Earlier reports suggested that galantamine, a drug approved to treat mild-to-moderate Alzheimer's disease (AD), and other centrally acting reversible acetylcholinesterase (AChE) inhibitors can serve as adjunct pretreatments against poisoning by organophosphorus compounds, including the nerve agent soman. The present study was designed to determine whether pretreatment with a clinically relevant oral dose of galantamine HBr mitigates the acute toxicity of 4.0×LD soman (15.
View Article and Find Full Text PDFThe translational capacity of data generated in preclinical toxicological studies is contingent upon several factors, including the appropriateness of the animal model. The primary objectives of this article are: 1) to analyze the natural history of acute and delayed signs and symptoms that develop following an acute exposure of humans to organophosphorus (OP) compounds, with an emphasis on nerve agents; 2) to identify animal models of the clinical manifestations of human exposure to OPs; and 3) to review the mechanisms that contribute to the immediate and delayed OP neurotoxicity. As discussed in this study, clinical manifestations of an acute exposure of humans to OP compounds can be faithfully reproduced in rodents and nonhuman primates.
View Article and Find Full Text PDFEleven patients with urologic cancer had an abnormal 99mTc (technetium-99m) bone scan as the sole evidence of metastatic disease. Potentially curative therapy should not be withheld on the basis of a "positive" bone scan if such an area is accessible to selected bone biopsy and proves to be negative for tumor histologically.
View Article and Find Full Text PDFThree cases of lymphocysts occurred in a series of 97 patients undergoing extension pelvic urological operations, an incidence rate of 3.1 per cent. This is the first report of this complication after urological lymphadenectomy.
View Article and Find Full Text PDFThe Snell dwarf mouse (dw/dw) is the result of a single recessive gene that is not sex-linked. The dwarfism is caused by the congenital deficiency of growth hormone, thyrotropin, and prolactin. This unique genetic model was selected to study compensatory renal hypertrophy.
View Article and Find Full Text PDFArch Biochem Biophys
November 1966