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Results for “inflammatory factor”

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At least 127 records · Page 7Linked to original sources
PubMed2002

[Changes of inflammatory factors in patients with coronary artery disease during perioperation].

OBJECTIVE: To investigate the proinflammatory cytocine factors in patients with coronary artery disease by different treatments during perioperation. METHODS: TNF-alpha, IL-6, c-reactive protein (CRP) were measured in 37 patients with coronary artery disease (CAD) and 10 patients with mitral valve replacement (MVR, control group) before operation and aortic clamping or before coronary artery bypass grafting (CABG) in the patients with cardiopulmonary bypass, or before transmyocardial laser reperfusion (TMLR), when aortic declamping and 3, 6, 24 hours after operation. RESULTS: The level of proinflammatory factors increased more significantly after operation than before operation. TNF-alpha increased more significantly in the patients with CPB than in those without CPB after operation [(4.10 +/- 0.71) pg/ml vs. (1.34 +/- 0.29) pg/ml, P < 0.05)]. IL-6 was not the different among all groups after operation. CRP was higher in the CAD patients with CPB than in the control group after operation [(12.89 +/- 0.29) pg/ml vs. (12.00 +/- 0.31) pg/ml, P < 0.05]. CONCLUSION: Inflammatory response can be seen after operation in all CAD patients. In patients undergoing CABG without CPB or undergoing TMLR, the changes in flammatory response are milder than those in patients with CPB. Thus patients should undergo CABG without CPB if they are indicated.

Aged↗
PubMed1985

Successful tumour immunotherapy: possible role of antibodies to anti-inflammatory factors produced by neoplasms.

Phenol-saline tumour extracts, active in the immunotherapy of bovine ocular squamous cell carcinoma (BOSCC), were used to immunize mice. The immunized mice became resistant to the depression of delayed type hypersensitivity (DTH) reactions by products of BOSCC cells or cultured mouse or rat tumour cells. They also showed partial resistance to the growth of an unrelated tumour. Monoclonal antibodies to a type C retrovirus protein, p15E, also induced resistance to the depression of DTH by products of BOSCC and mouse tumours. It is suggested that successful immunotherapy of BOSCC is associated with the induction of resistance to anti-inflammatory or immunosuppressive tumour cell products, allowing the operation of host defences, and that these products share antigenic determinants with a retrovirus protein.

Animals↗
PubMed2006

[Effects of the inhalable particle (PM10) on secretion of inflammatory factors in human lung fibroblasts and mouse alveolar macrophage cell].

OBJECTIVE: To study the effects of PM10 and the concentrated culture suspension of RAW264.7 cells treated with PM10 on the secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-6(IL-6) and interleukin-8(IL-8) in the human lung fibroblasts( HLF). METHODS: PM10 were collected during heating period in the urban area of Beijing. HLF and mouse alveolar macrophage cell (RAW264.7) were used. The two ways of exposed cells to PM10 were used: (1) HLF were treated with the different concentration of PM10 for 24h. (2) HLF were stimulated by the added the suspension of RAW264.7 cell exposed to different concentrations of PM10. Cytotoxicity of PM10 was measured by MTT assay. The levels of inflammatory cytokines TNF-alpha, IL-6 and IL-8 were determined by the radioimmunity assay. RESULTS: After treated for 24h, PM10 showed the cytotoxicity in HLF and RAW264.7 cells, which was characterized by increase of the viability of cells at low concentration of PM10, and decrease at high doses. PM10 induced the secretion of TNF-alpha, IL-6 and IL-8 in HLF in a dose-dependent manner. The concentrated culture medium of RAW264.7 cells treated with PM10 also stimulated the secretion of TNF-alpha, IL-6 and IL-8 in HLF. CONCLUSION: PM10 is cytotoxic to HLF and RAW264.7 cells. PM10 induced the secretion of TNF-alpha, IL-6 and IL-8 in HLF. This effect was also observed by treatment of HLF with the concentrated culture medium of RAW264.7 cell exposed to PM10.

Air Pollutants↗
PubMed2006

Are inflammatory factors related to retinal vessel caliber? The Beaver Dam Eye Study.

OBJECTIVE: To examine the relationship of systemic markers of inflammation, endothelial dysfunction, and serum folate level to retinal vessel diameter. METHODS: Cross-sectional analyses were completed for data from a random sample of 396 persons aged 50 to 86 years who underwent a baseline examination from 1988 to 1990. Standardized protocols for blood collection and measurement of markers were used. Diameters of arterioles and venules were measured from digitized photographs. Standard univariate and multivariate analyses were performed. RESULTS: While controlling for age, smoking status, diabetes status, serum high-density lipoprotein cholesterol, and hematocrit, wider retinal venular diameters were associated with higher serum high-sensitivity C-reactive protein, interleukin 6, and amyloid A levels. While controlling for age, systolic and diastolic blood pressure, smoking, serum high-density lipoprotein cholesterol level, and gout, smaller arteriolar diameters were associated with higher serum amyloid A and lower serum albumin and folate levels but not high-sensitivity C-reactive protein or interleukin 6 levels. Levels of serum soluble intercellular adhesion molecule-1 and serum soluble E-selectin, markers of endothelial dysfunction, were not associated with retinal arteriolar or venular diameters. CONCLUSIONS: These data show an association of inflammatory markers with larger retinal venular diameter, suggesting that retinal venular caliber may be a marker of systemic inflammation.

Aged↗
PubMed1995

[Rheumatoid disorders in Crohn disease and ulcerative colitis. Dominance of non-inflammatory factors].

82 consecutive outpatients with Crohn's disease (n = 52) and ulcerative colitis (n = 30) were examined ambulatory. Rheumatic complaints, objective results and diagnosis were correlated to the activity of the underlying illness and the extent of the bowel affected. 61% of the examined patients complaint about rheumatic pains. In two thirds this could be attributed to noninflammatory causes (30% insertion tendinitis. 16% degenerative arthritis, 16% wrong carriage), which appeared to be independent of the activity and severity of the underlying disease. One fourth of the rheumatic complaints was caused by inflammation (21% arthritis, 5% sacroileitis). In these cases a dependency on the disease activity and the extent of the colon involvement could be found. No cause was found for 12% of the rheumatic complaints. In patients with ulcerative colitis suffering from arthritis a significant increase of disease activity (Rachmilewitz index) could be shown as compared to ulcerative colitis patients without arthritis (p < 0.02). For patients with Crohn's disease no significant correlation between arthritis and disease activity could be established. In these cases the occurrence of arthritis was associated with the colon involvement (Chi2 = 8.48). The data indicate the high frequency of rheumatic complaints in inflammatory bowel diseases due to noninflammatory causes.

Adolescent↗
PubMed2006

Relationship between soluble P-selectin and inflammatory factors (interleukin-6 and C-reactive protein) in colorectal cancer.

BACKGROUND: Platelets are an important element in the thrombotic process, inflammation and cancer progression. We tested the hypothesis that there is a relationship between platelet activation and inflammation in colorectal cancer patients (CRC). PATIENTS/METHODS: We measured soluble (s) P-selectin (marker of platelet activation), interleukin-6 (IL-6) and C-reactive protein (CRP) (indexes of inflammation) in 42 CRC patients and 38 healthy subjects. CRC patients were divided into two groups: A-24 patients in stages I and II; B-18 patients in stage III. Soluble P-selectin, Interleukin-6 concentration was measured using commercially available immunoenzymatic methods. High sensitivity C-reactive protein (RCRP) concentration was measured by a high sensitivity latex particle turbidimetric immunoassay. RESULTS: Soluble P-selectin, CRP and IL-6 levels were significantly increased as compared to the control group (p<0.001). Plasma levels of sP-selectin, CRP and IL-6 were higher in group B (with metastases) than in group A (without metastases) (p<0.001). CRC patients had a positive correlation between IL-6 and CRP (r=0.7638, p<0.01) and between sP-selectin and IL-6 (r=0.5633, p<0.03). CONCLUSION: We observed hyperactivation of blood platelets and inflammatory response in patients with colorectal cancer, also the inflammatory process and platelet activation progress along with colorectal cancer advancement. Our results seem to confirm the relationship of platelet activation with inflammatory response in colorectal cancer patients.

Aged↗
PubMed1975

Naturally occurring anti-inflammatory factors in the synovial fluids of patients with rheumatic disease and their possible mode of action.

Evidence has been shown that pathological synovial fluid contained a substance capable of stabilizing rat liver lysosomes which was partly inactivated by treatment with trypsin and by storage. Such synovial fluid also appeared to contain a substance which labilized lysosomes and which was more stable than the stabilizing substance. (2) The lysosomal stabilizing substance described above was nondialysable and migrated electrophoretically with the alpha and beta globulins to which class it has been tentatively ascribed. (3) Pathological synovial fluid contained proteases which were active at acid pH and at neutral pH. It also appeared to contain a substance capable of inhibiting these proteases. (4) Alpha2-Macroglobulin has been detected in pathogenic synovial fluid.

Alpha-Globulins↗
PubMed2003

Downregulation of a rheumatoid arthritis-related antigen (RA-A47) by ra-a47 antisense oligonucleotides induces inflammatory factors in chondrocytes.

Previously we have shown that the expression of RA-A47 (rheumatoid arthritis-related antigen) which is identical to HSP47, a collagen-binding chaperon, is downregulated in chondrocytes by tumor necrosis factor alpha (TNFalpha). RA-A47 was also found on the surface of chondrocytes where it is recognized as an antigen in the serum of rheumatoid arthritis (RA) patients. Its translocation to the cell surface from endoplasmic reticulum membrane where it is normally located was also enhanced by TNFalpha. To understand the significance of RA-A47 downregulation in chondrocytes independent from other effects of TNFalpha, we used an antisense oligonucleotide approach and investigated the effect of this treatment on the expression of molecules related to matrix degradation and production of growth factors for chondrocytic, endothelial, and synovial cells. Here we show that treatment of rabbit chondrocyes and human chondrosarcoma cells HCS-2/8 by ra-a47 antisense S-oligonucleotides significantly reduced the expression of ra-a47 both at mRNA and protein level. Interestingly, this TNFalpha-independent RA-A47 downregulation was associated with a strong induction of matrix metalloproteinase (MMP)-9 mRNA and inducible NO synthase (iNOS) mRNA. The induction of active-type MMP-9 was further detected by gelatin zymography. Under the same conditions, the release of basic fibroblast growth factor (bFGF) and connective tissue growth factor (CTGF) from HCS-2/8 cells into the conditioned medium (CM) was strongly enhanced. These effects were not a result of TNFalpha upregulation, since the ra-a47 antisense oligonucleotide treatment did not enhance TNFalpha synthesis. These observations indicate that downregulation of RA-A47 induces TNFalpha-independent cartilage-degrading pathways involving iNOS and MMP-9. Furthermore, the stimulation of bFGF and CTGF release from chondrocytes may stimulate the proliferation of adjacent endothelial and/or synovial cells.

Animals↗
PubMed1986

Fahr's syndrome: local inflammatory factors in the pathogenesis of calcification.

Three cases of Fahr's syndrome are described. All patients had disturbances of calcium metabolism and had had a meningoencephalitis in childhood. It is suggested that gliovascular changes, induced by cerebral inflammation, can later facilitate the occurrence of calcification of the striopallidodentate system when abnormality of calcium metabolism develops.

Adult↗
PubMed1987

Glucocorticoid-induced low molecular mass anti-inflammatory factors which do not inhibit phospholipase A2.

The peritoneal lavage fluid of dexamethasone (DXM)-pretreated rats was filtered through an Amicon YM-10 membrane (cutsize 10 kD). The retentate inhibited dextran oedema. Its 40 kD fraction (lipocortin) obtained by molecular sieving on Sephadex (SG)-75, suppressed carrageenin-induced foot swelling and phospholipase A2 (PLA2) activity, but it had no effect on the dextran response. The Amicon filtrate was chromatographed on SG-25 gel and yielded 6 and 2 kD fractions suppressing dextran and serotonin (5-HT) oedema but not carrageenin inflammation and PLA2 activity. These fractions may be active fragments of vasocortin, a glucocorticoid-induced mediator regulating vascular permeability.

Adrenalectomy↗