08. Strengthening Karner Blue Butterfly Metapopulations

Wild lupine (Lupinus perennis) is the obligate host plant for larvae of the Karner blue butterfly (Lycaeides melissa samuelis). The purpose of this study was to determine whether planting wild lupine in dry prairie sites (areas previously devoid of wild lupine but having appropriate habitat structure for its growth) would result in colonization from existing populations of Karner blue butterflies over time, thereby adding to metapopulation stability. The newly planted sites were on private and public land and ranged in area from 0.81 to 8.1 ha (from 2 to 20 acres). They were located within about 3.2 km (2 mi) of existing Karner blue butterfly–occupied sites

INFORMATION SYSTEMS AND COST CONTROL

Information Systems Working Papers Serie

Current Use of Global Coronary Heart Disease Risk Assessment by a Sample of US Physicians

Background: Little is known about United States (US) physicians’ understanding and utilization of global CHD risk assessment in clinical practice. Purpose: To assess the current level of evidence regarding physicians’ use of global CHD risk assessment in primary prevention of cardiovascular disease by examining if there are valid and reliable tools available for clinicians to calculate patients’ global CHD risk scores, if calculation and communication of global risk scores translate into improved patient level outcomes, and if physicians understand/use global risk scoring in primary prevention of CVD. Methods: The MEDLINE database (from inception to 20 March 2010) was searched for studies involving physicians’ use of global CHD risk scores. Studies of any design were considered using the search terms, "global coronary heart disease risk score", "cardiovascular disease", "primary prevention", and "physicians". Reference lists from related systematic reviews and primary articles were searched and additional citations were provided by experts in the field of cardiovascular disease prevention. Studies were limited to those written in English. Results: The search resulted in one good quality recent systematic review that assessed the tools available for calculation of CHD risk scores, two good quality recent systematic reviews of the literature that assessed whether global CHD scoring results in improved patient outcomes, and three poor to fair quality original physician survey studies that examined physicians’ use of global CHD risk scores. Conclusion: Available evidence suggests that there are many accurate, easy to use tools available to physicians for calculation of patients CHD global risk score. Global CHD risk scoring may increase prescribing of preventive therapy (aspirin and lipid lowering therapy), reduce CHD risk 4 factors over the short-term, and improve the accuracy of risk perception with no reported clinical harm. Physicians may also overestimate the absolute risk of CHD events and effects of preventive therapy and could benefit from interventions to increase acceptance of tools used to calculate CHD risk.Master of Public Healt

Synaptic effects of ethanol on the agranular insunlar cortex

The purpose of this study was to provide the first examination of whether the agranular insular cortex (AIC) is a target for the actions of ethanol. Initially, we wished to determine whether basic excitatory and inhibitory synaptic transmission in the AIC are sensitive to acute ethanol. Therefore, we collected brain slices from ethanol-naïve adult male mice, obtained whole-cell recording configuration in layer 2/3 AIC pyramidal neurons, and bath-applied ethanol at pharmacologically relevant concentrations during electrophysiological assays of glutamatergic and γ-amino-butyric acid (GABA)ergic synaptic transmission and plasticity. We found that ethanol inhibited electrically evoked N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory postsynaptic currents (EPSCs) in a concentration-related fashion, and had little effect on other electrophysiological parameters of glutamatergic and (GABA)ergic synaptic transmission. Synaptic conditioning (low-frequency stimulation for 15 min at 1 Hz) induced a form of long-term depression (LTD) that was inhibited by a nonselective NMDAR antagonist (DL-2-amino-5-phosphonovaleric acid), and also by acute, intoxicating concentrations of ethanol. We then wished to determine whether NMDAR-dependent LTD in the AIC is sensitive to chronic ethanol. We utilized the Becker-Lopez chronic intermittent ethanol (CIE) exposure model to model chronic ethanol experience, and found that CIE vapor exposure disrupted the ability to induce NMDAR-dependent LTD in the AIC. Then, we wished to determine whether NMDAR-dependent LTD and other glutamatergic synaptic properties in the AIC are differentially modulated by conditions that promote aspects of alcohol use disorder (AUD) relative to conditions that do not. Therefore, groups of ethanol-drinking mice underwent either extended CIE (Drinking + CIE) or air (Drinking + Air) to generate AUD-like and non AUD-like phenotypes, respectively, before undergoing electrophysiological recordings testing for LTD and other glutamatergic synaptic properties. Drinking + CIE and Drinking + Air groups no longer displayed NMDAR-dependent LTD, but Drinking + CIE groups displayed a reduced NMDA/AMPA ratio relative to Drinking + Air groups. To verify the reduction in NMDA/AMPA ratio between Drinking + CIE and Drinking + Air groups, as well as determine whether modest amounts of ethanol drinking alter NMDA/AMPA ratio, we replicated the experiment with an additional ethanol-naïve handling control group. We found that ethanol drinking alone reduces NMDA/AMPA ratio relative to ethanol naïve animals. Finally, to verify whether AIC NMDAR-dependent LTD was not an age-dependent phenomenon, we tested for the presence of LTD in an additional ethanol-naïve group age-matched to the Drinking + CIE and Drinking + Air groups (≥14 weeks). We no longer observed the presence of LTD. These data indicate that glutamatergic transmission is sensitive to acute and chronic ethanol in AIC 2/3 pyramidal neurons, and that even moderate, non AUD-like ethanol drinking may alter age-dependent glutamatergic synaptic plasticity mechanisms.Pharmaceutical Science