The financial cost of carbon

Climate finance is first and foremost a risk-management problem, which means three things for investors. First, prudent investors will seek to hedge climate change risk by reducing their exposure to this risk. Second, investors will demand compensation for holding this risk. Third, investors will engage with companies to urge them to reduce this risk if they are not adequately compensated for it. For companies, the main implication of climate-risk management by investors is that the companies with greater carbon emissions will have to pay a higher financial cost of carbon (FCC). In their new study described in this article, the authors undertake a comprehensive analysis of the risk compensation implications of exposing investors to carbon transition risk. They explore how corporate GHG emissions have affected the price-to-earnings (P/E) ratios of listed companies in Europe and the U.S. over the period 2016 to 2020. Their main finding is that financial markets are beginning to broadly discount companies whose high carbon emissions are viewed as subjecting them to higher levels of political and regulatory risk, and providing them with what amounts to a higher cost of capital. Although price-earnings ratios are generally lower for companies with higher emissions, the discount varies significantly by sector and across firm size, with larger companies experiencing the larger discounts. Although the carbon discount is similar in the U.S. and in Europe, the authors find significantly higher discounts in industries in Europe that are directly covered by carbon pricing through the EU ETS. They even find a small price discount on corporate debt for smaller issuers. Overall, what emerges is a clear pattern of investors' growing concern over climate risk, which translates into an increasingly material FCC for companies with high GHG emissions. This growing valuation discount for companies with high emissions should encourage them to progress further along their decarbonization path, which our results suggest have large financial as well as other social benefits

Expression Of Glucocorticoid Receptor Beta (GCR Β) In Asthmatic Patients And Its Correlation With Clinical Severity And Pulmonary Functions

N e w Y o r k S c i e n c e J o u r n a l 2 0 1 0 ; 3 Expression Of Glucocorticoid Receptor Beta (GCR Β) In Asthmatic Patients And Its Correlation With Clinical Severity And Pulmonary Functions Engy Yousry Elsayed , Enas M Foda, khaled AH Mohammed, Hassan Shalaby, Amal Z. Abd El-Halem* and Eman Ramzy** Internal Medicine, Clinical Pathology* and Chest** Departments Faculty Of Medicine, Ain Shams University, cairo, Egypt. [email protected] ABSTRACT Background: Glucocorticoids are the gold standard treatment of bronchial asthma. Although the majority of patients with asthma respond favorably to inhaled and systemic steroid therapy, a subset of asthmatics failed to demonstrate a satisfactory response even to systemic glucocorticoid therapy. GCR β (glucocorticoid receptor beta) is a hormone binding deficit isoform of GCR (glucocorticoid receptor) which has been isolated in humans and when over expressed, it may function as a dominant negative modulator of GCR. Aim of the work: This study was designed to determine the percentage of expression of GCRβ on PBMCs: (peripheral blood mononuclear cells )of asthmatic patients and to correlate it with the clinical severity and pulmonary functions. Subjects and Methods: 60 asthmatic patients (41 males, 19 females) and 20 healthy controls were enrolled in this study. Asthmatics were classified according to GINA guidelines (2002) into mild, moderate and severe asthma. They were subdivided into asthmatic on inhaled corticosteroid (ICS) (n=35) and those not on ICS (n=25). For all studied groups, spirometeric pulmonary functions and immunohisto-chemistry staining of PBMC S were performed to analyze percentage of expression of GCRβ on PBMCs. Results: It showed that the percentage of expression of GCRβ on PBMC S were statistically higher in all asthmatic patient groups compared to control, with higher % of expression in those not on ICS. Also a statistical significant higher % of expression of GCR β in severe asthmatics compared to both mild and moderate groups was detected. In conclusion: This study highlights the importance of glucocorticoid receptor beta isoform in pathogenesis of bronchial asthma and this may be directly linked to asthma severity and can affect the response to medications especially ICS

Identification of Adropin as a Secreted Factor Linking Dietary Macronutrient Intake with Energy Homeostasis and Lipid Metabolism

Obesity and nutrient homeostasis are linked by mechanisms that are not fully elucidated. Here we describe a secreted protein, adropin, encoded by a gene, Energy Homeostasis Associated (Enho), expressed in liver and brain. Liver Enho expression is regulated by nutrition: lean C57BL/6J mice fed high-fat diet (HFD) exhibited a rapid increase, while fasting reduced expression compared to controls. However, liver Enho expression declines with diet-induced obesity (DIO) associated with 3 months of HFD or with genetically induced obesity, suggesting an association with metabolic disorders in the obese state. In DIO mice, transgenic overexpression or systemic adropin treatment attenuated hepatosteatosis and insulin resistance independently of effects on adiposity or food intake. Adropin regulated expression of hepatic lipogenic genes and adipose tissue peroxisome proliferator-activated receptor gamma, a major regulator of lipogenesis. Adropin may therefore be a factor governing glucose and lipid homeostasis, which protects against hepatosteatosis and hyperinsulinemia associated with obesity. © 2008 Elsevier Inc. All rights reserved

Transport properties of Ce-doped nickel oxide and relevance on the thermal growth of oxide scales on CeO2-coated nickel

International audienceThe growth of oxide scales on Ce02-coated Ni polycrystals, in the temperature range 800–1200 °C, is analyzed taking into account both the transport properties of Ce-doped Ni1-xO single crystals, under non-equilibrium conditions, and a formal analysis of transport properties of cation deficient p-type semi conducting oxides in presence of an external driving force. It was shown that a key feature of the beneficial influence of Ce02-coatings on the layer growth is the kinetic demixing of cations, leading to an enrichment of cerium in the inner oxidation scale. It follows a higher cationic vacancy concentration near the metal/oxide interface, leading to a lower vacancy concentration gradient across the layer and a decrease of the driving force of diffusion controlling the oxidation kinetics. Further, the lower cation mobility in the outer layer due to the depletion of Ce4+, leads to a blocking effect of the outward diffusion of cations. It follows a local excess of Ni2+ and the formation of new oxide units which also contribute to a decrease of the oxidation rate

Influence of CaO on the thermodynamic and transport properties of cobaltous oxide

International audienceThe electrical conductivity of Ca-doped Co_(1-x)O single crystals was measured as a function of oxygen partial pressure, over the temperature range 1273-1673 K. The results were analyzed using Seebeck coefficient measurements, microstructural characterizations, EELS, and X-ray diffraction experiments. From this set of results, we have shown that the influence of calcium on the thermodynamic and transport properties of cobaltous oxide is due to the reducing behavior of these solute cations, leading to both the shift of the Co/CoO phase boundary to higher P(O2) and the formation of singly ionized cobalt cations (Co +) in the stability range of CoO

Comparative study of low-cost fluoride removal by layered double hydroxides, geopolymers, softening pellets and struvite

Excessive F- in drinking water due to natural and anthropogenic activities is a serious health hazard affecting humans worldwide. In this study, a comparative assessment was made of eight mineral-based materials with advantageous structural properties for F- uptake: layered-double-hydroxides (LDHs), geopolymers, softening pellets and struvite. These materials are considered low-cost, for being either a waste or by-product, or can be locally-sourced. It can be concluded that Ca-based materials showed the strongest affinity for F- (Ca-Al-CO3 LDHs, slag-based geopolymer, softening pellets). The Langmuir adsorption capacity of Ca-Al-CO3 LDHs, slag-based geopolymer and softening pellets was observed to be 20.83, 5.23 and 1.20 mg/g, respectively. The main mechanism of F- uptake on Ca-Al-CO3 LDHs, Mg-Al-Cl LDHs, slag-based geopolymers and softening pellets was found to be sorption at low initial F- concentrations (<10 mg/L) whereas precipitation as CaF2 is proposed to play a major role at higher initial F- concentrations (>20 mg/L). Although the softening pellets had the highest Ca-content (96-97%; XRF), their dense structure and consequent low BET surface area (2–3 m2/g), resulted in poorer performance than the Ca-based LDHs and slag-based geopolymers. Nevertheless, geopolymers, as well as struvite, were not considered to be of interest for application in water treatment, as they would need modification due to their poor stability and/or F- leaching.Sanitary EngineeringMaterials and EnvironmentWater Managemen

Novel analogs of ghrelin: physiological and clinical implications.

International audienceGhrelin, the 28 amino acid peptide recently identified as the natural ligand for the growth hormone (GH) secretagogue (GHS) receptor, has multiple activities in addition to stimulation of GH secretion, including stimulation of feeding and weight gain. To utilize these actions for potential therapeutic benefit, we have produced analogs of human ghrelin with enhanced metabolic stability, affinity for the GHS receptor, and efficacy in stimulating weight gain. We have also discovered an analog of ghrelin, BIM-28163, that is an antagonist at the GHS receptor and that fully inhibits GHS receptor activation induced by native ghrelin. In vivo, BIM-28163 does not increase GH secretion but fully blocks ghrelin-induced GH secretion. In contrast, BIM-28163 acts as a full agonist with regard to the ghrelin actions of stimulating weight gain and food intake. These results suggest that a receptor other than the GHS receptor mediates the actions of ghrelin on feeding and weight gain. This concept is strengthened by our observation that at certain hypothalamic sites, BIM-28163 acts as an antagonist of ghrelin-induced neuronal activation, while at other sites, both ghrelin and BIM-28163 induce neuronal activation via the same receptor. Collectively, these results indicate the existence of a novel ghrelin receptor that may regulate the feeding activity of ghrelin. Using BIM-28163 as a tool to define the endogenous role of ghrelin in normal GH secretion, we have demonstrated that antagonism of the GHS receptor in normal rats does not impair the pulsatility of GH secretion but lowers the pulse amplitude and mean GH level. These results demonstrate that endogenous ghrelin acts to amplify the basic pattern of GH secretion established by the interplay of hypothalamic GH-releasing hormone and somatostatin. These studies demonstrate the feasibility of creating ghrelin analogs that are selective for specific activities, as well as their utility in dissecting the role of ghrelin in both normal physiology and specific pathologies

A novel growth hormone secretagogue-1a receptor antagonist that blocks ghrelin-induced growth hormone secretion but induces increased body weight gain

Ghrelin, the natural ligand for the growth hormone secretagogue-1a (GHS-1a) receptor, has received a great deal of attention due to its ability to stimulate weight gain and the hope that an antagonist of the GHS-1a receptor could be a treatment for obesity. We have discovered an analog of full-length human ghrelin, BIM-28163, which fully antagonizes GHS-1a by binding to but not activating the receptor. We further demonstrate that BIM-28163 blocks ghrelin activation of the GHS-1a receptor, and inhibits ghrelin-induced GH secretion in vivo. Unexpectedly, however, BIM-28163 acts as an agonist with regard to stimulating weight gain. These results may suggest the presence of an unknown ghrelin receptor that modulates ghrelin actions on weight gain. In keeping with our results on growth hormone (GH) secretion, BIM-28163 acts as an antagonist of ghrelin-induced Fos protein immunoreactivity (Fos-IR) in the medial arcuate nucleus, an area involved in the ghrelin modulation of GH secretion. However, in the dorsal medial hypothalamus (DMH), a region associated with regulation of food intake, both ghrelin and BIM-28163 act as agonists to upregulate Fos-IR. The observation that ghrelin and BIM-28163 have different efficacies in inducing Fos-IR in the DMH, and that concomitant administration of ghrelin and an excess of BIM-28163 results in the same level of Fos-IR as BIM-28163 administered alone may demonstrate that in the DMH both ghrelin and BIM-28163 act via the same receptor. If so, it is unlikely that this receptor is GHS-1a. Collectively, our findings suggest that the action of ghrelin to stimulate increased weight gain may be mediated by a novel receptor other than GHS-1a, and further imply that GHS-1a may not be the appropriate target for anti-obesity strategies. Copyrigh