Cadmium modulates intestinal Wnt/ß-catenin signaling ensuing intestinal barrier disruption and systemic inflammation.

The intricate architecture of the intestinal epithelium, crucial for nutrient absorption, is constantly threatened by environmental factors. The epithelium undergoes rapid turnover, which is essential for maintaining homeostasis, under the control of intestinal stem cells (ISCs). The central regulator, Wnt/ß-catenin signaling plays a key role in intestinal integrity and turnover. Despite its significance, the impact of environmental factors on this pathway has been largely overlooked. This study, for the first time, investigates the influence of Cd on the intestinal Wnt signaling pathway using a mouse model. In this study, male BALB/c mice were administered an environmentally relevant Cd dose (0.98 mg/kg) through oral gavage to investigate the intestinal disruption and Wnt signaling pathway. Various studies, including histopathology, immunohistochemistry, RT-PCR, western blotting, ELISA, intestinal permeability assay, and flow cytometry, were conducted to study Cd-induced changes in the intestine. The canonical Wnt signaling pathway experienced significant downregulation as a result of sub-chronic Cd exposure, which caused extensive damage throughout the small intestine. Increased intestinal permeability and a skewed immune response were also observed. To confirm that Wnt signaling downregulation is the key driver of Cd-induced gastrointestinal toxicity, mice were co-exposed to LiCl (a recognized Wnt activator) and Cd. The results clearly showed that the harmful effects of Cd could be reversed, which is strong evidence that Cd mostly damages the intestine through the Wnt/ß-catenin signalling axis. In conclusion, this research advances the current understanding of the role of Wnt/ß catenin signaling in gastrointestinal toxicity caused by diverse environmental pollutants.

Use of antioxidants to retard aging of bitumen: A review.

Oxidative aging of bitumen is an inevitable and irreversible phenomenon. Exposure to detrimental factors such as sunlight, oxygen, and UV radiations accelerates the aging of bitumen and bituminous pavement. The aging process induces hardening and embrittlement in bitumen, leading to premature pavement failure. Therefore, for constructing sustainable long-lasting pavements anti-aging additives are used. Among the available additives, the use of antioxidants has emerged as a promising solution to mitigate the aging of bitumen. The current review aims to summarise the existing literature for a comprehensive understanding of the effectiveness of these additives as aging inhibitors. It provides an overview of the chemical pathway involved during bitumen oxidation and various quantification techniques to measure the effect of aging. This review also highlights the potential use of antioxidants in bitumen and elaborates on the working mechanism of different types of antioxidants to prevent bitumen aging. Further, the effect of modification in bitumen at micro, macro, and mixture levels are discussed. Additionally, cost analysis and future prospects on the use of antioxidants for bitumen are presented.

Valorization of sugarcane bagasse with in situ grown MoS2 for continuous pollutant remediation and microbial decontamination.

In this study, sugarcane bagasse (SB) was strategically subjected to a delignification process followed by the in situ growth of multi-layered molybdenum disulfide (MoS2) nanosheets with hexagonal phase (2H-phase) crystal structure via hydrothermal treatment. The MoS2 nanosheets underwent self-assembly to form nanoflower-like structures in the aligned cellulose inter-channels of delignified sugarcane bagasse (DSB), the mechanism of which was understood through FTIR and XPS spectroscopic studies. DSB, due to its porous morphology and abundant hydroxyl groups, shows remediation capabilities of methylene blue (MB) dye through physio-sorption but shows a low adsorption capacity of 80.21 mg/g. To improve the removal capacity, DSB after in situ growth of MoS2 (DSB-MoS2) shows enhanced dye degradation to 114.3 mg/g (in the dark) which further improved to 158.74 mg/g during photodegradation, due to catalytically active MoS2. Interestingly, DSB-MoS2 was capable of continuous dye degradation with recyclability for three cycles, reaching an efficiency of > 83%, along with a strong antibacterial response against Gram-positive Staphylococcus aureus (S.aureus) and Gram-negative Escherichia coli (E. coli). The present study introduces a unique strategy for the up-conversion of agricultural biomass into value-added bio-adsorbents, which can effectively and economically address the remediation of dyes with simultaneous microbial decontamination from polluted wastewater streams.

Structural inscrutabilities of Histone (H2BK123) monoubiquitination: A systematic review.

Histone H2B monoubiquitination in budding yeast is a highly conserved post-translational modification. It is involved in normal functions of the cells like DNA Repair, RNA Pol II activation, trans-histone H3K and H79K methylation, meiosis, vesicle budding, etc. Deregulation of H2BK123ub can lead to the activation of proto-oncogenes and is also linked to neurodegenerative and heart diseases. Recent discoveries have enhanced the mechanistic underpinnings of H2BK123ub. For the first time, the Rad6's acidic tail has been implicated in histone recognition and interaction with Bre1's RBD domain. The non-canonical backside of Rad6 showed inhibition in polyubiquitination activity. Bre1 domains RBD and RING play a role in site-specific ubiquitination. The role of single Alaline residue in Rad6 activity. Understanding the mechanism of ubiquitination before moving to therapeutic applications is important. Current advancements in this field indicate the creation of novel therapeutic approaches and a foundation for further study.