Tuning of reduced graphene oxide thin film as an efficient electron conductive interlayer in a proven heterojunction photoanode for solar-driven photoelectrochemical water splitting

Although bismuth vanadate (BiVO4) has shown excellent photoelectrochemical (PEC) properties and is a good candidate of photoanode materials, the solar-driven PEC water splitting performance is still remained below its full potential due to the fast recombination and sluggish charge mobility of photogenerated charge carriers. Previously, we have communicated a proven Type II staggered vanadium pentoxide (V2O5)/BiVO4 heterojunction photoanode that could improve the photocurrent density. This study aimed to examine the effect of introducing an rGO thin film as an efficient electron conductive interlayer in a proven V2O5/BiVO4 heterojunction photoanode, and subsequently tuning the rGO film thickness in achieving the optimum PEC performance. The resultant ternary photoanode structure of V2O5/rGO/BiVO4 was characterised by using field emission-scanning electron microscopy (FE-SEM), high resolution-transmission electron microscopy (HR-TEM), UV–vis spectroscopy, X-ray diffractometer (XRD), Raman spectroscopy and photoluminescence (PL) measurements. Results showed that the interlayer rGO thin film arising from the sequential drop cast and electrochemical reduction of 320 μL ultrasonicated GO solution resulted in the optimal photocurrent density of 2.1 mA/cm2 at 1.5 V vs. Ag/AgCl. Furthermore, the chemical physics surrounding the photogenerated charge carrier transfer for heterojunction V2O5/BiVO4 was validated for the structure with and without the rGO interlayer. In particular, the electrochemical impedance spectroscopy (EIS) was used to measure multiple resistances at the FTO/semiconductor, semiconductor/semiconductor and semiconductor/electrolyte interfaces. Additionally, the charge transfer (Kt) and recombination (Kr) rate constants for the heterojunction V2O5/BiVO4 with the rGO interlayer were quantified using intensity modulated photocurrent spectroscopy (IMPS). Finally, the PEC H2 evolution rate from the ternary V2O5/rGO/BiVO4 photoanode was measured to be 32.7 μ mol/hr, which was about 3-fold higher than the bare V2O5/BiVO4 heterojunction photoanode

Endoplasmic reticulum stress and oxidative stress: A vicious nexus implicated in bowel disease pathophysiology

The endoplasmic reticulum (ER) is a complex protein folding and trafficking organelle. Alteration and discrepancy in the endoplasmic reticulum environment can affect the protein folding process and hence, can result in the production of misfolded proteins. The accumulation of misfolded proteins causes cellular damage and elicits endoplasmic reticulum stress. Under such stress conditions, cells exhibit reduced functional synthesis, and will undergo apoptosis if the stress is prolonged. To resolve the ER stress, cells trigger an intrinsic mechanism called an unfolded protein response (UPR). UPR is an adaptive signaling process that triggers multiple pathways through the endoplasmic reticulum transmembrane transducers, to reduce and remove misfolded proteins and improve the protein folding mechanism, in order to improve and maintain endoplasmic reticulum homeostasis. An increasing number of studies support the view that oxidative stress has a strong connection with ER stress. During the protein folding process, reactive oxygen species are produced as by-products, leading to impaired reduction-oxidation (redox) balance conferring oxidative stress. As the protein folding process is dependent on redox homeostasis, the oxidative stress can disrupt the protein folding mechanism and enhance the production of misfolded proteins, causing further ER stress. It is proposed that endoplasmic reticulum stress and oxidative stress together play significant roles in the pathophysiology of bowel diseases

Role of oxidative stress in the pathology and management of human tuberculosis

Copyright © 2018 Madhur D. Shastri et al. Tuberculosis (TB), caused by the bacterium Mycobacterium tuberculosis, is the leading cause of mortality worldwide due to a single infectious agent. The pathogen spreads primarily via aerosols and especially infects the alveolar macrophages in the lungs. The lung has evolved various biological mechanisms, including oxidative stress (OS) responses, to counteract TB infection. M. tuberculosis infection triggers the generation of reactive oxygen species by host phagocytic cells (primarily macrophages). The development of resistance to commonly prescribed antibiotics poses a challenge to treat TB; this commonly manifests as multidrug resistant tuberculosis (MDR-TB). OS and antioxidant defense mechanisms play key roles during TB infection and treatment. For instance, several established first-/second-line antitubercle antibiotics are administered in an inactive form and subsequently transformed into their active form by components of the OS responses of both host (nitric oxide, S-oxidation) and pathogen (catalase/peroxidase enzyme, EthA). Additionally, M. tuberculosis has developed mechanisms to survive high OS burden in the host, including the increased bacterial NADH/NAD+ ratio and enhanced intracellular survival (Eis) protein, peroxiredoxin, superoxide dismutases, and catalases. Here, we review the interplay between lung OS and its effects on both activation of antitubercle antibiotics and the strategies employed by M. tuberculosis that are essential for survival of both drug-susceptible and drug-resistant bacterial subtypes. We then outline potential new therapies that are based on combining standard antitubercular antibiotics with adjuvant agents that could limit the ability of M. tuberculosis to counter the host's OS response

The complex interplay between endoplasmic reticulum stress and the NLRP3 inflammasome: a potential therapeutic target for inflammatory disorders.

Inflammation is the result of a complex network of cellular and molecular interactions and mechanisms that facilitate immune protection against intrinsic and extrinsic stimuli, particularly pathogens, to maintain homeostasis and promote tissue healing. However, dysregulation in the immune system elicits excess/abnormal inflammation resulting in unintended tissue damage and causes major inflammatory diseases including asthma, chronic obstructive pulmonary disease, atherosclerosis, inflammatory bowel diseases, sarcoidosis and rheumatoid arthritis. It is now widely accepted that both endoplasmic reticulum (ER) stress and inflammasomes play critical roles in activating inflammatory signalling cascades. Notably, evidence is mounting for the involvement of ER stress in exacerbating inflammasome-induced inflammatory cascades, which may provide a new axis for therapeutic targeting in a range of inflammatory disorders. Here, we comprehensively review the roles, mechanisms and interactions of both ER stress and inflammasomes, as well as their interconnected relationships in inflammatory signalling cascades. We also discuss novel therapeutic strategies that are being developed to treat ER stress- and inflammasome-related inflammatory disorders

Intrusion detection routers: Design, implementation and evaluation using an experimental testbed

In this paper, we present the design, the implementation details, and the evaluation results of an intrusion detection and defense system for distributed denial-of-service (DDoS) attack. The evaluation is conducted using an experimental testbed. The system, known as intrusion detection router (IDR), is deployed on network routers to perform online detection on any DDoS attack event, and then react with defense mechanisms to mitigate the attack. The testbed is built up by a cluster of sufficient number of Linux machines to mimic a portion of the Internet. Using the testbed, we conduct real experiments to evaluate the IDR system and demonstrate that IDR is effective in protecting the network from various DDoS attacks. © 2006 IEEE.published_or_final_versio

Envelope Determinants of Equine Lentiviral Vaccine Protection

Lentiviral envelope (Env) antigenic variation and associated immune evasion present major obstacles to vaccine development. The concept that Env is a critical determinant for vaccine efficacy is well accepted, however defined correlates of protection associated with Env variation have yet to be determined. We reported an attenuated equine infectious anemia virus (EIAV) vaccine study that directly examined the effect of lentiviral Env sequence variation on vaccine efficacy. The study identified a significant, inverse, linear correlation between vaccine efficacy and increasing divergence of the challenge virus Env gp90 protein compared to the vaccine virus gp90. The report demonstrated approximately 100% protection of immunized ponies from disease after challenge by virus with a homologous gp90 (EV0), and roughly 40% protection against challenge by virus (EV13) with a gp90 13% divergent from the vaccine strain. In the current study we examine whether the protection observed when challenging with the EV0 strain could be conferred to animals via chimeric challenge viruses between the EV0 and EV13 strains, allowing for mapping of protection to specific Env sequences. Viruses containing the EV13 proviral backbone and selected domains of the EV0 gp90 were constructed and in vitro and in vivo infectivity examined. Vaccine efficacy studies indicated that homology between the vaccine strain gp90 and the N-terminus of the challenge strain gp90 was capable of inducing immunity that resulted in significantly lower levels of post-challenge virus and significantly delayed the onset of disease. However, a homologous N-terminal region alone inserted in the EV13 backbone could not impart the 100% protection observed with the EV0 strain. Data presented here denote the complicated and potentially contradictory relationship between in vitro virulence and in vivo pathogenicity. The study highlights the importance of structural conformation for immunogens and emphasizes the need for antibody binding, not neutralizing, assays that correlate with vaccine protection. © 2013 Craigo et al

Effects of an irregular bedtime schedule on sleep quality, daytime sleepiness, and fatigue among university students in Taiwan

<p>Abstract</p> <p>Background</p> <p>An irregular bedtime schedule is a prevalent problem in young adults, and could be a factor detrimentally affecting sleep quality. The goal of the present study was to explore the association between an irregular bedtime schedule and sleep quality, daytime sleepiness, and fatigue among undergraduate students in Taiwan.</p> <p>Methods</p> <p>A total of 160 students underwent a semi-structured interview and completed a survey comprising 4 parts: Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), Fatigue Severity Scale (FSS), and a rating of irregular bedtime frequency. Participants were grouped into 3 groups in terms of irregular bedtime frequency: low, intermediate, or high according to their 2-week sleep log. To screen for psychological disorders or distress that may have affected responses on the sleep assessment measures, the Chinese health questionnaire-12 (CHQ-12) was also administered.</p> <p>Results</p> <p>We found an increase in bedtime schedule irregularity to be significantly associated with a decrease in average sleep time per day (Spearman r = -0.22, p = 0.05). Multivariate regression analysis revealed that irregular bedtime frequency and average sleep time per day were correlated with PSQI scores, but not with ESS or FSS scores. A significant positive correlation between irregular bedtime frequency and PSQI scores was evident in the intermediate (partial r = 0.18, p = 0.02) and high (partial r = 0.15, p = 0.05) frequency groups as compared to low frequency group.</p> <p>Conclusion</p> <p>The results of our study suggest a high prevalence of both an irregular bedtime schedule and insufficient sleep among university students in Taiwan. Students with an irregular bedtime schedule may experience poor sleep quality. We suggest further research that explores the mechanisms involved in an irregular bedtime schedule and the effectiveness of interventions for improving this condition.</p