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A Kantarjian

Publications and source records attributed to A Kantarjian.

5 recordsLinked to original sources
PubMed1990

A possible role for cyclic guanosine monophosphate in the rat pineal gland.

Adrenergic stimulation of pinealocytes induces an increase of both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). However, for cGMP no biological effects have been demonstrated so far. Therefore we tested the effects of the analog 8-bromo-cGMP on synaptic ribbon numbers and on melatonin synthesis as reflected by N-acetyltransferase (NAT) activity in the rat pineal gland in vitro. Incubation for 6 h with 8-bromo-cGMP did not change the activity of serotonin NAT but it increased the number of synaptic ribbons. These results indicate that cGMP is involved as a second messenger in the regulation of synaptic ribbon numbers in the rat pineal gland.

Acetyltransferases↗
PubMed1987

Copper protects against galactosamine-induced hepatitis.

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.

Alanine Transaminase↗
PubMed1982

Liver disease in India.

One hundred and twenty-five children with chronic liver disease were seen in Pune in 13 months. Fifty-nine of them, aged 8-39 months, had Indian childhood cirrhosis histologically diagnosed. Their characteristics included an insidious onset of symptoms, a geographical clustering of cases in rural areas north-east of Pune, a high rate of parental consanguinity and affected siblings, and a very high hepatic copper concentration (790-6654 micrograms/g dry weight). Only 8 survived for 6 months, adverse prognostic features being jaundice, ascites, enlargement of the gall bladder, and severe anaemia at presentation. Clinical differentiation from other liver disorders in the same age group was clear in advanced cases but unreliable in earlier cases. Four asymptomatic siblings with hepatomegaly had a benign course. The need for non-invasive methods to diagnose early cases in the community is demonstrated. The other major diagnostic categories were: unresolved hepatitis (12); chronic active hepatitis (7); cryptogenic cirrhosis (6); neonatal hepatitis and biliary atresia (8).

Adolescent↗