Search PubMed⌕ Search

Biomedical subjects

S C Mann

Publications and source records attributed to S C Mann.

27 records · Page 2Linked to original sources
PubMed1986

Lethal catatonia.

Lethal catatonia, a life-threatening febrile neuropsychiatric disorder, was widely reported in this country and abroad before the introduction of modern psychopharmacologic treatments. A comprehensive review of the world literature indicates that although the prevalence of lethal catatonia may have declined, it continues to occur, now reported primarily in the foreign literature. Lack of recognition probably accounts for the scarcity of recent American reports. Furthermore, lethal catatonia is a syndrome rather than a specific disease and may develop in association with both functional and organic illnesses. Familiarity with the clinical features and varied etiologies is essential for effective management of this catastrophic reaction.

Adolescent↗
PubMed1978

Psychotropic drugs, summer heat and humidity, and hyperpyrexia: a danger restated.

The authors note an apparent unawareness of, as well as a paucity of recent literature pertaining to, hyperpyrexia as a complication of psychotropic drug treatment. They report a case of hyperpyrexia in a patient receiving psychotropic agents during a summer heat wave; massive muscle destruction (rhabdomyolysis) with myoglobinuria and acute renal failure make this case of particular interest. Causative mechanisms, preventive measures, and the benefits of prompt recognition and treatment of this condition are discussed.

Antipsychotic Agents↗
PubMedDate not supplied

[Lethal catatonia: clinical aspects and therapeutic intervention. A review of the literature].

Lethal catatonia continues to occur and represents a nonspecific syndrome associated with diverse organic as well as functional conditions. From this perspective, neuroleptic malignant syndrome may be conceptualized as a neuroleptic-induced toxic or iatrogenic form of organic lethal catatonia. Neuroleptics appear ineffective in the treatment of lethal catatonia and should be stopped whenever this disorder is suspected. Existing data suggest that ECT is a safe and effective treatment for lethal catatonia. ECT also appears effective in the treatment of neuroleptic malignant syndrome.

Antipsychotic Agents↗
PubMedDate not supplied

Comparison of lipid content, surface membrane fluidity, and temperature dependence of cis-diamminedichloroplatinum(II) accumulation in sensitive and resistant human ovarian carcinoma cells.

We conducted studies to determine whether the cisplatin (DDP)-resistant human ovarian carcinoma cell line designated 2008/DDP has membrane changes which could slow the passive diffusion of the drug into cells, thereby accounting for the observed reduction in DDP accumulation in 2008/DDP cells compared to the sensitive parental 2008 cells. To this end, we compared three indicators of membrane lipid composition and fluidity in the resistant and sensitive cells. In a comparison of major membrane lipid classes, the resistant line had a 17% increase in phosphatidyl choline, and an 11% increase in phosphatidyl ethanolamine relative to the sensitive line. There were no differences in the other major phospholipids or in the free cholesterol content of the cell lines. Secondly, results of fluorescence polarization measurements on whole cells of each line using the plasma membrane specific probe trimethylammonium diphenylhexatriene revealed no difference between the cell lines at both 28 degrees C and 37 degrees C. Finally, an examination of the temperature-dependence of DDP accumulation over 1 h produced Arrhenius plots of similar shape in 2008 and 2008/DDP cells. Both plots were linear from 40 degrees C down to a break point between 4 degrees C and 12 degrees C. The Q10's for DDP accumulation from 30 degrees C to 40 degrees C were greater than 2 in each cell line and were not significantly different. Results of these 3 comparisons point to substantial similarity in the bulk membrane lipid composition and fluidity of the two cell lines. We conclude that decreased DDP accumulation in our resistant cells is not due to membrane changes that would be expected to retard passive diffusion of the drug into the cells.

Biological Transport↗