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1. Plager DA, Leontovich AA, Henke SA, Davis MD, McEvoy MT, Sciallis GF 2nd, Pittelkow MR: Early cutaneous gene transcription changes in adult atopic dermatitis and potential clinical implications. Exp Dermatol; 2007 Jan;16(1):28-36
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  • [Title] Early cutaneous gene transcription changes in adult atopic dermatitis and potential clinical implications.
  • Therefore, we used high-density oligonucleotide arrays to identify cutaneous gene transcription changes associated with early AD inflammation as potential disease control targets.
  • Differential transcription occurring early in AD skin was indicated for (i) individual genes such as C-C chemokine ligand (CCL)18, CCL13, and interferon-alpha2 (IFNalpha2), (ii) genes associated with peroxisome proliferator-activated receptor (PPAR)alpha- and PPARgamma-regulated transcription, and possibly for (iii) immunoglobulin J-chain and heavy chain isotype transcripts.
  • These data suggest that local changes in immunoglobulin-associated transcription may favour IgE over secretory immunoglobulin (multimeric IgM and IgA) expression in AD skin.
  • [MeSH-minor] Adult. Biopsy. Case-Control Studies. Chemokines, CC / genetics. Chemokines, CC / metabolism. Female. Gene Expression Regulation. Humans. Immunoglobulin E / genetics. Immunoglobulin E / metabolism. Interferon-alpha / genetics. Interferon-alpha / metabolism. Male. Monocyte Chemoattractant Proteins / genetics. Monocyte Chemoattractant Proteins / metabolism. Oligonucleotide Array Sequence Analysis. PPAR alpha / genetics. PPAR alpha / metabolism. PPAR gamma / genetics. PPAR gamma / metabolism

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  • (PMID = 17181634.001).
  • [ISSN] 0906-6705
  • [Journal-full-title] Experimental dermatology
  • [ISO-abbreviation] Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / CCL13 protein, human; 0 / CCL18 protein, human; 0 / Chemokines, CC; 0 / Interferon-alpha; 0 / Monocyte Chemoattractant Proteins; 0 / PPAR alpha; 0 / PPAR gamma; 37341-29-0 / Immunoglobulin E
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2. Tokusashi Y, Asai K, Tamakawa S, Yamamoto M, Yoshie M, Yaginuma Y, Miyokawa N, Aoki T, Kino S, Kasai S, Ogawa K: Expression of NGF in hepatocellular carcinoma cells with its receptors in non-tumor cell components. Int J Cancer; 2005 Mar 10;114(1):39-45
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  • TrkA was detected in the smooth muscle cells of hepatic arteries, but it was negative in tumor cells as well as non-neoplastic hepatocytes. p75NTR and alpha-smooth muscle actin (alphaSMA) was expressed in HSCs in the background liver and fibroblast-like cells in stromal septa, whereas HSCs within the HCC tissues were mostly negative for p75NTR but positive for alphaSMA.
  • [MeSH-minor] Actins / analysis. Adult. Aged. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Hepatitis, Chronic / metabolism. Humans. Liver Cirrhosis / metabolism. Male. Middle Aged. RNA, Messenger / analysis. Receptor, Nerve Growth Factor. Receptor, trkA / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15523689.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptor, Nerve Growth Factor; 0 / Receptors, Nerve Growth Factor; 9061-61-4 / Nerve Growth Factor; EC 2.7.10.1 / Receptor, trkA
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3. Cassiani-Ingoni R, Coksaygan T, Xue H, Reichert-Scrivner SA, Wiendl H, Rao MS, Magnus T: Cytoplasmic translocation of Olig2 in adult glial progenitors marks the generation of reactive astrocytes following autoimmune inflammation. Exp Neurol; 2006 Oct;201(2):349-58
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  • Evidence of this process is found for months after disease initiation in the absence of new inflammatory infiltrates.
  • We further show that differentiation to astrocytes is induced in glial progenitors in vitro through exposure to the pro-inflammatory cytokine IFN-gamma, but not to TNF-alpha.
  • [MeSH-minor] Animals. Antigens / genetics. Antigens / metabolism. Cell Differentiation / drug effects. Cytoplasm / metabolism. Encephalomyelitis, Autoimmune, Experimental / immunology. Encephalomyelitis, Autoimmune, Experimental / metabolism. Encephalomyelitis, Autoimmune, Experimental / pathology. Glial Fibrillary Acidic Protein / genetics. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Interferon-gamma / pharmacology. Mice. Mice, Inbred C57BL. Microglia / cytology. Microglia / metabolism. Microscopy, Fluorescence. Proteoglycans / genetics. Proteoglycans / metabolism. RNA / genetics. RNA / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16814281.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [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 / Antigens; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glial Fibrillary Acidic Protein; 0 / Nerve Tissue Proteins; 0 / Olig2 protein, mouse; 0 / Proteoglycans; 0 / Tumor Necrosis Factor-alpha; 0 / chondroitin sulfate proteoglycan 4; 63231-63-0 / RNA; 82115-62-6 / Interferon-gamma
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4. Shabbeer J, Robinson M, Desnick RJ: Detection of alpha-galactosidase a mutations causing Fabry disease by denaturing high performance liquid chromatography. Hum Mutat; 2005 Mar;25(3):299-305
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  • [Title] Detection of alpha-galactosidase a mutations causing Fabry disease by denaturing high performance liquid chromatography.
  • Mutations in the alpha-galactosidase A (alpha-Gal A, GLA) gene cause Fabry disease, an X-linked recessive lysosomal storage disease.
  • Here we report the development and use of DHPLC to rapidly and cost-effectively screen for alpha-Gal A mutations.
  • Optimal DHPLC partial denaturing conditions for mutation detection were established for each PCR amplicon corresponding to the seven alpha-Gal A exons and their adjacent intronic/flanking sequences.
  • Sequencing all seven alpha-Gal A gene amplicons in the seven at-risk females who had normal DHPLC profiles excluded them as mutation carriers.
  • This DHPLC method should improve the rapidity and cost-effectiveness of alpha-Gal A mutation identification in affected males and carrier females for Fabry disease.
  • [MeSH-major] Chromatography, High Pressure Liquid. DNA Mutational Analysis / methods. Fabry Disease / genetics. alpha-Galactosidase / genetics
  • [MeSH-minor] Amino Acid Substitution. Cost-Benefit Analysis. Exons / genetics. Female. Gene Frequency. Genotype. Heterozygote Detection / methods. Humans. Introns / genetics. Lymphocytes / enzymology. Male. Mutation, Missense. Nucleic Acid Denaturation. Point Mutation. Polymerase Chain Reaction. Polymorphism, Genetic. Sequence Analysis, DNA

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15712228.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 M01RR00071; United States / NIDDK NIH HHS / DK / R37 DK34045
  • [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.; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.1.22 / alpha-Galactosidase
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5. Jaarsma D, Teuling E, Haasdijk ED, De Zeeuw CI, Hoogenraad CC: Neuron-specific expression of mutant superoxide dismutase is sufficient to induce amyotrophic lateral sclerosis in transgenic mice. J Neurosci; 2008 Feb 27;28(9):2075-88
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  • Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS), an adult-onset progressive paralytic disease characterized by loss of motor neurons, and cause an ALS-like disease when expressed in mice.
  • Recent data have suggested that motor neuron degeneration results from toxic actions of mutant SOD1 operating in both motor neurons and their neighboring glia, raising the question whether mutant SOD1 expression selectively in neurons is sufficient to induce disease.
  • In addition, we show that crossing our neuron-specific mutant SOD1 mice with ubiquitously wild-type SOD1-expressing mice leads to dramatic wild-type SOD1 aggregation in oligodendroglia after the onset of neuronal degeneration.
  • [MeSH-minor] Animals. Antigens, Thy-1 / physiology. Dendrites / metabolism. Dendrites / pathology. Dendrites / ultrastructure. Disease Models, Animal. Gene Expression Regulation / genetics. Humans. Mice. Mice, Transgenic. Microscopy, Electron, Transmission / methods. Nerve Tissue Proteins / metabolism. Oligodendroglia / metabolism. Oligodendroglia / pathology. Oligodendroglia / ultrastructure. Silver Staining / methods. Ubiquitin / metabolism. alpha-Crystallin B Chain / metabolism


6. Ladell K, Hellerstein MK, Cesar D, Busch R, Boban D, McCune JM: Central memory CD8+ T cells appear to have a shorter lifespan and reduced abundance as a function of HIV disease progression. J Immunol; 2008 Jun 15;180(12):7907-18
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  • [Title] Central memory CD8+ T cells appear to have a shorter lifespan and reduced abundance as a function of HIV disease progression.
  • Progressive HIV disease has been associated with loss of memory T cell responses to Ag.
  • HIV-negative subjects and antiretroviral-untreated HIV-infected subjects in varying stages of HIV disease were studied.
  • In pilot studies in HIV-infected subjects, T(CM) cells appeared to have a shorter half-life and reduced abundance, particularly in those with high viral loads; T(EMRA) cells, by contrast, retained a long half-life and accumulated in the face of progressive HIV disease.

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  • (PMID = 18523254.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / DPI OD 00329; United States / NIAID NIH HHS / AI / R37 AI043866; United States / NIAID NIH HHS / AI / R01 AI043866; United States / NCRR NIH HHS / RR / UL1 RR024131; United States / NIAID NIH HHS / AI / U01 AI 43641; United States / NCRR NIH HHS / RR / UL1 RR 024131-01; United States / NIH HHS / OD / DP1 OD000329; United States / NCRR NIH HHS / RR / UL1 RR024131-01; United States / NIH HHS / OD / DP1 OD000329-05; United States / NIAID NIH HHS / AI / R37 AI040312-14; United States / NIAID NIH HHS / AI / R37 AI040312; United States / NIAID NIH HHS / AI / R37 AI 40312; United States / NIAID NIH HHS / AI / R01 AI 43866
  • [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 / Antigens, CD57; 0 / IL18R1 protein, human; 0 / Interleukin-18 Receptor alpha Subunit; 0 / Receptors, Interleukin-7; 0 / interleukin-7 receptor, alpha chain
  • [Other-IDs] NLM/ NIHMS60180; NLM/ PMC2562545
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7. Kiyosue M, Fujisawa M, Kinoshita K, Hori M, Ozaki H: Different susceptibilities of spontaneous rhythmicity and myogenic contractility to intestinal muscularis inflammation in the hapten-induced colitis. Neurogastroenterol Motil; 2006 Nov;18(11):1019-30
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  • [Title] Different susceptibilities of spontaneous rhythmicity and myogenic contractility to intestinal muscularis inflammation in the hapten-induced colitis.
  • We examined the time-dependent changes in the immunoreactivity of the smooth muscle region and the accompanying motility disorder in a hapten-induced rat model of colitis.
  • The expression of proinflammatory cytokine mRNAs (TNF-alpha, IL-1beta and IL-6) and proteins in the muscle layer was increased at 2 days, then began to decrease, returning to control levels at 14 days.
  • [MeSH-major] Colitis / physiopathology. Gastrointestinal Motility / physiology. Intestinal Mucosa / physiology. Muscle Contraction / physiology. Muscle, Smooth / physiopathology
  • [MeSH-minor] Animals. Cytokines / metabolism. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Gene Expression. Haptens. Immunohistochemistry. Inflammation / chemically induced. Male. Peroxidase / metabolism. RNA, Messenger / analysis. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Trinitrobenzenesulfonic Acid / toxicity

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  • (PMID = 17040413.001).
  • [ISSN] 1350-1925
  • [Journal-full-title] Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
  • [ISO-abbreviation] Neurogastroenterol. Motil.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Haptens; 0 / RNA, Messenger; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid; EC 1.11.1.7 / Peroxidase
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8. Malamut G, Cabane C, Dubuquoy L, Malapel M, Dérijard B, Gay J, Tamboli C, Colombel JF, Desreumaux P: No evidence for an involvement of the p38 and JNK mitogen-activated protein in inflammatory bowel diseases. Dig Dis Sci; 2006 Aug;51(8):1443-53
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  • [Title] No evidence for an involvement of the p38 and JNK mitogen-activated protein in inflammatory bowel diseases.
  • Involvement of mitogen-activated protein (MAPK) in inflammatory bowel disease (IBD) remains enigmatic.
  • SB203580 decreased the p38 activity but displayed no clinical nor biological therapeutic effect.
  • [MeSH-major] Colitis, Ulcerative / metabolism. Inflammatory Bowel Diseases / metabolism. JNK Mitogen-Activated Protein Kinases / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Adult. Animals. Blotting, Western. Disease Models, Animal. Enzyme Inhibitors / therapeutic use. Female. Gene Expression. Humans. Imidazoles / therapeutic use. Interleukin-1 / genetics. Intestinal Mucosa / metabolism. Male. Mice. Mice, Inbred BALB C. Middle Aged. Polymerase Chain Reaction. Prognosis. Pyridines / therapeutic use. RNA, Messenger / genetics. Trinitrobenzenesulfonic Acid / toxicity. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16838116.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Interleukin-1; 0 / Pyridines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; OU13V1EYWQ / SB 203580
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9. Attanasio F, Cataldo S, Fisichella S, Nicoletti S, Nicoletti VG, Pignataro B, Savarino A, Rizzarelli E: Protective effects of L- and D-carnosine on alpha-crystallin amyloid fibril formation: implications for cataract disease. Biochemistry; 2009 Jul 14;48(27):6522-31
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  • [Title] Protective effects of L- and D-carnosine on alpha-crystallin amyloid fibril formation: implications for cataract disease.
  • Mildly denaturing conditions induce bovine alpha-crystallin, the major structural lens protein, to self-assemble into fibrillar structures in vitro.
  • The natural dipeptide l-carnosine has been shown to have potential protective and therapeutic significance in many diseases.
  • Here we report the inhibitory effect induced by the peptide (l- and d-enantiomeric form) on alpha-crystallin fibrillation and the almost complete restoration of the chaperone activity lost after denaturant and/or heat stress.
  • Scanning force microscopy (SFM), thioflavin T, and a turbidimetry assay have been used to determine the morphology of alpha-crystallin aggregates in the presence and absence of carnosine.
  • DSC and a near-UV CD assay evidenced that the structural precursors of amyloid fibrils are polypeptide chain segments that lack stable structural elements.
  • Moreover, we have found a disassembling effect of carnosine on alpha-crystallin amyloid fibrils.
  • [MeSH-major] Amyloid / chemistry. Carnosine / chemistry. Cataract / metabolism. alpha-Crystallins / chemistry

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  • (PMID = 19441807.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Molecular Chaperones; 0 / alpha-Crystallins; 8HO6PVN24W / Carnosine
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10. Imura K, Yoshioka T, Hikita I, Hirasawa T, Sakata T, Matsutani T, Horikawa T, Arimura A: Association of T-cell receptor Vbeta haplotypes with dry skin in DS-Nh mice. Clin Exp Dermatol; 2009 Jan;34(1):61-7
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  • BACKGROUND: Although dry skin and T cell-dependent disease exacerbation are characteristic features of atopic dermatitis (AD), the involvement of T cells in the development of dry skin remains unclear.
  • We analysed the TCRVbeta chain usage and cytokine response to antimouse CD3 monoclonal antibodies in the splenocytes from the two mouse substrains.
  • [MeSH-major] Dermatitis, Atopic / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology
  • [MeSH-minor] Animals. Cytokines / metabolism. Disease Models, Animal. Haplotypes. Immunohistochemistry. Mice. Mice, Inbred Strains. RNA, Messenger / metabolism

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  • (PMID = 19018787.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [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, Antigen, T-Cell, alpha-beta
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11. Koesters SA, Alimonti JB, Wachihi C, Matu L, Anzala O, Kimani J, Embree JE, Plummer FA, Fowke KR: IL-7Ralpha expression on CD4+ T lymphocytes decreases with HIV disease progression and inversely correlates with immune activation. Eur J Immunol; 2006 Feb;36(2):336-44
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  • [Title] IL-7Ralpha expression on CD4+ T lymphocytes decreases with HIV disease progression and inversely correlates with immune activation.
  • Many factors can influence the rate of HIV disease progression, including those that maintain T cell homeostasis.
  • The present study examined the expression of the IL-7Ralpha chain on naïve and memory T lymphocyte subsets of both HIV-positive and HIV-negative individuals from Nairobi, Kenya to assess the role of IL-7Ralpha in HIV disease.
  • [MeSH-minor] Apoptosis / immunology. CD4 Lymphocyte Count. Disease Progression. Humans. Immunologic Memory / immunology. Lymphocyte Activation. Male. Signal Transduction / immunology. Viral Load

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  • (PMID = 16421946.001).
  • [ISSN] 0014-2980
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Receptors, Interleukin-7; 0 / interleukin-7 receptor, alpha chain
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12. Hasegawa K: [Genetic basis for skeletal disease. Osteogenesis imperfecta and genetic abnormalities]. Clin Calcium; 2010 Aug;20(8):1190-5
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  • [Title] [Genetic basis for skeletal disease. Osteogenesis imperfecta and genetic abnormalities].
  • Patients with osteogenesis imperfecta (OI) represent various degrees of bone fragility and accompany many clinical manifestations such as dentinogenesis imperfecta, blue sclera, growth disturbance, hearing impairment and so on.
  • Although most OI is caused by genetic mutation of type I collagen gene ; COL1A1 and COL1A2, other genes that concerns post-translational modification of type I collagen molecules such as CRTAP, LEPRE1, PPIB, SERPINH1 and FKBP10 were found to be the causative candidates of OI.
  • On the other hand, genetic causes of type V and type VI OI are not identified.
  • [MeSH-minor] Collagen / genetics. Collagen Type I / genetics. Collagen Type I / metabolism. Cyclophilins / genetics. Extracellular Matrix Proteins / genetics. HSP47 Heat-Shock Proteins / genetics. Humans. Membrane Glycoproteins / genetics. Mutation. Proteoglycans / genetics. Tacrolimus Binding Proteins / genetics

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  • (PMID = 20675929.001).
  • [ISSN] 0917-5857
  • [Journal-full-title] Clinical calcium
  • [ISO-abbreviation] Clin Calcium
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CRTAP protein, human; 0 / Collagen Type I; 0 / Extracellular Matrix Proteins; 0 / HSP47 Heat-Shock Proteins; 0 / LEPRE1 protein, human; 0 / Membrane Glycoproteins; 0 / Proteoglycans; 0 / SERPINH1 protein, human; 0 / alpha 2(I) collagen; 0 / collagen type I, alpha 1 chain; 137497-17-7 / cyclophilin B; 9007-34-5 / Collagen; EC 5.2.1.- / Cyclophilins; EC 5.2.1.- / Tacrolimus Binding Proteins; EC 5.2.1.8 / FKBP10 protein, human
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13. Lin YL, Li M: Human cytomegalovirus and Epstein-Barr virus inhibit oral bacteria-induced macrophage activation and phagocytosis. Oral Microbiol Immunol; 2009 Jun;24(3):243-8
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  • INTRODUCTION: Periodontal disease is an inflammatory condition caused by periodontal microorganisms.
  • Viruses such as human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) are associated with certain types of periodontal disease, but their roles in promoting the disease are unclear.
  • Bacteria-induced macrophage activation was assayed by measuring the levels of tumor necrosis factor-alpha (TNF-alpha) produced in the media, and phagocytic activity was analysed by a phagocytosis assay with fluorescein isothiocyanate-labeled bacteria.
  • The virus-infected macrophages were also subjected to semi-quantitative polymerase chain reaction to measure the expression of toll-like receptor 9, which is involved in the activation of phagocytosis-related pathways.
  • RESULTS: Both HCMV and EBV significantly diminished the TNF-alpha production typically induced by oral bacteria, inhibited the phagocytic activity of macrophages, and downregulated the expression of toll-like receptor 9.
  • CONCLUSION: Infection by HCMV or EBV inhibits the functional ability of macrophages to respond to bacterial challenge, thereby suggesting their pathogenic role in the development of periodontal disease.

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  • (PMID = 19416455.001).
  • [ISSN] 1399-302X
  • [Journal-full-title] Oral microbiology and immunology
  • [ISO-abbreviation] Oral Microbiol. Immunol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR020145; United States / NCRR NIH HHS / RR / RFA-RR-03-014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / TLR9 protein, human; 0 / Toll-Like Receptor 9; 0 / Tumor Necrosis Factor-alpha; I223NX31W9 / Fluorescein-5-isothiocyanate
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14. Nadler EP, Patterson D, Violette S, Weinreb P, Lewis M, Magid MS, Greco MA: Integrin alphavbeta6 and mediators of extracellular matrix deposition are up-regulated in experimental biliary atresia. J Surg Res; 2009 Jun 1;154(1):21-9
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  • Human liver from patients with BA and those having a resection for nonfibrosing diseases was also evaluated.
  • Furthermore, integrin alpha(v) beta(6) mRNA expression was increased on days 7 (11-fold) and 14 (6-fold).
  • Presence of integrin alpha(v) beta(6) protein was confirmed by IHC in both mouse and human specimens in the proliferating biliary epithelium.
  • Furthermore, increased gene expression of integrin alpha(v)beta(6) was demonstrated and IHC confirmed protein expression.
  • Integrin alpha(v)beta(6) or the inhibitors of ECM breakdown may be attractive targets for future treatment strategies.
  • [MeSH-minor] Animals. Animals, Newborn. Disease Models, Animal. Immunohistochemistry. Matrix Metalloproteinase 7 / genetics. Mice. Mice, Inbred BALB C. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tissue Inhibitor of Metalloproteinase-1 / genetics. Up-Regulation

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  • (PMID = 19084240.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Integrins; 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / integrin alphavbeta6; EC 3.4.24.23 / Matrix Metalloproteinase 7
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15. Bitu CC, Sobral LM, Kellermann MG, Martelli-Junior H, Zecchin KG, Graner E, Coletta RD: Heterogeneous presence of myofibroblasts in hereditary gingival fibromatosis. J Clin Periodontol; 2006 Jun;33(6):393-400
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  • To characterize the presence of myofibroblasts, the expression of specific myofibroblast marker smooth muscle isoform of alpha-actin (alpha-SMA) was examined by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot, immunofluorescence, and flow cytometric analysis.
  • Immunohistochemistry against the alpha-SMA antigen was performed in the gingival tissue samples.
  • RESULTS: Our results demonstrated a significant increase in the expression of the myofibroblast marker alpha-SMA in cells from one HGF family (designed as HGF Family 2), which are also characterized by an elevated expression of type I collagen, TGF-beta1 and connective tissue growth factor (CTGF).
  • Additionally, alpha-SMA-positive cells were broadly detected in the gingival tissue samples from HGF Family 2 patients.
  • In contrast, alpha-SMA expression by HGF Family 1 cells was quite similar to NG cells and no myofibroblasts were detected immunohistochemically, despite the higher levels of TGF-beta1 and type I collagen in HGF Family 1 fibroblasts than in NG cells.
  • This could be an underlying reason for the high variable clinical expressivity of disease.
  • [MeSH-minor] Actins / analysis. Analysis of Variance. Blotting, Western. Connective Tissue Growth Factor. Humans. Immediate-Early Proteins / analysis. Intercellular Signaling Peptides and Proteins / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / analysis. Transforming Growth Factor beta1

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  • (PMID = 16677327.001).
  • [ISSN] 0303-6979
  • [Journal-full-title] Journal of clinical periodontology
  • [ISO-abbreviation] J. Clin. Periodontol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Actins; 0 / CTGF protein, human; 0 / Ctgf protein, rat; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / TGFB1 protein, human; 0 / Tgfb1 protein, rat; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / smooth muscle actin, rat; 139568-91-5 / Connective Tissue Growth Factor
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16. Schaefer N, Tahara K, Websky MV, Koscielny A, Pantelis D, Kalff JC, Abu-Elmagd K, Hirner A, Türler A: Acute rejection and the muscularis propria after intestinal transplantation: the alloresponse, inflammation, and smooth muscle function. Transplantation; 2008 May 27;85(10):1465-75
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  • [Title] Acute rejection and the muscularis propria after intestinal transplantation: the alloresponse, inflammation, and smooth muscle function.
  • BACKGROUND: It has been shown that in transplantation the intestinal muscularis may act as an immunologically active layer via the activation of resident macrophages and the recruitment of leukocytes.
  • Thus we hypothesized that inflammation within the intestinal muscularis is involved in the promotion of acute rejection in intestinal allografts and that this causes smooth muscle dysfunction.
  • METHODS: Orthotopic allogenic and small bowel transplantation (Brown-Norway rats-Lewis rats) was performed without immunosuppression.
  • Animals were sacrificed 1, 4, and 7 days after small bowel transplantation.
  • Mediator mRNA expression was determined by real-time reverse-transcriptase polymerase chain reaction.
  • Only allogenic transplanted animals exhibited a significant second molecular inflammatory peak in the muscularis during rejection (mRNA induction for interleukin (IL)-6, intercellular adhesion molecule-1, monocyte chemoattractant protein (MCP)-1, interferon-gamma, IL-2, tumor necrosis factor-alpha, IL-10, inducible nitric oxide synthase).
  • CONCLUSIONS: The data shows that transplantation results in an early and temporary inflammatory response within the intestinal graft muscularis, that is reactivated and intensified during acute allograft rejection.
  • The immunoreaction within the intestinal muscularis leads to intestinal allograft smooth muscle dysfunction.
  • [MeSH-minor] Acute Disease. Animals. Bethanechol / pharmacology. Inflammation / etiology. Muscle Contraction / drug effects. Muscle, Smooth / pathology. Muscle, Smooth / physiopathology. Muscle, Smooth / transplantation. Peroxidase / metabolism. Rats. Rats, Inbred BN. Rats, Inbred Lew. Transplantation, Isogeneic / pathology

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  • (PMID = 18497688.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 004F72P8F4 / Bethanechol; EC 1.11.1.7 / Peroxidase
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17. 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.

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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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18. Suffia I, Reckling SK, Salay G, Belkaid Y: A role for CD103 in the retention of CD4+CD25+ Treg and control of Leishmania major infection. J Immunol; 2005 May 1;174(9):5444-55
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  • Here, we show that expression of alpha(E)beta(7) integrin is necessary for the homing of T(reg) at site of Leishmania major infection.
  • The vast majority of T(reg) present in the dermis at steady-state conditions or during L. major infection express the alpha(E) chain (CD103) of alpha(E)beta(7).
  • Such susceptible phenotype can be restored when T(reg) from wild-type mice were transferred in CD103(-/-) mice.
  • [MeSH-major] Antigens, CD / physiology. Cell Movement / immunology. Integrin alpha Chains / physiology. Leishmania major / immunology. Leishmaniasis, Cutaneous / immunology. Receptors, Interleukin-2 / biosynthesis. T-Lymphocytes, Regulatory / cytology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adoptive Transfer. Animals. Cell Membrane / immunology. Cell Membrane / metabolism. Chronic Disease. Down-Regulation / immunology. Immunity, Innate / genetics. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Mice, SCID. Skin / cytology. Skin / immunology. Skin / metabolism


19. Cho W, Messing A: Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice. Exp Cell Res; 2009 Apr 15;315(7):1260-72
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  • Alexander disease is a fatal leukoencephalopathy caused by dominantly-acting coding mutations in GFAP.
  • Previous work has also implicated elevations in absolute levels of GFAP as central to the pathogenesis of the disease.
  • To provide new tools for investigating the nature of astrocyte dysfunction in Alexander disease, we have established primary astrocyte cultures from two mouse models of Alexander disease, a transgenic that over-expresses wild type human GFAP, and a knock-in at the endogenous mouse locus that mimics a common Alexander disease mutation.
  • We find that mutant GFAP, as well as excess wild type GFAP, promotes formation of cytoplasmic inclusions, disrupts the cytoskeleton, decreases cell proliferation, increases cell death, reduces proteasomal function, and compromises astrocyte resistance to stress.

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  • (PMID = 19146851.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P01 NS042803-06A20006; United States / NICHD NIH HHS / HD / P30 HD003352; United States / NICHD NIH HHS / HD / P30 HD003352-38; United States / NICHD NIH HHS / HD / HD03352; United States / NINDS NIH HHS / NS / R01 NS060120; United States / NINDS NIH HHS / NS / P01 NS042803; United States / NINDS NIH HHS / NS / NS42803; United States / NINDS NIH HHS / NS / NS042803-06A20006; United States / NINDS NIH HHS / NS / NS060120-02; United States / NINDS NIH HHS / NS / NS060120; United States / NINDS NIH HHS / NS / R01 NS060120-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Oxidants; 0 / alpha-Crystallin B Chain; BBX060AN9V / Hydrogen Peroxide; EC 3.4.22.- / Caspases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ NIHMS85017; NLM/ PMC2665202
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20. Chkalina AV, Zviagin IV, Mamedov IZ, Britanova OV, Staroverov DB, Lebedev IuB: [The oligoclonal expansion of T cells: study of its stability over time]. Bioorg Khim; 2010 Mar-Apr;36(2):206-14
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  • This approach is based on the wide-range sequencing of cDNA of the beta-chain of the T-cellular receptor (TcR).
  • The long-time stable expansion of these T clones was demonstrated during the development of the disease by specific monitoring.
  • [MeSH-major] Receptors, Antigen, T-Cell, alpha-beta / genetics. Spondylitis, Ankylosing / immunology. T-Lymphocytes / immunology

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  • (PMID = 20531479.001).
  • [ISSN] 0132-3423
  • [Journal-full-title] Bioorganicheskaia khimiia
  • [ISO-abbreviation] Bioorg. Khim.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / DNA, Complementary; 0 / Receptors, Antigen, T-Cell, alpha-beta
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21. Andersson D, Kotarsky K, Wu J, Agace W, Duan RD: Expression of alkaline sphingomyelinase in yeast cells and anti-inflammatory effects of the expressed enzyme in a rat colitis model. Dig Dis Sci; 2009 Jul;54(7):1440-8
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  • Alkaline sphingomyelinase (Alk-SMase) is a key enzyme in the intestinal tract for digestion of dietary sphingomyelin (SM), which generates lipid messengers with cell-cycle regulating effects.
  • We found a tendency for decreased tumor necrosis factor (TNF)-alpha expression in the Alk-SMase-treated group.
  • This study, for the first time, provides a method to produce the enzyme and shows the potential applicability of the enzyme in the treatment of inflammatory bowel diseases.
  • [MeSH-minor] Administration, Rectal. Animals. Colon / pathology. Dextran Sulfate / adverse effects. Disease Models, Animal. Female. Inflammation / prevention & control. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Pichia / cytology. Pilot Projects. Polymerase Chain Reaction. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18989780.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 9042-14-2 / Dextran Sulfate; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase; EC 3.1.4.12 / intestinal alkaline sphingomyelinase, human
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22. Brasnu E, Wechsler B, Bron A, Charlotte F, Bliefeld P, Lehoang P, Marcelin AG, Bodaghi B: Efficacy of interferon-alpha for the treatment of Kaposi's sarcoma herpesvirus-associated uveitis. Am J Ophthalmol; 2005 Oct;140(4):746-8
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  • [Title] Efficacy of interferon-alpha for the treatment of Kaposi's sarcoma herpesvirus-associated uveitis.
  • PURPOSE: To report cases of uveitis that are associated with human herpesvirus-8 (HHV-8) and the impact of interferon-alpha therapy on their visual outcome.
  • RESULTS: Two patients of Mediterranean origin were included.
  • Histopathologic examination of conjunctival biopsy specimens confirmed Kaposi's sarcoma in the second case, and quantitative polymerase chain reaction identified HHV-8 DNA in the biopsy specimen.
  • Disease was controlled by interferon-alpha2a in both cases, but maintenance therapy was mandatory to prevent relapses.
  • Interferon alpha seems to be a good candidate and may be proposed in these cases.
  • [MeSH-major] Eye Infections, Viral / drug therapy. Herpesvirus 8, Human / isolation & purification. Interferon-alpha / therapeutic use. Sarcoma, Kaposi / drug therapy. Uveitis / drug therapy
  • [MeSH-minor] Aged. Antiviral Agents / therapeutic use. Biopsy. Child. Conjunctivitis / pathology. Conjunctivitis / virology. DNA, Viral / analysis. Female. Humans. Polymerase Chain Reaction. Recombinant Proteins

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  • (PMID = 16226536.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / DNA, Viral; 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
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23. Claeys KG, van der Ven PF, Behin A, Stojkovic T, Eymard B, Dubourg O, Laforêt P, Faulkner G, Richard P, Vicart P, Romero NB, Stoltenburg G, Udd B, Fardeau M, Voit T, Fürst DO: Differential involvement of sarcomeric proteins in myofibrillar myopathies: a morphological and immunohistochemical study. Acta Neuropathol; 2009 Mar;117(3):293-307
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  • Myofibrillar myopathies (MFMs) are rare inherited or sporadic progressive neuromuscular disorders with considerable clinical and genetic heterogeneity.
  • Immunohistochemistry showed that in MFM only a subset of Z-disc proteins, such as filamin C and its ligands myotilin and Xin, exhibited significant alterations in their localization, whereas other Z-disc proteins like alpha-actinin, myopodin and tritopodin, did not.
  • We conclude that the presence of 'rubbed-out' fibers are a suggestive feature for desminopathy or alphaB-crystallinopathy, and that MFM is not a general disease of the myofibril, but primarily affects a subgroup of stress-responsive Z-disc proteins.
  • [MeSH-major] Contractile Proteins / metabolism. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / metabolism. Microfilament Proteins / metabolism. Muscle Proteins / genetics. Muscle Proteins / metabolism. Muscle, Skeletal / pathology. Muscular Diseases / pathology. Myofibrils / pathology. Nuclear Proteins / metabolism
  • [MeSH-minor] Actins / metabolism. Adaptor Proteins, Signal Transducing / genetics. Adult. Biopsy. Cohort Studies. Connectin. Desmin / genetics. Female. Filamins. Humans. Immunohistochemistry. LIM Domain Proteins. Male. Middle Aged. Muscle Fibers, Skeletal / pathology. Necrosis / pathology. Vacuoles / pathology. alpha-Crystallin B Chain / genetics

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  • (PMID = 19151983.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP04088
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / Adaptor Proteins, Signal Transducing; 0 / Connectin; 0 / Contractile Proteins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Desmin; 0 / Filamins; 0 / LDB3 protein, human; 0 / LIM Domain Proteins; 0 / MYOT protein, human; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Nuclear Proteins; 0 / SYNPO2 protein, human; 0 / XIRP1 protein, human; 0 / alpha-Crystallin B Chain
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24. Hölttä V, Klemetti P, Sipponen T, Westerholm-Ormio M, Kociubinski G, Salo H, Räsänen L, Kolho KL, Färkkilä M, Savilahti E, Vaarala O: IL-23/IL-17 immunity as a hallmark of Crohn's disease. Inflamm Bowel Dis; 2008 Sep;14(9):1175-84
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  • [Title] IL-23/IL-17 immunity as a hallmark of Crohn's disease.
  • BACKGROUND: We studied the balance between ileal T-effector cells versus T-regulatory cells in active and inactive Crohn's disease (CD).
  • METHODS: We compared effector and regulatory T-cell-related markers such as interleukin (IL)-17, interferon (IFN)-gamma, IL-4, and Foxp3 transforming growth factor (TGF)-beta CTLA-4 and markers for innate immune activation such as IL-6, IL-10, IL-18, IL-23, tumor necrosis factor (TNF)-alpha, and IL-12p70, studied with immunohistochemistry and RT-PCR in ileal biopsies from patients with active or inactive CD and from control subjects.
  • The effect of IL-17 on IL-8 and TNF-alpha mRNA expression in epithelial cell line Caco-2 was studied.
  • RESULTS: The numbers of IL-4-, IL-17-, and IL-23(p19)-positive cells in the lamina propria were higher in patients with CD, both active and inactive, than in the controls. mRNA expression of IL-17A, IL-6, and Foxp3 was increased in the biopsies both from patients with active disease and those in remission, whereas mRNA expression of IL-23 was increased only in active disease.
  • Fecal IL-17 concentration was increased in patients with active disease.
  • IL-17 enhanced the IL-8 and TNF-alpha response of the epithelial cell line to lipopolysaccharide (LPS) in vitro.
  • CONCLUSIONS: Our findings suggest that activation of the IL-23/IL-17 axis is fundamentally connected to the etiology of CD and may represent the basis for the relapsing nature of the disease by increasing the sensitivity of epithelium to microbial LPS.
  • [MeSH-major] Crohn Disease / immunology. Interleukin-17 / immunology. Interleukin-23 / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. Aged. Caco-2 Cells. Enzyme-Linked Immunosorbent Assay. Feces / chemistry. Female. Forkhead Transcription Factors / genetics. Forkhead Transcription Factors / immunology. Humans. Ileum / immunology. Immunoenzyme Techniques. Interferon-gamma / genetics. Interferon-gamma / immunology. Interleukin-4 / genetics. Interleukin-4 / immunology. Male. Middle Aged. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18512248.001).
  • [ISSN] 1536-4844
  • [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 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-17; 0 / Interleukin-23; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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25. Yin ZH, Huang RL, Lu HY, Liu XY: Are humoral factors involved in the colonic mucosal lesion in portal hypertensive rats? Acta Gastroenterol Belg; 2007 Jul-Sep;70(3):271-6
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  • AIMS: With a prehepatic portal hypertensive rat model, we explored the involvement of humoral factors to the occurrence of portal hypertensive colopathy (PHC), another clinical entity besides portal hypertensive gastropathy (PHG) in portal hypertension, by investigating the expression of inducible nitric oxide synthase (iNOS), endothelial constitutive NOS (ecNOS), endothelin-1 (ET-1), tumour necrosis factor alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) in the colonic and gastric mucosa.
  • Two weeks after complete obstruction of the portal vein, the portal pressure was measured and the expression of iNOS, ecNOS, ET-1, TNF-alpha and VEGF in the colonic and gastric mucosa were detected by RT-PCR and immunohistochemistry methods.
  • Significantly up-regulation of the mRNA levels of iNOS (P < 0.01), ET-1 (P < 0.05) and TNF-alpha (P < 0.01), but not ecNOS and VEGF, were detected in the colonic mucosa of portal hypertensive rats compared with control.
  • The mRNA of iNOS, ecNOS, ET-1, TNF-alpha and VEGF were all significantly increased at varied levels in the gastric mucosa as compared to control (P all < 0.05).
  • No difference of the appearance and localization of immunostaining of iNOS, ecNOS, ET-1, TNF-alpha and VEGF in the colonic and gastric mucosa were seen between two groups.
  • CONCLUSIONS: These data suggest the involvement of the upregulation of iNOS, ET-1 and TNF-alpha in the colonic mucosal lesion of portal hypertensive rats.
  • [MeSH-major] Colonic Diseases / metabolism. Hypertension, Portal / complications. Intestinal Mucosa / metabolism
  • [MeSH-minor] Adrenal Glands / blood supply. Animals. Disease Models, Animal. Endothelin-1 / analysis. Gastric Mucosa / blood supply. Gastric Mucosa / metabolism. Immunohistochemistry. Ligation. Male. Nitric Oxide Synthase Type II / analysis. Nitric Oxide Synthase Type III / analysis. Portal Pressure / physiology. Portal Vein / surgery. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / analysis. Up-Regulation. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 18074736.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, rat; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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26. Schmilovitz-Weiss H, Stemmer SM, Liberzon E, Avigad S, Sulkes J, Belinki A, Kazatsker A, Ben-Ari Z: Quantitation of alpha-fetoprotein messenger RNA for early detection of recurrent hepatocellular carcinoma: a prospective pilot study. Cancer Detect Prev; 2006;30(2):204-9
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  • [Title] Quantitation of alpha-fetoprotein messenger RNA for early detection of recurrent hepatocellular carcinoma: a prospective pilot study.
  • BACKGROUND: Alpha-fetoprotein (AFP) messenger RNA (mRNA) may be a potential marker of the dissemination of hepatocellular carcinoma (HCC) cells into the circulation.
  • METHODS: Peripheral blood samples were taken from seven patients before and after treatment for measurement of AFP mRNA levels by reverse-transcriptase polymerase chain reaction (RT-PCR).
  • The level of AFP mRNA in blood was serially determined, and the time course was related to the clinical course and disease outcome.
  • CONCLUSIONS: Although this is a small sample size pilot study these findings imply that quantitative measurement of AFP-expressing cells in peripheral blood may serve as a marker of HCC recurrence.
  • [MeSH-major] Carcinoma, Hepatocellular / blood. Carcinoma, Hepatocellular / diagnosis. Liver Neoplasms / blood. Liver Neoplasms / diagnosis. Neoplasm Recurrence, Local / blood. Neoplasm Recurrence, Local / diagnosis. RNA, Messenger / blood. alpha-Fetoproteins / analysis
  • [MeSH-minor] Aged. Catheter Ablation. Embolization, Therapeutic. Female. Humans. Male. Pilot Projects. Prognosis. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16638626.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / alpha-Fetoproteins
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27. Manzeniuk OIu, Malakho SG, Pekhov VM, Kosorukova IS, Poltaraus AB: [Characterization of the universal Russian reagent sets for real-time PCR and its application for molecular oncodiagnostic]. Mol Biol (Mosk); 2006 Mar-Apr;40(2):349-56
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  • No symptoms of minimal residual disease were found after 3.5 months since chemotherapy - fusion gene PML-RARalpha was not detected by real time PCR method.
  • These results are in agreement with clinical data.
  • [MeSH-major] DNA, Neoplasm / analysis. Leukemia, Promyelocytic, Acute / diagnosis. Neoplasm Proteins / analysis. Oncogene Proteins, Fusion / analysis. RNA, Neoplasm / analysis. Reagent Kits, Diagnostic
  • [MeSH-minor] Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Evaluation Studies as Topic. Humans. Neoplasm, Residual. Predictive Value of Tests. Reference Standards. Reverse Transcriptase Polymerase Chain Reaction / methods. Reverse Transcriptase Polymerase Chain Reaction / standards. Sensitivity and Specificity. Translocation, Genetic / genetics

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  • (PMID = 16637276.001).
  • [ISSN] 0026-8984
  • [Journal-full-title] Molekuliarnaia biologiia
  • [ISO-abbreviation] Mol. Biol. (Mosk.)
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / Reagent Kits, Diagnostic; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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28. Hamelet J, Maurin N, Fulchiron R, Delabar JM, Janel N: Mice lacking cystathionine beta synthase have lung fibrosis and air space enlargement. Exp Mol Pathol; 2007 Oct;83(2):249-53
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  • Severe hyperhomocysteinemia due to CBS deficiency confers diverse clinical manifestations, notably pulmonary thrombotic disease.
  • However, the association between hyperhomocysteinemia and chronic obstructive pulmonary disease is not well understood.
  • Analysis of profibrogenic factors was performed by real-time quantitative reverse transcription-polymerase chain reaction.
  • CBS-deficient mice develop fibrosis and air space enlargement in the lung, concomitant with an enhanced expression of heme oxygenase-1, pro(alpha)1 collagen type I, transforming growth factor-beta1 and alpha-smooth muscle actin.
  • The increased expression of alpha-smooth muscle actin and transforming growth factor-beta1 emphasizes the role of myofibroblasts differentiation in case of lung fibrosis due to CBS deficiency in mice.
  • [MeSH-minor] Animals. Cell Differentiation. Disease Models, Animal. Fibroblasts / pathology. Homocysteine / blood. Hyperhomocysteinemia / complications. Mice. Mice, Knockout. Polymerase Chain Reaction. Pulmonary Disease, Chronic Obstructive / etiology

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  • (PMID = 17543941.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0LVT1QZ0BA / Homocysteine; EC 4.2.1.22 / Cystathionine beta-Synthase
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29. Brell B, Temmesfeld-Wollbrück B, Altzschner I, Frisch E, Schmeck B, Hocke AC, Suttorp N, Hippenstiel S: Adrenomedullin reduces Staphylococcus aureus alpha-toxin-induced rat ileum microcirculatory damage. Crit Care Med; 2005 Apr;33(4):819-26
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  • [Title] Adrenomedullin reduces Staphylococcus aureus alpha-toxin-induced rat ileum microcirculatory damage.
  • The intestinal mucosa is very sensitive to tissue hypoxia.
  • Intestinal mucosa dysfunction may allow translocation of bacteria and their products, thereby perpetuating sepsis and inflammation.
  • Staphylococcus aureus alpha-toxin is a major pathogenicity determinant of this bacterium, provoking cardiovascular collapse.
  • Using alpha-toxin as a well-defined strong initiator of an inflammatory reaction, we tested the hypothesis that exogenously applied adrenomedullin stabilizes gut microcirculation.
  • INTERVENTIONS: Administration of S. aureus alpha-toxin before or after infusion of adrenomedullin.
  • MEASUREMENTS AND MAIN RESULTS: Injection of a bolus of 1 microg of alpha-toxin in the superior mesenteric artery in a constant-flow, blood-perfused preparation of rat ileum increased perfusion pressure and relative hemoglobin concentration and decreased mucosal hemoglobin oxygen saturation.
  • Continuous infusion of adrenomedullin (0.1 micromol/L) significantly reduced these alpha-toxin-related effects.
  • Severe microvascular hyperpermeability observed in alpha-toxin-exposed ileum was abolished by adrenomedullin pretreatment.
  • In addition, adrenomedullin blocked alpha-toxin-induced endothelial myosin light chain phosphorylation, endothelial cell contraction, and subsequent loss of endothelial barrier function in vitro.
  • Treatment of alpha-toxin (infusion of 0.05 microg/mL)-exposed ileum with adrenomedullin (0.1 micromol/L) started 10 mins after onset of toxin application also significantly reduced superior mesenteric artery pressure and permeability increase.
  • CONCLUSIONS: In summary, these data suggest that exogenous adrenomedullin protects ileum by reducing alpha-toxin-induced microcirculatory disturbances and by stabilizing endothelial barrier function.
  • [MeSH-minor] Actin Cytoskeleton / metabolism. Adrenomedullin. Animals. Capillary Permeability / drug effects. Disease Models, Animal. Infusions, Intravenous. Intestinal Mucosa / blood supply. Intestinal Mucosa / drug effects. Intestinal Mucosa / physiopathology. Male. Microcirculation / drug effects. Microcirculation / physiopathology. Myosin Light Chains / metabolism. Phosphorylation / drug effects. Prospective Studies. Rats. Rats, Sprague-Dawley. Treatment Outcome

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  • (PMID = 15818111.001).
  • [ISSN] 0090-3493
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Bacterial Toxins; 0 / Myosin Light Chains; 0 / Peptides; 148498-78-6 / Adrenomedullin
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30. Amirzargar A, Sadeghi M, Khosravi F, Dianat S, Naroueynejad M, Nicknam MH, Hatmi N, Ansaripour B, Moradi B, Nikbin B: Th1 and Th2 cytokine gene polymorphisms in two indigenous ethnic groups in Iran. Int J Immunogenet; 2006 Dec;33(6):429-37
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  • Cytokine single nucleotide polymorphisms have been extensively studied in different normal populations as well as in relation to diseases.
  • The polymorphisms of cytokine genes are potentially important as genetic predictors of the disease susceptibility and clinical outcome or as a tool for anthropological studies.
  • The allele and genotype frequencies of Th1 and Th2 cytokines SNP including interleukin (IL)-2, IL-4, IL-6, IL-10, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma have been investigated, using the polymerase chain reaction-sequence-specific primer method.
  • [MeSH-minor] Humans. Interferon-gamma / genetics. Interleukin-10 / genetics. Interleukin-2 / genetics. Interleukin-4 / genetics. Interleukin-6 / genetics. Iran / ethnology. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 17117953.001).
  • [ISSN] 1744-3121
  • [Journal-full-title] International journal of immunogenetics
  • [ISO-abbreviation] Int. J. Immunogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-2; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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31. Doss-Pepe EW, Chen L, Madura K: Alpha-synuclein and parkin contribute to the assembly of ubiquitin lysine 63-linked multiubiquitin chains. J Biol Chem; 2005 Apr 29;280(17):16619-24
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  • [Title] Alpha-synuclein and parkin contribute to the assembly of ubiquitin lysine 63-linked multiubiquitin chains.
  • Mutations in alpha-synuclein, Parkin, and UCH-L1 cause heritable forms of Parkinson disease.
  • Unlike alpha-synuclein, for which no precise biochemical function has been elucidated, Parkin functions as a ubiquitin E3 ligase, and UCH-L1 is a deubiquitinating enzyme.
  • The E3 ligase activity of Parkin in Parkinson disease is poorly understood and is further obscured by the fact that multiubiquitin chains can be formed through distinct types of linkages that regulate diverse cellular processes.
  • Because both Parkin and alpha-synuclein can regulate the activity of the dopamine transporter, we investigated whether they influenced ubiquitin lysine 63-linked chain assembly.
  • These studies revealed novel biochemical activities for both Parkin and alpha-synuclein.
  • Our results and the results of others indicate that Parkin can promote both lysine 48- and lysine 63-linked ubiquitin chains. alpha-Synuclein also stimulated the assembly of lysine 63-linked ubiquitin chains.
  • Because UCH-L1, a ubiquitin hydrolase, was recently reported to form lysine 63-linked conjugates, it is evident that three proteins that are genetically linked to Parkinson disease can contribute to lysine 63 multiubiquitin chain formation.
  • [MeSH-minor] Dimerization. Dopamine Plasma Membrane Transport Proteins. Endocytosis. Escherichia coli / metabolism. Glutathione Transferase / metabolism. Humans. Lysosomes / chemistry. Lysosomes / metabolism. Membrane Glycoproteins / chemistry. Membrane Transport Proteins / chemistry. Mutation. Parkinson Disease / metabolism. Proteasome Endopeptidase Complex / chemistry. Protein Binding. Ribosomes / chemistry. Synucleins. Time Factors. Ubiquitin / chemistry. Ubiquitin / metabolism. alpha-Synuclein

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  • (PMID = 15718234.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG01047; United States / NCI NIH HHS / CA / CA83875; United States / NINDS NIH HHS / NS / NS044081
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Plasma Membrane Transport Proteins; 0 / Membrane Glycoproteins; 0 / Membrane Transport Proteins; 0 / Nerve Tissue Proteins; 0 / SNCA protein, human; 0 / Synucleins; 0 / Ubiquitin; 0 / alpha-Synuclein; EC 2.5.1.18 / Glutathione Transferase; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / parkin protein; K3Z4F929H6 / Lysine
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32. Zhu MJ, Du M, Nathanielsz PW, Ford SP: Maternal obesity up-regulates inflammatory signaling pathways and enhances cytokine expression in the mid-gestation sheep placenta. Placenta; 2010 May;31(5):387-91
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  • MO increased mRNA levels of toll-like receptor (TLR) 2 (P < 0.05) and TLR4 (P = 0.06), macrophage markers cluster of differentiation (CD)11b (P = 0.06), CD14 and CD68 (P < 0.05), and proinflammatory cytokines tumor necrosis factor (TNF)alpha (P < 0.01), interleukin (IL)-6 (P < 0.05), IL-8(P < 0.01) and IL-18 (P = 0.06), in COT tissue.
  • Inflammatory c-Jun N-terminal kinase (JNK)/c-Jun and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) signaling pathways were up-regulated (P < 0.05) in COT of OB ewes.
  • [MeSH-minor] Animals. Antigens, CD / genetics. Antigens, CD / metabolism. Biomarkers / metabolism. Disease Models, Animal. Female. Fetal Blood / chemistry. Gene Expression Regulation, Developmental. Gestational Age. Lipids / analysis. Pregnancy. RNA, Messenger / metabolism. Signal Transduction / physiology. Toll-Like Receptors / genetics. Toll-Like Receptors / metabolism. Up-Regulation


33. Wikstrom ME, Batanero E, Smith M, Thomas JA, von Garnier C, Holt PG, Stumbles PA: Influence of mucosal adjuvants on antigen passage and CD4+ T cell activation during the primary response to airborne allergen. J Immunol; 2006 Jul 15;177(2):913-24
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  • We found a range of cell types acquired small amounts of fluorescent OVA in the DLN 4 h after per nasal administration.
  • Thus, we found no bias within the DLN in Ag handling or the primary T cell response associated with the eventual Th2 polarization induced by CT, and suggest that additional tissue-specific factors influence the development of allergic disease in the airways.

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  • (PMID = 16818746.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Allergens; 0 / Antigens; 0 / Antigens, CD8; 0 / CD8 antigen, alpha chain; 0 / Lipopolysaccharides; 9006-59-1 / Ovalbumin; 9012-63-9 / Cholera Toxin
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34. Ross OA, Braithwaite AT, Skipper LM, Kachergus J, Hulihan MM, Middleton FA, Nishioka K, Fuchs J, Gasser T, Maraganore DM, Adler CH, Larvor L, Chartier-Harlin MC, Nilsson C, Langston JW, Gwinn K, Hattori N, Farrer MJ: Genomic investigation of alpha-synuclein multiplication and parkinsonism. Ann Neurol; 2008 Jun;63(6):743-50
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  • [Title] Genomic investigation of alpha-synuclein multiplication and parkinsonism.
  • Herein we characterize five families with parkinsonism that have been identified to harbor multiplication of the chromosomal 4q21 locus containing the alpha-synuclein gene (SNCA).
  • The telomeric and centromeric breakpoints of each family were further narrowed using semiquantitative polymerase chain reaction with microsatellite markers and then screened for transposable repeat elements.
  • RESULTS: The severity of clinical presentation is correlated with SNCA dosage and does not appear to be overtly affected by the presence of other genes in the multiplicated region.
  • With the exception of the Lister kindred, in each family the multiplication event appears de novo.
  • The type and position of Alu/LINE repeats are also different at each breakpoint.
  • We hypothesize dysregulated expression of wild-type alpha-synuclein results in parkinsonism and may explain the recent association of common SNCA variants in sporadic Parkinson's disease.

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  • (PMID = 18571778.001).
  • [ISSN] 1531-8249
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 #NS40256; United States / NINDS NIH HHS / NS / P50 NS040256; United States / NIA NIH HHS / AG / P01 AG017216-090005; United States / NINDS NIH HHS / NS / N01-NS-2-2349; United States / NIA NIH HHS / AG / P01 AG17216; United States / NINDS NIH HHS / NS / P01 NS040256; United States / NIA NIH HHS / AG / P01 AG017216-05; United States / NIA NIH HHS / AG / P01 AG017216; United States / NIA NIH HHS / AG / P01 AG017216-09
  • [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 / alpha-Synuclein
  • [Other-IDs] NLM/ NIHMS110782; NLM/ PMC3850281
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35. Lavoie-Lamoureux A, Moran K, Beauchamp G, Mauel S, Steinbach F, Lefebvre-Lavoie J, Martin JG, Lavoie JP: IL-4 activates equine neutrophils and induces a mixed inflammatory cytokine expression profile with enhanced neutrophil chemotactic mediator release ex vivo. Am J Physiol Lung Cell Mol Physiol; 2010 Oct;299(4):L472-82
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  • Neutrophils are potent contributors to the lung pathophysiological changes occurring in allergic airway inflammation, which typically involve T helper type 2 (Th2) cytokine overexpression.
  • IL-4 type I receptor (IL-4Rα) and CD23 (FcεRII) expression were also upregulated by IL-4.
  • Importantly, disease as well as chronic antigenic exposure modified gene expression by PBN.
  • [MeSH-major] Asthma / metabolism. Interleukin-4 / metabolism. Interleukin-8 / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Chemotaxis, Leukocyte / immunology. Gene Expression Profiling. Horses. Immunoenzyme Techniques. Inflammation / genetics. Inflammation / immunology. Neutrophil Activation. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. STAT6 Transcription Factor / genetics. STAT6 Transcription Factor / metabolism. p38 Mitogen-Activated Protein Kinases / genetics. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 20639353.001).
  • [ISSN] 1522-1504
  • [Journal-full-title] American journal of physiology. Lung cellular and molecular physiology
  • [ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / RNA, Messenger; 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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36. Hong YB, Kim EY, Jung SC: Upregulation of proinflammatory cytokines in the fetal brain of the Gaucher mouse. J Korean Med Sci; 2006 Aug;21(4):733-8
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  • Gaucher disease is caused by a deficiency of glucocerebrosidase.
  • Patients with Gaucher disease are divided into three major phenotypes: chronic nonneuronopathic, acute neuronopathic, and chronic neuronopathic, based on symptoms of the nervous system, the severity of symptoms, and the age of disease onset.
  • The characteristics of patients with acute neuronopathic- and chronic neuronopathic-type Gaucher disease include oculomotor abnormalities, bulbar signs, limb rigidity, seizures and occasional choreoathetoid movements, and neuronal loss.
  • However, the mechanisms leading to the neurodegeneration of this disorder remain unknown.
  • To investigate brain dysfunction in Gaucher disease, we studied the possible role of inflammation in neurodegeneration during development of Gaucher disease in a mouse model.
  • Elevated levels of the proinflammatory cytokines, IL-1alpha, IL-1beta, IL-6, and TNF-alpha, were detected in the fetal brains of Gaucher mice.
  • Moreover, the levels of secreted nitric oxide and reactive oxygen species in the brains of Gaucher mice were higher than in wild-type mice.
  • [MeSH-major] Brain / metabolism. Cytokines / genetics. Gaucher Disease / genetics
  • [MeSH-minor] Animals. Cells, Cultured. Glucosylceramidase / genetics. Inflammation / immunology. Interleukin-1 / genetics. Interleukin-1 / secretion. Interleukin-6 / genetics. Interleukin-6 / secretion. Mice. Mice, Inbred C57BL. Mice, Inbred ICR. Mice, Knockout. Microglia / cytology. Microglia / metabolism. Nitric Oxide / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / secretion. Up-Regulation / genetics

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  • (PMID = 16891822.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; EC 3.2.1.45 / Glucosylceramidase
  • [Other-IDs] NLM/ PMC2729900
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37. Staals J, Bons JA, van Oostenbrugge RJ, Knottnerus IL, van Dieijen-Visser MP, Bouwman FG, Mariman EC, Delanghe JR, Lodder J, Wodzig WK: A SELDI-TOF-MS study in Lacunar Stroke with Subsequent Haptoglobin Phenotyping. Curr Neurovasc Res; 2008 May;5(2):93-8
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  • SELDI-TOF-MS, followed by protein identification, was performed in samples of 8 first-ever lacunar stroke patients with MR imaging showing a single symptomatic lacunar lesion (type 1), and 8 with multiple additional "silent" lacunar lesions and extensive white matter lesions (type 2).
  • A 16 kDa protein, identified as alpha-2-chain of haptoglobin (Hp), was found to be overrepresented in type 1 compared to type 2 (peak intensity 12.5 vs. 5.0; p=0.02).
  • As a polymorphism with two alleles, Hp-1 and Hp 2, determines the presence of alpha-1 and/or alpha-2-chains in the Hp-molecule, Hp phenotypic analysis was performed.
  • Hp 1 : Hp-2 allele frequency was 0.562 : 0.438 in type 1 and 0.812 : 0.188 in type 2 (population reference approximately 0.4 : 0.6).
  • We conclude that the overrepresentation of the alpha-2-chain in lacunar stroke type 1 compared to type 2 relates to a higher Hp-2 allele frequency in the former.
  • Our findings suggest a role for the Hp gene in the etiology of cerebral small vessel disease.

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  • (PMID = 18473824.001).
  • [ISSN] 1875-5739
  • [Journal-full-title] Current neurovascular research
  • [ISO-abbreviation] Curr Neurovasc Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Haptoglobins
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38. Wada T, Kenmochi H, Miyashita Y, Sasaki M, Ojima M, Sasahara M, Koya D, Tsuneki H, Sasaoka T: Spironolactone improves glucose and lipid metabolism by ameliorating hepatic steatosis and inflammation and suppressing enhanced gluconeogenesis induced by high-fat and high-fructose diet. Endocrinology; 2010 May;151(5):2040-9
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  • Recent evidence suggests that treatment with mineralocorticoid receptor antagonist suppressed local inflammation in vascular tissues or cardiomyocytes; therefore, we examined the effect of spironolactone on glucose and lipid metabolism in a mouse model with diet-induced diabetes and nonalcoholic fatty liver disease.
  • [MeSH-minor] Animals. Body Weight / drug effects. Cells, Cultured. Dietary Carbohydrates / administration & dosage. Dietary Fats / administration & dosage. Gene Expression / drug effects. Hep G2 Cells. Humans. Insulin / blood. Lipids / blood. Male. Mice. Mice, Inbred C57BL. Mineralocorticoid Receptor Antagonists / pharmacology. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Trans-Activators / genetics. Transcription Factors

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  • (PMID = 20211973.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Carbohydrates; 0 / Dietary Fats; 0 / Insulin; 0 / Lipids; 0 / Mineralocorticoid Receptor Antagonists; 0 / Ppargc1a protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 27O7W4T232 / Spironolactone; IY9XDZ35W2 / Glucose
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39. Kostelidou K, Trakas N, Zouridakis M, Bitzopoulou K, Sotiriadis A, Gavra I, Tzartos SJ: Expression and characterization of soluble forms of the extracellular domains of the beta, gamma and epsilon subunits of the human muscle acetylcholine receptor. FEBS J; 2006 Aug;273(15):3557-68
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  • Muscle AChR, formed by five homologous subunits (alpha2 beta gamma delta or alpha2 beta gamma epsilon), is the major antigen in the autoimmune disease, myasthenia gravis (MG), in which pathogenic autoantibodies bind to, and inactivate, the AChR.
  • The extracellular domain (ECD) of the human muscle alpha subunit has been heterologously expressed and extensively studied.
  • Our aim was to obtain satisfactory amounts of the ECDs of the non-alpha subunits of human muscle AChR for use as starting material for the determination of the 3D structure of the receptor ECDs and for the characterization of the specificities of antibodies in sera from patients with MG.
  • All three recombinant polypeptides were glycosylated and soluble; beta1-221 was mainly in an apparently dimeric form, whereas gamma1-218 and epsilon1-219 formed soluble oligomers.
  • CD studies of beta1-221 suggested that it has considerable beta-sheet secondary structure with a proportion of alpha-helix.
  • Conformation-dependent mAbs against the ECDs of the beta or gamma subunits specifically recognized beta1-221 or gamma1-218, respectively, and polyclonal rabbit antiserum raised against purified beta1-221 bound to (125)I-labeled alpha-bungarotoxin-labeled human AChR.
  • [MeSH-minor] Antibodies, Monoclonal / metabolism. Base Sequence. Chromatography, Gel. Chromatography, Liquid. Circular Dichroism. Cloning, Molecular. DNA Primers. Enzyme-Linked Immunosorbent Assay. Glycosylation. Humans. Polymerase Chain Reaction. Radioimmunoassay. Solubility

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  • (PMID = 16884496.001).
  • [ISSN] 1742-464X
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / DNA Primers; 0 / Receptors, Cholinergic
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40. Mueller S, Millonig G, Waite GN: The GOX/CAT system: a novel enzymatic method to independently control hydrogen peroxide and hypoxia in cell culture. Adv Med Sci; 2009;54(2):121-35
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  • Thus, the GOX/CAT system mimics a non-phosphorylating respiratory chain and allows to adjust H2O2 levels under hypoxic conditions truly simulating H2O2 release e.g. by inflammatory cells or intracellular sources.
  • Factors such as HIF1 alpha that respond both to hypoxia and H2O2 are an especially attractive target for the novel methodology.
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Diffusion. Humans. Hydrogen-Ion Concentration. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Models, Biological. Oxidation-Reduction. Oxygen Consumption / physiology. Procollagen-Proline Dioxygenase / metabolism. Signal Transduction / physiology. Time Factors

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  • (PMID = 20022860.001).
  • [ISSN] 1898-4002
  • [Journal-full-title] Advances in medical sciences
  • [ISO-abbreviation] Adv Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Oxidants; BBX060AN9V / Hydrogen Peroxide; EC 1.1.3.4 / Glucose Oxidase; EC 1.11.1.6 / Catalase; EC 1.14.11.2 / Procollagen-Proline Dioxygenase
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41. Lok CA, Jebbink J, Nieuwland R, Faas MM, Boer K, Sturk A, Van Der Post JA: Leukocyte activation and circulating leukocyte-derived microparticles in preeclampsia. Am J Reprod Immunol; 2009 May;61(5):346-59
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  • PROBLEM: Preeclampsia shows characteristics of an inflammatory disease including leukocyte activation.
  • These leukocytes showed up-regulation of Nuclear Factor of Kappa light chain gene enhancer in B cells inhibitor (NFkappaB-1A) and cyclin-dependent kinase inhibitor (CDKN)-1A compared with normotensive pregnant women.
  • [MeSH-minor] Adult. Biomarkers / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / immunology. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA-Binding Proteins / immunology. DNA-Binding Proteins / metabolism. Female. Gene Expression. Humans. I-kappa B Proteins. Interleukin 1 Receptor Antagonist Protein / immunology. Interleukin 1 Receptor Antagonist Protein / metabolism. L-Selectin / blood. Pancreatic Elastase / blood. Pregnancy. Receptors, Tumor Necrosis Factor, Type I / immunology. Receptors, Tumor Necrosis Factor, Type I / metabolism. Up-Regulation / immunology

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  • (PMID = 19341385.001).
  • [ISSN] 1600-0897
  • [Journal-full-title] American journal of reproductive immunology (New York, N.Y. : 1989)
  • [ISO-abbreviation] Am. J. Reprod. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Receptors, Tumor Necrosis Factor, Type I; 126880-86-2 / L-Selectin; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.4.21.36 / Pancreatic Elastase
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42. 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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43. Saxena V, Mathur A, Krishnani N, Dhole TN: Kinetics of cytokine profile during intraperitoneal inoculation of Japanese encephalitis virus in BALB/c mice model. Microbes Infect; 2008 Aug-Sep;10(10-11):1210-7
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  • We assessed iNOS, IFN-gamma, TNF-alpha, IL-10 and IL-4 production in spleen, brain and sera of intraperitoneally challenged BALB/c mice by RT-PCR and ELISA along with brain histopathology at different days post inoculation (d.p.i.).
  • At 5d.p.i., IL-10 expression outcompeted TNF-alpha, IFN-gamma and IL-4.
  • However, in the virus infected mice sera, IL-4 production predominated over TNF-alpha and IL-10 at 5d.p.i.

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  • (PMID = 18691668.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Viral; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse
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44. Royal W 3rd, Wang H, Jones O, Tran H, Bryant JL: A vitamin A deficient diet enhances proinflammatory cytokine, Mu opioid receptor, and HIV-1 expression in the HIV-1 transgenic rat. J Neuroimmunol; 2007 Apr;185(1-2):29-36
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  • The HIV-1 (HIV) transgenic (Tg) rat develops several immune abnormalities in association with clinical impairments that are similar to what are seen with HIV infection in humans.
  • In HIV infection, retinoids and opioids can have separate and potentially combined effects on the clinical course of HIV disease.
  • In these studies, the effects of a vitamin A deficient diet on T cell proinflammatory cytokine and mu opioid receptor (MOR) expression were examined in the Tg and in wild-type (WT) rats.
  • Phytohemagglutinin-stimulated T cells from WT rats on the vitamin A diet and from Tg rats on either diet were more likely to either produce increased percentages of T cells expressing intracytoplasmic IFN-gamma, secrete higher levels of TNF-alpha, and express higher levels of MOR mRNA and surface MOR.
  • All together, these data suggest that a vitamin A deficient diet can result in cellular effects that increase T cell proinflammatory responses and HIV expression, which may alter the course of disease in the HIV Tg rat model.

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  • (PMID = 17289162.001).
  • [ISSN] 0165-5728
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA015311; United States / NIDA NIH HHS / DA / R01 DA15311
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Receptors, Opioid, mu; 0 / Viral Proteins
  • [Other-IDs] NLM/ NIHMS21917; NLM/ PMC1885471
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45. Inagaki N, Hayashi T, Arimura T, Koga Y, Takahashi M, Shibata H, Teraoka K, Chikamori T, Yamashina A, Kimura A: Alpha B-crystallin mutation in dilated cardiomyopathy. Biochem Biophys Res Commun; 2006 Apr 7;342(2):379-86
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  • [Title] Alpha B-crystallin mutation in dilated cardiomyopathy.
  • However, disease-causing mutations can be identified only in a small proportion of the patients even in the familial cases, suggesting that there remains yet unidentified disease-causing gene(s) for DCM.
  • To explore the novel disease gene for DCM, we examined CRYAB encoding alphaB-crystallin for mutation in the patients with DCM, since alphaB-crystallin was recently reported to associate with the heart-specific N2B domain and adjacent I26/I27 domain of titin/connectin, and we previously reported a N2B mutation, Gln4053ter, in DCM.
  • A missense mutation of CRYAB, Arg157His, was found in a familial DCM patient and the mutation affected the evolutionary conserved amino acid residue among alpha-crystallins.
  • These observations suggest that the Arg157His mutation may be involved in the pathogenesis of DCM via impaired accommodation to the heart-specific N2B domain of titin/connectin and its disease-causing mechanism is different from the mutation found in desmin-related myopathy.
  • [MeSH-major] Cardiomyopathy, Dilated / genetics. Cardiomyopathy, Dilated / metabolism. Mutation, Missense. alpha-Crystallin B Chain / genetics


46. Eleftheriadis T, Kartsios C, Yiannaki E, Kazila P, Antoniadi G, Liakopoulos V, Markala D: Chronic inflammation and T cell zeta-chain downregulation in hemodialysis patients. Am J Nephrol; 2008;28(1):152-7
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  • [Title] Chronic inflammation and T cell zeta-chain downregulation in hemodialysis patients.
  • BACKGROUND: Clinical and experimental data indicate a deficient immune response in hemodialysis (HD) patients. zeta-Chain phosphorylation is an early and central event in the process that follows antigen recognition by the T cell antigen receptor (TCR).
  • T cell zeta-chain is downregulated in many chronic inflammatory states, such as cancer, autoimmune disease and chronic infection.
  • The aim of the present study was to evaluate T cell zeta-chain expression in HD patients.
  • T cell count, the percentage of zeta-chain-positive T cells, as well as T cell zeta-chain mean fluorescence intensity (MFI) were evaluated with flow cytometry.
  • The inflammatory markers C-reactive protein, interleukin-6 and tumor necrosis factor-alpha were measured in the serum by means of ELISA.
  • In these patients, T cell zeta-chain MFI was decreased.
  • CD3-epsilon MFI did not differ between the two groups indicating that among the TCR complex constituents, zeta-chain is selectively downregulated.
  • Like in other pathological chronic inflammatory conditions, T cell zeta-chain is downregulated in HD patients.
  • Since zeta-chain plays a key role in the transduction of the signal that follows antigen recognition by the TCR, its downregulation could be responsible for the deficient cellular immune response observed in HD patients.
  • [MeSH-minor] Aged. Antigens, CD3 / metabolism. C-Reactive Protein / metabolism. Chronic Disease. Down-Regulation / immunology. Female. Humans. Lymphocyte Count. Male. Middle Aged. Phosphorylation. Renal Dialysis

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  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • (PMID = 17951997.001).
  • [ISSN] 1421-9670
  • [Journal-full-title] American journal of nephrology
  • [ISO-abbreviation] Am. J. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / CD3 antigen, zeta chain; 0 / CD3E protein, human; 0 / Membrane Proteins; 0 / Receptors, Antigen, T-Cell; 0 / antigen T cell receptor, zeta chain; 9007-41-4 / C-Reactive Protein
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47. Trapé J, Franquesa J, Sala M, Domenech M, Montesinos J, Catot S, Buxó J, Casado E, Fígols C, Harillo S, Galobart J, Bella M: Determination of biological variation of α-fetoprotein and choriogonadotropin (β chain) in disease-free patients with testicular cancer. Clin Chem Lab Med; 2010 Dec;48(12):1799-801
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  • [Title] Determination of biological variation of α-fetoprotein and choriogonadotropin (β chain) in disease-free patients with testicular cancer.
  • The aim of this work is to determine the BV for total choriogonadotropin (β chain) (β-hCG) and α-fetoprotein (AFP) in patients diagnosed with testicular cancer but with no evidence of recurrence of disease.
  • RESULTS: The mean concentrations of α-fetoprotein and choriogonadotropin (β chain) were 3.9 μg/L and 0.79 IU/L, respectively.
  • Between-run analytical variation was 7.1% at 4.1 μg/L for α-fetoprotein, and 19% at 0.65 IU/L for choriogonadotropin (β chain).
  • BV obtained for α-fetoprotein and choriogonadotropin (β chain) was 12.4% and 16.7%, respectively, and the reference change value (RCV) for one-tail showed 38.2% and 60.7% for α-fetoprotein and choriogonadotropin (β chain), respectively.

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  • (PMID = 20828364.001).
  • [ISSN] 1437-4331
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin; 0 / alpha-Fetoproteins
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48. Rogers L, Burchat S, Gage J, Hasu M, Thabet M, Willcox L, Ramsamy TA, Whitman SC: Deficiency of invariant V alpha 14 natural killer T cells decreases atherosclerosis in LDL receptor null mice. Cardiovasc Res; 2008 Apr 01;78(1):167-74
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  • [Title] Deficiency of invariant V alpha 14 natural killer T cells decreases atherosclerosis in LDL receptor null mice.
  • Depletion of all populations of CD1d-dependent NKT cells has been shown by several groups to reduce atherosclerosis in two different mouse models of the disease.
  • In this study, we determined if removal of a single (V alpha 14) NKT cell population protects mice from the disease.
  • METHODS AND RESULTS: Targeted deletion of the J alpha 18 gene results in selective depletion of CD1d-dependent V alpha 14 NKT cells in C57BL/6 mice without affecting the population of other NKT, NK, and conventional T cells.
  • Therefore, to study the effect of V alpha 14 NKT cell depletion on the progression of atherosclerosis, we examined the extent of lesion formation using paired littermate LDL receptor null mice that were either +/+ or -/- for the J alpha 18 gene following the feeding of these mice a cholesterol- and fat-enriched diet for 8 weeks.
  • However, quantification of atherosclerosis revealed that V alpha 14 NKT cell deficiency significantly decreased lesion size in the aortic root (20-28%) and arch (28-38%) in both genders of mice.
  • By coupling the techniques of laser capture microdissection with quantitative real-time RT-PCR, we found that expression of the proatherogenic cytokine interferon (IFN)-gamma was significantly reduced in lesions from J alpha 18-/- mice.
  • [MeSH-major] Antigens, CD1 / metabolism. Atherosclerosis / prevention & control. Killer Cells, Natural / immunology. Receptors, Antigen, T-Cell, alpha-beta / metabolism. Receptors, LDL / metabolism. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Antigens, CD1d. Antigens, CD3 / metabolism. Cholesterol / blood. Disease Models, Animal. Down-Regulation. Female. Histocompatibility Antigens Class II / metabolism. Interferon-gamma / genetics. Interferon-gamma / metabolism. Interleukin-10 / genetics. Interleukin-10 / metabolism. Interleukin-4 / genetics. Interleukin-4 / metabolism. Male. Mice. Mice, Knockout. Microdissection / methods. Polymerase Chain Reaction. RNA, Messenger / metabolism

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  • [ErratumIn] Cardiovasc Res. 2009 Mar 1;81(4):814. Wilcox, Lindsay [corrected to Willcox, Lindsay]
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  • (PMID = 18192239.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Antigens, CD3; 0 / Histocompatibility Antigens Class II; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, LDL; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; 97C5T2UQ7J / Cholesterol
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49. Hendriksen SW, van Leengoed LA, Roest HI, van Nes A: [Neonatal diarrhoea in pigs: alpha- and beta2-toxin produced by Clostridium perfringens]. Tijdschr Diergeneeskd; 2006 Dec 15;131(24):910-3
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  • [Title] [Neonatal diarrhoea in pigs: alpha- and beta2-toxin produced by Clostridium perfringens].
  • [Transliterated title] Neonatale diarree bij biggen: alpha- en beta2-toxine producerende Clostridium perfringens.
  • Toxin typing by polymerase chain reaction led to the detection of genes encoding a-toxin (cpa) and beta2-toxin (cpb2).
  • Surprisingly, alpha- and beta2-toxin-producing C. perfringens was isolated from all tested herds with piglets with neonatal diarrhoea.
  • [MeSH-major] Bacterial Toxins / biosynthesis. Clostridium Infections / veterinary. Clostridium perfringens / metabolism. Diarrhea / veterinary. Swine Diseases / microbiology
  • [MeSH-minor] Animals. Animals, Newborn / microbiology. Calcium-Binding Proteins / genetics. Calcium-Binding Proteins / isolation & purification. Disease Outbreaks / veterinary. Netherlands / epidemiology. Polymerase Chain Reaction. Swine. Type C Phospholipases / genetics. Type C Phospholipases / isolation & purification. Vaccination / veterinary

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  • (PMID = 17278609.001).
  • [ISSN] 0040-7453
  • [Journal-full-title] Tijdschrift voor diergeneeskunde
  • [ISO-abbreviation] Tijdschr Diergeneeskd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Calcium-Binding Proteins; 0 / cpb2 protein, Clostridium perfringens; EC 3.1.4.- / Type C Phospholipases; EC 3.1.4.3 / alpha toxin, Clostridium perfringens
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50. Nakatsuji T, Shi Y, Zhu W, Huang CP, Chen YR, Lee DY, Smith JW, Zouboulis CC, Gallo RL, Huang CM: Bioengineering a humanized acne microenvironment model: proteomics analysis of host responses to Propionibacterium acnes infection in vivo. Proteomics; 2008 Aug;8(16):3406-15
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  • Acne is a human disease of the sebaceous hair follicle.
  • After P. acnes infection, four proteins including fibrinogen, alpha polypeptide, fibrinogen beta chain, S100A9, and serine protease inhibitor A3K showed altered concentrations in the mimicked acne microenvironment.

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  • (PMID = 18651708.001).
  • [ISSN] 1615-9861
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI052453-07; United States / PHS HHS / / R21-I58002-01; United States / NIAID NIH HHS / AI / R01 AI052453-07; United States / NIAMS NIH HHS / AR / 1R41AR056169-01; United States / NCRR NIH HHS / RR / RR020843; United States / NIAID NIH HHS / AI / R01-AI067395-01; United States / NIAID NIH HHS / AI / R01 AI052453; United States / PHS HHS / / R21-R022754-01; United States / NIAID NIH HHS / AI / R01 AI067395; United States / NIAMS NIH HHS / AR / R41 AR056169; United States / NCRR NIH HHS / RR / U54 RR020843
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Germany
  • [Number-of-references] 48
  • [Other-IDs] NLM/ NIHMS91863; NLM/ PMC2699546
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51. 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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52. Lv L, Zou HJ, Lin GW, Irons RR: [Genetic polymorphism of tumor necrosis factor-alpha in patients with chronic benzene poisoning]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi; 2005 Jun;23(3):195-8
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  • [Title] [Genetic polymorphism of tumor necrosis factor-alpha in patients with chronic benzene poisoning].
  • OBJECTIVE: To study the relationship between genetic polymorphism of tumor necrosis factor-alpha (TNF-alpha, sites at -238 nt and -308 nt) and susceptibility to chronic benzene poisoning.
  • METHOD: The polymorphism of TNF-alpha gene were detected by nested polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique from 50 benzene poisoning patients and 60 control individuals exposed to benzene.
  • RESULTS: The frequency of the TNF-alpha-238G/G, A/G and A/A in controls (95%, 5% and 0%, respectively), were not significantly different from those in patients (92%, 6% and 2%, respectively, P > 0.05).
  • The frequency of the TNF-alpha-308G/G, A/G and A/A in patients were 76%, 24% and 0% respectively, and that in control individuals were 93%, 7% and 0% respectively.
  • Chi(2) test showed that frequency of TNF-alpha-308A/G in patients was significantly higher than that in controls (chi(2) = 6.22, P = 0.013).
  • Logistic analysis showed that TNF-alpha-308A/G was the independent risk factor of benzene poisoning (OR = 5.3, P < 0.05).
  • CONCLUSION: Individuals with TNF-alpha-308A/G gene polymorphism are susceptible to benzene poisoning.
  • [MeSH-major] Benzene / poisoning. Occupational Diseases / genetics. Polymorphism, Genetic. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Chronic Disease. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length

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  • (PMID = 16124898.001).
  • [ISSN] 1001-9391
  • [Journal-full-title] Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases
  • [ISO-abbreviation] Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; J64922108F / Benzene
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53. Lemoli RM, Catani L, Talarico S, Loggi E, Gramenzi A, Baccarani U, Fogli M, Grazi GL, Aluigi M, Marzocchi G, Bernardi M, Pinna A, Bresadola F, Baccarani M, Andreone P: Mobilization of bone marrow-derived hematopoietic and endothelial stem cells after orthotopic liver transplantation and liver resection. Stem Cells; 2006 Dec;24(12):2817-25
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  • Here, we studied 24 patients undergoing orthotopic liver transplantation (OLT) for end-stage liver disease or hepatocellularcarcinoma, and 13 patients submitted to liver resection.
  • Reverse transcriptase-polymerase chain reaction and fluorescence-in situ hybridization were also used to characterize mobilized SC.
  • Cytogenetic and molecular analyses of CD34(+) cells showed the host origin of mobilized SC and the expression of transcripts for GATA-4, cytokeratin 19, and alpha-fetoprotein hepatocyte markers.


54. Hendryk S, Czuba Z, Jedrzejewska-Szypułka H, Bazowski P, Dolezych H, Król W: Increase in activity of neutrophils and proinflammatory mediators in rats following acute and prolonged focal cerebral ischemia and reperfusion. Acta Neurochir Suppl; 2010;106:29-35
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  • Neutrophils (PMNs) are one of the first factors in the chain of reactions of the immune system during focal cerebral ischemia.
  • Experimental and clinical studies have emphasized the important role of proinflammatory cytokines such as interleukin-1beta (IL-1beta) and tumor necrosis factor (TNFalpha), in addition to vasoactive peptide and endothelin-1 (ET-1), in the formation of cerebral ischemia.
  • [MeSH-major] Brain Ischemia / immunology. Brain Ischemia / pathology. Interleukin-1beta / metabolism. Neutrophils / physiology. Reperfusion. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cells, Cultured. Disease Models, Animal. Endothelin-1 / blood. Enzyme Activators / pharmacology. Male. Radioimmunoassay / methods. Rats. Rats, Wistar. Statistics, Nonparametric. Tetradecanoylphorbol Acetate / pharmacology. Time Factors. Vasoactive Intestinal Peptide / metabolism

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  • (PMID = 19812916.001).
  • [ISSN] 0065-1419
  • [Journal-full-title] Acta neurochirurgica. Supplement
  • [ISO-abbreviation] Acta Neurochir. Suppl.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / Enzyme Activators; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 37221-79-7 / Vasoactive Intestinal Peptide; NI40JAQ945 / Tetradecanoylphorbol Acetate
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55. Heron M, Grutters JC, van Moorsel CH, Ruven HJ, Huizinga TW, van der Helm-van Mil AH, Claessen AM, van den Bosch JM: Variation in IL7R predisposes to sarcoid inflammation. Genes Immun; 2009 Oct;10(7):647-53
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  • Sarcoidosis is a chronic granulomatous disorder characterized by a massive influx of Th1 lymphocytes.
  • Both naive and memory T cells express high levels of interleukin 7 receptor-alpha (IL7R alpha), encoded by the IL7R gene.
  • Replication of one significant associated SNP was carried out in 206 independent sarcoidosis patients, 127 controls and 126 patients with Löfgren's disease.
  • In addition, we report the same trend between variation in the IL7R gene and patients with Löfgren's disease, suggesting that variation in IL7R may confer general risk for developing granulomatous lung disease.
  • [MeSH-major] Genetic Predisposition to Disease. Lung Diseases / genetics. Lymphomatoid Granulomatosis / genetics. Receptors, Interleukin-7 / genetics. Sarcoidosis / genetics

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  • (PMID = 19626041.001).
  • [ISSN] 1476-5470
  • [Journal-full-title] Genes and immunity
  • [ISO-abbreviation] Genes Immun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Interleukin-7; 0 / interleukin-7 receptor, alpha chain
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56. Yanagisawa N, Shimada K, Miyazaki T, Kume A, Kitamura Y, Sumiyoshi K, Kiyanagi T, Iesaki T, Inoue N, Daida H: Enhanced production of nitric oxide, reactive oxygen species, and pro-inflammatory cytokines in very long chain saturated fatty acid-accumulated macrophages. Lipids Health Dis; 2008;7:48
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  • [Title] Enhanced production of nitric oxide, reactive oxygen species, and pro-inflammatory cytokines in very long chain saturated fatty acid-accumulated macrophages.
  • BACKGROUND: Deterioration of peroxisomal beta-oxidation activity causes an accumulation of very long chain saturated fatty acids (VLCSFA) in various organs.
  • We have recently reported that the levels of VLCSFA in the plasma and/or membranes of blood cells were significantly higher in patients with metabolic syndrome and in patients with coronary artery disease than the controls.
  • The levels of nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma), intracellular reactive oxygen species (ROS), and pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interluekin-6 (IL-6), and interleukin-12p70 (IL-12p70), were significantly higher in macrophages from ALDP-deficient mice than in those from wild-type mice.
  • CONCLUSION: These results suggested that VLCSFA accumulation in macrophages may contribute to the pathogenesis of inflammatory diseases through the enhancement of inflammatory and oxidative responses.
  • [MeSH-minor] Animals. Cells, Cultured. Interferon-gamma / pharmacology. Interleukin-12 / metabolism. Interleukin-6 / metabolism. Lipopolysaccharides / pharmacology. Male. Mice. Mice, Mutant Strains. Nitric Oxide Synthase Type II / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19038055.001).
  • [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 / Cytokines; 0 / Fatty Acids; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 31C4KY9ESH / Nitric Oxide; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II
  • [Other-IDs] NLM/ PMC2613382
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57. Rudakov N, Shpynov S, Fournier PE, Raoult D: Ecology and molecular epidemiology of tick-borne rickettsioses and anaplasmoses with natural foci in Russia and Kazakhstan. Ann N Y Acad Sci; 2006 Oct;1078:299-304
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  • The main results were obtained through genetic methods (PCR sequence) at the Université de la Mediterranée (Marseille, France).
  • We describe considerable heterogeneity of tick-borne alpha(1)-proteobacteria: 16 microorganisms the of the order Rickettsiales were detected in Russia and Kazakhstan. R. sibirica-caused North Asiatic tick-borne rickettsiosis is the main tick-borne rickettsiosis in Russia, with wide distribution in Siberia and the Russian Far East and high epidemic activity of natural foci of different landscape types.
  • The roles of more than 15 new genotypes of alpha(1)-proteobacteria in infectious disease in Russia and Kazakhstan are in need of further study.
  • [MeSH-major] Anaplasmosis / epidemiology. Rickettsia Infections / epidemiology. Tick-Borne Diseases / epidemiology
  • [MeSH-minor] Anaplasma / genetics. Anaplasma / isolation & purification. Genotype. Humans. Incidence. Kazakhstan / epidemiology. Polymerase Chain Reaction. Rickettsia / genetics. Rickettsia / isolation & purification. Russia / epidemiology

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  • (PMID = 17114725.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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58. Langerveld AJ, Mihalko D, DeLong C, Walburn J, Ide CF: Gene expression changes in postmortem tissue from the rostral pons of multiple system atrophy patients. Mov Disord; 2007 Apr 30;22(6):766-77
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  • Multiple system atrophy (MSA) is a neurodegenerative disease characterized by various degrees of Parkinsonism, cerebellar ataxia, and autonomic dysfunction.
  • The downregulated genes were primarily associated with biological functions known to be impaired in Parkinson's disease (PD) and other neurological diseases; for example, downregulation occurred in genes associated with mitochondrial function, ubiquitin-proteasome function, protein modification, glycolysis/metabolism, and ion transport.
  • Immunocytochemistry, in conjunction with quantitative image analysis, was carried out to characterize alpha-synuclein protein expression as glial cytoplasmic inclusions in the pontocerebellar tract in rostral pons tissue and to determine the relationship between the amount of aggregated alpha-synuclein protein and changes in specific gene expression.
  • Of the regulated genes, 86 were associated with the amount of observed aggregated alpha-synuclein protein in the rostral pons tissue.
  • These data indicate that cells in the pons of MSA patients show changes in gene expression previously associated with the substantia nigra of PD patients and/or other neurological diseases, with additional changes, for example related to oligodendrocyte function unique to MSA.
  • [MeSH-minor] Brain / pathology. Humans. Immunohistochemistry. Oligonucleotide Array Sequence Analysis. Postmortem Changes. RNA / genetics. RNA / isolation & purification. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. alpha-Synuclein / genetics

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  • (PMID = 17290454.001).
  • [ISSN] 0885-3185
  • [Journal-full-title] Movement disorders : official journal of the Movement Disorder Society
  • [ISO-abbreviation] Mov. Disord.
  • [Language] eng
  • [Publication-type] Journal Article; 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 / alpha-Synuclein; 63231-63-0 / RNA
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59. Nozawa K, Fujishiro M, Kawasaki M, Kaneko H, Iwabuchi K, Yanagida M, Suzuki F, Miyazawa K, Takasaki Y, Ogawa H, Takamori K, Sekigawa I: Connective tissue growth factor promotes articular damage by increased osteoclastogenesis in patients with rheumatoid arthritis. Arthritis Res Ther; 2009;11(6):R174
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  • Therefore, this study was conducted to investigate how CTGF is associated with the disease progression of RA.
  • METHODS: Serum samples were collected from RA patients in active or inactive disease stages, and before or after treatments with infliximab.
  • RESULTS: The serum concentrations of CTGF in RA were greater than in normal healthy controls and disease controls.
  • Furthermore, the CTGF levels significantly were decreased by infliximab concomitant with the disease amelioration.
  • In addition, tumour necrosis factor (TNF)alpha can induce the CTGF production from synovial fibroblasts even though TNFalpha can oppositely inhibit the production of CTGF from chondrocytes.
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antirheumatic Agents / therapeutic use. Blotting, Western. Cell Differentiation / physiology. Disease Progression. Enzyme-Linked Immunosorbent Assay. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Immunoprecipitation. Infliximab. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19922639.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antirheumatic Agents; 0 / Tumor Necrosis Factor-alpha; 139568-91-5 / Connective Tissue Growth Factor; B72HH48FLU / Infliximab
  • [Other-IDs] NLM/ PMC3003536
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60. Zou Z, Shi XY, Lü Y, Xu ZD, Shi D, Wang L, Liu G: [Role of alpha-adrenergic receptors in vascular hyperreactivity in rats with high level spinal injury]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue; 2006 Mar;18(3):176-9
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  • [Title] [Role of alpha-adrenergic receptors in vascular hyperreactivity in rats with high level spinal injury].
  • OBJECTIVE: To explore the vascular reactivity of abdominal aorta to agonists of alpha-adrenergic receptors in rat with high level transection of the spinal cord, and to quantify the expression of alpha-AR mRNA subtypes, in order to investigate relationship between alpha-AR and hyperreactivity of abdominal aorta.
  • METHODS: Four weeks after transection of the spinal cord at the level of 4th thoracic vertebra, the rats were sacrificed, and abdominal aorta rings were adopted to assay sensitivity to phenylephrine and clonidine with isolated organ perfusion system.
  • Alpha(1A)-AR, alpha(1B)-AR, alpha(1D)-AR, alpha(2A)-AR, alpha(2B)-AR, alpha(2C)-AR mRNA expressions were quantified by real time polymerase chain reaction (PCR).
  • RESULTS: Compared with abdominal aorta, of rat with sham operation, reactivity of aorta of rat after transection of spinal cord to clonidine was significantly higher (P<0.05 or P<0.01), but difference of vascular reactivity to phenylephrine between them was not significant (P>0.05).
  • Expressions of alpha(1A)-AR mRNA, alpha(1D)-AR mRNA, alpha(2A)-AR mRNA, alpha(2B)-AR mRNA, alpha(2C)-AR mRNA were significantly higher (P<0.05 or P<0.01), while the expression of alpha(1B)-AR mRNA did not vary significantly.
  • CONCLUSION: Vascular hyperreactivity to agonist of alpha(2)-AR may be the mechanism of hyperreactivity of abdominal aorta in rat after transection of spinal cord.
  • Although alpha(1)-AR mRNA expression is higher in aorta of rat with spinal cord injury, vascular hyperreactivity is not the result of upregulation of alpha(1)-AR sensitivity.
  • [MeSH-major] Aorta, Abdominal / physiopathology. Receptors, Adrenergic, alpha-1 / metabolism. Receptors, Adrenergic, alpha-2 / metabolism. Spinal Cord Injuries / physiopathology
  • [MeSH-minor] Adrenergic alpha-Agonists / pharmacology. Animals. Clonidine / pharmacology. Disease Models, Animal. Female. Male. Phenylephrine / pharmacology. RNA, Messenger / metabolism. Random Allocation. Rats. Rats, Wistar

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  • (PMID = 16524515.001).
  • [ISSN] 1003-0603
  • [Journal-full-title] Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
  • [ISO-abbreviation] Zhongguo Wei Zhong Bing Ji Jiu Yi Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adrenergic alpha-Agonists; 0 / RNA, Messenger; 0 / Receptors, Adrenergic, alpha-1; 0 / Receptors, Adrenergic, alpha-2; 1WS297W6MV / Phenylephrine; MN3L5RMN02 / Clonidine
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61. Hoe E, McKay FC, Schibeci SD, Gandhi K, Heard RN, Stewart GJ, Booth DR: Functionally significant differences in expression of disease-associated IL-7 receptor alpha haplotypes in CD4 T cells and dendritic cells. J Immunol; 2010 Mar 1;184(5):2512-7
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  • [Title] Functionally significant differences in expression of disease-associated IL-7 receptor alpha haplotypes in CD4 T cells and dendritic cells.
  • Common genetic variants of IL-7 receptor alpha (IL-7Ralpha) have recently been shown to affect susceptibility to multiple sclerosis (MS) and type 1 diabetes, and survival following bone marrow transplantation.
  • We have tested IL-7Ralpha mRNA expression in cell subsets and in models of T cell homeostasis, activation, tolerance, and differentiation into regulatory T cell/Th1/Th2/Th17, memory, and dendritic cells (DCs) under the hypothesis that the conditions in which haplotype differences are maximal are those likely to be the basis for their association with disease pathogenesis.
  • The TSLP/IL-7Ralpha interaction on DCs is known to be critical for production of thymic regulatory T cells, and reduced production of these cells in MS susceptibility haplotypes may be a basis for its association with this disease.
  • Because signaling through IL-7Ralpha controls T cell regulation, this haplotype difference is likely to affect the immunophenotype and disease pathogenesis.
  • [MeSH-minor] Alternative Splicing. Cells, Cultured. Cytokines / metabolism. Enzyme-Linked Immunosorbent Assay. Female. Genotype. Homeostasis / genetics. Humans. Interleukin-17 / metabolism. Male. Multiple Sclerosis / genetics. Protein Binding. Protein Isoforms / genetics. Protein Isoforms / metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes, Helper-Inducer / cytology. T-Lymphocytes, Helper-Inducer / metabolism. Th1 Cells / cytology. Th1 Cells / metabolism. Th2 Cells / cytology. Th2 Cells / metabolism

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  • (PMID = 20097866.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-17; 0 / Protein Isoforms; 0 / Receptors, Interleukin-7; 0 / interleukin-7 receptor, alpha chain; 0 / thymic stromal lymphopoietin
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62. Luhmann UF, Lin J, Acar N, Lammel S, Feil S, Grimm C, Seeliger MW, Hammes HP, Berger W: Role of the Norrie disease pseudoglioma gene in sprouting angiogenesis during development of the retinal vasculature. Invest Ophthalmol Vis Sci; 2005 Sep;46(9):3372-82
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  • [Title] Role of the Norrie disease pseudoglioma gene in sprouting angiogenesis during development of the retinal vasculature.
  • PURPOSE: To characterize developmental defects and the time course of Norrie disease in retinal and hyaloid vasculature during retinal development and to identify underlying molecular angiogenic pathways that may be affected in Norrie disease, exudative vitreoretinopathy, retinopathy of prematurity, and Coats' disease.
  • METHODS: Norrie disease pseudoglioma homologue (Ndph)-knockout mice were studied during retinal development at early postnatal (p) stages (p5, p10, p15, and p21).
  • The development of the superficial retinal vasculature was strongly delayed, whereas the deep retinal vasculature did not form because of the blockage of vessel outgrowth into the deep retinal layers.
  • They also suggest an early and a late phase of Norrie disease and may provide an explanation for similar phenotypic features of allelic retinal diseases in mice and patients as secondary consequences of pathologic hypoxia.
  • [MeSH-minor] Animals. Anoxia / metabolism. Blotting, Western. DNA-Binding Proteins / metabolism. Electroretinography. Enzyme-Linked Immunosorbent Assay. Fluorescein Angiography. Gene Expression / physiology. Humans. Hypoxia-Inducible Factor 1. Hypoxia-Inducible Factor 1, alpha Subunit. Infant, Newborn. Mice. Mice, Knockout. Nuclear Proteins / metabolism. Ophthalmoscopy. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16123442.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Eye Proteins; 0 / HIF1A protein, human; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ndph protein, mouse; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse
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63. Mitchell C, Robin MA, Mayeuf A, Mahrouf-Yorgov M, Mansouri A, Hamard M, Couton D, Fromenty B, Gilgenkrantz H: Protection against hepatocyte mitochondrial dysfunction delays fibrosis progression in mice. Am J Pathol; 2009 Nov;175(5):1929-37
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  • Analyses of mitochondrial DNA, respiratory chain complexes, and lipid peroxidation showed that Bcl-2 transgenic animals were protected against mitochondrial dysfunction and oxidative stress resulting from carbon tetrachloride injury.
  • Picrosirius red staining, alpha-smooth muscle actin immunohistochemistry, and real-time PCR for transforming growth factor-beta and collagen alpha-I revealed that Bcl-2 transgenic mice presented reduced fibrosis at early stages of fibrogenesis.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Biomarkers / metabolism. Carbon Tetrachloride / toxicity. Caspases / metabolism. Disease Progression. Fibrosis / metabolism. Fibrosis / pathology. Fibrosis / physiopathology. Lipid Peroxidation. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Oxidative Stress. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism


64. Bonofiglio D, Gabriele S, Aquila S, Catalano S, Gentile M, Middea E, Giordano F, Andò S: Estrogen receptor alpha binds to peroxisome proliferator-activated receptor response element and negatively interferes with peroxisome proliferator-activated receptor gamma signaling in breast cancer cells. Clin Cancer Res; 2005 Sep 1;11(17):6139-47
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  • [Title] Estrogen receptor alpha binds to peroxisome proliferator-activated receptor response element and negatively interferes with peroxisome proliferator-activated receptor gamma signaling in breast cancer cells.
  • This crosstalk could be taken into account in setting new pharmacologic strategies for breast cancer disease.
  • [MeSH-major] Breast Neoplasms / metabolism. Estrogen Receptor alpha / metabolism. PPAR gamma / metabolism. Response Elements / genetics. Signal Transduction
  • [MeSH-minor] Cell Proliferation / drug effects. Chromatin Immunoprecipitation. Electrophoretic Mobility Shift Assay. Estradiol / pharmacology. HeLa Cells. Humans. Ligands. PTEN Phosphohydrolase. Phosphatidylinositol 3-Kinases / metabolism. Phosphoric Monoester Hydrolases / drug effects. Phosphoric Monoester Hydrolases / metabolism. Phosphorylation. Promoter Regions, Genetic / genetics. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Reverse Transcriptase Polymerase Chain Reaction. Thiazolidinediones / pharmacology. Thymidine / metabolism. Transcription, Genetic. Transcriptional Activation. Tumor Suppressor Proteins / drug effects. Tumor Suppressor Proteins / metabolism. Vasodilator Agents / pharmacology

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  • (PMID = 16144913.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Ligands; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins; 0 / Thiazolidinediones; 0 / Tumor Suppressor Proteins; 0 / Vasodilator Agents; 05V02F2KDG / rosiglitazone; 4TI98Z838E / Estradiol; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; VC2W18DGKR / Thymidine
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65. Flego V, Radojcić Badovinac A, Bulat-Kardum L, Matanić D, Crnić-Martinović M, Kapović M, Ristić S: Primary lung cancer and TNF-alpha gene polymorphisms: a case-control study in a Croatian population. Med Sci Monit; 2009 Jul;15(7):CR361-5
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  • [Title] Primary lung cancer and TNF-alpha gene polymorphisms: a case-control study in a Croatian population.
  • BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine involved in the pathogenesis of various inflammatory and malignant diseases.
  • Previous studies investigating the role of the TNF-alpha gene polymorphisms in lung cancer have generated contradictory results.
  • The present study investigated whether the TNF-alpha-308 and TNF-alpha-238 polymorphisms are associated with risk and/or severity of disease in Croatian lung cancer patients.
  • MATERIAL/METHODS: In a case-control study, lung cancer patients (n=230) and appropriate age- and sex-matched controls (n=230) were genotyped by the polymerase chain reaction/restriction fragment length polymorphism method.
  • The chi-squared test was used to compare the observed numbers of different TNF-alpha genotypes for the population with those predicted by Hardy-Weinberg equilibrium.
  • RESULTS: There were no significant differences in the genotype and allele frequencies for the TNF-alpha-308 and TNF-alpha-238 polymorphisms between lung cancer patients and controls.
  • CONCLUSIONS: This study indicates that the TNF-alpha-308 and TNF-alpha-238 polymorphisms do not influence susceptibility to or severity of lung cancer in a Croatian population.
  • [MeSH-major] European Continental Ancestry Group / genetics. Lung Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Croatia. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Male. Middle Aged

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  • (PMID = 19564826.001).
  • [ISSN] 1643-3750
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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66. Gough MD, Ackroyd R, Majeed AW, Bird NC: Prediction of malignant potential in reflux disease: are cytokine polymorphisms important? Am J Gastroenterol; 2005 May;100(5):1012-8
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  • [Title] Prediction of malignant potential in reflux disease: are cytokine polymorphisms important?
  • OBJECTIVES: Esophageal reflux is common in the Western world and can lead to a number of diseases, such as esophagitis, Barrett's esophagus, and adenocarcinoma.
  • However, clinical methods only identify one patient in 15 with Barrett's esophagus.
  • PCR was used to determine the frequency of five functional cytokine polymorphisms: interleukin-1 receptor antagonist position +2018 (IL-1 Ra +2018), interleukin-1 beta position -511 (IL-1 beta-511), tumor necrosis factor-alpha position -238 (TNF-alpha-238), interleukin-10 position +1082 (IL-10 +1082), and interleukin-4 receptor position -1902 (IL-4R -1902).
  • There were no differences for the IL-1 beta-511, IL-4R -1902, and TNF-alpha-238 polymorphisms.
  • [MeSH-major] Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications. Interleukins / genetics. Polymorphism, Genetic / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / immunology. Adult. Aged. Aged, 80 and over. Barrett Esophagus / etiology. Barrett Esophagus / immunology. Esophagitis, Peptic / etiology. Esophagitis, Peptic / immunology. Female. Forecasting. Genotype. Humans. Interleukin-1 / genetics. Interleukin-10 / genetics. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Interleukin-1 / antagonists & inhibitors. Receptors, Interleukin-4 / genetics

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  • [CommentIn] Am J Gastroenterol. 2005 May;100(5):1019-20 [15842573.001]
  • (PMID = 15842572.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Interleukins; 0 / Receptors, Interleukin-1; 0 / Receptors, Interleukin-4; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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67. Fourcade S, López-Erauskin J, Galino J, Duval C, Naudi A, Jove M, Kemp S, Villarroya F, Ferrer I, Pamplona R, Portero-Otin M, Pujol A: Early oxidative damage underlying neurodegeneration in X-adrenoleukodystrophy. Hum Mol Genet; 2008 Jun 15;17(12):1762-73
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  • X-linked adrenoleukodystrophy (X-ALD) is a fatal neurodegenerative disorder, characterized by progressive cerebral demyelination cerebral childhood adrenoleukodystrophy (CCALD) or spinal cord neurodegeneration (adrenomyeloneuropathy, AMN), adrenal insufficiency and accumulation of very long-chain fatty acids (VLCFA) in tissues.
  • The disease is caused by mutations in the ABCD1 gene, which encodes a peroxisomal transporter that plays a role in the import of VLCFA or VLCFA-CoA into peroxisomes.
  • The Abcd1 knockout mice develop a spinal cord disease that mimics AMN in adult patients, with late onset at 20 months of age.
  • We find that the alpha-tocopherol analog Trolox is able to reverse oxidative lesions in vitro, thus providing therapeutic hope.


68. Nickel EA, Hsieh CH, Chen JG, Schwacha MG, Chaudry IH: Estrogen suppresses cardiac IL-6 after trauma-hemorrhage via a hypoxia-inducible factor 1 alpha-mediated pathway. Shock; 2009 Apr;31(4):354-8
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  • [Title] Estrogen suppresses cardiac IL-6 after trauma-hemorrhage via a hypoxia-inducible factor 1 alpha-mediated pathway.
  • Because hypoxia-inducible factor (HIF) 1 alpha is expressed during hypoxia and cellular stress and up-regulates the expression of IL-6, we hypothesized that HIF-1 alpha induces the increased cardiac IL-6 after trauma-hemorrhage and that estrogen suppresses this induction.
  • Vehicle, the HIF-alpha inhibitor YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole, a novel activator of platelet guanylate cyclase], or estrogen was administered to trauma-hemorrhage and sham groups during resuscitation.
  • Mice were killed at 2 h after resuscitation, and cardiac IL-6, HIF-1 alpha, and nuclear factor (NF) kappaB activities were measured.
  • IL-6, NF-kappaB, and HIF-1 alpha levels were markedly elevated after trauma-hemorrhage; all of these parameters were normalized by estrogen as well as YC-1 administration after trauma-hemorrhage.
  • Because elevated IL-6 levels after trauma-hemorrhage were decreased with YC-1 treatment, it indicates that IL-6 expression in cardiomyocytes is induced via HIF-1 alpha.
  • In addition, estrogen decreased the elevated HIF-1 alpha, NF-kappaB, and IL-6 levels after trauma-hemorrhage.
  • These results indicate that the beneficial effects of estrogen on cardiac function after trauma-hemorrhage seem to be mediated by the inhibition of HIF-1 alpha expression and activity.

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  • (PMID = 18791496.001).
  • [ISSN] 1540-0514
  • [Journal-full-title] Shock (Augusta, Ga.)
  • [ISO-abbreviation] Shock
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM037127-23; United States / NIGMS NIH HHS / GM / GM037127-23; United States / NIGMS NIH HHS / GM / R01 GM037127; United States / NIGMS NIH HHS / GM / R01 GM37127; United States / NIGMS NIH HHS / GM / R01 GM039519
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogens; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Interleukin-6; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS171172; NLM/ PMC2814124
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69. Leibetseder V, Humpeler S, Zuckermann A, Svoboda M, Thalhammer T, Marktl W, Ekmekcioglu C: Time dependence of estrogen receptor expression in human hearts. Biomed Pharmacother; 2010 Mar;64(3):154-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim was to quantify ER mRNA expression in left ventricular specimens from patients with coronary heart disease (CHD, n=15) and dilated cardiomyopathy (CMP, n=38) and compare their levels with those from healthy heart donors (n=9).
  • [MeSH-major] Cardiomyopathy, Dilated / metabolism. Coronary Disease / metabolism. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor beta / biosynthesis. Myocardium / metabolism. RNA, Messenger / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Circadian Rhythm. Computer Systems. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction. Time Factors. Young Adult

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  • [Copyright] Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 19944560.001).
  • [ISSN] 1950-6007
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / RNA, Messenger
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70. Madakamutil LT, Maricic I, Sercarz EE, Kumar V: Immunodominance in the TCR repertoire of a [corrected] TCR peptide-specific CD4+ Treg population that controls experimental autoimmune encephalomyelitis. J Immunol; 2008 Apr 1;180(7):4577-85
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  • We report, by sequencing of the TCR alpha- and beta-chain associated with CD4(+) Treg, that the TCR repertoire is limited and the majority of CD4(+) Treg use the TCR Vbeta14 and Valpha4 gene segments.
  • Furthermore, a higher frequency of CD4(+) Treg clones in the naive repertoire correlates with less severity and more rapid spontaneous recovery from disease in parental B10.PL or PL/J and (B10.PL x PL/J)F(1) mice.
  • Thus, a selective set of immunodominant Treg as well as pathogenic T cell clones can be targeted for potential intervention in autoimmune disease conditions.
  • [MeSH-major] Encephalomyelitis, Autoimmune, Experimental / immunology. Immunodominant Epitopes / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigens, Neoplasm / immunology. Disease Models, Animal. Female. Immunization. Mice. Molecular Sequence Data

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  • [ErratumIn] J Immunol. 2008 May 15;180(10):7048
  • (PMID = 18354180.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / B5 antigen; 0 / Immunodominant Epitopes; 0 / Receptors, Antigen, T-Cell, alpha-beta
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71. Zeissig S, Bergann T, Fromm A, Bojarski C, Heller F, Guenther U, Zeitz M, Fromm M, Schulzke JD: Altered ENaC expression leads to impaired sodium absorption in the noninflamed intestine in Crohn's disease. Gastroenterology; 2008 May;134(5):1436-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered ENaC expression leads to impaired sodium absorption in the noninflamed intestine in Crohn's disease.
  • BACKGROUND & AIMS: Crohn's disease (CD) is a chronic inflammatory bowel disease.
  • METHODS: Sodium transport via ENaC was investigated in Ussing chambers using biopsy specimens of sigmoid colon from controls and active CD limited to the small intestine.
  • ENaC messenger RNA expression and subcellular localization were studied by real-time polymerase chain reaction and confocal microscopy.
  • Exposure of rat distal colon to tumor necrosis factor alpha led to reduced electrogenic sodium absorption because of impaired transcriptional gamma-ENaC induction, which resembled the changes found in CD.
  • Tumor necrosis factor alpha effects were dependent on extracellular signal-regulated kinase 1/2 but not p38 or c-Jun-N-terminal kinase because inhibition of mitogen-activated protein kinase/extracellular regulated kinase (MEK)1/2 but not inhibition of p38 or c-Jun-N-terminal kinase prevented suppression of ENaC.
  • [MeSH-major] Colon / physiology. Crohn Disease / genetics. Epithelial Sodium Channels / genetics. Gene Expression. Intestinal Absorption / physiology. RNA / genetics. Sodium / metabolism
  • [MeSH-minor] Adult. Animals. Biopsy. Blotting, Western. Female. Follow-Up Studies. Humans. Immunohistochemistry. Ion Transport / physiology. Male. Middle Aged. Mitogen-Activated Protein Kinase 3 / metabolism. Patch-Clamp Techniques. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Spectrum Analysis. Tumor Necrosis Factor-alpha / biosynthesis


72. Liu DD, Lin HI, Hsieh NK, Chen HI: Enhancement effects of hypercapnia on the acute lung injury caused by acid aspiration. Chin J Physiol; 2009 Jun 30;52(3):115-27
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  • We employed reverse-transcriptase polymerase chain reaction to detect the expression of iNOS mRNA.
  • The insults also elevated LW/BW, LWG, PCBAL and dye leakage, plasma nitrate/nitrite, MG, MPO, PLA2, tumor necrosis factor(alpha), interleukin-beta and interleukin-6.
  • [MeSH-minor] Acid-Base Equilibrium / physiology. Administration, Inhalation. Animals. Blood Gas Analysis. Blood Pressure / drug effects. Blood Pressure / physiology. Carbon Dioxide / administration & dosage. Carbon Dioxide / pharmacology. Cytokines / metabolism. Disease Models, Animal. Heart Rate / drug effects. Heart Rate / physiology. Lung / metabolism. Lung / pathology. Lung / physiopathology. Male. Methylguanidine / blood. Nitric Oxide / metabolism. Nitric Oxide Synthase Type II / metabolism. Peroxidase / blood. Phospholipases A2 / blood. Rats. Rats, Sprague-Dawley

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  • (PMID = 19777797.001).
  • [ISSN] 0304-4920
  • [Journal-full-title] The Chinese journal of physiology
  • [ISO-abbreviation] Chin J Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Cytokines; 142M471B3J / Carbon Dioxide; 31C4KY9ESH / Nitric Oxide; 5L0H5Q9VAG / Methylguanidine; EC 1.11.1.7 / Peroxidase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 3.1.1.4 / Phospholipases A2
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73. Atencia R, Bustamante FJ, Valdivieso A, Arrieta A, Riñón M, Prada A, Maruri N: Differential expression of viral PAMP receptors mRNA in peripheral blood of patients with chronic hepatitis C infection. BMC Infect Dis; 2007;7:136
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  • In this work, we determined mRNA levels of two members of the Toll-like Receptors family, (TLR3 and TLR7) and the helicase RIG-I, all of three recognizing viral RNA products, in peripheral blood of healthy donors and hepatitis C virus (HCV) patients, to observe if their transcripts are altered in this disease.
  • METHODS: IFN-alpha, TLR3, TLR7 and RIG-I levels in peripheral blood from healthy controls (n = 18) and chronic HCV patients (n = 18) were quantified by real-time polymerase chain reaction.
  • RESULTS: Our results show that IFN-alpha, TLR3, TLR7 and RIG-I mRNA levels are significantly down-regulated in patients with chronic HCV infection when compared with healthy controls.
  • We also found that the measured levels of TLR3 and TLR7, but not RIG-I, correlated significantly with those of IFN-alpha CONCLUSION: Monitoring the expression of RNA-sensing receptors like TLR3, TLR7 and RIG-I during the different clinical stages of infection could bring a new source of data about the prognosis of disease.
  • [MeSH-minor] Adult. Aged. DEAD-box RNA Helicases / genetics. DEAD-box RNA Helicases / metabolism. Female. Hepacivirus / immunology. Hepacivirus / pathogenicity. Humans. Interferon-alpha / genetics. Interferon-alpha / metabolism. Male. Middle Aged. Prognosis. RNA, Viral / metabolism. Toll-Like Receptor 3 / genetics. Toll-Like Receptor 3 / metabolism. Toll-Like Receptor 7 / genetics. Toll-Like Receptor 7 / metabolism

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  • (PMID = 18021446.001).
  • [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 / Interferon-alpha; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Receptors, Pattern Recognition; 0 / Toll-Like Receptor 3; 0 / Toll-Like Receptor 7; EC 3.6.1.- / DDX58 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Other-IDs] NLM/ PMC2194715
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74. Welch MG, Anwar M, Chang CY, Gross KJ, Ruggiero DA, Tamir H, Gershon MD: Combined administration of secretin and oxytocin inhibits chronic colitis and associated activation of forebrain neurons. Neurogastroenterol Motil; 2010 Jun;22(6):654-e202
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  • BACKGROUND: The pathogenesis of inflammatory bowel disease is unknown; however, the disorder is aggravated by psychological stress and is itself psychologically stressful.
  • Chronic intestinal inflammation, moreover, has been reported to activate forebrain neurons.
  • Strikingly, S/OT decreased inflammatory infiltrates into the colon and colonic expression of tumor necrosis factor-alpha and interferon-gamma.
  • It is possible that S and OT, which are endogenous to the colon, might normally combine to restrict the severity of colonic inflammatory responses and that advantage might be taken of this system to develop novel means of treating inflammation-associated intestinal disorders.

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  • (PMID = 20210978.001).
  • [ISSN] 1365-2982
  • [Journal-full-title] Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
  • [ISO-abbreviation] Neurogastroenterol. Motil.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS012969-33; United States / NINDS NIH HHS / NS / R01 NS012969; United States / NINDS NIH HHS / NS / R01 NS015547; United States / NINDS NIH HHS / NS / R01 NS012969-33
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 1393-25-5 / Secretin; 50-56-6 / Oxytocin; 82115-62-6 / Interferon-gamma; 8T3HQG2ZC4 / Trinitrobenzenesulfonic Acid
  • [Other-IDs] NLM/ NIHMS174680; NLM/ PMC3068601
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75. Treszl A, Tulassay T, Vasarhelyi B: Genetic basis for necrotizing enterocolitis--risk factors and their relations to genetic polymorphisms. Front Biosci; 2006;11:570-80
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  • Necrotizing enterocolitis (NEC) is a common, life-threatening neonatal gastrointestinal disease; it affects approximately 11% of extremely premature neonates.
  • Risk factors may roughly be grouped into four main categories: prematurity; transient ischemia of the intestine; local/systemic inflammation predisposing the bowel to injury, and therapeutic interventions.
  • Positive findings indicate the implication of genetic polymorphisms of proinflammatory cytokines in premature birth; angiotensin converting enzyme in perinatal adaptation and angiotensin type 1 receptor in the closure of ductus arteriosus; surfactant proteins A and B in respiratory distress syndrome; interleukin (IL)-6 in sepsis, and IL-4-receptor alpha chain and IL-18 in NEC.

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  • (PMID = 16146753.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-18; 0 / Interleukin-6; 207137-56-2 / Interleukin-4; S88TT14065 / Oxygen
  • [Number-of-references] 108
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76. Li HT, Lin DH, Luo XY, Zhang F, Ji LN, Du HN, Song GQ, Hu J, Zhou JW, Hu HY: Inhibition of alpha-synuclein fibrillization by dopamine analogs via reaction with the amino groups of alpha-synuclein. Implication for dopaminergic neurodegeneration. FEBS J; 2005 Jul;272(14):3661-72
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  • [Title] Inhibition of alpha-synuclein fibrillization by dopamine analogs via reaction with the amino groups of alpha-synuclein. Implication for dopaminergic neurodegeneration.
  • Fibrillization of alpha-synuclein (alpha-Syn) is closely associated with the formation of Lewy bodies in neurons and dopamine (DA) is a potent inhibitor for the process, which is implicated in the causative pathogenesis of Parkinson's disease (PD).
  • The MS and NMR characterizations strongly demonstrate that DA and its analogs inhibit alpha-Syn fibrillization by a mechanism where the oxidation products (quinones) of DA analogs react with the amino groups of alpha-Syn chain, generating alpha-Syn-quinone adducts.
  • It is likely that the amino groups of alpha-Syn undergo nucleophilic attack on the quinone moiety of DA analogs to form imino bonds.
  • The covalently cross-linked alpha-Syn adducts by DA are primarily large molecular mass oligomers, while those by catechol and p-benzoquinone (or hydroquinone) are largely monomers or dimers.
  • The DA quinoprotein retains the same cytotoxicity as the intact alpha-Syn, suggesting that the oligomeric intermediates are the major elements that are toxic to the neuronal cells.
  • This finding implies that the reaction of alpha-Syn with DA is relevant to the selective dopaminergic loss in PD.
  • [MeSH-minor] Cross-Linking Reagents / chemistry. Cross-Linking Reagents / pharmacology. Flavonoids / chemistry. Flavonoids / pharmacology. Molecular Structure. Oxidation-Reduction. Phenols / chemistry. Phenols / pharmacology. Polyphenols. Protein Conformation / drug effects. Quinones / chemistry. Quinones / metabolism. Spectrometry, Mass, Electrospray Ionization. Synucleins. alpha-Synuclein

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  • (PMID = 16008565.001).
  • [ISSN] 1742-464X
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cross-Linking Reagents; 0 / Flavonoids; 0 / Nerve Tissue Proteins; 0 / Phenols; 0 / Polyphenols; 0 / Quinones; 0 / Synucleins; 0 / alpha-Synuclein; VTD58H1Z2X / Dopamine
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77. Meneghin A, Choi ES, Evanoff HL, Kunkel SL, Martinez FJ, Flaherty KR, Toews GB, Hogaboam CM: TLR9 is expressed in idiopathic interstitial pneumonia and its activation promotes in vitro myofibroblast differentiation. Histochem Cell Biol; 2008 Nov;130(5):979-92
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  • Infectious diseases can be cofactors in idiopathic interstitial pneumonias (IIP) pathogenesis; recent data suggests that toll-like receptors 9 (TLR9) ligands contribute to experimental chronic tissue remodeling.
  • Real-time TAQMAN and immunohistochemical analysis of IIP normal surgical lung biopsies (SLBs), primary fibroblast lines grown from both IIP and normal SLBs indicate that TLR9 is prominently and differentially expressed in a disease-specific manner.
  • TLR9 in fibroblasts appeared to be increased by profibrotic Th2 cytokines (IL-4 and IL-13) and this was true in fibroblasts cultured from the most severe form of IIP, idiopathic pulmonary fibrosis (IPF) SLBs, in non-specific interstitial pneumonia fibroblast lines, and in normal fibroblasts.
  • Finally, confocal microscopy studies have shown that TLR9 activation by its synthetic agonist CpG-ODN significantly increased the expression of alpha smooth muscle actin, the main marker of myofibroblast differentiation.
  • These data indicate that TLR9 expression may drive the abnormal tissue healing response in severe forms of IIP and its activation can have a key role in myofibroblast differentiation promoting the progression of disease during the terminal phase of IPF.
  • [MeSH-minor] Actins / metabolism. Cells, Cultured. Humans. Immunohistochemistry. Interleukin-13 / metabolism. Interleukin-4 / metabolism. Microscopy, Confocal. Oligodeoxyribonucleotides / pharmacology. Polymerase Chain Reaction. RNA, Messenger / metabolism. Recombinant Proteins / metabolism

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  • (PMID = 18633634.001).
  • [ISSN] 0948-6143
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P50 HL056402; United States / NHLBI NIH HHS / HL / P50 HL56402
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / CPG-oligonucleotide; 0 / Interleukin-13; 0 / Oligodeoxyribonucleotides; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / TLR9 protein, human; 0 / Toll-Like Receptor 9; 207137-56-2 / Interleukin-4
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78. Spirito F, Capt A, Del Rio M, Larcher F, Guaguere E, Danos O, Meneguzzi G: Sustained phenotypic reversion of junctional epidermolysis bullosa dog keratinocytes: Establishment of an immunocompetent animal model for cutaneous gene therapy. Biochem Biophys Res Commun; 2006 Jan 20;339(3):769-78
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  • Because gene therapy protocols require validation in animal models, we have phenotypically reverted by oncoretroviral transfer of the curative gene the keratinocytes isolated from dogs with a spontaneous form of JEB associated with a genetic mutation in the alpha3 chain of laminin 5.
  • (2) recover the adhesion, proliferation, and clonogenic capacity of wild-type keratinocytes;.
  • We validate an animal model that appears particularly suitable to demonstrate feasibility, efficacy, and safety of genetic therapeutic strategies for cutaneous disorders before undertaking human clinical trials.
  • [MeSH-major] Disease Models, Animal. Epidermolysis Bullosa / genetics. Epidermolysis Bullosa / therapy. Genetic Therapy / methods. Keratinocytes / metabolism. Laminin / genetics. Laminin / therapeutic use

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  • (PMID = 16316622.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Laminin; 0 / Recombinant Proteins; 170834-93-2 / laminin alpha 3
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79. Germain-Lee EL, Schwindinger W, Crane JL, Zewdu R, Zweifel LS, Wand G, Huso DL, Saji M, Ringel MD, Levine MA: A mouse model of albright hereditary osteodystrophy generated by targeted disruption of exon 1 of the Gnas gene. Endocrinology; 2005 Nov;146(11):4697-709
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  • Albright hereditary osteodystrophy is caused by heterozygous inactivating mutations in GNAS, a gene that encodes not only the alpha-chain of Gs (Galphas), but also NESP55 and XLalphas through use of alternative first exons.
  • This variant of Albright hereditary osteodystrophy is termed pseudohypoparathyroidism type 1a and is due to presumed tissue-specific paternal imprinting of Galphas.
  • Heterozygous mice were shorter and, when the disrupted allele was inherited maternally, weighed more than wild-type littermates.
  • These findings confirm the tissue-specific paternal imprinting of GNAS and demonstrate that Galphas deficiency alone is sufficient to account for the hormone resistance of pseudohypoparathyroidism type 1a.
  • [MeSH-major] Disease Models, Animal. Exons. Fibrous Dysplasia, Polyostotic / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mice, Knockout / genetics

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  • (PMID = 16099856.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56178; United States / NCRR NIH HHS / RR / MO1 RR00052; United States / NIAAA NIH HHS / AA / R01 AA09000; United States / NIDDK NIH HHS / DK / R01 DK34281; United States / NIDDK NIH HHS / DK / R01 DK56178; United States / NCRR NIH HHS / RR / RR00171
  • [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 / Parathyroid Hormone; 9002-71-5 / Thyrotropin; EC 3.6.1.- / GNAS protein, human; EC 3.6.1.- / Gnas protein, mouse; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; EC 4.6.1.1 / Adenylyl Cyclases
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80. Taura K, De Minicis S, Seki E, Hatano E, Iwaisako K, Osterreicher CH, Kodama Y, Miura K, Ikai I, Uemoto S, Brenner DA: Hepatic stellate cells secrete angiopoietin 1 that induces angiogenesis in liver fibrosis. Gastroenterology; 2008 Nov;135(5):1729-38
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  • In primary cultures, activated HSCs express and secrete angiopoietin 1 more abundantly than quiescent HSCs, and the inflammatory cytokine tumor necrosis factor-alpha stimulates its expression in an nuclear factor-kappaB-dependent manner.
  • [MeSH-minor] Animals. Antigens, CD31 / biosynthesis. Cells, Cultured. Disease Models, Animal. Electrophoresis, Polyacrylamide Gel. Enzyme-Linked Immunosorbent Assay. Gene Expression. Humans. Mice. Mice, Inbred BALB C. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptor, TIE-2 / metabolism. Signal Transduction. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18823985.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01GM041804
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiopoietin-1; 0 / Antigens, CD31; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Receptor, TIE-2
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81. Brezzi B, Del Prete D, Lupo A, Magistroni R, Gomez-Lira M, Bernich P, Anglani F, Mezzabotta F, Turco A, Furci L, Ceol M, Antonucci F, Abaterusso C, Bonfante L, D'Angelo A, Albertazzi A, Gambaro G: Primary IgA nephropathy is more severe in TGF-beta1 high secretor patients. J Nephrol; 2009 Nov-Dec;22(6):747-59
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  • [Title] Primary IgA nephropathy is more severe in TGF-beta1 high secretor patients.
  • BACKGROUND: IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and is characterized by extremely variable clinical and morphological features and outcome.
  • Glomerular and interstitial mRNA levels of TGF-beta1 were assessed by real-time PCR in 34 patients to seek relationships with clinical, renal histopathological features and outcome.
  • A higher interstitial immunodeposition was observed for TGF-beta1, collagen IV and alpha-SMA in patients with the COD 10 T allele (p=0.045, p=0.049, p=0.032, respectively).
  • CONCLUSIONS: In primary IgA nephropathy, the T allele of the TGF-beta1 COD 10 C/T polymorphism seems to be associated with more severe histological lesions, higher renal TGF-beta1 mRNA levels and a worse prognosis.
  • [MeSH-major] Glomerulonephritis, IGA / genetics. Kidney / secretion. Polymorphism, Genetic. Transforming Growth Factor beta1 / genetics
  • [MeSH-minor] Adult. Biopsy. Case-Control Studies. Disease Progression. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Italy. Kaplan-Meier Estimate. Male. Middle Aged. Phenotype. Prognosis. Proportional Hazards Models. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Risk Assessment. Risk Factors. Severity of Illness Index. Up-Regulation. Young Adult

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  • (PMID = 19967654.001).
  • [ISSN] 1121-8428
  • [Journal-full-title] Journal of nephrology
  • [ISO-abbreviation] J. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Transforming Growth Factor beta1
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82. Chakravarti A, Kumaria R: Circulating levels of tumour necrosis factor-alpha & interferon-gamma in patients with dengue & dengue haemorrhagic fever during an outbreak. Indian J Med Res; 2006 Jan;123(1):25-30
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  • [Title] Circulating levels of tumour necrosis factor-alpha & interferon-gamma in patients with dengue & dengue haemorrhagic fever during an outbreak.
  • Immune enhancement caused by cytokines, interferon and activated complement system is one of the hypotheses proposed to explain the haemorrhagic form of disease.
  • This study was undertaken to investigate the role of pro-inflammatory cytokines tumour necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) in dengue infection, and their possible association with disease severity.
  • All the patients were confirmed positive for dengue infection by serology or by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • Serum levels of TNF-alpha and IFN-gamma were determined by ELISA.
  • RESULTS: The levels of both the cytokines were significantly elevated in the disease group as compared to the control group.
  • Significantly higher levels of TNF-alpha; 258.02 pg/ml (P<0.005) were seen in patients having secondary infection, while patients with primary infection had higher level of IFN-gamma; 29.47 pg/ml (P<0.005).
  • TNF-alpha was elevated in the later phase of illness, while IFN-gamma was elevated in early phase also.
  • INTERPRETATION & CONCLUSION: Overproduction of TNF-alpha during secondary infection may have a role in immunopathogenesis of DHF, however, study of other cytokines produced along with IFN-gamma;, during the course of dengue infection is required to know the specific role of IFN-gamma in DI.
  • [MeSH-major] Dengue. Interferon-gamma / blood. Severe Dengue. Tumor Necrosis Factor-alpha / blood

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  • [CommentIn] Indian J Med Res. 2006 Jan;123(1):11-4 [16567861.001]
  • (PMID = 16567864.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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83. Flammer JR, Dobrovolna J, Kennedy MA, Chinenov Y, Glass CK, Ivashkiv LB, Rogatsky I: The type I interferon signaling pathway is a target for glucocorticoid inhibition. Mol Cell Biol; 2010 Oct;30(19):4564-74
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  • [Title] The type I interferon signaling pathway is a target for glucocorticoid inhibition.
  • Type I interferon (IFN) is essential for host defenses against viruses; however, dysregulated IFN signaling is causally linked to autoimmunity, particularly systemic lupus erythematosus.
  • Autoimmune disease treatments rely on glucocorticoids (GCs), which act via the GC receptor (GR) to repress proinflammatory cytokine gene transcription.
  • Conversely, cytokine signaling through cognate Jak/STAT pathways is reportedly unaffected or even stimulated by GR.
  • Unexpectedly, we found that GR dramatically inhibited IFN-stimulated gene (ISG) expression in macrophages.
  • The target of inhibition, the heterotrimeric STAT1-STAT2-IRF9 (ISGF3) transcription complex, utilized the GR cofactor GRIP1/TIF2 as a coactivator.
  • Consequently, GRIP1 knockdown, genetic ablation, or depletion by GC-activated GR attenuated ISGF3 promoter occupancy, preinitiation complex assembly, and ISG expression.
  • Furthermore, this regulatory loop was restricted to cell types such as macrophages expressing the GRIP1 protein at extremely low levels, and pharmacological disruption of the GR-GRIP1 interaction or transient introduction of GRIP1 restored RNA polymerase recruitment to target ISGs and the subsequent IFN response.
  • Thus, type I IFN is a cytokine uniquely controlled by GR at the levels of not only production but also signaling through antagonism with the ISGF3 effector function, revealing a novel facet of the immunosuppressive properties of GCs.

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  • (PMID = 20679482.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI059636-04; United States / NIAMS NIH HHS / AR / R01 AR050401-05; United States / NIAID NIH HHS / AI / R01 AI059636-03; United States / NIAID NIH HHS / AI / R01 AI046712-11; United States / NIAID NIH HHS / AI / R01 AI068820; United States / NIAID NIH HHS / AI / R01 AI059636; United States / NIAID NIH HHS / AI / R01 AI046712; United States / NIAMS NIH HHS / AR / AR050401-05; United States / NIAMS NIH HHS / AR / T32 AR007517; United States / NIAID NIH HHS / AI / AI046712-10; United States / NIAMS NIH HHS / AR / R01 AR050401-06A2; United States / NIAID NIH HHS / AI / R01 AI059636-04; United States / NIAID NIH HHS / AI / R01 AI046712-10; United States / NIAMS NIH HHS / AR / T32 AR07517; United States / NIAMS NIH HHS / AR / R01 AR050401; United States / NIAID NIH HHS / AI / AI059636-03
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Glucocorticoids; 0 / Grip1 protein, mouse; 0 / Interferon Type I; 0 / Interferon-Stimulated Gene Factor 3, alpha Subunit; 0 / Nerve Tissue Proteins; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC2950533
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84. Smits NC, Kurup S, Rops AL, ten Dam GB, Massuger LF, Hafmans T, Turnbull JE, Spillmann D, Li JP, Kennel SJ, Wall JS, Shworak NW, Dekhuijzen PN, van der Vlag J, van Kuppevelt TH: The heparan sulfate motif (GlcNS6S-IdoA2S)3, common in heparin, has a strict topography and is involved in cell behavior and disease. J Biol Chem; 2010 Dec 24;285(52):41143-51
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  • [Title] The heparan sulfate motif (GlcNS6S-IdoA2S)3, common in heparin, has a strict topography and is involved in cell behavior and disease.
  • Combined, our results demonstrate that NS4F5 is a powerful tool for elucidating the biological function of HS(NS4F5) and can be exploited as a probe to detect novel polysaccharide biomarkers of disease processes.
  • [MeSH-major] Amyloidosis / metabolism. Antibodies, Monoclonal / pharmacology. Endothelial Cells / metabolism. Heparitin Sulfate / metabolism. Neoplasms / metabolism. Single-Chain Antibodies / pharmacology
  • [MeSH-minor] Amyloidogenic Proteins / immunology. Amyloidogenic Proteins / metabolism. Animals. Biomarkers / metabolism. CHO Cells. Carbohydrate Sequence. Cell Proliferation / drug effects. Cricetinae. Cricetulus. Disease Models, Animal. Female. Humans. Male. Mice. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 20837479.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK079984; United States / NHLBI NIH HHS / HL / R01 HL079104
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloidogenic Proteins; 0 / Antibodies, Monoclonal; 0 / Biomarkers; 0 / Single-Chain Antibodies; 0 / Tumor Necrosis Factor-alpha; 9050-30-0 / Heparitin Sulfate
  • [Other-IDs] NLM/ PMC3003412
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85. Blaskó B, Kolka R, Thorbjornsdottir P, Sigurdarson ST, Sigurdsson G, Rónai Z, Sasvári-Székely M, Bödvarsson S, Thorgeirsson G, Prohászka Z, Kovács M, Füst G, Arason GJ: Low complement C4B gene copy number predicts short-term mortality after acute myocardial infarction. Int Immunol; 2008 Jan;20(1):31-7
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  • Previously, we found that the C4B*Q0 genotype (low copy number of the C4B gene that encodes the fourth component of complement) is strongly associated with morbidity and mortality of cardiovascular diseases (CVD).
  • The +252 G allele of the lymphotoxin-alpha (LTA) gene encoded close to the C4B gene was also reported to be related to CVD-related mortality in an Oriental population.
  • The number of the C4A and C4B genes was determined in genomic DNA samples by a newly developed real-time PCR-based method; lymphotoxin-alpha (LTA) +252 A>G polymorphism was determined by PCR-restriction fragment length polymorphism analysis.
  • [MeSH-major] Complement C4b / genetics. Gene Dosage. Genetic Predisposition to Disease. Myocardial Infarction / genetics. Myocardial Infarction / mortality. Smoking
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Iceland. Lymphotoxin-alpha / genetics. Male. Polymerase Chain Reaction / methods. Polymorphism, Single Nucleotide. Risk Factors. Survival Analysis

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  • (PMID = 18032375.001).
  • [ISSN] 1460-2377
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lymphotoxin-alpha; 80295-50-7 / Complement C4b
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86. Riediger ND, Othman RA, Suh M, Moghadasian MH: A systemic review of the roles of n-3 fatty acids in health and disease. J Am Diet Assoc; 2009 Apr;109(4):668-79
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  • [Title] A systemic review of the roles of n-3 fatty acids in health and disease.
  • Attention to the role of n-3 long-chain fatty acids in human health and disease has been continuously increased during recent decades.
  • Many clinical and epidemiologic studies have shown positive roles for n-3 fatty acids in infant development; cancer; cardiovascular diseases; and more recently, in various mental illnesses, including depression, attention-deficit hyperactivity disorder, and dementia.
  • Furthermore, additional controlled clinical trials are needed to document whether long-term consumption or supplementation with eicosapentaenoic acid/docosahexaenoic acid or the plant-derived counterpart (alpha-linolenic acid) results in better quality of life.
  • [MeSH-major] Cardiovascular Diseases / prevention & control. Child Development / physiology. Fatty Acids, Omega-3 / physiology. Mental Disorders / prevention & control. Neoplasms / prevention & control
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Attention Deficit Disorder with Hyperactivity / epidemiology. Attention Deficit Disorder with Hyperactivity / prevention & control. Child. Child, Preschool. Dementia / epidemiology. Dementia / prevention & control. Depression / epidemiology. Depression / prevention & control. Female. Food, Fortified. Humans. Infant. Infant, Newborn. Male. Middle Aged. Young Adult


87. Komen JC, Duran M, Wanders RJ: Characterization of phytanic acid omega-hydroxylation in human liver microsomes. Mol Genet Metab; 2005 Jul;85(3):190-5
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  • Phytanic acid is a 3-methyl branched-chain fatty acid which originates from dietary sources.
  • Since the 3-methyl group blocks regular beta-oxidation, it is broken down by peroxisomal alpha-oxidation.
  • Adult Refsum disease patients accumulate phytanic acid as a result of an impairment in peroxisomal alpha-oxidation, caused by the deficient activity of the enzyme phytanoyl-CoA hydroxylase in the majority of patients.
  • [MeSH-minor] Adult. Aldehyde Oxidoreductases / metabolism. Animals. Catalysis. Humans. Hydroxylation. NADP / metabolism. Oxidation-Reduction. Rats. Refsum Disease / metabolism

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  • (PMID = 15979030.001).
  • [ISSN] 1096-7192
  • [Journal-full-title] Molecular genetics and metabolism
  • [ISO-abbreviation] Mol. Genet. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 14721-66-5 / Phytanic Acid; 53-59-8 / NADP; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.2.- / Aldehyde Oxidoreductases
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88. Ates O, Musellim B, Ongen G, Topal-Sarikaya A: Interleukin-10 and tumor necrosis factor-alpha gene polymorphisms in tuberculosis. J Clin Immunol; 2008 May;28(3):232-6
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  • [Title] Interleukin-10 and tumor necrosis factor-alpha gene polymorphisms in tuberculosis.
  • Tuberculosis (TB), caused by Mycobacterium tuberculosis, is an infectious disease in humans killing nearly three million people and eight million cases annually.
  • The cytokines TNF-alpha and IL-10 have been implicated in the pathogenesis of TB.
  • Certain single nucleotide polymorphisms within the promoter region of the IL10 and TNF genes have been associated with altered levels of circulating IL10 and TNF-alpha.
  • We analyzed TNF-alpha (-308 G/A, -238 G/A, -376 G/A) and IL10 (-1,082 G/A, -819 C/T, -592 C/A) polymorphisms in 128 patients with TB and 80 healthy subjects using by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR).
  • No statistically significant association was found between IL-10 -819 C/T, TNF-alpha 308 G/A, -238 G/A, -376 G/A polymorphisms, functional TNFalpha/IL-10 genotypes and TB.
  • Our findings suggest that IL-10 1082 G/A alleles or haplotypes containing these alleles may influence the Th1/Th2 balance and hence may play a role in TB susceptibility and increase risk of developing disease.
  • This polymorphism may be one of the many genetic factors affecting disease outcome.
  • [MeSH-major] Interleukin-10 / genetics. Polymorphism, Genetic. Tuberculosis, Pulmonary / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Female. Genetic Predisposition to Disease. Haplotypes. Humans. Male. Middle Aged. Polymorphism, Single Nucleotide. Tuberculosis / genetics

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  • (PMID = 18071881.001).
  • [ISSN] 0271-9142
  • [Journal-full-title] Journal of clinical immunology
  • [ISO-abbreviation] J. Clin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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89. Brimil N, Barthell E, Heindrichs U, Kuhn M, Lütticken R, Spellerberg B: Epidemiology of Streptococcus agalactiae colonization in Germany. Int J Med Microbiol; 2006 Feb;296(1):39-44
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  • Implementation of CDC guidelines for group B streptococci (GBS) disease prevention resulted in a significant decline of invasive neonatal S. agalactiae infections in the USA.
  • The vast majority of all strains harbored genes for the major surface protein antigens, the alpha-C-protein or alpha-C-protein like antigens like Alp2-4, epsilon and Rib.
  • These data show that S. agalactiae colonization is common in Germany and strict adherence to the guidelines for the preventions of GBS disease will result in peripartal antibiotic prophylaxis in up to 20% of all deliveries.
  • [MeSH-minor] Bacterial Capsules / analysis. Bacterial Outer Membrane Proteins / chemistry. Bacterial Outer Membrane Proteins / genetics. DNA, Bacterial / chemistry. DNA, Bacterial / genetics. Female. Germany / epidemiology. Humans. Immunodiffusion. Polymerase Chain Reaction. Pregnancy. Rectum / microbiology. Serotyping. Vagina / microbiology

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  • (PMID = 16361113.001).
  • [ISSN] 1438-4221
  • [Journal-full-title] International journal of medical microbiology : IJMM
  • [ISO-abbreviation] Int. J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bacterial Outer Membrane Proteins; 0 / DNA, Bacterial
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90. Okada K, Fujii T, Ohtsuka Y, Yamakawa Y, Izumi H, Yamashiro Y, Shimizu T: Overfeeding can cause NEC-like enterocolitis in premature rat pups. Neonatology; 2010;97(3):218-24
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  • OBJECTIVES: To investigate the mechanisms of NEC in terms of inflammatory signaling in the intestine.
  • The premature rat pups, delivered by abdominal incision on day 20 of gestation (day 21 is considered as full term), were divided into three groups, and they were given a single administration of 0.05, 0.1, and 0.15 ml of formula milk via an orogastric catheter.
  • After 24 h, the development of enterocolitis was evaluated by the presence of hemorrhagic enterocolitis, and the expression of signaling molecules, inhibitor of nuclear factor-kappaB (IkappaB)-alpha/beta and peroxisome proliferator-activated receptor (PPAR)-gamma mRNA was examined by reverse transcription-polymerase chain reaction from inflamed and non-inflamed intestinal samples.
  • Expression of IkappaB-alpha/beta and PPAR-gamma mRNA increased in inflamed intestine.
  • CONCLUSIONS: Increased expression of IkappaB-alpha/beta suggested that the inflammatory mediator nuclear factor-kappaB is deeply involved in the pathogenesis of enterocolitis that can be easily introduced by overfeeding of milk ingestion in premature rat pups which mimic those seen in NEC.
  • [MeSH-major] Animals, Newborn. Disease Models, Animal. Enterocolitis, Necrotizing / etiology. Infant, Premature, Diseases / pathology. Overnutrition / complications. Rats
  • [MeSH-minor] Animals. Animals, Suckling. Enterocolitis / etiology. Enterocolitis / pathology. Female. Humans. I-kappa B Proteins / genetics. I-kappa B Proteins / metabolism. Infant, Newborn. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. PPAR gamma / genetics. PPAR gamma / metabolism. Pregnancy. Rats, Sprague-Dawley

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19887849.001).
  • [ISSN] 1661-7819
  • [Journal-full-title] Neonatology
  • [ISO-abbreviation] Neonatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / I kappa B beta protein; 0 / I-kappa B Proteins; 0 / PPAR gamma; 139874-52-5 / NF-kappaB inhibitor alpha
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91. Yousefipour GA, Salami Z, Farjadian S: Association of HLA-DQA1*0101/2 and DQB1*0502 with myasthenia gravis in southern Iranian patients. Iran J Immunol; 2009 Jun;6(2):99-102
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  • BACKGROUND: Myasthenia gravis is an autoimmune disorder of neuromuscular junction characterized by skeletal muscle weakness and fatigability.
  • Different genes may control the induction and clinical presentation of this disease.
  • METHODS: HLA-DQA1 and DQB1 alleles were determined in 104 sporadic patients with myasthenia gravis using polymerase chain reaction - restriction fragment length polymorphism method and the results were compared to 816 healthy controls.
  • These alleles revealed positive associations with the disease with relative risks of 1.69 and 2.41, respectively.
  • CONCLUSION: According to the results of this study, DQA1*0101/2 and DQB1*0502 alleles might be considered as predisposing genetic factors to myasthenia gravis while DQA1*0501, DQB1*0301 and *0602/3 show protective roles against this disease.
  • [MeSH-minor] Age of Onset. Early Diagnosis. Female. Gene Frequency. Genetic Predisposition to Disease. HLA-DQ alpha-Chains. HLA-DQ beta-Chains. Histocompatibility Testing. Humans. Iran. Male. Polymerase Chain Reaction

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  • (PMID = 19561379.001).
  • [ISSN] 1735-1383
  • [Journal-full-title] Iranian journal of immunology : IJI
  • [ISO-abbreviation] Iran J Immunol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / HLA-DQ Antigens; 0 / HLA-DQ alpha-Chains; 0 / HLA-DQ beta-Chains; 0 / HLA-DQA1 antigen; 0 / HLA-DQB1 antigen
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92. 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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93. Ehrlich S, Weiss D, Burghardt R, Infante-Duarte C, Brockhaus S, Muschler MA, Bleich S, Lehmkuhl U, Frieling H: Promoter specific DNA methylation and gene expression of POMC in acutely underweight and recovered patients with anorexia nervosa. J Psychiatr Res; 2010 Oct;44(13):827-33
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  • Proopiomelanocortin (POMC) and its derived peptides, in particular alpha-MSH, have been shown to play a crucial role in the regulation of hunger, satiety and energy homeostasis.
  • We hypothesised that POMC promoter specific DNA methylation and gene expression will be affected by malnutrition and therefore differ in AN patients at distinct stages of the disorder.
  • Expression of the truncated form and mean promoter DNA methylation was similar in all three subgroups.
  • [MeSH-minor] Adolescent. Adult. Body Mass Index. Body Weight. Disease-Free Survival. Female. Gene Expression. Humans. Leptin / blood. Malnutrition / blood. Malnutrition / genetics. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction. Young Adult. alpha-MSH / genetics. alpha-MSH / metabolism

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  • (PMID = 20176366.001).
  • [ISSN] 1879-1379
  • [Journal-full-title] Journal of psychiatric research
  • [ISO-abbreviation] J Psychiatr Res
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Leptin; 0 / RNA, Messenger; 581-05-5 / alpha-MSH; 66796-54-1 / Pro-Opiomelanocortin
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94. Degens H, Swisher AK, Heijdra YF, Siu PM, Dekhuijzen PN, Alway SE: Apoptosis and Id2 expression in diaphragm and soleus muscle from the emphysematous hamster. Am J Physiol Regul Integr Comp Physiol; 2007 Jul;293(1):R135-44
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  • During chronic obstructive pulmonary disease (COPD) diaphragm and peripheral muscle weakness occur.
  • The mRNA levels of TNF-alpha and markers of apoptosis were significantly elevated in the diaphragm and soleus muscles during emphysema.
  • Thus, despite the absence of muscle atrophy in emphysematous hamsters, there was evidence of increased TNF-alpha expression, apoptosis, and altered muscle-specific transcriptional regulation as reflected by decreased MyoD and elevated Id2 levels at least in the soleus and diaphragm muscle.
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Cell Nucleus / metabolism. Cricetinae. Cytosol / metabolism. DNA Fragmentation. Male. Mesocricetus. Muscle Fibers, Skeletal / chemistry. Muscle Fibers, Skeletal / physiology. MyoD Protein / genetics. Myosin Heavy Chains / metabolism. NF-kappa B / biosynthesis. Pulmonary Disease, Chronic Obstructive / metabolism. Pulmonary Disease, Chronic Obstructive / pathology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 17395785.001).
  • [ISSN] 0363-6119
  • [Journal-full-title] American journal of physiology. Regulatory, integrative and comparative physiology
  • [ISO-abbreviation] Am. J. Physiol. Regul. Integr. Comp. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inhibitor of Differentiation Protein 2; 0 / MyoD Protein; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 3; EC 3.6.4.1 / Myosin Heavy Chains
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95. Gholamiandekhordi AR, Ducatelle R, Heyndrickx M, Haesebrouck F, Van Immerseel F: Molecular and phenotypical characterization of Clostridium perfringens isolates from poultry flocks with different disease status. Vet Microbiol; 2006 Mar 10;113(1-2):143-52
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  • [Title] Molecular and phenotypical characterization of Clostridium perfringens isolates from poultry flocks with different disease status.
  • Due to the diminished use of growth-promoting antibiotics in the European Union, Clostridium perfringens induced necrotic enteritis and subclinical disease have become important threats to poultry health.
  • Animals from healthy flocks were sampled by cloacal swabs, while intestinal and liver samples of animals suffering from necrotic enteritis were analysed.
  • A total of 27 isolates was obtained from 23 broiler flocks without clinical problems and 36 isolates were obtained from 8 flocks with clinical problems.
  • Isolates derived from flocks where disease outbreaks occurred were clonal within each flock, but each flock harboured a different clone.
  • All isolates were of toxin type A.
  • In vitro alpha toxin production for all isolates was quantified by enzyme-linked immunosorbent assay.
  • It was shown that in vitro alpha toxin production of C. perfringens isolates from diseased flocks was not higher than in vitro alpha toxin production from isolates derived from healthy flocks.
  • [MeSH-major] Clostridium Infections / veterinary. Clostridium perfringens / genetics. Enteritis / veterinary. Poultry Diseases / microbiology
  • [MeSH-minor] Animals. Bacterial Toxins / analysis. Bacterial Toxins / classification. Bacterial Toxins / genetics. DNA Primers / chemistry. DNA, Bacterial / chemistry. DNA, Bacterial / isolation & purification. Electrophoresis, Gel, Pulsed-Field / methods. Phenotype. Phylogeny. Polymerase Chain Reaction / methods. Poultry

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  • (PMID = 16337097.001).
  • [ISSN] 0378-1135
  • [Journal-full-title] Veterinary microbiology
  • [ISO-abbreviation] Vet. Microbiol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / DNA Primers; 0 / DNA, Bacterial
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96. Miyauchi E, Morita H, Okuda J, Sashihara T, Shimizu M, Tanabe S: Cell wall fraction of Enterococcus hirae ameliorates TNF-alpha-induced barrier impairment in the human epithelial tight junction. Lett Appl Microbiol; 2008 Apr;46(4):469-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell wall fraction of Enterococcus hirae ameliorates TNF-alpha-induced barrier impairment in the human epithelial tight junction.
  • AIMS: The evaluation of the effects of Enterococcus hirae, an intestinal bacterium in the adjacent mucosa (mucosal bacterium), on tumour necrosis factor-alpha (TNF-alpha)-induced barrier impairment in human epithelial Caco-2 cells.
  • METHODS AND RESULTS: The filter-grown Caco-2 monolayers were used as an intestinal epithelial model system.
  • In Caco-2 cells, heat-killed E. hirae ATCC 9790(T) suppressed the TNF-alpha-induced barrier impairment and increase in interleukin-8 (IL-8) secretion, but lipase- and mutanolysin-treated E. hirae ATCC 9790(T) did not have these effects.
  • It was demonstrated that lipoteichoic acid (LTA) from E. hirae ATCC 9790(T) is responsible for Caco-2 cells' recovery from TNF-alpha-induced impairments.
  • Increased expression of zonula occludens-1 was observed by the addition of E. hirae ATCC 9790(T) to TNF-alpha-treated Caco-2 cells, and decreased expression of myosin light chain kinase was observed by the addition of LTA and Pam(3)Cys-Ser-(Lys)(4); this, in turn, led to barrier enforcement.
  • CONCLUSIONS: Enterococcus hirae ATCC 9790(T) cell wall fractions, such as LTA, protect against intestinal impairment by regulation of epithelial tight junction via TLR2 signalling.
  • SIGNIFICANCE AND IMPACT OF THE STUDY: Enterococcus hirae could be useful in the treatment of inflammatory bowel disease, as well as other intestinal disorders.
  • [MeSH-major] Cell Wall / immunology. Enterococcus / immunology. Epithelial Cells / microbiology. Tight Junctions / microbiology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Caco-2 Cells. Humans. Interleukin-8 / biosynthesis. Lipopeptides. Lipopolysaccharides / immunology. Lipopolysaccharides / isolation & purification. Membrane Proteins / biosynthesis. Myosin-Light-Chain Kinase / biosynthesis. Peptides / immunology. Phosphoproteins / biosynthesis. Teichoic Acids / immunology. Teichoic Acids / isolation & purification. Zonula Occludens-1 Protein

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