Illumination Intelligent Adaptation and Analysis Framework: A comprehensive solution for enhancing nighttime driving fatigue monitoring.

Nighttime driving presents a critical challenge to road safety due to insufficient lighting and increased risk of driver fatigue. Existing methods for monitoring driver fatigue, mainly focusing on behavioral analysis and biometric monitoring, face significant challenges under low-light conditions. Their effectiveness, especially in dynamic lighting environments, is limited by their dependency on specific environmental conditions and active driver participation, leading to reduced accuracy and practicality in real-world scenarios. This study introduces a novel 'Illumination Intelligent Adaptation and Analysis Framework (IIAAF)', aimed at addressing these limitations and enhancing the accuracy and practicality of driver fatigue monitoring under nighttime low-light conditions. The IIAAF framework employs a multidimensional technology integration, including comprehensive body posture analysis and facial fatigue feature detection, per-pixel dynamic illumination adjustment technology, and a light variation feature learning system based on Convolutional Neural Networks (CNN) and time-series analysis. Through this integrated approach, the framework is capable of accurately capturing subtle fatigue signals in nighttime driving environments and adapting in real-time to rapid changes in lighting conditions. Experimental results on two independent datasets indicate that the IIAAF framework significantly improves the accuracy of fatigue detection under nighttime low-light conditions. This breakthrough not only enhances the effectiveness of driving assistance systems but also provides reliable scientific support for reducing the risk of accidents caused by fatigued driving. These research findings have significant theoretical and practical implications for advancing intelligent driving assistance technology and improving nighttime road safety.

Simulation study on creep deformation of the impeller in lead-bismuth eutectic environment through fluid-solid coupling method.

Lead-based reactor is a new type of reactor using liquid lead or lead-bismuth alloy as a coolant. As the core working element of the main pump, the impeller is subjected to a huge load when conveying heavy metal liquids and is highly susceptible to damage. In this study, we used ANSYS and FLUENT software to investigate the stress, deformation, and creep deformation of the nuclear main pump impeller under a liquid lead-bismuth environment by the fluid-solid coupling method. The maximum equivalent force of the impeller was located at the junction of the blade and hub, which was prone to fatigue damage under the action of alternating load. The stress, deformation, and creep characteristics of the impeller blade were observed to generally increase with rotational speed. Particularly, the junction of the blade root and hub exhibited high susceptibility to stress concentration and fatigue damage. At a flow rate of 0.64 m/s and a speed of 690 r/min, the maximum equivalent force was 16.7 MPa, which was lower than the yield strength of 316L stainless steel. Additionally, the maximum deformation was less than 0.63 mm. Over a five-year period, the creep of the impeller ranged from a minimum of 0.228% to a maximum of 0.447%, indicating that the impeller can reliably operate in a liquid lead-bismuth environment for at least five years.

Exploring the mechanism of Astragali radix for promoting osteogenic differentiation based on network pharmacology, molecular docking, and experimental validation.

The present study used network pharmacology and molecular docking to predict the active ingredients and mechanisms of action of Astragalus radix (AR) to promote osteogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs), and cell experiments were conducted for verification. First, network pharmacology was used to predict the effective components, targets, and mechanisms of action of AR to promote osteogenic differentiation. The effective components and corresponding target proteins of AR, and the target proteins of osteogenic differentiation were collected through the database. The intersection targets of the two were used for the construction and analysis of a protein-protein interaction (PPI) network. Gene Oncology (GO) and Kyoto Encyclopedia of Genes, and Genomes (KEGG) enrichment analyses were conducted. Next, molecular docking technology was carried out to verify the interaction between the active ingredient and the target protein, and to select the appropriate effective active ingredient. Finally, the results of network pharmacology analysis were verified by in vitro experiments. A total of 95 potential targets were retrieved by searching the intersection of AR and osteogenic differentiation targets. PPI network analysis indicated that RAC-α-serine-threonine-protein kinase (Akt1) was considered to be the most reliable target for AR to regulate osteogenic differentiation. GO enrichment analysis included 21 biological processes, 21 cellular components and 100 molecular functions. KEGG enrichment analysis indicated that the class I phosphatidylinositol-3 kinase (PI3K)-serine-threonine kinase (Akt) signaling pathway may play an important role in promoting osteogenic differentiation. The results of molecular docking showed that quercetin's performance was improved compared with that of kaempferol. In vitro experiments showed that quercetin promoted the expression of osteogenic marker proteins (including collagen I, Runt-related transcription factor 2 and osteopontin) in BMSCs and activated the PI3K/Akt signaling pathway. AR acted on Akt1 targets through its main active component quercetin, and promoted the osteogenic differentiation of BM-MSCs by activating the PI3K/Akt signaling pathway.

Cellular senescence of renal tubular epithelial cells in renal fibrosis.

Renal fibrosis (RF) is the common pathological manifestation of virtually all chronic kidney diseases (CKD) and one of the major causes of end-stage renal disease (ESRD), but the pathogenesis of which is still unclear. Renal tubulointerstitial lesions have been identified as a key pathological hallmark of RF pathology. Renal tubular epithelial cells are the resident cells of the tubulointerstitium and play an important role in kidney recovery versus renal fibrosis following injury. Studies in recent years have shown that senescence of renal tubular epithelial cells can accelerate the progression of renal fibrosis. Oxidative stress(OS), telomere attrition and DNA damage are the major causes of renal tubular epithelial cell senescence. Current interventions and therapeutic strategies for cellular senescence include calorie restriction and routine exercise, Klotho, senolytics, senostatics, and other related drugs. This paper provides an overview of the mechanisms and the key signaling pathways including Wnt/ß-catenin/RAS, Nrf2/ARE and STAT-3/NF-κB pathway involved in renal tubular epithelial cell senescence in RF and therapies targeting renal tubular epithelial cell senescence future therapeutic potential for RF patients. These findings may offer promise for the further treatment of RF and CKD.

Understanding the mechanism of twenty-five ingredient decoction for setting a fracture in the treatment of fractures based on network pharmacology.

To study the mechanism of 25 ingredient decoction for setting a fracture (TDSF) in fracture treatment using network pharmacology. The TCMSP, BATMAN-TCM, HERB, and Uniprot protein databases were used to identify the active ingredients and targets of TDSF. Fracture-related targets were collected from the gene cards and the online mendelian inheritance in man databases. The acquisition of common genes of active compounds of TDSF and disease fractures was carried out using the Venny software. The Cytoscape 3.7.1 software and String database were used to construct a network diagram of drug-active ingredient-target-disease and the main core targets were obtained by protein interaction analysis. The Metascape platform was used to perform gene oncology functional and Kyoto encyclopedia of genes and genomes pathway enrichment analyses for common drug-disease targets. A total of 311 active ingredients and 348 targets were associated with TDSF, with 5197 targets related to fractures and 224 common targets between the 2 keywords. Key targets included serine/threonine protein kinase 1, tumor necrosis factor, interleukin 6, tumor protein 53, and vascular endothelial growth factor. Important roles of the following pathway were identified: cancer, lipid, and atherosclerosis; AGE-RAGE signaling pathway in diabetic complications; chemical carcinogenesis - receptor activation; PI3K -Akt signaling pathway; platinum drug resistance; cAMP signaling pathway; transcriptional mis regulation in cancer; serotonergic synapse; and malaria. TDSF mainly treats fractures by acting on multiple targets, such as serine/threonine protein kinase 1, tumor necrosis factor, interleukin 6, tumor protein 53, and vascular endothelial growth factor, and regulating the PI3K/AKT and cAMP signaling pathways.

Anti-apoptotic effect of HeidihuangWan in renal tubular epithelial cells via PI3K/Akt/mTOR signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Heidihuang Wan (HDHW) is a classic Chinese herbal formula, which was first recorded in the "Suwen Bingji Qiyi Baoming Collection" written by Liu Wansu during the Jin Dynasty (1115-1234 AD). It is commonly used clinically for the treatment of kidney diseases and its curative effect is stable. Previous animal experiments have confirmed that HDHW can effectively improve renal fibrosis. However, the underlying pharmacological mechanism remains unclear. AIMS OF THIS STUDY: Renal tubular epithelial cell (RTEC) apoptosis is one of the main pathological features of renal fibrosis. This study aimed to observe the effect and underlying mechanism of HDHW on the apoptosis of RTECs to further explore the pathological mechanism of HDHW against renal fibrosis. MATERIALS AND METHODS: We examined the HDHW composition in rat serum. In vitro, we first screened out the optimal intervention concentration of HDHW on RTECs using the MTT assay. Hypoxia/reoxygenation was then used to induce apoptosis of RTECs (H/R-RTECs), which were divided into H/R-RTEC, astragaloside IV (positive control), HDHW, and RTECs groups. After 48 h of drug intervention, apoptosis of RTECs was detected using flow cytometry and protein expression was detected by western blotting. The 5/6 nephrectomy rat model was constructed and divided into the normal control, 5/6 nephrectomy, HDHW, and astragaloside IV groups. After 8 weeks of treatment, TUNEL staining was used to detect cell apoptosis, and western blotting was used to detect protein expression. RESULTS: HDHW downregulated the expression of pro-apoptotic proteins Bax and Caspase3, up-regulated the expression of anti-apoptotic protein Bcl-2, activated the PI3K/Akt/mTOR signaling pathway, and reversed the early apoptosis of RTECs, thereby resisting the apoptosis of RTECs. CONCLUSION: HDHW inhibits apoptosis of RTECs by modulating the PI3K/Akt/mTOR signaling pathway. This study provides experimental evidence for the anti-fibrotic effect of HDHW on the kidneys and partially elucidates its pharmacological mechanism of action.

Heidihuangwan alleviates renal fibrosis in rats with 5/6 nephrectomy by inhibiting autophagy.

Renal fibrosis is a common pathway for the progression of various chronic kidney diseases (CKD), and the formation and deterioration will eventually lead to end-stage renal failure, which brings a heavy medical burden to the world. HeidihuangWan (HDHW) is a herbal formulation with stable and reliable clinical efficacy in the treatment of renal fibrosis. However, the mechanism of HDHW in treating renal fibrosis is not clear. In this study, we aimed to investigate the mechanism of HDHW to improve renal fibrosis. Wistar rats were randomly divided into the normal control group, 5/6 Nephrectomy group, astragaloside IV (AS-IV) group, HDHW group, and HDHW + IGF-1R inhibitor (JB1) group. Except for the normal control group, the rat renal fibrosis model was established by 5/6 nephrectomy and intervened with drugs for 8 weeks. Blood samples were collected to evaluate renal function. Hematoxylin-Eosin (HE), Periodic Acid-Schiff (PAS), Modified Masson's Trichrome (Masson) staining were used to evaluate the pathological renal injury, and immunohistochemistry and Western blotting were used to detect the protein expression of renal tissue. The results showed that HDHW was effective in improving renal function and reducing renal pathological damage. HDHW down-regulated the levels of fibrosis marker proteins, including α-smooth muscle actin (α-SMA), vimentin, and transforming growth factors-ß(TGF-ß), which in turn reduced renal fibrosis. Further studies showed that HDHW down-regulated the expression of autophagy-related proteins Beclin1 and LC3II, indicating that HDHW inhibited autophagy. In addition, we examined the activity of the class I phosphatidylinositol-3 kinase (PI3K)/serine-threonine kinase (Akt)/mTOR pathway, an important signaling pathway regulating autophagy, and the level of insulin-like growth factor 1 (IGF-1), an upstream activator of PI3K/Akt/mTOR. HDHW upregulated the expression of IGF-1 and activated the PI3K/Akt/mTOR pathway, which may be a vital pathway for its inhibition of autophagy. Application of insulin-like growth factor 1 receptor (IGF-1R) inhibitor further confirmed that the regulation of autophagy and renal fibrosis by HDHW was associated with IGF-1-mediated activation of the PI3K/Akt/mTOR pathway. In conclusion, our study showed that HDHW inhibited autophagy by upregulating IGF-1 expression, promoting the binding of IGF-1 to IGF-1R, and activating the PI3K/Akt/mTOR signaling pathway, thereby reducing renal fibrosis and protecting renal function. This study provides support for the application and further study of HDHW.