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Biomedical subjects

B A Davis

Publications and source records attributed to B A Davis.

At least 109 records · Page 6Linked to original sources
PubMed1986

Detection of Chlamydia trachomatis in genital specimens by the Microtrak direct specimen test.

The conventional cell culture method for detection of Chlamydia trachomatis requires two to six days and is technically difficult to perform. The authors evaluated a new, relatively simple, non-culture method (MicroTrak, Syva Co., Palo Alto, CA) that requires less than one hour to complete. Two hundred fifty-one cervical and 209 male urethral specimens from three Richmond health clinics were read by direct immunofluorescence staining and compared with cell culture technics using iodine staining. Patient specimens were applied directly onto microscope slides (8 mm well) and stained with a fluorescein-labeled monoclonal antibody. Slides were examined for 10-15 minutes at X1,000 using an AO epifluorescent microscope and were considered positive if five or more typical elementary bodies were seen. The sensitivity, specificity, positive and negative predictive values for the direct smear were 89%, 97%, 85%, and 98% for males, and 93%, 96%, 85%, and 98% for females, respectively. The rapid direct specimen test appears to be a satisfactory method for detecting chlamydia in male and female genital specimens.

Cervix Uteri↗
PubMed1985

The human glutathione S-transferases: developmental aspects of the GST1, GST2, and GST3 loci.

The expression of the GST1, GST2, and GST3 loci in fetal, neonatal, and infant tissues has been studied using starch gel electrophoresis and chromatofocusing. Each locus demonstrated developmental changes in expression, some of which were specific to a single tissue while others occurred in several tissues. GST1 was not usually expressed in any of the tissues studied before 30 weeks of gestation but steadily increased thereafter until adult levels were reached in late infancy. In neonates and older infants the frequencies of the GST1*0, GST1*1, and GST1*2 alleles were 0.79, 0.07, and 0.14, respectively. GST2 was always expressed in liver and adrenal but was only weakly expressed in spleen, cardiac muscle, and diaphragm. In kidney this locus was not usually expressed until nearly 1 year after birth. The GST3 isoenzymes were present in all fetal, neonatal, and infant tissues, although their expression in liver decreased after 30 weeks of gestation. Other isoenzymes with fast anodal mobilities were also identified in several tissues; these are believed to be GST3 isoenzymes that have undergone posttranslational modification rather than products of the putative GST4 locus. No specifically fetal isoenzymes were detected.

Chromatography↗
PubMed1984

The human glutathione S-transferases: studies on the tissue distribution and genetic variation of the GST1, GST2 and GST3 isozymes.

Three sets of isozymes of glutathione-S-transferase (GST) have been identified in human tissues. They differ in their tissue distribution, incidence of genetic variation, susceptibility to inactivation by N-ethylmaleimide and in their electrophoretic mobilities. The GST1 isozymes exhibit four phenotypes, including a common 'null' phenotype attributable to different combinations of three autosomal alleles GST1 1, GST1 2 and GST1 0 of frequency 0.13, 0.23 and 0.64, respectively, in the European population. The genetic polymorphism of GST1 is easily demonstrable in adult liver, kidney, adrenal and stomach but the isozymes are only weakly expressed in skeletal and cardiac muscle and not at all in fetal liver, fibroblasts, erythrocytes, lymphocytes and platelets. The GST2 isozymes also exhibit variant patterns but these are probably due to post-synthetic modification rather than allelic variation. The GST2 isozymes are not detectable in erythrocytes, platelets, cultured fibroblasts or lymphocytoid cells but are found in many other tissues, including fetal liver. GST3 isozymes were found as relatively strong components in every tissue examined except adult liver, with slight tissue to tissue variability in electrophoretic mobility.

Adrenal Glands↗
PubMed1983

Regulation of cardiac sarcoplasmic reticulum calcium transport by calcium-calmodulin-dependent phosphorylation.

Cardiac sarcoplasmic reticulum contains an endogenous calcium-calmodulin-dependent protein kinase and a 22,000-Da substrate, phospholamban. This kinase is half-maximally activated (EC50) by 3.8 +/- 0.3 microM calcium and is absolutely dependent on exogenous calmodulin (EC50 = 49 nM). To determine the effect of this phosphorylation on calcium transport, sarcoplasmic reticulum vesicles (0.5 mg/ml) were preincubated under conditions for optimal phosphorylation (50 mM potassium phosphate, pH 7.0, 10 mM MgCl2, 0.5 mM EGTA, 0.478 mM CACl2, 0.1 microM calmodulin, 0.5 mM ATP). Control sarcoplasmic reticulum was preincubated under identical conditions but in the absence of ATP to avoid phosphorylation. Both control and phosphorylated vesicles were centrifuged and resuspended in 0.3 M sucrose, 20 mM Tris-HCl, 100 mM KCl, pH 7.0, to remove calmodulin and subsequently assayed for calcium (45Ca) transport in the presence of 2.5 mM Tris-oxalate. Phosphorylation of sarcoplasmic reticulum vesicles by calcium-calmodulin-dependent protein kinase resulted in a significant increase (2- to 4-fold) in the rate of calcium transport at low calcium concentrations (less than 3 microM), while calcium transport was minimally affected at higher calcium. Hill coefficients (n) derived from Hill plots of transport data showed no difference between control and phosphorylated sarcoplasmic reticulum (n = 2.0), indicating that phosphorylation does not alter the cooperativity between calcium sites on the calcium pump. The EC50 for calcium activation of calcium transport by control vesicles was 0.86 +/- 0.1 microM calcium, and phosphorylation of phospholamban decreased this value to 0.61 +/- 0.07 microM calcium (n = 7, p less than 0.028), indicating an increase in the apparent affinity for calcium upon phosphorylation. These results were found to be specific for calcium-calmodulin-dependent phosphorylation of phospholamban. Control experiments on the effects of the reactants used in the phosphorylation assay and subsequent centrifugation of sarcoplasmic reticulum showed no alteration of the rate of calcium transport. Therefore, the calcium pump in cardiac sarcoplasmic reticulum appears to be regulated by an endogenous calcium-calmodulin-dependent protein kinase, and this may provide an important regulatory mechanism for the myocardium.

Adenosine Triphosphatases↗
PubMed1983

[3H]nimodipine specific binding to cardiac myocytes and subcellular fractions.

[3H]Nimodipine binding was studied in isolated myocytes from rat heart and in partially purified sarcolemma, sarcoplasmic reticulum and mitochondrial fractions from dog heart. In isolated myocytes, the density of [3H]nimodipine specific sites (10(6) per cell) was close to density of [3H]QNB sites (0.8 x 10(6) per cell) and higher than that of [3H]DHA sites (0.2 x 10(6) per cell). During subcellular fractionation, [3H]nimodipine binding did not copurify with plasma membrane markers. The highest densities were found in fractions enriched in sarcolemma or in sarcoplasmic reticulum. No specific binding was found in mitochondria. These results indicate that the localization of [3H]nimodipine sites is not restricted to areas of the plasma membrane rich in beta-adrenoceptors, muscarinic receptors and sodium pump sites.

Animals↗
PubMed1983

Potentiation of the biochemical effects of beta-phenylethylhydrazine by deuterium substitution.

The concentrations of dopamine (DA), m-tyramine (mTA), p-tyramine (pTA) and serotonin (5-HT) in the striata of rats 18 hr after the administration of three different doses (5, 50, or 100 mg/kg) of beta-phenylethylhydrazine (phenelzine, PEH) were measured. These concentrations were compared to those following the administration of the same doses of 1,1,2,2-tetradeutero-PEH (d4PEH). In general, PEH and d4PEH caused dose-dependent increases in the levels of mTA, pTA and 5-HT. The lowest dose of d4PEH caused greater increases than PEH in the levels of all four monoamines. The concentration of 5-HT was increased more by d4PEH than PEH at all three doses. The inhibition of mitochondrial MAO obtained from rat striatum by PEH or d4PEH in vitro revealed no differences. However, the inhibition of striatal MAO obtained from rats injected with d4PEH was found to be greater than that from rats injected with PEH. It was concluded that deuteration of PEH potentiates its ability to inhibit MAO following its administration to the rat by slowing its degradation in vivo.

Animals↗
PubMed1983

Trace acid levels in the plasma and MAO activity in the platelets of violent offenders.

The plasma concentrations of the unconjugated and conjugated so-called "trace acids," phenylacetic acid (PAA), m- and p-hydroxyphenylacetic acid (mHPA, pHPA), and platelet monoamine oxidase (MAO) activity were measured in 103 male prisoners detained in a psychiatric institution. Twenty-three had been convicted of violent crimes, 18 of sexual offenses, 24 of armed robbery, 27 of nonviolent property offenses, and 11 of miscellaneous nonviolent offenses. Unconjugated pHPA and conjugated PAA were found to be significantly reduced in the violent offenders when compared with those of the "nonviolent" groups. The levels of pHPA were also found to be low in sexual offenders. Platelet MAO activities to phenylethylamine, tryptamine, and p-tyramine between any of the categories of prisoners were not significantly different.

Adolescent↗
PubMed1983

Correlative relationship between biochemical activity and aggressive behaviour.

Correlative relationships were investigated between biogenic trace amines and histories of violence among offenders incarcerated in two federal penitentiaries. Plasma levels of unconjugated (U) and conjugated (C) trace acids (PAA, mHPA and pHPA) and platelet MAO activity to the substrates PE, TRYP and TA were assessed. A pilot study (N = 26) revealed a lower activity of MAO to TRYP among violent offenders. The factor analytically derived scale, Prison Disturbance, correlated with mHPA (U) .77 (p less than .001), mHPA(C) -.42 (p less than .05) and PAA (U) -.37 (p less than .10), controlling for time incarcerated. In the principal investigation (N = 103), PAA(C) (p less than .01), pHPA (U) (p less than .05) levels, and MAO activity to TRYP (p less than .05) were lower among violent offenders. Factor scores of biochemical activity produced even more significant results. However, when these results were cross validated with data from the pilot study, only minimal relationships were maintained.

Adult↗
PubMed1983

A study of the catabolism of trace amines in mentally disordered individuals with particular reference to agoraphobic patients with panic attacks.

Platelet MAO activity toward several trace amine substrates and the plasma levels of some trace acids have been investigated. Compared to controls, the agoraphobic patients were found to have significantly increased MAO activity. The substrate specificity in some of the patients appeared to be altered. The plasma levels of p-HPA and m-HPA were significantly lower than those of the control groups.

Adult↗
PubMed1983

Platelet monoamine oxidase activity and trace acid levels in plasma of agoraphobic patients.

Platelet monoamine oxidase activity and plasma trace acid levels in 29 patients classified as agoraphobics was estimated. MAO activity towards p-tyramine and beta-phenylethylamine was found to be significantly higher in agoraphobics than in non-agoraphobic depressed patients and healthy controls. In addition plasma p-hydroxyphenylacetic acid levels were low in both agoraphobic and depressed patient groups. All patients were also assessed by Spielberger State Anxiety and the short form of the Beck Depression Inventory scales. No significant correlations could be found between platelet MAO activity or plasma trace acid levels and the psychological scores.

Adult↗
PubMed1982

Plasma concentrations of p- and m-hydroxyphenylacetic acid and phenylacetic acid in humans: gas chromatographic--high-resolution mass spectrometric analysis.

Conjugated and unconjugated phenylacetic acid and m- and p-hydroxyphenylacetic acid have been determined in the plasma of normal, healthy subjects after fasting, consumption of a meal and ingestion of deuterium labelled amine precursors, by high-resolution gas chromatography--high resolution mass spectrometry with selected ion monitoring of their trifluoroethyl-pentafluoropropionyl derivatives. We observed tht all three conjugated acids are higher in fasting than in non-fasting subjects, and unconjugated phenylacetic acid was lower. Ingestion of deuterium-labelled amine precursors resulted in the appearance in the blood of the correspondingly labelled acids, a peak in the concentrations being reached about 1 h after consumption. Conjugated and unconjugated acids as expected increased following the consumption of a meal. Unconjugated phenylacetic acid was significantly higher in females than in males. Most values tended to increase with age, with male unconjugated and conjugated m-hydroxyphenylacetic acid and female conjugated phenylacetic and m-hydroxyphenylacetic acids increasing significantly.

Eating↗
PubMed1982

Deuterium isotope effects in the ninhydrin reaction of primary amines.

The rate of development of Ruhemann's purple in the ninhydrin reaction of two deuterated primary amines, aa-d2-p-tyramine and aa-d2-beta-phenylethylamine, is significantly reduced. It appears to be a primary isotope effect and indicates that the cleavage of the carbon-hydrogen bond at the a-position is involved in the rate-determining step of the color reaction.

Amines↗
PubMed1982

Alterations in trace amine and trace acid concentrations in isolated aggressive mice.

We have used an animal model of aggression, the isolation syndrome in mice, to examine the possible role of the trace amines, beta-phenylethylamine (PEA), meta-tyramine (m-TA) and para-tyramine (p-TA) in aggressive behaviour. The brain, plasma and urinary levels of PEA, m-TA and p-TA, and their respective major acid metabolites, phenylacetic acid (PAA), meta-hydroxyphenylacetic acid (m-HPA) and para-hydroxyphenylacetic acid (p-HPA) were measured in isolated aggressive mice (after fighting), and in group housed controls. The urinary levels of PEA, m-TA, PAA, m-HPA and p-HPA, and the plasma levels of PAA and p-HPA were significantly lower in isolated aggressive mice. Similarly, the whole brain levels of PEA, p-TA, PAA and p-HPA tended to be reduced. In contrast, the brain levels of m-TA and m-HPA tended to increase. It should be noted, however, that the present procedure did not dissociate the stress and aggression components of the isolation syndrome, and, therefore, further experiments are required to determine whether the observed neurochemical changes are functionally related to increased aggression.

Aggression↗
PubMed1982

Plasma levels of phenylacetic acid, m- and p-hydroxyphenylacetic acid, and platelet monoamine oxidase activity in schizophrenic and other patients.

Blood from chronic schizophrenic patients in two hospitals (A and B) and from institutional and noninstitutional controls was analyzed for platelet monoamine oxidase (MAO) activity toward three different substrates (tryptamine, phenylethylamine, and p-tyramine) and for plasma levels of conjugated and unconjugated phenylacetic acid (PAA) and m- and p-hydroxyphenylacetic acids (mHPA and pHPA). Compared to the controls, schizophrenic patients were found to have significantly reduced MAO activity. Although significant differences were found between unconjugated PAA (reduced) in Hospital B, conjugated pHPA (increased) in Hospital A, and conjugated PAA (increased) in Hospitals A and B and noninstitutional controls, the most consistent significant finding was a reduced unconjugated mHPA in both groups of schizophrenic patients compared with both control groups.

Antipsychotic Agents↗