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Biomedical subjects

J Pratt

Publications and source records attributed to J Pratt.

18 recordsLinked to original sources
PubMed1992

Neuroprotective actions of riluzole in rodent models of global and focal cerebral ischaemia.

Riluzole (2 amino 6-trifluoromethoxybenzothiazole), when administered at 4 and 8 mg/kg i.p., 0.5, 4.5, 24 and 28 h after the initiation of ischaemia, significantly reduced the prevalence of slow wave, and increased the proportion of higher frequency activity seen in the quantified electrocorticogram (ECoG), during the weeks that followed a 6 min bilateral occlusion of the common carotid arteries in the Mongolian gerbil. In focal ischaemia, provoked in Fischer rats following the occlusion of the middle cerebral artery, administration of riluzole (8 mg/kg) at 30 min and 24.5 h post occlusion significantly reduced the volume of infarcted cortex. These activities of riluzole could be related to its inhibition of sodium channel activity, which in turn inhibits glutamate release.

Animals↗
PubMed1992

The infant mortality rate at Cherbourg aboriginal community: an update.

The infant mortality rate (IMR) at Cherbourg Aboriginal Community in south-eastern Queensland remained high from 1906 to about 1955-60, but since then has dropped from over 200/1000 live births in 1956-60 to 16/1000 live births in 1986-90, compared with the 1987 rate for Queensland (9.2/1000) and Australia (8.6/1000). The rapid improvement in the IMR was associated with the installation of a piped and chlorinated water supply, sewerage and an intensive campaign to eradicate intestinal worms. There has also been a change in community attitudes towards routine health practices and it is likely that this has been a major factor in the changes.

Humans↗
PubMed1992

Multicenter evaluation of a new enzyme immunoassay for detection of Clostridium difficile enterotoxin A.

The Premier Clostridium difficile toxin A enzyme immunoassay (PTA EIA) (Meridian Diagnostics, Inc., Cincinnati, Ohio) for rapid diagnosis of antibiotic-associated colitis (AAC) was evaluated in a multicenter study. Stool samples from 421 patients suspected of having AAC were tested for toxin A by the PTA EIA and for toxin B by three tissue culture assays (TCA) employing WI-38 cells (New England Deaconess Hospital) in conventional tubes or foreskin fibroblasts (Children's Hospital) or Vero cells (Beth Israel Hospital) in microwells. The tubes and plates were examined at 24 and 48 h for cytotoxicity. Clinical criteria, repeat testing at another site, and culture of frozen stool samples for C. difficile were used to evaluate discrepant results. Of 504 samples, 66 were positive and 409 were negative by both tests. Eight samples had indeterminate PTA EIA results and were excluded from this analysis. Of 21 discrepancies, 9 were PTA EIA positive and TCA negative and 12 were PTA EIA negative TCA positive. Following resolution of the discrepancies, 11 of 12 PTA EIA-negative-TCA-positive and 5 of 9 PTA EIA-positive-TCA-negative samples were considered true positive for AAC. The sensitivity and specificity were, respectively, 86.6 and 99.0% for the PTA EIA and 93.9 and 99.8% for TCA. The predictive values of positive and negative tests were, respectively, 94.7 and 97.4% for the PTA EIA and 98.7 and 98.8% for TCA. We conclude that the PTA EIA is a rapid, simple EIA technique whose accuracy in detecting enterotoxin A approaches that of reference TCA methods for detection of cytotoxin B.

Bacterial Proteins↗
PubMed1991

Pathways of serotonin-induced electrolyte transport in rat distal colon.

Serotinin-stimulated electrolyte transport was examined in flat-sheet preparations of rat left colon with the Ussing chamber-voltage clamp technique. Transport was studied in tissues stripped of muscularis propria and in nonstripped tissue. In nonstripped colon, the action of serotonin (5-hydroxytrytamine [5-HT]) on short-circuit current was inhibited by a factor of 60% by tetrodotoxin (P less than 0.05; t test) and was also inhibited by the 5HT2 antagonist ketanserin (p less than 0.05 vs serotonin; t test) and the 5-HT3 antagonist ICS 205-930 (p less than 0.05 vs serotonin, t test). These compounds produced corresponding inhibition of serotonin-induced sodium and chloride flux in this preparation. The tetrodotoxin-sensitive component was not inhibited by atropine, hexamethonium, phentolamine, or propranolol. Histologic analysis of the stripped preparation showed that it consisted of mucosa and musclaris mucosa only. In this stripped preparation, serotonin-induced change in short-circuit current was tetrodotoxin insensitive and inhibited by ketanserin (p less than 0.05 vs serotonin, t test) but not by ICS 205-930. Serotonin-induced sodium and chloride flux was inhibited by ketanserin in the presence of tetrodotoxin in this preparation. These results suggest that serotonin-induced electrolyte transport in rat distal colon is mediated by nonneural 5HT2 receptors in the mucosa or muscularis mucosa and by 5-HT3 receptors located on enteric nonadrenergic, noncholinergic nerves.

Analysis of Variance↗
PubMed1988

A survey of the race profiles of cyclists in the pursuit and kilo track events.

A survey was made of national- and international-calibre men and women track cyclists who rode in three separate world-class competitions on the Argyll Velodrome, Edmonton, Canada. Race profiles were obtained from 222 riders who competed in the pursuit and 1000 m time trial (kilo) events. Mean lap times (MLT) and optimal race profiles (ORP) were constructed, and served as the bases of comparison between top- and bottom-ranked riders. The survey showed that riders whose race profile failed to approximate the ORP always lost to riders whose race profile did so. The most likely cause of poor race performances is the inefficient use of the cyclists' anaerobic energy resources.

Bicycling↗
PubMed1987

Effect of a hypoglycaemic agent M&B 39890A on glucagon secretion in isolated rat islets of Langerhans.

Administration of the compound M&B 39890A lowered serum glucose levels significantly (p less than 0.001) in genetically obese mice, while no effect on serum insulin levels was observed. In in vitro experiments with isolated rat islets of Langerhans M&B 39890A inhibited arginine-stimulated glucagon release at all concentrations tested (0.5, 5.0 and 50 mumol/l). Insulin secretion was not inhibited by M&B 39890A (0.5 and 5.0 mumol/l), but was slightly decreased at 50 mumol/l. M&B 39890A (5 mumol/l) also inhibited glucagon secretion in vitro in the presence of 2 mmol/l, 6 mmol/l and 20 mmol/l glucose, while exerting no effect on insulin secretion. These results suggest that the hypoglycaemic action of M&B 39890A may be due to its direct and selective effect on glucagon secretion; this appears to operate by a mechanism different to that of glucose.

Animals↗
PubMed1987

Effect of sodium 2-n-pentadecyl-benzimidazole-5-carboxylate (M & B 35347B), an inhibitor of acetyl-CoA carboxylase, on lipogenesis and fat deposition in obese hyperglycaemic (ob/ob) and lean mice.

A high rate of lipogenesis in obese mice plays a major role in their excessive deposition of body lipid. Inhibition of lipogenesis may decrease their obesity. Therefore, we have investigated the effects of sodium 2-n-pentadecyl-benzimidazole-5-carboxylate (M & B 35347B), an inhibitor of acetyl-CoA carboxylase, on in-vivo lipogenesis in obese and lean mice. It significantly inhibited hepatic cholesterol and fatty acid synthesis, measured using 3H2O, in both lean and obese mice, with or without a glucose load. Brown adipose tissue (scapular) lipogenesis was decreased by M & B 35347B in obese mice but not in lean mice. In white adipose tissue, M & B 35347B did not affect the rates of lipogenesis in either scapular white, inguinal or epididymal depots of obese mice, or the inguinal and scapular white depot of lean mice. However, it doubled lipogenesis in the epididymal fat pad of lean mice. After a glucose load, lipogenesis in the lean epididymal fat pad was not inhibited but that in the inguinal depot was. M & B 35347B inhibited acetyl CoA carboxylase of adipose tissue in vitro but only a small inhibition was detected after in-vivo treatment. These different responses according to type of mouse, treatment and tissue site appear to stem from differences in inhibitor concentration and the importance of acetyl CoA carboxylase as the rate-limiting enzyme of lipogenesis. The weight gain of obese mice dosed orally (200 mg M & B 35347B/kg daily) for 60 days was unaffected and they continued to deposit excess body fat. This presumably occurred because of the lack of inhibition of fatty acid synthesis in white adipose tissue.

Acetyl-CoA Carboxylase↗
PubMed1986

A study of glandular kallikrein in experimental diabetes.

Very high blood glucose concentrations were seen in rats one day after injection with alloxan or streptozotocin. Those levels fell (compared to day one, p less than 0.005) by the third day after injection and subsequently rose again during the ensuing days. In contrast, no significant differences between treated and control rats in concentrations of submandibular kallikrein were recorded until the tenth day after the initial injection. At that time the submandibular kallikrein concentrations in the alloxanized and streptozotocinized rats were less (p less than 0.01) than those of the untreated rats. A further fall (compared to day ten, p less than 0.005) took place over the next four days. Thus submandibular kallikrein would not seem to have been involved in the early stages of the experimental diabetes. In agreement with that conclusion were the results of a related series of experiments in which exogenous porcine pancreatic kallikrein was administered to alloxanized rats. The kallikrein did not bring about a reduction in the high blood glucose levels.

Animals↗
PubMed1986

Studies of the effects of insulin, bradykinin, and captopril on blood glucose levels of alloxan-diabetic rats.

Infusion of bradykinin (1 microgram/min) or saline vehicle for 30 minutes into alloxan-diabetic rats produced no change in the very high levels of blood glucose. Furthermore, intravenous injection of captopril (3 mg/Kg body weight) into the diabetic rats did not result in a significant change of glucose concentrations over a period of 60 minutes. However, infusion of bradykinin 15 minutes after intravenous injection of captopril resulted in a marked decrease of glucose levels (p less than 0.01, compared to pretreatment) by 20 minutes after the start of the infusion. Thus, the captopril potentiated the effect of the kinin, possibly by inhibition of kininase II. Using a spectrophotometric assay with Bz-Gly-Gly-Gly as substrate insulin was shown to be an inhibitor of kininase II purified from hog lungs with an I50 of 1.6 X 10(-5)M compared to captopril with I50 of 2.2 X 10(-9)M. Furthermore, it was found that in vivo infusion of as little as 50 mU insulin over a period of 30 minutes, a dose that by itself was ineffective, potentiated the glucose-lowering activity of a bradykinin infusion in alloxanized rats. Interestingly, the infusion of insulin 15 minutes after injection of captopril, at doses of each compound which alone were inactive, did produce a significant fall (p less than 0.005) in glucose concentrations. Overall, the results show that captopril, insulin and bradykinin can interact to promote a reduction in blood glucose of alloxan-diabetic rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

Comparison of media with and without 'Panmede' for the isolation of Streptobacillus moniliformis from blood cultures and observations on the inhibitory effect of sodium polyanethol sulphonate.

Fastidious anaerobe broth and brain-heart infusion cysteine broth supplemented with 'Panmede' (a papain digest of ox liver) 2.5% supported the recovery of five Streptobacillus moniliformis strains from simulated blood cultures. Other media tested in parallel--brain heart infusion cysteine broth without 'Panmede' and Brewer's thioglycollate broth--were unreliable. Sodium polyanethol sulphonate (Liquoid) 0.05%, inhibited five isolates of S. moniliformis, including isolates from patients with Haverhill Fever. Occasionally, Liquoid 0.025% was also inhibitory and a heavy inoculum of one strain, NCTC11194, was completely inhibited by Liquoid 0.012% in simulated nutrient-broth blood cultures. These results suggest that the choice of media included in each blood-culture set is critical for the optimal isolation of S. moniliformis. Brain-heart infusion cysteine broth supplemented with 'Panmede', or commercially available fastidious anaerobe broth, without Liquoid, is recommended.

Anaerobiosis↗
PubMed1984

A time-course study of submandibular kallikrein, blood glucose and insulin of alloxan-diabetic and streptozotocin-diabetic rats.

A time-course study was carried out of the levels of submandibular kallikrein, serum insulin and blood glucose of rats rendered diabetic by alloxan or streptozotocin. The permanent hyperglycemia seen one day after treatment and the subsequent relative changes in the levels of blood glucose recorded over the following nine days were in agreement with previous observations. A significant reduction in the concentration of submandibular kallikrein did not become apparent until ten days following the injection of alloxan or streptozotocin. Thus the enzyme would not appear to have played either a causal or a preventative role in the production of the hyperglycemic state. Furthermore, in disagreement with previous speculation, the submandibular gland had not compensated for the deficiency of insulin with an increase in production of kallikrein. The fall in the level of serum insulin had preceded the decrease in submandibular kallikrein. However, administration of exogenous insulin over a period of three days did not bring about an increase in the concentration of submandibular kallikrein of the diabetic rats. Thus insulin would not seem to be involved in controlling the level of kallikrein in the submandibular gland.

Alloxan↗