Community reactions to odors from pulp mills: A pilot study in Eureka, California.
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Biomedical subjects
Publications and source records attributed to G Sanders.
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We have observed the disappearance of rosette inhibitory factor (RIF) from the serum of 19 patients with acute hepatitis B virus infection. This occurred at a time coinciding with the detection of anti-HBs. In addition, levels of RIF activity were significantly greater (P less than 0.001) in 35 HBsAg carriers who lacked anti-HBs when compared to 15 carriers who regularly demonstrated this antibody. In all instances, RIF effect was partial affecting some, but not all, T-lymphocytes from healthy donors were separated into TM (helper), TG (suppressor), and T0 (null) subpopulations by an immunoglobulin-ox-cell rosette depletion method. The effect of RIF on erythrocyte rosette formation and Fc-receptor expression in these subpopulations was assessed. TG-lymphocytes were found to be refractory to RIF-mediated suppression of erythrocyte rosette formation while TM-lymphocytes demonstrated an enhanced sensitivity to RIF. Incubation of TG-lymphocytes, potential TM-percursor cells, with RIF resulted in a decreased expression of new IgM-Fc receptors. In order to determine if any functional significance could be derived from these findings, the effect of RIF on in vitro immunoglobulin secretion was tested. Using pokeweed mitogen-stimulated mononuclear cell cultures, purified RIF-low density lipoprotein was shown to suppress IgM, IgG, and IgA secretion by 75.3, 74.3, and 59.3%, respectively. These data are consistent with the hypothesis that RIF is a potential immunoregulatory protein which could contribute to the lack of anti-HBs noted during the acute phase of hepatitis B and in the majority of HBsAg carriers.
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This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
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