Behavioral treatment of angina-like chest pain in patients with hyperventilation syndrome

The hyperventilation syndrome is present in as many as 50% of patients with non-cardiac chest pain. This study evaluated a behavioral treatment of this disorder in three adult females. They had long histories of chest pain and were documented to be free of coronary artery disease. Each subject met the DSM-III-R diagnostic criteria for an anxiety disorder. Following treatment, all subjects showed a marked decrease in the frequency and intensity of chest pain episodes and in the frequency of shortness of breath episodes. Two subjects maintained their progress at one-year follow-up. The results lend support to the efficacy of controlled breathing and relaxation training for the treatment of hyperventilation-related chest pain and to the inclusion of a hyperventilation provocation test in the diagnosis of the syndrome as well as its role in changing cognitions regarding cardiac status. Also discussed is the rationale for treating hyperventilation related chest pain in a medical care setting.     

Left ventricular pseudoaneurysm as a late complication of mitral annuloplasty

A 59-year-old hypertensive male, 1 year after uncomplicatedmitral annuloplasty for regurgitation with MAZE procedure, witha history of chronic obstructive pulmonary disease and repeatedpulmonary     

Establishment and characterization of an in vitro model of acquired resistance to cisplatin in a human testicular nonseminomatous germ cell line.

Clinically, human testicular nonseminomatous germ cell tumors exhibit remarkable sensitivity to platinum-based chemotherapy. To define better the mechanistic basis for this unusual sensitivity, the biochemical determinants of platinum-induced cytotoxicity have been investigated in a human testicular tumor cell line (GCT27) established from a previously untreated patient and in an in vitro derived 5.6-fold cisplatin-resistant stable variant (GCT27cisR). Compared to 12 ovarian and 5 cervical human tumor cell lines, the parent GCT27 line was among the most sensitive to the cytotoxic effects of both cisplatin (dosage producing 50% inhibition, 0.2 microM) and carboplatin (dosage producing 50% inhibition, 2.9 microM), thus reflecting clinical data. A 4-day exposure sulforhodamine B-staining assay was used to determine that GCT27cisR was cross-resistant to carboplatin and iproplatin and the classical bifunctional alkylating agents melphalan and chlorambucil. Partial cross-resistance was observed to tetraplatin, methotrexate, and mitomycin C. No cross-resistance was observed to Adriamycin, etoposide, vinblastine, bleomycin, 1-beta-D-arabinofuranosylcytosine, and 5-fluorouracil. Intracellular cisplatin accumulation across the dose range 2.5-100 microM (for 2 h) was 1.6 +/- 0.39-fold (mean +/- SD) greater for the parent line. There was no significant difference in glutathione levels between the two lines. The acquired resistance line was 1.9-fold more resistant than the parent line to the cytotoxic effects of cadmium chloride. There was no significant difference between the two lines, however, in the total amounts of platinum bound to DNA after cisplatin exposure (25, 50, or 100 microM for 2 h). The removal of total platinum adducts from DNA was significantly faster for GCT27cisR compared to the parent line (half-times of removal, 32 and 67 h, respectively). These data suggest that the abnormal sensitivity of the parent testicular tumor cell line to platinum-containing anticancer drugs may be due predominantly to an inherent defect in the ability of these cells to remove platinum from their DNA. This defect is apparently lost in the acquired resistance counterpart. Reduced intracellular accumulation and increased cytoplasmic concentrations of metallothionein may also contribute, in part, to the acquisition of cisplatin resistance in this model.     

Hereditary Hypertriglyceridemic Rat: A New Animal Model of Metabolic Alterations in Hypertension

Hereditary hypertriglyceridemic rats (hHTg) were developed as a new genetic model for the study of relationships between blood pressure (BP) and metabolic abnormalities. This strain has been produced by selective inbreeding from Wistar rats according to the rise of plasma triglycerides induced by a high-sucrose diet. Though hHTg rats display hypertriglyceridemia, impaired glucose tolerrance, hyperinsulinemia, insulin resistance and increased BP even without nutritional stimuli, high sucrose feeding further aggravates these symptoms. High plasma triglycerides levels in hHTg rats seem to be a consequence of their hyperproduction. Impaired insulin action is responsible for the defective glucoregulation in this strain. The loss of insulin responsiveness might be due to a reduction in the number of glucose transporters. Highly significant relationships among plasma triglycerides, ouabain-resistant Na⁺ transport and BP were demonstrated in the hHTg rats. Segregating populations (F2 hybrids) should be used for genetic analysis of the primary role of lipid and/or ion transport abnormalities in the pathogenesis of this form of genetic hypertension.     

Gradient of alarm substance in the forced swimming test

Three studies were conducted with rats to study the effects of a proposed alarm substance released during the forced swimming test. In the first study, rats were retested in water previously swum in but which had been subsequently diluted to varying degrees. When water was diluted by more than 25% the proposed alarm substance could no longer be detected. In the second study, rats were retested at various times after initial testing. This study showed that the alarm substance was still active by eight days after it had been initially released. The final study tested animals to see if the alarm substance could be depleted by repeated testing. Testing animals for more than an hour did not result in depletion of the alarm substance. These three studies suggest that the proposed alarm substance secreted by rats during the forced swimming test has considerable biological significance.