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S Hood

Publications and source records attributed to S Hood.

44 records · Page 3Linked to original sources
PubMed1994

Coordinate induction of hepatic fatty acyl-CoA oxidase and P4504A1 in rat after activation of the peroxisome proliferator-activated receptor (PPAR) by sulphur-substituted fatty acid analogues.

1. In the liver of rat fed a single dose of 3-thia fatty acids, 3-dithiahexadecanedioic acid (3-thiadicarboxylic acid) and tetradecylthioacetic acid, steady-state levels of P4504A1 and fatty acyl-CoA oxidase mRNAs increased in parallel. The increases were significant 8 h after administration, reaching a maximum after 12 h and decreased from 12 to 24 h after administration. 2. The corresponding enzyme activities of P4504A1 and fatty acyl-CoA oxidase were also induced in a parallel manner by the 3-thia fatty acids. The enzyme activities were significantly increased 12 h after administration and increased further after 24 h. This may reflect a possible effect of the 3-thia fatty acids not only on mRNA levels, but also on the translation and degradation rate of the two enzymes. 3. Repeated administration of 3-thia fatty acids resulted in an increase of the specific P4504A1 protein accompanied with an increased lauric acid hydroxylase activity. The correlation between induction of P4504A1 and fatty acyl-CoA oxidase mRNAs and their enzyme activities may reflect a coordinated rather than a causative induction mechanism, and that these genes respond to a common signal. This suggests that the increased P450 activity may not be responsible or be a prerequisite for fatty acyl-CoA oxidase induction. 4. Since the peroxisome proliferator-activated receptor (PPAR) plays a role in mediating the induction of fatty acyl-CoA oxidase, we analysed the activation of PPAR by fatty acids and sulphur-substituted analogues utilizing a chimera between the N-terminal and DNA-binding domain of the glucocorticoid receptor and the putative ligand-binding domain of PPAR. Arachidonic acid activated this chimeric receptor in Chinese hamster ovary cells. Inhibitors of P450 did not affect the activation of PPAR by arachidonic acid. Furthermore, dicarboxylic acids including 1,12-dodecanedioic acid or 1,16-hexadecanedioic acid only weakly activated the chimera. 3-Thidicarboxylic acid, however, was a much more effective activator than the non-sulphur-substituted analogues. In conclusion, the data suggest that the most likely mechanism of the induction process is fatty acid-induced activation of PPAR, which then leads to a coordinated induction of P4504A1 and fatty acyl-CoA oxidase.

Acyl-CoA Oxidase↗
PubMed1990

One path to a comprehensive district psychiatric service.

Brighton, which never had its own large psychiatric hospital, now has a comprehensive community psychiatric service. Sarah Hood and Tony Whitehead describe the development of the service and argue that the closure of large hospitals need not and should not result in the neglect or exploitation of former patients.

Aged↗
PubMed1987

Cough with angiotensin converting-enzyme inhibitors.

Since there are isolated case reports linking cough with angiotensin converting-enzyme (ACE) inhibitor treatment, we reviewed the case notes of patients attending a hypertension outpatient clinic. Of 126 patients, 37 were on medications other than ACE inhibitors, and none complained of cough. In contrast, 12 of 89 patients receiving an ACE inhibitor had noted cough. The symptoms remained when one ACE inhibitor was substituted for another, but disappeared when the drug was withdrawn. Cough was sufficiently irritating to require cessation of treatment in two patients. We conclude that cough is not uncommon during treatment with ACE inhibitors.

Adult↗
PubMed1976

Inappropriate TSH secretion. Paradoxical rise in serum TSH in response to thyroxine therapy.

Serum thytropin (TSH) in a 45-year-old woman suffering from Hashimoto's thyroiditis and hypothyroidism rose over a period of 8 months from 23 to 98 muU/ml while on 0.15 mg of thyroxine daily. A significant pituitary tumor was excluded and the response of other anterior pituitary hormones to provocative stimuli were normal. The TSH response to thyrotropin releasing hormone (TRH) carried out after a year of therapy and while on 0.15 mg T4 was exaggerated and required 100 mug of triiodothyronine (T3) daily in addition to the thyroxine replacement to suppress it. After the completion of the T3 suppression test and while on 0.2 mg thyroxine, serum TSH rose from less than 0.5 to 27 muU/ml when seen last. It is postulated that in this patient there exists a partial selective resistance of the thyrotrophs to T4 and that the paradoxical increase in serum TSH associated with thyroxine therapy results from T4 dependent increase in the synthesis and secretion of endogenous TRH. Other possibilities include an as yet undetected pituitary microadenoma or a pituitary defect in the deiodination of T4.

Female↗
PubMed1976

The maintenance of the argasid tick Ornithodoros moubata (Murray) on embryonated hen eggs.

A laboratory colony of O. moubata was maintained entirely by feeding on the exposed membranes of embryonated hen eggs at the 17-19th day stage of incubation at 37 degrees C. There was no loss of either vigour or fecundity. The method gave markedly superior results to those obtained by feeding on rabbits, rats, mice and guinea-pigs. More convenient and economical than any alternative, the method has valuable advantages in its applicability to a wide range of pathogens.

Animals↗
PubMedDate not supplied

Intrinsic and extrinsic risk factors for anterior cruciate ligament injury in Australian footballers.

The aim of this study was to examine the interaction between intrinsic (player-related) and extrinsic (environment-related) variables as risk factors for anterior cruciate ligament injury in Australian football. Between 1992 and 1999, 100,820 player-match exposures were analyzed for risk of anterior cruciate ligament injury using logistic regression analysis. There were 63 surgically proven noncontact anterior cruciate ligament injuries. The strongest risk factors were a player history of anterior cruciate ligament reconstruction either in the previous 12 months (relative risk [RR], 11.33; 95% confidence interval [CI], 4.02 to 31.91) or before the previous 12 months (RR, 4.44; 95% CI, 2.46 to 8.01). Weather conditions that were associated with dry field conditions--high water evaporation in the month before the match (RR, 2.55; 95% CI, 1.44 to 4.52) and low rainfall in the year before the match (RR, 2.87; 95% CI, 1.30 to 6.32)--were also significantly associated with these injuries. The increased risk of injury in the first 12 months after reconstruction was associated with the reconstructed knee, whereas after 12 months there was an even distribution of new injuries to the reconstructed knee and contralateral knee. A history of anterior cruciate ligament reconstruction is a risk factor for further injury. Weather conditions of high evaporation and low rainfall before matches are associated with noncontact anterior cruciate ligament injury.

Adult↗