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Background: Researches have shown that chronic inhalation of cigarette smoke (CS) disrupts male reproductive system, but it is unclear about the mechanisms behind reproductive damages by tobacco toxicants in male rats. This study was designed to explore the effects of heated tobacco products (HTP) aerosols and CS exposure on the testicular health of rats. Materials and Methods: Experiments were performed on male SD rats exposed to filtered air, HTP aerosols at 10 μg/L, 23 μg/L, and 50 μg/L nicotine-equivalent contents, and also CS at 23 μg/L nicotine-equivalent content for 90 days in five exposure groups (coded as sham, HTP_10, HTP_23, HTP_50 and Cig_23). The expression of serum testosterone, testicular tissue inflammatory cytokines (IL-1β, IL-6, IL-10, TNF-α), reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA), NLRP3 inflammasome-related mRNAs and proteins (NLRP3, ASC, and Caspase-1), the degree of pyroptosis and histopathology were investigated. Results: The results demonstrated that HTP_50 and Cig_23 caused varying degrees of oxidative damage to rat testis, resulting in a decrease of sperm quantity and serum testosterone contents, an increase in the deformity rate, expression levels of proinflammatory cytokines, and NLRP3 inflammasome-related mRNA, and an increase in the NLRP3, ASC, and Caspase-1-immunopositive cells, pyroptosis cell indices, and histopathological damage in the testes of rats. Responses from the HTP_10 and HTP_23 groups were less than those found in the above two exposure groups. Conclusion: These findings indicate that HTP_50 and Cig_23 induced oxidative stress in rat testes, induced inflammation and pyroptosis through the ROS/NLRP3/Caspase-1 pathway, and destroyed the integrity of thetesticular tissue structure. [ABSTRACT FROM AUTHOR]

Interfacial fluids are ubiquitous in systems ranging from biological membranes to chemical droplets and exhibit a complex behavior due to their nonlinear, multiphase, and multicomponent nature. The development of accurate coarse-grained (CG) models for such systems poses significant challenges, as these models must effectively capture the intricate many-body interactions, both inter- and intramolecular, arising from atomic-level phenomena, and account for the diverse density distributions and fluctuations at the interface. In this study, we use advanced machine learning techniques incorporating force matching and diffusion probabilistic models to construct a robust CG model of interfacial fluids. We evaluate our model through simulations in various settings, including the water-air interface, bulk decane, and dipalmitoylphosphatidylcholine monolayer membranes. Our results show that our CG model accurately reproduces the essential many-body and interfacial properties of interfacial fluids and proves effective across different CG mapping strategies. This work not only validates the utility of our model for multiscale simulations, but also lays the groundwork for future improvements in the simulation of complex interfacial systems., (© 2024 Author(s). Published under an exclusive license by AIP Publishing.)

The endothelial glycocalyx layer (EGL) plays a crucial role in regulating blood flow in microvessels. Experimental evidence suggests that there is greater blood flow resistance in vivo compared to in vitro, partially due to the presence of the EGL. However, the complex relationship between EGL deformation and blood cell behavior in shear flow and its quantification remains incompletely understood. To address this gap, we employ a particle-based numerical simulation technique to examine the interaction of the EGL with flowing red blood cells (RBCs) in microtubes. We examine changes in EGL deformation in response to variations in shear rate, EGL graft density, and contour height. Our results indicate that the alterations in EGL height are influenced by the mechanical properties of the EGL, flow conditions, and the RBC-EGL interaction. The flowing RBC compresses the EGL, causing a notable reduction in EGL height near the RBC flow. Additionally, we find that the presence of the EGL in the microtube results in increased RBC deformation and a wider gap between the RBC and tube wall due to spatial occupancy. The significant impact of the EGL on RBC flow is particularly evident in microtubes with diameters ranging from 7 to 10µm, a range consistent with notable differences in vascular flow resistance observed between in vivo and in vitro experiments. The simulation results shed insight on the dynamic interplay between RBC and the EGL in microvascular blood flow.

The growing world population and increasing life expectancy are driving the need to improve the quality of blood transfusion, organ transplantation, and preservation. Here, to improve the ability of red blood cells (RBCs) for normothermic machine perfusion, a biocompatible blood silicification approach termed "shielding-augmenting RBC-in-nanoscale amorphous silica (SARNAS)" has been developed. The key to RBC surface engineering and structure augmentation is the precise control of the hydrolysis form of silicic acid to realize stabilization of RBC within conformal nanoscale silica-based exoskeletons. The formed silicified RBCs (Si-RBCs) maintain membrane/structural integrity, normal cellular functions (e.g., metabolism, oxygen-carrying capability), and enhance resistance to external stressors as well as tunable mechanical properties, resulting in nearly 100% RBC cryoprotection. In vivo experiments confirm their excellent biocompatibility. By shielding RBC surface antigens, the Si-RBCs provide universal blood compatibility, the ability for allogeneic mechanical perfusion, and more importantly, the possibility for cross-species transfusion. Being simple, reliable, and easily scalable, the SARNAS strategy holds great promise to revolutionize the use of engineered blood for future clinical applications., Competing Interests: Competing interests statement:The authors declare no competing interest.

Introduction: Smoking is one of the most important predisposing factors of intestinal inflammatory diseases. Heated tobacco product (HTP) is a novel tobacco category that is claimed to deliver reduced chemicals to human those reported in combustible cigarette smoke (CS). However, the effect of HTP on intestine is still unknown., Methods: In the framework of Organization for Economic Co-operation and Development guidelines 413 guidelines, Sprague-Dawley rats were exposed to HTP aerosol and CS for 13 weeks. The atmosphere was characterized and oxidative stress and inflammation of intestine were investigated after exposure. Furthermore, the faeces we performed with 16S sequencing and metabolomics analysis., Results: HTP aerosol and CS led to obvious intestinal damage evidenced by increased intestinal pro-inflammatory cytokines and oxidative stress in male and female rats After HTP and CS exposure, the abundance that obviously changed were Lactobacillus and Turiciacter in male rats and Lactobacillus and Prevotella in female rats. HTP mainly induced the metabolism of amino acids and fatty acyls such as short-chain fatty acids and tryptophan, while CS involved into the main metabolism of bile acids, especially indole and derivatives. Although different metabolic pathways in the gut mediated by HTP and CS, both to inflammation and oxidative stress were ultimately induced., Conclusions: HTP aerosol and CS induced intestinal damage mediated by different gut microbiota and metabolites, while both lead to inflammation and oxidative stress., Implications: The concentration of various harmful components in heated tobacco product aerosol is reported lower than that of traditional cigarette smoke, however, its health risk impact on consumers remains to be studied. Our research findings indicate that heated tobacco product and cigarette smoke inhalation induced intestinal damage through different metabolic pathways mediated by gut microbiome, indicating the health risk of heated tobacco product in intestine., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)