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Biomedical subjects

W Bean

Publications and source records attributed to W Bean.

7 recordsLinked to original sources
PubMed1992

Potential for hepatic and renal dysfunction during influenza B infection, convalescence, and after induction of secondary viremia.

Whether infection with influenza B virus alters hepatic function was examined in the ferret. Also, the possibility that viral-specific antibodies (Ab) could be produced well before their detection in serum was explored. During the febrile period of influenza, reductions in the serum potassium, anion gap, ammonia, albumin and CPK and elevations of the BUN, creatinine and the GGTP levels occurred. With convalescence, the electrolytes, BUN and creatinine normalized, FFA, SGPT and CPK levels rose and the serum GGTP rose even further. Hepatic fatty acid (FA) oxidation, ornithine transcarbamylase (OTC) and carnitine palmitoyltransferase (CPT) activities were minimally altered and liver ATP and total lipid content remained normal. Following experimental secondary viremia, serum FFA continued to rise, TG decreased and CPK remained elevated while SGPT and GGTP levels normalized. In the liver, FA oxidation and OTC rates remained unchanged but CPT activity was inhibited and the liver content of ATP was significantly reduced. Immune complex (IC) protein recovered from postmicrosomal supernatant fractions by polyethylene glycol precipitation was progressively increased in livers from convalescent and viremic animals. While the amount of IC protein recovered in the spleen also increases during convalescence, this is not the case after viremia when the IC formed seem to be processed largely by the liver. By SDS/PAGE, the major proteins identified in the IC were IgM and other viral proteins. However, the viral proteins could not be validated by immunoblot with Ab produced against purified influenza B hemagglutinin (HA) and neuraminidase (NA) most probably due to phagocytic alterations of glycoprotein immunodeterminants. These findings indicate that during influenza, convalescence and post viremia changes in the concentrations of several serum and liver components occur that reflect hepatic involvement. Also, antiviral Ab, largely IgM, appears to be produced early, complexes with Ag and can be found sequestered in both the liver and spleen at a time when Ab is not detectable in the serum.

Adenosine Triphosphate↗
PubMed1991

Acute alterations in the regulation of lipid metabolism after intravascular reexposure to a single bolus of homologous virus during influenza B infection in ferrets: possible model of epiphenomena associated with influenza.

Metabolic responses occurring 24 h following the secondary haematogenous dissemination of influenza B virus during convalescence from infection were examined in the ferret as a possible model for epiphenomena which can occur following infection with influenza. Among the major changes found were a further rise in the mean fasting serum free fatty acid (FFA) level to three times the control mean value and a 50% drop in the mean serum triglyceride (TG) concentration after the intravascular administration of a single bolus of virus compared to levels found in uninfected or convalescent animals. In adipose tissue, hormone-sensitive and lipoprotein lipase activities were increased six and three-fold, respectively, over mean control values, probably accounting for the changes that were observed in serum lipid concentrations. In the liver, total carnitine palmitoyltransferase (CPT) activity was affected only slightly and the total lipid content of the liver remained unchanged. These findings indicate that 24 h after the intravascular dissemination of homologous virus in a single bolus during convalescence from influenza B infection, major distortions in the regulation of lipid metabolism occur in the ferret. Loss of the synchronous regulation of the two adipose tissue lipases is a significant consequence leading to the mobilization of a large amount of FFA during fasting from both adipose tissue and the circulating plasma TG stores.

Adipose Tissue↗
PubMed1990

Hepatic steatosis during convalescence from influenza B infection in ferrets with postprandial hyperinsulinemia.

The possibility that postprandial hyperinsulinemia could play a role in the development of hepatic lipid disturbances during convalescence from influenza B infection was explored in the ferret as a possible model of the steatosis of Reye's syndrome. Postprandial hyperinsulinemia was produced by feeding young ferrets glucose/water and a regular diet (glucose-treated group), as reflected by the mean serum insulin levels attained, which were 57 and 135 microU/ml during control and postinfluenza periods, respectively. By comparison, ferrets fed water and a regular diet (untreated group) had mean insulin levels of 19 and 22 microU/ml, while postprandial glucose levels were comparable in the two groups of animals for each period. In contrast to untreated animals, grossly visible fatty livers were found in glucose-treated ferrets during convalescence. The total lipid content of these livers had doubled compared with preinfection samples and compared with livers of untreated ferrets. By electron microscopy hepatic mitochondria showed striking changes with diminution of matrix density and reduction in cristae surface area only in convalescent samples from glucose-treated animals. Serum free fatty acid (FFA) levels were considerably higher in the glucose-treated animals during fasting before influenza and also after feeding during convalescence. Serum triglyceride (TG) levels were also high during convalescence in the glucose-treated group. Adipose tissue lipoprotein lipase activities were similar between groups, but hormone-sensitive lipase activity was twelvefold higher in glucose-treated ferrets before and after influenza B. These findings indicate that for a given stimulus, glucose-treated ferrets would mobilize more FFA than untreated ferrets. The total capacity for beta-oxidation of FA by the mitochondrial pathway was identical in all groups of animals. Total carnitine palmitoyl transferase (CPT) activity was the same in both control groups, but was significantly diminished in glucose-treated animals during convalescence. As CPT regulates the entry of FA into the mitochondrial matrix, its reduction in response to higher insulin concentrations would limit the oxidation of FA and stimulate TG accumulation. Therefore, the accumulation of lipid in the liver in this model is regarded to have been caused by the simultaneous occurrence of increased lipolysis and increased hepatic TG synthesis owing, in part, to diversion of activated FA by CPT, which is reduced in activity due to the regulatory action of insulin. These findings may have pathophysiologic relevance for the lipid changes that occur in Reye's syndrome and to fatty liver formation in hyperinsulinemic states.

Adipose Tissue↗
PubMed1976

Some notes of an aging nail watcher.

Growth of deciduous tissues gives us a natural kymograph to record secular trends and in some instances makes the mark on the moving record. For the observant clinician, knowledge of the rate of nail growth may permit an occasional spectacular diagnosis, although much more often it merely adds a small bit to our understanding of simple but basic biological prenciples in health and disease.

Aging↗