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Biomedical subjects

M A Clark

Publications and source records attributed to M A Clark.

At least 235 records · Page 13Linked to original sources
PubMed1985

Multiple deaths resulting from shipboard exposure to trichlorotrifluoroethane.

During the course of dockside ship maintenance, a compartment was partially flooded with tricholotrifluoroethane gas. One sailor entered the compartment, collapsed, and was then rescued by two other men. All three victims then climbed a 11-m (36-ft) ladder and collapsed. They all experienced a rapid development of cardiac arrest. We report on the pathologic, toxicologic, and pathophysiologic aspects of the incident.

Accidents, Occupational↗
PubMed1984

Regulation of ligand binding to leukotriene D4 receptors: effects of cations and guanine nucleotides.

High affinity, stereoselective specific binding sites for [3H]leukotriene D4 [( 3H]LTD4) have been demonstrated in guinea pig lung membranes. Purine nucleotides quantitatively reduced [3H]LTD4 specific binding with a rank order potency of guanosine-5'-O-3-thiotriphosphate (GTP gamma S) = guanyl-5'-yl-imido-diphosphate [Gpp(NH)p] greater than GTP greater than ATP greater than GDP. In the presence of 1 microM Gpp(NH)p, the maximum number (Bmax) of [3H]LTD4 specific binding sites was reduced to 41 +/- 10 percent of the control level (950 +/- 150 fmol/mg membrane protein). In the presence of 3 microM Gpp(NH)p, the rate of association of [3H]LTD4 to the specific sites was estimated to have increased 2.5-fold. The rate of dissociation of [3H]LTD4 from the specific sites was also increased significantly in the presence of 50 microM Gpp(NH)p. The divalent cations, Ca2+ and Mg2+ (10 mM), increased the Bmax 2-fold and had minimal effects on the dissociation constant (Kd) of [3H]LTD4 specific binding. Sodium ions, at a concentration of 50 mM, reduced the Bmax, and had minimal effects on the Kd of [3H]LTD4 specific binding. These data indicate that guanine nucleotides, Na+, Mg2+ and Ca2+ regulate [3H]LTD4 binding to its receptors in guinea pig lung.

Animals↗
PubMed1984

Leukotriene C4 ([3H]-LTC4) binding to membranes isolated from a hamster smooth muscle cell line (DDT1MF2).

Leukotriene C4 (LTC4) has been demonstrated to induce contraction of the smooth muscle cell line DDT1MF2. A partially purified membrane fraction obtained from these cells exhibited a high affinity binding site for LTC4. Binding of [3H]-LTC4 was saturable, specific and reversible with a dissociation constant (Kd) of 21 +/- 4 nM. The maximum number of binding sites (Bmax) was 55 +/- 5 pmol/mg of protein. Specificity was demonstrated in competition studies in which the Ki of LTC4 against specifically bound [3H]-LTC4 was 12 nM whereas Leukotriene D4 (LTD4) and Leukotriene E4 (LTE4) had a Ki of 38 +/- 4 and 4.7 +/- 0.5 nM respectively. A previously described antagonist of leukotriene-induced smooth muscle contraction PFL 55712 had a Ki of 23 +/- 2 nM as determined by competition binding experiments.

Animals↗
PubMed1984

Characterization of the leukotriene D4 receptor in guinea-pig lung.

The effects of monovalent, divalent cations, buffere species and pH dependency on [3H]leukotriene D4 binding to the receptor have been characterized in vitro by using a radioligand binding assay. It was found that Ca2+, Mg2+, Co2+ and Mn2+ enhanced the specific binding. High concentrations of NaCl (150-300 mM) inhibited the specific binding to the receptor. The specific binding was also found to be higher in Pipes buffer (pH 6.5) than in Tris, Hepes and phosphate buffer at pH 7.0-8.0. Conversion of [3H]leukotriene D4 was minimized by inclusion of 1 mM cysteine, glycine in the incubation buffer and maintaining the temperature at 22 degrees C. Under the conditions employed, the dissociation constant (KD) and the receptor density (Bmax) were calculated to be 1.8 +/- 0.9 nM and 2100 +/- 375 fmol/mg protein respectively. The leukotriene antagonist FPL 55712, agonist 5R, 6S-LTD4 and LTE4 competed with the [3H]LTD4 binding to the receptor. Prostaglandins, alpha-, beta-adrenergic and dopaminergic receptor agonists and antagonists did not compete significantly.

Animals↗
PubMed1984

Identification of leukotriene D4 specific binding sites in the membrane preparation isolated from guinea pig lung.

A radioligand binding assay has been established to study leukotriene specific binding sites in the guinea pig and rabbit tissues. Using high specific activity [3H]-leukotriene D4 [( 3H]-LTD4), in the presence or absence of unlabeled LTD4, the diastereoisomer of LTD4 (5R,6S-LTD4), leukotriene E4 (LTE4) and the end-organ antagonist, FPL 55712, we have identified specific binding sites for [3H]-LTD4 in the crude membrane fraction isolated from guinea pig lung. The time required for [3H]-LTD4 binding to reach equilibrium was approximately 20 to 25 min at 37 degrees C in the presence of 10 mM Tris-HCl buffer (pH 7.5) containing 150 mM NaCl. The binding of [3H]-LTD4 to the specific sites was saturable, reversible and stereospecific. The maximal number of binding sites (Bmax), derived from Scatchard analysis, was approximately 320 +/- 200 fmol per mg of crude membrane protein. The dissociation constants, derived from kinetic and saturation analyses, were 9.7 nM and 5 +/- 4 nM, respectively. The specific binding sites could not be detected in the crude membrane fraction prepared from guinea pig ileum, brain and liver, or rabbit lung, trachea, ileum and uterus. In radioligand competition experiments, LTD4, FPL 55712 and 5R,6S-LTD4 competed with [3H]-LTD4. The metabolic inhibitors of arachidonic acid and SKF 88046, an antagonist of the indirectly-mediated actions of LTD4, did not significantly compete with [3H]-LTD4 at the specific binding sites. These correlations indicated that these specific binding sites may be the putative leukotriene receptors in the guinea-pig lung.

Animals↗
PubMed1984

Confusing wounds of entrance and exit with an unusual weapon.

A case of suicide where the victim used a four-barreled, concealable weapon firing 0.357 magnum ammunition is presented. Because of the extreme "blow back" effect caused by such a weapon, the direction of fire and manner of death were, at first, interpreted incorrectly by investigators.

Adult↗
PubMed1983

Effect of CO2 on neurons of the house cricket, Acheta domestica.

The effect of elevated levels of CO2 on the neurons of the metathoracic ganglion of the common house cricket was examined. Elevated CO2 produced a profound depolarization of the neurons without a substantial change in conductance. The depolarization was not due to CO2 acidification of the external solution since exposure of the neurons to a solution which was nominally CO2 free, but at an acid pH, produced little effect. The effect of elevated CO2 appeared to be due to intracellular acidification, since other treatments which acidified the cell interior also produced depolarization. Agents which block intracellular pH regulation also substantially enhance the effect and prevent recovery. The mechanism producing the depolarization appears to be blockage of a metabolic component of the resting potential, since the action of metabolic blockers mimics the effect of elevated CO2.

Animals↗
PubMed1982

Detrimental effect of mitochondria on hybrid cell survival.

A genetic technique has been developed for isolating nuclear hybrids which are products of fusion between karyoplasts and whole cells. Nuclear hybrids have greatly reduced mitochondrial component obtained from the nuclear donor and exhibit differences when compared to the corresponding whole-cell hybrids, such as better long-term survival and accelerated chromosome segregation. These results suggest that divergent mitochondria in a cell-fusion product may have adverse effects on survival.

Animals↗
PubMed1982

Long-lived cytoplasmic factors that suppress adrenal steroidogenesis.

Adrenal cells secrete steroids after stimulation with corticotropin (ACTH), whereas cells reconstructed by fusing adrenal cell nuclei to fibroblast cytoplasms are temporarily (2-3 wk) unresponsive to ACTH. In this report, we characterize this inhibition by using "cybrids" (cytoplasmic hybrids) isolated by either genetic selection or a new procedure that utilizes the fluorescence-activated cell sorter and the vital mitochondrial dye rhodamine 123. Such cybrids, which contain both adrenal and fibroblast cytoplasmic components, are unable to produce steroids, suggesting the existence of cytoplasmic inhibitory factors. In order to elucidate this cytoplasmic inhibition of steroidogenesis, techniques are described that test the contribution of fibroblast mitochondria to this phenomenon. The first technique utilizes purified mitochondria, isolated from chloramphenicol (CAP)-resistant fibroblasts, to confer CAP resistance on an otherwise sensitive adrenal cell. The resulting CAPr cells, termed mitochondrial transformants, are responsive to ACTH. The second technique utilizes a procedure for isolating small fragments of cytoplasm (microcytospheres) from fibroblasts. Microcytospheres, which do not contain mitochondria, are stained with rhodamine 18, a vital membrane dye, and then fused to unstained adrenal cells. The fusion products are then isolated with the fluorescence-activated cell sorter. Approximately 30% of the fusion products are inhibited in their ability to respond to ACTH. These results suggest that the fibroblast cytoplasm contains nonmitochondrial long-lived inhibitory factors that temporarily suppress steroidogenic function in adrenal cells.

Adrenal Gland Neoplasms↗
PubMed1982

Sudden death and partial absence of the right ventricular myocardium: a report of three cases and a review of the literature.

Three patients with congenital partial absence of the right ventricular myocardium were studied. These cases are unique in that all three patients died suddenly and none had clinical evidence of cardiovascular disease. Two of the three patients were active in sports, and both died suddenly while playing basketball. At the time of autopsy, the only significant abnormality was cardiomegaly, with right atrial and ventricular dilation and partial absence of the right ventricular myocardium.

Adolescent↗