproteinase-proteolytic phenotype in inflammatory bowel disease. Inflamm Bowel Dis; 2007 Feb;13(2):200-10
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  • [Title] Effect of the anti-tumor necrosis factor-alpha antibody infliximab on the ex vivo mucosal matrix metalloproteinase-proteolytic phenotype in inflammatory bowel disease.
  • BACKGROUND: Previous studies have shown an upregulation of matrix metalloproteinases (MMPs) in intestinal tissue of patients with inflammatory bowel disease (IBD) and significant clinical improvement after administration of the anti-TNF-a antibody infliximab.
  • The aims of our study were to determine expression and secretion of MMP-1, -2, -3, -9, and their inhibitors TIMP-1, -2 by IBD versus control intestinal mucosa ex vivo and to assess the regulatory capacity by infliximab of the proteolytic phenotype.
  • METHODS: Intestinal mucosal explants from 20 IBD and 15 control patients were cultured with or without infliximab and/or the T-cell activator pokeweed mitogen (PWM).
  • Explants and culture supernatants were analyzed for MMPs, TIMPs, and TNF-alpha protein, activity and/or mRNA levels.
  • All patients were genotyped for functional TNF-alpha, MMP, and TIMP single nucleotide polymorphism (SNP) loci.
  • CONCLUSIONS: The high expression of MMPs in patients with IBD suggests a role for these proteinases in the pathogenesis of this disease.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Colitis, Ulcerative / enzymology. Crohn Disease / enzymology. Intestinal Mucosa / enzymology. Matrix Metalloproteinases / metabolism. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Down-Regulation. Female. Humans. Infliximab. Male. Middle Aged. Phenotype. Polymorphism, Single Nucleotide. Reverse Transcriptase Polymerase Chain Reaction. Tissue Culture Techniques. Tissue Inhibitor of Metalloproteinases / genetics. Tissue Inhibitor of Metalloproteinases / metabolism

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  • (PMID = 17206679.001).
  • [ISSN] 1078-0998
  • [Journal-full-title] Inflammatory bowel diseases
  • [ISO-abbreviation] Inflamm. Bowel Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Tissue Inhibitor of Metalloproteinases; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; EC 3.4.24.- / Matrix Metalloproteinases
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27. 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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28. Hagge DA, Saunders BM, Ebenezer GJ, Ray NA, Marks VT, Britton WJ, Krahenbuhl JL, Adams LB: Lymphotoxin-alpha and TNF have essential but independent roles in the evolution of the granulomatous response in experimental leprosy. Am J Pathol; 2009 Apr;174(4):1379-89
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  • [Title] Lymphotoxin-alpha and TNF have essential but independent roles in the evolution of the granulomatous response in experimental leprosy.
  • Recent studies identified an association between genetic variants in the lymphotoxin-alpha (LTalpha) gene and leprosy.
  • Cellular responses to low-dose infection in cLTalpha(-/-) mice were dramatically different, with reduced accumulation of CD4(+) and CD8(+) lymphocytes and macrophages and failure to form granulomas.

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  • (PMID = 19246648.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / N01AI50027; United States / NIAID NIH HHS / AI / AI-50027
  • [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 / Cytokines; 0 / Lymphotoxin-alpha; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2671369
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29. Iannelli P, Zarrilli V, Varricchio E, Tramontano D, Mancini FP: The dietary antioxidant resveratrol affects redox changes of PPARalpha activity. Nutr Metab Cardiovasc Dis; 2007 May;17(4):247-56
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  • BACKGROUND AND AIMS: Gene-environment interaction is behind the pathogenesis of most widespread diseases, and nutrition is among the environmental factors with the highest impact on human health.
  • PPARalpha is a transcriptional factor that regulates gene expression when activated by endogenous or exogenous long-chain fatty acids.
  • Its activation results in significant protection from cardiovascular diseases in humans.
  • This finding could be relevant considering the important role of redox balance in pathological and physiological processes.
  • [MeSH-major] Antioxidants / administration & dosage. PPAR alpha / metabolism. Stilbenes / administration & dosage

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  • (PMID = 17134953.001).
  • [ISSN] 1590-3729
  • [Journal-full-title] Nutrition, metabolism, and cardiovascular diseases : NMCD
  • [ISO-abbreviation] Nutr Metab Cardiovasc Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Maleates; 0 / PPAR alpha; 0 / Stilbenes; 9007-49-2 / DNA; EC 1.3.3.6 / Acyl-CoA Oxidase; G81WQB56OL / diethyl maleate; GAN16C9B8O / Glutathione; Q369O8926L / resveratrol
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30. Sarfo FS, Phillips RO, Rangers B, Mahrous EA, Lee RE, Tarelli E, Asiedu KB, Small PL, Wansbrough-Jones MH: Detection of Mycolactone A/B in Mycobacterium ulcerans-Infected Human Tissue. PLoS Negl Trop Dis; 2010 Jan 05;4(1):e577
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Mycobacterium ulcerans disease (Buruli ulcer) is a neglected tropical disease common amongst children in rural West Africa.
  • On thin layer chromatography this molecule had a retention factor value of 0.23, MS analyses showed it had an m/z of 765.6 [M+Na(+)] and on MS:MS fragmented to produce the core lactone ring with m/z of 429.4 and the polyketide side chain of mycolactone A/B with m/z of 359.2.
  • Mycolactone A/B was detected in all of 10 tissue samples from patients with ulcerative and pre-ulcerative Mu disease.
  • [MeSH-minor] Adolescent. Adult. Animals. Cell Line. Child. Chromatography, Thin Layer. Female. Humans. Macrolides. Macrophages / drug effects. Macrophages / metabolism. Male. Mice. Skin / metabolism. Skin / microbiology. Skin / pathology. Spectrometry, Mass, Electrospray Ionization. Tumor Necrosis Factor-alpha / metabolism. Young Adult

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  • (PMID = 20052267.001).
  • [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 / Bacterial Toxins; 0 / Macrolides; 0 / Tumor Necrosis Factor-alpha; 0 / mycolactone
  • [Other-IDs] NLM/ PMC2791843
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31. Thompson BJ, Washington MK, Kurre U, Singh M, Rula EY, Emeson RB: Protective roles of alpha-calcitonin and beta-calcitonin gene-related peptide in spontaneous and experimentally induced colitis. Dig Dis Sci; 2008 Jan;53(1):229-41
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  • [Title] Protective roles of alpha-calcitonin and beta-calcitonin gene-related peptide in spontaneous and experimentally induced colitis.
  • Calcitonin gene-related peptide (CGRP) is thought to be involved in the regulation of gastric and mesenteric blood flow, in the control of gastric acid secretion and in the modulation of intestinal motility, yet the precise physiological roles of CGRP remain to be elucidated.
  • [MeSH-minor] Animals. Dextran Sulfate / toxicity. Disease Models, Animal. Disease Progression. Immunohistochemistry. Mice. Mice, Mutant Strains. Polymerase Chain Reaction. Severity of Illness Index

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  • (PMID = 17530400.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 63231-63-0 / RNA; 83652-28-2 / Calcitonin Gene-Related Peptide; 9042-14-2 / Dextran Sulfate
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32. Stefano JT, Correa-Giannella ML, Ribeiro CM, Alves VA, Massarollo PC, Machado MC, Giannella-Neto D: Increased hepatic expression of insulin-like growth factor-I receptor in chronic hepatitis C. World J Gastroenterol; 2006 Jun 28;12(24):3821-8
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  • METHODS: IGF-IR and IGF-I mRNA content were determined by semi-quantitative RT-PCR and IGF-IR protein expression was determined by immunohisto-chemistry in hepatic tissue obtained from patients with CHC before (34 patients) and after (10 patients) therapy with interferon-alpha and ribavirin.
  • Considering that liver is the organ with the highest levels of IGF-I, our finding of increased IGF-IR expression after both acute and chronic hepatic damage highlights the need for additional studies to elucidate the role of IGF-I in liver regeneration.
  • [MeSH-major] Hepatitis C, Chronic / genetics. Insulin-Like Growth Factor I / metabolism. Receptor, IGF Type 1 / metabolism
  • [MeSH-minor] Antiviral Agents / therapeutic use. Gene Expression Profiling. Hepatocytes / metabolism. Humans. Immunohistochemistry. Interferon-alpha / therapeutic use. Liver Regeneration / physiology. RNA, Messenger / analysis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Ribavirin / therapeutic use. Up-Regulation

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  • (PMID = 16804965.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / RNA, Messenger; 49717AWG6K / Ribavirin; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Other-IDs] NLM/ PMC4087928
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33. Alves Pedroso ML, Boldt AB, Pereira-Ferrari L, Steffensen R, Strauss E, Jensenius JC, Ioshii SO, Messias-Reason I: Mannan-binding lectin MBL2 gene polymorphism in chronic hepatitis C: association with the severity of liver fibrosis and response to interferon therapy. Clin Exp Immunol; 2008 May;152(2):258-64
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  • Hepatitis C virus (HCV) is a major cause of hepatic disease and of liver transplantation worldwide.
  • Six common single nucleotide polymorphisms in the MBL2 gene, three in the promoter (H/L, X/Y and P/Q) and three in exon 1 (A, the wild-type, and B, C or D also known as O) were evaluated using real-time polymerase chain reaction with fluorescent hybridization probes.
  • MBL2 polymorphisms may therefore be associated not only with the development of chronic hepatitis C, but also with its clinical evolution and response to treatment.
  • [MeSH-major] Antiviral Agents / therapeutic use. Hepatitis C, Chronic / genetics. Interferon-alpha / therapeutic use. Liver Cirrhosis / virology. Mannose-Binding Lectin / genetics
  • [MeSH-minor] Adult. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Polymorphism, Single Nucleotide. Severity of Illness Index. Treatment Outcome

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  • (PMID = 18336595.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / MBL2 protein, human; 0 / Mannose-Binding Lectin
  • [Other-IDs] NLM/ PMC2384100
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34. Sow FB, Gallup JM, Meyerholz DK, Ackermann MR: Gene profiling studies in the neonatal ovine lung show enhancing effects of VEGF on the immune response. Dev Comp Immunol; 2009 Jun;33(6):761-71
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  • We report that VEGF induced the expression of chemokines (IL-8, RANTES, MCP-1), cytokines (IFN-gamma, IL-6, TNF-alpha, GMCSF), Toll-like receptor (TLR)-4, complement family members (C3, CFB, CFH) and collectins (SP-A, SP-D).
  • These results suggest that VEGF can regulate local immune gene expression in vivo and should be further explored as a potential exogenous therapy for various lung diseases.
  • [MeSH-minor] Animals. Animals, Newborn. Chemokines / biosynthesis. Chemokines / genetics. Collectins / biosynthesis. Collectins / metabolism. Complement System Proteins / biosynthesis. Complement System Proteins / genetics. Cytokines / biosynthesis. Cytokines / genetics. Humans. Infant, Newborn. Polymerase Chain Reaction. RNA, Messenger / analysis. Respiratory Syncytial Virus Infections / immunology. Sheep. Toll-Like Receptors / biosynthesis. Toll-Like Receptors / genetics

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  • (PMID = 19189846.001).
  • [ISSN] 1879-0089
  • [Journal-full-title] Developmental and comparative immunology
  • [ISO-abbreviation] Dev. Comp. Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / K08 AI055499; United States / NIAID NIH HHS / AI / R01 AI062787; United States / NIAID NIH HHS / AI / R01 AI062787; United States / NIAID NIH HHS / AI / R01 AI062787-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines; 0 / Collectins; 0 / Cytokines; 0 / RNA, Messenger; 0 / Toll-Like Receptors; 0 / Vascular Endothelial Growth Factor A; 9007-36-7 / Complement System Proteins
  • [Other-IDs] NLM/ NIHMS160737; NLM/ PMC2791060
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35. Osman N, Adawi D, Ahrné S, Jeppsson B, Molin G: Endotoxin- and D-galactosamine-induced liver injury improved by the administration of Lactobacillus, Bifidobacterium and blueberry. Dig Liver Dis; 2007 Sep;39(9):849-56
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  • Samples were collected 24 h after induction for bacterial test, liver function test, short chain fatty acids, myeloperoxidase, cytokines, malondialdehyde and glutathione.
  • Bilirubin, liver TNF-alpha, myeloperoxidase and acetic acid in cecum content decreased significantly in all groups, while liver glutathione values increased significantly in all groups compared to liver injury control.
  • [MeSH-minor] Animals. Cecum / microbiology. Dietary Supplements. Disease Models, Animal. Endotoxins / adverse effects. Galactosamine / adverse effects. Inflammation / diet therapy. Rats

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  • (PMID = 17652039.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Endotoxins; 7535-00-4 / Galactosamine
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36. Patte-Mensah C, Kibaly C, Boudard D, Schaeffer V, Béglé A, Saredi S, Meyer L, Mensah-Nyagan AG: Neurogenic pain and steroid synthesis in the spinal cord. J Mol Neurosci; 2006;28(1):17-31
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  • In particular, an active form of cytochrome P450 sidechain cleavage (P450scc) has been localized in sensory networks of the rat SC dorsal horn (DH).
  • [MeSH-minor] 3-Hydroxysteroid Dehydrogenases / metabolism. 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / metabolism. 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) / metabolism. Animals. Cholesterol Side-Chain Cleavage Enzyme / metabolism. Humans. Ligation. Neurons / cytology. Neurons / metabolism. Pregnenolone / metabolism. Progesterone / analogs & derivatives. Progesterone / metabolism. Sciatic Nerve / surgery. Steroid 17-alpha-Hydroxylase / metabolism

  • MedlinePlus Health Information. consumer health - Pain.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 16632873.001).
  • [ISSN] 0895-8696
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Steroids; 4G7DS2Q64Y / Progesterone; 73R90F7MQ8 / Pregnenolone; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.50 / 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific); EC 1.14.14.19 / Steroid 17-alpha-Hydroxylase; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; EC 1.3.99.5 / 3-Oxo-5-alpha-Steroid 4-Dehydrogenase
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37. Akil O, Weber CM, Park SN, Ninkina N, Buchman V, Lustig LR: Localization of synucleins in the mammalian cochlea. J Assoc Res Otolaryngol; 2008 Dec;9(4):452-63
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  • Synucleins are widely expressed synaptic proteins within the central nervous system that have been implicated in such neurodegenerative disorders as Parkinson's disease.
  • In this study, an initial characterization of all three synucleins, alpha-, beta-, and gamma-synuclein, within the cochlea was undertaken.
  • Reverse transcriptase-polymerase chain reaction (PCR) demonstrated all three synuclein mRNA species within microdissected cochlear tissue.
  • Quantitative PCR suggests that beta-synuclein is the most abundantly expressed form, followed by gamma- and then alpha-synuclein.
  • Immunofluorescence localizes the three synucleins predominantly to the efferent neuronal system at the efferent outer hair cell synapse, with some additional localization within the efferent tunnel-crossing fibers (alpha- and gamma-synuclein), spiral ganglion (beta-synuclein), inner spiral bundle (gamma-synuclein), and stria vascularis (alpha- > beta-synuclein).
  • Developmentally, gamma-synuclein can be seen in the region of the outer hair cells by E19, while alpha- and beta-synuclein do not clearly appear there until approximately P10.
  • Additional studies in a null-mutant gamma-synuclein mouse show no histological changes in the organ of Corti with normal hair cell and spiral ganglion cell counts, and normal ABR and DPOAE thresholds in wild-type vs mutant littermates.
  • [MeSH-minor] Animals. Auditory Pathways / physiology. Blotting, Western. Evoked Potentials, Auditory, Brain Stem / physiology. Fluorescent Antibody Technique. Gene Expression Regulation, Developmental. Mammals. Mice. Mice, Inbred C57BL. Mice, Knockout. Otoacoustic Emissions, Spontaneous / physiology. Phenotype. Rats. Rats, Sprague-Dawley. Receptors, Nicotinic / physiology. Reverse Transcriptase Polymerase Chain Reaction. alpha-Synuclein / genetics. alpha-Synuclein / metabolism. beta-Synuclein / genetics. beta-Synuclein / metabolism. gamma-Synuclein / genetics. gamma-Synuclein / metabolism

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  • (PMID = 18665422.001).
  • [ISSN] 1525-3961
  • [Journal-full-title] Journal of the Association for Research in Otolaryngology : JARO
  • [ISO-abbreviation] J. Assoc. Res. Otolaryngol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 075615; United States / NIDCD NIH HHS / DC / K08 DC000189; United States / NIDCD NIH HHS / DC / K08 DC00189; United Kingdom / Wellcome Trust / /
  • [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 / Receptors, Nicotinic; 0 / Synucleins; 0 / alpha-Synuclein; 0 / beta-Synuclein; 0 / gamma-Synuclein
  • [Other-IDs] NLM/ PMC2580813
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38. Gensure RC, Mäkitie O, Barclay C, Chan C, Depalma SR, Bastepe M, Abuzahra H, Couper R, Mundlos S, Sillence D, Ala Kokko L, Seidman JG, Cole WG, Jüppner H: A novel COL1A1 mutation in infantile cortical hyperostosis (Caffey disease) expands the spectrum of collagen-related disorders. J Clin Invest; 2005 May;115(5):1250-7
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  • [Title] A novel COL1A1 mutation in infantile cortical hyperostosis (Caffey disease) expands the spectrum of collagen-related disorders.
  • Infantile cortical hyperostosis (Caffey disease) is characterized by spontaneous episodes of subperiosteal new bone formation along 1 or more bones commencing within the first 5 months of life.
  • A genome-wide screen for genetic linkage in a large family with an autosomal dominant form of Caffey disease (ADC) revealed a locus on chromosome 17q21 (LOD score, 6.78).
  • Affected individuals and obligate carriers were heterozygous for a missense mutation (3040Ctwo head right arrowT) in exon 41 of the gene encoding the alpha1(I) chain of type I collagen (COL1A1), altering residue 836 (R836C) in the triple-helical domain of this chain.
  • Individuals bearing the mutation, whether they had experienced an episode of cortical hyperostosis or not, had joint hyperlaxity, hyperextensible skin, and inguinal hernias resembling symptoms of a mild form of Ehlers-Danlos syndrome type III.
  • These findings extend the spectrum of COL1A1-related diseases to include a hyperostotic disorder.

  • Genetic Alliance. consumer health - Caffey Disease.
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  • (PMID = 15864348.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / K08 HD041512; United States / NICHD NIH HHS / HD / K08 HD41512; United States / PHS HHS / / R01 46718-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / collagen type I, alpha 1 chain
  • [Other-IDs] NLM/ PMC1087158
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39. Chow C, Kurt N, Murphy RM, Cavagnero S: Structural characterization of apomyoglobin self-associated species in aqueous buffer and urea solution. Biophys J; 2006 Jan 1;90(1):298-309
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  • Unlike the beta-sheet self-associated aggregates previously reported for this protein at high temperatures, the soluble aggregates detected here have either alpha-helical or random coil secondary structure, depending on solvent and solution conditions.
  • Hydrodynamic diameters range from 80 to 130 nm, with semiflexible chain-like morphology.

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  • (PMID = 16214860.001).
  • [ISSN] 0006-3495
  • [Journal-full-title] Biophysical journal
  • [ISO-abbreviation] Biophys. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoproteins; 0 / Buffers; 0 / Myoglobin; 0 / apomyoglobin; 059QF0KO0R / Water; 8W8T17847W / Urea
  • [Other-IDs] NLM/ PMC1367028
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40. 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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41. Kalivendi SV, Yedlapudi D, Hillard CJ, Kalyanaraman B: Oxidants induce alternative splicing of alpha-synuclein: Implications for Parkinson's disease. Free Radic Biol Med; 2010 Feb 1;48(3):377-83
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  • [Title] Oxidants induce alternative splicing of alpha-synuclein: Implications for Parkinson's disease.
  • alpha-Synuclein (alpha-syn) is a presynaptic protein that is widely implicated in the pathophysiology of Parkinson's disease (PD).
  • Emerging evidence indicates a strong correlation between alpha-syn aggregation and proteasomal dysfunction as one of the major pathways responsible for destruction of the dopamine neurons.
  • Using parkinsonism mimetics (MPP(+), rotenone) and related oxidants, we have identified an oxidant-induced alternative splicing of alpha-syn mRNA, generating a shorter isoform of alpha-syn with deleted exon-5 (112-syn).
  • We conclude that oxidant-induced alternative splicing of alpha-syn plays a crucial role in the mechanism of dopamine neuron cell death and thus contributes to PD.

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  • [Copyright] Copyright 2009. Published by Elsevier Inc.
  • (PMID = 19857570.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS039958; United States / NINDS NIH HHS / NS / NS39958
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic Agents; 0 / Dopamine Agents; 0 / Oxidants; 0 / RNA, Messenger; 0 / Uncoupling Agents; 0 / alpha-Synuclein; 03L9OT429T / Rotenone; 8HW4YBZ748 / Oxidopamine; 9P21XSP91P / 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
  • [Other-IDs] NLM/ NIHMS640838; NLM/ PMC4485429
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42. Taylor MD, Liu Y, Nagji AS, Theodosakis N, Jones DR: Combined proteasome and histone deacetylase inhibition attenuates epithelial-mesenchymal transition through E-cadherin in esophageal cancer cells. J Thorac Cardiovasc Surg; 2010 May;139(5):1224-32, 1232.e1
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  • Cells were treated with tumor necrosis factor alpha (to simulate proinflammatory tumor milieu) and transforming growth factor beta (cytokine critical for induction of epithelial-mesenchymal transition).
  • Quantitative reverse transcriptase polymerase chain reaction and Western blot analyses revealed robust rescue of E-cadherin transcription and protein expression after combined therapy.
  • [MeSH-minor] Boronic Acids / pharmacology. Bortezomib. Cell Death. Cell Line, Tumor. Cell Movement / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Histone Deacetylase Inhibitors / pharmacology. Humans. Hydroxamic Acids / pharmacology. Neoplasm Invasiveness. Protease Inhibitors / pharmacology. Proteasome Endopeptidase Complex / metabolism. Pyrazines / pharmacology. RNA, Messenger / metabolism. Spheroids, Cellular. Time Factors. Transfection. Transforming Growth Factor beta / metabolism. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation

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  • [Copyright] 2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
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  • (PMID = 20412959.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007849
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / CDH1 protein, human; 0 / Cadherins; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 58IFB293JI / vorinostat; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ NIHMS638631; NLM/ PMC4219566
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43. Zhu J, Wu X, Goel S, Gowda NM, Kumar S, Krishnegowda G, Mishra G, Weinberg R, Li G, Gaestel M, Muta T, Gowda DC: MAPK-activated protein kinase 2 differentially regulates plasmodium falciparum glycosylphosphatidylinositol-induced production of tumor necrosis factor-{alpha} and interleukin-12 in macrophages. J Biol Chem; 2009 Jun 5;284(23):15750-61
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  • [Title] MAPK-activated protein kinase 2 differentially regulates plasmodium falciparum glycosylphosphatidylinositol-induced production of tumor necrosis factor-{alpha} and interleukin-12 in macrophages.
  • In this study, we investigated the role of MAPK-activated protein kinase 2 (MK2) in the regulation of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12, two of the major inflammatory cytokines produced by macrophages stimulated with GPIs.
  • We show that MK2 differentially regulates the GPI-induced production of TNF-alpha and IL-12.
  • Although TNF-alpha production was markedly decreased, IL-12 expression was increased by 2-3-fold in GPI-stimulated MK2(-/-) macrophages compared with wild type (WT) cells.
  • MK2(-/-) macrophages produced markedly decreased levels of TNF-alpha than WT macrophages mainly because of lower mRNA stability and translation.
  • Using the protein kinase inhibitors SB203580 and U0126, we also show that the ERK and p38 pathways regulate TNF-alpha and IL-12 production, and that both inhibitors can reduce phosphorylation of MK2 in response to GPIs and other toll-like receptor ligands.
  • These results may have important implications for developing therapeutics for malaria and other infectious diseases.

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  • (PMID = 19359247.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI041139-11; United States / NIAID NIH HHS / AI / R01 AI041139; United States / NIAID NIH HHS / AI / AI41139; United States / NIAID NIH HHS / AI / R01 AI041139-11
  • [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 / DNA Primers; 0 / Glycosylphosphatidylinositols; 0 / NF-kappa B; 0 / Protozoan Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 63231-63-0 / RNA; EC 2.7.12.2 / MAP Kinase Kinase 2
  • [Other-IDs] NLM/ PMC2708872
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44. Gaborit N, Le Bouter S, Szuts V, Varro A, Escande D, Nattel S, Demolombe S: Regional and tissue specific transcript signatures of ion channel genes in the non-diseased human heart. J Physiol; 2007 Jul 15;582(Pt 2):675-93
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  • Transcripts that were more strongly expressed in epicardium (versus endocardium) included Cav1.2, KChIP2, SERCA2, CALM3 and calcineurin-alpha.
  • [MeSH-minor] Adult. Blotting, Western. Carrier Proteins / genetics. Cluster Analysis. Endocardium / metabolism. Female. Heart Atria. Heart Ventricles. Humans. Male. Middle Aged. Pericardium / metabolism. Protein Isoforms / genetics. Purkinje Fibers / metabolism. RNA, Messenger / metabolism. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Tissue Distribution

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  • (PMID = 17478540.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Ion Channels; 0 / Protein Isoforms; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2075332
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45. Knight RL, Booth C, Wilcox HE, Fisher J, Ingham E: Tissue engineering of cardiac valves: re-seeding of acellular porcine aortic valve matrices with human mesenchymal progenitor cells. J Heart Valve Dis; 2005 Nov;14(6):806-13
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  • Phenotypic analysis of the cells in the re-seeded matrix revealed the cells to have a similar phenotype to native valve interstitial cells (vimentin+, alpha-smooth muscle actin+, heavy chain myosin slow-, desmin-).

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  • (PMID = 16359063.001).
  • [ISSN] 0966-8519
  • [Journal-full-title] The Journal of heart valve disease
  • [ISO-abbreviation] J. Heart Valve Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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46. Ishida T, Yoshida M, Arita M, Nishitani Y, Nishiumi S, Masuda A, Mizuno S, Takagawa T, Morita Y, Kutsumi H, Inokuchi H, Serhan CN, Blumberg RS, Azuma T: Resolvin E1, an endogenous lipid mediator derived from eicosapentaenoic acid, prevents dextran sulfate sodium-induced colitis. Inflamm Bowel Dis; 2010 Jan;16(1):87-95
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  • RESULTS: RvE1 treatment led to inhibition of proinflammatory cytokines including TNF-alpha and IL-12p40.
  • In HEK293 cells, pretreatment with RvE1 inhibited TNF-alpha-induced nuclear translocation of NF-kappaB in a ChemR23-dependent manner.
  • RvE1 and its receptor may therefore be useful as therapeutic targets in the treatment of human inflammatory bowel disease and other inflammatory disorders.

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  • (PMID = 19572372.001).
  • [ISSN] 1536-4844
  • [Journal-full-title] Inflammatory bowel diseases
  • [ISO-abbreviation] Inflamm. Bowel Dis.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R37 DK044319; United States / NIDDK NIH HHS / DK / DK51362; United States / NIDDK NIH HHS / DK / DK051362-12; United States / NIDDK NIH HHS / DK / DK44319; United States / NIDDK NIH HHS / DK / R01 DK051362; United States / NIDDK NIH HHS / DK / R01 DK044319-12; United States / NIDDK NIH HHS / DK / R01 DK053056; United States / NIDDK NIH HHS / DK / R01 DK053056-12; United States / NIDDK NIH HHS / DK / R01 DK53056; United States / NIDDK NIH HHS / DK / R01 DK051362-12; United States / NIDDK NIH HHS / DK / DK044319-12; United States / NIDDK NIH HHS / DK / R01 DK044319
  • [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 / 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid; 0 / Inflammation Mediators; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Chemokine; 9042-14-2 / Dextran Sulfate; AAN7QOV9EA / Eicosapentaenoic Acid
  • [Other-IDs] NLM/ NIHMS144953; NLM/ PMC3070396
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47. Srinoun K, Svasti S, Chumworathayee W, Vadolas J, Vattanaviboon P, Fucharoen S, Winichagoon P: Imbalanced globin chain synthesis determines erythroid cell pathology in thalassemic mice. Haematologica; 2009 Sep;94(9):1211-9
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  • [Title] Imbalanced globin chain synthesis determines erythroid cell pathology in thalassemic mice.
  • BACKGROUND: beta-thalassemia occurs from the imbalanced globin chain synthesis due to the absence or inadequate beta-globin chain production.
  • The excessive unbound alpha-globin chains precipitate in erythroid precursors and mature red blood cells leading to ineffective erythropoiesis and hemolysis.
  • DESIGN AND METHODS: In vitro globin chain synthesis in reticulocytes from different types of thalassemic mice was performed.
  • The effect of imbalanced globin chain synthesis was assessed from changes of red blood cell properties including increased numbers of red blood cells vesicles and apoptotic red blood cells, increased reactive oxygen species and decreased red blood cell survival.
  • RESULTS: The alpha/beta-globin chain ratio in beta(IVSII-654)-thalassemic mice, 1.26+/-0.03, was significantly higher than that of wild type mice, 0.96+/-0.05.
  • These values were improved significantly in doubly heterozygous thalassemic mice harboring 4 copies of human beta(E)-globin transgene, with a more balanced globin chain synthesis, 0.92+/-0.05.
  • Moreover, transgenic mice harboring 8 extra copies of the human beta(E)-globin transgene showed inversely imbalanced alpha/beta-globin synthesis ratio, 0.83+/-0.01, that resulted in a mild beta-thalassemia phenotype due to the excessive beta-globin chains.
  • The degree of ineffective erythropoiesis also correlated with the degree of imbalanced globin chain synthesis.
  • CONCLUSIONS: Imbalanced alpha/beta-globin chain as a consequence of either reduction or enhancement of beta-globin chain synthesis can cause abnormal red blood cell properties in mouse models.
  • [MeSH-major] Erythrocytes, Abnormal / metabolism. Erythrocytes, Abnormal / pathology. alpha-Globins / biosynthesis. beta-Globins / biosynthesis. beta-Thalassemia / metabolism. beta-Thalassemia / pathology

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  • (PMID = 19608680.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / alpha-Globins; 0 / beta-Globins
  • [Other-IDs] NLM/ PMC2738712
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48. Tinoco SM, Sichieri R, Setta CL, Moura AS, Carmo MG: n-3 polyunsaturated fatty acids in milk is associate to weight gain and growth in premature infants. Lipids Health Dis; 2009;8:23
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  • BACKGROUND: Linoleic 18:2 (n-6) and alpha-linolenic 18:3 (n-3) essential fatty acids and long-chain polyunsaturated fatty acids (LC-PUFA) are essential nutrients for growth and neonatal development.

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  • (PMID = 19558659.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated
  • [Other-IDs] NLM/ PMC2707376
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49. Bai L, Mao GP, Cao CP: Effects of inflammatory cytokines on the recurrence of liver cancer after an apparently curative operation. J Dig Dis; 2007 Aug;8(3):154-9
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  • OBJECTIVE: To investigate the effects of inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and vascular cell adhesion molecule (VCAM-1), on the recurrence of liver cancer after apparently curative surgical resection of the tumor.
  • The expression of inflammatory cytokines as TNF-alpha, IL-1beta, IL-6 and VCAM-1 were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • RESULTS: Compared with SH, a significant augmented metastatic effect was observed in the mice with PH (P < 0.01), and higher mRNA expressions of TNF-alpha, IL-1beta, IL-6 and VCAM-1 were also observed.
  • Among them, TNF-alpha expression was found immediately increasing after 4 h and kept at a high level till 96 h after PH.
  • The expression of TNF-alpha, IL-1beta, IL-6 and VCAM-1 showed a significantly positive correlation with the augmenting effect of liver metastasis in the mice model.
  • CONCLUSION: The results indicate that pro-inflammatory cytokines, TNF-alpha, IL-1beta, IL-6 and VCAM-1 might be involved in promoting the enhanced metastasis of liver cancer after surgical operation, especially the PH.
  • [MeSH-minor] Animals. Disease Models, Animal. Female. Hepatectomy. Mice

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  • (PMID = 17650228.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Cytokines
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50. Bhangoo A, Paris F, Philibert P, Audran F, Ten S, Sultan C: Isolated micropenis reveals partial androgen insensitivity syndrome confirmed by molecular analysis. Asian J Androl; 2010 Jul;12(4):561-6
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  • We studied the association of isolated micropenis with the genetic defects resulting in androgen resistance, that is, AR gene defects and 5-alpha reductase type 2 (SRD5A2) deficiency.
  • DNA was extracted from peripheral leukocytes, and all exons of the SRD5A2 and AR genes were amplified by polymerase chain reaction and sequenced.
  • [MeSH-major] 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / genetics. Androgen-Insensitivity Syndrome / genetics. Receptors, Androgen / genetics

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  • (PMID = 20305676.001).
  • [ISSN] 1745-7262
  • [Journal-full-title] Asian journal of andrology
  • [ISO-abbreviation] Asian J. Androl.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Chorionic Gonadotropin; 0 / Receptors, Androgen; 3XMK78S47O / Testosterone; EC 1.3.99.5 / 3-Oxo-5-alpha-Steroid 4-Dehydrogenase
  • [Other-IDs] NLM/ PMC3739378
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51. Sawaya BE, Deshmane SL, Mukerjee R, Fan S, Khalili K: TNF alpha production in morphine-treated human neural cells is NF-kappaB-dependent. J Neuroimmune Pharmacol; 2009 Mar;4(1):140-9
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  • [Title] TNF alpha production in morphine-treated human neural cells is NF-kappaB-dependent.
  • The cytokine tumor necrosis factor alpha (TNFalpha) is a key factor in several inflammatory diseases and its levels increase in response to a variety of internal or external stimuli.
  • Using reverse transcriptase polymerase chain reaction, we demonstrated the presence of morphine receptors in these cells.
  • The use of a small interfering RNA directed against p65, a subunit of NF-kappaB, demonstrated that TNFalpha induction by morphine is NF-kappaB-dependent.
  • [MeSH-major] Analgesics, Opioid / pharmacology. Morphine / pharmacology. NF-kappa B / physiology. Neuroglia / metabolism. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Astrocytes / drug effects. Astrocytes / metabolism. Blotting, Western. Cells, Cultured. HIV Infections / virology. HIV-1. Humans. Microglia / drug effects. Microglia / metabolism. Naloxone / pharmacology. Narcotic Antagonists / pharmacology. Promoter Regions, Genetic / genetics. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells

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  • (PMID = 19023660.001).
  • [ISSN] 1557-1904
  • [Journal-full-title] Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
  • [ISO-abbreviation] J Neuroimmune Pharmacol
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS040673-04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 0 / NF-kappa B; 0 / Narcotic Antagonists; 0 / Tumor Necrosis Factor-alpha; 36B82AMQ7N / Naloxone; 76I7G6D29C / Morphine
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52. Seo HS, Nahm MH: Lipoprotein lipase and hydrofluoric acid deactivate both bacterial lipoproteins and lipoteichoic acids, but platelet-activating factor-acetylhydrolase degrades only lipoteichoic acids. Clin Vaccine Immunol; 2009 Aug;16(8):1187-95
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  • Changes in the structures of the two synthetic proteins and the LTAs were monitored by mass spectrometry, and biological activity changes were evaluated by measuring tumor necrosis factor alpha production by mouse macrophage cells (RAW 264.7) following stimulation.
  • LPL also removed an acyl chain from the LTA and reduced its activity.

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  • (PMID = 19553557.001).
  • [ISSN] 1556-679X
  • [Journal-full-title] Clinical and vaccine immunology : CVI
  • [ISO-abbreviation] Clin. Vaccine Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / N01AI30021; United States / NIAID NIH HHS / AI / AI-30021; United States / NIAID NIH HHS / AI / AI-69695
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Lipopolysaccharides; 0 / Lipoproteins; 0 / Teichoic Acids; 56411-57-5 / lipoteichoic acid; EC 3.1.1.34 / Lipoprotein Lipase; EC 3.1.1.47 / 1-Alkyl-2-acetylglycerophosphocholine Esterase; RGL5YE86CZ / Hydrofluoric Acid
  • [Other-IDs] NLM/ PMC2725534
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53. Matsushita T, Horikawa M, Iwata Y, Tedder TF: Regulatory B cells (B10 cells) and regulatory T cells have independent roles in controlling experimental autoimmune encephalomyelitis initiation and late-phase immunopathogenesis. J Immunol; 2010 Aug 15;185(4):2240-52
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  • Experimental autoimmune encephalomyelitis (EAE) is a T lymphocyte-mediated autoimmune disease of the CNS.
  • B10 cell numbers expanded quickly within the spleen, but not CNS following myelin oligodendrocyte glycoprotein(35-55) immunization, which paralleled B10 cell regulation of disease initiation.
  • The adoptive transfer of myelin oligodendrocyte glycoprotein(33-35)-sensitized B10 cells into wild-type mice reduced EAE initiation dramatically.
  • However, B10 cells did not suppress ongoing EAE disease.
  • Rather, Treg numbers expanded significantly within the CNS during disease progression, which paralleled their negative regulation of late-phase disease.
  • Likewise, the preferential depletion of B10 cells in vivo during disease initiation enhanced EAE pathogenesis, whereas Treg depletion enhanced late-phase disease.
  • B10 cells did not regulate T cell proliferation during in vitro assays, but significantly altered CD4(+) T cell IFN-gamma and TNF-alpha production.
  • Thus, B10 cells predominantly control disease initiation, whereas Tregs reciprocally inhibit late-phase disease, with overlapping B10 cell and Treg functions shaping the normal course of EAE immunopathogenesis.

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  • (PMID = 20624940.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / U19 AI056363; United States / NIAID NIH HHS / AI / U54 AI057157; United States / NIAID NIH HHS / AI / AI56363
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Cd22 protein, mouse; 0 / Cytokines; 0 / Glycoproteins; 0 / Myelin-Oligodendrocyte Glycoprotein; 0 / Peptide Fragments; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / myelin oligodendrocyte glycoprotein (35-55); 130068-27-8 / Interleukin-10
  • [Other-IDs] NLM/ NIHMS495305; NLM/ PMC3717968
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54. Hung YH, Ou TT, Lin CH, Li RN, Lin YC, Tsai WC, Liu HW, Yen JH: IkBα promoter polymorphisms in patients with ankylosing spondylitis. Rheumatol Int; 2009 Nov;30(1):93-7
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  • The IκBα-881A/G, -826C/T, -550A/T, -519C/T, and -297C/T polymorphisms were determined by the polymerase chain reaction/restriction fragment length polymorphism method.
  • [MeSH-minor] Adult. Case-Control Studies. Chi-Square Distribution. Female. Gene Frequency. Genetic Predisposition to Disease. Haplotypes. Humans. Male. Middle Aged. NF-KappaB Inhibitor alpha. Odds Ratio. Phenotype. Polymerase Chain Reaction. Risk Assessment. Risk Factors. Taiwan / epidemiology

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  • (PMID = 19363678.001).
  • [ISSN] 1437-160X
  • [Journal-full-title] Rheumatology international
  • [ISO-abbreviation] Rheumatol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / NFKBIA protein, human; 139874-52-5 / NF-KappaB Inhibitor alpha
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55. Jiang L, Wei XF, Yi DH, Xu P, Liu H, Chang Q, Yang SM, Li ZF, Gao HB, Hao GJ: Synergistic effects of cyclic strain and Th1-like cytokines on tenascin-C production by rheumatic aortic valve interstitial cells. Clin Exp Immunol; 2009 Feb;155(2):216-23
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  • Tenascin-C (TN-C) is a key component of extracellular matrix (ECM) and its expression process is poorly understood during rheumatic heart valvular disease (RHVD).
  • In this study, we found that interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and TN-C concentrations in patients with RHVD were significantly higher than in normal controls.
  • Antibodies neutralizing IFN-gamma or TNF-alpha could attenuate patients' sera-induced TN-C transcription by isolated rheumatic aortic valves interstitial cells.
  • By application with different protein kinase inhibitors, we found that combined with cyclic strain, TNF-alpha and IFN-gamma induced TN-C transcription through the RhoA/ROCK signalling pathway.
  • At the same time, p38 mitogen-activated protein kinase was involved in TNF-alpha and IFN-gamma induced TN-C transcription.
  • TNF-alpha also increased TN-C mRNA level by additional PKC and ERK 1/2 activation.
  • Our finding revealed a new insight into ECM remodelling during RHVD pathogenesis and new mechanisms involved in the clinical anti-IFN-gamma and anti-TNF-alpha therapy.
  • [MeSH-major] Aortic Valve / metabolism. Cytokines / physiology. Rheumatic Heart Disease / metabolism. Tenascin / biosynthesis
  • [MeSH-minor] Adult. Cells, Cultured. Female. Heart-Assist Devices. Humans. Interferon-gamma / blood. Male. Middle Aged. RNA, Messenger / genetics. Receptors, Interferon / metabolism. Receptors, Tumor Necrosis Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Stress, Mechanical. Transcriptional Activation / immunology. Tumor Necrosis Factor-alpha / blood. Young Adult

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  • (PMID = 19040616.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Receptors, Interferon; 0 / Receptors, Tumor Necrosis Factor; 0 / Tenascin; 0 / Tumor Necrosis Factor-alpha; 0 / interferon gamma receptor; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2675252
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56. Davis NA, Crowe JE Jr, Pajewski NM, McKinney BA: Surfing a genetic association interaction network to identify modulators of antibody response to smallpox vaccine. Genes Immun; 2010 Dec;11(8):630-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The variation in antibody response to vaccination likely involves small contributions of numerous genetic variants, such as single-nucleotide polymorphisms (SNPs), which interact in gene networks and pathways.
  • To accumulate the bits of genetic information relevant to the phenotype that are distributed throughout the interaction network, we develop a network eigenvector centrality algorithm (SNPrank) that is sensitive to the weak main effects, gene-gene interactions and small higher-order interactions through hub effects.
  • Analogous to Google PageRank, we interpret the algorithm as the simulation of a random SNP surfer (RSS) that accumulates bits of information in the network through a dynamic probabilistic Markov chain.