Hadronic Decays of Charm

Recent hadronic charm decay results from fixed-target experiments are presented. New measurements of the D0 to K-K+K-pi+ branching ratio are shown as are recent results from Dalitz plot fits to D+ to K-K+pi+, pi+pi-pi+, K-pi+pi+, K+pi-pi+ and D_s+ to pi+pi-pi+, K+pi-pi+. These fits include measurements of the masses and widths of several light resonances as well as strong evidence for the existence of two light scalar particles, the pipi resonance sigma and the Kpi resonance kappa.Comment: 8 pages, 9 figures, to appear in the proceedings for the 9th International Symposium on Heavy Flavors, Caltech, Pasadena, 10-13 Sept. 200

From mass to structure: An aromaticity index for high-resolution mass data of natural organic matter

Recent progress in Fourier transform ion cyclotron resonance mass spectrometry (FTICRMS) provided extensive molecular mass data for complex natural organic matter (NOM). Structural information can be deduced solely from the molecular masses for ions with extreme molecular element ratios, in particular low H/C ratios, which are abundant in thermally altered NOM (e.g. black carbon). In this communication we propose a general aromaticity index (AI) and two threshold values as unequivocal criteria for the existence of either aromatic (AI > 0.5) or condensed aromatic structures (AI >= 0.67) in NOM. AI can be calculated from molecular formulae which are derived from exact molecular masses of naturally occurring compounds containing C, H, O, N, S and P and is especially applicable for substances with aromatic cores and few alkylations. In order to test the validity of our model index, AI is applied to FTICRMS data of a NOM deep-water sample from the Weddell Sea (Antarctica), a fulvic acid standard and an artificial dataset of all theoretically possible molecular formulae. For graphical evaluation a ternary plot is suggested for four-dimensional data representation. The proposed aromaticity index is a step towards structural identification of NOM and the molecular identification of black carbon in the environment

Dual-Species Plasmas Illustrate MHD Flows

Plasma loops created in the laboratory strongly resemble structures observed in the solar corona. For example, both solar coronal loops and experimental loops exhibit remarkably uniform axial cross sections. A magnetohydrodynamic theory that was proposed to explain this phenomenon predicts that a plasma loop whose axial magnetic field is constricted at both footpoints will experience bulk flows into the loop from both ends. To test this theory, dual-species plasma loops were formed by supplying a different neutral gas to each of the two footpoints. Optical filters were then used to separately image the motion of different sections of the plasma. Bulk flows were, in fact, observed

The Role of Collaboration in Defining and Maintaining a Safety Culture: Australian Perspectives in the Construction Sector

The nature of the Australian construction industry, with strict time and work demands, serves to challenge construction organisations in how they can develop and maintain a positive site safety culture. Much research has examined the role management has in influencing culture, however more is needed to specifically elucidate the attributes required by leaders within organisations (Cox, Tomas, Cheyne, & Oliver 1998; Glendon & Stanton 2000; Williamson, Feyer, Cairns & Biancotti 1997). To answer this question, focus groups were held with eleven of the twelve largest construction companies across Australia. Discussion centred around safety culture and the attributes required by those who hold ‘safety critical roles’ i.e. key safety positions. Data was analysed qualitatively to identify key themes. The results indicated the strong role that leadership style, communication and workplace collaboration had in influencing the ability of organisations to develop and maintain a positive safety culture. Specifically, the participants indicated that leadership and communication styles that served to reduce conflict and work demands, and sought to involve workers in decision making and problem solving appeared to increase personalisation, which in turn increased safety awareness and safety performance

Planning for the mobile library: a strategy for managing innovation and transformation at the University of Glasgow Library

Modern mobile devices have powerful features that are transforming access to information. Lippincott argues that as mobile devices such as smartphones become ‘key information devices’ for our users, libraries will want to have a significant presence in offering content and services that are suitable for this medium. This article outlines the process of development and implementation of a mobile strategy at the University of Glasgow Library. What began as an investigation into a mobile interface to the library catalogue evolved into a comprehensive strategic review of how we deliver services now and in the future in this rapidly changing mobile environment

Beyond Basic Exercise Guidelines: Is Sitting Really the New Smoking?

The Just Stand movement has recently gained a foothold at CSB|SJU with the addition of sit-stand workstations in Clemens Library, Murray Hall, and several faculty and staff offices. Researchers have been studying sitting disease, more formally termed sedentary physiology, for over a decade and have begun to conclude that simply meeting exercise guidelines is not enough to reduce risk for chronic diseases. An individual can be physically active and lead a sedentary lifestyle. The two are not mutually exclusive. The average American adult, even those who meet the general exercise guidelines, spends 55% of their waking hours sedentary. Sedentary behaviors are characterized by wakeful activities that require little physical movement, low energy expenditure, and are performed in a sitting or lying position. Sedentary time is closely related to adverse health risks even if individuals perform physical activity on a daily basis. So what exactly happens when we sit and how can moving more help us decrease our risk for chronic diseases like cardiovascular disease and diabetes? During this presentation, I discuss why too much sitting can be detrimental to health, examine how sedentary time impacts our students, faculty, and staff, and share simple ways you can decrease your sedentary time both at work and at home

Studies of LXR and CIDEA function in human adipocytes

Obesity, defined as a body mass index of 30 or above, is the result of an imbalance of energy intake and energy expenditure. In the last decade, the obesity prevalence has truly reached epidemic proportions with major effects on public health. Obesity is closely associated with insulin resistance, type 2 diabetes, hyperlipidemia and atherosclerosis. On the other end of the spectra, cancer cachexia is a poor diagnostic factor in cancer patients. It is characterized by a state of unintentional weight loss, primarily of body fat but also of lean body mass. Although the mechanisms behind the loss of adipose tissue are not completely understood, lipolysis seems to be a major factor. Adipose tissue is an important metabolic and endocrine organ. One of the most important functions of the adipocyte is lipolysis, the hydrolysis of triglycerides to free fatty acids (FFA) and glycerol. This is a tightly regulated process of great importance to the whole-body metabolism. The FFAs can either be released into the circulation, to be used as energy substrate by other organs and tissues, or utilized within the adipocyte for re-esterification or lipid oxidation. The process of lipid oxidation in adipocytes is controlled in part by the pyruvate dehydrogenase complex (PDC), an important regulator of substrate oxidation in adipocytes. This complex is inactivated when phosphorylated by pyruvate dehydrogenase kinases (PDKs), which promotes lipid oxidation rather than glucose oxidation. The aim of this thesis was to investigate how two factors, the liver x receptor (LXR) and cell death-inducing DNA fragmentation factor-α-like effector A (CIDEA) affect adipose tissue metabolism. LXR is a nuclear receptor and a known regulator of cholesterol, lipid and carbohydrate metabolism. CIDEA is almost exclusively expressed in white adipocytes in humans and can affect critical metabolic functions such as lipolysis. In paper I, we investigated the role of CIDEA in cancer cachexia. We measured levels of CIDEA in subcutaneous adipose tissue from subjects suffering from cancer cachexia and compared these to weight-stable cancer patients and noncancer patients. Levels of CIDEA mRNA were increased in cancer cachexia and correlated with elevated levels of FFAs and weight loss. Over-expression of CIDEA increased fatty acid oxidation in human adipocytes in culture and decreased glucose oxidation. Furthermore, augmented levels of CIDEA enhanced the expression of PDK1 and PDK4, and the phosphorylation of PDC. In accordance with this, mRNA levels of PDK1 and PDK4 in the clinical material correlated with CIDEA expression. In conclusion, CIDEA is involved in loss of adipose tissue in cancer cachexia at least in part due to its ability to inactivate PDC and thereby switch substrate oxidation in human adipocytes from glucose to lipids. In papers II and III, the role of LXR in human adipocyte function was studied, with focus on substrate oxidation (paper II) and lipolysis (paper III). In paper II, we treated human adipocytes with the LXR agonist GW3965 and observed an increased fatty acid and decreased glucose oxidation. We showed that LXR activation can increase the mRNA level of PDK4 and thereby the phosphorylation of PDC. We also showed a decreased activity of PDC, which was found to be dependent on PDK4. Furthermore, we could establish that the effect of GW3965 on lipid oxidation was specific for LXR, since it was abolished upon knockdown of LXR. In conclusion, we suggest that LXR has an important role in the regulation of substrate oxidation in human adipocytes, at least in part by influencing the phosphorylation status of PDC. In paper III, LXR activation was shown to up-regulate glycerol release from human adipocytes. Based on microarray analysis we found a strong impact of LXR activation on known lipolysis-regulating genes. We showed differences in expression and localization of perilipin 1 (PLIN1) and hormone sensitive lipase (HSL). When PLIN1 is depleted, the effect of LXR is abolished. Furthermore, we showed binding of LXR and its heterodimerizing partner Retinoid X Receptor to the promoters of HSL and PLIN1 upon LXR activation. We also demonstrated that LXRα is the predominant isoform involved in regulation of adipocyte lipolysis within this context. In conclusion, we proposed that LXR activation up-regulates adipocyte lipolysis, at least in part through LXR binding to the promoter of PLIN1 and down-regulation of PLIN1 expression. In conclusion, we suggest that CIDEA and LXR can affect central functions of adipocyte metabolism, namely lipolysis and substrate oxidation. We show that CIDEA is involved in the loss of adipose tissue in cancer cachexia and that this is at least in part due to a shift in substrate oxidation. Activation of LXR in human adipocytes increases fatty acid oxidation and lipolysis, through effects on PDC and PLIN1. The findings in this thesis are of importance for conditions of dysregulated adipose tissue metabolism, such as obesity and cachexia

Impact of environmental risk factors for schizophrenia on the developing brain, characterisation of the effects of polyIC and THC on functional neural systems and behaviour

Strathclyde theses - ask staff. Thesis no. : T13455Cannabis abuse can produce deficits in cognition and has been implicated as a 'late' environmental risk factor in the pathogenesis of the poly-factorial disorder schizophrenia. Evidence suggests an age-related susceptibility to the deleterious effects of cannabis as early onset of use may increase the vulnerability of the brain to the adverse consequences of cannabis abuse. Animal models are crucial for exploration of mechanistic and causative theories, and long-term behavioural consequences of adolescent cannabis abuse in a controlled experimental environment. This thesis evaluates the vulnerability of the adolescent/peripubertal brain to Δ9-tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis, and explores the potential interplay between this schizophrenia-related 'late' environmental risk factor and an 'early' environmental risk factor (prenatal infection - maternal immune activation (MIA)) on functional neural systems and behaviours relevant to schizophrenia. Cannabinoid CB1 receptor ontogeny (activated in the brain by the receptor ligand THC) within important cognitive substrates, the prefrontal cortex (PFC) and hippocampus, was investigated to delineate a period of neurodevelopmental vulnerability for peripubertal THC treatment. CB1 receptor ligand binding revealed that the PFC and hippocampus follow differential late maturational trajectories throughout the peripubertal period. The 'vulnerability window' for peripubertal THC treatment was defined as post-natal day (PD) 35-56 to encompass the dynamic peripubertal ontogenetic patterns of the CB1 receptor in both these regions. Furthermore, age-related alterations in cerebral metabolism and regional functional connectivity profiles were evident in the hippocampus and important neuromodulatory nuclei including the ventral tegmental area, dorsal raphe, locus coeruleus and the diagonal band of Broca.;Acute THC administration (5mg/kg) produced hypometabolism in the thalamus and an altered functional connectivity profile between thalamic nuclei and the PFC, hippocampus and the nucleus accumbens. THC-induced anomalistic neural activity was evident in key neuromodulatory nuclei and produced perturbed functional connectivity within acetylcholine, noradrenaline, and dopamine neural pathways. Acute THC treatment resulted in alterations in cerebral metabolism in the amygdala and aberrant functional connectivity profiles between amygdaloid nuclei and the hippocampus, PFC and nucleus accumbens. There appeared to be an age-related sensitivity to THC in several thalamic, neuromodulatory and amygdaloid nuclei. Peripubertal low-dose intermittent THC (3.5mg/kg, 3 times a week), mimetic of light, recreational adolescent cannabis use, produced long-term cognitive inflexibility, as measured by the attentional-set shifting task, perturbed cerebral metabolism in the dorsolateral orbital cortex and the nucleus accumbens core and altered functional coupling between both these regions and neural substrates subserving reward-related learning including prefrontal, septal and amygdala subfields. High-dose daily THC (7mg/kg) throughout the peripubertal period, mimetic of heavy daily cannabis abuse, did not precipitate any schizophrenia-related behaviours in adulthood. MIA induced by prenatal exposure to the immune-stimulating agent polyriboinosinic-polyribocytidilic acid (PolyIC) did not produce any schizophrenia-related phenotypes in adulthood. However, prenatal PolyIC exposure produced residual hypermetabolism within discrete components of the prefrontal cortex dorsolateral orbital and cingulate cortices and hypometabolism within the CA3 subfield of the hippocampus. The functional connectivity signatures of all these regions indicated a unified MIA effect of aberrant mesocorticolimbic functional coupling in adulthood. Furthermore, chronic intermittent treatment with low-dose THC during the peripubertal period caused an increase in sensitivity to amphetamine (indicative of aberrant mesolimbic dopamine transmission) in PolyIC-treated offspring compared to PBS-treated offspring, suggestive of a synergistic effect of these two environmental risk factors. In conclusion, the findings presented in this thesis have provided clear evidence of dose-specific detrimental effects of 'adolescent' THC exposure on behaviour and the functional neural systems that may underpin these deficits which impact on behaviour and neural systems into adulthood.Cannabis abuse can produce deficits in cognition and has been implicated as a 'late' environmental risk factor in the pathogenesis of the poly-factorial disorder schizophrenia. Evidence suggests an age-related susceptibility to the deleterious effects of cannabis as early onset of use may increase the vulnerability of the brain to the adverse consequences of cannabis abuse. Animal models are crucial for exploration of mechanistic and causative theories, and long-term behavioural consequences of adolescent cannabis abuse in a controlled experimental environment. This thesis evaluates the vulnerability of the adolescent/peripubertal brain to Δ9-tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis, and explores the potential interplay between this schizophrenia-related 'late' environmental risk factor and an 'early' environmental risk factor (prenatal infection - maternal immune activation (MIA)) on functional neural systems and behaviours relevant to schizophrenia. Cannabinoid CB1 receptor ontogeny (activated in the brain by the receptor ligand THC) within important cognitive substrates, the prefrontal cortex (PFC) and hippocampus, was investigated to delineate a period of neurodevelopmental vulnerability for peripubertal THC treatment. CB1 receptor ligand binding revealed that the PFC and hippocampus follow differential late maturational trajectories throughout the peripubertal period. The 'vulnerability window' for peripubertal THC treatment was defined as post-natal day (PD) 35-56 to encompass the dynamic peripubertal ontogenetic patterns of the CB1 receptor in both these regions. Furthermore, age-related alterations in cerebral metabolism and regional functional connectivity profiles were evident in the hippocampus and important neuromodulatory nuclei including the ventral tegmental area, dorsal raphe, locus coeruleus and the diagonal band of Broca.;Acute THC administration (5mg/kg) produced hypometabolism in the thalamus and an altered functional connectivity profile between thalamic nuclei and the PFC, hippocampus and the nucleus accumbens. THC-induced anomalistic neural activity was evident in key neuromodulatory nuclei and produced perturbed functional connectivity within acetylcholine, noradrenaline, and dopamine neural pathways. Acute THC treatment resulted in alterations in cerebral metabolism in the amygdala and aberrant functional connectivity profiles between amygdaloid nuclei and the hippocampus, PFC and nucleus accumbens. There appeared to be an age-related sensitivity to THC in several thalamic, neuromodulatory and amygdaloid nuclei. Peripubertal low-dose intermittent THC (3.5mg/kg, 3 times a week), mimetic of light, recreational adolescent cannabis use, produced long-term cognitive inflexibility, as measured by the attentional-set shifting task, perturbed cerebral metabolism in the dorsolateral orbital cortex and the nucleus accumbens core and altered functional coupling between both these regions and neural substrates subserving reward-related learning including prefrontal, septal and amygdala subfields. High-dose daily THC (7mg/kg) throughout the peripubertal period, mimetic of heavy daily cannabis abuse, did not precipitate any schizophrenia-related behaviours in adulthood. MIA induced by prenatal exposure to the immune-stimulating agent polyriboinosinic-polyribocytidilic acid (PolyIC) did not produce any schizophrenia-related phenotypes in adulthood. However, prenatal PolyIC exposure produced residual hypermetabolism within discrete components of the prefrontal cortex dorsolateral orbital and cingulate cortices and hypometabolism within the CA3 subfield of the hippocampus. The functional connectivity signatures of all these regions indicated a unified MIA effect of aberrant mesocorticolimbic functional coupling in adulthood. Furthermore, chronic intermittent treatment with low-dose THC during the peripubertal period caused an increase in sensitivity to amphetamine (indicative of aberrant mesolimbic dopamine transmission) in PolyIC-treated offspring compared to PBS-treated offspring, suggestive of a synergistic effect of these two environmental risk factors. In conclusion, the findings presented in this thesis have provided clear evidence of dose-specific detrimental effects of 'adolescent' THC exposure on behaviour and the functional neural systems that may underpin these deficits which impact on behaviour and neural systems into adulthood