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Biomedical subjects

W J Jenkins

Publications and source records attributed to W J Jenkins.

At least 37 records · Page 2Linked to original sources
PubMed1982

Diclofenac hepatitis.

Explore the source record for details and available documents.

Chemical and Drug Induced Liver Injury↗
PubMed1982

Rh(D) fraction incompatibility causing hemolytic disease of the newborn. Report of two cases in a Chinese family.

Two cases of hemolytic disease of new born in a Chinese family are reported. The hemolysis was due to the production in the mother of antibodies against fractions A, C, and D of Rh(D) antigen. The fractions were absent in the mother's red blood cells which are Rh(DB) but present in her babies. Rh(DB) may be detected by the use of two types of anti-D sera, one with and the other without anti-DB activity. For transfusion purpose, all DB patients so tested, would be regarded as Rh(D) negative.

Adult↗
PubMed1982

Impaired acetaldehyde oxidation in alcoholics.

High blood acetaldehyde levels in alcoholics after ethanol ingestion are due to reduced acetaldehyde oxidation rather than to an increased rate of its formation from ethanol. This is associated with low hepatic acetaldehyde dehydrogenase activity in alcoholic subjects and may represent a specific abnormality in them.

Acetaldehyde↗
PubMed1982

Serum glutamate dehydrogenase is not a reliable marker of liver cell necrosis in alcoholics.

Serum glutamate dehydrogenase (EC 1.4.1.3.) activity was measured in 73 hospital patients who had a history of chronic alcohol abuse and who all had a liver biopsy performed. High levels of serum GDH activity occurred in those patients with recent excess alcohol consumption independently of the underlying liver histology, and did not discriminate between those patients with and those without alcoholic hepatitis.

Ethanol↗
PubMed1982

Guillain-Barré syndrome associated with hepatitis A in a male homosexual.

A 48-year-old male homosexual developed the Guillain-Barré syndrome in association with acute hepatitis. The hepatitis A virus was almost certainly transmitted sexually. Since the incidence of viral hepatitis is high in active male homosexuals, they are particularly at risk of developing such complications.

Hepatitis A↗
PubMed1981

Subcellular localisation of vitamin B12 during absorption in the guinea-pig ileum.

The subcellular distribution of vitamin B12 was studied during its absorption in the guinea-pig ileum. Animals were fed either (57Co) or (58Co) cyanocobalamin and killed two or four hours later. At two hours labelled cyanocobalamin was concentrated in brush border and lysosomal fractions of ileal homogenates, with some remaining in the sample layer. In contrast, at four hours labelled cyanocobalamin was concentrated predominantly in the cytosol with much smaller peaks in the brush border and lysosomal fractions. These findings are consistent with vitamin B12 absorption by receptor-mediated endocytosis. It is suggested that, after binding at the brush border, vitamin B12 is first sequestrated within lysosomes, and then released into the cytosol, from where it leaves the cell to enter the portal blood.

Animals↗
PubMed1981

Genetic factors in determining susceptibility to alcohol dependence and development of alcohol-induced liver disease.

There is considerable evidence in favour of genetic factors influencing excessive drinking behaviour and development of alcohol dependence (alcoholism), although readily identified markers of these genes have not been established. In addition, environmental factors undoubtedly play an important role. Although the probability of developing a significant liver disease (alcohol-induced hepatitis with or without cirrhosis) is related to the amount of alcohol ingested, there is a great variation in susceptibility which presumably stems from either genetic or additional environmental influences. The probable linkage of development of severe alcohol-induced liver disease with alleles of the HLA-B locus would suggest the influence of a gene(s) on chromosome 6. Such a gene may determine the rate or type of metabolism of alcohol or, since the immune response genes are present on chromosome 6, may indicate genetically controlled variation in the level of the immune and inflammatory response to alcohol-induced changes in liver membrane antigenicity. Further studies are needed to confirm these associations and to determine the type of factor involved.

Alcohol Oxidoreductases↗
PubMed1980

Selectively reduced hepatic acetaldehyde dehydrogenase in alcoholics.

Acetaldehyde dehydrogenase activity in liver biopsy specimens was considerably lower in 12 non-cirrhotic alcoholics than in 11 control subjects. It is suggested that reduced enzyme activity may cause the impaired metabolism of acetaldehyde reported in alcoholics and may play a part in the pathophysiology of alcoholism. Subcellular fractionation studies showed that acetaldehyde dehydrogenase was localised in the mitochondrial and cytosolic fractions of the liver cell, but in alcoholics the cytosolic component was selectively depleted. This deficiency may be a primary defect in alcoholics, reflecting the genetic aspect of alcoholism.

Acetaldehyde↗
PubMed1978

Analytical subcellular fractionation of jejunal biopsy specimens: enzyme activities, organelle pathology and response to corticosteroids in patients with non-responsive coeliac disease.

1. Jejunal biopsies from five patients with non-responsive coeliac disease have been subjected to analytical subcellular fractionation and enzymic microassay in order to compare the organelle pathology of this group with untreated but glutensensitive patients. 2. Compared with the gluten-sensitive group these non-responsive patients showed marked reduction of the endoplasmic reticulum enzymes, normal activities of lysosomal enzymes and slightly less severely reduced brush border activities. 3. It is suggested that the present biochemical studies in combination with previous clinical reports and measurements of DNA and protein synthesis by cultured mucosal biopsies delineate non-responsive coeliac disease as a distinct entity. 4. The patients were treated with oral prednisolone (20 mg daily) for between 5 and 9 weeks and the properties of the jejunal biopsies restudied. 5. Although morphologically there was only a partial restoration of the villus architecture the enzymic alterations and organelle abnormalities returned essentially to normal values.

Adult↗
PubMed1978

Mitochondrial enzyme activities in liver biopsies from patients with alcoholic liver disease.

The hypothesis that mictochondrial damage is a significant factor in the pathogenesis of alcoholic liver disease (ALD) was investigated by enzymic analysis of mitochondrial fractions isolated from needle biopsy specimens from control patients, patients with fatty liver due to chronic alcoholism, and from patients with other forms of liver disease. Enzymes associated with the inner and outer mitochondrial membranes showed normal levels in ALD. Enzymes associated with the mitochondrial matrix, glutamate dehydrogenase, malate dehydrogenase and aspartate aminotransferase showed significantly raised levels in ALD, but the levels in patients with non-alcoholic liver disease was normal. In addition, analysis of the mitochondria by sucrose density gradient centrifugation revealed no differences between control tissue and liver from patients with alcoholic liver disease. These results do not indicate that there is significant mitochondrial damage in ALD. The raised mitochondrial matrix enzymes may represent an adaptive response to the ethanol load.

Aspartate Aminotransferases↗
PubMed1975

Mechanized blood grouping: a hospital trial using an 8-channel grouping machine.

ABO and Rh (D) groups of 6403 blood samples were assessed on an 8/9-channel autoanalyser in the Serology Department of the London Hospital; the results were independently checked at the Regional Blood Transfusion Centre, Brentwood, using the routine methods for grouping donor blood. Results of this comparative study are given and instances are described in which anomalous results or incorrect groupings occurred; the possible causes are discussed. The 8/9-channel automated blood group analyser is evaluated in terms of routine hospital laboratory practice.

ABO Blood-Group System↗