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Biomedical subjects

W Perry

Publications and source records attributed to W Perry.

At least 73 records · Page 4Linked to original sources
PubMed1982

Calcium metabolism during rifampicin and isoniazid therapy for tuberculosis.

Calcium metabolism was studied in 83 patients during eighteen months' rifampicin and isoniazid therapy for tuberculosis by measurements including calcium, alkaline phosphatase and 25-hydroxycholecalciferol (25-HCC). Five out of 52 Indian patients in the series were found to have osteomalacia, a prevalence probably no higher than in the Asian population in the UK at large. Moreover, osteomalacia responded to physiological supplementation with vitamin D. One European out of 31 had osteomalacia due to low vitamin D intake. Serum calcium was compared in 17 patients before and after six months of antituberculous chemotherapy but no significant difference was detected (P greater than 0.1). Two Indian patients were in positive calcium balance with low to normal plasma 25-HCC levels, indicating that an effect on 1,25 dihydroxyvitamin D activity during therapy was unlikely. It is concluded that rifampicin when combined with isoniazid has no significant effect on calcium metabolism over an eighteen-month treatment period.

Adolescent↗
PubMed1981

Effect of partial hepatectomy on removal of O6-methylguanine from alkylated DNA by rat liver extracts.

1. The activity of an enzyme catalysing the loss of O6-methylguanine from methylated DNA was increasing during liver regeneration after partial hepatectomy. Activity was increased 3-fold by 24h and was maximal (6-fold increase) over the period 48-72h after operation. 2. This activity could also be induced by chronic treatment with dimethylnitrosamine, but the maximal response amounted to a 2-3-fold change (with the greater effect in male rats) after 4-6 weeks of exposure to daily doses of 2 mg of dimethylnitrosamine/kg. 3. Neither partial hepatectomy nor treatment with dimethylnitrosamine increased the activities of two other enzymes repairing alkylated DNA, DNA (7-methylguanine-)glycosylase and DNA (3-methyladenine-)glycosylase. 4. These results therefore indicate that there is a selective induction of the O6-methylguanine removal system during hepatocyte proliferation. Since this product is known to lead to mutations and its persistence in DNA throughout cell replication has been implicated in tumour initiation, this induction may play a role in resistance to carcinogenesis by alkylating agents.

Alkylation↗
PubMed1981

Effects of chronic naloxone treatment on brain-stimulation reward.

Rats were tested on a rate-free psychophysical procedure in order to determine the absolute reinforcement thresholds for self-stimulation behavior. The administration of naloxone (16 mg/kg) for five days failed to alter the reinforcement thresholds on this procedure. To the extent that naloxone is an effective antagonist of endogenous opioids, we conclude that central endorphin systems are not necessary to support self-stimulation behavior.

Animals↗
PubMed1981

Stimulation of transfer of methyl groups from O6-methylguanine in DNA to protein by rat liver extracts in response to hepatotoxins.

An enzymatic activity present in rat liver extracts catalyzes the transfer of methyl groups from O6-methylguanine in DNA to protein. This activity was stimulated by treatment of rats with thioacetamide, carbon tetrachloride, 1,2-dimethylhydrazine, diethylnitrosamine, dimethylnitrosamine and by partial hepatectomy but not by treatment with N-methyl-N-nitrosourea or streptozotocin. These results suggest that an enhancement of this activity accompanies the increase in cell division brought about by these agents and is not necessarily a specific response to the presence of alkylated bases in DNA.

Animals↗
PubMed1981

Emergence of gentamicin- and methicillin-resistant Staphylococcus aureus strains in New York City hospitals.

Gentamicin- and methicillin-resistant strains of Staphylococcus aureus have been isolated from Spring 1979 to the present from many hospitals in New York City. A large proportion of the strains were resistant to the majority of antistaphylococcal antibiotics. The ratio of multiply resistant strains was highest among tetracycline-resistant strains. There were significant differences in phage susceptibility patterns and the resistance spectrum of strains isolated at different hospitals, whereas strains isolated at the same hospital often showed a marked degree of similarity. This suggests multiple origins of gentamicin- and methicillin-resistant strains isolated in New York City.

Bacteriophage Typing↗
PubMed1980

Effects of d-amphetamine and naloxone on brain stimulation reward.

Self-stimulation thresholds were determined in rats by means of a modification of the psychophysical method of limits. Reinforcement values were determined after the administration of d-amphetamine alone, naloxone alone, and naloxone administered concurrently with d-amphetamine. d-Amphetamine yielded dose-related decreases in the threshold (0.25--2.00 mg/kg IP), while naloxone alone (2.0--16 mg/kg IP) caused no consistent changes. For each animal, a dose of d-amphetamine that substantially lowered the threshold was then selected to be administered with varying doses of naloxone. The threshold-lowering effect of d-amphetamine was blocked by naloxone at doses as low as 2.0 or 4.0 mg/kg. This finding suggests the possible involvement of an opiate receptor in the mediation of the enhancement by d-amphetamine of brain stimulation reward.

Animals↗
PubMed1980

Effects of quinidine on serum digoxin concentration: a prospective study.

Results of studies of 15 adults placed on quinidine therapy after their serum digoxin concentrations were stabilized showed significantly increased digoxin concentrations. The average digoxin concentration before quinidine therapy was 0.75 +/- 0.28 ng/mL and after 4 days of quinidine therapy was 1.41 +/- 0.43 ng/mL. During this period, the renal clearance of digoxin decreased from 53.4 +/- 21 mL/min . 1.73 m to 35.3 +/- 12.6 mL/ min . 1.73 m. No significant correlation was found between the individual rise in serum digoxin concentrations and the rise in serum quinidine concentrations. These results suggest that serum digoxin concentration should be monitored closely for at least the first 4 days of quinidine therapy.

Aged↗
PubMed1979

Methicillin-resistant strains of Staphylococcus aureus phage type 92.

Methicillin-resistant (Mec(r)) strains of Staphylococcus aureus received for phage typing from several hospitals in New York City were resistant to the international set of typing phages but susceptible to experimental phage 92. Subsequently, strains of type 92 were detected in two outbreaks with Mec(r) strains in two other locations in the United States. In all instances, type 92 was predominant among the Mec(r) strains isolated in each hospital. With the exception of one strain, the methicillin resistance of the Mec(r) strains investigated was homogeneous. In most instances, isolates from the same hospital were closely similar in their antibiotic resistance patterns. The strains isolated in New York City could be divided into three groups by the host range of their lysogenic phages and by antigenic structure. Transduction experiments indicated that the transfer of chromosomal tetracycline resistance from Mec(r) strains into a strain susceptible to several international typing phages renders the latter nontypable. However, the acceptor strain remains susceptible to experimental phages 92 and 88. Transduction of methicillin resistance had no effect on the phage susceptibility of the acceptor strain. It is possible that the presence of chromosomal tetracycline resistance is a determining factor in the phage susceptibility of Mec(r) strains isolated in New York City.

Bacteriophage Typing↗
PubMed1978

Hereditary hypophosphataemic rickets with autosomal recessive inheritance and severe osteosclerosis. A report of two cases.

We have observed congenital hypophosphataemic rickets in two sons of a marriage between first cousins, their mother being clinically and biochemically normal. Both patients are now approaching middle age. In addition to severe childhood rickets and lifelong hypophosphataemia, their disease is characterised by gross osteosclerosis with extraskeletal ossification, clinically persistent osteomalacia in one and spinal cord compression in the other. The genetics of this disease can be satisfactorily explained only on the basis of autosomal recessive inheritance, a mode which has only once before been reported in the literature. The severity of certain features, which would be expected in a homozygous state, may help our understanding of the more usual X-linked form.

Adult↗