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Biomedical subjects

M A Ansari

Publications and source records attributed to M A Ansari.

At least 73 records · Page 4Linked to original sources
PubMed1989

Urinary enzyme output during detoxification of chronic alcoholic patients.

The urinary excretion of N-acetylglucosaminidase, gamma-glutamyl transferase and lactate dehydrogenase was elevated by two to three fold in chronic alcoholic patients when compared to normal controls. After 4 weeks of alcohol abstention, the urinary excretion of these enzymes returned to control values. Increased urinary enzyme excretion was not related to malnutrition or pathological glomerular filtration and is due most probably to a direct effect of alcohol on the renal proximal tubule.

Acetylglucosaminidase↗
PubMed1989

Relationship between beta-endorphin/beta-lipotropin, hyperglycemia, and hyperinsulinemia in obese male Zucker rats.

The relationship between beta-endorphin(beta-EP)/beta-lipotropin(beta-LP) and insulin secretion in the basal state and after glucose challenge was studied in obese male Zucker rats and their lean littermates. Baseline plasma beta-EP/beta-LP concentrations were similar in the two groups of animals. Baseline plasma insulin and serum glucose concentrations were significantly higher in the obese animals. Following glucose challenge, the increase in plasma beta-EP/beta-LP concentrations was significantly lower in the obese animals than in their lean littermates. Opioid blockade with naloxone failed to alter the baseline hyperinsulinemia and hyperglycemia seen in the obese animals. The data suggest that the hyperinsulinemia in the obese Zucker rat is not due to endogenous hyperendorphinemia as shown in humans with polycystic ovary syndrome. The obese rats showed dissociation between glucose-stimulated plasma levels of beta-EP/beta-LP and insulin levels which may contribute to the hyperinsulinemia and insulin resistance in these animals.

Animals↗
PubMed1989

Insecticide impregnated ropes as mosquito repellent.

Ropes were impregnated with different dosages of deltamethrin and burnt throughout the night in human dwellings and cattlesheds. Smoke from smouldering ropes treated with various dose levels gradually saturated rooms and prevented the entry of mosquitoes. This method provided very good protection from mosquito bites including the principal vector of malaria, A. culicifacies. Results of ropes impregnated with 80 ppm deltamethrin were more consistent than at the lower dosage. The technique is indigenous, cost-effective, simple and appropriate for rural areas and does not require any special skills in its application.

Animals↗
PubMed1989

Evaluation of Bacillus sphaericus to control breeding of malaria vectors.

Bacillus sphaericus formulations (Solvay liquid 2362 and Abbott granules 2297) were tested in the laboratory and field for the control of mosquito breeding. Results of laboratory evaluation revealed that both formulations had good larvicidal activity against Culex quinquefasciatus, at 0.04 ml and 1 gm/sq m dosages respectively. Higher dosages at 5 ml liquid or 5 gm/sq m granules were required to control A. stephensi and A. subpictus. A. culicifacies required still higher dosages of Solvay (25 ml/sq m) to achieve same levels of control whereas Abbott granules were not effective even at 20 gm/sq m.

Animals↗
PubMed1988

Endogenous opioids and TSH secretion in azotemic male rats.

The role of endogenous opioids in the control of thyroid-stimulating hormone (TSH) secretion in uremic male rats was investigated using the narcotic antagonist naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of altered TSH secretion in uremia, we also studied a group of normal control animals who were pair-fed with the uremic animals, so that their weights were comparable to that of the uremic animals. Naloxone administration produced a significant increase in the basal concentration of TSH response to TRH (5 micrograms i.v.) was significantly blunted in the uremic animals compared to the normal controls and the starved animals. Naloxone administration did not alter the peak thyrotropin-releasing hormone (TRH) stimulated TSH response in any of the experimental groups of rats. Because of the possibility that the effects of naloxone on TSH secretion in the uremic rats were related to impaired clearance of the naloxone in those animals, an additional group of normal rats was given twice the dose of naloxone administered to the uremic animals. The higher dose of naloxone was similarly without effect on the basal or TRH-stimulated TSH secretion in this group. The data suggest that experimental renal failure is associated with diminished sensitivity of the thyrotroph to TRH stimulation and that this blunted sensitivity cannot be abolished by blockade of endogenous opioids by naloxone. Opioid blockade does, however, increase basal TSH secretion in uremic animals, suggesting an increase in endogenous opioidergic tone in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Gonadotropin secretion in azotemic male rats--effect of opioid blockade.

The role of endogenous opioids in the control of gonadotropin secretion in uremic male rats was investigated using the narcotic antagonist, naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of previously described altered gonadotropin secretion in uremia, we also studied a group of normal pair-fed control animals who exhibited a weight loss comparable to that of the uremic animals. Naloxone administration had no effect on the basal or LRH-stimulated peak concentrations of LH and FSH in the normal or the uremic rats. Basal and LRH-stimulated gonadotropin responses in the pair-fed rats were comparable to those seen in the normal rats. Similarly, opioid blockade produced no change in the basal or LRH-stimulated gonadotropin responses in the pair-fed animals. Testosterone concentrations were significantly lower in the uremic and pair-fed animals compared to the normal rats. The data suggest that experimental renal failure is not associated with altered opioidergic tone, as it relates to gonadotropin secretion, or to diminished sensitivity of the gonadotroph to LRH stimulation. The decreased testosterone concentration seen in the uremic and pair-fed rats may reflect abnormalities in gonadal hormone secretion due to primary pathology occurring at the level of the gonad. These abnormalities may be reflected as diminished Leydig cell sensitivity to LH. The inappropriately low concentrations of LH in the presence of low testosterone together with normal gonadotropin response to exogenous LRH also suggest an abnormal secretion of endogenous LRH. It is not clear whether this presumed abnormality in LRH secretion is a primary event or is related to decreased testosterone production by the testes in the uremic and pair-fed rats.

Animals↗
PubMed1988

Atrial natriuretic peptide, arginine vasopressin, and the renin-angiotensin system in carbon tetrachloride-induced hepatitis in rats.

The concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP) and hormones of the renin-angiotensin axis were studied in male rats with carbon tetrachloride-induced hepatitis and the results compared to normal control animals. The rats with hepatitis exhibited lower concentrations of ANP, plasma renin activity (PRA), and angiotensin I (AI) than did the control animals. Plasma concentrations of AVP and aldosterone were not significantly different in the two groups. The results suggest that experimental hepatitis is associated with renal hyperperfusion together with reduction in atrial pressures.

Aldosterone↗
PubMed1987

Dopamine and TSH secretion in uremic male rats.

The role of dopamine in the dysregulation of TSH secretion in uremic male rats was investigated using the dopamine antagonist, pimozide. In order to obviate the effect of weight loss due to uremia-induced anorexia as a cause of altered TSH secretion in uremia, we also studied a group of normal animals whose food intake was restricted and who demonstrated weight loss comparable to that of the uremic animals. Baseline TSH concentrations were not significantly different in the normal, uremic or starved animals. Pimozide administration produced no change in the baseline TSH concentrations in any of the groups of rats. The peak TSH response to TRH (5 micrograms IV) was significantly blunted in the uremic animals compared to the normal controls and the starved animals. Pimozide administration did not alter the peak TRH-stimulated TSH response in either the normal animals or the starved animals. However, the peak TRH-stimulated TSH response was significantly increased in the uremic animals and was comparable to the peak TSH response seen in the pimozide-untreated control animals. The data suggest that experimental renal failure in rats is associated with diminished sensitivity of the thyrotroph to TRH stimulation, and that this blunted sensitivity may be dopamine-dependent since it can be abolished by pharmacologic dopamine blockade.

Animals↗
PubMed1987

Gamma-aminobutyric acid and dysregulation of TSH secretion in uremic male rats.

The role of gamma-aminobutyric acid (GABA) in the abnormal secretion of thyrotropic hormone (TSH) in uremia was studied in male Sprague-Dawley rats rendered renally insufficient by subtotal nephrectomy. Baseline TSH concentrations in normal control animals and in the uremic animals were similar. The peak TSH response to thyrotropin-releasing hormone (TRH; 5 micrograms i.v.) was significantly blunted in the uremic animals compared to the controls. Pretreatment of the uremic animals with the specific GABA antagonist, bicuculline (1.5 mumol i.v.) resulted in normalization of the peak TSH response to TRH. Bicuculline pretreatment, however, did not alter the basal secretion of TSH in either the normal or the uremic animals, and it also did not augment the TRH-stimulated TSH response in the normal animals. Sham-operated animals demonstrated basal and TRH-stimulated TSH responses comparable to the control group. In order to assess whether the weight loss associated with uremia could have accounted for the blunted TRH-stimulated TSH secretion in the uremic animals, a group of rats were starved so that their weights were comparable to those of the uremic animals. Basal and TRH-stimulated TSH responses in this group were not significantly different from the controls. Bicuculline pretreatment of the starved animals also failed to alter the basal and TRH-stimulated TSH responses. These data indicate that an increase in central gabaergic tone may be partly responsible for the blunted TSH response to TRH seen in uremia, but that GABA is not an important modulator of TSH secretion in the normal rat.

Animals↗