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Dysregulation of tumour necrosis factor alpha (TNF alpha) production is thought to be important in rheumatoid arthritis. Since pentoxifylline and thalidomide inhibit endotoxin induced TNF production in vitro, these drugs were tested in an open study in rheumatoid arthritis patients to assess toxicity, the effect on TNF production, and the antiarthritic effects.
In 14 patients with stable angina pectoris we examined the effect of pentoxifyline (PTX) on oxidative metabolism of TNF-alpha-priming neutrophils. The control group consisted of 21 patients with stable angina pectoris without pentoxifylline administration. Blood samples for examination were taken from basilic vein (peripheral blood) and coronary sinus immediately before PTCA procedure. In PTX-group was found the significant decrease in spontaneous CL of TNF-alpha-priming neutrophils from coronary sinus blood (1231.0 +/- 119.4 mV x min), in comparison to the control group (1374 +/- 124.4 mV x min). In PTX-group was found the significant decrease in fMLP stimulated CL of TNF-alpha-priming neutrophils from peripheral blood (4219.0 +/- 707.2 mV x min) and coronary sinus blood (4322.0 +/- 664.4 mV x min), in comparison to the control group (5248.0 +/- 595.8 mV x min and 4973.0 +/- 536.5 mV x min; respectively). There were no differences between both groups in PMA stimulated CL of TNF-alpha-priming neutrophils.
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Prescribers should always seek a history of intolerance to caffeine and related compounds prior to use of pentoxifylline, as severe life threatening reactions can occur.
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Two reviewers independently applied the inclusion criteria. Trial quality was assessed.
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C3Hf/Sed/Kam mice were given midbrain or whole-body irradiation. Cerebral expression of interleukins (IL-1 alpha, IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6), interferon (IFN-gamma), tumor necrosis factors (TNF-alpha and TNF-beta), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthetase (iNOS), von Willebrand factor (vWF), alpha 1-antichymotrypsin (EB22/5.3), and glial fibrillary acidic protein (GFAP) was measured at various times after various radiation doses by ribonuclease (RNase) protection assay. The effects of dexamethasone or pentoxifylline treatment of mice on radiation-induced gene expression were also examined.
The aim of this study was to determine the effect of pentoxifylline (PTX) on angiogenesis and the healing of a critical-sized segmental defect of the radius diaphysis in a rat model, using radiological and histological grading systems.
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Pentoxifylline (PTX) has potential usefulness in HIV-seropositive patients due to its beneficial effects on renal function, its inhibitory effects on tumor necrosis factor alpha, and its vascular effects on microcirculatory disturbances. The present study prospectively evaluated the effects of multiple oral doses of PTX (400 mg three times daily for 12 weeks) on renal function in 11 HIV-seropositive patients compared with 14 control patients. Four of these patients had HIV-associated nephropathy, manifested by high urinary microalbumin outputs (72 +/- 56 micrograms/min; mean +/- SD). Ambulatory 24-h urine collections were analyzed for creatinine, electrolytes, and immunological markers at weekly intervals for 12 weeks. Urine flow rates diminished to one-half baseline values by week 12; changes were related to both time and treatment sequences. There were significant decreases in creatinine clearances and electrolyte excretion rates over the study period that were not associated with treatment regimens. No differences were found in fractional electrolyte, uric acid, microalbumin, and neopterin excretion rates either between or within groups. One subject with high microalbumin excretion rates had a significant drop over the 12 weeks (133 to 4 micrograms/min); the other 3 subjects had similar or elevated microalbumin outputs by the end of the study. Although well tolerated, therapeutic doses of PTX did not significantly affect renal function in HIV-seropositive patients.
In the Per Protocol Set (PPS), PWT of the intervention group increased 1.6±1.6 minutes after treatment (p<0.05). With PLC treatment, CT was significantly decreased in the treatment group. ABI was increased in both treatment and control groups. However, no statistical significance was found. In the Safety Analysis Set (SS), there were 110 adverse events during the course of the study (67 in PLC group vs. 43 in control group). There were two serious adverse events in the PLC group and four in the placebo group. All of the SAEs were assessed as unrelated to the study drug which indicated that PLC was well-tolerated in PAD patients.
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This in vitro study was designed to examine changes of red cell microrheological parameters (red cell aggregation and their suspension viscosity) after cell incubation with some drugs having phosphodiesterase (PDE) inhibitory activity (pentoxifylline - 25.0 microg/ml; drotaverine - 10.0 microg/ml; vinpocetine - 5.0 microg/ml; papaverine - 10.0 microg/ml; caffeine - 25.0 microg/ml; 3-isobutyl-1-methylxanthine [IBMX] - 10.0 microg/ml). Concentrations of used drugs for in vitro red cell microrheology study were the similar with those which it could be possible in blood of patient after intravenous therapeutic infusion. Red blood cells were separated from the blood by centrifugation at 1400 g for 15 min and washed 3 times with phosphate buffered saline (PBS). The washed RBCs were then resuspended in PBS at a hematocrit of approximately 40%. In each of the research sessions these RBC suspensions were divided into two aliquots and exposed to: one of the drug at 37 degrees C for 15 min; remaining aliquot (red cell suspension with PBS) was kept at 37 degrees C for 15 min and served as the control. It was found that all of used drugs decreased red cell aggregation and their suspension viscosity significantly. Since IBMX and vinpocetine are the specific inhibitor PDE activity it might be suppose that cellular PDE is molecular target in RBCs for this class of drugs. The obtained data reveals evidence that drugs, acting as PDE inhibitors, might be considered as microrheologically positive remedies.
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The objective of this study was to determine the effect of nonspecific phosphodiesterase inhibition on transcription factor activation and tumor necrosis factor-alpha (TNF-alpha) production in lipopolysaccharide (LPS)-stimulated human mononuclear cells.
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The question whether progressive sensorineural hearing loss during childhood is the fateful course of a main illness has been discussed controversially over 60 years. No medicamentous therapy with satisfactory results has been described in the literature. The goal of this study was to determine whether an infusion therapy, developed for the treatment of sudden hearing loss in the elderly, can induce recovery after progression in sensorineural hearing loss during childhood.
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Ciprofloxacin works through interfering with replication and transcription of bacterial DNA, which leads to increased oxidative stress, and death of bacterial cells. Drugs with strong antioxidant such as tempol, melatonin and pentoxifylline might interfere with the antibacterial activity of ciprofloxacin. In the current study, the effect of these drugs on the cytotoxicity of ciprofloxacin was investigated against several reference bacteria. Standard bacterial strains included Escherichia coli ATCC 35218, Staphylococcus aureus ATCC29213, Pseudomonas aeruginosa ATCC 9027, Staphylococcus epidermidis ATCC 12228, Acinetobacter baumannii ATCC 17978, Proteus mirabilis ATCC 12459, Klebsiella pneumoniae ATCC 13883, methicillin-resistant Staphylococcus aureus (MRSA) (ATCC 43300), and Streptococcus pneumoniae (ATCC 25923). The antibacterial activity of ciprofloxacin with or without treatment of bacterial cells by tempol, melatonin or pentoxifylline was assessed using the disc diffusion method and by measuring the minimum inhibitory concentration (MIC) and zones of inhibition of bacterial growth. All of the tested bacterial strains were sensitive to ciprofloxacin. When treated with tempol, melatonin or pentoxifylline, all bacterial strains showed significantly smaller zones of inhibition and larger MIC values compared ciprofloxacin alone. In correlation, reactive oxygen species (ROS) generation induced by ciprofloxacin antibacterial action was diminished by treatment of bacterial cells with tempol, melatonin or pentoxifylline. In conclusion, results indicate the possible antagonistic properties for agents with antioxidant properties such as tempol, melatonin and pentoxifylline when they are used concurrently with flouroquinolones. This could be related to the ability of these agents to inhibit oxidative stress in bacterial cells.
Using guinea pigs, a study was conducted on the effects of KBT-3022, a new anti-platelet agent, on hemorheological properties in various tests including blood filterability, blood viscosity, shear stress-induced red blood cell (RBC) deformability and contents of ATP and 2,3-diphosphoglycerate (2,3-DPG). Oral administration of KBT-3022 at 1 and 10 mg/kg significantly increased blood filterability, and significantly reduced blood viscosity at 10 mg/kg without changing the hematocrit, plasma fibrinogen concentration or plasma viscosity. KBT-3022 (10 mg/kg, p.o.) improved RBC deformability in response to shear stress, which was evoked by passing the blood through a thin tube. This dose of KBT-3022 also increased the contents of ATP and 2,3-DPG in RBC. These findings indicate that KBT-3022 may reduce blood viscosity as a sequel to improvement of RBC deformability through direct action on RBC. The increase in the intracellular levels of ATP and 2,3-DPG was considered to be involved in this improvement of hemorheological properties. These hemorheological effects of KBT-3022 appear to be promising for the treatment of patients with ischemic vascular disease.
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Whole blood was incubated with HBSS, LPS (100 microg/mL), leukoreduced PRBC supernatant + LPS, or supernatant + LPS + PTX (2 mmol/L). TNF-alpha levels were measured by ELISA. MMP-9 was evaluated with zymography. Neutrophil CD66b expression was determined by flow cytometry in blood treated with HBSS, fMLP (1 micromol/L), supernatant + fMLP, or supernatant + fMLP + PTX.
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This study was conducted to determine whether pentoxifylline has an in vitro effect on sperm motion characteristics in normozoospermic men. The subjects of the study were 15 male volunteers. After the spermatozoa were washed with mBWW medium, the sperm suspension was divided into two aliquots: one was treated with 1 mg/ml pentoxifylline, the other was used as a control. The sperm motion characteristics were examined by an HT-M2030 at 30, 60, 120, 180, 240 and 300 min during continuous exposure to the drug. As results, pentoxifylline increased the curvilinear velocity and the lateral head displacement. However, it did not affect sperm motility, the straight line velocity. Pentoxifylline may improve sperm fertilizing ability by altering the characteristics of sperm motion, not by increasing the number of motile spermatozoa.
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Blood viscosity was measured using a cone-plate viscometer and whole blood filterability was determined by a filtration method. Cardiac index and portal venous inflow were measured using radioactive microspheres. Measurements were performed 30 min after double-blind administration of placebo or pentoxifylline (25 mg/kg, intravenously).
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It was found that the constructed SVR model fitted better to the release data than the MLR model (higher coefficients of determination, R( 2), lower prediction error sum of squares, narrower range of residuals, and lower mean relative error), outlining its advantages in handling complex nonlinear problems. Superimposed contour plots derived by using the SVR model and describing the effects of polymer and sodium alginate content on pentoxifylline release showed that formulation of optimal release profiles, according to United States Pharmacopeia limitations, could be located at drug : matrix ratio of 1 and sodium alginate content 25% w/w in the matrix-former.
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Pruritic papular eruption (PPE) of HIV/AIDS is a common manifestation of HIV infection. Unfortunately, treatments for the unremitting pruritus have yielded only partial relief.
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Serum levels of liver enzymes, blood ammonia and prothrombin time and the stage of hepatic encephalopathy were significantly improved in rats treated with dimethylsulfoxide or dimethylthiourea compared to the other treatment groups (p<0.001). Liver histology and the survival rate in these rats were not adversely affected by thioacetamide administration (p<0.001), while in all the other treatment groups those parameters were similar to control rats with fulminant hepatic failure. Furthermore, dimethylsulfoxide ameliorated liver damage and improved survival even when its administration was initiated 8 and 16 h after the first thioacetamide injection. The hepatic concentration of methanesulfinic acid, which is produced after direct interaction of dimethylsulfoxide with hydroxyl radicals, was increased five-fold in rats treated with thioacetamide+dimethylsulfoxide (p<0.001), suggesting a role for hydroxyl radical scavenging in the protection from fulminant hepatic failure in this model. In the group of thioacetamide-treated rats that were pretreated with L-NAME, liver enzymes, blood ammonia levels and the mortality rate were higher than in the control group, treated with thioacetamide only.
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A mature-onset diabetic patient who developed microangiopathic hemolytic anemia (MHA) is presented. Although numerous causes of hemolysis are reported in the literature, MHA is a rare complication of diabetes. The proposed mechanism of hemolytic anemia is thought to be related to the abnormal formation of cell membranes in the diabetic environment. The ratio of cholesterol to phospholipid in the core of the membrane is altered in diabetics; as a result, the red blood cell wall becomes rigid and nondeformable. The abnormal cells becomes disrupted as they circulate through the microangiopathic blood vessels. The mechanism of action of the antiplatelet agents is to enhance cell membrane compliance. With improved cell-wall compliance, one can expect a reduction in hemolysis, as occurred in our patient. The literature on diabetes mellitus-related microangiopathic hemolytic anemia is reviewed.
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The mechanism of the early stage of metastasis formation by sticky blood-born cancer cells is discussed. Abnormal platelet aggregation to circulating and lodged cancer cells, as well as alterations of blood coagulation and fibrinolysis play an important role. The reducing effect of several platelet aggregation inhibitors on cancer cell stickiness and tumor embolism mortality has been investigated in rats after intravenous transplantation of 1 X 10(6) Walker-256 carcinosarcoma cells. The tested substances diminished platelet aggregation to circulating cancer cells, leading to a dose-dependent inhibition of cancer cell lodgment to the endothelium. Furthermore, some of the substances prevented lethal pulmonary tumor cell embolism which was observed in 60% of the controls. These results are interpreted by assuming an inhibition of disseminated intravascular coagulation which occured after intravenous transplantation of Walker-256 carcinosarcoma. On this basis a clinical long-term study for metastasis prophylaxis was started more than 4 years ago with one of the tested substances, the dipyridamole derivative RA 233, in 40 patients with sarcoma or malignant lymphoma of the head and neck region. The provisional results obtained in matched pairs are discussed.
Events of the recent past have focused attention on the possibility of radiological (nuclear) terrorism and on the implications of such terrorist threats for radiation accident preparedness. This review discusses recent advances in the knowledge about how radiation injuries from such events might be treated pharmacologically, and the practical barriers to clinical utilization of these approaches.