The effects of the Na+/H+ exchange blocking drug diethylamiloride (DEA) on mechanical function have been studied in the rabbit isolated, arterially perfused interventricular septum. At concentrations of 10(-6)-10(-5) M, DEA induced a significant, dose-dependent, negative inotropic effect (a 54% decrease from control values at the highest concentration), which was slow to develop. After a 45 min washout, recovery was almost complete (95 +/- 3.4%). At concentrations greater than 5 x 10(-5) M, DEA induced a rapid and marked decrease in developed tension, associated with a progressive decrease in excitability and incomplete recovery. Resting tension was not significantly modified at any of the concentrations tested. At greater than 10(-6) M DEA enhanced significantly the transient negative inotropic effect of the brief intracellular acidosis induced by removal of NH4Cl perfusion, both by decreasing the minimal value of developed tension and by increasing the time required to produce this effect. These effects suggest that the dose-dependent DEA negative inotropic effect could be mediated by a progressive intracellular acidosis produced by inhibition of the Na+/H+ exchange system.

Amiloride↗

PubMed1990

[Adenocarcinoma of the ovary in the ovarian remnant syndrome].

Explore the source record for details and available documents.

Adenocarcinoma↗

PubMed1987

Isospora belli infection in patients with AIDS in Catalunya, Spain.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

[Molecular control of the cellular cycle and apoptosis: new treatments for gliomas].

Cancer represents perhaps the most formidable challenge in medicine and science in general. Currently, gliomas are one of the most deadly cancers. Despite aggressive therapy using surgery, radiotherapy and chemotherapy, the prognosis of glioma patients is very poor. The design of new therapies for these tumors is therefore mandatory. Molecular medicine is based on the discovery of fundamental molecular components that determine normal cellular behavior, and are aberrant in cancer cells, and in the subsequent exploitation of these new uncovered targets to generate specific and nontoxic treatments for cancer. In addition with the activation or amplification of oncogenes, progressive inactivation of tumor suppressor genes is one of the characteristics of the malignant progression of gliomas. One of the most promising approaches of gene therapy is the transfer of such tumor suppressor genes to cancer cells. In gliomas, p53, p16 and Rb abnormalities are present in the vast majority of gliomas. Restoration of the wild-type functions of these genes results in either apoptosis or suppression of glioma growth with very low toxicity. This review highlights a small sample of areas where conceptual and practical advances in molecular biology are changing our understanding of the pathogenesis of these tumors.

Apoptosis↗