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For both the B2O3-Bi2O3-CaO and B2O3-Bi2O3-SrO glass systems, γ-ray and neutron attenuation qualities were evaluated. Utilizing the Phy-X/PSD program, within the 0.015-15 MeV energy range, linear attenuation coefficients (µ) and mass attenuation coefficients (μ/ρ) were calculated, and the attained μ/ρ quantities match well with respective simulation results computed by MCNPX, Geant4, and Penelope codes. Instead of B2O3/CaO or B2O3/SrO, the Bi2O3 addition causes improved γ-ray shielding competence, i.e., rise in effective atomic number (Zeff) and a fall in half-value layer (HVL), tenth-value layer (TVL), and mean free path (MFP). Exposure buildup factors (EBFs) and energy absorption buildup factors (EABFs) were derived using a geometric progression (G-P) fitting approach at 1-40 mfp penetration depths (PDs), within the 0.015-15 MeV range. Computed radiation protection efficiency (RPE) values confirm their excellent capacity for lower energy photons shielding. Comparably greater density (7.59 g/cm3), larger μ, μ/ρ, Zeff, equivalent atomic number (Zeq), and RPE, with the lowest HVL, TVL, MFP, EBFs, and EABFs derived for 30B2O3-60Bi2O3-10SrO (mol%) glass suggest it as an excellent γ-ray attenuator. Additionally, 30B2O3-60Bi2O3-10SrO (mol%) glass holds a commensurably bigger macroscopic removal cross-section for fast neutrons (ΣR) (=0.1199 cm-1), obtained by applying Phy-X/PSD for fast neutrons shielding, owing to the presence of larger wt% of 'Bi' (80.6813 wt%) and moderate 'B' (2.0869 wt%) elements in it. 70B2O3-5Bi2O3-25CaO (mol%) sample (B 17.5887 wt%, Bi 24.2855 wt%, Ca 11.6436 wt%, and O 46.4821 wt%) shows high potentiality for thermal or slow neutrons and intermediate energy neutrons capture or absorption due to comprised high wt% of 'B' element in it.Recent epidemiological studies suggest that prenatal exposure to acetaminophen (APAP) is associated with increased risk of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder affecting 1 in 59 children in the US. Maternal and prenatal exposure to pesticides from food and environmental sources have also been implicated to affect fetal neurodevelopment. However, the underlying mechanisms for ASD are so far unknown, likely with complex and multifactorial etiology. The aim of this study was to explore the potential effects of APAP and pesticide exposure on development with regards to the etiology of ASD by highlighting common genes and biological pathways. Genes associated with APAP, pesticides, and ASD through human research were retrieved from molecular and biomedical literature databases. The interaction network of overlapping genetic associations was subjected to network topology analysis and functional annotation of the resulting clusters. These genes were over-represented in pathways and biological processes (FDR p less then 0.05) related to apoptosis, metabolism of reactive oxygen species (ROS), and carbohydrate metabolism. Since these three biological processes are frequently implicated in ASD, our findings support the hypothesis that cell death processes and specific metabolic pathways, both of which appear to be targeted by APAP and pesticide exposure, may be involved in the etiology of ASD. This novel exposures-gene-disease database mining might inspire future work on understanding the biological underpinnings of various ASD risk factors.Taking as a starting point the frequent characterisation of self-harm as "an adolescent thing for girls," this paper offers a sociologically informed, qualitative exploration of self-harm as a gendered practice. We move beyond statistical constructions of this "reality," and critically examine how this characterisation comes to be, and some of its effects. Our data are drawn from a pilot study that developed a collaborative arts-based inquiry into meanings of self-harm. The authors worked with two groups one of practitioners and another of people who had self-harmed, meeting over six sessions to discuss and make art in response to a range of themes relating to the interpretation and explanation of self-harm. Through data generation and analysis, we collaboratively seek to make sense of the gendering of self-harm, focusing on a series of dualistic Cartesian "cuts" between male and female, violence and vulnerability, and inside and outside. In conclusion, we call for more multi- and interdisciplinary explorations of self-harm, and greater use of diverse, arts-based, and qualitative methodologies, in order to further expand and nuance understandings and ethical engagements with self-harm, and those who are affected by it.Chlamydia are Gram-negative, intracellular pathogens colonizing epithelial mucosa. They cause primarily atypical pneumonia and have recently been associated with chronic diseases. Diagnostics relies almost exclusively on serological methods; PCR tests are used rarely because in patients with positive ELISA, it is nearly impossible to identify chlamydial DNA. This paradox is associated with DNA degradation in sputum samples, low abundance, and low sensitivity of PCR systems. see more In a newly designed and validated "nested" PCR (NPCR) assay, it was possible to amplify DNA of Chlamydia known to infect humans in 31% samples. The reliability of the assay was confirmed by DNA sequencing, and all PCR products belonged exclusively to the Chlamydiales, mainly recognized as Chlamydia pneumoniae. Three samples were related to Ca. Rhabdochlamydia porcellionis and Ca. Renichlamydia lutjani, which infect arthropods. In one case, samples were taken from sick individual, indicating the potential as a human pathogen.S-nitrosylation is a selective and reversible post-translational modification of protein thiols by nitric oxide (NO), which is a bioactive signaling molecule, to exert a variety of effects. These effects include the modulation of protein conformation, activity, stability, and protein-protein interactions. S-nitrosylation plays a central role in propagating NO signals within a cell, tissue, and tissue microenvironment, as the nitrosyl moiety can rapidly be transferred from one protein to another upon contact. This modification has also been reported to confer either tumor-suppressing or tumor-promoting effects and is portrayed as a process involved in every stage of cancer progression. In particular, S-nitrosylation has recently been found as an essential regulator of the tumor microenvironment (TME), the environment around a tumor governing the disease pathogenesis. This review aims to outline the effects of S-nitrosylation on different resident cells in the TME and the diverse outcomes in a context-dependent manner.
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