Disturbance and organisms on boulders

Summary The tops of intertidal boulders on the east coast of Australia may carry a half-dozen algae, while the undersides may support a dozen or more species of sessile animals; mobile forms such as molluscs, crustaceans, and echinoderms are also common. These organisms are disturbed when boulders are moved by waves or buried in sand. Experiments were done to test the hypothesis that these disturbances are responsible for the reduced diversity and abundance of the assemblages on the undersides of small boulders. Boulders on one shore were bolted to the substratum to prevent movement by waves. In two separate experiments on another shore, boulders with and without attached organisms were buried in a few centimetres of sand. All experiments included relevant controls and were done high and low on the shore using rocks of several sizes.The assemblages of algae developing on the tops of all stabilised boulders, regardless of size, were similar to those on boulders free to roll indicating that, in contrast to results elsewhere, disturbance by waves was too infrequent or slight to affect these species. The tops of rocks were also rarely buried in sand and the main influences on the community in this situation were apparently exposure at low-tide and grazing gastropods.More species, however, did settle or survive on the undersides of rocks which were free of sand or could not be moved by waves; thus disturbances were important in this situation. In the absence of disturbance low on the shore, much or all space was occupied and sessile species such as sponges and ascidians overgrew other forms and reduced diversity. This did not happen higher on the shore and here diversity was simply an increasing function of rock-size. Overall disturbance played a similar role in all places — it killed organisms and created free space — but the final effects on the community varied depending upon the species present and the actions of other factors.     

Fructose augments infection-impaired net hepatic glucose uptake during TPN administration

During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) and net hepatic lactate release (NHLR) are markedly reduced (downward arrow approximately 45 and approximately 65%, respectively) with infection. Because small quantities of fructose are known to augment hepatic glucose uptake and lactate release in normal fasted animals, the aim of this work was to determine whether acute fructose infusion with TPN could correct the impairments in NHGU and NHLR during infection. Chronically catheterized conscious dogs received TPN for 5 days via the inferior vena cava at a rate designed to match daily basal energy requirements. On the third day of TPN administration, a sterile (SHAM, n = 12) or Escherichia coli-containing (INF, n = 11) fibrin clot was implanted in the peritoneal cavity. Forty-two hours later, somatostatin was infused with intraportal replacement of insulin (12 +/- 2 vs. 24 +/- 2 microU/ml, SHAM vs. INF, respectively) and glucagon (24 +/- 4 vs. 92 +/- 5 pg/ml) to match concentrations previously observed in sham and infected animals. After a 120-min basal period, animals received either saline (Sham+S, n = 6; Inf+S, n = 6) or intraportal fructose (0.7 mg x kg(-1) x min(-1); Sham+F, n = 6; Inf+F, n = 5) infusion for 180 min. Isoglycemia of 120 mg/dl was maintained with a variable glucose infusion. Combined tracer and arteriovenous difference techniques were used to assess hepatic glucose metabolism. Acute fructose infusion with TPN augmented NHGU by 2.9 +/- 0.4 and 2.5 +/- 0.3 mg x kg(-1) x min(-1) in Sham+F and Inf+F, respectively. The majority of liver glucose uptake was stored as glycogen, and NHLR did not increase substantially. Therefore, despite an infection-induced impairment in NHGU and different hormonal environments, small amounts of fructose enhanced NHGU similarly in sham and infected animals. Glycogen storage, not lactate release, was the preferential fate of the fructose-induced increase in hepatic glucose disposal in animals adapted to TPN.     

Characterizing Latino anglers' environmental risk perceptions,sport fish consumption,and advisory awareness

Sport fish advisories for the Great Lakes states suggest limiting consumption of fish taken from the lakes and their tributaries because of chemical contamination. It appears, however, that minority anglers are less aware of the advisories and also consume greater amounts of sport fish than white anglers. We conducted focus groups in western New York with Latino anglers and partners of anglers to explore these patterns. Analysis revealed that older anglers believed local waters were of good quality and that it was safe to consume fish taken from them. They based their evaluation of both water and fish primarily on visual inspection. In contrast, younger Latinos believed that area waters were highly polluted because of dumping of waste from local industries. They fished away from urban areas in an effort to find cleaner, more swiftly moving waters. They considered consuming sport fish from urban areas highly risky, given their occasional illness experiences following meals of what they thought were polluted fish. For all Latino anglers, however, state-sponsored advisories were minimally effective because of their limited distribution and complex wording. Results point to differences in lay and scientific models of pollution and a need to bridge this gap in future risk-communication strategies.     

Infection impairs insulin-dependent hepatic glucose uptake during total parenteral nutrition

Total parenteral nutrition (TPN) markedly augments net hepatic glucose uptake (NHGU) and hepatic glycolysis in the presence of mild hyperglycemia and hyperinsulinemia. This increase is impaired by an infection. We determined whether the adaptation to TPN alters the responsiveness of the liver to insulin and whether infection impairs that response. Chronically catheterized dogs received TPN for 5 days. On day 3 of TPN, either a nonlethal hypermetabolic infection was induced (INF, n = 5) or a sham surgery was performed (SHAM, n = 5). Forty-two hours after clot implantation, somatostatin and glucagon (34 +/- 3 vs. 84 +/- 11 pg/ml in artery, SHAM vs. INF) were infused, and a three-step (120 min each) isoglycemic (approximately 120 mg/dl) hyperinsulinemic (approximately 12, 25, and 50 microU/ml) clamp was performed to simulate levels seen in normal, infected, and exogenous insulin treatment states. In SHAM, NHGU (3.5 +/- 0.2 to 4.2 +/- 0.4 to 4.6 +/- 0.5 mg x kg(-1) x min(-1)) modestly increased. In INF, NHGU was consistently lower at each insulin step (1.1 +/- 0.5 to 2.6 +/- 0.5 to 2.8 +/- 0.7 mg x kg(-1) x min(-1)). Although NHGU increased from the first to the second step in INF, it did not increase further with the highest dose of insulin. Despite increases in NHGU, net hepatic lactate release did not increase in SHAM and fell in INF. In summary, in the TPN-adapted state, liver glucose uptake is unresponsive to increases in insulin above the basal level. Although the infection-induced increase in insulin sustains NHGU, further increments in insulin enhance neither NHGU nor glycolysis.     

Dechlorination of Pesticides by a Specific Bacterial Glutathione S‐transferase,BphKLB400: Potential for Bioremediation

The bphK gene located in the bph operon of Burkholderia xenovorans LB400 encodes a protein, BphK^LB400, with significant sequence similarity to glutathione‐S‐transferases (GSTs). GSTs are a superfamily of enzymes involved in the detoxification of many endobiotic and xenobiotic substances. Recently, BphK^LB400 was shown to catalyze the dechlorination of a number of toxic chlorinated organic compounds. Comparison of the amino acid sequence of BphK^LB400 with GSTs from other bacteria that degrade polychlorinated biphenyls identified a number of highly conserved amino acids in the C‐terminal region of the protein thought to be associated with substrate specificity. Mutating the conserved amino acid at position 180 of BphK^LB400 from an alanine to a proline residue resulted in an increase in GST activity of bacterial cell extracts towards a number of chlorinated organic substrates tested including commonly used pesticides. Laboratory scale plant protection experiments suggested that E. coli expressing BphK^LB400 [wildtype and mutant (Ala180Pro)] could protect pea plants from the effects of chloromequat chloride. Therefore, BphK^LB400, identified as having dechlorination activity towards toxic chlorinated organic compounds used in the environment, could have potential in bioremediation.     

Differences in regeneration between hurricane damaged and clear-cut mangrove stands 25 years after clearing

The effect of human disturbance on mangrove forest may be substantially different from the effects of natural disturbances. This paper describes differences in vegetation composition and structure of five vegetation types in two mangrove areas near Darwin, Australia, 25 years after disturbance. The vegetation in clear-felled forest showed more adult Avicennia marina than in the hurricane-affected forest, and a virtual absence of A. marina juveniles and saplings. This indicates that A. marina will be replaced by other species in the canopy, showing a multi-phase vegetation development in mangrove forest after human disturbance. The mechanism of disturbance and the conditions after clearing therefore affects the vegetation composition for at least 25 years after this disturbance took place.     

Monoclonal antibody antagonists of hypothalamic FGFR1 cause potent but reversible hypophagia and weight loss in rodents and monkeys

We generated three fully human monoclonal antibody antagonists against fibroblast growth factor receptor-1 (FGFR1) that potently block FGF signaling. We found that antibodies targeting the c-splice form of the receptor (FGFR1c) were anorexigenic when administered intraperitoneally three times weekly to mice, resulting in rapid, dose-dependent weight loss that plateaued (for doses>4 mg/kg) at 35-40% in 2 wk. Animals appeared healthy during treatment and regained their normal body weights and growth trajectories upon clearance of the antibodies from the bloodstream. Measurements of food consumption and energy expenditure indicated that the rapid weight loss was induced primarily by decreased energy intake and not by increased energy expenditure or cachexia and was accompanied by a greater reduction in fat than lean body mass. Hypophagia was not caused through malaise or illness, as indicated by absence of conditioned taste aversion, pica behavior, and decreased need-induced salt intake in rats. In support of a hypothalamic site of action, we found that, after intraperitoneal injections, anti-FGFR1c (IMC-A1), but not a control antibody, accumulated in the median eminence and adjacent mediobasal hypothalamus and that FGFR1c is enriched in the hypothalamus of mice. Furthermore, a single intracerebroventricular administration of 3 microg of IMC-A1 via the 3rd ventricle to mice caused an approximately 36% reduction in food intake and an approximately 6% weight loss within the ensuing 24 h. Our data suggest that FGF signaling through FGFR1c may play a physiological role in hypothalamic feeding circuit and that blocking it leads to hypophagia and weight loss.