Home About us Contact
|
Home About us Contact | ||
|
|
||
Serum Tumor Necrosis Factor (serum + tumor_necrosis_factor)
Selected AbstractsPTHrP-independent hypercalcemia with increased proinflammatory cytokines and bone resorption in two children with CD19-negative precursor B acute lymphoblastic leukemiaPEDIATRIC BLOOD & CANCER, Issue 7 2007Hidetaka Niizuma MD Abstract Hypercalcemia in childhood acute lymphoblastic leukemia (ALL) is rare and occasionally associated with parathyroid hormone-related protein (PTHrP). However, the pathogenesis of PTHrP-independent hypercalcemia remains unclear. We report two children with precursor B ALL who had marked hypercalcemia (15.8 and 16.6 mg/dl, respectively) and disseminated osteolysis. Serum tumor necrosis factor-, (TNF-,) and IL-6 were markedly elevated, whereas 1,25(OH)2 vitamin D3, intact PTH and PTHrP were decreased or undetected. Analysis of urinary deoxypyridinoline (DPY) or bone biopsy of the osteolytic lesion showed an increased bone resorption, and administration of bisphosphonate improved the hypercalcemia. Patients had ALL with immunophenotype positive for CD10, CD34, and HLA-DR but negative for CD19 and obtained remission with chemotherapy. These findings suggest that increased osteoclastic bone resorption via stimulation with TNF-, and IL-6 may be mechanism causing PTHrP-independent hypercalcemia in some patients with precursor B ALL lacking CD19 expression. Pediatr Blood Cancer 2007;49:990,993. © 2006 Wiley-Liss, Inc. [source] Interleukin 6 alleviates hepatic steatosis and ischemia/reperfusion injury in mice with fatty liver diseaseHEPATOLOGY, Issue 4 2004Feng Hong Fatty liver, formerly associated predominantly with excessive alcohol intake, is now also recognized as a complication of obesity and an important precursor state to more severe forms of liver pathology including ischemia/reperfusion injury. No standard protocol for treating fatty liver exists at this time. We therefore examined the effects of 10 days of interleukin 6 (IL-6) injection in 3 murine models of fatty liver: leptin deficient ob/ob mice, ethanol-fed mice, and mice fed a high-fat diet. In all 3 models, IL-6 injection decreased steatosis and normalized serum aminotransferase. The beneficial effects of IL-6 treatment in vivo resulted in part from an increase in mitochondrial , oxidation of fatty acid and an increase in hepatic export of triglyceride and cholesterol. However, administration of IL-6 to isolated cultured steatotic hepatocytes failed to decrease lipid contents, suggesting that the beneficial effects of IL-6 in vivo do not result from its effects on hepatocytes alone. IL-6 treatment increased hepatic peroxisome proliferator-activated receptor (PPAR) , and decreased liver and serum tumor necrosis factor (TNF) ,. Finally, 10 days of treatment with IL-6 prevented the susceptibility of fatty livers to warm ischemia/reperfusion injury. In conclusion, long-term IL-6 administration ameliorates fatty livers and protects against warm ischemia/reperfusion fatty liver injury, suggesting the therapeutic potential of IL-6 in treating human fatty liver disease. Supplementary material for this article can be found on the Hepatology website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html). (HEPATOLOGY 2004;40:933,941.) [source] The effect of sildenafil, a phosphodiesterase-5 inhibitor, on acetic acid-induced colonic inflammation in the ratJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2009Sevgin Ozlem Iseri Abstract Background and Aim:, Sildenafil, a selective and potent inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase (PDE)5, has a relaxant effect on the smooth muscle cells of the arterioles supplying the human corpus cavernosum acting via nitric oxide (NO)-dependent mechanism. This study aimed to investigate the possible protective effect of sildenafil citrate on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Methods:, Colitis was induced by intrarectal administration of 1 mL of 5% acetic acid to Sprague-Dawley rats (200,250 g; n = 7,8/group). Control rats received an equal volume of saline intrarectally. In treatment groups, the rats were treated with either sildenafil citrate (5 mg/kg/day; subcutaneously) or saline for 3 days. After decapitation, distal colon was weighed and scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and oxidant production. Trunk blood was collected for the assessment of serum tumor necrosis factor (TNF)-, and interleukin (IL)-1, levels. Results:, In the colitis group, the colonic tissue was characterized by lesions, increased lipid peroxidation with a concomitant reduction in GSH content, increased MPO activity and oxidant production. Serum TNF-, and IL-1, levels were higher in the colitis group compared to control values. Sildenafil reversed these inflammatory parameters nearly back to control values. Conclusions:, Sildenafil citrate administration to rats with acetic acid-induced colitis seems to be beneficial via prevention of lipid peroxidation, oxidant generation, cytokine production and neutrophil accumulation. [source] Changes in serum concentrations of tumor necrosis factor , and adhesion molecules in normal pregnant women and those with pregnancy-induced hypertensionJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 6 2003Keiichi Matsubara Abstract Aim:, To study whether serum tumor necrosis factor , gene (TNF,) and adhesion molecule levels are indicators of the onset of pregnancy-induced hypertension (PIH), we compared levels of these molecules between normal pregnant women and PIH patients from the first to the third trimester. Methods:, We serially measured serum concentrations of TNF,, soluble intercellular adhesion molecule-1 (sICAM-1), soluble E-selectin (sE-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble P-selectin (sP-selectin) using enzyme immunoassay kits in 10 normal pregnant women and 10 pregnant women who developed PIH late in gestation. Results:, Serum TNF,, sICAM-1 and sE-selectin levels in PIH affected women were significantly higher from the first trimester compared with those in normal pregnancy. sVCAM-1 and sP-selectin levels were not significantly changed. Conclusion:, Serum TNF,, sE-selectin and sICAM-1 levels might be effective indicators of the onset of PIH. [source] Effects of inflammatory response on in vivo transgene expression by plasmid DNA in miceJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 8 2008Keiko Kako Abstract To examine the effects of inflammatory response to plasmid DNA (pDNA) on transgene expression, serum tumor necrosis factor-, (TNF-,) was measured after intravenous injection of pDNA or calf thymus DNA (CT DNA) in the naked or complexed form with cationic liposomes (lipoplex). pDNA with many CpG motifs induced TNF-, production regardless of the forms. No significant TNF-, production was detected when CT DNA or methylated pDNA was injected. Clodronate liposomes and dexamethasone were used to deplete phagocytes or to inhibit inflammatory responses, respectively. Transient depletion of phagocytes, such as liver Kupffer cells and splenic macrophages, by clodronate liposomes slightly altered the tissue distribution of 32P-pDNA lipoplex, but significantly reduced the TNF-, production and transgene expression. Dexamethasone significantly inhibited the initial transgene expression, but increased the duration of the expression slightly. Use of NF-,B activity-dependent plasmid vector suggested that the inhibition of NF-,B activation is involved in the reduced expression by these treatments. These findings indicate that tissue macrophages are closely involved in the CpG motif-dependent TNF-, production. It is also suggested that TNF-, activates NF-,B and increases transgene expression by pDNA having many NF-,B binding sites, but TNF-, also reduces transgene expression at later time periods, leading to short-term transgene expression. © 2007 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 97: 3074,3083, 2008 [source] Protective effects of Ginkgo biloba extract against mercury(II)-induced cardiovascular oxidative damage in ratsPHYTOTHERAPY RESEARCH, Issue 1 2007Tugba Tunali-Akbay Abstract This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) against Hg II-induced oxidative damage and also thromboplastic activity in the aorta and heart tissues. Wistar albino rats of either sex (200,250 g) were divided into four groups. Rats were injected intraperitoneally with (1) control (C) group: 0.9% NaCl; (2) EGb group: Ginkgo biloba extract (Abdi Ibrahim Pharmaceutical Company, Istanbul, Turkey) at a dose of 50 mg/kg/day; (3) Hg group: a single dose of 5 mg/kg mercuric chloride (HgCl2); and (4) Hg + EGb group: First day EGb at a dose of 50 mg/kg/day, i.p., 1 hour after HgCl2 (5 mg/kg) injection; following four days EGb at a dose 50 mg/kg/day, i.p. After decapitation of the rats, trunk blood was obtained and serum tumor necrosis factor- , (TNF- ,), lactate dehydrogenase (LDH) activity, and malondialdehyde (MDA) and glutathione (GSH) levels were analysed. In the aorta and heart tissues total protein, MDA, GSH levels and thromboplastic activity were determined. The results revealed that HgCl2 induced oxidative tissue damage, as evidenced by increases in MDA levels and decreased GSH levels both in serum and tissue samples. Thromboplastic activity was increased significantly following Hg administration, which verifies the cardiotoxic effects of HgCl2. Serum LDH and TNF- , were elevated in the Hg group compared with the control group. Since EGb treatment reversed these responses, it seems likely that Ginkgo biloba extract can protect the cardiovascular tissues against HgCl2 -induced oxidative damage. Copyright © 2006 John Wiley & Sons, Ltd. [source] Therapeutic Effects and Anti-inflammatory Mechanisms of Heparin on Acute Lung Injury in RabbitsACADEMIC EMERGENCY MEDICINE, Issue 7 2008Meitang Wang MD Abstract Objectives:, The objectives were to investigate the potential beneficial effects and molecular mechanisms of heparin and low-molecular-weight heparin (LMWH) on acute lung injury (ALI). Methods:, Forty-eight rabbits were randomized into four groups: normal control group (Group A), lipopolysaccharide (LPS) group (Group B), LPS + heparin group (Group C), and LPS + LMWH group (Group D). The rabbit ALI model was established by intravenous (IV) injection with LPS. Alveolar,arterial O2 difference (PA-aO2), serum tumor necrosis factor , (TNF-,), circulating p38 mitogen-activated protein kinase (p38 MAPK) levels, lung nuclear factor (NF)-,B levels, and lung dry/wet (D/W) ratio were measured, and the lung injury scores were calculated. Results:, Lipopolysaccharide caused significant increases in PA-aO2, serum TNF-,, expression of p38 MAPK in polymorphonuclear neutrophils (PMNs), the lung injury scores, and nuclear factor-,B (NF-,B) activity in the lung tissue and caused a decrease in lung D/W ratio. A positive linear correlation was found between p38 MAPK and TNF-, at 1, 2, 4, and 6 hours (r = 0.68, 0.92, 0.93, and 0.93, respectively) and between NF-,B and p38 MAPK and TNF-, at 6 hours (r = 0.94 and 0.83, respectively). IV heparin or LMWH given after LPS treatment attenuated these changes in inflammatory response, oxygenation, p38 MAPK expression, and NF-,B activation. Conclusions:, The anti-inflammatory mechanisms of heparin in ALI may be inhibiting p38 MAPK and NF-,B activities, and then TNF-, overexpression, thus alleviating the inflammatory reaction. [source] | ||||||||||