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Biomedical subjects

G Treisman

Publications and source records attributed to G Treisman.

12 recordsLinked to original sources
PubMed1997

AIDS mania.

Twenty patients with HIV infection and mania were grouped according to whether their first manic episode occurred when CD4 count was < 200 (late onset) or > or = 200 (early onset). The late-onset patients were less likely to have personal or family histories of mood disorder and more likely to have dementia or cognitive slowing. They also exhibited a different manic symptom profile. The different sociodemographic and symptom profiles associated with early-onset and late-onset mania may reflect differences in pathophysiology.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Sertraline in the treatment of severe aggressiveness in Huntington's disease.

Sertraline, a selective serotonin reuptake inhibitor, was used to treat two consecutive cases of genetically confirmed Huntington's disease in which severe irritability and aggressiveness required inpatient admission. The complete cessation of aggressive behavior in both cases has been maintained on follow-up. This report adds to the literature implicating serotonergic mechanisms in irritability and aggressiveness in both neuropsychiatric and idiopathic psychiatric disorders.

1-Naphthylamine↗
PubMed1995

Psychiatric issues and emergencies in HIV infection.

Emergency departments are frequently the entry point for patients infected with HIV. Psychiatric conditions may be the initial predominant presentation or an important concomitant factor. Because of the complexities of HIV infection, the serious medical nature of its associated psychiatric complications, the frequent presence of comorbid substance use and other behavioral disorders, and the multiple sites of treatment involved, psychiatrists, emergency physicians, and other professionals must work in collaboration in screening patients infected with HIV for mental disorders and in providing careful and rational care.

AIDS Dementia Complex↗
PubMed1984

Calmodulin stimulates adenylate cyclase activity and increases dopamine activation in bovine retina.

Adenylate cyclase activity in bovine retina is highly responsive to Ca2+ and the endogenous Ca2+-binding protein, calmodulin (CaM). CaM stimulated adenylate cyclase activity in washed particulate fractions of bovine retina by 6.6-fold in a Ca2+-dependent manner. Activation of adenylate cyclase activity by CaM was maximal at 0.12 microM free Ca2+. The apparent Ka for calmodulin stimulation of adenylate cyclase was 67 nM and the apparent Vmax was 116 pmol/min/mg of protein above basal activity. Adenylate cyclase activity in bovine retina was stimulated approximately 50% by guanosine 5'-triphosphate (GTP), but the nonhydrolyzable GTP analogue, guanosine-5'-(beta, gamma-imido)triphosphate (Gpp(NH)p), was able to activate the enzyme nearly 5-fold. CaM and Gpp(NH)p appeared to be partially competitive activators of adenylate cyclase in the retina particulate fraction. Dopamine stimulated adenylate cyclase activity in the presence of GTP with an apparent Ka of 1.0 microM and an apparent Vmax of 66 pmol/min/mg of protein. Ca2+ and CaM increased the apparent Vmax of the dopamine-stimulated adenylate cyclase activity more than 2-fold to a level of 146 pmol/min/mg of protein but did not alter the apparent Ka. This suggests that CaM is an endogenous modulator of dopamine-stimulated adenylate cyclase activity in the retina. CaM-stimulated adenylate cyclase activity may be a common component to retina since we found this activity in retinas from rabbit, rat, and goldfish as well as cow.

Adenylyl Cyclases↗
PubMed1983

Calmodulin level in whole blood correlates with the percentage of reticulocytes.

We studied the calmodulin-like activity (CaM) level in hemolyzed samples of whole blood after determining the percentage and absolute number of reticulocytes present. Twenty-six samples from 25 people with a range of reticulocyte counts were studied. CaM levels correlated with the percentage (r = 0.63, P less than .01) and absolute number (r = 0.64, P less than .01) of reticulocytes present, indicating that the calmodulin-like activity level in whole blood was inversely related to erythrocyte age.

Adult↗
PubMed1983

Chronic sulpiride treatment produces supersensitivity of striatal adenylate cyclase to dopamine in sexually immature or adult castrated rats.

Sulpiride, a substituted benzamide antipsychotic drug, is considered to be a selective antagonist at dopamine D-2 receptors, largely because it does not inhibit dopamine-stimulated adenylate cyclase activity. It was found that sulpiride in vitro can block dopamine-stimulated adenylate cyclase activity in rat striatum from sexually immature or adult castrated male rats. Chronic treatment with sulpiride (20 mg/kg i.p. twice daily for 15 days) resulted in supersensitivity of dopamine-stimulated adenylate cyclase activity in striatum from sexually immature (3-4 weeks old) as well as adult castrated rats. The apparent Ka was decreased 4-fold in the sulpiride-treated animals, whereas the apparent Vmax remained unchanged. This treatment did not alter dopamine-stimulated adenylate cyclase activity in the striatum from adult male rats. Acute treatment with sulpiride was slightly inhibitory to dopamine-stimulated adenylate cyclase in striatum from the immature rat, suggesting that the supersensitivity after repeated injections could be a compensatory increase. In in vitro studies it was found that sulpiride at nanomolar levels could inhibit the ability of low concentrations of dopamine to stimulate adenylate cyclase activity in striatal particulate fractions from sexually immature or adult castrated rats. Sulpiride did not affect dopamine-stimulated adenylate cyclase in the adult rat striatum. Our results indicate that sulpiride can affect dopamine-stimulated adenylate cyclase activity in animals that are lacking testosterone, or perhaps estrogen. This suggests that sex hormones could regulate the sensitivity and pharmacological profile of dopamine receptors for their ligands.

Adenylyl Cyclases↗
PubMedDate not supplied

The effectiveness of psychiatric treatment for HIV-infected patients.

The study sought to determine the effectiveness of a model program of psychiatric care for human immunodeficiency virus (HIV)-infected patients. This was a cohort study of 126 HIV-positive outpatients referred for psychiatric evaluation and treatment (average follow up of 14 months) in a HIV-dedicated primary-care outpatient clinic in the inner city. A global outcome measure (encompassing symptom relief, functioning, and HIV-risk behaviors), and a measure of abstinence from alcohol and illicit substances were used. Fifty percent of patients improved, with 19% "nearly well" at follow-up. Abstinence was achieved 48% of the time. Good compliance with treatment and the absence of injection drug use were the primary predictors of good outcomes. Of the compliant patients, 94% improved, with 45.7% being nearly well. Psychiatric treatment of HIV-infected patients is effective when located in the HIV primary-care setting and administered by a multidisciplinary team under the direction of a psychiatrist, using evidence-based interventions.

Adult↗