Hydrogen peroxide (H202) contributes to renal cellular injury.

The activation state of T and B lymphocytes in the peripheral blood of periodontitis patients may be a reflection of disease activity. We have utilized 2- and 3-color flow cytometric analyses using a new chromophore, peridinin chlorophyll A protein, and conventional dyes, fluorescein isothiocyanate and phycoerythrin, conjugated to monoclonal antibodies against activated lymphocyte surface markers to measure blood lymphocyte subsets from 18 periodontitis patients and 16 periodontally healthy control subjects. Two-color flow cytometric analysis demonstrated that the frequency of CD4+ and CD5+ T cells, CD20+ B cells, and CD16+ NK (natural killer) cells were increased in periodontitis patients. Of particular interest, CD4+ activated "memory" T cells, CD5+ B cells, and CD56+ NK effector cells were increased significantly in periodontitis patients (p less than 0.05). While the relationship of lymphocyte activation to periodontal disease activity remains unclear, there may be potential for using 2- and 3-color flow cytometry to subcategorize periodontitis patients into high- and moderate-risk groups.

We describe a case of peritonitis caused by Aureobasidium pullulans in a patient on continuous ambulatory peritoneal dialysis (CAPD). This dematiaceous fungus rarely causes infection in humans and to date has not been reported as an etiology of CAPD-associated peritonitis. The patient was managed successfully with peritoneal catheter removal and a prolonged course of intravenous amphotericin B, allowing resumption of CAPD. In vitro susceptibility testing confirmed sensitivity of this organism to amphotericin B.

We studied the roles of acidosis, plasma osmolality, and organic osmolytes in the pathogenesis of cerebral edema in an animal model of diabetes mellitus. Normonatremic rats with streptozotocin-induced non-ketotic (NKD) and ketotic (DKA) diabetes were sacrificed before or after treatment with hypotonic saline and insulin. Brains were analyzed for water, electrolyte, and organic osmolyte content. Brain water decreased by 2% in untreated DKA and NKD despite a 12% increase in plasma osmolality due to hyperglycemia. After treatment of both NKD and DKA, brain water increased equivalently by 8%. The cerebral edema that occurred after treatment was associated with decreased brain sodium content and no change in total major brain organic osmolytes in both NKD and DKA. However, brain content of the individual osmolytes glutamine and taurine increased after treatment of DKA. In a separate study, brain water and solute content of rats with DKA were compared after treatment with either hypotonic or isotonic fluid. Animals treated with isotonic fluid had significantly less cerebral edema and higher brain sodium content than those treated with hypotonic fluid. In our studies, brain swelling after treatment of DKA and NKD was primarily due to a rapid reduction of plasma glucose and osmolality, and was not caused by sodium movement into the brain. Acidosis did not appear to play a major role in the pathogenesis of cerebral edema after treatment of DKA.