Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five healthy male adults were deprived of food for a short period (40 hr) and biochemical studies and urinalyses were done before and after fasting to determine the effects on liver and renal functions. Acceleration in lipid metabolism was seen with an increase of about 90% in NEFA and about 20% in TG. GOT, GPT and LDH showed elevations of about 40 to 100% indicating a slight effect of 40 hr fasting on liver functions. BUN, HDL-C and ALP showed increases of about 30% while, CPK and TC showed decreases of about 20%. In the other parameters changes of about 10% were seen. After a fasting with water intake of about 1,000 ml/day, a body weight loss of 1.2 kg was observed at 40 hr. During the short-term fasting (40 hr) as done in our study, changes were seen in glucose and lipid metabolism. However, since no abnormalities were seen in general biochemical parameters, we consider that a fasting of this duration is valuable for use as one of the fastings.
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PMID:Effect of short-term fasting treatment on liver and renal function. 134 10

The reasons of fat embolism as well as the following fat embolism syndrome are most likely long bone fractures, especially if the femur is participated. On the other hand there are cases, where a severe concussion of the entire body caused fat embolism. But it is also supposed, that intramedullary reaming as well as the insertion of knee- and hip-prostheses could be a releasing factor, because the applicated pressure on the medullary canal can cause a fat release in the systemic blood system. The morbidity depends on age and fracture, which is on fractures between 0.9 and 2%. The most affected group are people between 18 and 28 years of age. The fat embolism is manifesting at 46-60% of the patients in the first 24 hours and over 90% of the patients are affected in the first three days. If you look at the metabolic changes, you will find shortly after the fracturing process a rapid increase of free fatty acids (FFA), as well as an increase of the plasmatic enzyme levels (lipase, GPT, GOT, GLDH, LDH, etc.), catecholamines and glucocorticoids. In order to discuss the pathogenesis in a fairly complete way, you have to take different theories into consideration, because several parallel running processes--which are influencing each other--are leading to the syndrome. Infloating theory: Proceeding on the assumption that contents of the bone marrow are floating out of the fracture gap into the venous system and are leading to fat embolism in the lungs. Lipase theory: You can diagnose in 50-70% of the fracture patients an increase of the lipase level, which is correlating with the manifestation of the fat embolism. The lipase releases fat from the body depositories in addition to the fat, who is coming out of the fracture gap. Shock and coagulation theory: During shock the microcirculation is decelerated, the blood viscosity is increased and the suspension stability of the cellular blood components is decreased, which is leading to the sludging phenomenon. So the capillaries of the lungs and the brain are a kind of sludge filter of the blood, that is changed in its suspensions stability. Free fatty acids theory: Primary existing capillary defects are reasonable caused by free fatty acids (FFA). They are hydrolyzed of the neutral fats and are histotoxic for the walls of the blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Fat embolism and fracture, a review of the literature]. 135 89

As far as the pathogenesis of poisonings with organophosphorus pesticides is concerned, in addition to irreversible inhibition of acetylcholinesterase (AGE) in tissues, of importance are changes in the other systems which essentially determine the outcome of intoxication. The purpose of the present study was to examine the nature of changes occurring in total protein and protein fractions, free amino acids (aspartic and glutamic acids, glycine, isoleucine, leucine) and in certain enzymes (AST, ALT, CP, GGTP, GDH) in the cerebrospinal fluid (CSF) of patients with acute Malathion insecticide poisoning. 137 patients aged 20 to 50 years were placed under observation. There were 77 men and 60 women. 40 persons had poisoning of medium gravity and 97 were severely poisoned. The intake of the CSF was performed on days 1, 3, 10, 14 and 21 since the disease onset. It has been established that in acute Malathion insecticide poisoning, the CSF content of the stimulating mediator amino acids, aspartic and glutamic, rises within the early periods, whereas the concentration of the inhibitory mediator glycine decreases. The changes in protein fractions of the CSF are characterized by a fall of the content of globulins and a rise of albumins, thus attesting to the predominance of pathological processes in the brain, especially in the initial period of intoxication, and to the impairment of the blood-brain barrier. The development of intoxication is associated with activation in the CSF of LDN, CP, GGTP and GDH as well as by activation of LDH isozymes which is viewed as the result of the membranotoxic effect of a Malathion insecticide.
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PMID:[Changes in the biochemical composition of the cerebrospinal fluid in acute carbophos poisoning]. 135 42

The present study was designed to elucidate the effect of FK506 on 90 min of warm ischemia of the liver and reperfusion in 30 dogs. Three groups of animals were studied. Group 1 animals received FK (0.15 mg/kg/day) for three days prior to the ischemia and group 2 animals got 2 ml of saline solution for three days instead of FK and were considered controls. In group 3 FK (0.15 mg/kg/day) was injected immediately upon reperfusion and two days thereafter. Evaluation of the effectiveness of the drug was monitored by measuring the serum activities of AST, ALT, LDH, serum total bilirubin, malondialdehyde, and by histopathological examinations of the liver specimens and survival of the animals for 7 days after reperfusion. The 7 day survival of the animals in group 1 (80%) was significantly (P < 0.05) improved compared with those in group 2 (30%) and group 3 (20%). The serum activities of AST, ALT, and LDH and total bilirubin were significantly lower in group 1 than in group 2 and group 3. FK pretreatment significantly prevented hepatocellular necrosis and neutrophilic infiltration in group 1 in comparison with those in group 2 and group 3. Although the malondialdehyde level in hepatic venous blood was relatively lower in group 1, this difference was not statistically significant. Three days FK pretreatment prevented hepatocellular injury and enzyme leakage after 90 min of hepatic ischemia, whereas FK treatment immediately upon reperfusion failed to do so. In conclusion, donor organ pretreatment with FK may become a promising strategy for improved allograft survival in liver transplantation.
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PMID:The salutary effect of FK506 in ischemia-reperfusion injury of the canine liver. 138 88

The effects of d-catechin (d-CTC) on carbon tetrachloride- and d-galactosamine (d-Ga1N)-induced cytotoxicity in primary cultured rat hepatocytes were examined. After 1.5 h preincubation, d-CTC was added at doses of 0.1-5.0 mg/ml to culture medium together with 10 mmol/L CCl4 or 5 mmol/L d-GalN, respectively. GOT, GPT and LDH levels were measured 1.5 h after treatment. The results showed that d-CTC at doses of 0.6 to 5.0 mg/ml could protect the hepatocytes against the toxic effects of CCl4 and d-GalN. At the higher doses (2.5-5.0 mg/ml), d-CTC showed weak inhibition of LDH and GPT activities, but these did not influence its anti-hepatotoxic activity.
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PMID:[Effect of d-catechin on carbon tetrachloride- and d-galactosamine-induced cytotoxicity in primary cultured rat hepatocytes]. 139 38

The normal values (clinical references range) of the laboratory tests differs among hospitals due to the differences in: (1) the kinds of instruments and reagents used, (2) how the population for study was selected and the size of the population was, (3) when the specimens were taken, (4) how they were stored until use, and (5) how the data obtained were calculated and (6) who evaluated the results. In this study, questionnaires regarding the above-mentioned points were sent to the heads of the clinical laboratories in 80 university hospitals in Japan. Answers were received from 71 laboratories (the rate of recovery was 88.8%). The normal range of potassium, uric acid, total cholesterol, enzyme activities [ALP, LDH, CHE, AST (GOT) and ALT (GPT)] in the university hospitals in Japan varied. It is not ideal to use different reference values in different hospitals. However, it is impossible to prepare a standard manual to obtain the normal range at present. When the inter-hospital differences become small enough to obtain one normal range for the Japanese peoples, a standard manual for normal values should be made.
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PMID:[Present status and problems of the normal values (clinical reference range) of the laboratory tests--results of a questionnaire survey in university hospitals in Japan]. 140 53

Many modifications of the UW solution have been reported to yield successful results in rat liver preservation and transplantation. One solution used histidine, in combination with lactobionate (HL-I), and gave superior preservation of the rat liver when compared with the UW solution. In this study we have compared the HL-I solution with 90 mM histidine, HL-II solution with 30 mM histidine, and the UW solution in dog liver preservation and transplantation. Dog livers were preserved for 48 hr in one of the three solutions and transplanted. The peak AST and ALT values were highest in livers preserved in HL-I, intermediate in UW solution, and lowest in HL-II. However, there were no significant differences among survival rates (average 5-7 days per group), posttransplant serum concentration of liver enzymes (AST, ALT, LDH, and alk-phos), clotting factors (PT and PTT), bilirubin, and fibrinogen concentration for each group. Dogs were sacrificed or died within 5-7 days due to rejection in nonimmunosuppressed dogs. Also, rat livers were preserved in the HL-II solution or in a solution in which histidine was replaced by isoleucine (IL-I). Isoleucine is an amino acid with a molecular mass similar to that of histidine, but is not as good a hydrogen ion buffer as histidine at the pH used for liver preservation (7.4). The buffer capacity of the IL-I solution was similar to the UW solution, but about one-half as much as the HL-II solution. Rats receiving a liver preserved for 30 hr in HL-II or IL-I were 100% viable. Rats receiving a liver preserved for 40-44 hr in HL-II or IL-I showed less survival (33% and 25%, respectively). This shows that histidine can be effectively replaced by isoleucine in a preservation solution and gives equivalent preservation results. Thus, the mechanism of improvement of liver preservation with histidine is not due to its action as a hydrogen ion buffer. These studies show that, although the HL solutions are superior for preservation of the rat liver, they are not superior to the UW solution for preservation of the dog liver. However, as others have shown in the rat liver transplant model, a simplified UW solution (HL-II) appears effective in dog liver preservation. The dog liver transplant model remains a more appropriate model for testing new preservation solutions prior to initiation of clinical trials.
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PMID:A comparison of histidine-lactobionate and UW solution in 48-hour dog liver preservation. 141 52

Clinical usefulness of ondansetron as an antiemetic for the treatment of nausea and vomiting induced by anticancer drugs including cisplatin (> or = 50 mg/m2) was evaluated by a multi-institutional, double-blind comparative study with placebo with inpatients with various malignancies. In this study, efficacy, safety and usefulness of single dose of ondansetron (4 mg) or placebo (physiological saline), given intravenously for initial nausea and vomiting were observed for 24 hours after treatment. Clinically, very effective or effective response was seen in 64% (16/25) of the group O (ondansetron) and 5.9% (1/17) of the group P (placebo). No clinically significant adverse effects or abnormal laboratory test values were reported in the group of O. Diarrhea (1 case) and the elevation of laboratory test values (GOT.GPT, T-bilirubin, LDH, in 3 cases) were reported in the group of P. General safety assessment was considered "safe" in 100% of both group O and group P, and there was no statistical difference between two groups. Usefulness was considered as "useful" in 64% (16/25) of group O and 6.3% (1/16) of group P, and O was significantly better than group P (p < 0.001) level. In conclusion, ondansetron provides a safe and effective antiemetic measure when employed therapeutically against nausea and vomiting induced by regimens including cisplatin.
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PMID:[Evaluation of SN-307 (ondansetron), given intravenously in the treatment of nausea and vomiting caused by anticancer drugs including cisplatin--a placebo-controlled, double-blind comparative study]. 141 15

One hundred and eighty seven patients (155 males, 32 females) with histologically proven and previously untreated head and neck cancer were entered in the study. A total of 222 cycles of therapy were analyzed (cisplatin 100 mg m-2 on day 1 and 5-day continuous intravenous infusion of 5-FU 550-1069 mg m-2 day-1, mean 875.5 mg m-2 day-1). Significant interpatient variability for various 5-FU pharmacokinetic parameters was observed including an almost ten-fold range in 5-FU clearance (5-FU Cl, ml min-1 m-2 = 791-7769, mean 2820.7). Log 5-FU Cl was not modified by 5-FU dose (r = -0.1034, P = 0.124, n = 222). Poor linear correlations between log 5-FU Cl and hepatic function tests were observed (respective r and P values for 222 cycles, log AST:0.0526, 0.4365; Log ALT: -0.1167, 0.0842; Log A1K. Phos.:0.154, 0.0214; Log GGT: 0.0652, 0.3436; Log LDH: -0.0984, 0.1563; Log bilirubin: 0.1278, 0.0601). The log 5-FU Cl was also poorly correlated with the serum concentration of various nutritional proteins (respective r and P values for 222 cycles, Albumin: 0.0110, 0.8714; prealbumin: -0.1067, 0.1129; transferrin: 0.0439, 0.5226). Laboratory data including indices of hepatic function and nutritional status cannot account for the interpatient variability in 5-FU disposition.
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PMID:No effect of dose, hepatic function, or nutritional status on 5-FU clearance following continuous (5-day), 5-FU infusion. 849 17

Male and female Sprague-Dawley rats were administered drinking water containing 300, 600, 1200, or 2400 mg/L chloral hydrate for 90 days. A control group received distilled water only. No animals died during the study and no differences were observed in body weight gain or food and water consumption, except for males at the highest-dose level. Minor treatment-related effects were observed for organ weights and hematological parameters and these did not appear to be of toxicological significance. Some indications of toxicity were evident in the 2400 mg/L male group (equivalent to 168 mg/kg-day) including a significant decrease in food and water consumption and in weight gain. In addition, histopathological examination of these animals revealed an apparent increase in the incidence of focal hepatocellular necrosis. Increases in AST, ALT, and LDH, which occurred at several dose levels in males, but particularly at 200 mg/L, are consistent with the hepatocellular necrosis of minimal to mild severity diagnosed by microscopic examination. These liver changes, except for sporadic enzyme changes, were not seen in the female rats which actually consumed higher doses of chloral hydrate (e.g., 288 mg/kg-day at 2400 mg/L). On the basis of the mild liver toxicity (histopathological and clinical) observed in males at the highest doses (168 mg/kg-day), the no observed adverse effect level (NOAEL) for oral exposure of rats to chloral hydrate for 90 days is considered to be 96 mg/kg-day (600 mg/L).
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PMID:Ninety-day toxicity study of chloral hydrate in the Sprague-Dawley rat. 142 61


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