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Biomedical subjects

B J Williams

Publications and source records attributed to B J Williams.

At least 109 records · Page 6Linked to original sources
PubMed1983

Reduction of 4-nitroquinoline 1-oxide to 4-hydroxyaminoquinoline 1-oxide in lysates of cytomegalovirus-infected cells.

The rates of virus inactivation by 4-nitroquinoline 1-oxide (NQO) and 4-hydroxyaminoquinoline 1-oxide (HAQO) were compared and samples of cytomegalovirus (CMV)-infected cell lysates to which NQO had been added were examined for the presence of HAQO. These experiments demonstrated that (i) CMV inactivation by HAQO was more rapid than with NQO, (ii) virus inactivation by either NQO or HAQO failed to demonstrate a photodynamic component, and (iii) NQO-treated stocks contained HAQO, indicating reduction of NQO to HAQO. The results support the concept that metabolism of NQO to HAQO enhances the genotoxic effect of NQO.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1983

Pulmonary and systemic vascular effects of SKF-82526-J, a new specific peripheral dopamine receptor agonist, in unanesthetized neonatal lambs.

We examined the circulatory effects of SKF-82526-J, a new specific dopamine receptor agonist, using chronically instrumented neonatal lambs. Serial infusion of doses ranging from 1.4 to 337 micrograms/kg/min did not change cardiac output, heart rate, left atrial pressure, systemic arterial pressure (SAP) or vascular resistance (SVR). Pulmonary pressure (PAP) increased from 22.6 +/- 1.1 to 35.8 +/- 4.0 mm Hg at 337 micrograms/kg/min (p less than 0.005) and pulmonary resistance (PVR) changed from 0.099 +/- 0.01 to 0.15 +/- 0.03 mm Hg/ml/kg/min (p less than 0.025). After 3-12 min of recovery, SAP increased in all lambs (range 6-57 mm Hg), while PAP fell, without change in cardiac output. Thus, the ratio of PVR/SVR returned more quickly to baseline (4 min) than either PVR or SVR alone. We conclude, based on physiologic evidence, that the newborn lamb pulmonary circulation has no vasodilating dopamine receptors.

Animals↗
PubMed1983

The effect of alpha-adrenergic blockade on the pulmonary vascular response to dopamine in neonatal lambs.

The effect of alpha-adrenergic blockade by phentolamine on the pulmonary vascular response to dopamine was studied in chronically prepared newborn lambs. Dopamine was administered at doses of 2.7 micrograms . kg-1 . min-1, 27 micrograms . kg-1 . min-1 and 270 micrograms . kg-1 . min-1 with and without alpha-adrenergic blockade. Dopamine infusion at 270 micrograms . kg-1 . min-1 caused a rise in the mean pulmonary artery pressure from 22 +/- 3.2 mmHg (mean +/- S.E.) at baseline to 36 +/- 4.1 mmHg (P less than 0.001). This rise was unaffected by alpha-adrenergic blockade. Dopamine infusion alone did not change pulmonary blood flow, but, in the presence of alpha-adrenergic blockade, pulmonary blood flow rose from 190 +/- 12 ml . min-1 . kg-1 at baseline to 280 +/- 13 ml . min-1 . kg-1 at the maximum dopamine infusion rate (P less than 0.001). Pulmonary vascular resistance was the same before and after alpha-adrenergic blockade and did not change from the baseline value during dopamine infusion.

Adrenergic alpha-Antagonists↗
PubMed1983

Cardiac effects of lead.

Symptoms consistent with cardiac disease have been noted as part of the syndrome of lead (Pb) intoxication. All types of cardiotoxicity noted in patients have been reproduced in experimental animals exposed acutely to high concentrations of Pb, or chronically exposed to lower levels. Types of cardiac effects observed include negative inotropism and electrocardiogram abnormalities, particularly conduction defects. Neonatal rats exposed to Pb via the milk of dams provided a drinking solution of lead acetate exhibit approximately four times the sensitivity to the arrhythmogenic effect of norepinephrine as adults compared with controls. Cardiotoxicity occurs after exposure as short as the first 10 postnatal days, but is not expressed until the rats are adult. Increased sensitivity to the arrhythmogenic effect of norepinephrine was seen in Pb-exposed animals in vivo and in isolated hearts from Pb-exposed animals in vitro. Norepinephrine arrhythmogenesis in vivo was attenuated by atropine or vagotomy, which indicates vagal nerve involvement. Possible mechanisms including interference with central gamma-aminobutyric acid systems, alteration of adrenergic nerve development, and Pb-Ca interaction are discussed.

Animals↗
PubMed1982

Tissue distribution of lead in rat pups nourished by lead-poisoned mothers.

Lead accumulation was studied in rats treated with Pb through the dam's milk from birth to weaning. Dams of experimental litters received lead acetate in drinking water, while dams of control litters received a sodium solution. Fluid consumption by dams and pup weight were monitored daily. No differences were seen in the dams' fluid consumption or in mortality or growth rate of pups. Rats were sacrificed after 5, 10, 16, or 21 d of Pb treatment, or 3 and 3.5 mo after weaning. Samples of heart, brain, liver, kidney, intestine, and bone were solubilized in concentration nitric acid and analyzed for Pb by atomic absorption spectrophotometry. Nitric acid digests of blood samples from pups 10 and 21 d old and from animals allowed a Pb-free period of 3-3.5 mo after treatment were also analyzed for Pb concentration. Levels of Pb in all tissues analyzed progressively increased during the first 10 d of treatment. After the Pb-free period only bone Pb concentration remained elevated. The results indicate that treatment of lactating dams is an efficient method of producing chronic Pb exposure of rat pups. The results also provide a means of comparing studies of Pb toxicity in which different treatment paradigms are used.

Animal Population Groups↗
PubMed1982

Acid-labile resin linkage agents for use in solid phase peptide synthesis.

Details are given of the preparation of two acid-labile peptide-resin linkage agents for use in solid phase peptide synthesis, viz. 4-hydroxymethylphenoxy-acetic acid and 3-methoxy-4-hydroxymethylphenoxyacetic acid. The latter is suitable for the preparation of peptide fragments bearing t-butyl-based side chain protecting groups.

Glycolates↗
PubMed1981

Induction of swimming in the high spinal stingray by L-DOPA.

Stingrays with high spinal transections, which do not spontaneously locomote, can be induced to swim by intravenous injection of L-DOPA. The L-DOPA-induced swim of the spinal animal is associated with patterns of EMG activity that appear similar to those of the spontaneous swim of the decerebrate preparation. However, in contrast to the decerebrate condition, the L-DOPA-induced cycles of swimming are slower and less vigorous. Furthermore, secondary periodicites and altered intersegmental timing relationships are also evident.

Animals↗
PubMed1980

An interdisciplinary teacher education program.

In 1975 the faculty of the University of Washington School of Dentistry, in conjunction with the College of Education and the affiliated Children's Orthopedic Hospital and Medical Center, developed a 36-month formal teacher education program in combination with joint specialty training in pedodontics and orthodontics. The program goal was to produce a professional dental educator/administrator who could function primarily in the teaching and practice of child and adolescent comprehensive care. After four years and three graduates, the faculty terminated this program. This paper outlines the rationale and structure of the original program and discusses the reasons for its termination.

Curriculum↗
PubMed1979

A factor necessary for normal morphogenetic function of anuran endoderm.

Cytoplasmic preparations obtained from late blastulae and early gastrulae of normal R. pipiens eggs contain factors which induce delayed lethal effects when injected into normal eggs at the beginning of cleavage. The same preparations can rescue some defective eggs which occur spontaneously (NS eggs), or are produced experimentally (ES eggs), by relieving the specific developmental syndrome displayed by either type of egg. The syndrome involves abnormal endoderm in which cytolysis is time-programmed. The lethal factors as well as the rescue factors are absent in the normal egg cytoplasm prior to the late blastula stage.

Animals↗
PubMed1979

Time and level of perinatal lead exposure for development of norepinephrine cardiotoxicity.

Neonatal lead exposure produces an enhanced susceptibility of the adult rat heart to the arrhythmogenic effects of norepinephrine. The present study examines the relationship of time and level of exposure to the extent of cardiac abnormality produced. The results indicate that the level of lead exposure required to produce norepinephrine cardiotoxicity without overt growth retardation is quite narrow, and lead must be present during the first ten days of life to cause these effects on the heart. A critical concentration of lead achieved during the early time period after birth appears necessary for the production of this cardiac abnormality, suggesting that lead interferes with neonatal cardiac and/or autonomic development.

Animals↗
PubMed1978

The protective effect of phentolamine against cardiac arrhythmias in the rat.

Norepinephrine was given by continuous infusion at a rate of 80 microgram/kg/min for 2 min. Norepinephrine caused the appearance of cardiac arrhythmias, primarily ventricular extrasystoles. The prior administration of phentolamine, even in a dose which did not antagonize the pressor effect of norephinephrine, prevented extrasystole production by norepinephrine. Tolazoline and yohimbine, in doses which did not affect the vasopressor action of norepinephrine, also suppressed extrasystole production. It is concluded that the antiarrhythmic effect of phentolamine, does not require antagonism of alpha-adrenoceptors of the type found in the vasculature, but may involve effects on a different type of alpha-adrenoceptors in the heart.

Angiotensin II↗