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Biomedical subjects

H Drexler

Publications and source records attributed to H Drexler.

270 records · Page 15Linked to original sources
PubMed1973

Transduction of Gal+ by coliphage T1. 3. Requirement for transcription and translation in recipient cells.

A 10- to 15-min derepression of a lambda prophage in a Gal(-) recipient during early infection with a transducing lysate of coliphage T1am will cause an increase in the efficiency of transduction of Gal(+). An increase in the efficiency of transduction occurs when the donor is either nonlysogenic or lysogenic for lambda; the increase is blocked by rifampin or chloramphenicol. With strain R901 it has been shown that efficient transduction can be blocked by treatment with rifampin after all chloramphenicol-sensitive steps have occurred.

Chloramphenicol↗
PubMed1972

Transduction of Gal+ by coliphage T1. I. Role of hybrids of bacterial and prophage lambda deoxyribonucleic acid.

Hybrids of lambda and adjacent bacterial deoxyribonucleic acid carried in T1 particles were able to transduce Gal(+) with a greatly increased efficiency to strains which were not immune to lambda compared to immune strains. The enhanced transduction was dependent on a functional recA(+) gene in the recipient. Mutations of the donor's lambda prophage which abolished the function of either the cI, O, or P genes in the recipients led to a further enhancement of transduction. The rate of transduction of a nonlysogenic recipient such as W3350 by the hybrid particles may be as much as 140 times greater than transduction of the lysogenic recipient W3350(lambda). In addition to the effect of lambda immunity in blocking enhanced transduction, mutations of the N gene of the donor's lambda prophage abolished enhanced transduction. Mutations in the red, int, xis, and Q genes of the donor's prophage had no significant effect on transduction. The hybrids which mediated the enhanced transduction are called (lambda-gal)T1.

Chromosomes, Bacterial↗
PubMed1972

Transduction of Gal+ by coliphage T1. II. Role of lambda transcription control in the efficiency of transduction.

One of the crossovers leading to the transduction of Escherichia coli W3350 or one of its derivatives for the Gal(+) marker by T1 grown on donors lysogenic for lambda must occur to the right of the galactose operon. The location of this crossover determined both the rate of transduction and the lambda genes which control the transduction by (lambda-gal)T1. When the crossover occurred either to the left of gene N or the right of the cI gene, it was affected in a positive fashion by the gene product of the N(+) gene. When the crossover occurred either to the left of gene N or between N and gene Q, its efficiency was not significantly affected by the expression of Q(+). However, crossovers to the right of gene Q were greatly stimulated by the presence of a functioning Q gene on the chromosome of (lambda-gal)T1 hybrid. The repressor made by the cI(+) gene of lambda blocked efficient transduction. Therefore, the control of efficient transduction by (lambda-gal)T1 is the same as the control of transcription of lambda. It is concluded that the increased efficiency of transduction by (lambda-gal)T1 in nonimmune recipients is not caused by any particular product of a gene but rather by the process of transcription itself.

Chromosomes, Bacterial↗
PubMed1970

Transduction by bacteriophage T1.

Amber mutants of the virulent coliphage T1 are able to transduce a wide variety of genetic characteristics from permissive to nonpermissive K strains of Escherichia coli.

Coliphages↗
PubMed1969

Nature of Escherichia coli B(P1) yielder cells at the time of infection with restricted T1.

In the infection of Escherichia coli B(P1) with restricted T1, it was shown that yielder cells consist of both special and nonspecial cells. Special or predetermined yielders occurred only among the earliest yielders. In most instances, yielder-cell formation was most easily explained by assuming that the first step was a chance escape of the restricted phage DNA from the degrading enzyme of the restricting cell.

Coliphages↗
PubMedDate not supplied

Systemic and regional vascular effects of atrial natriuretic peptide in a rat model of chronic heart failure.

To characterize the systemic and regional vascular effects of atrial natriuretic peptide (ANP) in chronic heart failure, central hemodynamics, regional blood flow and plasma ANP levels were determined in a rat model of myocardial infarction and failure and in sham-operated animals. Measurements were made in the conscious state before and after intravenous rANP [99-126] (8 micrograms bolus followed by continuous infusion of 1.0 microgram/kg/min). With this protocol, ANP significantly decreased cardiac output, right atrial, left ventricular end-diastolic and arterial pressures and there were increases in heart rate, systemic and intestinal vascular resistances in sham animals. Renal blood flow per gram of tissue was unchanged with ANP, but when expressed as a percentage of cardiac output, increased significantly, indicating a preferential renal vasodilatory effect of ANP. In rats with infarction and failure, this dose did not alter cardiac output or arterial pressure, but decreased right atrial and left ventricular blood flow. Although significantly reduced as compared to the control group, renal blood flow was not improved with ANP in the heart failure group. ANP plasma levels of the heart failure group were elevated at baseline (p less than 0.01), and increased 5-10 times after infusion of rANP. Thus, in rats with chronic heart failure, the renal vascular effects of ANP are blunted, which may, in part, explain the failure of ANP to restore the altered volume homeostasis in heart failure despite elevated ANP plasma levels. However, the effects on venous return were preserved which, in turn, improved cardiac performance via a reduction of preload.

Animals↗
PubMedDate not supplied

Cardiocirculatory adjustments to exercise following myocardial infarction in rats.

The sequential changes of the cardiocirculatory response to exercise over time in rats with myocardial infarction and failure were studied. Hemodynamics and regional blood flow (RBF, radioactive microspheres) were determined at rest and during exercise either at 1, 10 or 42 days after infarction (MI, infarct size 41.4 +/- 2.6% of LV) or sham procedures (SH). Whereas the response to exercise was attenuated one day after surgery in MI and SH, cardiocirculatory recovery was present in SH at 10 days and LV systolic and end-diastolic pressures separated SH and MI groups. Renal vasoconstriction during exercise occurred 10 days after MI and BF to working muscle during exercise was significantly lower in MI as compared to SH. At 42 days after MI manifest heart failure was present and despite significant blood flow redistribution (p less than 0.05 MI vs SH in renal and cutaneous beds) impaired skeletal muscle flow was observed along with increased vascular resistance in working muscle during exercise. We conclude that the cardiocirculatory response to exercise following large MI follows a distinctive time-dependent pattern, which differs from that observed at rest. Besides exaggerated sympathetically mediated vasoconstriction during exercise, impaired vasodilatation in skeletal muscle at exercise emerged.

Animals↗
PubMedDate not supplied

Correction of endothelial dysfunction in coronary microcirculation of hypercholesterolaemic patients by L-arginine.

Hypercholesterolaemia impairs endothelial function, possibly by interference with the intracellular formation of endothelium-derived relaxing factor from its precursor L-arginine. Whether L-arginine reverses hypercholesterolaemia-induced endothelial dysfunction in the coronary circulation was thus investigated. Epicardial artery cross-sectional area and coronary blood flow velocity were measured in 8 hypercholesterolaemic patients (mean serum cholesterol 7.8 [SE 0.3] mmol/l) and 7 age-matched controls before and after graded intracoronary infusions of the endothelium-dependent agent acetylcholine (0.036, 0.36, 3.6 micrograms/min). The effect of intracoronary infusion of L-arginine (160 mumol/min via the guiding catheter) on these measurements was then examined. In controls, acetylcholine induced a moderate dose-dependent constriction of the epicardial artery segment of the left anterior descending artery and increased coronary blood flow (by 239% [SE 57] at the highest dose). In patients with hypercholesterolaemia, the vasoconstrictive effect of acetylcholine on epicardial segments was similar to that in controls, but the increase in coronary blood flow with acetylcholine was significantly attenuated (highest dose: 61%, p less than 0.02 vs controls). L-arginine restored the acetylcholine-induced increase in blood flow in patients with hypercholesterolaemia (198% [61] vs baseline) but did not affect coronary blood flow in controls. The findings suggest that hypercholesterolaemia impairs endothelium-dependent dilatation of the coronary microcirculation and that this impairment can be restored by short-term administration of L-arginine. The possibility that L-arginine might form the basis of treatment for coronary endothelial abnormalities induced by hypercholesterolaemia could be worth investigating.

Acetylcholine↗
PubMedDate not supplied

Endothelial dysfunction: clinical implications.

The endothelium is involved in the control of vascular tone and homeostasis. Risk factors for arteriosclerosis, as well as other conditions have been shown to be associated with a dysfunctional endothelium. Clinically, endothelial function and dysfunction have been mostly evaluated by the assessment of endothelial dependent relaxation, for example in response to acetylcholine or increase inflow. The functional implications of endothelial dysfunction in cardiovascular disease are not well defined, but recent clinical trials have suggested that endothelial dysfunction may affect vascular tone and organ perfusion particularly during stress situations such as exercise. Moreover, endothelial dysfunction may represent an early event in the development of arteriosclerosis. Therefore, recent clinical studies have been performed to restore normal endothelial function in patients, using interventions such as L-arginine, lipid lowering drugs, vitamin C, other antioxidants, or exercise.

Acetylcholine↗
PubMedDate not supplied

Determination of carbon disulfide at the workplace by sampling on charcoal tubes--problems and solutions.

The aim of the study was to check the reliability and comparability of different analytical methods for ambient monitoring of carbon disulfide (CS2). A stationary sampling system, consisting of a charcoal sampling tube and pump, and two personal sampling systems, consisting of a charcoal sampling tube and a portable pump and of a diffusive charcoal sampler have been compared. The limits of quantification, within-series precision, between-series precision, recovery, and comparability of the methods were investigated. For passive sampling the recovery was determined by three different techniques. For a sampling time of 6 hours the limit of quantification was 0.2 ppm for the personal sampling and 0.01 ppm for the stationary sampling system. The within-series precision was between 5 and 8%. For personal sampling the between-series precision was between 9 and 12% using a passive sampler. The recovery ranged between 45 and 85% depending on the quotient of eluent volume and charcoal mass. The comparison of the two personal sampling methods in a field study using linear regression demonstrated with statistical certainty an excellent concordance of the methods. The study shows that particularly the method for determining air levels of carbon disulfide by passive sampling is associated with high systematic errors. If these errors are unknown or ignored they will result in highly underestimated exposure data for carbon disulfide.

Carbon Disulfide↗
PubMedDate not supplied

Regional vascular and hemodynamic effects of orally administered nisoldipine in conscious rats.

This study examined the hemodynamic and regional vascular effects of orally administered nisoldipine, a new dihydropyridine derivative (0.3 mg/kg) in normal conscious rats (n = 10). Nisoldipine significantly reduced systemic vascular resistance (0.58 to 0.38 mm Hg kg min/ml, p less than 0.05) and mean arterial pressure (122 to 108 mm Hg, p less than 0.05), and increased heart rate (395 to 447 beats/min, p less than 0.01) and cardiac index (225 to 326 ml/beat/kg, p less than 0.05). Left ventricular end-diastolic pressure was slightly decreased by nisoldipine (9.6 to 3.8 mm Hg, p less than 0.05). Blood flow (radioactive microspheres, 15 +/- 5 micron in diameter) to heart, gut, kidney, and brain was significantly increased. Improvement of blood flow was most pronounced in the coronary circulation (+ 58%) followed by the gut and renal circulatory beds. We conclude that nisoldipine represents a new orally effective calcium antagonist with highly selective effects in vascular smooth muscle as compared with its direct cardiac effects. The results are compared with our previous study utilizing intravenous nisoldipine.

Administration, Oral↗
PubMedDate not supplied

Differential effects of quinaprilat and enalaprilat on endothelial function of conduit arteries in patients with chronic heart failure.

BACKGROUND: Chronic heart failure (CHF) is associated with endothelial dysfunction, including impaired flow-dependent (endothelium-mediated) dilation (FDD). We have previously shown that ACE inhibition improves endothelium-mediated vasodilation in healthy volunteers. The present study was designed to determine whether ACE inhibition improves the impaired FDD in patients with CHF. Because their affinity to tissue ACE may influence the ability of ACE inhibitors to affect endothelial function, we compared the effects of quinaprilat (high affinity to tissue ACE) and enalaprilat (low affinity to tissue ACE) on FDD in patients with CHF. METHODS AND RESULTS: High-resolution ultrasound and Doppler were used to measure radial artery diameter and blood flow in patients with CHF. The effects of intra-arterial infusion of quinaprilat 1.6 microg/min (n=15) and enalaprilat 5 microg/min (n=15) were determined at rest and during reactive hyperemia (causing endothelium-mediated dilation) before and after N-monomethyl-L-arginine (L-NMMA) to inhibit endothelial synthesis of nitric oxide. Quinaprilat improved FDD by >40% (10.2+/-0.6% versus 6.9+/-0.6%; P<0.01), whereas enalaprilat had no effect. In particular, the part of FDD mediated by nitric oxide (ie, inhibited by L-NMMA) was increased by >100% with quinaprilat (5.6+/-0.5% versus 2.5+/-0.5%; P<0.01). Enalaprilat had no effect on FDD even when it was infused twice in the same dose (5 microg/min) and up to 30 microg/min. The effect of sodium nitroprusside on radial artery diameter and blood flow was similar in patients treated with quinaprilat, enalaprilat, and placebo. CONCLUSIONS: Quinaprilat improves FDD in patients with CHF as the result of increased availability of nitric oxide, whereas enalaprilat does not. This observation suggests that intrinsic differences exist between quinaprilat and enalaprilat that determine the ability to improve endothelium-mediated vasodilation, ie, their different affinity to tissue ACE.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

External quality assurance program for biological monitoring in occupational and environmental medicine.

Biological monitoring of chemical exposure in the workplace and in the environment has become increasingly important in assessing health risk. The analysis must be carried out under a quality assurance scheme to guarantee that the results obtained in biological monitoring are comparable with the threshold limit values and results from other laboratories. Since 1982, the German Society for Occupational and Environmental Medicine has offered 28 intercomparison programs. These programs cover 96 analytes in urine, blood, and plasma for 47 substances and cover most parameters that are relevant in occupational and environmental medicine. The data obtained in these programs provide a good overview of the current quality of the determination of analytes that are assessed in occupational and environmental toxicological laboratories. For the analyses of inorganic substances in blood and urine, the tolerable variation ranges from 7.5% to 43.5%. For organic substances in urine, the tolerable variation ranges from 12% to 48%. For organic substances in urine, the tolerable variation ranges from 12% to 48%. The highest variations (36% to 60%) were found for the analysis of organochlorine compounds in plasma. The tolerable variations for determining solvents in blood by head space gas chromatography range from 26% to 57%. The overall average success rates for the participants of the external quality programs range from 65% to 75%.

Environmental Monitoring↗