Physiological Effects of Chronic Copper Exposure to Rainbow Trout (\u3cem\u3eOncorhynchus Mykiss\u3c/em\u3e) in Hard and Soft Water: Evaluation of Chronic Indicators

Effects of chronic copper exposure on a suite of indicators were examined: acute toxicity, acclimation, growth, sprint performance, whole-body electrolytes, tissue residues, and gill copper binding characteristics. Juvenile rainbow trout were exposed for 30 d to waterborne copper in hard water (hardness = 120 μg/L as CaCO3, pH = 8.0, Cu = 20 and 60 μg/L) and soft water (hardness = 20 μg/L as CaCO3, pH = 7.2, Cu = 1 and 2 μg/L). Significant acclimation to the metal occurred only in fish exposed to 60 mg/L, as seen by an approx. twofold increase in 96-h LC50 (153 vs 91 μg Cu/L). Chronic copper exposure had little or no effect on survival, growth, or swimming performance in either water hardness, nor was there any initial whole-body electrolyte loss (Na+ and Cl-). The present data suggest that the availability of food (3% wet body weight/day, distributed as three 1% meals) prevented growth inhibition and initial ion losses that usually result from Cu exposure. Elevated metal burdens in the gills and livers of exposed fish were measures of chronic copper exposure but not of effect. Initial gill binding experiments revealed the necessity of using radiolabeled Cu (64Cu) to detect newly accumulated Cu against gill background levels. Using this method, we verified the presence of saturable Cu-binding sites in the gills of juvenile rainbow trout and were able to make estimates of copperbinding affinity (log Kgill=Cu) and capacity (Bmax). Furthermore, we showed that both chronic exposure to Cu and to low water calcium had important effects on the Cu-binding characteristics of the gills

Medication decision making and patient outcomes in GP, nurse and pharmacist prescriber consultations

UNLABELLED: Aim The aims of this study were twofold: (a) to explore whether specific components of shared decision making were present in consultations involving nurse prescribers (NPs), pharmacist prescribers (PPs) and general practitioners (GPs) and (b) to relate these to self-reported patient outcomes including satisfaction, adherence and patient perceptions of practitioner empathy.BACKGROUND: There are a range of ways for defining and measuring the process of concordance, or shared decision making as it relates to decisions about medicines. As a result, demonstrating a convincing link between shared decision making and patient benefit is challenging. In the United Kingdom, nurses and pharmacists can now take on a prescribing role, engaging in shared decision making. Given the different professional backgrounds of GPs, NPs and PPs, this study sought to explore the process of shared decision making across these three prescriber groups.METHODS: Analysis of audio-recordings of consultations in primary care in South England between patients and GPs, NPs and PPs. Analysis of patient questionnaires completed post consultation. Findings A total of 532 consultations were audio-recorded with 20 GPs, 19 NPs and 12 PPs. Prescribing decisions occurred in 421 (79%). Patients were given treatment options in 21% (102/482) of decisions, the prescriber elicited the patient's treatment preference in 18% (88/482) and the patient expressed a treatment preference in 24% (118/482) of decisions. PPs were more likely to ask for the patient's preference about their treatment regimen (χ 2=6.6, P=0.036, Cramer's V=0.12) than either NPs or GPs. Of the 275 patient questionnaires, 192(70%) could be matched with a prescribing decision. NP patients had higher satisfaction levels than patients of GPs or PPs. More time describing treatment options was associated with increased satisfaction, adherence and greater perceived practitioner empathy. While defining, measuring and enabling the process of shared decision making remains challenging, it may have patient benefit

Solving Tree Problems with Category Theory

Artificial Intelligence (AI) has long pursued models, theories, and techniques to imbue machines with human-like general intelligence. Yet even the currently predominant data-driven approaches in AI seem to be lacking humans' unique ability to solve wide ranges of problems. This situation begs the question of the existence of principles that underlie general problem-solving capabilities. We approach this question through the mathematical formulation of analogies across different problems and solutions. We focus in particular on problems that could be represented as tree-like structures. Most importantly, we adopt a category-theoretic approach in formalising tree problems as categories, and in proving the existence of equivalences across apparently unrelated problem domains. We prove the existence of a functor between the category of tree problems and the category of solutions. We also provide a weaker version of the functor by quantifying equivalences of problem categories using a metric on tree problems.Comment: 10 pages, 4 figures, International Conference on Artificial General Intelligence (AGI) 201

Regulation of Cytosolic Phospholipase A 2 Activation and Cyclooxygenase 2 Expression in Macrophages by the β-Glucan Receptor

Phagocytosis of non-opsonized microorganisms by macrophages initiates innate immune responses for host defense against infection. Cytosolic phospholipase A(2) is activated during phagocytosis, releasing arachidonic acid for production of eicosanoids, which initiate acute inflammation. Our objective was to identify pattern recognition receptors that stimulate arachidonic acid release and cyclooxygenase 2 (COX2) expression in macrophages by pathogenic yeast and yeast cell walls. Zymosan- and Candida albicans-stimulated arachidonic acid release from resident mouse peritoneal macrophages was blocked by soluble glucan phosphate. In RAW264.7 cells arachidonic acid release, COX2 expression, and prostaglandin production were enhanced by overexpressing the beta-glucan receptor, dectin-1, but not dectin-1 lacking the cytoplasmic tail. Pure particulate (1, 3)-beta-D-glucan stimulated arachidonic acid release and COX2 expression, which were augmented in a Toll-like receptor 2 (TLR2)-dependent manner by macrophage-activating lipopeptide-2. However, arachidonic acid release and leukotriene C(4) production stimulated by zymosan and C. albicans were TLR2-independent, whereas COX2 expression and prostaglandin production were partially blunted in TLR2(-/-) macrophages. Inhibition of Syk tyrosine kinase blocked arachidonic acid release and COX2 expression in response to zymosan, C. albicans, and particulate (1, 3)-beta-D-glucan. The results suggest that cytosolic phospholipase A(2) activation triggered by the beta-glucan component of yeast is dependent on the immunoreceptor tyrosine-based activation motif-like domain of dectin-1 and activation of Syk kinase, whereas both TLR2 and Syk kinase regulate COX2 expression

Regulation of Cytosolic Phospholipase a\u3csub\u3e2\u3c/sub\u3e Activation and Cyclooxygenase 2 Expression in Macrophages by the β-Glucan Receptor

Phagocytosis of non-opsonized microorganisms bymacrophages initiates innate immune responses for host defense against infection. Cytosolic phospholipase A2 is activated during phagocytosis, releasing arachidonic acid for production of eicosanoids, which initiate acute inflammation. Our objective was to identify pattern recognition receptors that stimulate arachidonic acid release and cyclooxygenase 2 (COX2) expression in macrophages by pathogenic yeast and yeast cell walls. Zymosan- and Candida albicans-stimulated arachidonic acid release from resident mouse peritoneal macrophages was blocked by soluble glucan phosphate. In RAW264.7 cells arachidonic acid release, COX2 expression, and prostaglandin production were enhanced by overexpressing the β-glucan receptor, dectin-1, but not dectin-1 lacking the cytoplasmic tail. Pure particulate (1, 3)-β-D-glucan stimulated arachidonic acid release and COX2 expression, which were augmented in a Toll-like receptor 2 (TLR2)-dependent manner by macrophage-activating lipopeptide-2. However, arachidonic acid release and leukotriene C4 production stimulated by zymosan and C. albicans were TLR2-independent, whereas COX2 expression and prostaglandin production were partially blunted in TLR2-/- macrophages. Inhibition of Syk tyrosine kinase blocked arachidonic acid release and COX2 expression in response to zymosan, C. albicans, and particulate (1, 3)-β-D-glucan. The results suggest that cytosolic phospholipase A2 activation triggered by the β-glucan component of yeast is dependent on the immunoreceptor tyrosine-based activation motif-like domain of dectin-1 and activation of Syk kinase, whereas both TLR2 and Syk kinase regulate COX2 expression

Experimental electronic heat capacities of α−\alpha- and δ−\delta-Plutonium; heavy-fermion physics in an element

We have measured the heat capacities of $\delta-$Pu$_{0.95}$Al$_{0.05}$ and $\alpha-$Pu over the temperature range 2-303 K. The availability of data below 10 K plus an estimate of the phonon contribution to the heat capacity based on recent neutron-scattering experiments on the same sample enable us to make a reliable deduction of the electronic contribution to the heat capacity of $\delta-$Pu$_{0.95}$Al$_{0.05}$; we find $\gamma = 64 \pm 3$ mJK$^{-2}$mol$^{-1}$ as $T \to 0$. This is a factor $\sim 4$ larger than that of any element, and large enough for $\delta-$Pu$_{0.95}$Al$_{0.05}$ to be classed as a heavy-fermion system. By contrast, $\gamma = 17 \pm 1$ mJK$^{-2}$mol$^{-1}$ in $\alpha-$Pu. Two distinct anomalies are seen in the electronic contribution to the heat capacity of $\delta-$Pu$_{0.95}$Al$_{0.05}$, one or both of which may be associated with the formation of the $\alpha'-$ martensitic phase. We suggest that the large $\gamma$-value of $\delta-$Pu$_{0.95}$Al$_{0.05}$ may be caused by proximity to a quantum-critical point.Comment: 4 pages, 4 figure

Spatially Resolved PAH Emission Features in Nearby, Low Metallicity, Star-Forming Galaxies

Low-resolution, mid-infrared Spitzer/IRS spectral maps are presented for three nearby, low-metallicity dwarf galaxies (NGC 55, NGC 3109 and IC 5152) for the purpose of examining the spatial distribution and variation of polycyclic aromatic hydrocarbon (PAH) emission. The sample straddles a metallicity of 12+log(O/H)~8.0, a transition point below which PAH intensity empirically drops and the character of the interstellar medium changes. We derive quantitative radiances of PAH features and atomic lines on both global and spatially-resolved scales. The Spitzer spectra, combined with extensive ancillary data from the UV through the mid-infrared, allow us to examine changes in the physical environments and in PAH feature radiances down to a physical scale of 50 pc. We discuss correlations between various PAH emission feature and atomic line radiances. The (6.2 micron)/(11.3 micron), (7.7 micron)/(11.3 micron), (8.6 micron)/(11.3 micron), (7.7 micron)/(6.2 micron), and (8.6 micron)/(6.2 micron) PAH radiance ratios are found to be independent of position across all three galaxies, although the ratios do vary from galaxy to galaxy. As seen in other galaxies, we find no variation in the grain size distribution as a function of local radiation field strength. Absolute PAH feature intensities as measured by a ratio of PAH/(24 micron) radiances are seen to vary both positionally within a given galaxy, and from one galaxy to another when integrated over the full observed extent of each system. We examine direct comparisons of CC mode PAH ratios (7.7 micron)/(6.2 micron) and (8.6 micron)/(6.2 micron) to the mixed (CC/CH) mode PAH ratio (7.7 micron)/(11.3 micron). We find little variation in either mode, and no difference in trends between modes. While the local conditions change markedly over the observed regions of these galaxies, the properties of PAH emission show a remarkable degree of uniformity.Comment: Astrophysical Journal, in pres

High Performance InGaAsSb TPV Cells

Lattice-matched 0.52 eV InGaAsSb/GaSb thermophotovoltaic (TPV) cells are grown using a multi-wafer metal-organic-chemical-vapor-deposition (MOCVD) system. MOCVD growth series of P/N junction epitaxial structures consisting of as many as 30 wafers demonstrate good run-to-run reproducibility, good uniformity across the wafer and exhibit high performance with open circuit voltages of {approx}300mV and fill factors of 70% at 25 C. Growth parameters, including temperature, surface preparation and substrate orientation, that directly affect growth have been optimized for the active 0.52 eV InGaAsSb region and GaSb confinement layers. Focus is on increasing TPV diode performance through architectural improvements, specifically by reducing the minority carrier recombination velocity at the emitter and base front and back interfaces. Work in support of incorporating a back surface reflector (BSR) including the growth of N/P diode architectures and the addition of a lattice-matched InAsSb etch stop layer for substrate removal and wafer bonding, is reported. The lattice matched InAsSb stop etch exhibits resiliency to the substrate removal and wafer bonding processes. Substantial improvement in carrier lifetime on test structures with P-type AlGaAsSb layers indicated incorporation of these layers into the TPV cell structure should provide significant improvement in open-circuit voltage. Addition of AlGaAsSb confinement layers to the standard P/N cell structure gave some of the best InGaAsSb TPV cell results to date

Bostonia: The Boston University Alumni Magazine. Volume 9

Founded in 1900, Bostonia magazine is Boston University's main alumni publication, which covers alumni and student life, as well as university activities, events, and programs

Pathways Regulating Cytosolic Phospholipase a\u3csub\u3e2\u3c/sub\u3e Activation and Eicosanoid Production in Macrophages by Candida Albicans

Resident tissue macrophages are activated by the fungal pathogen Candida albicans to release eicosanoids, which are important modulators of inflammation and immune responses. Our objective was to identify the macrophage receptors engaged by C. albicans that mediate activation of group IVA cytosolic phospholipase A2 (cPLA2α), a regulatory enzyme that releases arachidonic acid (AA) for production of prostaglandins and leukotrienes. A comparison of peritoneal macrophages from wild type and knock-out mice demonstrates that the β-glucan receptor Dectin-1 and MyD88 regulate early release of AA and eicosanoids in response to C. albicans. However, cyclooxygenase 2 (COX2) expression and later phase eicosanoid production are defective in MyD88-/- but not Dectin-1-/- macrophages. Furthermore, C. albicans-stimulated activation of MAPK and phosphorylation of cPLA2α on Ser-505 are regulated by MyD88 and not Dectin-1. In contrast, Dectin-1 mediates MAPK activation, cPLA 2α phosphorylation, and COX2 expression in response to particulate β-glucan suggesting that other receptors engaged by C. albicans preferentially mediate these responses. Results also implicate the mannan-binding receptor Dectin-2 in regulating cPLA2α. C. albicans-stimulated MAPK activation and AA release are blocked by D-mannose and Dectin-2-specific antibody, and overexpression of Dectin-2 in RAW264.7 macrophages enhances C. albicans-stimulated MAPK activation, AA release, and COX2 expression. In addition, calcium mobilization is enhanced in RAW264.7 macrophages overexpressing Dectin-1 or -2. The results demonstrate that C. albicans engages both β-glucan and mannan-binding receptors on macrophages that act with MyD88 to regulate the activation of cPLA2α and eicosanoid production