891 resultados para BILE-SALT HYDROLASE
Resumo:
The purpose of this study was to determine the relative rate of corrosion of iron-tin alloys containing low percentages of tin. Since in the world today, a great deal of work is being done to develop large tin deposits and new methods devised to treat these ores, it is possible that the metal will become abundant and will obtain a more important position in the metal industry.
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The Salt Chuck, Rush and Brown, and adjacent mines and claims form an area of approximately 15 square miles near the head of Kasaan Bay about 10 miles northwest of the village of Kasaan on Prince of Wales Island in southeastern Alaska. It is an area of moderate relief in which the hills rise from the water’s edge to heights of some 500 feet. Most of the area is covered with dense vegetation and muskeg.
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ABSTRACT: There is a high frequency of diarrhea and vomiting in childhood. As a consequence the focus of the present review is to recognize the different body fluid compartments, to clinically assess the degree of dehydration, to know how the equilibrium between extracellular fluid and intracellular fluid is maintained, to calculate the effective blood osmolality and discuss both parenteral fluid requirments and repair.
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Patients with neurosurgical disorders often present with hyponatraemia. Two mechanisms account for hyponatraemia in these patients: the Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) and Cerebral Salt Wasting Syndrome (CSWS). The two entities differ in their volume status. In SIADH, volume is expanded due to ADH-mediated renal water retention, but in CSWS, volume is diminished as a consequence of renal salt wasting, most likely attributable to an increased secretion of Brain Natriuretic Peptide (BNP) and Artrial Natriuretic Peptide (ANP). Since it is clinically difficult to distinguish between these two entities, fluid management has to be performed carefully. Salt and fluid replacement appears to be indicated in CSWS, whereas fluid restriction might be the primary approach in patients with SIADH.
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Pharmaceuticals are ubiquitous in surface waters as a consequence of discharges from municipal wastewater treatment plants. However, few studies have assessed the bioavailability of pharmaceuticals to fish in natural waters. In the present study, passive samplers and rainbow trout were experimentally deployed next to three municipal wastewater treatment plants in Finland to evaluate the degree of animal exposure. Pharmaceuticals from several therapeutic classes (in total 15) were analyzed by liquid chromatography-tandem mass spectrometry in extracts of passive samplers and in bile and blood plasma of rainbow trout held at polluted sites for 10 d. Each approach indicated the highest exposure near wastewater treatment plant A and the lowest near that of plant C. Diclofenac, naproxen, and ibuprofen were found in rainbow trout, and their concentrations in bile were 10 to 400 times higher than in plasma. The phase I metabolite hydroxydiclofenac was also detected in bile. Hence, bile proved to be an excellent sample matrix for the exposure assessment of fish. Most of the monitored pharmaceuticals were found in passive samplers, implying that they may overestimate the actual exposure of fish in receiving waters. Two biomarkers, hepatic vitellogenin and cytochrome P4501A, did not reveal clear effects on fish, although a small induction of vitellogenin mRNA was observed in trout caged near wastewater treatment plants B and C.
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Inspissated bile syndrome in a 6Â week old boy was unresponsive to oral ursodesoxycholic acid. Intraoperative cholangiography revealed complete obstruction of the common bile duct. Therefore, the gallbladder fundus was pulled out through a laparoscopy port site and sutured to the fascia. A catheter was positioned into the infundibulum for irrigation with ursodesoxycholic acid. At day 8 complete resolution of the plug and free passage of contrast medium into the duodenum was documented radiologically. The catheter was removed, skin closed spontaneously without a second surgery for closure of the gall bladder.
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Intraductal papillary neoplasms of the bile duct are still poorly characterized regarding (1) their molecular alterations during the development to invasive carcinomas, (2) their subtype stratification and (3) their biological behavior. We performed a multicenter study that analyzed these issues in a large European cohort. Intraductal papillary neoplasms of the bile duct from 45 patients were graded and subtyped using mucin markers and CDX2. In addition, tumors were analyzed for common oncogenic pathways, and the findings were correlated with subtype and grade. Data were compared with those from 22 extra- and intrahepatic cholangiocarcinomas. Intraductal papillary neoplasms showed a development from preinvasive low- to high-grade intraepithelial neoplasia to invasive carcinoma. Molecular and immunohistochemical analysis revealed mutated KRAS, overexpression of TP53 and loss of p16 in low-grade intraepithelial neoplasia, whereas loss of SMAD4 was found in late phases of tumor development. Alterations of HER2, EGFR, β-catenin and GNAS were rare events. Among the subtypes, pancreato-biliary (36%) and intestinal (29%) were the most common, followed by gastric (18%) and oncocytic (13%) subtypes. Patients with intraductal papillary neoplasm of the bile duct showed a slightly better overall survival than patients with cholangiocarcinoma (hazard ratio (cholangiocarcinoma versus intraductal papillary neoplasm of the bile duct): 1.40; 95% confidence interval: 0.46-4.30; P=0.552). The development of biliary intraductal papillary neoplasms of the bile duct follows an adenoma-carcinoma sequence that correlates with the stepwise activation of common oncogenic pathways. Further large trials are needed to investigate and verify the finding of a better prognosis of intraductal papillary neoplasms compared with conventional cholangiocarcinoma.
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Electrolyte disorders are common and potentially fatal laboratory findings in emergency patients. Approximately 20 % of patients in the emergency department present with either hyponatremia or hypernatremia. Recently it was shown that disorders of serum sodium are not only an expression of the severity of the underlying disease but independent predictors for the outcome of patients. They directly influence patient daily life by causing not only gait and concentration disturbances but also an increased tendency to fall together with a reduced bone mass. Given these new data it is even more important to detect and adequately correct dysnatremia in patients in the emergency department. Acute, symptomatic dysnatremia should be corrected promptly by use of 3 % NaCl for hyponatremia and 5 % glucose for hypernatremia. A close monitoring of serum sodium concentration is, however, essential in any case of correction of hyponatremia or hypernatremia in order to avoid rapid overcorrection and subsequent complications. A profound knowledge of the mechanisms underlying the development of hyponatremia, e.g. diuretics, syndrome of inappropriate antidiuretic hormone secretion (SIADH), heart failure and cirrhosis of the liver and hypernatremia, e.g. dehydration, infusions, diuretics and osmotic diuresis is essential. The present article describes the epidemiology, etiology and correction of hyponatremia and hypernatremia on the basis of current knowledge with special emphasis on emergency department patients.
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PURPOSE Hyponatremia is frequently observed in intensive care unit (ICU) patients, but there is still lack information on the physiological mechanisms of development. MATERIALS AND METHODS In this retrospective analysis we performed tonicity balances in 54 patients with ICU acquired hyponatremia. We calculated fluid and solute in and outputs during 24 hours in 106 patient days with decreasing serum-sodium levels. RESULTS We could observe a positive fluid balance as a single reason for hyponatremia in 25% of patients and a negative solute balance in 57%. In 18% both factors contributed to the decrease in serum-sodium. Hyponatremic patients had renal water retention, measured by electrolyte free water clearance calculation in 79% and positive input of free water in 67% as reasons for decline of serum-sodium. The theoretical change of serum sodium during 24 hours according to the calculations of measured balances correlated well with the real change of serum sodium (r = 0.78, P < .01). CONCLUSIONS Balance studies showed that renal water retention together with renal sodium loss and high electrolyte free water input are the major contributors to the development of hyponatremia. Control of renal water and sodium handling by urine analysis may contribute to a better fluid management in the ICU population.
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The injurious effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in the small intestine was not appreciated until the widespread use of capsule endoscopy. Animal studies found that NSAID-induced small intestinal injury depends on the ability of these drugs to be secreted into the bile. Because the individual toxicity of amphiphilic bile acids and NSAIDs directly correlates with their interactions with phospholipid membranes, we propose that the presence of both NSAIDs and bile acids alters their individual physicochemical properties and enhances the disruptive effect on cell membranes and overall cytotoxicity. We utilized in vitro gastric AGS and intestinal IEC-6 cells and found that combinations of bile acid, deoxycholic acid (DC), taurodeoxycholic acid, glycodeoxycholic acid, and the NSAID indomethacin (Indo) significantly increased cell plasma membrane permeability and became more cytotoxic than these agents alone. We confirmed this finding by measuring liposome permeability and intramembrane packing in synthetic model membranes exposed to DC, Indo, or combinations of both agents. By measuring physicochemical parameters, such as fluorescence resonance energy transfer and membrane surface charge, we found that Indo associated with phosphatidylcholine and promoted the molecular aggregation of DC and potential formation of larger and isolated bile acid complexes within either biomembranes or bile acid-lipid mixed micelles, which leads to membrane disruption. In this study, we demonstrated increased cytotoxicity of combinations of bile acid and NSAID and provided a molecular mechanism for the observed toxicity. This mechanism potentially contributes to the NSAID-induced injury in the small bowel.
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Hypertension and chronic kidney disease (CKD) are complex traits representing major global health problems1,2. Multiple genome-wide association studies have identified common variants in the promoter of the UMOD gene3–9, which encodes uromodulin, the major protein secreted in normal urine, that cause independent susceptibility to CKD and hypertension. Despite compelling genetic evidence for the association between UMOD risk variants and disease susceptibility in the general population, the underlying biological mechanism is not understood. Here, we demonstrate that UMOD risk variants increased UMOD expression in vitro and in vivo. Uromodulin overexpression in transgenic mice led to salt-sensitive hypertension and to the presence of age-dependent renal lesions similar to those observed in elderly individuals homozygous for UMOD promoter risk variants. The link between uromodulin and hypertension is due to activation of the renal sodium cotransporter NKCC2. We demonstrated the relevance of this mechanism in humans by showing that pharmacological inhibition of NKCC2 was more effective in lowering blood pressure in hypertensive patients who are homozygous for UMOD promoter risk variants than in other hypertensive patients. Our findings link genetic susceptibility to hypertension and CKD to the level of uromodulin expression and uromodulin’s effect on salt reabsorption in the kidney. These findings point to uromodulin as a therapeutic target for lowering blood pressure and preserving renal function.