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The influence of stress on the structure of the gastric mucosal capillary network was investigated in an experimental model using scanning electron microscopy (SEM) to study corrosion casts of the gastric microvasculature. An index of microcirculatory patency was devised to improve the objectivity of SEM. Stress (mean score 42.4 +/- 4.7) severely disrupted the structure of the mucosal capillary network when compared with controls (mean 5.0 +/- 2.9) (P < 0.01). Disruption of the microvascular network was significantly reduced by pretreatment with allopurinol, cimetidine, and misoprostol, these groups having mean damage scores of 17.4 +/- 5.8, 21.2 +/- 7.9, and 28.6 +/- 9.3, respectively, when compared with untreated stressed controls in which the mean score was 42.4 +/- 4.7 (P < 0.02). Microvascular disruption is a significant factor in stress ulceration and the efficacy of allopurinol in minimizing the stress-induced disruption of the microvascular network provides further indirect evidence for the role of ischemia and oxygen-derived free radical generation in its etiology.
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We report a case of a 34-year-old male, who had urinary tract calculus, caused by complete deficiency of adenine phosphoribosyltransferase. Ureterolithotomy was performed on February 28, 1983. Infrared spectroanalysis revealed a 2,8-dihydroxyadenine calculus. APRT activity was less than 1% of the normal level, and it was found to be complete deficiency of APRT. Since the operation, 300 mg/day of allopurinol is being administered without any sign of recurrence.
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To study the beneficial and harmful effects of electro-coagulation compared with no intervention, to other ablation methods, or systemic treatments in patients with liver metastases.
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In the early phases, HRUW solution decreased oxidative stress, tubular apoptosis, and interstitial macrophage infiltration in the kidney grafts. Consequently, HRUW solution improved renal function and prolonged recipient survival rate compared with simple cold storage using UW solution. Histopathologically, HRUW treatment alleviated tubular injury and suppressed development of interstitial fibrosis.
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Shock wave lithotripsy is believed to cause renal damage directly through cellular injury from high energy shock waves and indirectly through vascular injury and resultant ischemia, which gives rise to oxygen free radical compounds. The transient and volatile nature of free radicals and derived products makes their detection difficult. Moreover, certain medications may provide a protective effect against shock wave lithotripsy induced renal parenchymal injury. We introduced an innovative microdialysis system for in vivo sampling of interstitial fluids that can be analyzed for free radical mediated lipid peroxidation products after shock wave lithotripsy treatment in the swine model. In addition, this system was used to test the antioxidant or renoprotective action of allopurinol.
Free radical (FR) formation in the rat intestinal lumen was measured using the spin-trapping technique and electron paramagnetic resonance spectroscopy. Intestinal ischemia was produced by occluding the celiac and the superior mesenteric arteries for 30 min followed by reperfusion. The lumen was filled with a solution of PBN (N-tert-butyl-alpha-phenyl-nitrone) and the intestine was squeezed to enhance the interaction between the PBN solution and the intestinal mucosal cells. Free radicals were produced upon reperfusion, with peaks at 5 and 90 min. Post-ischemic treatment with superoxide dismutase (20 mg.kg(-1)) inhibited the increase of FR production during the second peak by 36%. In a single study in a group of leucocytopenic rats (WBC < 1500/mm(3)), the increase of FR production during the second peak was decreased by 80%. However, these treatments did not inhibit the FR production during the first peak in either group. In contrast, pretreatment with allopurinol (40 and 100 mg.kg(-1) injection at 24 and 3 hours before ischemia, respectively) inhibited the FR production during the first peak by 76%, but did not inhibit during the second peak. The changes in lipid peroxidation in the intestinal mucosa, specific gravity of the intestine and in the hematocrit were correlated to the FR production in the second peak. These results suggest that a major cause of tissue injury after reperfusion in the ischemic intestine may largely be produced by neutrophils.
The effect of glucose infusion on renal handling of purine bases and oxypurinol was examined in 6 normal subjects. Five hundred milliliters of 1.1 M glucose solution were administered intravenously in 1 h. Fractional clearances of uric acid, xanthine and oxypurinol were significantly increased during glucose infusion, but that of hypoxanthine was not changed, while a 1-hour infusion of 500 ml of 1.1 M mannitol had no effect on the fractional clearances of purine bases and oxypurinol. These data indicate that the effect of glucose infusion on the renal clearances of uric acid, xanthine and oxypurinol was not related to osmotic diuresis but induced by glycosuria and/or hyperglycemia. Accordingly, the glycosuria- and/or hyperglycemia-induced decrease in the biological half-life of oxypurinol must be considered in the administration of allopurinol to gouty patients with uncontrolled diabetes mellitus.
A nonsignificant decrease was found in both daily UNOx excretion and creatinine clearance when pretreated ARF groups and the ARF group without pretreatment were compared (p > 0.05). Significantly lower plasma sodium values (139.5 +/- 4.86 mmol/l) in the allopurinol-pretreated ARF group were found than in the ARF group without pretreatment, in the ARF group pretreated with enalapril, and in the sham SHR group (p = 0.029). The urinary sodium loss was greater in the enalapril-pretreated than in the allopurinol-pretreated ARF group (p = 0.047). Allopurinol and/or enalapril pretreatment decreased total vascular resistance (p = 0.003) in comparison with the sham SHR group.
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To assess the short-term effects of allopurinol on intestinal permeability, oxidative stress and endotoxin-dependent cytokines in patients with cirrhosis.
We isolated cDNA encoding a multispecific organic anion transporter 2 (OAT2) from the mouse kidney cDNA library. Isolated mouse OAT2 (mOAT2) consisted of 1623 base pairs that encoded a 540-amino acid residue protein with 12 putative membrane-spanning domains, and the amino acid sequence was 87% identical to that of rat OAT2 (rOAT2). The gene coding for mOAT2, Slc22a7, is found on chromosome 17C. Northern blot analysis revealed that the mOAT2 mRNA is abundantly expressed in the male mouse kidney, whereas it was predominantly expressed in both the liver and kidney of female mice. When expressed in Xenopus laevis oocytes, mOAT2 mediated the high affinity transport of glutarate (K(m) = 15.8 +/- 3.2 microM) and prostaglandin E2 (K(m) = 5.2 +/- 0.5 nM) in a sodium-independent manner. mOAT2-expressing oocytes also mediated the uptake of alpha-ketoglutarate, glutarate, prostaglandin E2, p-aminohippuric acid, methotrexate, ochratoxin A, valproate, and allopurinol. However, we did not observe mOAT2-mediated uptake of salicylate. A wide range of structurally unrelated organic anions inhibited mOAT2-mediated glutarate uptake especially erythromycin, a potent inhibitor. These results indicate that isolated mOAT2 is a multispecific organic anion transporter having some differences in substrate specificity compared with rOAT2. In addition, we found that there exists a sex- and species-related differential gene expression of the OAT2 isoform.
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The electron transport chain of the mitochondria is highly sensitive to myocardial ischemia. As free oxygen radicals take part in the damage that occurred during ischemia, this study was undertaken to determine if allopurinol and deferrioxamine had any beneficial effect on mitochondrial function. Our results showed that perfusion with allopurinol did not improve the mitochondrial function, but that reperfusion with allopurinol and deferrioxamine had a beneficial effect. We came to the conclusion that xanthine oxidase, as a generator of superoxide anions, is of minor importance in comparison with the hydroxyl radicals, which are probably formed in the presence of iron in the cell.
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Donors criteria were worse in the Celsior group for age, male sex, creatinemia, and cold ischemia. Populations of recipients were comparable. There were no differences at 1 and 12 months in creatinine levels (p=0.9 and 0.8, respectively) and in number of delayed graft functions (DGF) (p=0.8 and relative risk =0.9) between groups. There were no differences in post-transplantation outcomes for all variables. At 5 years, graft survival was 90.4% for UW and 93.5% for Celsior (p=0.44).
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To compare the efficacy of combined low dose of hypouricemic drugs (Allopurinol 100 mg and benzbromarone 20 mg; Allomaron) and standard dose 300 mg of allopurinol in hyperuricemia.
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The effect of adding allopurinol and catalase to hypothermic cardioplegia for ischemic-reperfusion injury was investigated in the isolated rabbit heart. Hearts were divided into two groups, namely: Group C (n = 7), which received a hypothermic crystalloid cardioplegic solution alone (4 degrees C), and group T (n = 7), which received the hypothermic cardioplegic solution with allopurinol (148 mumol/L)13 and catalase (37 nmol/L).12 The cardioplegic solution was infused continuously into the isolated hearts, which had been placed in ice-cold saline, during a 12 h preservation. Subsequently, the hearts were mounted on a noncirculating, nonpulsatile perfusion circuit using Krebs-Henseleit buffer solution at 37 degrees C for 1 h at a constant perfusion pressure of 75 mm Hg. The left ventricular developed pressure (LVDP), maximum rate of pressure change (max dp/dt), and percent recovery of coronary flow were higher, while the creatine phosphokinase concentration and left ventricular end diastolic pressure (LVEDP) were lower in group T. The tissue malondialdehyde concentration and water content were similar in both groups. Thus, cardiac function after a 12 h preservation was enhanced by the added combination of allopurinol and catalase to the cardioplegic solution, supporting its role in the prevention of free radical reperfusion injury in cardiac preservation.
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Subjects (n=1086) in this open-label extension study were assigned to fixed-dose daily urate-lowering treatment (ULT) with febuxostat (80 mg or 120 mg) or allopurinol (300 mg). ULT reassignment was permitted during months 1 to 6 to achieve serum urate (SUA) concentrations between 3.0 and <6.0 mg/dl. Flares requiring treatment, tophus size, safety, and SUA levels were monitored during up to 40 months of ULT maintenance.
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With a view to modifying misonidazole (MISO) neurotoxicity, we initiated a randomized clinical study to assess a possible drug interaction and toxicity protection when dexamethasone (DXM) is administered concomittantly with MISO. The ongoing study consists of: 1. Pharmacokinetic evaluation; 2. Assessment of toxicity. Fourteen patients undergoing radiation therapy for different types of malignant neoplasia (excluding brain tumors) have been randomized to receive either MISO alone, or DXM one week prior and during treatment with MISO. Five of seven patients receiving MISO alone developed peripheral neuropathies while only one out of 7 patients that received MISO with DXM coverage developed a transient and mild neuropathy. Pharmacokinetic evaluation of MISO in plasma and urine of those patients receiving DXM has shown no evidence of drug interaction. It is postulated that the mechanism of action of DXM is at the nerve cell membrane level, restoring and stabilizing cell surface properties. In future studies we will investigate the use of DXM with increasing doses of MISO above the recommended maximum dose of 12 gm/m2, hoping to achieve a higher tumor tissue level of MISO while avoiding unacceptable toxicity. The effect of Allopurinol on the plasma kinetics of MISO was studied in four additional patients, observing also no evidence of drug interaction.
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Theophylline kinetics after intravenous aminophylline were determined in 5 nonsmoking healthy males before and after allopurinol for 1 wk. There was no significant alteration in theophylline disposition.
Nicotine, which is tobacco alkaloid, still induces interests for researchers because of smokers addiction to nicotine. Nicotine having influence on the neuronal acetylcholine receptors (nAChRs) increases release of most certain neurotransmitters from the nerve endings. Also, nicotine, affecting the mitochondrial respiratory chains, contributes to the formation of reactive oxygen species. In the present study, we investigated the effects of nicotine on smooth muscles of gastric fundus on the electrical field stimulation (EFS) that induces transition contraction via stimulation nAChRs. In addition, we aimed to investigate the interaction between release of acetylcholine, induced by nicotine, and the effects of reactive oxygen species. Therefore, the effects of allopurinol (10(-6)-10(-5) M), deferoxamine (10(-4) M) and mannitol (10(-4)-5 x 10(-3) M) were tested on the transient contraction induced by nicotine. In conclusion, mannitol (5 x 10(-3) M) significantly reduced contractile response to nicotine on EFS only in high concentration. Whereas in small concentrations mannitol (10(-4) M) statistically did not cause any results. Deferoxamine and allopurinol also did not have any significant response.
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We conducted a retrospective analysis of prospectively collected data in 45 patients with DRESS syndrome diagnosed between September 2009 and August 2011.
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Allopurinol is an effective urate lowering drug, which is usually well-tolerated with no adverse effects in most cases, but about 2% of the treated patients develop a skin rash, and patients may experience severe allopurinol-induced hypersensitivity syndrome.
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We investigated the effects of nicotinamide (NA) supplementation of the processing medium during islet isolation. One hundred and two human pancreata were processed for clinical transplantation after preservation either in the University of Wisconsin (UW) or using the two-layer method (TLM). Pancreata were then divided into four groups and retrospectively analyzed. Group I: UW preservation followed by processing without NA, Group II: UW preservation and processing with NA, Group III: TLM preservation without NA, Group IV: TLM preservation with NA. We observed a significant increase in islet yield in Group II (4343+/-348 IEQ/g) [mean+/-SEM], compared to Group I (2789+/-348 IEQ/g) (p=0.005). Similarly, a significant increase in islet yield was observed when NA was used in the processing of organs preserved with TLM (Group IV: 5538+/-413 vs. Group III: 3500+/-629; p=0.02). Furthermore islet yield was higher in Group IV than in Group II (p<0.05). The percentages of preparations that qualified for transplantation were 25, 47, 45, 69% in Groups I, II, III, IV, respectively. Addition of NA to the processing medium significantly improved islet yields in both the UW and TLM preservation protocols, allowing for a higher percentage of islet preparations to qualify for clinical transplantation.
Allopurinol is an inhibitor of xanthine oxidase (XO), and XO is an enzyme that generates great amounts of reactive oxygen species. The aim of this work was to evaluate the efficacy of allopurinol to prevent experimental cirrhosis. Fibrosis and cirrhosis were induced by common bile duct ligation (BDL) for 4 weeks in rats. Animals were divided into 4 groups: sham-operated rats (SHAM); BDL group; BDL plus allopurinol (100 mg·kg⁻¹, p.o.), and SHAM plus allopurinol treatment. Alanine aminotransferase, γ-glutamyl transpeptidase, and alkaline phosphatase were increased in BDL rats but were preserved normal by allopurinol. XO activity was prevented by allopurinol; however, lipophilic and hydrophilic oxidative stress was not prevented by the drug. Allopurinol partially suppresses nuclear factor-κB (NF-κB) nuclear translocation and transforming growth factor-β (TGF-β) expression, and increased the active form of matrix metalloproteinase-13 (MMP-13). Moreover, collagen production induced by BDL was partially but significantly reduced by allopurinol. These findings suggest that allopurinol possesses a hepatoprotective effect probably by modulating proteins such as NF-κB, TGF-β, and MMP-13, helping to protect against liver damage induced by chronic cholestasis and a mechanism independent of oxidative stress.
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The distribution of xanthine dehydrogenase throughout the soybean plant as well as the intercellular localization of xanthine dehydrogenase within soybean nodules was determined. Polyclonal antibodies against purified xanthine dehydrogenase were prepared and used in an enzymelinked immunosorbent assay to determine whether xanthine dehydrogenase is a nodule-specific protein. This immunological assay showed that xanthine dehydrogenase is present in far greater concentration in the nodule than in any other plant organ. Immunodiffusion tests showed that anti-soybean nodule xanthine dehydrogenase would cross-react with nodule crude extracts from the ureide producers, soybean, cowpea, and lima bean, but would not cross-react with those of the amide producers, alfalfa and lupine. A crude extract from pea nodules cross-reacted slightly with anti-soybean xanthine dehydrogenase. Anti-soybean xanthine dehydrogenase did not cross-react with buttermilk xanthine oxidase either by enzyme-linked immunosorbent assay or by immunodiffusion test.Fresh nodule sections from the ureide-producers, soybean, cowpea, and lima bean, all stained positively for xanthine dehydrogenase. The substrate-dependent stain was inhibited by allopurinol and was observed only in the infected nodule cells of these species. Nodules from the amideproducers, alfalfa and white lupine, did not stain for xanthine dehydrogenase.
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Gout is a common cause of inflammatory arthritis in the United States, and its prevalence has increased in recent decades, especially among older adults. Older adults with gout are of particular interest because they tend to experience higher rates of tophi, an advanced stage of gout, than do younger patients.
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Bioartificial liver support systems, which use freshly isolated primary hepatocytes (PH), present severe logistical difficulties. Stored frozen PH that are thawed as required could answer this problem. The aim of this study was to develop a cryopreservation protocol for large-scale preparation of porcine PH. We cryopreserved single and spheroid hepatocytes. Harvested hepatocytes were cryopreserved in various concentrations of dimethyl sulfoxide (DMSO) using hormonally defined medium (HDM) and various presentation solutions, such as University of Wisconsin (UW) and fetal bovine serum. After thawing the hepatocytes, we measured the viability, plating efficiency, ammonia removal, urea synthesis, and albumin secretion. UW solution was most effective for cryopreservation, as evidenced by the viability and liver-specific functions of the thawed hepatocytes. The optimal DMSO concentration for porcine hepatocyte cryopreservation was 15%. After cryopreservation, spheroid hepatocytes maintained greater viability and functional activity compared with single hepatocytes. Moreover, spheroid hepatocytes showed native cell structures and maintained high levels of liver-specific functions. In conclusion, cryopreserved spheroid hepatocytes were superior to cryopreserved single hepatocytes in terms of viability and liver-specific functions.
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High-resolution HLA genotyping was performed for 65 patients of European ancestry treated with lamotrigine (22 cases with lamotrigine-induced SCARs and 43 controls on lamotrigine without SCAR-related symptoms). Association of HLA genetic variants with SCARs in these patients were evaluated by contrasting allele frequencies between the cases and the controls for each of 112 HLA four-digit alleles.
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In humans, uric acid (UA) is the main urinary metabolite of purines, whereas in other species (avians) it is the chief nitrogen compound excreted in the urine. The absence of uricase, due to nonsense or splice mutations occurring during the evolution of primates, results in blood urate levels much higher in humans than in other mammalians. This could have favorable implications, including protection from oxidative damage, as well as possibly allowing better blood pressure (BP) control in settings of low dietary Na+ intake. UA is a stimulus of the renin-angiotensin system (RAS). Moreover, blood UA levels are a major marker of proximal tubular function and overall volume status. On the other hand, hyperuricemia is a co-factor in Na+ -sensitive arterial hypertension, a marker and perhaps itself responsible for microvascular and systemic damage through RAS stimulation, inhibitory effects on endothelial cells, and the proliferation of perivascular smooth muscle cells. Recent studies in rats rendered hyperuricemic through administration of oxonic acid demonstrate the induction of hypertension and severe microvascular damage when associated with subtotal nephrectomy or chronic cyclosporine treatment. The opportunity to pharmacologically manipulate blood UA levels through inhibitors of synthesis (allopurinol), uricosuric agents (benziodarone), or recombinant urate oxidase (rasburicase) provides a relevant therapeutic potential in UA metabolism disorders, tumor lysis syndrome, and possibly in essential hypertension, as well as chronic progressive renal disease.
The hypouricemic actions of exopolysaccharide produced by Cordyceps militaris (EPCM) in potassium oxonate-induced hyperuricemia in mice were examined. Hyperuricemic mice were administered intragastrically with EPCM (200, 400 and 800 mg/kg body weight) or allopurinol (5 mg/kg body weight) once daily. Serum uric acid, blood urea nitrogen and liver xanthine oxidase (XOD) activities of each treatment were measured after administration for 7 days. EPCM showed dose-dependent uric acid-lowering actions. EPCM at a dose of 400 mg/kg body weight and allopurinol showed the same effect in serum uric acid, blood urea nitrogen and liver XOD activities in hyperuricemic mice. An increase in liver XOD activities was observed in hyperuricemic mice due to administration of EPCM at a dose of 200 mg/kg body weight. EPCM at a dose of 800 mg/kg body weight did not show significant effects on serum uric acid and XOD activities. We conclude that EPCM has a hypouricemic effect caused by decreases in urate production and the inhibition of XOD activities in hyperuricemic mice, and this natural product exhibited more potential efficacy than allopurinol in renal protection.