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Biomedical subjects

W J Jenkins

Publications and source records attributed to W J Jenkins.

At least 19 recordsLinked to original sources
PubMed2001

The role of dopamine in the nucleus accumbens and striatum during sexual behavior in the female rat.

Dopamine in dialysate from the nucleus accumbens (NAcc) increases during sexual and feeding behavior and after administration of drugs of abuse, even those that do not directly activate dopaminergic systems (e.g., morphine or nicotine). These findings and others have led to hypotheses that propose that dopamine is rewarding, predicts that reinforcement will occur, or attributes incentive salience. Examining increases in dopamine in NAcc or striatum during sexual behavior in female rats provides a unique situation to study these relations. This is because, for the female rat, sexual behavior is associated with an increase in NAcc dopamine and conditioned place preference only under certain testing conditions. This experiment was conducted to determine what factors are important for the increase in dopamine in dialysate from NAcc and striatum during sexual behavior in female rats. The factors considered were the number of contacts by the male, the timing of contacts by the male, or the ability of the female to control contacts by the male. The results indicate that increased NAcc dopamine is dependent on the timing of copulatory stimuli, independent of whether the female rat is actively engaged in regulating this timing. For the striatum, the timing of copulatory behavior influences the magnitude of the increase in dopamine in dialysate, but other factors are also involved. We conclude that increased extracellular dopamine in the NAcc and striatum conveys qualitative or interpretive information about the rewarding value of stimuli. Sexual behavior in the female rat is proposed as a model to determine the role of dopamine in motivated behavior.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2001

Role of the striatum and nucleus accumbens in paced copulatory behavior in the female rat.

Female rats engage in a series of approach and avoidance behaviors (pacing behavior) directed at the male in order to achieve a preferred rate of intromissions that make pregnancy more likely to occur with insemination. The striatum and nucleus accumbens have been implicated in the modulation of pacing behavior. It is unclear, however, whether these areas of the brain are necessary for the display of pacing behavior. To address this question, ovariectomized female rats received either bilateral quinolinic acid lesions of the striatum or nucleus accumbens or sham surgeries. After hormone priming, rats were allowed to engage in mating behaviors in an apparatus in which they could pace the rate of the copulatory bout. There was a significant reduction in pacing efficiency after striatal lesions, in that females were less likely to leave the male's side of the chamber after a contact. Animals with lesions of the nucleus accumbens that included the shell were more likely to avoid sexual interaction altogether than animals with control lesions. Therefore, it is concluded that the striatum and nucleus accumbens modulate specific aspects of pacing behavior in the female rat.

Animals↗
PubMed2000

Critical periods for the effects of alcohol exposure on brain weight, body weight, activity and investigation.

Using an animal model of fetal alcohol syndrome - which equates peak blood alcohol concentrations across different developmental periods - critical periods for the effect of alcohol on brain weight, activity and investigative behavior were examined. The periods of alcohol exposure were from gestational day (GD) 1 through 10, GD 11 through 22, postnatal day (PD) 2 through 10, or all three periods combined. The critical period of alcohol exposure for an increase in activity in juveniles was GD 11 through 22. This pattern was not seen in the same animals in adulthood; instead, increases in both activity and investigation were seen in animals exposed from PD 2 through 10 and not seen in animals exposed during all three periods combined. Brain weight was reduced by alcohol exposure from GD 11 through 22, PD 2 through 10 and all three periods combined. The period from PD 2 through 10 was the only period when the brain weight to body weight ratio was reduced. In conclusion, exposure to alcohol during the periods in the latter half of gestation or early postnatal period seem to have the most deleterious effects on the brain, activity and investigation in the rat. In addition, the effects of alcohol exposure over both the prenatal and postnatal period cannot be easily predicted from the effects of shorter periods of exposure.

Animals↗
PubMed1987

A preliminary study of hepatitis B virus replication during short-term (7-day) social drinking.

The purpose of this study is to determine the effect of short-term social drinking on hepatitis B virus (HBV) replication as measured by serum levels of hepatitis B virus DNA (HBV-DNA). We studied five male carriers of hepatitis B e antigen who were social drinkers. Levels of HBV-DNA, blood alcohol, and aspartate aminotransferase (AST) were measured during abstinence from alcohol, before and during a test dose (29.8 g) of alcohol which followed one week of abstinence, and before and during the same test dose which followed social drinking for one week. We observed no significant changes in HBV-DNA or AST levels. These data suggest that a single one-week period of social drinking in patients with chronic HBV infection does not cause enhanced viral replication. The risks of repeated ingestion of moderate amounts of alcohol by such patients have not been established. Interpretation of our data is limited by the small number of subjects, and further studies are needed. Nevertheless, our results are consistent with published recommendations that social drinking by nonalcoholic HBV carriers should be restricted but need not be totally forbidden.

Adult↗
PubMed1987

Effect of chronic ethanol ingestion on enterocyte turnover in rat small intestine.

Whether chronic ethanol ingestion significantly damages the small intestine remains controversial. To clarify this we have analysed the morphology of the small intestinal epithelium and quantified its renewal in chronically ethanol fed rats. Twenty adult male rats were pair fed for 28 days a nutritionally adequate liquid diet containing either ethanol as 36% of total calories or an isocaloric diet in which fat substituted for ethanol. Crypt cell production rate was determined in the jejunum and ileum by the metaphase arrest method. Weight gain and small intestinal morphology were similar in ethanol fed and control rats, but enterocyte turnover was significantly reduced in the jejunum (p less than 0.05) and ileum (p less than 0.01) of the ethanol fed rats. This effect of ethanol on the small intestine is probably systemic rather than local, because the changes in jejunum and ileum were similar, and it may contribute to the development of malnutrition in chronic alcoholics.

Animals↗
PubMed1987

Effect of chronic ethanol intake on lactase activity and active galactose absorption in rat small intestine.

The effects of feeding a nutritionally adequate liquid diet containing 5% ethanol to rats over a four week period on intestinal lactase activity and the kinetics of jejunal galactose absorption in vivo have been determined. Both lactase activity and the maximum capacity for active, saturable galactose absorption (Jmax) were increased significantly after chronic ethanol ingestion. In contrast, uptake of the sugar via the phlorhizin-insensitive (passive) route was unaffected by ethanol. Our results imply the presence of an increased maturity of the enterocyte population on the villus surface in response to ethanol. The relevance of this work to uptake studies in alcoholics is briefly discussed.

Animals↗
PubMed1986

Platelet function defects in chronic alcoholism.

Platelet function in alcoholic patients was assessed on admission and during abstinence in hospital. On admission platelets from these patients were significantly less responsive (percentage aggregation and thromboxane A2 release) to conventional in vitro aggregating agents (adrenaline, adenosine diphosphate, and collagen) than platelets from healthy, moderate drinkers. Initially, platelet counts in platelet rich plasma tended to be low and the Simplate II bleeding times frequently prolonged. Platelet aggregation and thromboxane A2 release, however, were inhibited even in patients with normal platelet counts on admission. Platelet aggregation and thromboxane A2 release returned to normal or became hyper-responsive during two to three weeks of abstinence. Platelet counts rose during this period, the largest responses occurring in those patients with the lowest counts on admission. Bleeding times reverted to normal during abstinence and correlated significantly with changes in platelet aggregation, thromboxane A2 release, and platelet count and with the estimated ethanol consumption during the week before admission. Chronic, heavy alcohol ingestion evidently exerts an inhibitory effect on platelet function even in the absence of alcohol in the blood, and this phenomenon is reversible on abstaining. The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal haemorrhage associated with excessive alcohol intake.

Adult↗
PubMed1985

Absent ileal uptake of IF-bound vitamin B12 in vivo in the Imerslund-Grasbeck syndrome (familial vitamin B12 malabsorption with proteinuria).

A Syrian family is described with three children who had inherited selective vitamin B12 malabsorption associated with proteinuria. (Imerslund-Grasbeck syndrome). Although inherited the defect was apparently not present at birth. A third child had less severe vitamin B12 malabsorption, was not vitamin B12 deficient and had no proteinuria. Studies on two of the affected children with subcellular fractionation of the uptake of radioactive vitamin B12 by ileal tissue in vivo indicate a defect in the ileal receptors for IF-bound vitamin B12. These findings are different from the single in vitro experiment on a patient with this condition that has been previously reported.

Adolescent↗
PubMed1984

The preparation of human intrinsic factor-cobalamin complex from human gastric juice by immunoadsorption.

Immune complexes of human intrinsic factor were prepared by mixing gastric juice saturated with vitamin B12, and sera from patients with pernicious anaemia that had a high proportion of binding (Type II) antibody. The complexes were isolated by sodium sulphate precipitation followed by Sephadex G-150 gel filtration. Acid conditions dissociated the immune complexes and allowed separation of specific antibody and purified antigen bound to vitamin B12 by Sephadex G-200 gel filtration. Specific antibody was covalently attached to Protein A Sepharose CL-4B by coupling with water soluble carbodiimide which allowed intrinsic factor-B12 complex to be purified directly from gastric juice. The intrinsic factor obtained after iodination, ran as a single band on SDS-polyacrylamide gel electrophoresis and was biologically active.

Anemia, Pernicious↗
PubMed1984

Effect of alcohol consumption on hepatic aldehyde dehydrogenase activity in alcoholic patients.

Two liver biopsies were performed 6 months apart in each of 29 patients with alcoholic liver disease. Hepatic aldehyde dehydrogenase activity was measured on each occasion. The patients were seen regularly and their alcohol consumption was assessed independently. Hepatic aldehyde dehydrogenase activity was unchanged in 17 patients who continued to drink to excess; it rose in 10 patients who significantly reduced their alcohol intake; and it fell dramatically in 2 patients who were virtually abstinent initially, but then began drinking heavily. These results clearly demonstrate that alcohol consumption itself depresses hepatic aldehyde dehydrogenase activity. It is unlikely that the low hepatic aldehyde dehydrogenase activity reported in alcoholics represents a primary abnormality predisposing to alcoholism or alcoholic liver disease.

Acetaldehyde↗
PubMed1983

Controlled trial of propranolol for the prevention of recurrent variceal hemorrhage in patients with cirrhosis.

We conducted a prospective randomized trial of propranolol for the prevention of recurrent variceal bleeding in 48 patients with cirrhosis of the liver. During a follow-up period of up to 21 months, 12 of 26 patients in the propranolol group and 11 of 22 in the control group had rebleeding from esophageal varices. There was no significant difference in rebleeding between the two groups. This contrasts with a previous report of the efficacy of propranolol in preventing recurrent gastrointestinal bleeding in alcoholic cirrhosis. The difference in results may be due to the inclusion in our study of patients with other causes of cirrhosis and more severe liver disease. Propranolol may not be indicated for the prophylaxis of variceal rebleeding in such patients, and we advocate that its use be limited at present to controlled clinical trials.

Adult↗
PubMed1983

Subcellular localization of acetaldehyde dehydrogenase in human liver.

The subcellular distribution of aldehyde dehydrogenase activity was determined in human liver biopsies by analytical sucrose density-gradient centrifugation. There was bimodal distribution of activity corresponding to mitochondrial and cytosolic localizations. At pH 9.6 cytosolic aldehyde dehydrogenase had a lower apparent Kappm for NAD (0.03 mmol l-1), than the mitochondrial enzyme (Kappm NAD = 1.1 mmol l-1). Also, the pH optimum for cytosolic aldehyde dehydrogenase activity (pH 7.5) was lower than that for the mitochondrial enzyme activity (pH 9.0), and the cytosolic enzyme activity was more sensitive to inhibition by disulfiram in vitro. Disulfiram (40 mumol l-1) caused a 70% reduction in cytosolic aldehyde dehydrogenase activity, but only a 30% reduction in mitochondrial enzyme activity after 10 min incubation. The liver cytosol may therefore be the major site of acetaldehyde oxidation in vivo in man.

Aldehyde Oxidoreductases↗
PubMed1983

Efficacy of clonidine in treatment of alcohol withdrawal state.

Clonidine hydrochloride 5 micrograms/kg and placebo were given orally to 11 patients experiencing well-developed alcohol withdrawal states. Active drug and placebo were given in a randomised, cross-over double blind fashion 2 h apart. Clonidine significantly suppressed heart rate (P = 0.002), arterial blood pressure (P = 0.006), and an accumulated score of withdrawal symptoms and signs (P = 0.004). These data suggest that clonidine may be useful in the management of alcohol withdrawal states, and that the underlying pathophysiology of at least some of these manifestations may be sympathetic nervous system hyperactivity.

Adult↗
PubMed1983

Nuclear magnetic resonance (NMR) imaging in Wilson disease.

Nuclear magnetic resonance (NMR) scans of the head and liver were obtained in 13 patients with Wilson disease, and the results were compared with computed tomography (CT). Twelve age and sex matched normal controls were also scanned with NMR. The subjects were scanned using repeated free induction decay (RFID), inversion-recovery (IR), and spin-echo (SE) sequences. The IR scans of the brain provided excellent anatomical localisation while SE scans highlighted pathological areas. Within the brain, NMR demonstrated abnormalities in two patients with normal CT scans. More extensive involvement was shown with NMR in three additional cases. In the liver, NMR and CT showed similar abnormalities of morphology. T1 values were within the normal range in all cases, including three patients with high liver copper levels at the time of NMR examination.

Adolescent↗
PubMed1983

The effect of ranitidine on the plasma clearance and hepatic extraction of indocyanine green in patients with chronic liver disease.

Since hepatic clearance of ICG is reduced by H2-receptor antagonists in normal subjects, it has been suggested that they reduce liver blood flow. We have studied the effect of intravenous ranitidine on ICG clearance in twelve patients with chronic liver disease. Wedged and free hepatic venous pressure were measured before and after intravenous ranitidine in nine of the patients, and the hepatic extraction of ICG was determined in six patients. ICG clearance fell by 22 +/- 11% (s.e. mean) 60 min after ranitidine. In patients in whom ICG clearance fell after intravenous ranitidine the hepatic extraction of ICG was also reduced. There was no significant change in the gradient between wedged and free hepatic venous pressure after ranitidine. It is therefore unlikely that ranitidine lowers liver blood flow.

Adolescent↗