The Highly Durable Antibacterial Gel-like Coatings for Textiles.

Hospital-acquired infections are considered a priority for public health systems since they pose a significant burden for society. High-touch surfaces of healthcare centers, including textiles, provide a suitable environment for pathogenic bacteria to grow, necessitating incorporating effective antibacterial agents into textiles. This paper introduces a highly durable antibacterial gel-like solution, Silver Shell™ finish, which contains chitosan-bound silver chloride microparticles. The study investigates the coating's environmental impact, health risks, and durability during repeated washing. The structure of the Silver Shell™ finish was studied using transmission electron microscopy (TEM) and energy-dispersive X-ray spectroscopy (EDX). The TEM images showed a core-shell structure, with chitosan forming a protective shell around groupings of silver microparticles. The field-emission scanning electron microscopy (FESEM) demonstrated the uniform deposition of Silver Shell™ on the surfaces of the fabrics. AATCC Test Method 100 was employed to quantitatively analyze the antibacterial properties of the fabrics coated with silver microparticles. Two types of bacteria, Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli), were used in this study. The antibacterial results showed that after 75 wash cycles, a 100% reduction for both S. aureus and E. coli in the coated samples using crosslinking agents was observed. The coated samples without a crosslinking agent exhibited 99.88% and 99.81% reductions for S. aureus and E. coli after 50 washing cycles. To compare the antibacterial properties toward non-pathogenic and pathogenic strains of the same species, MG1655 model E. coli strain (ATCC 29213) and a multidrug-resistant clinical isolate were used. The results showed the antibacterial efficiency of the Silver ShellTM solution (up to 99.99% reduction) coated on cotton fabric. AATCC-147 was performed to investigate the coated samples' leaching properties and the crosslinking agent's effects against S. aureus and E. coli. All coated samples demonstrated remarkable antibacterial efficacy, even after 75 wash cycles. The crosslinking agent facilitated durable attachment between the silver microparticles and cotton substrate, minimizing the release of particles from the fabrics. Color measurements were conducted to assess the color differences resulting from the coating process. The results indicated fixation values of 44%, 32%, and 28% following 25, 50, and 75 washing cycles, respectively.

The Highly Durable Antibacterial Gel-like Coatings for Textiles.

Hospital-acquired infections are considered a priority for public health systems, which poses a significant burden for society. High-touch surfaces of healthcare centers, including textiles, provide a suitable environment for pathogenic bacteria to grow, necessitating incorporating effective antibacterial agents into textiles. This paper introduces a highly durable antibacterial gel-like solution, Silver Shell finish, which contains chitosan-bound silver chloride microparticles. The study investigates the coating's environmental impact, health risks, and durability during repeated washing. The structure of the Silver Shell finish was studied using Transmission Electron Microscopy (TEM) and Energy-Dispersive X-ray Spectroscopy (EDX). TEM images showed a core-shell structure, with chitosan forming a protective shell around groupings of silver micro-particles. Field Emission Scanning Electron Microscopy (FESEM) demonstrated the uniform deposition of Silver Shell on the surface of fabrics. AATCC Test Method 100 was employed to quantitatively analyze the antibacterial properties of fabrics coated with silver microparticles. Two types of bacteria, Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) were used in this study. The antibacterial results showed that after 75 wash cycles, a 100% reduction for both S. aureus and E. coli in the coated samples using crosslinking agents was observed. The coated samples without a crosslinking agent exhibited a 99.88% and 99.81% reduction for S. aureus and E. coli after 50 washing cycles. AATCC-147 was performed to investigate the coated samples' leaching properties and the crosslinking agent's effect against S. aureus and E. coli. All coated samples demonstrated remarkable antibacterial efficacy even after 75 wash cycles.

1-deoxysphingolipids bind to COUP-TF to modulate lymphatic and cardiac cell development.

Identification of physiological modulators of nuclear hormone receptor (NHR) activity is paramount for understanding the link between metabolism and transcriptional networks that orchestrate development and cellular physiology. Using libraries of metabolic enzymes alongside their substrates and products, we identify 1-deoxysphingosines as modulators of the activity of NR2F1 and 2 (COUP-TFs), which are orphan NHRs that are critical for development of the nervous system, heart, veins, and lymphatic vessels. We show that these non-canonical alanine-based sphingolipids bind to the NR2F1/2 ligand-binding domains (LBDs) and modulate their transcriptional activity in cell-based assays at physiological concentrations. Furthermore, inhibition of sphingolipid biosynthesis phenocopies NR2F1/2 deficiency in endothelium and cardiomyocytes, and increases in 1-deoxysphingosine levels activate NR2F1/2-dependent differentiation programs. Our findings suggest that 1-deoxysphingosines are physiological regulators of NR2F1/2-mediated transcription.

Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility.

Dioxins are a group of highly persistent chemicals that are generated as by-products of industrial and natural processes. Reduction in sperm counts is among the most sensitive endpoints of dioxin toxicity. The exact mechanism by which dioxins reduce sperm counts is not known. Recent data implicate the role of epididymal factors rather than disruption of spermatogenesis. Studies reviewed here demonstrate that dioxins induce the transfer of environmental conditions to the next generation via male germline following exposures during the window of epigenetic reprogramming of primordial germ cells. Increased incidence of birth defects in offspring of male veterans exposed to dioxin containing, Agent Orange, suggest that dioxins may induce epigenomic changes in male germ cells of adults during spermatogenesis. This is supported by recent animal data that show that environmental conditions can cause epigenetic dysregulation in sperm in the context of specific windows of epigenetic reprogramming during spermatogenesis.

Developmental Exposure to 2,2',4,4'-Tetrabromodiphenyl Ether Induces Long-Lasting Changes in Liver Metabolism in Male Mice.

Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives in a wide range of polymers. The generations born when environmental concentrations of PBDEs reached their maximum account in the United States for one-fifth of the total population. We hypothesized that exposure to PBDEs during sensitive developmental windows might result in long-lasting changes in liver metabolism. The present study was based on experiments with CD-1 mice and human hepatocellular carcinoma cells (human hepatoma cell line, HepG2). Pregnant mice were exposed to 0.2 mg/kg 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) from gestation day 8 until postnatal day 21. The metabolic health-related outcomes were analyzed on postnatal day 21 and postnatal week 20 in male offspring. Several groups of metabolic genes, including ribosomal and mitochondrial genes, were significantly upregulated in the liver at both points. Genes regulated via mechanistic target of rapamycin (mTOR) pathway, the gatekeeper of metabolic homeostasis, were whether up- or downregulated at both measurement points. On postnatal day 21, but not week 20, both mTOR complexes in the liver were activated, as measured by phosphorylation of their targets. mTOR complexes were also activated by BDE-47 in HepG2 cells in vitro. The following changes were observed at week 20: a decreased number of polyploid hepatocytes, suppressed cytoplasmic S6K1, twofold greater blood insulin-like growth factor-1 and triglycerides, and 2.5-fold lower expression of fatty acid uptake membrane receptor CD36 in liver tissue. Thus, perinatal exposure to environmentally relevant doses of BDE-47 in laboratory mice results in long-lasting changes in liver physiology. Our evidence suggests involvement of the mTOR pathway in the observed metabolic programming of the liver.

Perinatal exposure to 2,2',4'4' -Tetrabromodiphenyl ether induces testicular toxicity in adult rats.

Since 1965, polybrominated diphenyl ethers (PBDEs) have been used internationally as flame-retardant additives. PBDEs were recently withdrawn from commerce in North America and Europe due to their environmental persistence, bioaccumulative properties and endocrine-disrupting effects. Generations exposed perinatally to the highest environmental doses of PBDE account for one-fifth of the total United States population. While, toxicity of PBDE for the male reproductive system has been demonstrated in several human and animal studies, the long-lasting effects of perinatal exposures on male reproduction are still poorly understood. In this study, pregnant Wistar rats were exposed to 0.2mg/kg 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) from gestation day 8 until postnatal day 21. Male reproductive outcomes were analyzed on postnatal day 120 in offspring. Exposed animals had significantly smaller testes, displayed decreased sperm production per testis weight, had significantly increased percentage of morphologically abnormal spermatozoa, and showed an increase in spermatozoa head size. Perinatal BDE-47 exposure led to significant changes in testes transcriptome, including suppression of genes essential for spermatogenesis and activation of immune response genes. In particular, we observed a 4-fold average decrease in expression of protamine and transition protein genes in testes, suggesting that histone-protamine exchange may be dysregulated during spermatogenesis, resulting in an aberrant sperm epigenome. The possibility of long-lasting effects of developmental PBDE exposures calls for additional studies to build a foundation for the development of preventive and protective interventions against the environmentally-induced decline in fertility.