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Biomedical subjects

J B Hudson

Publications and source records attributed to J B Hudson.

At least 91 records · Page 5Linked to original sources
PubMed1980

Moonshine-related arsenic poisoning.

Twelve sequential cases of arsenic poisoning were reviewed for possible sources of ingestion. Contaminated illicit whiskey (moonshine) appeared to be the source in approximately 50% of the patients. An analysis of.confiscated moonshine revealed that occasional specimens contained high levels of arsenic as a contaminant. Although arsenic poisoning occurs relatively infrequently, contaminated moonshine may be an important cause of the poisoning in some areas of the country.

Adult↗
PubMed1980

Parathyroid hormone and 25-hydroxycholecalciferol levels in hypercalcemia of acute renal failure.

A 38-year-old man developed symptomatic hypercalcemia during the diuretic phase of acute renal failure secondary to rhabdomyolysis. Although early secondary hyperparathyroidism was documented, parathyroid hormone levels fell when hypercalcemia occurred. The 25-hydroxycholecalciferol level was normal on two separate occasions during the hypercalcemia. Remobilization of muscle calcium deposits during diuresis is proposed as the cause of the hypercalcemia in this syndrome.

Acute Kidney Injury↗
PubMed1979

Isolated ultrafiltration in the therapy of volume overload accompanying oliguric vascular shock states.

Isolated ultrafiltration (removal of plasma water and solute without dialysis) was used as a "last resort" therapy in three patients with diuretic and pressor resistant oliguria complicating severe volume overload and vascular shock. The improvement in clinical and hemodynamic parameters is reported and the possible mechanisms of action (decreased pulmonary capillary wedge pressure and increased colloid osmotic pressure) are discussed.

Anuria↗
PubMed1979

Vertical transmission of murine cytomegalovirus.

Congenital abnormalities induced by murine cytomegalovirus have previously been suggested to be an indirect effect of maternal illness as no infectious virus has been isolated from the foetus. However, in this article we report that latent virus detectable by immunofluorescence and in situ hybridization, may frequently be present in foetal tissues.

Animals↗
PubMed1979

Interaction of murine cytomegalovirus with separated populations of spleen cells.

Mouse spleen cultures were infected with murine cytomegalovirus, either before or after separating the cells into various classes, and the growth of virus and production of infectious centers were measured in each cell class. The separation techniques, which were used in various combinations, comprised: adherence to plastic surfaces; adherence to nylon wool columns; gamma irradiation; and treatment with anti-immunoglobulin serum plus complement. The "macrophage population" took up most of the input virus, as shown by autoradiography of spleen cells infected with radioactive virus. These cells formed infectious centers but replicated the virus only transiently. In contrast, the "B-lymphocyte population" contained a minor cell fraction which was permissive for replication. The "T-lymphocyte population" appeared to be nonpermissive for replication and did not produce infectious centers.

Animals↗
PubMed1979

Isolated ultrafiltration in the treatment of fluid overload in cardiogenic shock.

Dramatic improvement in measured hemodynamic values, arterial blood gas values, and renal function was quickly achieved by the use of isolated ultrafiltration in a patient with cardiogenic shock refractory to medical management. Swift venous access was obtained by femoral catheterization, and the rapid removal of 3,500 mL of ultrafiltrate was well tolerated. This technique may afford another mode of therapy in patients with refractory cardiogenic shock associated with severe volume overload.

Catheterization↗
PubMed1978

Multiple interactions between murine cytomegalovirus and lymphoid cells in vitro.

Spleen cultures from various strains of mice were infected in vitro with murine cytomegalovirus (MCMV). Infectious centres were established in a small proportion (not greater than 1%) of the cells. Virus could be rescued from these cells by co-cultivation with syngeneic or allogeneic fibroblasts, but the frequency of rescue could not be altered by incubation with cyclic nucleotide analogues, iododeoxyuridine, cortisol, or allogeneic spleen cells. In addition a smaller fraction of the cell population, possibly a sub-population of the infectious centres, replicated virus spontaneously. The presence of mitogens did not affect these interactions qualitatively or quantitatively. A third response to infection was an inhibition in DNA synthesis, which was suffered by unstimulated cultures and by cells transformed by concanavalin A and bacterial lipopolysaccharides, although overall cell viability was maintained. This response was also mediated by u.v.-inactivated virus.

Animals↗
PubMed1978

Regulation of murine cytomegalovirus gene expression. I. Transcription during productive infection.

Murine cytomegalovirus RNA synthesis in productively infected mouse embryo cultures was measured by reassociation kinetics with iodinated viral DNA. The data were analyzed by a computer program and indicated the following: before DNA replication approximately 25% of the genome was transcribed into asymmetric transcripts, of which slightly fewer than half of the sequences were recovered from the cytoplasm. After viral DNA replication, approximately 38% of the genome was transcribed (5% as symmetric transcripts), and again less than half of the sequences appeared in the cytoplasm. Both early and late RNA comprised two abundance classes differing about 8- to 10-fold in concentration. Early RNA was a subset of late RNA. The RNE sequences synthesized in late-infected cells in the presence of cytosine arabinoside or cycloheximide were similar to early RNA. Thus, murine cytomegalovirus displays temporal, quantitative, and post-transcriptional controls over gene expression, but the pattern differs considerably from herpes simplex virus.

Animals↗
PubMed1978

Chronic renal insufficiency from cortical necrosis induced by arsenic poisoning.

A 39-year-old man had anuria and azotemia and was found to be suffering from acute arsenic poisoning. After two peritoneal dialyses, partial renal function returned, and the patient has survived for five years without dialysis. Renal cortical necrosis was demonstrated by renal biopsy and renal calcification. We suggest that arsenic be added to the list of substances capable of causing renal cortical necrosis and recommend consideration of this complication in cases of arsenical poisoning.

Acute Disease↗