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Biomedical subjects

W D Reed

Publications and source records attributed to W D Reed.

At least 55 records · Page 3Linked to original sources
PubMed1984

Thymus-dependence of autoantibody responses to liver specific lipoprotein in the mouse.

Proposed mechanisms for the induction of autoantibodies to liver specific lipoprotein (LSP) assume that the autoantibody response is T-dependent. This hypothesis was tested in the athymic nude mouse. Athymic homozygote (nu/nu) nude mice and appropriate control mouse strains were immunized with rabbit or human LSP and infected with murine cytomegalovirus (MCMV) in an attempt to induce autoantibodies to LSP. Antibodies to LSP were measured by passive haemagglutination and by an enzyme linked immunosorbent assay. Nude mice did not produce antibodies to either foreign LSP species or autoantibodies to mouse LSP when immunized with either rabbit or human LSP. Control heterozygote (nu/+) mice and C57BL/6J mice produced antibody to foreign LSP and autoantibody to mouse LSP when immunized with xenogeneic LSP. Athymic nu/nu mice also failed to produce autoantibody to mouse LSP following infection with MCMV, in contrast to control nu/+ and C57BL/6J mice which produced LSP autoantibody after infection with MCMV. It is concluded that the autoantibody response to LSP is T-dependent.

Animals↗
PubMed1983

Autoantibodies to liver-specific lipoprotein following hepatitis induced by mouse cytomegalovirus.

Autoantibodies to liver specific lipoprotein (LSP) are produced following acute non-fatal hepatitis in murine cytomegalovirus (MCMV) infected mice. Both C57B1 and BALB/c mice produced a transient LSP autoantibody response demonstrated by passive haemagglutination and enzyme linked immunosorbent assay. C57Bl mice produced both IgM and IgG LSP autoantibody and BALB/c mice produced only IgM autoantibody. The autoantibody was species non-specific, reacting with both mouse and rabbit LSP. Plasma containing LSP autoantibody reacted with the surface of normal mouse hepatocytes by immunofluorescence. This model provides an opportunity for study of LSP autoantibody production during viral hepatitis.

Animals↗
PubMed1981

Intracranial complications of sphenoidal sinus inflammation.

A young man who presented with bacterial meningitis and visual disturbance developed a left sixth nerve palsy due to an isolated sphenoidal sinus inflammation caused by Corynebacterium haemolyticum. Sphenoidal sinusitis and intracranial infection by C. haemolyticum are uncommon complications.

Adult↗
PubMed1981

Selective carnitine palmitoyltransferase deficiency in fibroblasts from a patient with muscle CPT deficiency.

A 13-year-old boy developed cramps and myoglobinuria following exertion. Mitochondrial preparations from a skeletal muscle biopsy were deficient in carnitine palmitoyltransferase (CPT) activity when assayed by the hydroxamate and kinetic assays. The patient's fibroblasts were also deficient when assayed by the hydroxamate and kinetic assays, but not when tested by the DTNB (5,5'-dithiobis-[nitrobenzoic acid]) method. This disparity probably indicates a specific deficiency in fibroblasts of one of the two carnitine palmitoyltransferases, presumably CPT II.

Acyltransferases↗
PubMed1981

Ketone bodies, glucose and glutamine as lipogenic precursors in human diploid fibroblasts.

Incorporation of [14C] from acetoacetate, D(-)- and L(+)-3-hydroxybutyrate, glucose, glutamine, acetate and palmitate in cellular lipids were studied in cultures in human diploid fibroblasts (HDF). The results showed that acetoacetate was 2-10 times more effective as a lipogenic precursor than was either D- or L-3-hydroxybutyrate. Its extent of incorporation into lipids was 2- to 8-fold more than the other precursors examined under conditions when the overall rates of nonsaponifiable and saponifiable lipogenesis as measured by 3H2O incorporation were essentially unchanged. Acetoacetate supported both saponifiable and nonsaponifiable lipid synthesis with half-saturation values (Km app.) of 185 microM and 30 microM, respectively. Glucose stimulated acetoacetate incorporation into lipids whereas, conversely, acetoacetate inhibited [14C]glucose incorporation into lipids. The presence of low density lipoproteins (LDL) cholesterol (40 microgram cholesterol/mL) inhibited the incorporation of [14C] from acetoacetate 56% into nonsaponifiable lipids; the inhibition was consistently higher (75%) when [14C]glucose or glutamine were the precursors. The loss of 3-hydroxy-3-methyl-glutaryl CoA (HMG CoA) reductase activity upon addition of LDL-cholesterol was greater than the suppression of [14C] incorporation from acetoacetate or glucose into nonsaponifiable lipids. In the presence of glucose, [14C]acetoacetate was incorporated into 3-beta OH sterols (digitonin precipitable) 7.7 +/- 1.1 times more effectively than was [14C]glucose. The results suggest that HDF would be a suitable model to investigate the effects of various precursors of HMG CoA on the rate of cholesterol biosynthesis.

3-Hydroxybutyric Acid↗
PubMed1981

Comparison of the oxidation of glutamine, glucose, ketone bodies and fatty acids by human diploid fibroblasts.

The contribution of glutamine, glucose, ketone bodies and fatty acids to the oxidative energy metabolism of human diploid fibroblasts ws studied. The rate of glutamine oxidation by fibroblasts was 98 nmol/h per mg cell protein compared to 2 nmol/h per mg cell protein or less for glucose, acetoacetate, D-3-hydroxybutyrate, octanoic acid and palmitic acid. Glucose inhibited glutamine oxidation by 85%, while the other substrates had no effect. Therefore, these cells meet their energy requirement almost solely by anaerobic glycolysis and glutamine oxidation.

Cell Line↗
PubMed1981

Autoantibody responses to liver-specific lipoprotein in mice.

Autoantibody to the hepatocyte membrane antigen, liver-specific lipoprotein (LSP) was induced in mice by immunization with LSP-containing protein preparations from human, rat, rabbit and mouse liver and also with purified allogeneic LSP. Each of the strains of mice used (C57B1, BALB/c, C3H) showed the capacity to produce high titre autoantibody to LSP. Autoantibody to LSP demonstrated by passive haemagglutination was absorbed by normal mouse hepatocytes but not by kidney or spleen cells and reacted with the cell membrane of normal mouse hepatocytes by immunofluorescence. The liver was examined histologically in all mice and where inflammation was found it was attributable to the Freund's complete adjuvant used in immunization rather than liver protein immunogen. The demonstration of high titre autoantibody to LSP in mice without associated hepatitis contrasts with chronic hepatitis in man and experimental chronic hepatitis in rabbits where autoantibodies to LSP have been implicated in the pathogenesis of the disease.

Animals↗
PubMed1980

A case of filariasis diagnosed on gastric cytology.

Cytological examination of gastric washings or brushing is a widely accepted technique used as a diagnostic aid in the detection of gastric malignancy. Occasionally, cytology may also provide valuable information concerning a variety of non-neoplastic disorders. This brief report is of the exceptional experience of finding numerous microfilariae of Loa loa type in a gastric lavage specimen. This observation led to appropriate further investigation and successful treatment.

Cytodiagnosis↗
PubMed1980

Epidemiology of chronic hepatitis in Perth, Western Australia.

A survey was made on 50 patients with active chronic hepatitis (ACH) seen in Perth, Western Australia. The aetiology varied: three cases followed metabolic disease, 8 drugs or alcohol, 12 were due to hepatitis B and no cause in 27. There was a male preponderance in the first three groups and a female preponderance in the idiopathic group. The drug dependent group had a greater mean age than the other groups. Autoantibodies were present in 40 of the cases--the most frequent were antismooth muscle antibody in 24 cases and antinuclear factor in 13 cases. Six patients (12%) improved and are well following discontinuation of therapy. Seven (14%) have died. The rest (74%) remain on treatment.

Adolescent↗
PubMed1979

The effects of maternal ethanol consumption in the rat on the development of their offspring.

The effects of ethanol on the physical development and maturation of the CNS in the offspring of lactating rats were investigated. Dams were fed: 1) regular stock diet (control), 2) liquid diet containing 35% of the calories as ethanol (ETOH) or 3) liquid diet with maltose-dextrin substituted for the calories supplied by ethanol (isoenergetic = IE). Diets were administered from the 14th day of gestation until 3 weeks post-partum (pre- and post-natal exposure) or from birth until 3 weeks post-partum (post-natal exposure). Body weight, crown-rump length and tail length, as well as brain weight were followed longitudinally in the pups. The growth in the pups of dams fed ETOH diet and those fed IE diet were significantly less than that observed in the pups of control dams. Furthermore, pups of dams fed the ETOH diet showed retardation in growth indices and brain weight at various ages when compared to pups of equivalent age from dams fed the IE diet. Therefore, administration of ethanol to pregnant or lactating dams impaired the physical growth, including central nervous systems (CNS), of their offspring more than those changes caused by nitritional deprivation.

Animals↗
PubMed1978

Effect of L-alanine infusion on gluconeogenesis and ketogenesis in the rat in vivo.

1. In 48 h-starved 6-week-old rats the 14C incorporation in vivo into blood glucose from a constant-specific-radioactivity pool of circulating [14c]actateconfirmed that lactate is the preferred gluconeogenic substrate. 2. Increasing the blood [alanine] to that occurrring in the fed state increased 14C incorporation into blood glucose 2.3-fold from [14c]alanine and 1.7-fold from [14c]lactate. 3. When the blood [alanine] was increased to that in the fed state, the 14C incorporation into liver glycogen from circulating [14c]alanine or [14c]lactate increased 13.5- and 1.7-fold respectively. 4. The incorporation of 14C into blood acetoacetate and 3-hydroxybutyrate from a constant-specific-radioactivity pool of circulating [14c]oleate was virtually abolished by increasing the blood [alanine] to that existing in the fed state. However, the [acetoacetate] remained unchanged, whereas [3-hydroxybutyrate] decreased, although less rapidly than did its radiochemical concentration. 5. It is concluded that during starvation in 6-week-old rats, the blood [alanine] appears to influence ketogenesis for circulating unesterfied fatty acids and inversely affects gluconeogenesis from either lactate or alanine. A different pattern of gluconeogenesis may exist for alanine and lactate as evidenced by comparative 14C incorporation into liver glycogen and blood glucose.

Acetoacetates↗
PubMed1977

Hypoketonaemic effect of L-alamine. Specific decrease in blood concentrations of 3-hydroxybutyrate in the rat.

1. The injection of L-alanine (50-100 mg/kg) into 35-day-old rats that had been starveed for 48 h increased blood L-alanine concentration to values observed in fed animals and lowered the blood concentration of 3-hydroxybutyrate within 2 min. 2. This hypoketon aemic action of L-alanine was specific for 3-hydroxybutyrate, since the acetoacetate concentrations did not change significantly. 3. The decrease in 3-hydroxybutyrate elicited by L-alanine was not related to changes in the blood concentrations of insulin, glucagon, growth hormone, glucose, unesterified fatty acids, lactate or pyruvate. 4. The injection of L-alanine resulted in a decrease in total ketones that was apparently unrelated to their increased peripheral utilization. These results are interpreted as an anti-ketogenic action of L-alanine. 5. The data suggest that L-alamine lowers ketone-body formation in starved rats, possibly via an alteration in hepatic redox equilibrium.

Acetates↗
PubMed1977

Effects of starvation and development on mitochondrial acetoacetyl-coenzyme A thiolase of rat liver.

The activity of the putative ketogenic beta-oxoacyl-CoA thiolase from mitochondria of rat liver increases with starvation, during neonatal life, and after the injection of glucagon. These changes are associated with alteration in ketonaemia. The changes in activities of this species of thiolase are not associated with significant alterations in the apparent affinity (Km) for the ketogenic substrate, acetyl-CoA. These results support a role for thiolase in the regulation of ketogenesis.

Acetyl-CoA C-Acetyltransferase↗