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Biomedical subjects

M Lowe

Publications and source records attributed to M Lowe.

At least 55 records · Page 3Linked to original sources
PubMed1989

Glutamate release from guinea-pig synaptosomes: stimulation by reuptake-induced depolarization.

Glutamate (10-100 microM) reversibly depolarizes guinea-pig cerebral cortical synaptosomes. This does not appear to be because of a conventional autoreceptor. Neither kainate at 1 mM, 100 microM N-methyl-D-aspartate (NMDA), 100 microM L-2-amino-4-phosphonobutanoate (APB), nor 100 microM quisqualate affects the Ca2+-dependent release of glutamate from suboptimally depolarized synaptosomes. However, kainate, quisqualate, and the quisqualate agonists beta-N-oxalylamino-L-alanine and alpha-amino-3-hydroxy-5-methylisoxazole propionate cause a slow Ca2+-independent release of glutamate from polarized synaptosomes. However, unlike kainate, quisqualate does not inhibit the acidic amino acid carrier. APB, NMDA, and the NMDA receptor-mediated neurotoxin beta-N-methylamino-L-alanine do not influence Ca2+-independent release at 100 microM. The depolarization of the plasma membrane by glutamate can be mimicked by D-aspartate, can be blocked by the transport inhibitor dihydrokainate, and is accompanied by the net uptake of acidic amino acids. L-Glutamate or D-aspartate at 100 microM increases the cytoplasmic free Ca2+ concentration. D-aspartate at 100 microM causes a Ca2+-dependent release of endogenous glutamate, superimposed on the Ca2+-independent heteroexchange with glutamate through the acidic amino acid carrier. The results suggest that the glutamatergic subpopulation of synaptosomes can be depolarized by exogenous glutamate.

Amino Acids↗
PubMed1989

Evaluation of normal erectile function with color flow Doppler sonography.

To understand better the vascular events that occur during normal erection, we used color flow Doppler sonography to examine the erectile process in seven normal subjects. The relationship of systolic/diastolic velocities and spectral waveform changes in the penile arteries was studied in response to increasing pressure within the corpora cavernosa (tumescence) before and after the intracorporal administration of drugs to induce erection. A characteristic spectral waveform pattern was identified throughout the erectile cycle, and the pattern was correlated with increasing pressure. Both systolic and diastolic velocities were elevated during the initiation of erection, at which time the pressure within the corpora cavernosa was low (11-25 mm Hg). Systolic velocities remained elevated until the last phase of erection (83-106 mm Hg). Diastolic velocity decreased as the intracorporal pressure increased from 25 to 40 mm Hg. Between 40 and 63 mm Hg, diastolic velocity approximated zero. With increasing pressure (63-83 mm Hg), diastolic flow reversed. As the corpora cavernosa approached full erection (83-105 mm Hg), both the forward systolic and reverse diastolic flow components diminished. At approximately 106 mm Hg (systolic occlusion pressure), flow ceased. Systolic/diastolic velocity and waveform phase relationships could be used to define the integrity of both the cavernosal artery inflow and the venous sinusoidal outflow occlusion mechanisms. Color flow Doppler sonography enhanced our ability to observe and quantify dynamic erectile events and provided new insights into understanding normal erectile function.

Adult↗
PubMed1988

Surgical aspects of international drug smuggling.

The internal concealment of cocaine and other drugs in packets by "body packers"--those who swallow packets of drugs or hide them in their vagina or rectum--to avoid detection by customs officials has been increasing in both the United States and Europe. The types of package and how they are concealed are changing as the traffickers become more sophisticated in their methods. The latest parcels are less likely to burst, but obstruction of the bowel may occur. Awareness of the problem is important for staff of emergency medical services near international ports of arrival.

Adult↗
PubMed1988

Sequence analyses of herpesviral enzymes suggest an ancient origin for human sexual behavior.

Comparison of the amino acid sequences of the deoxythymidine kinases of herpes simplex (HSV) and of marmoset herpes viruses (MHV) suggests a divergence time of 8 to 10 million years ago for HSV-1 and -2. Like MHV, HSV-1 and -2 cause local infections in their natural hosts, and direct contact between two individuals during the brief period of infectivity is needed for transmission. Because B virus, a nearer relative of HSV, depends on both oral and genital routes of transmission, we postulate that ancestral HSV (aHSV) was similar, and that for HSV-1 and -2 to diverge, genital and oral sites had to become microbiologically somewhat isolated from each other, while oral--oral and genital--genital contact had to be facilitated to maintain both aHSV strains. We propose that acquisition of continual sexual attractiveness by the ancestral human female and the adoption of close face-to-face mating, two hallmarks of human sexual behavior, provided the conditions for the divergence.

Animals↗
PubMed1988

Cloning and characterization of Bacillus subtilis homologs of Escherichia coli cell division genes ftsZ and ftsA.

The Bacillus subtilis homolog of the Escherichia coli ftsZ gene was isolated by screening a B. subtilis genomic library with anti-E. coli FtsZ antiserum. DNA sequence analysis of a 4-kilobase region revealed three open reading frames. One of these coded for a protein that was about 50% homologous to the E. coli FtsZ protein. The open reading frame just upstream of ftsZ coded for a protein that was 34% homologous to the E. coli FtsA protein. The open reading frames flanking these two B. subtilis genes showed no relationship to those found in E. coli. Expression of the B. subtilis ftsZ and ftsA genes in E. coli was lethal, since neither of these genes could be cloned on plasmid vectors unless promoter sequences were first removed. Cloning the B. subtilis ftsZ gene under the control of the lac promoter resulted in an IPTGs phenotype that could be suppressed by overproduction of E. coli FtsZ. These genes mapped at 135 degrees on the B. subtilis genetic map near previously identified cell division mutations.

Amino Acid Sequence↗
PubMed1986

Investigation of alternative mechanisms of collagen-induced platelet activation by using monoclonal antibodies to glycoprotein IIb-IIIa and fibrinogen.

Anti-HuPl-ml (reactive with IIIa) and anti-C2G7 (reactive with the carboxyl terminal of the alpha chain of fibrinogen) were used to investigate platelet aggregation, fibrinogen binding and thromboxane synthesis induced by low dose collagen (LDC) or high dose collagen (HDC) in normal or aspirin treated platelets. Anti-HuPl-ml and anti-C2G7 inhibited LDC induced platelet aggregation almost completely whilst abolishing fibrinogen binding; thromboxane production although reduced, still occurred. Thus LDC activation was dependent on fibrinogen binding to Gp IIIa. Aggregation of platelets induced by HDC was inhibited with anti-C2G7 or anti-HuPl-ml by 15-35% in association with a modest reduction in thromboxane (TxB2) production (with anti-HuPl-ml) and total inhibition of fibrinogen binding. When anti-HuPl-ml was added to aspirin treated platelets, aggregation with HDC although substantially reduced was not totally abolished. Collagen appears to activate platelets in a dose related manner in which there are at least three possible mechanisms via: (i) GpIIb-IIIa and associated fibrinogen binding; (ii) prostaglandin pathway; (iii) an alternate pathway responsible for approximately 20%-30% of platelet aggregation.

Antibodies, Monoclonal↗
PubMed1986

Overproduction of FtsZ suppresses sensitivity of lon mutants to division inhibition.

Escherichia coli lon mutants are sensitive to UV light and other DNA-damaging agents. This sensitivity is due to the loss of the lon-encoded ATP-dependent proteolytic activity which results in increased stability of the cell division inhibitor SulA. Introduction of the multicopy plasmid pZAQ containing the ftsZ gene, which is known to increase the level of FtsZ, suppressed the sensitivity of lon mutants to the DNA-damaging agents UV and nitrofurantoin. Alterations of pZAQ which reduced the expression of ftsZ reduced the ability of this plasmid to suppress the UV sensitivity. Examination of the kinetics of cell division revealed that pZAQ did not suppress the transient filamentation seen after exposure to UV, but did suppress the long-term inhibition that is normally observed. lon strains carrying pZAQ could stably maintain a multicopy plasmid carrying sulA (pBS2), which cannot otherwise be introduced into lon mutants. In addition, the increased temperature sensitivity of lexA(Ts) strains containing pBS2 was suppressed by pZAQ. These results suggest that SulA inhibits cell division by inhibiting FtsZ and that this interaction is stoichiometric.

Alleles↗