Peritoneal dialysis in the rat: its application as an effective teaching aid.
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Biomedical subjects
Publications and source records attributed to K D Gardner.
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BALB/c mice develop fatal illness following infection with Leishmania major despite expansion of helper L3T4+ T cells in the draining lymph nodes and spleen. Healer mice, either genetically resistant C57BL/6 or BALB/c that have been pretreated with monoclonal antibody GK 1.5, also develop expanded numbers of L3T4+ T cells at the time of healing. Lymph node cells from healer mice produce gamma-interferon in vitro and message for gamma-interferon can be recovered from the lymph nodes during healing in vivo. Conversely, cells harvested from non-healer mice during the course of infection produce minimal gamma-interferon in vitro and have little message for gamma-interferon detectable in vivo. When the same Northern blots are hybridized for IL-4, large amounts of IL-4 message are detected only in cells from non-healer mice. The data are consistent with the expansion of type 1 helper cells (Th1) during healing and type 2 helper cells (Th2) during progressive leishmania infection.
UNLABELLED: We followed sequentially the plasma potassium concentration in five, essentially anuric, hyperglycemic patients with no known abnormality of potassium metabolism and treated only with insulin. Acid-base balance, external potassium and fluid balance, and weights did not change during observation. The following changes in plasma potassium concentration (delta K) were noted: In initial hyperkalemia (three patients) delta K was -1.8 +/- 0.1 mmol/l (p less than 0.005). In normokalemia (one patient) delta K was -1.3 mmol/l. In hypokalemia (one patient) delta K was +0.1 mmol/l. The correlation between the starting potassium concentration and the change in potassium concentration was -0.88 (p = 0.05). CONCLUSIONS: When only parenteral insulin is used for treatment and acid-base balances and body weights do not change during treatment in anuric hyperglycemia: a) The change in potassium concentration is dependent on the starting plasma potassium concentration, b) hyperkalemic patients will drop their plasma potassium concentration toward normal, and c) hypokalemic patients may not need potassium replacement.
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