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Biomedical subjects

E Lear

Publications and source records attributed to E Lear.

At least 19 recordsLinked to original sources
PubMed1991

A mechanism for maintaining an up-to-date GenBank database via Usenet.

In this paper, we describe an automated system for distributing updates to the GenBank nucleic acid sequence database, using the Usenet news system as the underlying transport mechanism. Our system allows new loci to be distributed as soon as the sequences are available, over existing networks, using existing Usenet software and infrastructure currently available on a wide range of computer systems.

Amino Acid Sequence↗
PubMed1991

The effects of oxytocin on intracranial pressure.

The commonly used vasodilators sodium nitroprusside and nitroglycerine increase the intracranial pressure (ICP). Oxytocin is also a vasodilator although its primary effect is contraction of uterine smooth muscle. We therefore studied the effect of oxytocin on the ICP of cats. Twelve cats were assigned to two equal groups. One group had normal ICP and in the other the ICP was artificially increased by inflating a balloon placed in the extradural space. All of the cats initially received an oxytocin infusion for 15 min. After a period of stabilization, an additional dose of oxytocin was injected as a bolus. Oxytocin administered as an infusion did not change the ICP significantly in any of the cats. Oxytocin administered as a bolus increased the ICP from 27 +/- 4 to 31 +/- 2 mm Hg in the cats with artificially increased ICP. There were no significant changes in the mean blood pressure or heart rate in either group.

Journal Article↗
PubMed1988

Effect of suxamethonium on the ICP of cats with and without thiopentone pretreatment.

Twelve cats were assigned equally to two groups, one with normal, and the other with artificially-increased intracranial pressure. When suxamethonium was administered to these animals, the intracranial pressure increased in both groups, irrespective of their baseline intracranial pressure. When the same dose of suxamethonium was administered after pretreatment with thiopentone in both groups of animals, the intracranial pressure again increased from the control values.

Animals↗
PubMed1987

Toxicity of chloroprocaine and sodium bisulfite on human neuroblastoma cells.

The effects of commercial and crystalline solutions of chloroprocaine (CP) (1.6 X 10(-3)-0.4 X 10(-3)M) and sodium bisulfite (SB) (0.8 X 10(-3)-0.08 X 10(-3)M) were studied on the multiplication of human neuroblastoma cells. These cells were chosen because of putative neurotoxicity associated with CP; cell multiplication (measured as colony-forming ability-CFA) was studied because CFA is a reliable in vitro test for drug toxicity at the cellular level. CFA was dramatically reduced (86%) after 20-hr exposure to commercial solutions of CP. Shorter exposure times (3 hr) resulted in a marginal toxic effect (32%). At similar concentrations and after 20-hr exposure time, CP crystalline solutions induced a 37.5% inhibition that decreased with decreased time in culture. Sodium bisulfite reduced cell multiplication to a degree that varied with different samples of SB. With a 3-hr exposure time, CFA was reduced 72-92% by SB-1 and 57-72% by SB-2. The variability of SB toxicity and the difference in toxicity with commercial and crystalline solutions of CP are discussed in terms of possible clinical toxicity.

Cell Division↗
PubMed1986

Effect of diltiazem-induced hypotension on normal and increased intracranial pressure of cats.

The commonly used vasodilators sodium nitroprusside and nitroglycerin increase intracranial pressure (ICP) and cause tachycardia. Since diltiazem is also a vasodilator, we designed this experiment in cats to study its effect on intracranial pressure and heart rate (HR). Twelve cats were assigned to two equal groups. One group had normal ICP (N-ICP), while in the other the ICP was raised artificially (AR-ICP) by placing a balloon into the intracranial extradural space. Both groups received an infusion of diltiazem to decrease the mean blood pressure (BP), which was maintained 30 per cent below the baseline value for 15 minutes. Diltiazem caused no significant change in ICP (5.7 +/- 1 to 6.7 +/- 1.5 mmHg, p less than 0.01) in cats with N-ICP while in cats with AR-ICP, the increase from 26.9 +/- 0.5 to 34.0 +/- 1.9 mmHg was significant (p less than 0.006). HR decreased significantly during the diltiazem infusion in both groups.

Animals↗
PubMed1986

In vitro induction of somatic cell hybridization by the local anesthetic chloroprocaine.

Chloroprocaine, an aminoester local anesthetic commonly used for epidural block, has been found to induce interspecies somatic cell hybrids in vitro. Mixed cultures of human amniocytes and mouse hepatoma cells, deficient in hypoxanthine phosphoribosyl transferase, were exposed to 1.6, 0.8, or 0.4 X 10(-3)M chloroprocaine for 3 hr at 37 degrees C, then maintained for 3 weeks in a double-selective medium of hypoxanthine, aminopterin, and thymidine (HAT) and ouabain to eliminate the unfused parental cells. Clones of actively multiplying cells appeared in cultures exposed to 1.6 and 0.8 X 10(-3)M chloroprocaine. Chromosome analysis confirmed they were hybrids. Cultures treated with 0.8 X 10(-3)M chloroprocaine exhibited the highest frequency of cell hybridization (8.8 X 10(-5). The hybrid clones bore the morphologic characteristics of both parents although their growth pattern closely resembled the mouse parent. Procaine, sodium bisulfite (the antioxidant present in the commercial solutions of chloroprocaine), and the two chloroprocaine metabolites, chloroaminobenzoic acid and diethylaminoethanol, were nonfusogenic. The hybridogenic effect of chloroprocaine has not been previously described with other local anesthetics.

Animals↗
PubMed1984

Cell membrane fusion by chloroprocaine.

The cytotoxicity of the local anesthetics chloroprocaine, procaine, and lidocaine was studied in murine and human cells. Murine glial and hepatic cells, and human fibroblasts were individually exposed to chloroprocaine, procaine, and lidocaine in concentrations ranging from 1.6 X 10(-3) M to 0.2 X 10(-3) M. The cells of all three cell lines underwent membrane fusion after exposure to chloroprocaine as indicated by the presence of the high number of multinucleated cells in the cultures. The 0.8 X 10(-3) M concentration was the most fusogenic, and caused multinucleation in 30% of glial and hepatic cells, and in 23% of fibroblasts. Membrane fusion and multinucleation also occurred in mixed human and murine cell cultures that were exposed to 0.8 X 10(-3) M concentration of both commercial and crystalline solutions of chloroprocaine, with a portion of multinucleated cells that was 27 and 17%, respectively. Cell membrane fusion was not caused by procaine, lidocaine, sodium bisulfite (the antioxidant present in the commercial solutions of chloroprocaine), or chloro-aminobenzoic acid and diethylamino-ethanol (the two chloroprocaine metabolites). The fusogenic effect of chloroprocaine on cell membrane has not been previously described for any local anesthetic.

Anesthetics, Local↗