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Biomedical subjects

A J Ryan

Publications and source records attributed to A J Ryan.

At least 145 records · Page 8Linked to original sources
PubMed1976

Traumatic injuries: office treatment of lacerations.

Every laceration should be explored to its depth to locate foreign bodies and damage to tissues. Debridement should be thorough except on the face, where conservation of skin is important. Deep lacerations are closed in layers, using different sutures for each layer; if tissue has been lost, plastic tecnhiques of closure are necessary. Lacerations that are carefully repaired rarely become infected, and tetanus prophylaxis is the only required safeguard against infection.

Anti-Bacterial Agents↗
PubMed1976

Traumatic injuries: office treatment of deep bruises.

Local application of cold, compression, and elevation of the injured part are the mainstays of emergency care of a suspected deep bruise. Lack of treatment may have unpleasant consequences, such as muscle shortening.

Contusions↗
PubMed1976

Hepatic and extrahepatic metabolism of 14C-styrene oxide.

With 8-(14)C-styrene oxide as substrate, specific glutathione S-transferase and epoxide hydrase activities were determined in subcellular fractions of liver, lungs, kidney, and intestinal mucosa from rabbit, rat, and guinea pig. Liver had the highest enzyme activities in each species. Rat and guinea pig had higher glutathione S-transferase activity in both liver and kidney than rabbit. Rat testis also had appreciable glutathione S-transferase activity. The perinatal development of epoxide hydrase and glutathione S-transferase was followed in liver and several extrahepatic tissues of fetal and neonatal guinea pigs and rabbits. The rates at which enzyme activities reached adult levels in the extrahepatic tissues differed from the liver in both species. Epoxide hydrase and glutathione S-transferases developed at different rates in each organ, demonstrating that the relative importance of these two detoxifying pathways for styrene oxide may shift before and after birth. The effects of pretreating male and female rats with phenobarbital (PB), 1,2,3,4-dibenzanthracene (DBA), pregnenolone-16alpha-carbonitrile (PCN), or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on hepatic and extrahepatic epoxide hydrase and glutathione S-transferase activities toward styrene oxide were determined. PB increased both enzyme activities in liver of both sexes. PCN induced only glutathione S-transferase activity in female liver. Extrahepatic epoxide hydrase and glutathione S-transferase activities were unaffected except that TCDD doubled female renal epoxide hydrase activity and PB increased intestinal epoxide hydrase activity in both sexes. Styrene oxide biotransformation was studied in isolated, perfused rat liver and rabbit lung preparations. Conjugation with glutathione was a major metabolic pathway although significant amounts of diol were also formed in each instance. In rat liver, 27-40% of the administered styrene oxide was excreted via the bile mainly as S-(1-phenyl-2-hydroxyethyl)glutathione.

Aging↗
PubMed1975

Inhibitors of hepatic mixed function oxidases. I. The metabolism of 2,6-dihydroxy-,2-hydroxy-6-methoxy- and 2,6-dimethoxyacetophenones.

1. 2,6-Dihydroxyacetophenone, its mono- and di-methyl ethers are inhibitors of hepatic mixed function oxidases. The dimethyl ether is a competitive inhibitor of aminopyrine demethylase with the others displaying mixed kinetics. The metabolism of all three ketones has been studied. 2. 2,6-Dihydroxyacetophenone is excreted unchanged and as conjugates. 3. 2-Hydroxy-6-methoxyacetophenone is largely excreted unchanged and conjugated but small amounts of the 3- and 5-hydroxylated derivatives are formed. 4. 2,6-Dimethoxyacetophenone is demethylated to 2-hydroxy-6-methoxy-acetophenone. In addition 3-hydroxy-2,5-dimethoxyacetophenone and 2,3-dihydroxy-6-methoxyacetophenone were identified as metabolites. 5. Quantitative data on the excretion of metabolites were obtained with 14C-labelled ketones.

Acetophenones↗