Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:021525 (albumin)
 60,984 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A major avenue of our research has been to develop molecular probes (cDNAs) for studying the pathogenesis of liver disease (i.e., applied molecular pathophysiology). During the last 2-3 yr, we have developed and used molecular hybridization to study regulation of albumin synthesis in normal, protein-calorie deprived, uremic, and cirrhotic rat liver. Our current work is directed toward cloning the albumin gene to permit further analysis of albumin transcriptional and posttranscriptional control. Molecular hybridization, DNA cloning, related techniques can be utilized to study the function of virtually any gene. Incorporation of such advances in basic research into meaningful studies of liver disease is an exciting challenge to modern academic hepatology.
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PMID:Molecular hybridization probes for research in liver disease: studies with albumin cDNA. 9 41

The action of lecithin:cholesterol acyltransferase (LCAT) was studied on an abnormal lipoprotein (LP-X) rich in phosphatidylcholine and cholesterol from the plasma of patients with obstructive liver disease. 60 mg LP-X isolated free of other lipoproteins and subsequently labelled with 3H-cholesterol were incubated with 1 mg highly purified enzyme in the presence of albumin. After 45 h at 37 degrees C, the incubation mixture was subjected to zonal ultracentrifugation. 3H-cholesterol and 3H-cholesteryl esters were quantified in each fraction of the zonal gradient. More than 95% of the lipoproteins in this mixture banded in the density range of LP-X with no change in size distribution, but did contain 593 nmoles of newly formed cholesteryl esters. Agarose electrophoresis revealed an alpha-migrating band in addition to the original beta-band. Also on agar, the typically cathode migrating LP-X was changed to anode moving material. These studies indicate that LP-X can serve as a substrate for LCAT.
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PMID:Lipoprotein-X: a substrate for lecithin: cholesterol acyltransferase. 19 60

The mortality of patients with bleeding esophageal varices was studied in a private hospital where the modalities of treatment are considered optimal. Of the sixty-two patients in the study, twenty (32 per cent) died. Mortality was higher (p is less than 0.02) for those who had ascites or bilirubin more than 5 mg/dl, albumin less than 3 gm/dl, prothrombin time more than 4 seconds of control, or blood transfusions of more than 5 liters. The lower mortality in this study as compared with other studies among indigent population is the result of either private patients having less severe liver disease or having more effective care of both.
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PMID:The mortality of bleeding esophageal varices in a private university hospital. 30 87

Variations in body weight, behaviour of lipidaemic fractions proteinaemia, uricaemia and uricuria, and lipid and protein absorption were studied preoperatively and at varying times following operation in five subjects who had undergone jejuno-ileal bypass for obesity. The results showed high serous NEFA and a definite, early and persistent reduction in all lipidaemic fractions after operation. The post-operative levels of serous proteins, particularly albumin, which were reduced in all subjects, reached pathological levels in two patients where proteic malnutrition following on the operation was associated with serious liver disease. The results agree with reported data. The variations in lipidic and proteic malabsorption proved to be in agreement with weight drop and the serous parameters considered. The reduction in uricaemia encountered in the five patients studied failed to agree with data reported in the Anglo-Saxon literature. This may be explained by alimentary and racial differences between the two populations of patients.
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PMID:[Behavior of serum proteins and lipids after jejuno-ileal bypass for obesity]. 35 86

Arterial plasma levels and hepatic extraction of renin and aldosterone (ALDO) were measured in 24 patients with alcoholic liver disease and in 14 normal subjects being evaluated as prospective kidney donors. Patients with liver disease had higher plasma concentrations and lower fractional hepatic extractions of both renin and ALDO than the normal subjects. The quantity of renin extracted by the liver was highly correlated with plasma renin in both normal subjects and patients. Plasma ALDO concentration was positively correlated with plasma renin (p less than 0.001) but not with serum sodium, potassium or albumin concentration, inferior vena cava pressure, corrected hepatic venous wedge pressure, plasma volume or sulfobromophthalein storage or transport. Sixteen patients were restudied after one month. Six had received 40 mg/day of prednisolone, and the remaining 10 had received a placebo. Neither group had a change in plasma volume, corrected hepatic venous wedge pressure, plasma concentration or hepatic extraction of renin or ALDO. Serum albumin concentration increased and inferior vena cava pressure decreased with prednisolone therapy. These studies document high plasma levels and impaired hepatic extraction of renin and ALDO in patients with liver disease that are not corrected by short-term prednisolone therapy.
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PMID:Plasma levels and hepatic extraction of renin and aldosterone in alcoholic liver disease. 44 56

After observing alterations in the activity of the serum complement in patients undergoing periodic hemodialysis, the authors performed a preliminary study to determine repeatedly the activity of C3, C4, and CH50 in 44 patients. They discovered a consistent drop in C3 and CH50 while C4 remained normal. An attempt to explain these findings with information from the literature offered no more than a hypothesis for further study. While the possibility of a decline in the synthesis of the complement factors cannot be disregarded, the authors believe it is much more probable that they are consumed at a rate higher than normal. Since the C4 factor does not appear to be involved, activation is probably along the alternative pathway. Defective synthesis cannot be attributed to liver disease because the latter is not always present and because there is no relationship between C3 levels and levels of albumin or the presence of hepatopathy. The literature was reviewed for data that might support the idea that the complements in these patients are activated continuously by some process in connection with dialysis, by chemical products employed for to clean the machines, by commonly administered drugs, etc. Because so few data could be found on the subject, the authors consider that is necessary to study these mechanisms and their repercussions over a longer period of time.
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PMID:[Hemodialysis and complement (author's transl)]. 45 95

In this investigation we have shown that severe liver disease with cerebral involvement can be followed by the presence of BB creatine kinase isoenzyme in serum. Groups of rats were injected with a bile acid mixture, oleic acid, albumin and normal saline respectively. Bile acids or/and oleic acid induced BB isoenzyme to leak from central nervous tissue and this can be measured in serum. Albumin binding prevented this leakage. The experiments support our hypothesis, based on biochemical findings in human liver failure, that detergent and surface activity properties of the above mentioned components are able to produce this specific brain isoenzyme leakage.
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PMID:Brain specific creatine kinase isoenzyme behavior in rat serum after bile acid, sodium oleate and albumin injection. 48 11

Serum bile acid measurements now available by radioimmunoassay have proven to be the most sensitive procedure developed to date to assess diseases of the hepatobiliary system in both adult and pediatric liver disease. Their clinical utility appears to hold particular promise in establishing the early diagnosis of liver disease when conventional liver function test such as SGOT, alkaline phosphatase, bilirubin and albumin are still normal. Serum bile acid determinations have been shown to be particularly useful in the diagnosis of alcoholic liver disease, drug-induced liver disease, viral hepatitis and cholestasis of intra- and extrahepatic origin. In infants, serum bile acid measurements can be used to establish the diagnosis of biliary atresia. When serum bile acids are determined post-prandially, they are the most sensitive indicator of liver dysfunction developed to date.
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PMID:Serum bile acids (a new advance in the diagnosis of liver disease). 49 9

The plasma concentrations and urinary excretion of paracetamol and its glucuronide, sulphate, cysteine and mercapturic acid conjugates were measured in eight normal subjects, eight patients with mild liver disease and seven patients with severe liver disease following an oral dose of 1.5 g of paracetamol. The mean plasma paracetamol half-life was similar in normal subjects (2.43 h +/- 0.19) but was significantly prolonged in all patients with severe liver disease (4.25 h +/- 1.15:p = less than 0.001). Prolongation of the paracetamol half-life was related to reduced plasma albumin and increased prothrombin time. The mean ratios of plasma concentrations of unchanged paracetamol to paracetamol glucoronide and sulphate were significantly greater in patients with sever liver disease than the normal subjects. There were no significant differences in the overall 24-h urinary excretion of paracetamol and its glucuronide, sulphate, cysteine and mercapturic acid conjugates in the three groups. The glutathione conjugation of paracetamol did not seem to be impaired in patients with severe liver disease as evidence by the production of normal amounts of the cysteine and mercapturic acid conjugates. There is thus no evidence that they are at increased risk of hepatotoxicity when given a single therapeutic dose of paracetamol.
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PMID:Paracetamol metabolism in chronic liver disease. 49 92

We have selected for this study a well-defined group of patients with moderately advanced but compensated alcoholic cirrhosis. They were well-nourished and had no ascites, varices, azotemia, or encephalopathy. Liver biopsy showed little or no necrosis and inflammation despite wide-spread fibrosis. Serum bilirubin, transaminase, alkaline phosphatase, albumin and globulins were essentially normal. Biochemical evidence for liver disease was restricted to modest elevation of BSP retention, gamma GTP, serum bile acid concentrations, and urinary bile acid excretion. Except for changes in the interrelationships among the three biliary lipids, they were generally spared the abnormalities of sterol metabolism described in other patients with more advanced, more active liver disease. Thus, striking abnormalities in the metabolism of cholesterol and bile acids probably require severe reductions in functioning hepatocellular mass, major portal-systemic shunting, high disease activity, or all three to become manifest.
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PMID:Cholesterol and bile acid metabolism in moderately advanced, stable cirrhosis of the liver. 49 6


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