Primary hyperparathyroidism and monoclonal gammopathy

Coexistent primary hyperparathyroidism and monoclonal gammopathy, although rare, has been reported previously by a number of investigators. We report four patients with such an occurrence who were seen between 1976 and 1988. Another patient with primary hyperparathyroidism also had multiple myeloma and was in remission for 12 years. These patients represent approximately 1% of the 386 patients with primary hyperparathyroidism seen during the same 12-year period. Although several mechanisms have been proposed to explain this concurrence, we believe it is the result of a chance occurrence. A review of the literature, an estimate of the chance occurrence of coincidental monoclonal gammopathy, benign or malignant, in patients with primary hyperparathyroidism, and some practical implications of this interesting coexistence are presented.     

Estimated causes of death in Thailand, 2005: implications for health policy

Background  

Almost 400,000 deaths are registered each year in Thailand. Their value for public health policy and planning is greatly diminished by incomplete registration of deaths and by concerns about the quality of cause-of-death information. This arises from misclassification of specified causes of death, particularly in hospitals, as well as from extensive use of ill-defined and vague codes to attribute the underlying cause of death. Detailed investigations of a sample of deaths in and out of hospital were carried out to identify misclassification of causes and thus derive a best estimate of national mortality patterns by age, sex, and cause of death.     

重组人白细胞介素-1β对小鼠骨髓粒系细胞和红系细胞的正负调节作用

为阐明IL-1对粒系细胞和红系细胞的作用,我们通过对小鼠骨髓及外周血的研究探讨了IL-1对粒系和红系造血细胞的调节作用.结果表明:IL-1单剂量腹腔注射后第7天红系造血细胞明显减少,外周血网织红细胞在第8天显著下降.在5～10万U/kg剂量范围内IL-1明显促进粒系细胞的增殖.应用流式细胞仪对DNA分析显示IL-1并不引起全骨髓细胞DNA的变化,但大体积细胞在注射IL-1后第3天S期细胞明显增多.我们的结果表明IL-1抑制红系造血细胞的分化增殖,在适当的剂量范围内促进粒系细胞的增殖和分化成熟.其作用的分子基础是诱导造血细胞的细胞周期变化.     

Modulation of carbohydrate metabolism in the selected tissues of marine prawn, Penaeus indicus (H. Milne Edwards), under phosphamidon-induced stress

Changes in carbohydrate metabolism were studied in midgut gland, muscle, and gill tissues of marine prawn Penaeus indicus exposed to a sublethal concentration (0.3 ppm) of phosphamidon. A significant decrease in glycogen and pyruvate and an increase in lactate content were observed in all phosphamidon-exposed prawn tissues after 96 hr. An increase in phosphorylase a and aldolase activity levels suggested the increased formation of triose sugars during phosphamidon toxicity. LDH activity was considerably decreased and an increment in lactate content was observed which indicates reduced mobilization of pyruvate into the citric acid cycle. Glucose-6-phosphate dehydrogenase activity was considerably increased, suggesting the enhanced oxidation of glucose in the hexose monophosphate shunt pathway. Krebs cycle enzymes such as NAD-isocitrate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase were found to be decreased, suggesting the impairment in mitochondrial oxidative metabolism due to the acute toxic impact of phosphamidon. Cytochrome-c oxidase and Mg2+ ATPase activity levels were also decreased considerably, suggesting impaired energy synthesis and breakdown during phosphamidon toxicity, as a result of reduced oxidation of glucose aerobically. The increase in acid and alkaline phosphatase activities indicates the enhanced breakdown of phosphate to release energy in view of inhibiton or impairment in the ATPase system during phosphamidon-induced stress. These results suggest that phosphamidon has a profound effect on the oxidative metabolism of prawn which results in the triggering of compensatory metabolic pathways for survivability.