Node thickening is a way to strengthen the nodes of a geogrid. Increasing the node thickness in conventional biaxial geogrids enhances the interface frictional strength parameters and improves its ...three-dimensional reinforcement effect. Based on the triaxial tests of aeolian sand, single-rib strip tests of geogrids, and pull-out tests of geogrid in aeolian sand, a three-dimensional discrete element pull-out model for geogrids with strengthened nodes was developed to investigate the mechanical performance of an aeolian sand-geogrid interface. The influences of increasing node thickness, the number of strengthened nodes, and the spacing between adjacent nodes on the mechanical performance of the geogrid-soil interface were extensively studied used the proposed model. The results demonstrated that strengthened nodes effectively optimize the reinforcing performance of the geogrid. Among the three node-thickening methods, that in which both the upper and lower sides of nodes are thickened showed the most significant improvement in ultimate pull-out resistance and interface friction angle. Moreover, when using the same node-thickening method, the ultimate pull-out resistance increase shows a linear relationship with the node thickness increase and the strengthened node quantity. In comparison with the conventional geogrid, the strengthened nodes in a geogrid lead to a wider shear band and a stronger ability to restrain soil displacement. When multiple strengthened nodes are simultaneously applied, there is a collective effect that is primarily influenced by the spacing between adjacent nodes. The results provide a valuable reference for optimizing the performance of geogrids and determining the spacing for geogrid installation.
Sevoflurane exposures were demonstrated to induce neurotoxicity in the developing brain in both human and animal studies. However, there is no effective approach to reverse it. The present study ...aimed to evaluate the feasibility of utilizing docosahexaenoic acid (DHA) to prevent sevoflurane-induced neurotoxicity. P6 (postnatal 6 days) mice were administrated DHA after exposure to 3% sevoflurane for two hours daily in three consecutive days. Molecular expressions of synaptic makers (PSD95, synaptophysin) and synaptic morphological changes were investigated by Western blot analysis and transmission electron microscopy, respectively. Meanwhile, Morris water maze test was used to assess spatial memory of mice at P31 (postnatal 31 days). DHA restored sevoflurane-induced decreased level of PSD95 and synaptophysin expressions and increased PSD areas and also improved long-term spatial memory. These results suggest that DHA could rescue synaptogenesis impairment and long-term memory deficits in postnatal caused by multiple sevoflurane exposures.
A simulation framework combining the coupling fluid method (CFM) and flexible coupling boundary method was developed to simulate drained and undrained triaxial tests. The discrete element method ...(DEM) model was calibrated using consolidated drained (CD) triaxial tests on saturated silt and then used to calculate the drained response of specimens with different initial porosity in both rigid and flexible boundaries. Subsequently, consolidated undrained (CU) triaxial tests were simulated and compared to the constant volume method. The bulk modulus of water was determined, and the reliability of the CFM was verified. On this basis, the DEM model was used to calculate the undrained response of the specimens with different initial porosity by simulating CU triaxial tests. The computed drained/undrained responses, including stress path, deviatoric stress, and shear-induced volumetric strain/pore water pressure, were consistent with the known behavior of silt. This study has promising potential to further enhance the understanding of granular behavior.
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•Flexible coupling boundary was extended to undrained triaxial simulations.•A simulation framework for drained and undrained triaxial tests was developed.•A contact model considering Vander Waals forces was developed for saturated silt.•The effects of porosity and boundary on granular materials were analyzed.
•Methylprednisolone (MP) shows promise in alleviating lung injury in sepsis.•MP regulates the miR-151-5p/USP38 pathway in acute lung injury.•MP enhances pulmonary function and reduces inflammation in ...ALI.•miR-151-5p levels decrease after MP treatment, targeting USP38.•Inhibition of miR-151-5p or overexpression of USP38 enhances MP's effects.
Acute lung injury (ALI) is manifested by increased blood vessel permeability within the lungs and subsequent impairment of alveolar gas exchange. Methylprednisolone (MP) is commonly used as a treatment for ALI to reduce inflammation, yet its molecular mechanism remains unclear. This study aims to explore the underlying mechanisms of MP on ALI in a model induced by lipopolysaccharide (LPS).
The proliferation, viability, apoptosis, and miR-151-5p expression of alveolar type II epithelial cells (AECII) were detected using the cell EdU assay, Annexin V/PI Apoptosis Kit, counting kit-8 (CCK-8) assay, and RT-qPCR. Western blot analysis was used to detect the Usp38 protein level. IL-6 and TNF-α were measured by ELISA. The combination of miR-151-5p and USP38 was determined by chromatin immunoprecipitation (ChIP)-PCR and dual-luciferase reporter assay.
MP greatly improved pulmonary function in vivo, reduced inflammation, and promoted the proliferation of the alveolar type II epithelial cells (AECII) in vitro. By comparing the alterations of microRNAs in lung tissues between MP treatment and control groups, we found that miR-151-5p exhibited a significant increase after LPS-treated AECII, but decreased after MP treatment. Confirmed by a luciferase reporter assay, USP38, identified as a downstream target of miR-151-5p, was found to increase after MP administration. Inhibition of miR-151-5p or overexpression of USP38 in AECII significantly improved the anti-inflammatory, anti-apoptotic, and proliferation-promotive effects of MP.
In summary, our data demonstrated that MP alleviates the inflammation and apoptosis of AECII induced by LPS, and promotes the proliferation of AECII partially via miR-151-5p suppression and subsequent USP38 activation.
BACKGROUND Brain injuries induced by hypoxia-ischemia in neonates contribute to increased mortality and lifelong neurological dysfunction. The specific PKR inhibitor C16 has been previously ...demonstrated to exert a neuroprotective role in adult brain injuries. However, there is no recent study available concerning its protective role in hypoxia-ischemia-induced immature brain damage. Therefore, we investigated whether C16 protects against neonatal hypoxia-ischemia injuries in a neonatal rat model. MATERIAL AND METHODS Postnatal day 7 (P7) rats were used to establish classical hypoxia-ischemia animal models, and C16 postconditioning with 100 ug/kg was performed immediately after hypoxia. Western blot analysis was performed to quantify the phosphorylation of the PKR at 0 h, 3 h, 6 h, 12 h, 24 h, and phosphorylation of NF-κB 24h after hypoxia exposure. The TTC stain for infarction area and TUNEL stain for apoptotic cells were assayed 24 h after the brain hypoxia. Gene expression of IL-1β, IL-6, and TNF-α was performed at 3 h, 6 h, 12 h, and 24 h. RESULTS The level of PKR autophosphorylation was increased dramatically, especially at 3 h (C16 group vs. HI group, P<0.01). Intraperitoneal C16 administration reduced the infarct volume and apoptosis ratio after this insult (C16 group vs. HI group<0.01), and C16 reduced proinflammatory cytokines mRNA expression, partly through inhibiting NF-κB activation (C16 group vs. HI group<0.05). CONCLUSIONS C16 can protect immature rats against hypoxia-ischemia-induced brain damage by modulating neuroinflammation.
In mammals, the most remarkable T cell variations with aging are the shrinking of the naïve T cell pool and the enlargement of the memory T cell pool, which are partially caused by thymic involution. ...However, the mechanism underlying the relationship between T‐cell changes and aging remains unclear. In this study, we find that T‐cell‐specific Rip1 KO mice show similar age‐related T cell changes and exhibit signs of accelerated aging‐like phenotypes, including inflammation, multiple age‐related diseases, and a shorter lifespan. Mechanistically, Rip1‐deficient T cells undergo excessive apoptosis and promote chronic inflammation. Consistent with this, blocking apoptosis by co‐deletion of Fadd in Rip1‐deficient T cells significantly rescues lymphopenia, the imbalance between naïve and memory T cells, and aging‐like phenotypes, and prolongs life span in T‐cell‐specific Rip1 KO mice. These results suggest that the reduction and hyperactivation of T cells can have a significant impact on organismal health and lifespan, underscoring the importance of maintaining T cell homeostasis for healthy aging and prevention or treatment of age‐related diseases.
Synopsis
T‐cell specific Rip1 KO mice show signs of accelerated aging‐like phenotypes, along with premature death. Blocking apoptosis by co‐deleting Fadd in Rip1tKO mice significantly rescues aging‐like phenotypes and prolongs shortened lifespan.
Rip1tKO mice show similar age‐related T cell changes and exhibit signs of accelerated aging and a shorter lifespan.
Rip1‐deficient T cells undergo excessive apoptosis, promoting chronic inflammation.
Blocking necroptosis has little effect on the multimorbidity and premature aging seen in Rip1tKO mice.
Blocking T cell apoptosis by co‐deleting Fadd rescues premature aging and multimorbidity in Rip1tKO mice.
T‐cell specific Rip1 KO mice show signs of accelerated aging‐like phenotypes, along with premature death. Blocking apoptosis by co‐deleting Fadd in Rip1tKO mice significantly rescues aging‐like phenotypes and prolongs shortened lifespan.
Acute lung injury (ALI) is characterized by dramatic lung inflammation and alveolar epithelial cell death. Although protein kinase R (PKR) (double-stranded RNA-activated serine/threonine kinase) has ...been implicated in inflammatory response to bacterial cell wall components, whether it plays roles in lipopolysaccharide (LPS)-induced ALI remains unclear. This study was aimed to reveal whether and how PKR was involved in LPS-induced ALI pathology and the potential effects of its specific inhibitor, C16 (C
13
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OS). During the experiment, mice received C16 (100 or 500 ug/kg) intraperitoneally 1 h before intratracheal LPS instillation. Then, whole lung lavage was collected for analysis of total protein levels and proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6. The lungs were tested for Western blot, transferase-mediated dUTP nick-end labeling (TUNEL) stain and immunohistochemistry. Results showed that PKR phosphorylation increased significantly after LPS instillation. Furthermore, PKR specific inhibition attenuated LPS-induced lung injury (hematoxylin and eosin stain), reduced lung protein permeability (total protein levels in whole lung lavage) and suppressed proinflammatory cytokines (TNF-α, IL-1β and IL-6) and lung apoptosis (TUNEL stain and caspase3 activation). Moreover, mechanism-study showed that C16 significantly suppressed I kappa B kinase (IKK)/I kappa B alpha (IκBα)/NF-κB signaling pathway after LPS challenge. These findings suggested that PKR inhibition ameliorated LPS-induced lung inflammation and apoptosis in mice by suppressing NF-κB signaling pathway.
Layered materials have great potential as cathodes for aqueous zinc‐ion batteries (AZIBs) because of their facile 2D Zn2+ transport channels; however, either low capacity or poor cycling stability ...limits their practical applications. Herein, two classical layered materials are innovatively combined by intercalating graphene into MoS2 gallery, which results in significantly enlarged MoS2 interlayers (from 0.62 to 1.16 nm) and enhanced hydrophilicity. The sandwich‐structured MoS2/graphene nanosheets self‐assemble into a flower‐like architecture that facilitates Zn‐ion diffusion, promotes electrolyte infiltration, and ensures high structural stability. Therefore, this novel MoS2/graphene nanocomposite exhibits exceptional high‐rate capability (285.4 mA h g−1 at 0.05 A g−1 with 141.6 mA h g−1 at 5 A g−1) and long‐term cycling stability (88.2% capacity retention after 1800 cycles). The superior Zn2+ migration kinetics and desirable pseudocapacitive behaviors are confirmed by electrochemical measurements and density functional theory computations. The energy storage mechanism regarding the highly reversible phase transition between 2H‐ and 1T‐MoS2 upon Zn‐ion insertion/extraction is elucidated through ex situ investigations. As a proof of concept, a flexible quasi‐solid‐state zinc‐ion battery employing the MoS2/graphene cathode demonstrates great stability under different bending conditions. This study paves a new direction for the design and on‐going development of 2D materials as high‐performance cathodes for AZIBs.
A novel sandwich‐like heterostructure of intercalating graphene into a MoS2 gallery significantly enlarges the MoS2 interlayer spacing from 0.62 to 1.16 nm and simultaneously enhances the hydrophilicity. These structural merits enable facilitated Zn‐ion diffusion kinetics and a highly reversible phase transition between 2H‐ and 1T‐MoS2 upon Zn2+ insertion/extraction, thus rendering a splendid high‐rate capability and long‐term cycling stability in aqueous Zn‐ion batteries.
Aqueous Zn‐ion batteries (AZIBs) are considered as promising large‐scale energy storage devices due to their high safety and low cost. Transition metal dichalcogenides (TMDs) as the potential aqueous ...Zn‐storage cathode materials are under the research spotlight because of their facile 2D ion‐transport channels and weak electrostatic interactions with Zn2+. In this concept article, we summarize the intrinsic structural features and aqueous Zn‐storage mechanisms of the TMDs‐based electrodes. More significantly, the latest design concepts of TMDs materials for high‐performance AZIBs are discussed in detail from three aspects of interlayer expansion engineering, phase transition engineering, and structure defects engineering. Finally, the current challenges facing TMDs cathodes and possible remedies are outlined for future developments towards efficient, rapid, and stable aqueous Zn‐ion storage.
Transition metal dichalcogenides (TMDs) are widely investigated as cathodes for aqueous Zn‐ion batteries (AZIBs) due to their facile 2D Zn‐ion transport channels and weak electrostatic interactions with Zn2+. This concept article discusses the latest design strategies of TMDs cathodes for high‐performance AZIBs from the aspects of Zn‐storage mechanism optimization, interlayer expansion, phase transition, and structure defects creation.
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