The power of the CEO and environmental decoupling

This paper examines the impact of the power of the chief executive officer (CEO) on environmental decoupling. We define environmental decoupling as a gap between firm's claims about the environmental sustainability and actual environmental sustainability performance. Based on the managerial power theory, we argue that powerful managers are more involved in environmental decoupling and use environmental reporting in a more opportunistic manner than their less powerful peers. We analyse a dataset of 4576 firm-year observations of US-listed firms for the period 2002–2017. We find that powerful CEOs decouple firm's environmental performance from environmental reporting. These findings are robust to a battery of analyses and show that powerful CEOs do not show true commitment towards corporate environmental sustainability. The results provide important implications for investors, policymakers and fund managers. Useful future research recommendations are also provided to guide the research in the domain of environmental sustainability

Walking the Talk? A Corporate Governance Perspective on Corporate Social Responsibility Decoupling

Information asymmetry and the pressure to conform to stakeholders’ expectations cause firms to engage in corporate social responsibility (CSR) decoupling – a practice that has severe socioeconomic consequences for firms. Adopting a corporate governance perspective, this paper answers a novel question: whether board gender diversity (BGD) curbs CSR decoupling. Using a battery of sophisticated analyses and robustness tests on 9276 firm-year observations for the period 2002–2017, our results confirm that BGD is negatively associated with CSR decoupling. Analysis of the composition of gender-diverse boards further reveals that this effect is stronger for balanced boards than for skewed and tilted boards. Furthermore, we note that independent female directors are more effective monitors of decoupling than executive female directors. We also document that the relationship between BGD and CSR decoupling is stronger when the overall governance is weak. This implies that gender-diverse boards could act as a substitute mechanism for corporate governance that would otherwise be weak. Our study offers important theoretical and policy implications for the field of corporate governance and CSR

Huh-7 cell line as an alternative cultural model for the production of human like erythropoietin (EPO)

Erythropoietin (EPO) is a glycoprotein hormone which is required to regulate the production of red blood cells. Deficiency of EPO is known to cause anemia in chronically infected renal patients and they require regular blood transfusion. Availability of recombinant EPO has eliminated the need for blood transfusion and now it is extensively used for the treatment of anemia. Glycosylation of erythropoietin is essential for its secretion, stability, protein conformation and biological activity. However, maintenance of human like glycosylation pattern during manufacturing of EPO is a major challenge in biotechnology. Currently, Chinese hamster ovary (CHO) cell line is used for the commercial production of erythropoietin but this cell line does not maintain glycosylation resembling human system. With the trend to eliminate non-human constituent from biopharmaceutical products, as a preliminary approach, we have investigated the potential of human hepatoma cell line (Huh-7) to produce recombinant EPO.Initially, the secretory signal and Kozak sequences was added before the EPO mature protein sequence using overlap extension PCR technique. PCR-amplified cDNA fragments of EPO was inserted into mammalian expression vector under the control of the cytomegalovirus (CMV) promoter and transiently expressed in CHO and Huh-7 cell lines. After RT-PCR analysis, ELISA and Western blotting was performed to verify the immunochemical properties of secreted EPO.Addition of secretory signal and Kozak sequence facilitated the extra-cellular secretion and enhanced the expression of EPO protein. Significant expression (P < 0.05) of EPO was observed in the medium from Huh-7 cell line.Huh-7 cell line has a great potential to produce glycosylated EPO, suggesting the use of this cell line to produce glycoproteins of the therapeutic importance resembling to the natural human system

HCV genotype-specific correlation with serum markers: Higher predictability for genotype 4a

Several factors have been proposed to assess the clinical outcome of HCV infection. The correlation of HCV genotypes to possible serum markers in clinical prediction is still controversial. The main objective of this study was to determine the existence of any correlation between HCV genotypes to viral load and different clinical serum markers.We performed a prospective cross-sectional and observational study. About 3160 serum HCV RNA positive patients were chosen from 4020 randomly selected anti-HCV positive patients. Statistical analysis was performed using the SPSS 16 software package. ROC (receiver operating characteristics) curves were used to compare diagnostic values of serum markers to predict genotypes.The most prevalent genotype was 3a (73.9%) followed by 1a (10.7%), 4a (6.4%) and 3b (6.1%) in Pakistani population. No correlation was found between viral load and serum markers for genotype 3a in a large no. of sample (n = 2336). While significant correlation was observed between viral load and AST in genotype 3b, ALP with viral load and ALT for genotype 1a. Patients with genotype 4a showed a significant inverse correlation with viral load and Hb level and AST with ALP. For genotype 4a, AUC (area under the curve) of ALT, ALP, AST, bilirubin, Hb level and viral load was 0.790, 0.763, 0.454, 0.664, 0.458 and 0.872 respectively.In conclusion, there was a significant variable response of HCV genotypes with serum markers. Severity of disease is independent of serum marker level in genotype 3a, while the liver damage in genotype 4a may associate with viral cytopathic effect as well as the immune-mediated process. An index using six serum markers may correctly predict genotype 4a in patients with ≥ 75% accuracy

Claudin-1 required for HCV virus entry has high potential for phosphorylation and O-glycosylation

HCV is a leading cause of hepatocellular carcinoma and cirrhosis all over the world. Claudins belong to family of tight junction's proteins that are responsible for establishing barriers for controlling the flow of molecules around cells. For therapeutic strategies, regulation of viral entry into the host cells holds a lot of promise. During HCV infection claudin-1 is highly expressed in liver and believed to be associated with HCV virus entry after HCV binding with or without co-receptor CD81. The claudin-1 assembly with tight junctions is regulated by post translational modifications. During claudins assembly and disassembly with tight junctions, phosphorylation is required at C-terminal tail. In cellular proteins, interplay between phosphorylation and O-β-GlcNAc modification is believed to be functional switch, but it is very difficult to monitor these functional and vibrant changes in vivo. Netphos 2.0 and Disphos 1.3 programs were used for potential phosphorylation; NetPhosK 1.0 and KinasePhos for kinase prediction; and YinOYang 1.2 and OGPET to predict possible O-glycosylation sites. We also identified Yin Yang sites that may have potential for O-β-GlcNAc and phosphorylation interplay at same Ser/Thr residues. We for the first time proposed that alternate phosphorylation and O-β-GlcNAc modification on Ser 192, Ser 205, Ser 206; and Thr 191 may provide an on/off switch to regulate assembly of claudin-1 at tight junctions. In addition these phosphorylation sites may be targeted by novel chemotherapeutic agents to prevent phosphorylation lead by HCV viral entry complex

A brief review on molecular, genetic and imaging techniques for HCV fibrosis evaluation

<p>Abstract</p> <p>Background</p> <p>Chronic HCV is one of the major causes of morbidity and mortality in the present day world. The assessment of disease progression not only provides useful information for diagnosis and therapeutic supervision judgment but also for monitoring disease. Different invasive and non invasive methods are applied to diagnose the disease from initial to end stage (mild fibrosis to cirrhosis). Although, liver biopsy is still considered as gold standard to identify liver histological stages, an assessment of the disease development based on non-invasive clinical findings is also emerging and this may replace the need of biopsy in near future. This review gives brief insight on non-invasive methods currently available for predicting liver fibrosis in HCV with their current pros and cons to make easier for a clinician to choose better marker to assess liver fibrosis in HCV infected patients.</p> <p>Methods</p> <p>More than 200 studies regarding invasive and noninvasive markers available for HCV liver disease diagnosis were thoroughly reviewed. We examined year wise results of these markers based on their sensitivity, specificity, PPV, NPV and AUROCs.</p> <p>Results</p> <p>We found that in all non-invasive serum markers for HCV, FibroTest, Forn's Index, Fibrometer and HepaScore have high five-year predictive value but with low AUROCs (0.60~0.85) and are not comparable to liver biopsy (AUROC = 0.97). Even though from its beginning, Fibroscan is proved to be best with high AUROCs (> 0.90) in all studies, no single noninvasive marker is able to differentiate all fibrosis stages from end stage cirrhosis. Meanwhile, specific genetic markers may not only discriminate fibrotic and cirrhotic liver but also differentiate individual fibrosis stages.</p> <p>Conclusions</p> <p>There is a need of marker which accurately determines the stage based on simplest routine laboratory test. Genetic marker in combination of imaging technique may be the better non invasive diagnostic method in future.</p

NS4A protein as a marker of HCV history suggests that different HCV genotypes originally evolved from genotype 1b

<p>Abstract</p> <p>Background</p> <p>The 9.6 kb long RNA genome of Hepatitis C virus (HCV) is under the control of RNA dependent RNA polymerase, an error-prone enzyme, for its transcription and replication. A high rate of mutation has been found to be associated with RNA viruses like HCV. Based on genetic variability, HCV has been classified into 6 different major genotypes and 11 different subtypes. However this classification system does not provide significant information about the origin of the virus, primarily due to high mutation rate at nucleotide level. HCV genome codes for a single polyprotein of about 3011 amino acids which is processed into structural and non-structural proteins inside host cell by viral and cellular proteases.</p> <p>Results</p> <p>We have identified a conserved NS4A protein sequence for HCV genotype 3a reported from four different continents of the world i.e. Europe, America, Australia and Asia. We investigated 346 sequences and compared amino acid composition of NS4A protein of different HCV genotypes through Multiple Sequence Alignment and observed amino acid substitutions C₂₂, V₂₉, V₃₀, V₃₈, Q₄₆and Q₄₇in NS4A protein of genotype 1b. Furthermore, we observed C₂₂and V₃₀as more consistent members of NS4A protein of genotype 1a. Similarly Q₄₆and Q₄₇in genotype 5, V₂₉, V₃₀, Q₄₆and Q₄₇in genotype 4, C₂₂, Q₄₆and Q₄₇in genotype 6, C₂₂, V₃₈, Q₄₆and Q₄₇in genotype 3 and C₂₂in genotype 2 as more consistent members of NS4A protein of these genotypes. So the different amino acids that were introduced as substitutions in NS4A protein of genotype 1 subtype 1b have been retained as consistent members of the NS4A protein of other known genotypes.</p> <p>Conclusion</p> <p>These observations indicate that NS4A protein of different HCV genotypes originally evolved from NS4A protein of genotype 1 subtype 1b, which in turn indicate that HCV genotype 1 subtype 1b established itself earlier in human population and all other known genotypes evolved later as a result of mutations in HCV genotype 1b. These results were further confirmed through phylogenetic analysis by constructing phylogenetic tree using NS4A protein as a phylogenetic marker.</p

3D models of radiatively driven colliding winds in massive O+O star binaries - II. Thermal radio to sub-mm emission

In this work the thermal emission over cm to sub-mm wavelengths from the winds in short-period O+O-star binaries is investigated (potential non-thermal emission is presently ignored). The calculations are based on three-dimensional hydrodynamical models which incorporate gravity, the driving of the winds, orbital motion of the stars, and radiative cooling of the shocked plasma. The thermal emission arises from the stellar winds and the region where they collide. We investigate the flux and spectrum from a variety of models as a function of orbital phase and orientation of the observer, and compare to the single star case. The emission from the wind-wind collision region (WCR) is strongly dependent on its density and temperature, being optically thick in radiative systems, and optically thin in adiabatic systems. The flux from systems where the WCR is highly radiative, as investigated for the first time in this work, can be over an order of magnitude greater than the combined flux from identically typed single stars. This excess occurs over a broad range of wavelengths from cm to sub-mm. In contrast, when the WCR is largely adiabatic, a significant excess in the thermal flux occurs only below 100 GHz. Eccentric systems may show order of magnitude or greater flux variability, especially if the plasma in the WCR transitions from an adiabatic to a radiative state and vice-versa - in such cases the flux can display significant hysteresis with stellar separation. We further demonstrate that clumping can affect the variability of radio lightcurves. We investigate the spectral index of the emission, and often find indices steeper than +0.6. Our predictions are of interest to future observations with the next generation of radio and sub-mm telescopes (abridged).Comment: 25 pages, 21 figures, accepted for publication in MNRA

Observed Consequences of Presupernova Instability in Very Massive Stars

This chapter concentrates on the deaths of very massive stars, the events leading up to their deaths, and how mass loss affects the resulting death. The previous three chapters emphasized the theory of wind mass loss, eruptions, and core collapse physics, but here we emphasize mainly the observational properties of the resulting death throes. Mass loss through winds, eruptions, and interacting binaries largely determines the wide variety of different types of supernovae that are observed, as well as the circumstellar environments into which the supernova blast waves expand. Connecting these observed properties of the explosions to the initial masses of their progenitor stars is, however, an enduring challenge and is especially difficult for very massive stars. Superluminous supernovae, pair instability supernovae, gamma ray bursts, and "failed" supernovae are all end fates that have been proposed for very massive stars, but the range of initial masses or other conditions leading to each of these (if they actually occur) are still very certain. Extrapolating to infer the role of very massive stars in the early universe is essentially unencumbered by observational constraints and still quite dicey.Comment: 39 pages, 5 figures, to appear as chapter in the book "Very Massive Stars in the Local Universe", ed. J. Vin