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6. Roumestan C, Michel A, Bichon F, Portet K, Detoc M, Henriquet C, Jaffuel D, Mathieu M: Anti-inflammatory properties of desipramine and fluoxetine. Respir Res; 2007;8:35
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  • We also analysed whether antidepressants act directly on peripheral cell types that participate in the inflammatory response in these diseases.
  • Circulating levels of tumour necrosis factor (TNF)-alpha and mortality rate were measured.
  • In vitro production of TNF-alpha and Regulated upon Activation, Normal T cell Expressed and presumably Secreted (RANTES) from activated monocytes and lung epithelial cells, respectively, was analysed by immunoassays.
  • Reporter gene assays were used to measure the effect of antidepressants on the activity of nuclear factor-kappaB and activator protein-1 which are involved in the control of TNF-alpha and RANTES expression.
  • RESULTS: In the septic shock model, all three drugs given preventively markedly decreased circulating levels of TNF-alpha and mortality (50% mortality in fluoxetine treated group, 30% in desipramine and prednisolone treated groups versus 90% in controls).
  • In vitro, desipramine and fluoxetine dose-dependently inhibited the release of TNF-alpha from LPS-treated monocytes.
  • In lung epithelial cells, these compounds decreased TNF-alpha-induced RANTES expression as well as the activity of nuclear factor-kappaB and activator protein-1.
  • These antidepressants act directly on relevant peripheral cell types to decrease expression of inflammatory mediators probably by affecting their gene transcription.
  • [MeSH-minor] Animals. Asthma / complications. Asthma / metabolism. Cells, Cultured. Cytokines / drug effects. Cytokines / metabolism. Disease Models, Animal. Humans. Inflammation / drug therapy. Inflammation / etiology. Mice. Mice, Inbred BALB C. Monocytes / drug effects. Prednisolone / therapeutic use. Rats. Respiratory Mucosa / drug effects. Shock, Septic / complications. Shock, Septic / metabolism. Treatment Outcome

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  • (PMID = 17477857.001).
  • [ISSN] 1465-993X
  • [Journal-full-title] Respiratory research
  • [ISO-abbreviation] Respir. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antidepressive Agents; 0 / Cytokines; 01K63SUP8D / Fluoxetine; 9PHQ9Y1OLM / Prednisolone; TG537D343B / Desipramine
  • [Other-IDs] NLM/ PMC1876225
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7. Choy EH: Selective modulation of T-cell co-stimulation: a novel mode of action for the treatment of rheumatoid arthritis. Clin Exp Rheumatol; 2009 May-Jun;27(3):510-8
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  • [Title] Selective modulation of T-cell co-stimulation: a novel mode of action for the treatment of rheumatoid arthritis.
  • Disease-modifying antirheumatic drug therapy, including biological treatments that act via tumour necrosis factor (TNF)-alpha blockade, have benefited numerous patients suffering from rheumatoid arthritis (RA).
  • These factors illustrate the requirement for additional therapy options, with novel modes of action, in order to treat this chronic and disabling disease.
  • Activated T cells predominate in the disease processes of RA.
  • Therefore, one rational approach to therapy is to modulate or target T cells.
  • Abatacept is a first-in-class agent that targets T-cell modulation via the co-stimulatory CD80/CD86:CD28 pathway.
  • Preclinical studies and clinical trials have demonstrated both the rationale and efficacy of using T-cell modulation as a therapeutic approach and, as a result, abatacept is currently approved in the European Union for the treatment of RA in adults with moderately to severely active disease who have not responded to TNF-alpha antagon-ist therapy.
  • This review will highlight abatacept as an important treatment option in the therapeutic repertoire for RA that selectively modulates T-cell co-stimulation.

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  • (PMID = 19604448.001).
  • [ISSN] 0392-856X
  • [Journal-full-title] Clinical and experimental rheumatology
  • [ISO-abbreviation] Clin. Exp. Rheumatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / Antirheumatic Agents; 0 / Immunoconjugates; 7D0YB67S97 / Abatacept
  • [Number-of-references] 64
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8. Willhauck-Fleckenstein M, Moehler TM, Merling A, Pusunc S, Goldschmidt H, Schwartz-Albiez R: Transcriptional regulation of the vascular endothelial glycome by angiogenic and inflammatory signalling. Angiogenesis; 2010 Mar;13(1):25-42
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  • Vascular endothelial cells undergo many molecular changes during pathological processes such as inflammation and tumour development.
  • Tumours such as malignant lymphomas affecting bone marrow are dependent on interactions with endothelial cells for (1) site-specific homing and (2) tumour-induced angiogenesis.
  • In order to gain a comprehensive insight into the regulation of the endothelial glycome, comprising genes encoding for sugar transporters (sugar s/t), glycosyltransferases (GT), glycan-degrading enzymes (GD) and lectins (GBP), we performed gene profiling analysis of the human bone marrow-derived microvascular endothelial cell line HBMEC-60 that resembles closely in its biological behaviour primary bone marrow endothelial cells.
  • Approximately 48% (207 genes) of the 432 glycome genes tested were found to be expressed in HBMEC-60 cells.
  • [MeSH-minor] Biomarkers / metabolism. Bone Marrow Cells / cytology. Cell Line. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Glycoconjugates / chemistry. Glycoconjugates / metabolism. Glycoproteins / genetics. Glycoproteins / metabolism. Glycosyltransferases / metabolism. Humans. N-Acetylneuraminic Acid / metabolism. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 20162350.001).
  • [ISSN] 1573-7209
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Glycoconjugates; 0 / Glycoproteins; 0 / Polysaccharides; 0 / Receptors, Cell Surface; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; EC 2.4.- / Glycosyltransferases; GZP2782OP0 / N-Acetylneuraminic Acid
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9. Kindt S, Van Oudenhove L, Broekaert D, Kasran A, Ceuppens JL, Bossuyt X, Fischler B, Tack J: Immune dysfunction in patients with functional gastrointestinal disorders. Neurogastroenterol Motil; 2009 Apr;21(4):389-98
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  • There is increasing evidence for involvement of the immune system in functional gastrointestinal disorder (FGID), including onset after acute gastrointestinal infections, genotypes resulting in altered cytokine expression and abnormal presence of immune cells.
  • Our aim was to assess cellular and humoral immune responses in (i) FGIDs, compared to healthy subjects and (ii) acute vs unspecified onset FGIDs.
  • Lymphocytic [interleukin (IL)-5, IL-10, IL-13 and interferon gamma (IFN-gamma)] and monocytic [IL-10, IL-12, tumour necrosis factor (TNF)-alpha] cytokine production was characterized at baseline and after stimulation with phytohemagglutinine and anti-CD28 or lipopolysaccharide (LPS) in controls (n = 32), irritable bowel syndrome (IBS) (n = 30), functional dyspepsia (FD) (n = 23) and non-cardiac chest pain (NCCP) (n = 15).
  • Serum IL-6 and IL-10 concentrations were compared, and the immunophenotype was assessed using fluorescent-activated cell sorter.
  • Findings were compared for acute vs unspecified onset FGID.
  • Except for an increase in the numbers of CD3(+)CD45RA(+)CD45RO(+) cells, no distinct cellular profile was detected.
  • Patients with a presumed acute onset of their symptoms had higher serum IL-10 levels and more CD3(+)CD45RA(+)CD45RO(+) cells, while TNF-alpha levels following stimulation with LPS were higher in FD patients reporting an acute onset.

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  • (PMID = 19126184.001).
  • [ISSN] 1365-2982
  • [Journal-full-title] Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
  • [ISO-abbreviation] Neurogastroenterol. Motil.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cytokines
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10. Soilleux EJ, Turley H, Tian YM, Pugh CW, Gatter KC, Harris AL: Use of novel monoclonal antibodies to determine the expression and distribution of the hypoxia regulatory factors PHD-1, PHD-2, PHD-3 and FIH in normal and neoplastic human tissues. Histopathology; 2005 Dec;47(6):602-10
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  • METHODS AND RESULTS: Immunohistochemistry of normal tissues with these monoclonal antibodies demonstrated a wide distribution in epithelial cells, stromal cells and leucocytes, with cytoplasmic staining predominating over nuclear staining.
  • A preliminary study of tumours showed variable staining in tumour, stromal and inflammatory cells.
  • While all tumour types showed some positive staining with each antibody, the overall pattern suggested a slight decrease in the amount of staining seen with PHD-1, -2 and -3 and an increase in FIH staining in neoplasia compared with corresponding normal tissues.
  • [MeSH-major] Antibodies, Monoclonal / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immediate-Early Proteins / metabolism. Neoplasms / metabolism. Procollagen-Proline Dioxygenase / metabolism. Repressor Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. COS Cells. Cell Line. Cell Line, Tumor. Cercopithecus aethiops. Dioxygenases. Humans. Hypoxia-Inducible Factor-Proline Dioxygenases. Immunohistochemistry. Mixed Function Oxygenases. Tissue Distribution

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  • (PMID = 16324198.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Immediate-Early Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; EC 1.- / Mixed Function Oxygenases; EC 1.13.11.- / Dioxygenases; EC 1.14.11.- / HIF1AN protein, human; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
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11. Heilmann K, Hoffmann U, Witte E, Loddenkemper C, Sina C, Schreiber S, Hayford C, Holzlöhner P, Wolk K, Tchatchou E, Moos V, Zeitz M, Sabat R, Günthert U, Wittig BM: Osteopontin as two-sided mediator of intestinal inflammation. J Cell Mol Med; 2009 Jun;13(6):1162-74
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  • However, OPN-(/-) mice showed increased serum levels of tumour necrosis factor (TNF)-alpha, which could be due to systemically present lipopolysaccharide translocated to the gut.
  • Lastly, we demonstrate that in patients with active Crohn's disease OPN serum concentration correlated significantly with disease activity.
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Animals. Crohn Disease / blood. Crohn Disease / pathology. Cytokines / genetics. Cytokines / metabolism. Dextran Sulfate. Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry. Inflammatory Bowel Diseases / blood. Inflammatory Bowel Diseases / pathology. Macrophage Activation / immunology. Mice. Mice, Inbred C57BL. Mice, Knockout. Middle Aged. Phagocytosis / immunology. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 18627421.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 106441-73-0 / Osteopontin; 9042-14-2 / Dextran Sulfate
  • [Other-IDs] NLM/ PMC4496111
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12. Enarsson K, Lundin BS, Johnsson E, Brezicka T, Quiding-Järbrink M: CD4+ CD25high regulatory T cells reduce T cell transendothelial migration in cancer patients. Eur J Immunol; 2007 Jan;37(1):282-91
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  • [Title] CD4+ CD25high regulatory T cells reduce T cell transendothelial migration in cancer patients.
  • Cell-mediated immunity is thought to be the main mechanism of anti-tumour responses of the host, but it is not known if cancer disease affects T cell recruitment from blood to tissues.
  • Therefore, we compared Heliobacter pylori-induced T cell transendothelial migration (TEM) in H. pylori-infected gastric carcinoma patients, colon and lung carcinoma patients and healthy volunteers. H. pylori induced significant T cell migration from all groups.
  • However, there was a dramatic reduction of T cell TEM in gastric carcinoma patients (80%) compared to healthy individuals.
  • We found significantly increased frequencies of T(reg) cells in the blood of gastric carcinoma patients compared to healthy individuals, and depletion of T(reg) cells from the blood of these patients prior to TEM restored T cell migration.
  • The effect of T(reg) cells was largely dependent on cell-cell contact, but not on IL-10 or TGF-beta.
  • In addition, the presence of T(reg) cells led to reduced T cell attachment to endothelium and decreased production of T cell-recruiting chemokines during TEM.
  • In conclusion, T(reg) cell-mediated reduction of T cell TEM may reduce T cell recruitment in patients with epithelial malignancies, thereby hampering anti-tumour responses.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / immunology. Cell Migration Inhibition. Colonic Neoplasms / immunology. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lung Neoplasms / immunology. Stomach Neoplasms / immunology. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Adhesion / immunology. Cell Movement / immunology. Contact Inhibition / immunology. Endothelium, Vascular / cytology. Endothelium, Vascular / immunology. Endothelium, Vascular / metabolism. Female. Helicobacter pylori / immunology. Humans. Male. Middle Aged

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  • (PMID = 17163448.001).
  • [ISSN] 0014-2980
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interleukin-2 Receptor alpha Subunit
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13. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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1
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4. Gómez-Laguna J, Millán Y, Reymundo C, Domingo V, Martín de Las Mulas J: Bilateral retiform Sertoli-Leydig cell tumour in a bitch. Alpha-inhibin and epithelial membrane antigen as useful tools for differential diagnosis. J Comp Pathol; 2008 Aug-Oct;139(2-3):137-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral retiform Sertoli-Leydig cell tumour in a bitch. Alpha-inhibin and epithelial membrane antigen as useful tools for differential diagnosis.
  • Sertoli-Leydig cell tumours with a retiform pattern similar to the pattern of the rete testis are a subtype of sex cord-stromal tumours recognized in the human WHO histological classification of ovarian tumours but not in the equivalent classification for domestic animals.
  • The morphology of the tumour may be confused with that of the more common ovarian epithelial tumours.
  • The gross, microscopical and immunohistochemical features of a canine retiform Sertoli-Leydig cell tumour and its comparison with the human counterpart are presented in this report.
  • Microscopically, the tumour was cystic with tubulopapillary growth characterized by narrow, elongated branching tubules.
  • Immunohistochemically, the tumour cells expressed alpha-inhibin, while epithelial membrane antigen was not detected, indicating a sex cord-stromal origin of the tumour.
  • Additionally, the tumour cells expressed cytokeratin and vimentin in addition to oestrogen receptor alpha and progesterone receptor.
  • [MeSH-major] Dog Diseases / metabolism. Dog Diseases / pathology. Inhibins / biosynthesis. Mucin-1 / biosynthesis. Ovarian Neoplasms / veterinary. Sertoli-Leydig Cell Tumor / veterinary
  • [MeSH-minor] Animals. Diagnosis, Differential. Dogs. Female. Immunohistochemistry. Neoplasms, Glandular and Epithelial / pathology

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  • (PMID = 18620701.001).
  • [ISSN] 0021-9975
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mucin-1; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
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15. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Through its well-characterized functionality in regulating the activity of bioactive peptides by removal of the N-terminal dipeptide, DPP-IV activity may have profound effects upon metastatic potential and cell growth.
  • Although DPP-IV/CD26 (EC 3.4.14.5) is the canonical representative of the group, a number of other proteins including DPP-7, 8, 9, and seprase/fibroblast activation protein-alpha (FAP-alpha) have been shown to have similar enzymatic activity.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • In parallel, expression of CXCR4, receptor for glioma cell growth stimulator chemokine SDF-1alpha known to be a DPP-IV substrate, was investigated.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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16. Boost KA, Flondor M, Hofstetter C, Platacis I, Stegewerth K, Hoegl S, Nguyen T, Muhl H, Zwissler B: The beta-adrenoceptor antagonist propranolol counteracts anti-inflammatory effects of isoflurane in rat endotoxemia. Acta Anaesthesiol Scand; 2007 Aug;51(7):900-8
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  • After 4 h of endotoxemia, levels of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-10 (IL-10) in plasma and bronchoalveolar fluid (BALF) were analysed.
  • RESULTS: Inhalation of isoflurane reduced the release of TNF-alpha (P < 0.05) and IL-1beta (P < 0.05) in plasma and IL-1beta (P < 0.05) in BALF.
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Blotting, Western. Bronchoalveolar Lavage Fluid / cytology. Cell Count. Enzyme-Linked Immunosorbent Assay. Heart Rate / drug effects. Inflammation / metabolism. Inflammation / pathology. Interleukin-10 / metabolism. Interleukin-1beta / metabolism. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / enzymology. Male. Nitric Oxide / biosynthesis. Nitric Oxide Synthase Type II / metabolism. Nitrites / blood. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17635398.001).
  • [ISSN] 0001-5172
  • [Journal-full-title] Acta anaesthesiologica Scandinavica
  • [ISO-abbreviation] Acta Anaesthesiol Scand
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic beta-Antagonists; 0 / Anesthetics, Inhalation; 0 / Anti-Inflammatory Agents; 0 / Interleukin-1beta; 0 / Nitrites; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 31C4KY9ESH / Nitric Oxide; 9Y8NXQ24VQ / Propranolol; CYS9AKD70P / Isoflurane; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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17. Ceccarelli M, Bani D, Cinci L, Nistri S, Uliva C, Ragazzo E, Vannacci A, Manoni M, Gori AM, Abbate R, Gensini GF, Masini E: Anti-inflammatory effects of low molecular weight heparin derivative in a rat model of carrageenan-induced pleurisy. J Cell Mol Med; 2009 Aug;13(8B):2704-12
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  • A 30-min. pre-treatment with K5NOSepiLMW (0.1, 0.5 and 1 mg/kg b.wt., given intrapleurally) attenuated the recruitment of leucocytes in the lung tissue and the pleural exudate, inhibited the induction of inducible nitric oxide synthase and cyclooxygenase-2 (COX-2), thereby abating the generation of nitric oxide and pro-inflammatory prostaglandins such as PgE(2) and PGF(1alpha), reduced the inflammation-induced nitroxidative lung tissue injury, as shown by tissue thiobarbituric acid-reactive substances and nitrotyrosine, and blunted the local generation of cytokines such as interleukin-1beta and tumour necrosis factor-alpha.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Carrageenan / toxicity. Disease Models, Animal. Heparin, Low-Molecular-Weight / pharmacology. Pleurisy / pathology

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  • (PMID = 20141620.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Heparin, Low-Molecular-Weight; 0 / Thiobarbituric Acid Reactive Substances; 9000-07-1 / Carrageenan
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18. Dong LF, Low P, Dyason JC, Wang XF, Prochazka L, Witting PK, Freeman R, Swettenham E, Valis K, Liu J, Zobalova R, Turanek J, Spitz DR, Domann FE, Scheffler IE, Ralph SJ, Neuzil J: Alpha-tocopheryl succinate induces apoptosis by targeting ubiquinone-binding sites in mitochondrial respiratory complex II. Oncogene; 2008 Jul 17;27(31):4324-35
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  • [Title] Alpha-tocopheryl succinate induces apoptosis by targeting ubiquinone-binding sites in mitochondrial respiratory complex II.
  • Alpha-tocopheryl succinate (alpha-TOS) is a selective inducer of apoptosis in cancer cells, which involves the accumulation of reactive oxygen species (ROS).
  • The molecular target of alpha-TOS has not been identified.
  • Here, we show that alpha-TOS inhibits succinate dehydrogenase (SDH) activity of complex II (CII) by interacting with the proximal and distal ubiquinone (UbQ)-binding site (Q(P) and Q(D), respectively).
  • This is based on biochemical analyses and molecular modelling, revealing similar or stronger interaction energy of alpha-TOS compared to that of UbQ for the Q(P) and Q(D) sites, respectively.
  • CybL-mutant cells with dysfunctional CII failed to accumulate ROS and underwent apoptosis in the presence of alpha-TOS.
  • Reconstitution of functional CII rendered CybL-mutant cells susceptible to alpha-TOS.
  • We propose that alpha-TOS displaces UbQ in CII causing electrons generated by SDH to recombine with molecular oxygen to yield ROS.
  • Our data highlight CII, a known tumour suppressor, as a novel target for cancer therapy.

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  • (PMID = 18372923.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R29 CA073612; United States / NCI NIH HHS / CA / CA073612-07; United States / NCI NIH HHS / CA / R01 CA100045-03; United States / NCI NIH HHS / CA / R01-CA100045; United States / NCI NIH HHS / CA / R01 CA073612; United States / NCI NIH HHS / CA / R56 CA073612; United States / NCI NIH HHS / CA / R01-CA73612; United States / NCI NIH HHS / CA / R01 CA100045; United States / NCI NIH HHS / CA / R01 CA100045-05; United States / NCI NIH HHS / CA / R01 CA073612-07; United States / NCI NIH HHS / CA / CA073612-08; United States / NCI NIH HHS / CA / R01 CA073612-08; United States / NCI NIH HHS / CA / R01 CA100045-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Reactive Oxygen Species; 1339-63-5 / Ubiquinone; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols; EC 1.3.5.1 / Electron Transport Complex II; EC 1.6.5.3 / respiratory complex II
  • [Other-IDs] NLM/ NIHMS100471; NLM/ PMC2668987
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19. Ludwig A, Schulte A, Schnack C, Hundhausen C, Reiss K, Brodway N, Held-Feindt J, Mentlein R: Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells. J Neurochem; 2005 Jun;93(5):1293-303
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  • [Title] Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells.
  • The transmembrane chemokine CXCL16 is expressed by dendritic and vascular cells and mediates chemotaxis and adhesion of activated T cells via the chemokine receptor CXCR6/Bonzo.
  • Here we describe the expression and shedding of this chemokine by glioma cells in situ and in vitro.
  • By quantitative RT-PCR and immunohistochemistry, we show that CXCL16 is highly expressed in human gliomas, while expression in normal brain is low and mainly restricted to brain vascular endothelial cells.
  • In cultivated human glioma cells as well as in activated mouse astroglial cells, CXCL16 mRNA and protein is constitutively expressed and further up-regulated by tumour necrosis factor alpha (TNFalpha) and interferon-gamma (IFNgamma).
  • CXCL16 is continuously released from glial cells by proteolytic cleavage which is rapidly enhanced by stimulation with phorbol-12-myristate-13-acetate (PMA).
  • In addition to the chemokine, its receptor CXCR6 could be detected by quantitative RT-PCR in human glioma tissue, cultivated murine astrocytes and at a lower level in microglial cells.
  • Functionally, recombinant soluble CXCL16 enhanced proliferation of CXCR6-positive murine astroglial and microglial cells.
  • Thus, the transmembrane chemokine CXCL16 is expressed in the brain by malignant and inflamed astroglial cells, shed to a soluble form and targets not only activated T cells but also glial cells themselves.
  • [MeSH-minor] Animals. Cell Line, Tumor. Chemokine CXCL6. Humans. Interferon-gamma / pharmacology. Metalloproteases / metabolism. Mice. Microglia / metabolism. Neuroglia / metabolism. RNA, Messenger / metabolism. Receptors, Scavenger. Recombinant Proteins / pharmacology. Solubility. Tissue Culture Techniques. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation

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  • (PMID = 15934948.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL16 protein, human; 0 / Chemokine CXCL6; 0 / Chemokines, CXC; 0 / Cxcl16 protein, mouse; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Immunologic; 0 / Receptors, Scavenger; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 3.4.- / Metalloproteases
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20. Wu J, Wu MC, Zhang LF, Lei JY, Feng L, Jin J: Identification of binding peptides of the ADAM15 disintegrin domain using phage display. J Biosci; 2009 Jun;34(2):213-20
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  • ADAM15 plays an important role in tumour development by interacting with integrins.
  • First, we successfully produced the recombinant human ADAM15 disintegrin domain (RADD) that could inhibit melanoma cell adhesion by using Escherichia coli.
  • By using the BLAST software and a relevant protein database, integrin alpha v beta 3 was found to be homologous to peptide A.
  • Synthetic peptide A had a highly inhibitory effect on RADD-integrin alpha v beta 3 binding.
  • [MeSH-minor] Cell Adhesion. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Escherichia coli / metabolism. Humans. Integrins / metabolism. Melanoma / metabolism. Models, Biological. Peptide Library. Peptides / chemistry. Protein Binding. Protein Structure, Tertiary. Proteomics / methods

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  • (PMID = 19550037.001).
  • [ISSN] 0250-5991
  • [Journal-full-title] Journal of biosciences
  • [ISO-abbreviation] J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Integrins; 0 / Membrane Proteins; 0 / Peptide Library; 0 / Peptides; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAM15 protein, human
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21. Iyer A, Hatta M, Usman R, Luiten S, Oskam L, Faber W, Geluk A, Das P: Serum levels of interferon-gamma, tumour necrosis factor-alpha, soluble interleukin-6R and soluble cell activation markers for monitoring response to treatment of leprosy reactions. Clin Exp Immunol; 2007 Nov;150(2):210-6
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  • [Title] Serum levels of interferon-gamma, tumour necrosis factor-alpha, soluble interleukin-6R and soluble cell activation markers for monitoring response to treatment of leprosy reactions.
  • Identifying pathogen and host-related laboratory parameters are essential for the early diagnosis of leprosy reactions.
  • The present study aimed to clarify the validity of measuring the profiles of serum cytokines [interleukin (IL)-4, IL-6, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha], the soluble IL-6 receptor (sIL-6R), soluble T cell (sCD27) and macrophage (neopterin) activation markers and Mycobacterium leprae-specific anti-PGL-I IgM antibodies in relation to the leprosy spectrum and reactions.
  • Levels of IFN-gamma, TNF-alpha and sIL-6R declined significantly upon corticosteroid treatment of ENL.
  • Thus, although the present study suggests limited applicability of serial measurement of IFN-gamma, TNF-alpha and sIL-6R in monitoring treatment efficacy of ENL, reactions it recommends a search for a wider panel of more disease-specific markers in future studies.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Bacterial / blood. Antigens, Bacterial / immunology. Biomarkers / blood. Child. Cross-Sectional Studies. Female. Glycolipids / immunology. Humans. Immunoglobulin M / blood. Inflammation Mediators / blood. Interferon-gamma / blood. Interleukin-10 / blood. Interleukin-4 / blood. Male. Middle Aged. Mycobacterium leprae / immunology. Neopterin / blood. Prednisolone / therapeutic use. Receptors, Interleukin-6 / blood. Solubility. Treatment Outcome. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17937676.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Antigens, Bacterial; 0 / Biomarkers; 0 / Cytokines; 0 / Glucocorticoids; 0 / Glycolipids; 0 / Immunoglobulin M; 0 / Inflammation Mediators; 0 / Receptors, Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 0 / phenolic glycolipid I, Mycobacterium leprae; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 670-65-5 / Neopterin; 82115-62-6 / Interferon-gamma; 9PHQ9Y1OLM / Prednisolone
  • [Other-IDs] NLM/ PMC2219358
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22. Leung TF, Wong KY, Wong CK, Fung KP, Lam CW, Fok TF, Leung PC, Hon KL: In vitro and clinical immunomodulatory effects of a novel Pentaherbs concoction for atopic dermatitis. Br J Dermatol; 2008 Jun;158(6):1216-23
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  • [Title] In vitro and clinical immunomodulatory effects of a novel Pentaherbs concoction for atopic dermatitis.
  • BACKGROUND: Our group recently reported a randomized and placebo-controlled clinical trial on the efficacy of a twice-daily concoction of five herbal ingredients (Pentaherbs formulation, PHF) in treating children with atopic dermatitis (AD).
  • METHODS: We investigated the effects of PHF on cytotoxicity and proliferation of phytohaemagglutinin (PHA)- and staphylococcal enterotoxin B (SEB)-stimulated peripheral blood mononuclear cells (PBMC) isolated from buffy coat of blood donors.
  • The effects of a 3-month, open-label study of PHF on circulating inflammatory mediators in children with AD were also assessed.
  • The addition of PHF to cultured PBMC reduced supernatant concentrations of brain-derived neurotrophic factor (BDNF), interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha in response to PHA, and BDNF and thymus and activation-regulated chemokine (TARC) following SEB stimulation.
  • PHF increased epithelial cell-derived neutrophil activating peptide-78 levels in culture supernatants.
  • At the RNA level, PHF suppressed the transcription of BDNF, TARC, IFN-gamma and TNF-alpha.
  • Twenty-eight children with AD were treated with PHF for 3 months, and their mean plasma concentrations of BDNF and TARC decreased significantly from 1798 pg mL(-1) and 824 pg mL(-1) at baseline to 1378 pg mL(-1) and 492 pg mL(-1) (P = 0.002 and 0.013, respectively) upon study completion.
  • CONCLUSIONS: PHF possesses in vitro and in vivo immunomodulatory properties that may mediate the clinical efficacy observed in AD treatment.

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  • (PMID = 18341655.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Drugs, Chinese Herbal; 0 / Phytohemagglutinins
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23. Seeber S, Issinger OG, Holm T, Kristensen LP, Guerra B: Validation of protein kinase CK2 as oncological target. Apoptosis; 2005 Aug;10(4):875-85
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  • Protein kinase CK2 is a highly conserved enzyme composed of two catalytic subunits alpha and/or alpha' and two regulatory subunits beta whose activity is elevated in diverse tumour types as well as in highly proliferating tissues.
  • To better elucidate the role of CK2 in programmed cell death, we have depleted cells of CK2 catalytic subunits by the application of antisense oligodeoxynucleotides and siRNAs techniques, respectively.
  • In addition, we show that despite the effectiveness of the methods applied in lowering CK2 kinase activity in all cells investigated, CK2 might not by itself be sufficient to trigger enhanced drug-induced apoptosis in cells.
  • [MeSH-minor] Apoptosis / drug effects. Catalytic Domain. Cell Transformation, Neoplastic. Flow Cytometry. HCT116 Cells. HeLa Cells. Humans. Jurkat Cells. Nocodazole / pharmacology. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / antagonists & inhibitors. RNA, Small Interfering / pharmacology. Reproducibility of Results

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  • (PMID = 16133877.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 2.7.11.1 / Casein Kinase II; SH1WY3R615 / Nocodazole
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24. Krimmer DI, Loseli M, Hughes JM, Oliver BG, Moir LM, Hunt NH, Black JL, Burgess JK: CD40 and OX40 ligand are differentially regulated on asthmatic airway smooth muscle. Allergy; 2009 Jul;64(7):1074-82
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  • BACKGROUND: CD40 and OX40 Ligand (OX40L) are cell-surface molecules expressed on airway smooth muscle (ASM) that can enhance inflammatory cell activation and survival.
  • The aim of this study was to examine the effect of tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) on ASM CD40 and OX40L expression.
  • METHODS: CD40 and OX40L expression on human ASM cells from asthmatic and nonasthmatic donors following stimulation with TNF-alpha and/or IFN-gamma was measured using cell-surface enzyme-linked immunosorbent assay (ELISA) and flow cytometry.
  • RESULTS: Interferon-gamma and TNF-alpha synergistically increased CD40 expression to a greater extent on asthmatic than on nonasthmatic ASM.
  • In contrast, IFN-gamma reduced TNF-alpha-induced OX40L expression to a similar extent in both cell types.
  • TNF-alpha and IFN-gamma induced CD40 via nuclear factor-kappaB (NF-kappaB) and signal transducer and activator of transcription-3 in both cell types and modulated OX40L via NF-kappaB and c-Jun N terminal kinase in nonasthmatic cells.
  • Similar effects on the induction of OX40L in asthmatic cells were seen with NF-kappaB, but these were not statistically significant.
  • The reduced OX40L expression with TNF-alpha and IFN-gamma involved extracellular regulated kinase 1/2 activation.
  • [MeSH-major] Antigens, CD40 / metabolism. Asthma / immunology. Interferon-gamma / pharmacology. Myocytes, Smooth Muscle / drug effects. OX40 Ligand / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 19220210.001).
  • [ISSN] 1398-9995
  • [Journal-full-title] Allergy
  • [ISO-abbreviation] Allergy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / OX40 Ligand; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4
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25. Passalacqua R, Buzio C, Buti S, Porta C, Labianca R, Pezzuolo D, Camisa R, Sabbatini R, Benecchi L, Messina C, Cengarle R, Vaglio A, Dalla Chiesa M, Tomasello G, Caminiti C: Phase III, randomised, multicentre trial of maintenance immunotherapy with low-dose interleukin-2 and interferon-alpha for metastatic renal cell cancer. Cancer Immunol Immunother; 2010 Apr;59(4):553-61
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  • [Title] Phase III, randomised, multicentre trial of maintenance immunotherapy with low-dose interleukin-2 and interferon-alpha for metastatic renal cell cancer.
  • This is the first phase III randomised trial to evaluate maintenance immunotherapy in metastatic renal cell cancer (mRCC).
  • Patients were randomised to receive treatment with a 4-week cycle of subcutaneous low doses IL-2 + IFN in months 1, 3 and 5, and then every 3 months until the first documented disease progression (arm A, suspension), or the same regimen, with chronic maintenance of immunotherapy, regardless of tumour response, until death or intolerable toxicity (arm B, maintenance).
  • Chronic maintenance immunotherapy after disease progression is feasible, but does not significantly increase OS or the TFPTD.
  • [MeSH-major] Carcinoma, Papillary / drug therapy. Carcinoma, Renal Cell / drug therapy. Immunotherapy. Interferon-alpha / therapeutic use. Interleukin-2 / therapeutic use. Kidney Neoplasms / drug therapy

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  • (PMID = 19779715.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Interleukin-2
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26. Maass DR, Sepulveda J, Pernthaner A, Shoemaker CB: Alpaca (Lama pacos) as a convenient source of recombinant camelid heavy chain antibodies (VHHs). J Immunol Methods; 2007 Jul 31;324(1-2):13-25
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  • Alpacas were immunized with ovine tumour necrosis factor alpha (TNFalpha) and a VHH phage display library was prepared from a lymph node that drains the sites of immunizations and successfully employed in the isolation of VHHs that bind and neutralize ovine TNFalpha.

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  • (PMID = 17568607.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21 AI061517; United States / NIAID NIH HHS / AI / AI061517-01; United States / NIAID NIH HHS / AI / N01AI30050; United States / NIAID NIH HHS / AI / R21 AI061517-01; United States / NIAID NIH HHS / AI / N01-AI-30050
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Recombinant Proteins
  • [Other-IDs] NLM/ NIHMS27515; NLM/ PMC2014515
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27. Olsnes C, Stavang H, Olofsson J, Aarstad HJ: TNF-alpha is secreted by monocytes in transit to become macrophages, but not by peripheral blood monocytes, following OK-432 (lyophilized S. pyogenes) stimulation. Scand J Immunol; 2007 Dec;66(6):684-93
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  • [Title] TNF-alpha is secreted by monocytes in transit to become macrophages, but not by peripheral blood monocytes, following OK-432 (lyophilized S. pyogenes) stimulation.
  • We have studied proinflammatory interleukin (IL) secretion following OK-432 stimulation of total blood, peripheral blood mononuclear cell (PBMC) and purified monocytes in vitro.
  • OK-432 stimulation of purified monocytes gave IL-1beta, IL-1RA, IL-6, IL-12p40 and tumour necrosis factor (TNF)-alpha response.
  • OK-432 stimulation of cells within blood did, however, not yield TNF-alpha secretion.
  • When PBMC or monocytes were cultured in low-attachment wells a decreased IL secretion was observed compared to adherent cells.
  • This shows that beta(1-3)-integrin receptor function is not necessary for monocyte OK-432-stimulated TNF-alpha secretion.
  • In conclusion, TNF-alpha secretion is only found in monocytes removed from blood.
  • This TNF-alpha secretion is not mediated through the beta(1-3)-integrin receptors.
  • OK-432 may act as a target-seeking substance whereby only monocytes adhered, e.g. to a tumour cell, become cytotoxic in part explaining why OK-432 is well suited as a cancer treatment drug.
  • [MeSH-major] Head and Neck Neoplasms / blood. Macrophages / immunology. Monocytes / secretion. Picibanil / administration & dosage. Tumor Necrosis Factor-alpha / secretion
  • [MeSH-minor] Adult. Cell Adhesion / immunology. Cell Differentiation / drug effects. Cells, Cultured. Cytotoxicity, Immunologic / drug effects. Enzyme Inhibitors. Humans. Immunity, Cellular / drug effects. Interferon-gamma / immunology. Interleukins / immunology. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Leukocytes, Mononuclear / cytology. Leukocytes, Mononuclear / immunology. Lipopolysaccharides / administration & dosage. Lipopolysaccharides / chemistry. Lipopolysaccharides / pharmacology. Lymphocyte Activation / drug effects. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Reference Values

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  • (PMID = 18021366.001).
  • [ISSN] 1365-3083
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Interleukins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 39325-01-4 / Picibanil; 82115-62-6 / Interferon-gamma; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase
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28. de Bie P, van de Sluis B, Burstein E, Duran KJ, Berger R, Duckett CS, Wijmenga C, Klomp LW: Characterization of COMMD protein-protein interactions in NF-kappaB signalling. Biochem J; 2006 Aug 15;398(1):63-71
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  • This interaction was verified by independent techniques, appeared to be direct and could be detected throughout the whole cell, including the nucleus.
  • Both proteins inhibit TNF (tumour necrosis factor)-induced NF-kappaB activation in a non-synergistic manner.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Amino Acid Sequence. Animals. Carrier Proteins. Cells, Cultured. Conserved Sequence / genetics. Dogs. Exons / genetics. Fluorescence. Gene Expression Profiling. Gene Expression Regulation. Humans. I-kappa B Proteins / metabolism. Molecular Sequence Data. Mutation / genetics. Protein Binding. RNA, Messenger / genetics. RNA, Messenger / metabolism. Sequence Alignment. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16573520.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / COMMD1 protein, human; 0 / COMMD6 protein, human; 0 / Carrier Proteins; 0 / I-kappa B Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / NF-kappa B; 0 / Proteins; 0 / RNA, Messenger; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha
  • [Other-IDs] NLM/ PMC1525016
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29. Schram MT, Chaturvedi N, Schalkwijk CG, Fuller JH, Stehouwer CD, EURODIAB Prospective Complications Study Group: Markers of inflammation are cross-sectionally associated with microvascular complications and cardiovascular disease in type 1 diabetes--the EURODIAB Prospective Complications Study. Diabetologia; 2005 Feb;48(2):370-8
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  • [Title] Markers of inflammation are cross-sectionally associated with microvascular complications and cardiovascular disease in type 1 diabetes--the EURODIAB Prospective Complications Study.
  • RESULTS: C-reactive protein, interleukin-6 and tumour necrosis factor-alpha levels, which were combined in an inflammatory marker Z-score, were associated with albuminuria, retinopathy and cardiovascular disease.
  • Calculated means (95% confidence intervals) of the marker Z-score were -0.15 (-0.22 to -0.07), 0.10 (-0.05 to 0.25), and 0.28 (0.15 to 0.41), p for trend <0.0001, in individuals with normo-, micro- and macroalbuminuria; -0.23 (-0.33 to -0.13), 0.14 (0.02 to 0.25) and 0.20 (0.07 to 0.32), p for trend <0.0001, in individuals with no, non-proliferative and proliferative retinopathy; and -0.28 (-0.39 to -0.18) and 0.06 (-0.08 to 0.20), p<0.001, in individuals without and with cardiovascular disease.
  • CONCLUSIONS/INTERPRETATION: We have shown that markers of inflammation are strongly and independently associated with microvascular complications and cardiovascular disease in type 1 diabetes.


30. Horwich A, Dearnaley D, Huddart R, Graham J, Bessell E, Mason M, Bliss J: A randomised trial of accelerated radiotherapy for localised invasive bladder cancer. Radiother Oncol; 2005 Apr;75(1):34-43
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  • Eligible patients had clinical stage T2 or T3, N0 or N1, M0 transitional cell carcinoma.
  • The primary endpoint of the trial was local control and the trial was powered to detect a 20% difference (alpha 0.05, power 90%).
  • There was no significant difference in analysis of time to loss of local tumour control comparing the two treatment arms; local recurrence was recorded in 29 of the 100 patients treated with CF and in 41 of 129 patients treated with AF (logrank P=0.86).
  • There was also no significant difference between the treatment arms comparing disease-free survival and overall survival.

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  • (PMID = 15878099.001).
  • [ISSN] 0167-8140
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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31. Pollara G, Handley ME, Kwan A, Chain BM, Katz DR: Autocrine type I interferon amplifies dendritic cell responses to lipopolysaccharide via the nuclear factor-kappaB/p38 pathways. Scand J Immunol; 2006 Mar;63(3):151-4
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  • [Title] Autocrine type I interferon amplifies dendritic cell responses to lipopolysaccharide via the nuclear factor-kappaB/p38 pathways.
  • The central role of dendritic cells (DC) in the initiation of immune responses requires these cells to be able to determine the degree of danger in their microenvironment.
  • At a higher concentration of LPS, while changes in surface phenotype are not dependent on type I IFN, this cytokine is required for maximal secretion of interleukin-12 (IL-12) and tumour necrosis factor-alpha (TNFalpha) by DC.
  • [MeSH-major] Dendritic Cells / immunology. Interferon Type I / physiology. Lipopolysaccharides / pharmacology. NF-kappa B / metabolism
  • [MeSH-minor] Antigens, CD86 / metabolism. Cell Differentiation. Humans. Tumor Necrosis Factor-alpha / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism. p38 Mitogen-Activated Protein Kinases / physiology

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  • (PMID = 16499567.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD86; 0 / Interferon Type I; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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32. Wu CJ, Conze DB, Li T, Srinivasula SM, Ashwell JD: Sensing of Lys 63-linked polyubiquitination by NEMO is a key event in NF-kappaB activation [corrected]. Nat Cell Biol; 2006 Apr;8(4):398-406
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  • Here, we show that NEMO binds to Lys 63- but not Lys 48-linked polyubiquitin, and that single point mutations in NEMO that prevent binding to Lys 63-linked polyubiquitin also abrogates the binding of NEMO to RIP in tumour necrosis factor (TNF)-alpha-stimulated cells, the recruitment of IKK to TNF receptor (TNF-R) 1, and the activation of IKK and NF-kappaB.
  • RIP is also destabilized in the absence of NEMO binding and undergoes proteasomal degradation in TNF-alpha-treated cells.
  • [MeSH-minor] Electrophoretic Mobility Shift Assay. HeLa Cells. Humans. Immunoprecipitation. Point Mutation. Protein-Serine-Threonine Kinases / metabolism. Receptor-Interacting Protein Serine-Threonine Kinases. Receptors, Tumor Necrosis Factor, Type I / metabolism. Saccharomyces cerevisiae. Signal Transduction. Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Two-Hybrid System Techniques


33. Brahimi-Horn C, Pouysségur J: The role of the hypoxia-inducible factor in tumor metabolism growth and invasion. Bull Cancer; 2006 Aug;93(8):E73-80
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  • [Title] The role of the hypoxia-inducible factor in tumor metabolism growth and invasion.
  • HIF is a transcription factor that, in hypoxia, drives the induction or repression of a myriad of genes controlling multiple cell functions such as angiogenesis, metabolism, invasion/metastasis and apoptosis/survival.
  • Thus, the level of oxygen in a cell dictates the molecular response of cells through modulation of gene expression.
  • Here we review the central role of HIF in cancer progression through the tumour response to hypoxia.
  • Within this context the following aspects will be discussed: i) the mechanism by which oxygen deprivation inhibits two oxygen-sensor hydroxylases, thereby releasing the alpha subunit of HIF from programmed destruction by the ubiquitin-proteasome system and from a lock on its transcriptional activity;.
  • ii) the way in which the bi-transcriptional activity of HIF-alpha, which is regulated by the interplay between an oxygen-sensor attenuator and co-activators, determines the repertoire of gene expression; and iii) the role that HIF plays in tumour metabolism, in particular in glycolysis, and consequent acidification of the microenvironment, which influences both cell survival and cell death.
  • Finally, the direct link of HIF to tumourigenesis and metastasis will be investigated and approaches for fighting tumour progression through a better understanding of HIF-mediated modulation of tumour metabolism and cell death will be considered.
  • [MeSH-major] Cell Hypoxia / physiology. Hypoxia-Inducible Factor 1 / physiology. Neoplasms
  • [MeSH-minor] Cell Death / physiology. Cell Survival / physiology. Enzyme Stability. Erythropoietin / metabolism. Gene Expression Regulation. Homeostasis. Hydroxylation. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Neoplasm Invasiveness. Neoplasm Metastasis / physiopathology. Neovascularization, Pathologic / etiology. Oxygen / metabolism. Procollagen-Proline Dioxygenase / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16935775.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 11096-26-7 / Erythropoietin; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; S88TT14065 / Oxygen
  • [Number-of-references] 38
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34. Trøseid M, Lappegård KT, Mollnes TE, Arnesen H, Seljeflot I: Changes in serum levels of E-selectin correlate to improved glycaemic control and reduced obesity in subjects with the metabolic syndrome. Scand J Clin Lab Invest; 2005;65(4):283-90
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  • [Title] Changes in serum levels of E-selectin correlate to improved glycaemic control and reduced obesity in subjects with the metabolic syndrome.
  • Cellular adhesion molecules (CAMs) such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are involved in the rolling, adhesion and extravasation of monocytes and T-lymphocytes into the atherosclerotic plaque.
  • MATERIAL AND METHODS: The study was designed as an unmasked randomized 2x2 factorial trial of 12 weeks duration in 32 subjects with the metabolic syndrome.
  • Changes from baseline were studied, and correlations between changes in CAMs, anthropometric measures, regional fat distribution, glycaemic control and the adipocytokine tumour necrosis factor-a (TNF-a) and adiponectin were investigated.
  • CONCLUSION: Changes in glycaemic control and obesity, rather than regional fat distribution, seem to influence the levels of E-selectin in subjects with the metabolic syndrome.
  • [MeSH-major] Biomarkers / blood. E-Selectin / blood. Hyperglycemia / blood. Metabolic Syndrome X / blood. Obesity / blood
  • [MeSH-minor] Adiponectin. Adipose Tissue / metabolism. Adult. Aged. Blood Glucose / metabolism. Humans. Intercellular Adhesion Molecule-1 / blood. Intercellular Signaling Peptides and Proteins / metabolism. Male. Middle Aged. Predictive Value of Tests. Tumor Necrosis Factor-alpha / metabolism. Vascular Cell Adhesion Molecule-1 / blood

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  • (PMID = 16076683.001).
  • [ISSN] 0036-5513
  • [Journal-full-title] Scandinavian journal of clinical and laboratory investigation
  • [ISO-abbreviation] Scand. J. Clin. Lab. Invest.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Biomarkers; 0 / Blood Glucose; 0 / E-Selectin; 0 / Intercellular Signaling Peptides and Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1
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35. Gómez-Puerta JA, Burlingame RW, Cervera R: Anti-chromatin (anti-nucleosome) antibodies: diagnostic and clinical value. Autoimmun Rev; 2008 Sep;7(8):606-11
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  • Anti-chromatin (nucleosome) autoantibodies were one of the first autoantibodies ever detected since they make up the majority of antibodies causing LE Cell formation.
  • The prevalence of anti-chromatin antibodies in systemic lupus erythematosus (SLE) varies from 50% to 100%, being similar to that of the classical positive LE cell.
  • The presence of these antibodies can be used, in conjunction with clinical findings and other laboratory tests, to help in the diagnosis of SLE and drug-induced lupus.
  • Anti-chromatin antibodies have also been found in a lesser percentage of other autoimmune disorders such as primary Sjögren's syndrome and primary antiphospholipid syndrome.
  • The presence of anti-chromatin antibodies has also been linked to glomerulonephritis and disease activity in SLE patients.
  • Recent studies demonstrated the induction of anti-chromatin (anti-nucleosome) antibodies after an anti-tumour necrosis factor (TNF)-alpha agent treatment.
  • [MeSH-minor] Animals. Humans. Lupus Erythematosus, Systemic / diagnosis. Lupus Erythematosus, Systemic / immunology

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  • (PMID = 18606252.001).
  • [ISSN] 1568-9972
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Chromatin; 0 / Nucleosomes
  • [Number-of-references] 39
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36. Din FV, Stark LA, Dunlop MG: Aspirin-induced nuclear translocation of NFkappaB and apoptosis in colorectal cancer is independent of p53 status and DNA mismatch repair proficiency. Br J Cancer; 2005 Mar 28;92(6):1137-43
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  • However, the molecular basis for this anti-tumour activity has not been fully elucidated.
  • We previously reported that aspirin induces signal-specific IkappaBalpha degradation followed by NFkappaB nuclear translocation in CRC cells, and that this mechanism contributes substantially to aspirin-induced apoptosis.
  • We have also reported the relative specificity of this aspirin-induced NFkappaB-dependent apoptotic effect for CRC cells, in comparison to other cancer cell types.
  • It is now important to establish whether there is heterogeneity within CRC, with respect to the effects of aspirin on the NFkappaB pathway and apoptosis. p53 signalling and DNA mismatch repair (MMR) are known to be deranged in CRC and have been reported as potential molecular targets for the anti-tumour activity of NSAIDs.
  • We specifically compared the effects of aspirin treatment on cell viability, apoptosis and NFkappaB signalling in an HCT-116 CRC cell line with the p53 gene homozygously disrupted (HCT-116(p53-/-)) and an HCT-116 cell line rendered MMR proficient by chromosomal transfer (HCT-116(+ch3)), to the parental HCT-116 CRC cell line.
  • [MeSH-major] Active Transport, Cell Nucleus / drug effects. Apoptosis / drug effects. Aspirin / pharmacology. Base Pair Mismatch. Colorectal Neoplasms / drug therapy. NF-kappa B / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Carrier Proteins. Cell Line, Tumor. Humans. I-kappa B Proteins / metabolism. Neoplasm Proteins / physiology. Nuclear Proteins. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 15770215.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / I-kappa B Proteins; 0 / MLH1 protein, human; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p53; 139874-52-5 / NF-kappaB inhibitor alpha; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ PMC2361954
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37. Juengel E, Engler J, Mickuckyte A, Jones J, Hudak L, Jonas D, Blaheta RA: Effects of combined valproic acid and the epidermal growth factor/vascular endothelial growth factor receptor tyrosine kinase inhibitor AEE788 on renal cell carcinoma cell lines in vitro. BJU Int; 2010 Feb;105(4):549-57
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  • [Title] Effects of combined valproic acid and the epidermal growth factor/vascular endothelial growth factor receptor tyrosine kinase inhibitor AEE788 on renal cell carcinoma cell lines in vitro.
  • OBJECTIVE: To evaluate adhesion and growth inhibiting effects of the multiple receptor tyrosine kinase inhibitor AEE788 and the histone deacetylase (HDAC) inhibitor valproic acid (VPA) on renal cell carcinoma (RCC) cells.
  • MATERIALS AND METHODS: Caki-1 cells were treated with AEE788 and VPA, either alone or in combination, to investigate RCC cell adhesion to vascular endothelial cells or to immobilized extracellular matrix proteins.
  • Tumour cell proliferation was examined by MTT dye reduction assay.
  • Effects of drug treatment on cell signalling pathways were determined by Western blotting.
  • The expression levels of integrin alpha and beta subtypes were evaluated by flow cytometry (surface expression) and Western blotting (intracellular protein expression).
  • RESULTS: RCC cell treatment with AEE788 and VPA in combination resulted in a stronger inhibition of tumour cell proliferation than that caused by either drug alone.
  • There were also additive effects of the combined treatment on tumour cell adhesion to endothelial cells and to immobilized laminin (but not to immobilized fibronectin and collagen).
  • Both compounds altered integrin alpha and beta subtype expression, in particular alpha1, alpha3 and beta4, and blocked integrin-dependent integrin-linked kinase and focal-adhesion kinase (total and phosphorylated) signalling.
  • CONCLUSIONS: Both AEE788 and VPA profoundly block the interaction of RCC cells with endothelium and extracellular matrix and reduce tumour growth in vitro.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Renal Cell / drug therapy. Integrin alpha Chains / metabolism. Integrin beta Chains / metabolism. Kidney Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Adhesion / drug effects. Cell Line, Tumor. Drug Screening Assays, Antitumor / methods. Endothelium, Vascular. Extracellular Matrix Proteins / metabolism. Flow Cytometry. Humans. Purines / administration & dosage. Valproic Acid / administration & dosage

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  • (PMID = 19594733.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AEE 788; 0 / Extracellular Matrix Proteins; 0 / Integrin alpha Chains; 0 / Integrin beta Chains; 0 / Purines; 614OI1Z5WI / Valproic Acid
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38. Johannessen LN, Nilsen AM, Løvik M: The mycotoxins citrinin and gliotoxin differentially affect production of the pro-inflammatory cytokines tumour necrosis factor-alpha and interleukin-6, and the anti-inflammatory cytokine interleukin-10. Clin Exp Allergy; 2005 Jun;35(6):782-9
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  • [Title] The mycotoxins citrinin and gliotoxin differentially affect production of the pro-inflammatory cytokines tumour necrosis factor-alpha and interleukin-6, and the anti-inflammatory cytokine interleukin-10.
  • OBJECTIVE: We hypothesized that the mycotoxins citrinin and gliotoxin could cause an imbalance between the secretion of the pro-inflammatory cytokines TNF-alpha and IL-6 and the anti-inflammatory cytokine IL-10.
  • METHODS: We investigated the influence of citrinin and gliotoxin on the human monocytic cell line Mono-Mac-6 (MM6) with and without lipopolysaccharide -stimulation.
  • The levels of IL-10, IL-6 and TNF-alpha were analysed in cell culture supernatants by ELISA.
  • Cell viability and cell apoptosis were measured by flow cytometry.
  • IL-6 levels were found to decrease in a dose-dependent manner along with reduced cell viability.
  • TNF-alpha levels increased with low gliotoxin exposure (less than 100 ng/mL), but decreased significantly at 375 ng/mL and higher along with increased cell apoptosis and reduced cell viability.
  • TNF-alpha levels were not reduced by citrinin exposure.
  • CONCLUSION: We observed a cytokine imbalance with a more pronounced reduction of IL-10 concentrations compared with those of TNF-alpha and IL-6.
  • We suggest that low exposure doses of citrinin and gliotoxin (corresponding to less than 100 ng/mL gliotoxin and less than 10 mug/mL citrinin) may inhibit IL-10 and lead to increased risk of an inflammatory response with relative overproduction of TNF-alpha and IL-6.
  • [MeSH-major] Citrinin / immunology. Gliotoxin / immunology. Interleukin-10 / immunology. Interleukin-6 / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Air Pollution, Indoor. Anti-Bacterial Agents / immunology. Apoptosis / immunology. Cell Line. Cell Survival / immunology. Dose-Response Relationship, Immunologic. Humans. Immunosuppressive Agents / immunology. Lipopolysaccharides / immunology. Monocytes / immunology. Respiratory Hypersensitivity / immunology

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  • (PMID = 15969670.001).
  • [ISSN] 0954-7894
  • [Journal-full-title] Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • [ISO-abbreviation] Clin. Exp. Allergy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Immunosuppressive Agents; 0 / Interleukin-6; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 3S697X6SNZ / Citrinin; 67-99-2 / Gliotoxin
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39. Xiaofang Y, Yue Z, Xialian X, Zhibin Y: Serum tumour markers in patients with chronic kidney disease. Scand J Clin Lab Invest; 2007;67(6):661-7
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  • [Title] Serum tumour markers in patients with chronic kidney disease.
  • OBJECTIVE. Tumour markers are widely used for monitoring cancer patients and for screening certain tumours.
  • It has recently been shown that the concentrations of some tumour markers are higher in patients with chronic kidney disease (CKD) than in healthy subjects.
  • We analysed the influence of renal function and hemodialysis treatment on the serum levels of CA19-9, CA125, alpha fetoprotein (AFP), CA15.3, CA72.4, CYFRA 21-1, neuron-specific enolase (NSE) and squamous cell carcinoma antigen (SCC-Ag).
  • CONCLUSIONS: The increase in the serum levels of CA19-9, CA125 (in males), CYFRA 21-1, NSE and SCC-Ag in patients with CKD affects the specificity of these markers in the diagnosis of cancer.
  • [MeSH-major] Biomarkers, Tumor / blood. Kidney Failure, Chronic / blood
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / blood. CA-125 Antigen / blood. CA-19-9 Antigen / blood. Female. Glomerular Filtration Rate. Humans. Keratin-19. Keratins / blood. Male. Middle Aged. Mucin-1 / blood. Renal Dialysis / statistics & numerical data. alpha-Fetoproteins / analysis

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  • (PMID = 17852811.001).
  • [ISSN] 0036-5513
  • [Journal-full-title] Scandinavian journal of clinical and laboratory investigation
  • [ISO-abbreviation] Scand. J. Clin. Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / CA-19-9 Antigen; 0 / Keratin-19; 0 / Mucin-1; 0 / alpha-Fetoproteins; 0 / antigen CYFRA21.1; 68238-35-7 / Keratins
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40. Chang JH, Park JY, Kim SK: Dependence on p38 MAPK signalling in the up-regulation of TLR2, TLR4 and TLR9 gene expression in Trichomonas vaginalis-treated HeLa cells. Immunology; 2006 Jun;118(2):164-70
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  • [Title] Dependence on p38 MAPK signalling in the up-regulation of TLR2, TLR4 and TLR9 gene expression in Trichomonas vaginalis-treated HeLa cells.
  • Our hypothesis is that T. vaginalis-infected epithelial cells are major effector cells in the skin barrier.
  • These cells function as a central regulator of TLR gene expression, thus accelerating the process of barrier dysfunction via increased release of chemokines and proinflammatory cytokines.
  • To test this hypothesis, RT-PCR was performed on TLRs, interleukin (IL)-8 and tumour necrosis factor (TNF)-alpha.
  • Stimulation of HeLa cells by T. vaginalis was observed to up-regulate TLR2, 4 and 9 mRNA expression as well as that of IL-8 and TNF-alpha.
  • To further clarify the molecular mechanism of barrier devastation triggered by these up-regulatory stimuli, we examined the profiles of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB activation in HeLa cells using specific inhibitors.
  • Interestingly, pretreatment of HeLa cells with the p38 MAPK inhibitor SB203580 demonstrated inhibition of T. vaginalis-induced up-regulation of TLR2, 4, and 9 mRNA expression.
  • In addition, pretreatment with SB203580 reduced epithelium-derived IL-8 and TNF-alpha release evoked by T. vaginalis.
  • Our results show that T. vaginalis infection of the mucocutaneous barrier could up-regulate TLR2, 4 and 9 gene expression via the p38 MAPK signalling pathway in epithelial cells; this process then leads to modulation of p38 MAPK-dependent IL-8 and TNF-alpha release from the epithelium.
  • [MeSH-minor] Animals. Extracellular Signal-Regulated MAP Kinases / immunology. HeLa Cells. Humans. Interleukin-8 / biosynthesis. Interleukin-8 / genetics. NF-kappa B / immunology. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Signal Transduction / immunology. Toll-Like Receptor 2 / biosynthesis. Toll-Like Receptor 2 / genetics. Toll-Like Receptor 4 / biosynthesis. Toll-Like Receptor 4 / genetics. Toll-Like Receptor 9 / biosynthesis. Toll-Like Receptor 9 / genetics. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics. Up-Regulation / immunology

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  • (PMID = 16771851.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4; 0 / Toll-Like Receptor 9; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1782292
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41. Hosoya M, Kawasaki Y, Katayose M, Sakuma H, Watanabe M, Igarashi E, Aoyama M, Nunoi H, Suzuki H: Prognostic predictive values of serum cytochrome c, cytokines, and other laboratory measurements in acute encephalopathy with multiple organ failure. Arch Dis Child; 2006 Jun;91(6):469-72
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  • RESULTS: Cytochrome c, tumour necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), soluble TNF-receptor 1 (sTNF-R1), and aspartate aminotransferase (AST) concentrations at the initial phase were high and correlated well with patient outcome.
  • High concentrations of serum cytochrome c (>45 ng/ml), sTNF-R1 (>2000 pg/ml), AST (>58 IU/dl), IL-6 (>60 pg/ml), and TNF-alpha (>15 pg/ml) predicted an unfavourable prognosis (sequelae and death) at 93%, 79%, 82%, 77%, and 60%, respectively.
  • [MeSH-minor] Acute Disease. Area Under Curve. Aspartate Aminotransferases / blood. Biomarkers / blood. Brain Edema / blood. Child. Child, Preschool. Critical Care. Female. Humans. Infant. Interleukin-6 / blood. Male. Prognosis. ROC Curve. Receptors, Tumor Necrosis Factor / blood. Sensitivity and Specificity. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 16443616.001).
  • [ISSN] 1468-2044
  • [Journal-full-title] Archives of disease in childhood
  • [ISO-abbreviation] Arch. Dis. Child.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cytokines; 0 / Interleukin-6; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 9007-43-6 / Cytochromes c; EC 2.6.1.1 / Aspartate Aminotransferases
  • [Other-IDs] NLM/ PMC2082805
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42. Skogseth H, Larsson E, Halgunset J: The invasive behaviour of prostatic cancer cells is suppressed by inhibitors of tyrosine kinase. APMIS; 2006 Jan;114(1):61-6
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  • [Title] The invasive behaviour of prostatic cancer cells is suppressed by inhibitors of tyrosine kinase.
  • Proteolytic enzymes, and especially urokinase plasminogen activator (uPA), play an important role in tumour invasion and metastasis.
  • Previously we demonstrated that the production of urokinase plasminogen activator (uPA) was decreased by several tyrosine kinase inhibitors (TKI) in two prostatic carcinoma cell lines.
  • The effect of the two TKI genistein and tyrphostin AG-1478 was investigated in the prostate carcinoma cell lines PC-3 and DU-145.
  • Cell invasion was increased by plasminogen, but this enhanced cell migration was counteracted by TKI treatment.
  • The increased cell invasion induced by plasminogen was decreased by at least 60% in both cell lines when alpha-2 anti-plasmin was added to the assay.
  • Cells in the absence of plasminogen were not affected by TKI.
  • External uPA failed to regenerate the decreased cell invasion caused by TKI.
  • Our results indicate a possible role of TKI as inhibitors of cancer cell invasion by inhibiting uPA and MMP production.
  • [MeSH-minor] Basement Membrane / chemistry. Basement Membrane / pathology. Biological Assay. Cell Movement / drug effects. Collagen / chemistry. Drug Combinations. Humans. Laminin / chemistry. Male. Matrix Metalloproteinases / metabolism. Neoplasm Invasiveness. Plasminogen / pharmacology. Plasminogen Activators / antagonists & inhibitors. Proteoglycans / chemistry. Quinazolines

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  • (PMID = 16499663.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Matrix Metalloproteinase Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Proteoglycans; 0 / Quinazolines; 0 / Tyrphostins; 119978-18-6 / matrigel; 170449-18-0 / tyrphostin AG 1478; 9001-91-6 / Plasminogen; 9007-34-5 / Collagen; DH2M523P0H / Genistein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.4.21.- / Plasminogen Activators; EC 3.4.24.- / Matrix Metalloproteinases
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43. Khuda II, Koide N, Noman AS, Dagvadorj J, Tumurkhuu G, Naiki Y, Komatsu T, Yoshida T, Yokochi T: Astrocyte elevated gene-1 (AEG-1) is induced by lipopolysaccharide as toll-like receptor 4 (TLR4) ligand and regulates TLR4 signalling. Immunology; 2009 Sep;128(1 Suppl):e700-6
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  • Astrocyte elevated gene-1 (AEG-1) is induced by human immunodeficiency virus 1 (HIV-1) infection and involved in tumour progression, migration and invasion as a nuclear factor-kappaB (NF-kappaB) -dependent gene.
  • AEG-1 was induced via NF-kappaB activation in LPS-stimulated U937 human promonocytic cells.
  • The prevention of AEG-1 expression inhibited LPS-induced tumour necrosis factor-alpha and prostaglandin E(2) production.
  • [MeSH-major] Cell Adhesion Molecules / biosynthesis. Lipopolysaccharides / immunology. Monocytes / immunology. Toll-Like Receptor 4 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Dinoprostone / biosynthesis. Dinoprostone / immunology. Humans. NF-kappa B / agonists. NF-kappa B / metabolism. Signal Transduction. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 19740331.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Lipopolysaccharides; 0 / MTDH protein, human; 0 / NF-kappa B; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2753960
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44. Butler LM, Rainger GE, Rahman M, Nash GB: Prolonged culture of endothelial cells and deposition of basement membrane modify the recruitment of neutrophils. Exp Cell Res; 2005 Oct 15;310(1):22-32
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  • [Title] Prolonged culture of endothelial cells and deposition of basement membrane modify the recruitment of neutrophils.
  • We tested whether endothelial cell conditioning during prolonged culture and deposition of basement membrane (BM) could modify neutrophil recruitment induced by the inflammatory cytokine, tumour necrosis factor-alpha (TNF).
  • Confluent endothelial cells (EC) from human umbilical veins were cultured for 1 to 20 days and then stimulated with 1, 10 or 100 U/ml of TNF for 4 h.
  • When isolated neutrophils were settled on EC stimulated with the lower doses of TNF, the levels of adhesion and the proportion of adherent cells that transmigrated increased markedly with time of culture.
  • Prolonged culture was also associated with deposition of a distinct BM.
  • [MeSH-major] Basement Membrane / metabolism. Endothelial Cells / cytology. Neutrophil Infiltration / physiology. Neutrophils / cytology. Neutrophils / physiology
  • [MeSH-minor] Cell Adhesion / physiology. Cells, Cultured. Coculture Techniques. Humans. Time Factors. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16109405.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [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
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45. Andersson AK, Feldmann M, Brennan FM: Neutralizing IL-21 and IL-15 inhibits pro-inflammatory cytokine production in rheumatoid arthritis. Scand J Immunol; 2008 Jul;68(1):103-11
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  • We have analysed the effects of blocking IL-21 and IL-15 on spontaneous production of pro-inflammatory cytokines in RA synovial cell cultures.
  • RA synovial membrane cells were cultured in the presence of an IL-21R-Fc chimera or a neutralizing IL-15 antibody and production of tumour necrosis factor (TNF)alpha, IL-6 and IL-1beta was measured by enzyme-linked immunosorbent assay (ELISA).
  • Expression of IL-21 and IL-15 in RA synovium was measured by RT-PCR and ELISA. mRNA for IL-21 and IL-21R was detected in the culture cell lysates.
  • Protein for IL-15 was found at detectable levels in the cell lysates.
  • [MeSH-minor] Adult. Aged. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Female. Humans. Inflammation Mediators / immunology. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Synovial Membrane / cytology. Synovial Membrane / immunology


46. Ao C, Huo Y, Qi L, Xiong Z, Xue L, Qi Y: Pioglitazone suppresses the lipopolysaccharide-induced production of inflammatory factors in mouse macrophages by inactivating NF-kappaB. Cell Biol Int; 2010 Jul;34(7):723-30
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  • We have investigated the effects of pioglitazone on LPS (lipopolysaccharide)-induced production of TNF-alpha (tumour necrosis factor alpha), sPLA2-V and -X (groups V and X sPLA2) in RAW 264.7 macrophages.
  • TNF-alpha, sPLA2-V and -X mRNA and protein expression were determined by RT-PCR (reverse transcriptase-PCR) and Western blot analysis, respectively.
  • LPS induced TNF-alpha, sPLA2-V and sPLA2-X mRNA and protein expression.
  • Pretreatment with 10 mumol/l pioglitazone significantly suppressed LPS-induced TNF-alpha, sPLA2-V and sPLA2-X mRNA and protein expression.
  • Our findings indicate that pioglitazone inhibits production of inflammatory factors induced by LPS in murine macrophage cells by inactivating NF-kappaB.
  • [MeSH-minor] Animals. Cell Line. Group V Phospholipases A2 / genetics. Group V Phospholipases A2 / immunology. Group X Phospholipases A2 / genetics. Group X Phospholipases A2 / immunology. Humans. Mice. PPAR gamma / agonists. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 19947950.001).
  • [ISSN] 1095-8355
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / PPAR gamma; 0 / Thiazolidinediones; 0 / Tumor Necrosis Factor-alpha; EC 3.1.1.4 / Group V Phospholipases A2; EC 3.1.1.4 / Group X Phospholipases A2; X4OV71U42S / pioglitazone
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47. Wang JZ, Li XA, Mayr NA: Dose escalation to combat hypoxia in prostate cancer: a radiobiological study on clinical data. Br J Radiol; 2006 Nov;79(947):905-11
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  • Using the concept of the clinical oxygen enhancement ratio (COER), the linear-quadratic (LQ) model was extended to account for the effect of tumour hypoxia.
  • The clinical data collected at the Fox Chase Cancer Center for prostate cancer were analysed based on the LQ model as well as the tumour control probability (TCP) model.
  • The LQ and TCP parameters (alpha = 0.15 Gy (-1), alpha/beta = 3.1 Gy and the number of clonogens K = 10(6) approximately 10(7) cells) determined in earlier studies were used to derive the COER for prostate cancer: COER = 1.4 with a standard confidence interval (CI) of (1.2, 1.8).
  • The result is consistent with the in vitro OER measurements of human tumour cell lines under chronic hypoxia conditions.
  • This implies that a higher dose is needed to overcome tumour hypoxia.
  • For prostate tumours, the prescription dose required to overcome tumour hypoxia is 165 Gy (CI: 153 approximately 186 Gy) for permanent 125I implants and 88 Gy (CI: 74 approximately 118 Gy) in 2 Gy fractions for external-beam radiotherapy.
  • This study provides a preliminary estimate of the dose escalation needed to overcome tumour hypoxia based on clinical data.

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  • (PMID = 16885177.001).
  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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48. Sanders PM, Russell ST, Tisdale MJ: Angiotensin II directly induces muscle protein catabolism through the ubiquitin-proteasome proteolytic pathway and may play a role in cancer cachexia. Br J Cancer; 2005 Aug 22;93(4):425-34
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  • Both Ang I and Ang II stimulated an increased proteasome 'chymotrypsin-like' enzyme activity as well as an increase in protein expression of 20S proteasome alpha-subunits, the 19S subunits MSS1 and p42, at the same concentrations as those inducing protein degradation.
  • The highly lipophilic ACE inhibitor imidapril (Vitortrade mark) (30 mg kg(-1)) attenuated the development of weight loss in mice bearing the MAC16 tumour, suggesting that Ang II may play a role in the development of cachexia in this model.
  • [MeSH-minor] Angiotensin I / physiology. Angiotensin-Converting Enzyme Inhibitors / pharmacology. Animals. Cell Culture Techniques. Imidazolidines / pharmacology. Male. Mice. Muscle Fibers, Skeletal / metabolism

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  • (PMID = 16052213.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Imidazolidines; 0 / Muscle Proteins; 0 / Ubiquitin; 11128-99-7 / Angiotensin II; 9041-90-1 / Angiotensin I; BW7H1TJS22 / imidapril; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC3217221
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49. Notebaert S, Carlsen H, Janssen D, Vandenabeele P, Blomhoff R, Meyer E: In vivo imaging of NF-kappaB activity during Escherichia coli-induced mammary gland infection. Cell Microbiol; 2008 Jun;10(6):1249-58
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  • This systemic reaction was confirmed by increased circulating levels of the acute phase protein serum amyloid A, tumour necrosis factor-alpha and interleukin-6.
  • [MeSH-minor] Animals. Epithelium / metabolism. Female. Immunohistochemistry. Interleukin-6 / metabolism. Liver / metabolism. Luciferases / genetics. Mice. Mice, Transgenic. Microscopy, Fluorescence. Serum Amyloid A Protein / metabolism. Transcription Factor RelA / isolation & purification. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18241210.001).
  • [ISSN] 1462-5822
  • [Journal-full-title] Cellular microbiology
  • [ISO-abbreviation] Cell. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / NF-kappa B; 0 / Rela protein, mouse; 0 / Serum Amyloid A Protein; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; EC 1.13.12.- / Luciferases
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50. Kim S, Kim HO, Kim HJ, Lee K, Kim HS: Generation of functionally mature dendritic cells from elutriated monocytes using polyinosinic : polycytidylic acid and soluble CD40 ligand for clinical application. Clin Exp Immunol; 2008 Dec;154(3):365-74
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  • [Title] Generation of functionally mature dendritic cells from elutriated monocytes using polyinosinic : polycytidylic acid and soluble CD40 ligand for clinical application.
  • Despite the increasing use of dendritic cell (DC) vaccination in clinical trials, optimal conditions for the generation of functionally mature DCs remain to be established.
  • The current standard DC maturation protocol for clinical trials has been used as an inflammatory cytokine cocktail [tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6 and prostaglandin E(2)], but this cocktail induced insufficient maturation of DCs derived from elutriated monocytes when cultured in X-VIVO 15.
  • We compared the functional capacity of DCs in response to all possible pairwise combinations of four different classes of stimuli: TNF-alpha, peptidoglycan, polyinosinic : polycytidylic acid [poly(I:C)] and soluble CD40 ligand (CD40L).
  • Maturation status of DCs stimulated with combination of four stimuli was similar to that of the cytokine cocktail as assessed by the cell surface phenotype.
  • [MeSH-major] CD40 Ligand / immunology. Dendritic Cells / immunology. Poly I-C / immunology
  • [MeSH-minor] Cell Differentiation / immunology. Cell Polarity / immunology. Chemotaxis, Leukocyte / immunology. Cytokines / biosynthesis. Humans. Immunophenotyping. Interferon Inducers / immunology. Leukapheresis / methods. Lymphocyte Culture Test, Mixed. Monocytes / immunology. Th1 Cells / immunology. Th2 Cells / immunology. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18782327.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interferon Inducers; 0 / Tumor Necrosis Factor-alpha; 147205-72-9 / CD40 Ligand; 24939-03-5 / Poly I-C
  • [Other-IDs] NLM/ PMC2633224
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51. Weibel S, Stritzker J, Eck M, Goebel W, Szalay AA: Colonization of experimental murine breast tumours by Escherichia coli K-12 significantly alters the tumour microenvironment. Cell Microbiol; 2008 Jun;10(6):1235-48
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  • [Title] Colonization of experimental murine breast tumours by Escherichia coli K-12 significantly alters the tumour microenvironment.
  • The successful application of live bacteria in cancer therapy requires a more detailed understanding of bacterial interaction with the tumour microenvironment.
  • Here, we analysed the effect of Escherichia coli K-12 colonization on the tumour microenvironment by immunohistochemistry and fluorescence microscopy in the murine 4T1 breast carcinoma model.
  • We described the colonization of tumour-bearing mice, as well as the spatiotemporal distribution of E. coli K-12 in the 4T1 tumour tissue over a period of 14 days.
  • The colonization resulted within 3 days in large avascular necrotic tissue, redistribution of hypoxic areas and an enhanced collagen IV deposition within the colonized tumour tissue, which changed the tumoral perfusion of systemically injected immunoglobulins.
  • In addition, E. coli K-12 colonization led to the redistribution of tumour-associated macrophages, forming a granulation tissue around bacterial colonies, and also to an increase in TNFalpha and matrix metalloproteinase 9 expression.
  • These new insights will contribute to the general understanding of the tumour-microbe cross-talk and to the design of bacterial strains with enhanced anticancer efficiency.
  • [MeSH-minor] Animals. Cell Line, Tumor. Collagen Type IV / metabolism. Colony Count, Microbial. Female. Humans. Immunohistochemistry. Liver / microbiology. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Macrophages / pathology. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Microscopy, Fluorescence. Necrosis / pathology. Oxygen / metabolism. Spleen / microbiology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18208564.001).
  • [ISSN] 1462-5822
  • [Journal-full-title] Cellular microbiology
  • [ISO-abbreviation] Cell. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Collagen Type IV; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.35 / Matrix Metalloproteinase 9; S88TT14065 / Oxygen
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52. Kalt A, Schneider T, Ring S, Hoffmann J, Zeitz M, Stallmach A, Persing DH, Marth T: Decreased levels of interleukin-12p40 in the serum of patients with Whipple's disease. Int J Colorectal Dis; 2006 Mar;21(2):114-20
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  • [Title] Decreased levels of interleukin-12p40 in the serum of patients with Whipple's disease.
  • BACKGROUND: An impaired production of interleukin (IL)-12 and T cell interferon-gamma (IFN-gamma) of in vitro stimulated monocytes has been discussed as a pathogenic factor in Whipple's disease (WD).
  • METHODS: We analyzed the serum of 40 patients with Whipple's disease in various degrees of disease activity by sandwich enzyme-linked immunosorbent assay for differences in cytokine and cell adhesion molecule concentrations compared with age- and sex-matched controls.
  • RESULTS: We observed a highly significant reduction of IL-12p40 levels (patients, 0.18+/-0.05 ng/ml (mean+/-SEM); controls, 3.19+/-0.39 ng/ml; p<0.01) in all stages of disease activity, whereas the concentration of IL-12p70 was comparable with controls.
  • Furthermore, we observed a slight decrease in tumour necrosis factor alpha (TNF-alpha) concentrations in the serum of patients (patients, 6.36+/-0.90 pg/ml; controls, 10.5+/-1.23 pg/ml; p<0,05).
  • The levels of other cytokines such as IFN-gamma, IL-2, IL-13 and transforming growth factor beta, as well as soluble cell adhesion molecules lymphocyte function-associated antigen 3 and intercellular adhesion molecule 1, were not significantly different compared with controls.
  • CONCLUSION: Our data demonstrate a persistent defect of the cellular immune response with decreased serum concentrations of IL-12p40 and TNF-alpha and decreased IgG2 levels in a large group of WD patients.
  • These data support as in vivo finding the results obtained in previous investigations with stimulated monocytes/lymphocytes.
  • [MeSH-major] Interleukin-12 Subunit p40 / blood. Whipple Disease / blood
  • [MeSH-minor] Biomarkers / blood. Disease Progression. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunoglobulin G / blood. Interleukin-12 / blood. Male. Middle Aged. Severity of Illness Index. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 15875203.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Immunoglobulin G; 0 / Interleukin-12 Subunit p40; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12
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53. Juanes PP, Ferreira L, Montero JC, Arribas J, Pandiella A: N-terminal cleavage of proTGFalpha occurs at the cell surface by a TACE-independent activity. Biochem J; 2005 Jul 1;389(Pt 1):161-72
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  • [Title] N-terminal cleavage of proTGFalpha occurs at the cell surface by a TACE-independent activity.
  • ProTGFalpha (transforming growth factor alpha precursor) maturation and conversion into soluble TGFalpha is a complex process that involves three proteolytic steps.
  • In vivo treatment with the hydroxamate-based metalloprotease inhibitors BB3103 or TAPI-2 (tumour necrosis factor-alpha protease inhibitor 2) reversibly induced accumulation of forms of proTGFalpha that included the N-terminal extension.
  • N-terminal shedding was rapid, and occurred at the cell surface.
  • Experiments of proTGFalpha expression and maturation in cells deficient in TACE (tumour-necrosis-factor-alpha-converting enzyme) activity indicated that this protease was dispensable for N-terminal processing of proTGFalpha in vivo, but was required for regulated cleavage at the C-terminus.
  • [MeSH-major] ADAM Proteins / metabolism. Cell Membrane / metabolism. Protein Precursors / metabolism. Transforming Growth Factor alpha / metabolism
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Animals. Aspartic Acid Endopeptidases. CHO Cells. Cricetinae. Dose-Response Relationship, Drug. Endopeptidases / metabolism. Endoplasmic Reticulum / metabolism. HeLa Cells. Humans. Hydroxamic Acids / pharmacology. Protease Inhibitors / pharmacology. Protein Processing, Post-Translational / drug effects

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  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydroxamic Acids; 0 / Protease Inhibitors; 0 / Protein Precursors; 0 / Transforming Growth Factor alpha; 0 / protransforming growth factor alpha; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  • [Other-IDs] NLM/ PMC1184548
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54. Hartgring SA, Bijlsma JW, Lafeber FP, van Roon JA: Interleukin-7 induced immunopathology in arthritis. Ann Rheum Dis; 2006 Nov;65 Suppl 3:iii69-74
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  • Interleukin (IL)-7 is a potent immunoregulatory cytokine that is detected in joints of patients with rheumatoid and juvenile idiopathic arthritis and which correlates with parameters of disease.
  • Several synovial cell types that play an important role in inflammation and immunopathology, such as macrophages, dendritic cells, and fibroblasts, produce IL-7.
  • IL-7 induces cytokines produced by arthritogenic T cells (for example, interferon gamma (IFNgamma), IL-17), T cell differentiating factors (for example, IL-12), chemokines capable of attracting inflammatory cells (for example, macrophage induced gene (MIG), macrophage inflammatory protein (MIP)-1alpha) as well as molecules involved in cell adhesion, migration, and costimulation (for example, lymphocyte function associated antigen (LFA)-1, CD40, CD80).
  • IL-7 induces tumour necrosis factor alpha (TNFalpha) secretion by T cells and by monocytes after T cell dependent monocyte/macrophage activation.
  • [MeSH-minor] Animals. Antirheumatic Agents / therapeutic use. Autoimmune Diseases / immunology. CD4-Positive T-Lymphocytes / immunology. Humans. Mice. Monocytes / immunology. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 17038478.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Interleukin-7; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 65
  • [Other-IDs] NLM/ PMC1798384
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55. Szlosarek PW, Grimshaw MJ, Wilbanks GD, Hagemann T, Wilson JL, Burke F, Stamp G, Balkwill FR: Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer. Int J Cancer; 2007 Jul 01;121(1):6-11
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  • [Title] Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer.
  • The pro-inflammatory cytokine, tumour necrosis factor-alpha, TNF-alpha, is dysregulated in malignant compared with normal ovarian surface epithelium (OSE).
  • Several epidemiological studies have associated inflammation with ovarian tumorigenesis, with TNF-alpha playing a key role in modulating invasion, angiogenesis and metastasis.
  • Here, we show that TNF-alpha also induces expression of arate-limiting enzyme in arginine synthesis, argininosuccinate synthetase (AS), thereby linking inflammation with several arginine-dependent metabolic pathways, implicated in accelerated carcinogenesis and tumour progression.
  • Having identified AS mRNA induction in TNF-alpha-treated IGROV-1 ovarian cancer cells, using RNA-arbitrarily primed-PCR, we then observed differential regulation of AS mRNA and protein in malignant, compared with normal, OSE cells.
  • A cDNA cancer profiling array with matched normal ovarian and ovarian tumour samples revealed increased expression of AS mRNA in the latter.
  • Moreover, AS protein co-localised with TNF-alpha in ovarian cancer cells, with significantly higher levels of AS in malignant compared with normal ovarian tissue.
  • Increased co-expression of AS and TNF-alpha mRNA was also observed in 2 other epithelial tumours, non-small cell lung and stomach cancer, compared with normal corresponding tissues.
  • In summary, high levels of AS expression, which may be required for several arginine-dependent processes in cancer, including the production of nitric oxide, proline, pyrimidines and polyamines, is regulated by TNF-alpha and may provide an important molecular pathway linking inflammation and metabolism to ovarian tumorigenesis.
  • [MeSH-major] Argininosuccinate Synthase / metabolism. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Ovarian Neoplasms / enzymology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Female. Health. Humans. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 17354225.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974; United Kingdom / Medical Research Council / / G0601867
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 6.3.4.5 / Argininosuccinate Synthase
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56. Henderson EA, Bavetsias V, Theti DS, Wilson SC, Clauss R, Jackman AL: Targeting the alpha-folate receptor with cyclopenta[g]quinazoline-based inhibitors of thymidylate synthase. Bioorg Med Chem; 2006 Jul 15;14(14):5020-42
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  • [Title] Targeting the alpha-folate receptor with cyclopenta[g]quinazoline-based inhibitors of thymidylate synthase.
  • The alpha-FR has been reported to be overexpressed in many carcinomas, in particular those of the ovary and uterus.
  • The high expression of alpha-FR in some tumours compared with normal tissues has been exploited over the last decade for folate-mediated targeting of macromolecules, anticancer drugs, imaging agents and nucleic acids to cancer cells.
  • CB300638, a cyclopenta[g]quinazoline-based inhibitor of thymidylate synthase (TS), has been reported to have high affinity for the receptor and selectivity for alpha-FR overexpressing tumour cell lines.
  • In this study, the structural features of the molecule, in particular modifications at the 2-position, have been investigated with respect to TS inhibition, affinity for the alpha-FR and reduced folate carrier (RFC) and activity in A431-FBP cells (transfected with human alpha-FR) compared with neo-transfected A431 cells.
  • It was found that the 2-substituent does not affect the affinity for the alpha-FR; however, it greatly affects selectivity for A431-FBP cells, and suggests that there are factors other than TS inhibition and alpha-FR affinity that are important for the activity of these compounds.
  • Compound 2b (2-CH2OH derivative) displayed the highest selectivity for the A431-FBP cells compared with A431 cells.
  • [MeSH-major] Carrier Proteins / antagonists & inhibitors. Enzyme Inhibitors / chemistry. Enzyme Inhibitors / pharmacology. Quinazolines / chemistry. Quinazolines / pharmacology. Receptors, Cell Surface / antagonists & inhibitors. Thymidylate Synthase / antagonists & inhibitors
  • [MeSH-minor] Cell Line. Cyclopentanes / chemistry. Cyclopentanes / pharmacology. Folate Receptors, GPI-Anchored. Humans. In Vitro Techniques. Recombinant Proteins / antagonists & inhibitors. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Structure-Activity Relationship. Transfection

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  • (PMID = 16554160.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CB300638; 0 / Carrier Proteins; 0 / Cyclopentanes; 0 / Enzyme Inhibitors; 0 / Folate Receptors, GPI-Anchored; 0 / Quinazolines; 0 / Receptors, Cell Surface; 0 / Recombinant Proteins; EC 2.1.1.45 / Thymidylate Synthase
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57. Choi JH, Choi EK, Park SJ, Ko HM, Kim KJ, Han SJ, Choi IW, Im SY: Impairment of p38 MAPK-mediated cytosolic phospholipase A2 activation in the kidneys is associated with pathogenicity of Candida albicans. Immunology; 2007 Feb;120(2):173-81
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  • In studying the mechanisms underlying the susceptibility of the kidney to candidal infection, we previously reported that the reduced production of cytokines [i.e. tumour necrosis factor-alpha (TNF-alpha)] via platelet-activating factor (PAF)-induced activation of nuclear factor-kappaB (NF-kappaB) renders the organ susceptible to the fungal burden.
  • In this study, we investigated the possibility that pathogenic Candida albicans may evade clearance and perhaps even multiply by inhibiting elements in the signalling pathway that lead to the production of TNF-alpha.
  • The fungal burden of pathogenic C. albicans in the kidneys was 10(4)-10(5)-fold higher than that of a non-pathogenic strain.
  • PAF-induced early activation of NF-kappaB and TNF-alpha mRNA expression were both observed in the kidneys of mice infected with non-pathogenic strains of C. albicans, but not in mice infected with pathogenic strains.
  • [MeSH-minor] Animals. Enzyme Inhibitors / pharmacology. Female. Gene Expression Regulation. Mice. Mice, Inbred BALB C. NF-kappa B / metabolism. Phospholipases A2. Phosphorylation. Platelet Activating Factor / antagonists & inhibitors. Platelet Activating Factor / physiology. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / genetics. Virulence

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  • (PMID = 17054728.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / Platelet Activating Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Phospholipases A2
  • [Other-IDs] NLM/ PMC2265852
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58. Zeine R, Salwen HR, Peddinti R, Tian Y, Guerrero L, Yang Q, Chlenski A, Cohn SL: Presence of cancer-associated fibroblasts inversely correlates with Schwannian stroma in neuroblastoma tumors. Mod Pathol; 2009 Jul;22(7):950-8
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  • [Title] Presence of cancer-associated fibroblasts inversely correlates with Schwannian stroma in neuroblastoma tumors.
  • Stromal cells have a central function in the regulation of tumor angiogenesis.
  • Recent studies have shown that stromal myofibroblasts (cancer-associated fibroblasts) actively promote tumor growth and enhance tumor angiogenesis in many types of adult carcinomas.
  • To evaluate the function cancer-associated fibroblasts have in neuroblastoma angiogenesis and investigate their relationship to stromal Schwann cells, we quantified cancer-associated fibroblasts in 60 primary neuroblastoma tumors and in a novel neuroblastoma xenograft model in which murine Schwann cells were induced to infiltrate into the tumor stroma.
  • Tumor sections were examined for presence of microvascular proliferation, a hallmark of tumor angiogenesis.
  • Cancer-associated fibroblasts were characterized by positive immunostaining for alpha-smooth muscle actin (alpha-SMA) and were distinguished from pericytes by staining negatively for high-molecular-weight caldesmon. alpha-SMA-positive cells were quantified and their number was defined as high when >1.0% of the area was positive.
  • Thirty-seven (80%) of the 46 Schwannian stroma-poor tumors had high numbers of cancer-associated fibroblasts in the tumor stroma compared to only 2 (14%) of the 14 Schwannian stroma-rich/dominant tumors (P<0.001).
  • Thirty-three (89%) of 37 tumors with microvascular proliferation had high numbers of cancer-associated fibroblasts compared to 9 (40%) of 22 tumors without microvascular proliferation (P<0.001).
  • In the xenografts with infiltrating Schwann cells (n=10), the number of cancer-associated fibroblasts per mm(2) was approximately sevenfold less than in the control xenografts without stromal Schwann cells (n=9) (mean of 51+/-30 vs 368+/-105, respectively; P<0.001).
  • Thus, cancer-associated fibroblasts were inversely associated with presence of Schwann cells, suggesting that Schwann cells may prevent the activation of fibroblasts.
  • [MeSH-major] Fibroblasts / pathology. Neovascularization, Pathologic / pathology. Neuroblastoma / pathology. Schwann Cells / pathology. Stromal Cells / pathology
  • [MeSH-minor] Actins / metabolism. Animals. Biomarkers / metabolism. Calmodulin-Binding Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Disease Models, Animal. Female. Humans. Infant. Male. Mice. Mice, Nude. Neoplasm Transplantation. Pericytes / metabolism. Pericytes / pathology. Sciatic Nerve / pathology. Sciatic Nerve / surgery

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  • (PMID = 19407854.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS049814; United States / NINDS NIH HHS / NS / R01 NS049814-04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers; 0 / Calmodulin-Binding Proteins
  • [Other-IDs] NLM/ NIHMS97522; NLM/ PMC3347894
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59. Brennan PA, Quintero M: Hunterian Lecture. Regulation of hypoxia-inducible factor 1 (HIF-1) by nitric oxide in oral squamous cell carcinoma. Ann R Coll Surg Engl; 2005 May;87(3):153-8
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  • [Title] Hunterian Lecture. Regulation of hypoxia-inducible factor 1 (HIF-1) by nitric oxide in oral squamous cell carcinoma.
  • INTRODUCTION: Hypoxia is a common feature of many cancers, contributing to tumour progression as well as potentially compromising radiotherapy and chemotherapy.
  • METHOD: Three oral cancer cell lines were used to investigate the effects of NO synthase enzymes (NOS) on HIF-1alpha expression under both normal oxygen and hypoxic conditions.
  • The effect of NOS inhibition was evaluated with the drug L-NMMA.
  • RESULTS & CONCLUSIONS: HIF-1alpha expression occurred following exposure of cells to 3% oxygen for 8 h in all three cell lines, and its expression was found to be dependent on NOS activity, being reduced or inhibited by L-NMMA.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. DNA-Binding Proteins / metabolism. Mouth Neoplasms / metabolism. Nitric Oxide / physiology. Nuclear Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Cell Hypoxia / physiology. Enzyme Inhibitors / pharmacology. Humans. Hypoxia-Inducible Factor 1. Hypoxia-Inducible Factor 1, alpha Subunit. Neoplasm Proteins / metabolism. Nitric Oxide Synthase / antagonists & inhibitors. Nitric Oxide Synthase / metabolism. Tumor Cells, Cultured. omega-N-Methylarginine / pharmacology

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  • (PMID = 15901372.001).
  • [ISSN] 0035-8843
  • [Journal-full-title] Annals of the Royal College of Surgeons of England
  • [ISO-abbreviation] Ann R Coll Surg Engl
  • [Language] eng
  • [Publication-type] Lectures; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 27JT06E6GR / omega-N-Methylarginine; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase
  • [Other-IDs] NLM/ PMC1963906
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60. Holohan C, Szegezdi E, Ritter T, O'Brien T, Samali A: Cytokine-induced beta-cell apoptosis is NO-dependent, mitochondria-mediated and inhibited by BCL-XL. J Cell Mol Med; 2008 Apr;12(2):591-606
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  • [Title] Cytokine-induced beta-cell apoptosis is NO-dependent, mitochondria-mediated and inhibited by BCL-XL.
  • Pro-inflammatory cytokines are implicated as the main mediators of beta-cell death during type 1 diabetes but the exact mechanisms remain unknown.
  • This study examined the effects of interleukin-1beta (IL-1beta), interferon-gamma (IFNgamma) and tumour necrosis factor alpha (TNFalpha) on a rat insulinoma cell line (RIN-r) in order to identify the core mechanism of cytokine-induced beta-cell death.
  • Treatment of cells with a combination of IL-1beta and IFNgamma (IL-1beta/IFNgamma)induced apoptotic cell death.
  • TNFalpha neither induced beta-cell death nor did it potentiate the effects of IL-1beta, IFNgamma or IL-1beta/IFNgamma .
  • The broad range caspase inhibitor, Boc-D-fmk, blocked IL-1beta/IFNgamma -induced caspase activity, but not nitric oxide production nor cell death.
  • However, pre-treatment with L-NIO, a NOS inhibitor, prevented nitric oxide production, caspase activity and reduced apoptosis.
  • Transduction of cells with Ad-Bcl-X(L) blocked both iNOS and cytokine-mediated mitochondrial changes and subsequent apoptosis, downstream of nitric oxide.
  • We conclude that cytokine-induced nitric oxide production is both essential and sufficient for caspase activation and beta-cell death, and have identified Bcl-X(L) as a potential target to combat beta-cell apoptosis.
  • [MeSH-minor] Adenoviridae / genetics. Animals. Caspases / metabolism. Cell Line, Tumor. Enzyme Activation / drug effects. Insulinoma / pathology. Membrane Potential, Mitochondrial / drug effects. Microscopy, Fluorescence. Models, Biological. Nitric Oxide / biosynthesis. Nitric Oxide Synthase Type II / metabolism. Rats

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  • (PMID = 18081694.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Cytokines; 0 / bcl-X Protein; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC3822546
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61. Reinhardt P, Cybulski M, Miller SM, Ferrarotto C, Wilkins R, Deslauriers Y: Broad-spectrum sunscreens prevent the secretion of proinflammatory cytokines in human keratinocytes exposed to ultraviolet A and phototoxic lomefloxacin. Can J Physiol Pharmacol; 2006 Feb;84(2):221-6
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  • The present study measured the ability of sunscreens to prevent cytokine secretion in human keratinocytes following cotreatment of these cells with a known photoreactive drug and UVA.
  • NOR, owing to the absence of a fluorine atom in position 8, was non-phototoxic and used as a negative control.
  • Cell viability and the release of 3 cytokines were assessed, namely interleukin-1alpha (IL-1alpha), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-alpha).
  • To measure their ability to prevent cytokine secretion, various sunscreens were inserted between the UVA source and the cells.
  • Treatment with NOR, NOR plus UVA, or LOM had no effect on the cells.
  • LOM plus UVA, however, had an effect on cell viability and on cytokine secretion.
  • The release of TNF-alpha and IL-6 followed the same pattern at lower concentrations of LOM but peaked at 15 micromol/L and decreased at higher concentrations.
  • Sunscreens protected the cells from the effects of LOM plus UVA, as cell viability and levels of cytokines remained the same as in the control cells.
  • [MeSH-minor] Cell Survival / drug effects. Cell Survival / physiology. Cell Survival / radiation effects. Cells, Cultured. Dermatitis, Phototoxic / prevention & control. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Humans

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  • (PMID = 16900948.001).
  • [ISSN] 0008-4212
  • [Journal-full-title] Canadian journal of physiology and pharmacology
  • [ISO-abbreviation] Can. J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Cytokines; 0 / Fluoroquinolones; 0 / Inflammation Mediators; 0 / Quinolones; 0 / Sunscreening Agents; L6BR2WJD8V / lomefloxacin
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62. Amat M, Benjamim CF, Williams LM, Prats N, Terricabras E, Beleta J, Kunkel SL, Godessart N: Pharmacological blockade of CCR1 ameliorates murine arthritis and alters cytokine networks in vivo. Br J Pharmacol; 2006 Nov;149(6):666-75
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  • EXPERIMENTAL APPROACH: Compound J-113863 was tested in collagen-induced arthritis (CIA) and three models of acute inflammation; Staphylococcus enterotoxin B (SEB)-induced interleukin-2 (IL-2), delayed-type hypersensitivity (DTH) response, and lipopolysaccharide (LPS)-induced tumour necrosis factoralpha (TNFalpha) production.
  • KEY RESULTS: Treatment of arthritic mice with J-113863 improved paw inflammation and joint damage, and dramatically decreased cell infiltration into joints.
  • The compound did not inhibit mouse TNFalpha in vitro, but did induce a trend towards increased TNFalpha release in cells from synovial membranes of rheumatoid arthritis patients.
  • CONCLUSIONS AND IMPLICATIONS: CCR1 blockade improves the development of CIA, probably via inhibition of inflammatory cell recruitment.
  • [MeSH-major] Arthritis / drug therapy. Receptors, Chemokine / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism. Xanthenes / therapeutic use

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  • (PMID = 17016504.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0700128; United States / NHLBI NIH HHS / HL / HL074024; United States / NHLBI NIH HHS / HL / P50 HL074024; United States / NHLBI NIH HHS / HL / HL031237; United States / NHLBI NIH HHS / HL / R01 HL031237
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR1 protein, human; 0 / Ccr1 protein, mouse; 0 / Receptors, CCR1; 0 / Receptors, Chemokine; 0 / Tumor Necrosis Factor-alpha; 0 / UCB 35625; 0 / Xanthenes
  • [Other-IDs] NLM/ PMC2014657
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63. Parry S, Zhang J, Koi H, Arechavaleta-Velasco F, Elovitz MA: Transcytosis of Human immunodeficiency virus 1 across the placenta is enhanced by treatment with tumour necrosis factor alpha. J Gen Virol; 2006 Aug;87(Pt 8):2269-78
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  • [Title] Transcytosis of Human immunodeficiency virus 1 across the placenta is enhanced by treatment with tumour necrosis factor alpha.
  • It was hypothesized that the pro-inflammatory mediator tumour necrosis factor alpha (TNF-alpha), which promotes HIV-1 transmission across endothelial membranes, increases HIV-1 transmission across the placenta.
  • Flow cytometry and immunostaining studies were performed, which demonstrated that the HIV-1 receptors CD4, CCR5 and CXCR4 were not expressed by villous trophoblast cells.
  • Consequently, primary villous trophoblast cells were not infected with cell-free HIV-1 isolates, as measured by in situ PCR and quantitative PCR, but villous trophoblast cells were infected by HIV-1-infected peripheral blood mononuclear cells (PBMC).
  • HIV-1 from infected PBMC was rapidly transported across confluent transformed trophoblast cell monolayers by transcytosis, and TNF-alpha significantly upregulated transcytosis of HIV-1 across the trophoblast layer without disrupting cell viability or confluency.
  • Inhibitors of TNF-alpha (antibodies against TNF-alpha and TNF-alpha receptors) and an anti-inflammatory drug (tenidap) significantly reduced transcytosis rates.
  • It was concluded that the villous trophoblast is resistant to infection by cell-free HIV-1 but susceptible to transcytosis of HIV-1 from infected PBMC, and inflammatory mediators such as TNF-alpha may play a critical role in promoting maternal-fetal transmission of HIV-1.
  • [MeSH-major] HIV-1 / physiology. Leukocytes, Mononuclear / virology. Placenta / virology. Trophoblasts / virology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antigens, CD4 / analysis. Cell Line. Cells, Cultured. Flow Cytometry. HIV Core Protein p24 / analysis. HIV Infections / immunology. HIV Infections / transmission. Humans. Immunohistochemistry. Indoles / pharmacology. Polymerase Chain Reaction. RNA, Viral / analysis. Receptors, CCR5 / analysis. Receptors, CXCR4 / analysis

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  • (PMID = 16847123.001).
  • [ISSN] 0022-1317
  • [Journal-full-title] The Journal of general virology
  • [ISO-abbreviation] J. Gen. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antigens, CD4; 0 / HIV Core Protein p24; 0 / Indoles; 0 / RNA, Viral; 0 / Receptors, CCR5; 0 / Receptors, CXCR4; 0 / Tumor Necrosis Factor-alpha; 9K7CJ74ONH / tenidap
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64. Tsukamoto K, Huang YC, Dorsey WC, Carns B, Sharma V: Juxtacrine function of interleukin-15/interleukin-15 receptor system in tumour derived human B-cell lines. Clin Exp Immunol; 2006 Dec;146(3):559-66
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  • [Title] Juxtacrine function of interleukin-15/interleukin-15 receptor system in tumour derived human B-cell lines.
  • Interleukin-15 (IL-15) is a cytokine that induces proliferation and promotes cell survival of human T, B and NK cells.
  • IL-15 and interleukin-2 (IL-2) exhibit a similar spectrum of immune effects and share the IL-2 receptor (IL-2R) subunits IL-2Rbeta and IL-2Rgamma(c) for signalling in haematopoietic cells.
  • Furthermore, each cytokine has a private alpha receptor, namely IL-2Ralpha for IL-2 and IL-15Ralpha for IL-15, that functions in ligand binding.
  • Using reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) methods, the expression and secretion of IL-15 and IL-15Ralpha in tumour-derived B-cell lines were studied.
  • The results as presented in this study identify that IL-15 mRNA is predominantly expressed in EBV positive (EBV(+)) B-cell lines, although IL-15Ralpha is ubiquitously and constitutively expressed in all these B-cell lines.
  • Although no detectable levels of IL-15 protein secretion were observed in any of these cell lines, we were able to detect membrane-bound expression of IL-15 protein by FACS analysis in some cell lines.
  • [MeSH-major] B-Lymphocytes / immunology. Interleukin-15 / immunology. Lymphoma, B-Cell / immunology. Receptors, Interleukin-15 / immunology
  • [MeSH-minor] Cell Membrane / immunology. Enzyme-Linked Immunosorbent Assay / methods. Humans. Polymorphism, Genetic. RNA, Messenger / genetics. RNA, Neoplasm. Reverse Transcriptase Polymerase Chain Reaction / methods. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 17100778.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-15; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Interleukin-15
  • [Other-IDs] NLM/ PMC1810416
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65. Ruggieri R, Nahum AE: The impact of hypofractionation on simultaneous dose-boosting to hypoxic tumor subvolumes. Med Phys; 2006 Nov;33(11):4044-55
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  • [Title] The impact of hypofractionation on simultaneous dose-boosting to hypoxic tumor subvolumes.
  • In a previous study, the dependence of the therapeutic ratio on the number of fractions (n), including both acute and chronic hypoxia, was investigated for homogeneously irradiated tumors.
  • The present study further develops the model to include simultaneous dose-boosting to the hypoxic tumour subvolumes.
  • The acutely hypoxic (ah) tumor subvolume was partitioned into a large number (10(2)-10(3)) of oxygenation subvolumes, modelled through rectangular pO2(t) waves all with the same frequency and fractional time spent below the hypoxic threshold, but with randomly distributed phases.
  • Three quite different assumptions were considered for the effect of prolonged hypoxia on the radiosensitivity (alpha) of the chronically hypoxic (ch) clonogens, ranging from equal radiosensitivity to that of the ah-cells to an even greater radiosensitivity than that of the well-oxygenated (ox) cells.
  • The linear-quadratic model, including tumor repopulation, intertumor alpha-heterogeneity, and dependence of the oxygen enhancement ratio on the dose per fraction, was adopted for tumor control probability (TCP) computation.
  • For those 1(fr/d) x 5(d/w) schedules yielding 50% TCP with homogeneous irradiation (our reference benchmark), we estimated the gain in TCP and the corresponding NTD(L) from dose boosting only the ch-subvolume, both the ah- and the ch-subvolumes, or 50% of the pretreatment tumor volume without specific targeting to tumor hypoxia.
  • In conclusion, a strategy of dose-boosting tumor hypoxia, guided by nuclear medicine techniques that substantially map chronic hypoxia, is expected to yield optimal gains in TCP via severely hypofractionated delivery.
  • [MeSH-major] Apoptosis / radiation effects. Cell Survival / radiation effects. Models, Biological. Neoplasms / pathology. Neoplasms / physiopathology
  • [MeSH-minor] Animals. Cell Hypoxia / radiation effects. Cell Size / radiation effects. Computer Simulation. Dose Fractionation. Dose-Response Relationship, Radiation. Humans. Lethal Dose 50. Models, Statistical. Radiation Dosage

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  • (PMID = 17153384.001).
  • [ISSN] 0094-2405
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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66. Ni W, Zhang X, Bi H, Iteku J, Ji L, Sun C, Fang J, Tai G, Zhou Y, Zhao J: Preparation of a glucan from the roots of Rubus crataegifolius Bge. and its immunological activity. Carbohydr Res; 2009 Dec 14;344(18):2512-8
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  • [Title] Preparation of a glucan from the roots of Rubus crataegifolius Bge. and its immunological activity.
  • A water-soluble glucan (RCP-1) was prepared from the roots of Rubus crataegifolius Bge. by extraction with hot-water, deproteination by Sevag reagent, alpha-amylase treatment and ultrafiltration.
  • Fourier transform infra-red spectroscopy (FT-IR), nuclear magnetic resonance spectroscopy (NMR), methylation and periodate oxidation analyses indicated that RCP-1 was an alpha-d-glucan.
  • Its main chains were composed of (1-->4)- and (1-->6)-linked alpha-glucopyranosyls, and side chains were single alpha-glucopyranosyl residues attached to the O-6 of glucosyls in the main chains.
  • RCP-1 could increase both cytotoxic activity against B16 melanoma cells and the production of nitric oxide (NO) of macrophages in vitro.
  • Furthermore, in vivo bioassay tests indicated that RCP-1 could remarkably enhance T and B lymphocyte proliferations, augment the phagocytosis of macrophages and increase the tumour necrosis factor-alpha (TNF-alpha) levels in serum.
  • [MeSH-minor] Animals. Antineoplastic Agents / isolation & purification. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Glucose / analysis. Glucose / chemistry. Humans. Immunotherapy. Lymphocytes / drug effects. Macrophages, Peritoneal / immunology. Macrophages, Peritoneal / metabolism. Male. Melanoma / drug therapy. Melanoma / pathology. Mice. Mice, Inbred C57BL. Nitric Oxide / biosynthesis. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 19853841.001).
  • [ISSN] 1873-426X
  • [Journal-full-title] Carbohydrate research
  • [ISO-abbreviation] Carbohydr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucans; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; IY9XDZ35W2 / Glucose
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67. Lau KW, Tian YM, Raval RR, Ratcliffe PJ, Pugh CW: Target gene selectivity of hypoxia-inducible factor-alpha in renal cancer cells is conveyed by post-DNA-binding mechanisms. Br J Cancer; 2007 Apr 23;96(8):1284-92
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  • [Title] Target gene selectivity of hypoxia-inducible factor-alpha in renal cancer cells is conveyed by post-DNA-binding mechanisms.
  • Inactivation of the von Hippel-Lindau tumour suppressor in renal cell carcinoma (RCC) leads to failure of proteolytic regulation of the alpha subunits of hypoxia-inducible factor (HIF), constitutive upregulation of the HIF complex, and overexpression of HIF target genes.
  • However, recent studies have indicated that in this setting, upregulation of the closely related HIF-alpha isoforms, HIF-1alpha and HIF-2alpha, have contrasting effects on tumour growth, and activate distinct sets of target genes.
  • Using chromatin immunoprecipitation to probe binding to hypoxia response elements in vivo, and expression of chimaeric molecules bearing reciprocal domain exchanges between HIF-1alpha and HIF-2alpha molecules, we show that selective activation of HIF-alpha target gene expression is not dependent on selective DNA-binding at the target locus, but depends on non-equivalent C-terminal portions of these molecules.
  • Our data indicate that post-DNA binding mechanisms that are dissimilar for HIF-1alpha and HIF-2alpha determine target gene selectivity in RCC cells.
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors. Chromatin Immunoprecipitation. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / physiology

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  • (PMID = 17387348.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/127; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / endothelial PAS domain-containing protein 1; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2360163
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68. Lansbury L, Leonardi-Bee J, Perkins W, Goodacre T, Tweed JA, Bath-Hextall FJ: Interventions for non-metastatic squamous cell carcinoma of the skin. Cochrane Database Syst Rev; 2010 Apr 14;(4):CD007869
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  • [Title] Interventions for non-metastatic squamous cell carcinoma of the skin.
  • BACKGROUND: Squamous cell carcinoma (SCC) is the second most common skin cancer, and is becoming increasingly common around the world.
  • Surgical excision is the first line of treatment for most skin SCCs, although other forms of treatment are also used depending upon the nature and site of the tumour and individual participant factors.
  • OBJECTIVES: To assess the effects of treatments for primary non-metastatic squamous cell carcinoma of the skin.
  • This compared the time to recurrence in participants with aggressive skin SCC who were randomised to receive either adjuvant 13-cis-retinoic acid and interferon alpha after surgery with or without radiation treatment, or no adjuvant therapy after their initial treatment.
  • There was no significant difference in time to recurrence of tumour between the two groups (hazard ratio 1.08, 95% confidence intervals 0.43 to 2.72).Most studies identified from the searches were excluded as they were either uncontrolled case series, did not include participants with invasive primary SCC, or included only participants with recurrent or metastatic disease.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Skin Neoplasms / therapy

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  • (PMID = 20393962.001).
  • [ISSN] 1469-493X
  • [Journal-full-title] The Cochrane database of systematic reviews
  • [ISO-abbreviation] Cochrane Database Syst Rev
  • [Language] eng
  • [Grant] United Kingdom / Department of Health / / RP-PG-0407-10177
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 75
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69. Reuter S, Heinz A, Sieren M, Wiewrodt R, Gelfand EW, Stassen M, Buhl R, Taube C: Mast cell-derived tumour necrosis factor is essential for allergic airway disease. Eur Respir J; 2008 Apr;31(4):773-82
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  • [Title] Mast cell-derived tumour necrosis factor is essential for allergic airway disease.
  • Mast cells are thought to contribute to allergic airway disease.
  • However, the role of mast cell-produced mediators, such as tumour necrosis factor (TNF), for the development of allergic airway disease is unclear.
  • In order to define the role of mast cells in acute allergic airway disease two strains of mast cell-deficient mice (Kit(W/Wv) and Kit(W-sh/W-sh)) were studied.
  • Compared with their wild-type littermates, Kit(W/Wv) and Kit(W-sh/W-sh) mice developed significantly lower airway responsiveness to methacholine and less airway inflammation and goblet cell metaplasia, following sensitisation in the absence of adjuvant and airway challenge.
  • Transfer of bone marrow-derived mast cells (BMMCs) from wild-type mice to Kit(W-sh/W-sh) mice reconstituted both airway responsiveness and inflammation to levels similar to those in sensitised and challenged wild-type mice.
  • In contrast, sensitised Kit(W-sh/W-sh) mice reconstituted with BMMCs from TNF-deficient mice were still severely impaired in their ability to develop airway hyperresponsiveness, inflammation or goblet cell metaplasia following allergen challenge.
  • The present results demonstrate the significance of mast cells in the development of airway disease and highlight the importance of mast cell-derived tumour necrosis factor in these responses.
  • [MeSH-major] Asthma / immunology. Mast Cells / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Allergens / immunology. Animals. Bronchial Hyperreactivity / immunology. Disease Models, Animal. Goblet Cells / immunology. Goblet Cells / pathology. Immunization. Inflammation / pathology. Mice. Mice, Knockout

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  • (PMID = 18094004.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Allergens; 0 / Tumor Necrosis Factor-alpha
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70. Hozawa S, Nakamura T, Nakano M, Adachi M, Tanaka H, Takahashi Y, Tetsuya M, Miyata N, Soma H, Hibi T: Induction of matrix metalloproteinase-1 gene transcription by tumour necrosis factor alpha via the p50/p50 homodimer of nuclear factor-kappa B in activated human hepatic stellate cells. Liver Int; 2008 Dec;28(10):1418-25
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  • [Title] Induction of matrix metalloproteinase-1 gene transcription by tumour necrosis factor alpha via the p50/p50 homodimer of nuclear factor-kappa B in activated human hepatic stellate cells.
  • BACKGROUND/AIMS: Liver injury results in the activation of hepatic stellate cells (HSCs), which in turn produce matrix metalloproteinase (MMP) in response to pro-inflammatory cytokines for tissue remodelling.
  • This study explored the transcriptional induction of the MMP-1 gene by tumour necrosis factor-alpha (TNF-alpha) in HSCs.
  • Deletional or site-directed mutations were introduced into the promoter region and transiently transfected into LI90 cells to determine the cis-acting elements necessary for TNF-alpha inducibility.
  • Gel shift mobility assays were used to determine the transcriptional factors involved in the TNF-alpha responsiveness.
  • RESULTS: TNF-alpha upregulated MMP-1 protein and mRNA expression in a dose-dependent manner.
  • A time-course experiment revealed a rapid induction of MMP-1 mRNA expression after TNF-alpha treatment.
  • Mutation in a putative nuclear factor (NF)-kappaB-binding site at -2541 bp almost completely abolished the TNF-alpha response to MMP-1 gene-promoter activity, suggesting transcriptional regulation of MMP-1 expression by TNF-alpha via this site.
  • CONCLUSIONS: MMP-1 gene expression might be induced by TNF-alpha via the p50/p50 homodimer of NF-kappaB in activated human HSCs.
  • [MeSH-major] Enzyme Induction / physiology. Hepatic Stellate Cells / metabolism. Matrix Metalloproteinase 1 / metabolism. NF-kappa B p50 Subunit / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Blotting, Northern. Cell Line. Electrophoretic Mobility Shift Assay. Enzyme-Linked Immunosorbent Assay. Humans. Mutagenesis, Site-Directed

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  • (PMID = 19055644.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B p50 Subunit; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.7 / Matrix Metalloproteinase 1
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71. Morel S, Burnier L, Roatti A, Chassot A, Roth I, Sutter E, Galan K, Pfenniger A, Chanson M, Kwak BR: Unexpected role for the human Cx37 C1019T polymorphism in tumour cell proliferation. Carcinogenesis; 2010 Nov;31(11):1922-31
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  • [Title] Unexpected role for the human Cx37 C1019T polymorphism in tumour cell proliferation.
  • Connexins are a large family of proteins that form gap junction channels allowing exchange of ions and small metabolites between neighboring cells.
  • They have been implicated in pathological processes such as tumourigenesis in which they may act as tumour suppressors.
  • In this study, we have used communication-deficient HeLa and SK-HEP-1 cells transfected with Cx37-319S, Cx37-319P or empty vector.
  • We showed that the expression of Cx37-319P limited proliferation of HeLa and SK-HEP-1 cells, whereas Cx37-319S expression was without effect.
  • Using an in vitro kinase assay, we demonstrated phosphorylation of Cx37 CT by glycogen synthase kinase-3 (GSK-3), a kinase known to be implicated in cell proliferation and cancer.
  • This latter effect on GJIC involved the beta and not the alpha isoform of GSK-3.
  • In contrast, GSK-3 inhibitors were without effect on HeLa cells expressing Cx37-319S.
  • In conclusion, our data indicate functional effects of the Cx37 C1019T polymorphism on GJIC that might contribute to tumour cell growth.
  • [MeSH-major] Cell Proliferation. Connexins / genetics. Neoplasms / genetics. Neoplasms / pathology. Polymorphism, Genetic / physiology
  • [MeSH-minor] Blotting, Western. Cell Communication. Cell Cycle. Fluorescent Antibody Technique. Gap Junctions. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Glycogen Synthase Kinase 3 / metabolism. HeLa Cells. Humans. Phosphorylation. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20705954.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Connexins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / connexin 37; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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72. Mathsson L, Lampa J, Mullazehi M, Rönnelid J: Immune complexes from rheumatoid arthritis synovial fluid induce FcgammaRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-alpha by peripheral blood mononuclear cells. Arthritis Res Ther; 2006;8(3):R64
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  • [Title] Immune complexes from rheumatoid arthritis synovial fluid induce FcgammaRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-alpha by peripheral blood mononuclear cells.
  • Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors.
  • We investigated whether and how polyethylene glycol (PEG) precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells.
  • The precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-alpha levels were measured after 20 hours.
  • In separate cell culture experiments FcgammaRIIa and FcgammaRIII were blocked and monocytes were depleted or enriched.
  • In two separate investigations, we demonstrated a correlation between RF, PEG-precipitated IgG levels and induction of the proinflammatory cytokine TNF-alpha by PEG-precipitated SF ICs.
  • TNF-alpha levels induced by SF precipitates, but not serum precipitates, correlated with the number of swollen and tender joints.
  • Monocytes/macrophages were shown to be the main responder cells, and blockade of FcgammaRIIa, but not blockade of FcgammaRIII, inhibited TNF-alpha production in cultures stimulated with precipitated ICs.
  • Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG precipitates or with precipitate-induced TNF-alpha levels.
  • Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcgammaRIIa receptor might be ways to reduce IC-induced TNF-alpha production in the joints of seropositive RA patients.
  • [MeSH-major] Antigen-Antibody Complex / immunology. Antigens, CD / immunology. Arthritis, Rheumatoid / immunology. Leukocytes, Mononuclear / immunology. Receptors, IgG / immunology. Rheumatoid Factor / immunology. Synovial Fluid / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antirheumatic Agents / therapeutic use. Cells, Cultured. Cytokines / immunology. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Middle Aged. Reference Values

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  • (PMID = 16569263.001).
  • [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 / Antigen-Antibody Complex; 0 / Antigens, CD; 0 / Antirheumatic Agents; 0 / Cytokines; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG; 0 / Tumor Necrosis Factor-alpha; 9009-79-4 / Rheumatoid Factor
  • [Other-IDs] NLM/ PMC1526644
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73. Farah CS, Hu Y, Riminton S, Ashman RB: Distinct roles for interleukin-12p40 and tumour necrosis factor in resistance to oral candidiasis defined by gene-targeting. Oral Microbiol Immunol; 2006 Aug;21(4):252-5
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  • [Title] Distinct roles for interleukin-12p40 and tumour necrosis factor in resistance to oral candidiasis defined by gene-targeting.
  • Cell-mediated immunity is important for anti-Candida host defence in mucosal tissues.
  • Knockout mice used in this study included interleukin-4 (IL-4), IL-10, IL-12p40, interferon-gamma (IFN-gamma), and tumour necrosis factor (TNF).
  • The role of IL-12p40, and its relation to T-cell-mediated responses remain to be determined.
  • [MeSH-major] Candidiasis, Oral / immunology. Gene Targeting. Interleukin-12 / immunology. Protein Subunits / immunology. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Animals. Brain / microbiology. Candida albicans / immunology. Disease Susceptibility / immunology. Female. Fungemia / microbiology. Immunity, Cellular / immunology. Immunity, Innate / immunology. Interferon-gamma / immunology. Interleukin-10 / immunology. Interleukin-12 Subunit p40. Interleukin-4 / immunology. Kidney / microbiology. Mice. Mice, Knockout. Mouth Mucosa / microbiology. Specific Pathogen-Free Organisms. Th1 Cells / immunology. Th2 Cells / immunology

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  • (PMID = 16842510.001).
  • [ISSN] 0902-0055
  • [Journal-full-title] Oral microbiology and immunology
  • [ISO-abbreviation] Oral Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Interleukin-12 Subunit p40; 0 / Protein Subunits; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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74. Chowdhury P, Sacks SH, Sheerin NS: Toll-like receptors TLR2 and TLR4 initiate the innate immune response of the renal tubular epithelium to bacterial products. Clin Exp Immunol; 2006 Aug;145(2):346-56
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  • Renal tubular epithelial cells (TECs) respond diffusely to local infection, with the release of multiple cytokines, chemokines and other factors that are thought to orchestrate the cellular constituents of the innate immune response.
  • Cell monolayers were stimulated with lipopolysaccharide (LPS) and synthetic TLR2 and 4 agonists.
  • The innate immune response was quantified by measurement of the cytokines tumour necrosis factor (TNF)-alpha and KC (IL-8 homologue) in cell supernatants by enzyme-linked immunosorbent assay.
  • Cultured TECs grown from healthy mice produced the cytokines TNF-alpha and KC in response to stimulation by LPS and synthetic TLR2 and TLR4 agonists.
  • Cells lacking the respective TLRs had a reduced response to stimulation.
  • Finally, apical stimulation of these TLRs elicited basal surface secretion of TNF-alpha and KC (as well as the reverse), consistent with the biological response in vivo.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Animals. Antigens, CD14 / genetics. Cell Polarity. Cells, Cultured. Cytokines / immunology. Epithelial Cells / immunology. Gene Expression. Lipopolysaccharides. Lymphocyte Antigen 96 / genetics. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. Mice, Knockout. Myeloid Differentiation Factor 88. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16879256.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD14; 0 / Cytokines; 0 / Lipopolysaccharides; 0 / Lymphocyte Antigen 96; 0 / Myd88 protein, mouse; 0 / Myeloid Differentiation Factor 88; 0 / Tlr2 protein, mouse; 0 / Tlr4 protein, mouse; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 4
  • [Other-IDs] NLM/ PMC1809678
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75. Przybyło M, Lityńska A, Pocheć E: Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation. Biochimie; 2005 Feb;87(2):133-42
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  • [Title] Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation.
  • In tumour cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • This study used cell lines having very different behaviour in vivo: HCV29 non-malignant transitional epithelium and T24 bladder transitional cell carcinoma.
  • The functional role of carbohydrates was studied by treating these cells with swainsonine, an inhibitor of Golgi alpha-mannosidase II, and in vitro adhesion and migration assays.
  • The adhesion of swainsonine-treated HCV29 and T24 cells was increased on fibronectin and type IV collagen by 1.5- and 2-fold, respectively, whereas adhesion on laminin was virtually unchanged after swainsonine-treatment in HCV29 cells and was increased in T24 cells.
  • Swainsonine treatment reduced the rate of T24 cell migration by 20%.
  • We concluded that beta1-6 branched tri- and tetraantennary complex-type glycans have an important function in adhesion and migration in the studied cell lines.
  • [MeSH-major] Cell Movement. Epithelial Cells / metabolism. Polysaccharides / biosynthesis. Ureter / metabolism. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Glycosylation / drug effects. Humans. Male. Species Specificity. Swainsonine / pharmacology

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  • (PMID = 15760705.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Polysaccharides; RSY4RK37KQ / Swainsonine
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76. Calafat M, Larocca L, Roca V, Hauk V, Pregi N, Nesse A, Pérez Leirós C: Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands. Arthritis Res Ther; 2009;11(2):R53
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  • [Title] Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands.
  • INTRODUCTION: The role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction is currently explored in Sjogren's syndrome patients and in the nonobese diabetic (NOD) mouse model.
  • Our goal was to analyse the effect of TNF-alpha on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP.
  • METHODS: Acinar cells were isolated from submandibular glands of 16-week-old NOD females with salivary flow decline.
  • Apoptotic mediators and TNF-alpha receptor expression were assessed by immunoblotting and RT-PCR, caspase 3 activity was assessed by optical density at 405 nm with Ac-DEVD-pNA as a substrate and chromatin condensation by Hoechst stain.
  • They were evaluated in resting conditions and after a 3.5 or 6 hours of culture with TNF-alpha.
  • VIP effects in acinar cells were assessed at 100 nM in TNF-alpha-treated cultures and VIP receptor functional assays by radio immunoassay (cAMP) or enzymatic detection (amylase).
  • RESULTS: NOD acinar cells at 16 weeks present an increased expression of TNF-alpha receptor1 together with increased Bax, tumour protein 53-induced nuclear protein1alpha (TP53INP1alpha), caspase 3 activity and chromatin condensation.
  • Acini from NOD mice were more sensitive to TNF-alpha-induced increases of apoptotic mediators than control cells.
  • VIP inhibited TNF-alpha-induced apoptotic events through functional VPAC1 receptors coupled to the protein kinase A (PKA) signalling pathway.
  • CONCLUSIONS: Our results indicate that acinar cells isolated from submandibular glands of NOD mice with salivary dysfunction are more sensitive to apoptosis induced by TNF-alpha which could be prevented by VIP through a PKA-mediated pathway.
  • [MeSH-major] Apoptosis / physiology. Sjogren's Syndrome / metabolism. Submandibular Gland / metabolism. Tumor Necrosis Factor-alpha / metabolism. Vasoactive Intestinal Peptide / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cyclic AMP-Dependent Protein Kinases / metabolism. Disease Models, Animal. Female. Mice. Mice, Inbred BALB C. Mice, Inbred NOD. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / physiology

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  • (PMID = 19356238.001).
  • [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 / Tumor Necrosis Factor-alpha; 37221-79-7 / Vasoactive Intestinal Peptide; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC2688204
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77. Wellnitz O, Baumert A, Saudenowa M, Bruckmaier RM: Immune response of bovine milk somatic cells to endotoxin in healthy quarters with normal and very low cell counts. J Dairy Res; 2010 Nov;77(4):452-9
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  • [Title] Immune response of bovine milk somatic cells to endotoxin in healthy quarters with normal and very low cell counts.
  • Low somatic cell count (SCC) is a reliable indicator of high-quality milk free of pathogenic microorganisms.
  • The cells in milk are, however, predominantly immune cells with important immune functions.
  • To investigate the mammary immune competence of quarters with very low SCC, healthy udder quarters of cows with normal SCC of (40-100) x 10³ cells/ml and very low SCC of < 20 x 10³ cells/ml were challenged with lipopolysaccharide (LPS) from Escherichia coli.
  • In the first experiment, SCC and cell viability after a challenge with 50 ng of LPS/quarter was investigated.
  • In the second experiment, tumour necrosis factor α (TNF-α) concentration and lactate dehydrogenase (LDH) activity in milk, and mRNA expression of various innate immune factors in milk cells were measured after a challenge with 100 μg LPS/quarter.
  • The viability of cells and the LDH activity in milk increased in response to LPS challenge, however, without a difference between the groups.
  • The mRNA expression of IL-1β and IL-8 was increased in milk cells at 12 h after LPS challenge, whereas that of TNF-α and lactoferrin was not increased at the measured time points (12, 24 and 36 h after LPS challenge).
  • However, the immune competence of the cells themselves based on mRNA expression of TNF-α, IL-8, IL-1β, and lactoferrin, did not differ.
  • The results may indicate that very low SCC can impair the immune competence of udder quarters, because the immune response in udder quarters with lower SCC is less efficient as fewer cells contribute to the production of immunoregulators.
  • [MeSH-minor] Animals. Cattle. Cell Count / veterinary. Female. Interleukin-1beta / analysis. Interleukin-1beta / metabolism. Interleukin-8 / analysis. Interleukin-8 / metabolism. Lactoferrin / analysis. Lactoferrin / metabolism. Time Factors. Tumor Necrosis Factor-alpha / analysis. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20822558.001).
  • [ISSN] 1469-7629
  • [Journal-full-title] The Journal of dairy research
  • [ISO-abbreviation] J. Dairy Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Interleukin-8; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; EC 3.4.21.- / Lactoferrin
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78. Pavan B, Biondi C, Dalpiaz A: Nuclear retinoic acid receptor beta as a tool in chemoprevention trials. Curr Med Chem; 2006;13(29):3553-63
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  • They play this role as ligands of the RAR and RXR nuclear retinoic acid receptors, including the RA receptor isoforms alpha, beta, and gamma.
  • Among these target genes, the RARbeta gene is of great interest, being able to encode a potential tumour suppressor.
  • It should be emphasized that most breast carcinomas and breast cancer cell lines show loss or down-regulation of RARbeta receptor expression, whereas RARalpha and gamma, as well as retinoid X receptors, appear to be variably expressed in both normal and tumour cells.
  • It is also interesting to note that basal and RA-induced RARbeta mRNA levels tend to increase with senescence of normal cells.
  • This information provides further support for the hypothesis that genetic events involved in cellular senescence may also play a significant role in tumour suppression in humans.

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  • (PMID = 17168722.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta
  • [Number-of-references] 72
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79. McNulty J, Nair JJ, Codina C, Bastida J, Pandey S, Gerasimoff J, Griffin C: Selective apoptosis-inducing activity of crinum-type Amaryllidaceae alkaloids. Phytochemistry; 2007 Apr;68(7):1068-74
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  • Biological screening indicated crinamine 4 and haemanthamine 9 to be potent inducers of apoptosis in tumour cells at micromolar concentrations.
  • Structure-activity relationships demonstrated the requirement for both an alpha-C2 bridge and a free hydroxyl at the C-11 position as pharmacophoric requirements for this activity.
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / chemical synthesis. Antineoplastic Agents, Phytogenic / chemistry. Antineoplastic Agents, Phytogenic / isolation & purification. Antineoplastic Agents, Phytogenic / pharmacology. Cell Line. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Molecular Structure

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  • (PMID = 17331551.001).
  • [ISSN] 0031-9422
  • [Journal-full-title] Phytochemistry
  • [ISO-abbreviation] Phytochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amaryllidaceae Alkaloids; 0 / Antineoplastic Agents, Phytogenic; 639-41-8 / crinamine
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80. Jongbloed SL, Lebre MC, Fraser AR, Gracie JA, Sturrock RD, Tak PP, McInnes IB: Enumeration and phenotypical analysis of distinct dendritic cell subsets in psoriatic arthritis and rheumatoid arthritis. Arthritis Res Ther; 2006;8(1):R15
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  • [Title] Enumeration and phenotypical analysis of distinct dendritic cell subsets in psoriatic arthritis and rheumatoid arthritis.
  • Dendritic cells (DCs) comprise heterogeneous subsets of professional antigen-presenting cells, linking innate and adaptive immunity.
  • Functional analysis revealed that both SF DC subsets matured following toll-like receptor stimulation. pDCs from PB and SF produced interferon alpha and tumour necrosis factor alpha on TLR9 stimulation, but only SF pDCs produced IL-10.
  • Similarly, mDCs from PB and SF produced similar tumour necrosis factor alpha levels to TLR2 agonism, whereas SF mDCs produced more IL-10 than PB controls.
  • [MeSH-major] Arthritis, Psoriatic / immunology. Arthritis, Rheumatoid / immunology. Cytokines / blood. Dendritic Cells / immunology


81. Oremek GM, Sauer-Eppel H, Bruzdziak TH: Value of tumour and inflammatory markers in lung cancer. Anticancer Res; 2007 Jul-Aug;27(4A):1911-5
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  • [Title] Value of tumour and inflammatory markers in lung cancer.
  • The aim of this study was to evaluate the individual diagnostic utility of tumour and inflammatory markers in patients with different pulmonary diseases.
  • The usefulness of neuron-specific enolase (NSE), carcino-embryonic antigen (CEA), serum pro-gastrin releasing peptide (ProGRP) and CYFRA 21-1, as tumour markers, and C-reactive protein (CRP) and tumour necrosis factor-alpha (TNFalpha) as inflammatory markers for diagnosis, treatment and monitoring of patients with different pulmonary afflictions was investigated.
  • Moreover, serum marker levels were analyzed in 139 patients with different pulmonary malignancies: 29 patients with adenocarcinoma, 30 patients with squamous cell carcinoma, 80 patients with small cell lung cancer (SCLC).
  • All tumour markers showed significantly elevated values in malignant diseases.
  • In conclusion, when serum tumour markers are abnormally elevated in patients with lung cancer, CEA, CYFRA 21-1, NSE and ProGRP are useful clinical markers, good indicators of disease extent and may have important prognostic value.
  • [MeSH-major] Biomarkers, Tumor / blood. Inflammation / blood. Lung Neoplasms / diagnosis
  • [MeSH-minor] Antigens, Neoplasm / blood. Area Under Curve. C-Reactive Protein / analysis. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Small Cell / blood. Carcinoma, Small Cell / diagnosis. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / diagnosis. Humans. Immunoassay. Keratin-19. Keratins / blood. Lung Diseases / blood. Lung Diseases / diagnosis. Peptide Fragments / blood. Peptides / blood. Phosphopyruvate Hydratase / blood. ROC Curve. Recombinant Proteins / blood. Sensitivity and Specificity. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17649794.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / antigen CYFRA21.1; 0 / pro-gastrin-releasing peptide (31-98); 68238-35-7 / Keratins; 9007-41-4 / C-Reactive Protein; EC 4.2.1.11 / Phosphopyruvate Hydratase
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82. Nee L, Tuite N, Ryan MP, McMorrow T: TNF-alpha and IL-1 beta-mediated regulation of MMP-9 and TIMP-1 in human glomerular mesangial cells. Nephron Exp Nephrol; 2007;107(2):e73-86
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  • [Title] TNF-alpha and IL-1 beta-mediated regulation of MMP-9 and TIMP-1 in human glomerular mesangial cells.
  • BACKGROUND: Renal cells such as mesangial cells are known to secrete metalloproteinases that are capable of degrading the constituents of the glomerular basement membrane (GBM).
  • Disruption of the GBM via cytokine-induced alterations in matrixmetalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) may be an important mechanism in the renal disease process.
  • In renal disease, both resident renal cells and infiltrating immune cells are capable of secreting pro-inflammatory cytokines including tumour necrosing factor-alpha (TNFalpha) and interleukin-1 beta (IL-1 beta).
  • In this study, we examine the potential of these cytokines to alter levels of MMPs and TIMPs in human mesangial cells.
  • METHODS: The T-HMC human mesangial cell line was cultured in RPMI 1640 containing 5% serum.
  • Cells at confluency were serum starved for 24 h prior to exposure to TNF-alpha (0.1-100 ng/ml) or IL-1 beta (0.1-100 ng/ml) or a combination of both for 48 h.
  • RESULTS: TNF-alpha but not IL-1 beta resulted in a dose-dependent increase in the latent form of MMP-9 and a decrease in TIMP-1 production.
  • Co-treatment with IL-1 beta had no effect on the induction of MMP-9 but increased the inhibition of TIMP-1 in the presence of TNF-alpha.
  • Inhibition of PKC provided evidence of the importance of this pathway in mediating the TNF-alpha-induced suppression of TIMP-1.
  • Activation of the ERK 1/2 MAPK mediated both the upregulation of MMP-9 and the inhibition of TIMP-1 following TNF-alpha treatment. p38 MAPK activation was also found to be involved in the TNF-alpha-stimulated MMP-9.
  • CONCLUSION: The cytokine TNF-alpha causes different effects on human mesangial MMP-9 and TIMP-1 expression which are mediated through the TNF-RI, and the different signalling pathways of PKC, ERK 1/2 and p38 MAPK.
  • This suggests an important role for pro-inflammatory cytokines in renal disease progression.
  • [MeSH-major] Interleukin-1beta / physiology. Matrix Metalloproteinase 9 / biosynthesis. Mesangial Cells / enzymology. Tissue Inhibitor of Metalloproteinase-1 / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Transformed. Dose-Response Relationship, Drug. Down-Regulation / physiology. HL-60 Cells. Humans. Receptors, Tumor Necrosis Factor, Type I / physiology. Signal Transduction / drug effects. Signal Transduction / physiology. Up-Regulation / physiology

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  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • (PMID = 17890880.001).
  • [ISSN] 1660-2129
  • [Journal-full-title] Nephron. Experimental nephrology
  • [ISO-abbreviation] Nephron Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.35 / Matrix Metalloproteinase 9
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83. Tang Y, Xu X, Song H, Yang S, Shi S, Wei J, Pan B, Zhao F, Liao C, Luo C: Early diagnostic and prognostic significance of a specific Th1/Th2 cytokine pattern in children with haemophagocytic syndrome. Br J Haematol; 2008 Oct;143(1):84-91
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  • [Title] Early diagnostic and prognostic significance of a specific Th1/Th2 cytokine pattern in children with haemophagocytic syndrome.
  • The haemophagocytic syndrome (HPS) is a rare but frequently fatal disorder of immune regulation caused by hypercytokinemia.
  • Using cytometric bead array technique, the serum T-helper cell type 1 (Th1) and 2 (Th2) cytokines including interferon-gamma (IFN-gamma), tumour necrosis factor (TNF), interleukin (IL)-10, IL-6, IL-4 and IL-2 were determined in 24 children with de novo HPS and 87 children as control.
  • [MeSH-major] Cytokines / blood. Lymphohistiocytosis, Hemophagocytic / diagnosis. Th1 Cells / immunology. Th2 Cells / immunology
  • [MeSH-minor] Adolescent. Biomarkers / blood. Case-Control Studies. Chi-Square Distribution. Child. Child, Preschool. Female. Humans. Infant. Interferon-gamma / immunology. Interleukin-10 / immunology. Interleukin-2 / immunology. Interleukin-4 / immunology. Interleukin-6 / immunology. Kaplan-Meier Estimate. Male. Prognosis. Survival Analysis. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18673367.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 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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84. Lau YS, Adamopoulos IE, Sabokbar A, Giele H, Gibbons CL, Athanasou NA: Cellular and humoral mechanisms of osteoclast formation in Ewing's sarcoma. Br J Cancer; 2007 Jun 4;96(11):1716-22
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  • Cellular mechanisms that account for tumour osteolysis associated with Ewing's sarcoma are uncertain.
  • Osteoclasts are marrow-derived multinucleated cells (MNCs) that effect tumour osteolysis.
  • In this study, our aim has been to determine whether tumour-associated macrophages (TAMs) isolated from Ewing's sarcoma are capable of differentiating into osteoclasts and to characterise the cellular and humoral mechanisms whereby this occurs.
  • Tumour-associated macrophages were isolated from two Ewing's sarcomas and cultured on both coverslips and dentine slices for up to 21 days with soluble RANKL and macrophage colony stimulating factor (M-CSF).
  • Both Ewing's sarcoma-derived fibroblasts and some bone stromal cells expressed RANKL and supported osteoclast formation by a contact-dependent mechanism.
  • We also found that osteoclast differentiation occurred when Ewing's TAMs were cultured with tumour necrosis factor (TNF)-alpha in the presence of M-CSF and that TC71 Ewing's sarcoma cells stimulated osteoclast formation through the release of a soluble factor, the action of which was abolished by an antibody to TNF-alpha.
  • These results indicate that TAMs in Ewing's sarcoma are capable of osteoclast differentiation by both RANKL-dependent and TNF-alpha-dependent mechanisms and that Ewing's sarcoma cells produce osteoclastogenic factor(s).
  • [MeSH-minor] Adolescent. Adult. Aged. Bone Resorption / pathology. Bone and Bones / cytology. Bone and Bones / pathology. Cell Differentiation. Female. Humans. Macrophages / physiology. Male. Middle Aged. Osteoprotegerin / metabolism. Osteoprotegerin / pharmacology. RANK Ligand / metabolism. RANK Ligand / pharmacology. Stromal Cells / cytology. Stromal Cells / pathology. TNF-Related Apoptosis-Inducing Ligand / metabolism. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 17533390.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF11B protein, human; 0 / TNFSF10 protein, human; 0 / TNFSF11 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2359921
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85. Waterston AM, Gumbrell L, Bratt T, Waller S, Gustav-Aspland J, L'hermenier C, Bellenger K, Campbell M, Powles T, Highley M, Bower M, Mouritsen S, Feldmann M, Coombes RC: Phase I study of TNFalpha AutoVaccIne in patients with metastatic cancer. Cancer Immunol Immunother; 2005 Sep;54(9):848-57
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  • We evaluated the safety and immunogencity of a novel vaccine directed against autologous TNFalpha in a Phase I fixed dose escalation trial.
  • The vaccine consisted of two recombinant TNFalpha proteins, with specific peptides replaced by foreign immunodominant T cell epitopes from tetanus toxoid.
  • Secondary objectives were improvements in body weight and tumour response.
  • Eleven patients (33%) had mild grade1/2 injection site reactions at the higher doses.
  • However, since the antibodies were only able to cross-react with partly denatured TNFalpha, evaluation of safety and tumour responses to the TNFalpha vaccine was compromised.
  • [MeSH-major] Cancer Vaccines / immunology. Epitopes, T-Lymphocyte / immunology. Immunodominant Epitopes / immunology. Immunoglobulin G / blood. Tetanus Toxoid / immunology. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 15754205.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Epitopes, T-Lymphocyte; 0 / Immunodominant Epitopes; 0 / Immunoglobulin G; 0 / Recombinant Proteins; 0 / Tetanus Toxoid; 0 / Tumor Necrosis Factor-alpha
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91. Plater-Zyberk C, Joosten LA, Helsen MM, Hepp J, Baeuerle PA, van den Berg WB: GM-CSF neutralisation suppresses inflammation and protects cartilage in acute streptococcal cell wall arthritis of mice. Ann Rheum Dis; 2007 Apr;66(4):452-7
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  • [Title] GM-CSF neutralisation suppresses inflammation and protects cartilage in acute streptococcal cell wall arthritis of mice.
  • We have investigated the therapeutic effect of GM-CSF neutralisation in the streptococcal cell wall (SCW) arthritis model in mice.
  • In this model, the pathogenic contribution of tumour necrosis factor (TNF)alpha is minor and is expressed only on joint swelling, whereas cartilage proteoglycan depletion is independent of this cytokine.
  • Treatments (mAb 22E9 at 300, 100, 30 microg; or Enbrel 300 microg) were given twice intraperitoneally 2 h before and 3 days after disease induction.
  • CONCLUSIONS: Our findings show a pathogenic role for GM-CSF in this arthritis model, support the therapeutic potential of neutralising this cytokine, and may indicate therapeutic activity of an anti-GM-CSF mAb in TNFalpha-independent disease situations.
  • [MeSH-minor] Acute Disease. Animals. Cartilage, Articular / metabolism. Cell Wall / immunology. Dose-Response Relationship, Immunologic. Interleukin-1beta / biosynthesis. Male. Mice. Mice, Inbred C57BL. Proteoglycans / metabolism. Streptococcus pyogenes / immunology. Synovial Membrane / pathology

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  • (PMID = 17020908.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Interleukin-1beta; 0 / Proteoglycans; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC1856054
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92. Majumder N, Bhattacharjee S, Bhattacharyya Majumdar S, Dey R, Guha P, Pal NK, Majumdar S: Restoration of impaired free radical generation and proinflammatory cytokines by MCP-1 in mycobacterial pathogenesis. Scand J Immunol; 2008 Apr;67(4):329-39
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  • Mycobacterium tuberculosis exerts its pathogenic effects mainly via its cell wall glycolipid called Mannosylated Lipoarabinomannan (Man-LAM), which subverts the cellular inflammatory responses by the suppression of superoxide anion generation in earlier hours, and nitric oxide (NO) generation at later hours of pathogenic invasion.
  • In this paper, we have shown the prophylactic effect of C-C chemokines, both in vitro and in vivo.
  • Exogenous administration of C-C chemokines, particularly monocyte chemoattractant protein (MCP)-1, led to the induction of superoxide anion generation via the restoration of impaired protein kinase C (PKC) signalling in Man-LAM-treated macrophages.
  • Monocyte chemoattractant protein-1 could also potently induce NO generation by upregulation of the proinflammatory cytokines tumour necrosis factor-alpha and interleukin-12 from Man-LAM-treated macrophages accompanied by inhibition of anti-inflammatory responses.
  • [MeSH-minor] Animals. Antigens, Bacterial / pharmacology. Chemokine CCL3 / genetics. Colony Count, Microbial. Interleukin-12 / metabolism. Lipopolysaccharides / pharmacology. Lung / microbiology. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / immunology. Macrophages, Peritoneal / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Nitric Oxide / metabolism. Protein Kinases / metabolism. Recombinant Proteins / pharmacology. Signal Transduction / drug effects. Spleen / microbiology. Superoxides / metabolism. Tumor Necrosis Factor-alpha / metabolism. Virulence

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  • (PMID = 18282229.001).
  • [ISSN] 1365-3083
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Chemokine CCL3; 0 / Lipopolysaccharides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / lipoarabinomannan; 11062-77-4 / Superoxides; 187348-17-0 / Interleukin-12; 31C4KY9ESH / Nitric Oxide; EC 2.7.- / Protein Kinases
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93. Simons PJ, van den Pangaart PS, Aerts JM, Boon L: Pro-inflammatory delipidizing cytokines reduce adiponectin secretion from human adipocytes without affecting adiponectin oligomerization. J Endocrinol; 2007 Feb;192(2):289-99
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  • Therefore, we investigated the effect of long-term exposure of tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1beta, and interferon (IFN)-gamma on total insulin-sensitizing adiponectin secretion and adiponectin complex formation from human adipocytes.
  • The present study demonstrates that TNF-alpha, IL-1beta, and IFN-gamma dose and time dependently suppressed total adiponectin secretion within 7 days (60, 70, and 35% reduction respectively).
  • Despite this reduction of lipid-laden adipocytes, TNF-alpha, IL-6/sIL-6R, and IL-1beta stimulated leptin release.
  • Furthermore, delipidizing adipocytes and preadipocytes are active leptin producers when stimulated by TNF-alpha, IL-6/sIL-6R, and IL-1beta.
  • [MeSH-minor] Adult. Analysis of Variance. Azo Compounds. Cell Proliferation. Cells, Cultured. Coloring Agents. Depression, Chemical. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay / methods. Female. Humans. Insulin Resistance. Interferon-gamma / pharmacology. Interleukin-1beta / pharmacology. Interleukin-6 / pharmacology. Leptin / secretion. Lipid Metabolism. Middle Aged. Protein Isoforms / metabolism. Receptors, Interleukin-6 / metabolism. Subcutaneous Fat. Time Factors. Tumor Necrosis Factor-alpha / pharmacology

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  • [ErratumIn] J Endocrinol. 2007 Mar;192(3):683
  • (PMID = 17283229.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Azo Compounds; 0 / Coloring Agents; 0 / Cytokines; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Leptin; 0 / Protein Isoforms; 0 / Receptors, Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 1320-06-5 / oil red O; 82115-62-6 / Interferon-gamma
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94. Tull SP, Yates CM, Maskrey BH, O'Donnell VB, Madden J, Grimble RF, Calder PC, Nash GB, Rainger GE: Omega-3 Fatty acids and inflammation: novel interactions reveal a new step in neutrophil recruitment. PLoS Biol; 2009 Aug;7(8):e1000177
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  • Inflammation is a physiological response to tissue trauma or infection, but leukocytes, which are the effector cells of the inflammatory process, have powerful tissue remodelling capabilities.
  • In this process, peptide agonists of the chemokine family are assumed to provide a chemotactic stimulus capable of supporting the migration of neutrophils across vascular endothelial cells, through the basement membrane of the vessel wall, and out into the tissue stroma.
  • Here, we show that, although an initial chemokine stimulus is essential for the recruitment of flowing neutrophils by endothelial cells stimulated with the inflammatory cytokine tumour necrosis factor-alpha, transit of the endothelial monolayer is regulated by an additional and downstream stimulus.
  • This alternative series eicosanoid inhibited the migration of neutrophils across endothelial cells by antagonising the PGD(2) receptor.
  • Here, we describe a new step in the neutrophil recruitment process that relies upon a lipid-mediated signal to regulate the migration of neutrophils across endothelial cells.
  • PGD(2) signalling is subordinate to the chemokine-mediated activation of neutrophils, but without the sequential delivery of this signal, neutrophils fail to penetrate the endothelial cell monolayer.
  • [MeSH-minor] Cell Adhesion. Cells, Cultured. Chemokine CCL2 / genetics. Chemokine CXCL1 / genetics. Chemokine CXCL2 / genetics. Chromatography, Liquid. Cyclooxygenase Inhibitors. E-Selectin / metabolism. Eicosapentaenoic Acid / metabolism. Endothelial