Evidence for beta adrenergic receptor involvement in the immunomodulatory effects of morphine

The present study assessed the involvement of the beta adrenergic system in the immunomodulatory effects of morphine. Male Lewis rats were administered either the nonselective beta adrenergic antagonist nadolol, the beta 1-selective adrenergic antagonist atenolol or the beta 2-selective adrenergic antagonist erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylaminobuta n-2-ol (ICI-118,551) in doses of 0, 0.125, 0.5, 2.0 or 8.0 mg/kg s.c. before the administration of 15 mg/kg morphine or saline s.c. After sacrifice, the spleen was removed and blood was collected from each rat and multiple in vitro immune assays were performed. Pretreatment with all three beta adrenergic antagonists completely antagonized the suppressive effects of morphine on the proliferative responses of splenic leukocytes to concanavalin-A (Con-A), phytohemagglutinin (PHA), lipopolysaccharide (LPS) and the combination of ionomycin and phorbol myristate acetate (PMA). None of the antagonists blocked the suppressive effects of morphine on the proliferative responses of blood leukocytes to concanavalin-A or phytohemagglutinin, splenic natural killer (NK) cell activity, total splenic leukocyte counts and blood leukocyte counts per milliliter. These results demonstrate the involvement of beta adrenergic receptors in certain of morphine's immunosuppressive effects. Moreover, because both nadolol and atenolol are peripherally acting compounds, these data implicate peripheral beta adrenergic receptors specifically in morphine's immunomodulatory effects.     

Shallow groundwater mercury supply in a Coastal Plain stream

Fluvial methylmercury (MeHg) is attributed to methylation in up-gradient wetland areas. This hypothesis depends on efficient wetland-to-stream hydraulic transport under nonflood and flood conditions. Fluxes of water and dissolved (filtered) mercury (Hg) species (FMeHg and total Hg (FTHg)) were quantified in April and July of 2009 in a reach at McTier Creek, South Carolina to determine the relative importance of tributary surface water and shallow groundwater Hg transport from wetland/floodplain areas to the stream under nonflood conditions. The reach represented less than 6% of upstream main-channel distance and 2% of upstream basin area. Surface-water discharge increased within the reach by approximately 10%. Mean FMeHg and FTHg fluxes increased within the reach by 23-27% and 9-15%, respectively. Mass balances indicated that, under nonflood conditions, the primary supply of water, FMeHg, and FTHg within the reach (excluding upstream surface water influx) was groundwater discharge, rather than tributary transport from wetlands, in-stream MeHg production, or atmospheric Hg deposition. These results illustrate the importance of riparian wetland/floodplain areas as sources of fluvial MeHg and of groundwater Hg transport as a fundamental control on Hg supply to Coastal Plain streams.     

Foreign serum-induced pancreatitis in mice. II. Secretory disturbances of acinar cells

As previously reported, pancreatic acinar cell necrosis and inflammation develop in mice a few hours after one intraperitoneal injection of foreign serum. However, sublethally injured acinar cells exhibited notable increases in both zymogen granule numbers and amylase activity, observed within 3 hours and increasing with time. These two changes were coupled with a progressive decrease in the secretory response to pilocarpine and were preceded by significant disturbances in pancreatic tissue concentrations of sodium and potassium. We conclude that (1) the granule increase results from an induced disturbance of the granule exocytosis mechanism while granule formation continues and, therefore, (2) the granule secretory process is more sensitive to the serum injury mechanism than is the zymogen synthesis process. Although the granule increases developed in acinar cells throughout most of the nonnecrotic gland and persisted for at least 24 hours, acinar cell necrosis was maximal in extent--approximately 25% of the gland in severest form--by 12 to 15 hours. We conclude, therefore, that the increase in granules is neither the primary determinant nor initiator of acinar cell death. The latter is likely caused by disturbed plasma membrane functions, sufficient in some cells to result in lethal changes in ion and fluid composition. The injury mechanism, which permits granule formation to go on in the face of impaired granule exocytosis, is yet to be worked out. The possibilities are discussed in relationship to the reactivity of foreign sera for target cell plasma membranes.     

Cancer mortality in relation to asbestos in municipal water supplies

The mortality experience of twenty-two municipalities in Quebec grouped by evidence of exposure to asbestos fibers in water supplies (known high, possible high, and probable low exposures) was evaluated. Excess mortality due to cancer of the stomach (males), pancreas (females), and lung (males) was observed in the two municipalities with known high exposures. The excesses among males have been due to occupational exposure to asbestos. The absence of excess mortality due to pancreatic cancer among males suggested that the excess among females was not due to waterborne asbestos. The study therefore did not reveal evidence of excess cancer mortality that could be attributed to exposure to asbestos in drinking water.