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Biomedical subjects

L Forman

Publications and source records attributed to L Forman.

At least 37 records · Page 2Linked to original sources
PubMed1987

Effect of oxalate and malonate on red cell metabolism.

The addition of oxalate to blood stored in Citrate-phosphate-dextrose (CPD) produces a marked improvement in 2,3-diphosphoglycerate (2,3-DPG) preservation; an increase in 2,3-DPG levels can also be documented in short-term incubation studies. Oxalate is a potent in vitro inhibitor of red cell lactate dehydrogenase, monophosphoglycerate mutase, and pyruvate kinase (PK). In the presence of fructose 1,6-diphosphate the latter inhibitory effect is competitive with phospho(enol)pyruvate (PEP). Determination of the levels of intermediate compounds in red cells incubated with oxalate suggest the presence of inhibition at the PK step, indicating that this is the site of oxalate action. Apparent inhibition at the glyceraldehyde phosphate dehydrogenase step is apparently due to an increase in the NADH/NAD ratio. Oxalate had no effect on the in vivo viability of rabbit red cells stored in CPD preservatives for 21 days. Greater understanding of the toxicity of oxalate is required before it can be considered suitable as a component of preservative media, but appreciation of the mechanism by which it affects 2,3-DPG levels may be important in design of other blood additives. Malonate, the 3-carbon dicarboxylic acid analogue of oxalate late did not inhibit pyruvate kinase nor affect 2,3-DPG levels.

2,3-Diphosphoglycerate↗
PubMed1986

G-6-PD Walter Reed: possible insight into "structural" NADP in G-6-PD.

A new G-6-PD variant, G-6-PD Walter Reed, causing hereditary nonspherocytic hemolytic anemia is characterized. This variant is unusual in that its stability requires the presence of high concentrations of NADP, while its Km for NADP is normal. This finding is consistent with the suggestion that G-6-PD has two separate binding sites, a high affinity "structural" site and a lower affinity catalytic site. The mutation in G-6-PD Walter Reed, like that of the previously described variant, G-6-PD Torrance, may be due to a mutation of the "structural" site for NADP.

Anemia, Hemolytic, Congenital↗
PubMed1986

Genetic variation within and among lion tamarins.

The golden lion tamarin Leontopithecus rosalia rosalia, one of the rarest and most endangered of New World primates, has been the focus of an intensive research and conservation effort for two decades. During that period, managed breeding from 44 founders has brought the captive population to over 400 individuals, a number that equals or exceeds the estimated number of free-ranging golden lion tamarins. The extent of genetic variation among golden lion tamarins was estimated with an electrophoretic survey of 47 allozyme loci from 67 captive and 73 free-ranging individuals. The amount of variation was low, compared to 15 other primate species, with 4% of the loci being polymorphic (P), and with an average heterozygosity H estimate of 0.01 in these callitrichids. Electrophoretic analyses of captive and free-ranging animals (N = 31) of two allopatric morphotypes, Leontopithecus rosalia chrysopygus and L. r. chrysomelas, were similar to the L. r. rosalia findings insofar as they also revealed limited genetic polymorphism. Computation of the Nei-genetic distance measurements showed that the three morphotypes were genetically very similar, although discernible differentiation had occurred at two loci. These data are consistent with the occurrence of recent reproductive isolations of these subspecies.

Animals↗
PubMed1983

Coexistence of alpha-thalassemia and a new pyruvate kinase variant: PK Fukien.

A 12-year-old male of Chinese ancestry had life-long hemolytic anemia attributed to alpha-thalassemia. Restriction endonuclease mapping of his DNA revealed that in reality, he had three alpha-globin loci, but he was homozygous for pyruvate kinase deficiency. The new pyruvate kinase variant carried by this patient was characterized and designated PK Fukien.

Blood Protein Electrophoresis↗
PubMed1983

Metabolic compensation for profound erythrocyte adenylate kinase deficiency. A hereditary enzyme defect without hemolytic anemia.

A child with hemolytic anemia was found to have severe erythrocyte adenylate kinase (AK) deficiency, but an equally enzyme-deficient sibling had no evidence of hemolysis. No residual enzyme activity was found in erythrocytes by spectrophotometric methods that could easily have detected 0.1% of normal activity. However, concentrated hemolysates were shown to have the capacity to generate small amounts of ATP and AMP from ADP after prolonged incubation. Hemolysates could also catalyze the transfer of labeled gamma-phosphate from ATP to ADP. Intact erythrocytes were able to transfer phosphate from the gamma-position of ATP to the beta-position, albeit at a rate substantially slower than normal. They could also incorporate 14C-labeled adenine into ADP and ATP. Thus, a small amount of residual AK-like activity representing about 1/2,000 of the activity normally present could be documented in the deficient erythrocytes. The residual activity was not inhibited by N-ethylmaleimide, which completely abolishes the activity of the normal AK1 isozyme of erythrocytes. The minute amount of residual activity in erythrocytes could represent a small amount of the AK2 isozyme, which has not been thought to be present in erythrocytes, or the activity of erythrocyte guanylate kinase with AMP substituting as substrate for GMP. Peripheral blood leukocytes, cultured skin fibroblasts, and transformed lymphoblasts from the deficient subject manifested about 17, 24, and 74%, respectively, of the activity of the concurrent controls. This residual activity is consistent with the existence of genetically independent AK isozyme, AK2, which is known to exist in these tissues. The cause of hemolysis in the proband was not identified. Possibilities include an unrelated enzyme deficiency or other erythrocyte enzyme defect and intraction of another unidentified defect with AK deficiency.

Adenine↗
PubMed1982

Polymorphonuclear cell chemotaxis to secretions of pathogenic and nonpathogenic Trichomonas vaginalis.

Polymorphonuclear cell chemotaxis to secretions of pathogenic and nonpathogenic strains of Trichomonas vaginalis were investigated. Cells from three groups, laboratory workers, patients with urogenital symptoms, and asymptomatic patients attending an antenatal clinic, all showed greater response to secretions of pathogenic strains, when the secretion was dilute. At higher concentrations of secretion, responses to both strains were similar, except in the pregnant group, where increased chemotaxis to pathogenic strains was still evident.

Animals↗
PubMed1980

In vitro attraction of polymorphonuclear leucocytes by Trichomonas vaginalis.

Boyden chambers were used to investigate the attraction of polymorphonuclear leucocytes to T. vaginalis. Chemotaxis to live organisms was demonstrated, and chemotaxis to T. vaginalis supernatant was shown to be concentration dependent. Both chemokinesis and true chemotaxis characterized the response to supernatants. There was no chemotaxis to the supernatant after it had been heated to 60 C for 1 hr, or to the supernatant from formalin-fixed T. vaginalis. The chemotactic factor in the supernatant did not pass through a dialysis membrane. Protein was found in the supernatant of T. vaginalis suspensions.

Adult↗
PubMed1979

Actinic chickenpox. Light-distributed varicella eruption.

When areas of the skin which are normally covered become sunburnt just before chickenpox eruption, there occurs a marked intensification of the rash on the freshly burnt parts. This phenomenon is not widely known. Its history, published reports and our original observations on this 'actinic' chickenpox are presented, with comment on its pathogenesis.

Adult↗
PubMed1977

Oral non-dystrophic bullous eruption mainly limited to the gingivae: a mechano bullous response. A variant of cicatricial mucous membrane pemphigoid?

Fourteen patients with recurrent blistering entirely restricted to the mouth have been observed for up to 7 years. Their average age was 52 years, and there was a predilection for females (ratio 2-5:1). Patients presented with thick-roofed blisters and denuded, red, boggy areas of mucosa. The area of maximal involvement with the labial gingiva, and whilst the blisters would arise spontaneously, mechanical trauma was the obvious provocative factor in all patients. Gentle friction on normal looking mucosa would produce a bulla which became blood filled. Re-epithelialization usually occurred within 1-3 weeks, with no scarring. Biopsies showed subepithelial bullae, and direct immunofluorescence was positive in the basement membrane zone of 2 of the 5 cases examined. The most striking feature was the extreme fragility of the epithelial attachment to the underlying corium, as shown by a useful clinical test with a probe. In 10 patients, the condition gradually remitted and the probe test became difficult to perform. The term acquired oral non-dystrophic epidermolysis bullosa was considered for the diagnosis, although a forme fruste of cicatricial mucous membrane pemphigoid remained an alternative.

Adult↗
PubMed1975

Bloom's syndrome: a probable new case with cytogenetic findings.

A 19-year-old Jordanian girl, born to first-cousin parents, has most features of Bloom's syndrome but is tall and has secondary amenorrhoea. Blood and skin cultures revealed a normal diploid female complement but about one-quarter of the cells show chromosome or chromatid gaps, breaks and rearrangements. These abnormalities were localized after trypsin banding and having been found non-randomly distributed along the chromosomes.

Abnormalities, Multiple↗