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Biomedical subjects

A Chandra

Publications and source records attributed to A Chandra.

At least 127 records · Page 7Linked to original sources
PubMed1986

Serological relationship between reverse transcriptases from human T-cell lymphotropic viruses defined by monoclonal antibodies. Evidence for two forms of reverse transcriptases in the AIDS-associated virus, HTLV-III/LAV.

The immunological relationship between reverse transcriptases purified from human T-cell lymphotropic viruses (HTLV-I, HTLV-II, HTLV-III) was defined using monoclonal antibodies specific for HTLV-III reverse transcriptase, secreted by a mouse/mouse hybridoma clone (4F8) developed in our laboratory. The viral proteins from HTLV-I and HTLV-II do not bear any cross-reactive epitope to antibodies secreted by this clone. These antibodies specifically cross-react with HTLV-III reverse transcriptase. The antibodies failed to neutralize the catalytic activity of reverse transcriptase; however, after immunoprecipitation with a magnetic conjugate of goat anti-mouse IgG, the residual activity was completely inhibited. This shows that the antibodies are not directed towards the catalytic active center of the enzyme. Using an immunoblotting technique (Western blotting), we have found two cross-reactive proteins with HTLV-III lysate with molecular masses of 53 and 66 kDa. This suggests that HTLV-III possesses two reverse transcriptase activities with a common determinant recognized by the same epitope.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Biochemical heterogeneity of reverse transcriptase purified from the AIDS virus, HTLV-III.

The reverse transcriptase from AIDS virus, HTLV-III, was purified and characterized. The purified enzyme has a very high affinity for template primers (rC)n X (dG)12 and (rCm)n X (dG)12 compared to that for (rA)n X (dT)12. In addition, the HTLV-III reverse transcriptase was able to transcribe (rAm)n X (dT)12 very efficiently. The ionic requirements are unique in the sense that HTLV-III reverse transcriptase prefers Mg2+ as divalent ions to transcribe (rC)n X (dG)12 and (rA)n X (dT)12. The Mr of the enzyme is 95 000-98 000. Unlike the HTLV-I reverse transcriptase, the HTLV-III enzyme is highly stable and has a much higher activity in the presence of (rC)n X (dG)12; the Vmax for HTLV-III reverse transcriptase is several-fold higher than that for HTLV-I enzyme. The enzyme activity of the purified reverse transcriptase from HTLV-III was resolved into two peaks on a preparative isoelectric column, one at pH 5.75 and the other at pH 6.25. This leads us to conclude that the reverse transcriptase of HTLV-III is biochemically heterogeneous.

Cations, Divalent↗
PubMed1986

The effect of 17-alpha-estradiol, a possible endogenous opiate antagonist, on D-ala2-met5-enkephalinamide-induced blood pressure responses in conscious, unrestrained rats.

D-ala2-met5-enkephalinamide (DAME) produced a dose-related increase in the mean arterial blood pressure of conscious, unrestrained rats. Intravenous injection of DAME (0.5, 1, 2, and 4 mg/kg) resulted in mean systemic arterial blood pressures of 138 +/- 2, 146 +/- 5, 141 +/- 4, 156 +/- 5 mmHg, respectively. 17-alpha-estradiol and its derivatives are known to be inactive in target tissues responsive to estrogenic hormones such as 17-beta-estradiol. However, LaBella et al. (1978) found after testing a large number of steroid hormones and their metabolites that only 17-alpha-estradiol significantly inhibited binding of 3H-naloxone, an opiate antagonist, in rat-brain homogenates. The present study was designed to determine whether 17-alpha-estradiol could antagonize the cardiovascular responses elicited by intravenous injections of DAME. Intravenous infusion of 17-alpha-estradiol (1.5 mg/kg) every 2 hours for 24 hours (total infusion time was 2 minutes for each infusion) did not change the mean systemic arterial blood pressure (94 +/- 5 mmHg) compared to the blood pressure prior to infusion of 17-alpha-estradiol (99 +/- 7 mmHg). Intravenous infusion of 17-alpha-estradiol (1.5 mg/kg) 10 minutes prior to DAME (1 mg/kg, i.v.) resulted in a blood pressure of 106 +/- 9 mmHg, which is significantly less than the blood pressure of 146 +/- 5 mmHg seen with DAME (1 mg/kg, i.v.) alone. Intravenous injection of DAME (1 mg/kg) 8 hours after the last infusion of 17-alpha-estradiol produced an increase in mean systemic arterial blood pressure of 136 +/- 8 mmHg. These results indicate that 17-alpha-estradiol may function as an opiate antagonist.

Animals↗
PubMed1984

Inhibitors of phenylethanolamine-N-methyltransferase: effects on brain catecholamine content and blood pressure in DOCA-salt hypertensive rats.

Inhibitors [2-cyclooctyl-2-hydroxyethylamine (CONH), 1 aminomethylcycloundecanol (CUNH), 7,8-dichloro-1,2,3,4-tetrahydroisoquinoline (SKF64139), 2,3-dichloro-alpha-methylbenzylamine (DCMB), 8,9-dichloro-2,3,4,5-tetrahydro-1H-2-benzazepine(LY134046)] of phenylethanolamine N-methyltransferase (PNMT) were found to reduce blood pressure in deoxycorticosterone-salt (DOCA-salt) hypertensive rats. CONH, CUNH and DCMB, but not SKF64139 and LY134046, also lowered blood pressure in normotensive control rats. All of the PNMT inhibitors tested lowered hypothalamic epinephrine (Epi) content in both DOCA-salt hypertensive and normotensive rats. DCMB, SKF64139 and LY134046 also lowered brainstem Epi in both animal groups. From these data a good correlation could not be made between the blood pressure lowering effects of PNMT inhibitors and their effects on hypothalamic Epi content as had been observed in other animal models of hypertension (e.g. spontaneously hypertensive rats).

Animals↗
PubMed1982

Hypothalamic and striatal dopamine receptor activation inhibits heat production in the rat.

Direct injection of dopaminergic agonist apomorphine into the lateral cerebral ventricle, the preoptic anterior hypothalamus, the caudate-putamen complex, or the globus pallidus caused hypothermia, decreased metabolism and cutaneous vasoconstriction at ambient temperature (Ta) 8 and 22 degrees C, and hyperthermia and cutaneous vasoconstriction in the rat at Ta 30 degrees C. On the other hand, local injection of dopaminergic antagonists such as haloperidol and pimozide into the preoptic anterior hypothalamus and the striatal nuclei caused hyperthermia, increased metabolism and cutaneous vasoconstriction at Ta 8, 22, and 30 degrees C. However, there was no change in respiratory evaporative heat loss in response to administration of either dopaminergic agonist or antagonists in the rat at all Ta studied. The data indicate that hypothalamic and striatal dopaminergic receptor activation inhibits metabolic heat production in rats. In addition, intrahypothalamic injection of 5-hydroxytryptamine caused hypothermia, decreased metabolism and cutaneous vasodilatation in the rat at Ta 8 and 22 degrees C, whereas at Ta 30 degrees C caused an insignificant change in the thermoregulatory responses. Furthermore, the thermal responses induced by intrahypothalamic injection of apomorphine were not altered by depletion of hypothalamic 5-hydroxytryptamine. These observations do not support the contention that there is a dopamineserotonin link in the hypothalamic pathways that mediate heat loss mechanisms in the rat.

5,7-Dihydroxytryptamine↗
PubMed1982

A norepinephrine-cyclic AMP link in the hypothalamic pathways which mediate fever induced by endotoxin and prostaglandin E2 in the rat.

The changes in rectal temperature, metabolic rate, cutaneous temperatures and respiratory evaporative heat loss produced by an injection of a bacterial endotoxin piromen (4-40 ng in 1 microliter) into the anterior hypothalamus were assessed in conscious rats in both sexes from a wide range of body mass and at various ambient temperatures (TaS). Intrahypothalamic injection of piromen increased metabolism and decreased cutaneous temperatures which led to fever in rats at Ta 8-30 degrees C. The monophasic fever was not significantly correlated with either body mass, sex difference of the Ta at which the experiments are carried out. Furthermore, daily intrahypothalamic injections of piromen produced no pyrogenic tolerance. Intrahypothalamic injections of either prostaglandin E2, norepinephrine, aminophylline or dibutyryl cyclic AMP also produced increased metabolism and decreased cutaneous temperature which led to fever at Ta 8-30 degrees C. In addition, the fever induced by intrahypothalamic injections of piromen, prostaglandin E2 or nor-epinephrine was greatly antagonized by pretreatment with intrahypothalamic injections of alpha or beta adrenergic antagonist. However, the fever induced by dibutyryl cyclic AMP or aminophylline was not affected by pretreatment with adrenergic receptor blockade. The data indicate that a norepinephrine- cyclic AMP link occurs in the hypothalamic pathways which mediate the piromen-induced or the prostaglandin E2-induced fever in rats.

Aminophylline↗
PubMed1981

Activation of striatal dopamine receptors induces pain inhibition in rats.

In the rat, elevating dopamine content in corpus striatum with electrical stimulation of substantia nigra or direct administration of apomorphine (50-200 micrograms) into the lateral cerebral ventricle or apomorphine (2-10 microgram) into the caudate-putamen complex decreased pain sensitivity (as shown by an increase in the latency to hind-paw lick in the hot plate test). Furthermore, the decreased pain sensitivity after the central administration of apomorphine was antagonized by pretreatment with haloperidol (a dopamine antagonist). On the other hand, lowering dopamine content in corpus striatum with electrolytic destruction of substantia nigra and 6-hydroxydopamine lesions to the substantia nigra, as well as direct injection of haloperidol into the lateral cerebral ventricle or caudate-putamen complex increased pain sensitivity. The data indicate that activation of striatal dopamine receptors in rat brain induces pain inhibition.

Animals↗
PubMed1981

Effects of adenosine 3',5'-cyclic monophosphate on thermoregulation in both rats and rabbits.

The effects of intraventricular administration of dibutyryl adenosine 3',5'-cyclic monophosphate (db cyclic AMP) on the thermoregulatory responses of unanesthetized rats and rabbits to different ambient temperatures (Ta) were assessed. Administration of db cyclic AMP (10-60 mM) produced dose-dependent hypothermia in both rats and rabbits at Ta 2-22 degrees C. The hypothermia in response to db cyclic AMP was due to decreased metabolic heat production and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. In contrast, in the heat (30-32 degrees C), db cyclic AMP administration produced dose-dependent hyperthermia in these animals. The hyperthermia was due to increased metabolism (due to muscular shivering) and decreased heat losses. The reduction in heat losses was shown by a decrease in both cutaneous circulation and respiratory evaporative heat loss. The data demonstrate that the thermoregulatory responses induced by central administration of db cyclic AMP are Ta-dependent.

Animals↗