Increase in quantal transmitter release by calcium- and sodium-containing phosphatidylcholine liposomes [proceedings].
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Biomedical subjects
Publications and source records attributed to H Meiri.
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We studied the in vitro and in vivo effects of calcitriol (1,25D) on the cellular immune responses in 19 hemodialysis (HD) patients. In vitro 5-day treatment with 1,25D markedly reduced the HLA-DR expression by peripheral blood CD14(+) monocytes from both HD patients and normal subjects in a similar fashion. The HLA-DR expression by monocytes and the phorbol myristate acetate (PMA)-induced superoxide production (SOP) by neutrophils were significantly higher in the HD patients than in the normal subjects (p < 0.01 and p < 0.05, respectively). The phagocytic activity in the HD patients was significantly lower than that in the normal subjects (p < 0.05). Moreover, the mitogen response of HD peripheral blood lymphocytes against pokeweed mitogen (PWM) was significantly lower than that of the controls (p < 0.01) but was only slightly and insignificantly lower against Con A. Oral 1,25D pulse therapy resulted in a marked decrease in the HLA-DR expression by peripheral blood monocytes 2 and 4 days after the first 1,25D administration (p < 0.01) in HD patients. Moreover, the treatment significantly enhanced the PMA-induced SOP 2 days after the treatment (p < 0.01). However, the phagocytic activity by neutrophils and the mitogen responses to Con A and PWM by lymphocytes were not significantly affected by this treatment. These results suggest that 1,25D plays a significant role in the regulation of both the monocyte and neutrophil functions in HD patients.
Elevated levels of aluminum in brain tissue have been found in demented patients with Alzheimer's disease, with ALS-PD complex of Guam and with dialysis encephalopathy. A possible etiological relationship between enhanced aluminum exposure and impaired mental function was suggested both for ALS-PD of Guam (a region where high contents of aluminum in water are found) and for dialysis encephalopathy which appears in dialyzed patients exposed to high doses of aluminum in medications and in dialysate fluid. The role of aluminum in Alzheimer's disease is not known as is the question of life-long aluminum accumulation in healthy human beings. In this review we have limited ourselves to the issue of oral aluminum ingestion and the possible neurotoxic consequences of such exposure. The following topics are summarized: 1. Physiological mechanisms involved in ingestion and intestinal absorption of aluminum and the influences of pH and available organic complexing agents on these processes. 2. Effects of an aluminum-enriched diet on behavior and on brain metabolism. 3. Dietary sources of aluminum and elevated loads of this substance due to prolonged intake of aluminum-containing medications. The main conclusion of this summary is that aluminum is absorbed and may accumulate in different organs in both adults and infants. Two groups seem to be at particular risk for aluminum related toxicity: people with chronic renal failure treated with aluminum-containing medications and pre-term infants fed on aluminum containing formulate. It seems probable that at least upon short term exposure the healthy human body can defend itself adequately from aluminum's toxic effects. However, not enough information is available on possible effects of life-long exposure to aluminum in the environment, diet and medications, which over decades may lead to accumulation of this substance with expressions of toxicity. Therefore, the question of aluminum's relevance to dementive diseases cannot yet be adequately answered.
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