Objective To elucidate the changes in the gut microbiota and molecular mechanism of huaier in enhancing the efficacy of oxaliplatin (OXA) chemotherapy in gastric cancer (GC). Methods The effects of huaier on the gut microbiota structure and intestinal barrier function in MKN45-bearing mice were analyzed by using 16S rRNA sequencing, RT-qPCR, and IHC. UPLC-MS and network pharmacology, as well as in vivo experimental approaches, were employed to investigate the key bioactive constituents of huaier systematically and elucidate the underlying mechanisms by which huaier exerts therapeutic effects against GC. The expression of the PI3K/AKT/SREBP pathway was detected in cancer cells and tissues via Western blot analysis. The safety profile of huaier combined with OXA was verified through serum biochemistry and HE-stained tissue section analyses. Results Huaier inhibited the PI3K/AKT/SREBP pathway by increasing the abundance of Akkermansia muciniphila, reduced lipid droplet deposition, and ultimately enhanced the sensitivity to OXA in the treatment of GC. Conclusion This study demonstrates the value of huaier in gastric cancer treatment by enhancing chemosensitivity and provides novel insights into its systemic therapeutic effects through molecular mechanisms and gut microbiota modulation.

Coagulation factor XIa (FXIa) plays a crucial role in thrombus formation; therefore, the development of potent and safe FXIa inhibitors is of great significance. In this study, compound F22, previously discovered by our group, was selected as the lead compound. Based on the principles of bioisosterism and fragment-based drug design, four series comprising 14 novel Asundexian derivatives not previously reported in the literature were designed and synthesized. The structures of the target compounds were confirmed by 1H NMR and HRMS, and their inhibitory activities against FXIa were evaluated using chromogenic substrate assay. Results showed that compound FD-1 exhibited the most potent activity, with an IC50 value of 2.8 nmol/L, which was superior to that of the lead compound F22 (IC50 = 4.5 nmol/L) and the reference drug Asundexian (IC50 = 5.0 nmol/L). Furthermore, in the activated partial thromboplastin time (aPTT) assay, compound FD-1 demonstrated excellent anticoagulant activity, outperforming Asundexian, showing no significant effect on prothrombin time (PT). These findings provide valuable insights for further structural optimization and rational design of small-molecule FXIa inhibitors.

BACKGROUND: Serum osmolality is a prognostic indicator in critically ill patients. This study aimed to evaluate the association between high osmolality and 28-day mortality in patients with cardiac arrest (CA) admitted to the intensive care unit (ICU). METHODS: Baseline data of adult patients with CA who were admitted to the ICU from 2008 to 2019 were collected from the Medical Information Mart for Intensive Care (MIMIC)-IV. Patients were divided into survivor and non-survivor groups according to the 28-day prognosis. Serum concentrations of sodium, potassium, glucose, and urea nitrogen on the first day of ICU admission were used to determine serum osmolarity. The primary endpoint of this study was 28-day all-cause mortality. Propensity score matching (PSM) analysis was performed to reduce bias between the survivor and non-survivor groups. RESULTS: Among the 798 included CA patients, the high osmolarity on the first day of ICU admission remained significantly associated with increased 28-day mortality (62.0% vs. 35.5%, P<0.001) and reduced cumulative survival (log-rank P<0.05) after PSM. Cox regression identified the high osmolarity on the first day of ICU admission as an independent predictor. High serum osmolarity on the first day of ICU admission effectively predicted 1-, 3-, 7-, and 28-day all-cause mortality, with the strongest predictive performance for 1-day mortality both before and after PSM (all P<0.05). CONCLUSION: In this study, elevated serum osmolarity on the first day of ICU admission was independently associated with increased 28-day mortality in CA patients and could serve as a prognostic marker.

Background: Influenza A virus (IAV) is a negative-sense RNA virus of the Orthomyxoviridae family and is the etiological agent of a highly contagious acute respiratory disease that can lead to acute lung injury. Objective: To elucidate the molecular mechanisms of IAV infection, an integrative research approach combining gene expression profiling, multinetwork analysis, and in vivo experimental validations was employed. Methods: First, a series of network-based analyses were performed, including protein-protein interaction network construction, weighted gene co-expression network analysis, and subsequent gene set enrichment analysis, to identify the major underlying mechanisms of IAV infection. Following gene expression analysis, core targets, both direct and indirect regulators, were screened. An IAV (H1N1) strain A/PR/8/34-induced acute lung injury mouse model was constructed for in vivo validations. Batch one included two groups to evaluate findings from the multi-network analysis: Mock (n = 10; 5 males and 5 females) and IAV (n = 10; 5 males and 5 females). Batch two included three groups to assess the role of toll-like receptor 3 (TLR3) in IAV infection: Mock (n = 6; 3 males and 3 females), IAV (n = 6; 3 males and 3 females), and TLR3 inhibitor (n = 6; 3 males and 3 females). Body weight was measured on days 0, 3, and 5 after infection. On day 5, lung tissues were collected to assess viral load and histopathological changes. Key targets were examined using enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining, both in sera and lung tissues. Results: IAV infection was significantly associated with dysregulation of the immune-inflammation system, such as the LTR, nucle-otide-binding oligomerization domain-(NOD) like receptor, retinoic acid-inducible gene I-like receptor, and nuclear factor kappa-B signaling pathways. Gene set enrichment analysis further indicated that the TLR and necroptosis signaling pathways played crucial roles in the progression of IAV infection (TLR signaling pathway normalized enrichment score = 2.3941, P = 1.00 × 10 ⁻¹⁰; necroptosis normalized enrichment score = 1.9421, P = 6.21 × 10 ⁻⁷). Among the core targets, TLR3 and mixed lineage kinase domain-like protein (MLKL) may regulate gene expression at the transcriptional level (all P < 0.05). In vivo validation using an IAV (PR8) infected acute lung injury mouse model demonstrated increased viral load and lung index, alveolar structural damage, and inflammatory cell infiltration. Immunofluorescence staining exhibited large gaps in Lamin B1 staining and breaches in Emerin signals following IAV-PR8 infection. Expression levels of TLR3, p-receptor-interacting serine/threonine-protein kinase 3 (RIPK3)/RIPK3, and p-mixed lineage kinase domain-like protein (MLKL)/MLKL proteins in lung tissues, as well as proinflammatory factors and mediators in sera, were significantly elevated after IAV infection. Moreover, enhanced neutrophil infiltration (myeloperoxidase) and citrullinated histone H3 (a neutrophil extracellular trap-specific marker), both established indicators of neutrophil extracellular trap formation, were observed. Notably, treatment with a TLR3 inhibitor significantly ameliorated IAV-induced acute lung injury by regulating necroptosis-related targets. Conclusion: Our study provides network-based in vivo evidence that TLR3-receptor-interacting serine/threonine-protein kinase 3-MLKL-mediated necroptosis may underlie IAV-induced acute lung injury and could serve as a potential therapeutic target in severe influenza cases.

Prolonged standing work can lead to various lower limb health issues. Footwear, as a convenient and noninvasive intervention, plays a key role in foot protection. The purpose of this review was to evaluate the impact of footwear characteristics on foot comfort among workers engaged in prolonged standing occupations. A systematic search of PubMed, Web of Science, Scopus, and the Cochrane Library was conducted until March 2025 for experimental and observational studies; the review is registered in International Prospective Register of Systematic Reviews (CRD420251003253).Given the diversity of study designs, participant characteristics, and outcome measures, results were synthesized narratively, organizing findings by footwear design factors. The synthesis indicated that soft soles reduce foot impact and fatigue but offer limited support, whereas hard soles enhance stability but may cause localized pressure and discomfort. Sole hardness should balance cushioning and support based on activity: hard soles for standing and soft soles for walking. Insole hardness must be carefully considered as semirigid arch supports can cause discomfort. Most insoles improve pressure distribution by adjusting arch loading, and some enhance intrinsic foot muscles by promoting toe engagement, reducing leg swelling. Custom orthotic insoles outperform standard ones in comfort and balance. Future research should promote interdisciplinary collaboration with footwear designers to explore key design parameters and establish a scientific framework for protective footwear.

Objective To assess the stability of the molluscicidal activity of the fermentation broth supernatant of Bacillus indicus F19, so as to provide insights into development of novel molluscicides derived from this isolate. Methods Healthy Oncomelania hupensis snails free from Schistosoma japonicum infections and acclimated in the laboratory for 7 days were selected. The fermentation broth supernatant of B. indicus F19 was prepared. For each treatment condition, four experimental groups and one control group were established, with 10 mL of the fermentation broth supernatant each group. O. hupensis snails were exposed to different pH values (3, 6, 9 and 12), temperatures (40, 60, 80 °C and 100 °C), and ultraviolet (UV) exposure durations (1, 2, 3 h and 4 h). Then, the supernatant was diluted with dechlorinated water to concentrations of 50%, 10%, and 5% (v/v), and 10 mL of each dilution solution was added to three separate tubes, with an equal volume of dechlorinated water as a blank control. Twenty O. hupensis snails were transferred to each tube, immersed for 48 h and 72 h, and collected for viability assessment using the shell-tapping method. The mortality of O. hupensis snails was calculated and compared among dilution groups and the blank control group to evaluate the molluscicidal activity of the fermentation broth supernatant of B. indicus F19. Results There was a significant difference in the mortality of O. hupensis snails immersed in 5% fermentation broth supernatants of B. indicus F19 for 48 h at various pH levels (χ² = 11.556, P < 0.05), and the mortality reduced to 13.33% (8/60) in the experimental groups at a pH value of 12, which was significantly lower than in the blank control group [33.33% (20/60)] (χ² = 6.708, P < 0.05). There was a significant difference in the mortality of O. hupensis snails immersed in 10% fermentation broth supernatants of B. indicus F19 for 72 h at various pH levels (χ² = 31.691, P < 0.001), and the mortality reduced to 71.67% (43/60) and 65.00% (39/60) in the experimental group at pH values of 9 and 12, which was significantly lower than in the blank control group [100.00% (60/60)] (χ² = 8.571 and 12.110, both P values < 0.01). The mortality of O. hupensis snails both reduced to 23.33% (14/60) following immersion in 5% fermentation broth supernatants of B. indicus F19 heated in a water bath at 80 °C and 100 °C for 48 h, which was lower than that of unheated O. hupensis snails [33.33% (20/60)] and snails heated in a water bath at 40 °C [35.00% (21/60)] and 60 °C [33.33% (20/60)], and there was no significant difference in the mortality of O. hupensis snails among groups (χ² = 3.898, P > 0.05). The mortality of O. hupensis snails was 68.33% (41/60), 66.67% (40/60), 65.00% (39/60), and 68.33% (41/60) following immersion in fermentation broth supernatants heated in a water bath at 40, 60, 80 °C and 100 °C for 72 h, which was all lower than that of snails in the control group [71.70% (43/60)]; however, there was no significant difference seen in the snail mortality among groups (χ² = 0.674, P > 0.05). The mortality of O. hupensis snails was 73.33% (44/60), 71.67% (43/60), 71.67% (43/60), and 75.00% (45/60) following 48 h immersion in 10% fermentation broth supernatants of B. indicus F19 irradiated by UV for 1, 2, 3 h and 4 h, 33.33% (20/60), 31.67% (19/60), 35.00% (21/60), and 33.33% (20/60) following 48 h immersion in 10% fermentation broth supernatants of B. indicus F19 irradiated by UV for 1, 2, 3 h and 4 h, and 71.67% (43/60) and 33.33% (20/60) following 48 h immersion in 10% fermentation broth supernatants of B. indicus F19 without UV irradiation, and no significant differences were found among groups (χ² = 0.229 and 0.150, both P values > 0.05). In addition, the mortality of O. hupensis snails was 76.67% (46/60), 71.67% (43/60), 70.00% (42/60), and 76.67% (46/60) following 72 h immersion in 5% fermentation broth supernatants of B. indicus F19 irradiated by UV for 1, 2, 3 h and 4 h, and 71.67% (43/60) in the control group, and there was no significant difference in the snail mortality among groups (χ² = 1.193, P > 0.05). Conclusion The molluscicidal action of the fermentation broth supernatants of B. indicus F19 is tolerant to high temperature and UV irradiation; however, the activity is attenuated under alkaline conditions.

ObjectiveTo evaluate the Effect of Guishen Wan on learning and memory ability in D-galactose-induced aging model mice and to explore the application of the "Kidney-Brain Coordination" theory in traditional Chinese medicine （TCM）. MethodsAn subacute aging mouse model was established by subcutaneous injection of D-galactose （200 mg·kg^-1·d^-1） into the neck and back of KM mice. The mice were then administered GuiShen Wan at high， medium， and low doses （18， 9， 4.5 g·kg^-1·d^-1） or donepezil（2 mg·kg^-1·d^-1）， a standard clinical therapeutic agent for Alzheimer's disease， served as the positive control in this study，for 4 consecutive weeks. Learning and memory abilities were evaluated using the Morris water maze. The degree of renal fibrosis was observed via Masson staining. Hippocampal neuron injury was assessed by hematoxylin-eosin（HE） staining. Damage to Nissl bodies in the hippocampus was examined using Nissl staining. The fluorescence expression intensity of Klotho in the hippocampus was detected by immunofluorescence. Western blot was used to detect the protein expression of Klotho in the kidneys， as well as proteins related to the hippocampal inflammatory pathway and inflammatory factor-related signaling pathways. ResultsResults from the water maze test showed that compared with the blank group， the number of platform crossings and the time spent in the target quadrant were significantly decreased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan significantly increased the number of platform crossings and the time spent in the target quadrant in model mice （P<0.01）.Masson staining results showed that compared with the blank group， the collagen volume fraction was significantly increased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan significantly reduced the collagen volume fraction in the model group （P<0.01）. Kidney Western blot analysis showed that compared with the blank group， the Klotho protein was significantly decreased in the model group （P<0.01）. Compared with the model group， Guishen Wan elevated the klotho protein （P<0.01）.Neuronal cell count results showed that compared with the blank group， the number of neurons was significantly reduced in the model group （P<0.01）. Compared with the model group， Guishen Wan exhibited a dose-dependent trend in repairing neuronal damage and increasing the number of neuronal cells （P<0.01）.Immunofluorescence intensity results showed that compared with the blank group， the positive expression of Klotho was significantly decreased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan enhanced Klotho fluorescence expression （P<0.01）.Hippocampal Western blot analysis showed that compared with the blank group， the ratios of interleukin（IL）-1β and IL-6 proteins were significantly increased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan significantly reduced the ratios of IL-1β and IL-6 proteins（P<0.01）. Compared with the blank group， the ratio of phosphorylated-nuclear transcription factor-κB（p-NF-κB） protein was significantly increased （P<0.01）， while the klotho protein was significantly decreased （P<0.01） in the model group. Compared with the model group， all Guishen Wan groups significantly reduced the p-NF-κB protein （P<0.05， P<0.01） and significantly increased the Klotho protein（P<0.01）. ConclusionGuishen Wan effectively ameliorates D-galactose-induced aging in model mice. Its mechanism of action may be related to upregulating Klotho concentration and inhibiting inflammatory factors associated with the NF-κB signaling pathway.

ObjectiveTo investigate the effect and mechanism of Banxia Shumitang plus Zhizichi Tang （BZ） on PTEN-induced kinase 1 （PINK1）/Parkin signaling pathway in regulating mitochondrial autophagy in preventing insomnia with depression. MethodsSeventy-two 6-week-old male Kunming mice were randomized into a normal group， a model group， low-dose， medium-dose， and high-dose BZ groups （BZ-L， BZ-M， BZ-H， 2.92， 5.85， 11.7 g·kg^-1）， and an estazolam （0.21 mg·kg^-1） group. Insomnia model was established on days 1 to 3. p-Chlorophenylalanine （PCPA） was injected intraperitoneally at a dose of 400 mg·kg^-1 into mice of the model group and administration groups for 3 consecutive days. Then， the classic depression model was established with chronic unpredictable mild stress （CUMS） for 28 consecutive days. Administration and modeling were performed simultaneously. After gavage， 24 h spontaneous activity test was performed to test sleep state， and sugar preference test and open field test were performed to evaluate anxiety-like state. The morphological changes of the hypothalamus were observed by hematoxylin-eosin （HE） staining， and the number of Nissl bodies was observed by Nissl staining. The ultrastructure of mitochondria was observed by transmission electron microscopy. The mitochondrial membrane potential assay kit （JC-1） was used to examine the mitochondrial function， and a biochemical assay kit was used to measure the ATP content in the hypothalamus. The level of reactive oxygen species （ROS） was determined by the immunofluorescence assay， and the serum levels of 5-hydroxytryptamine （5-HT）， noradrenalin （NE）， and cortisol （CORT） were determined by enzyme-linked immunosorbent assay （ELISA）. Western blot and Real-time quantitative polymerase chain reaction （Real-time PCR） were employed to determine the expression of PINK1， Parkin， microtubule-associated protein 1 light chain 3 （LC3）， and isolator protein 1 （p62） at protein and mRNA levels， respectively. ResultsThe 24 h spontaneous activity test showed that compared with the normal group， the model group did not exhibit circadian rhythm characteristics in their spontaneous activity time， while the circadian rhythm characteristics were restored in each treatment group （P<0.05）. The sucrose preference test indicated that compared with that in the normal group， the sucrose preference rate in the model group reduced （P<0.01）， and compared with that in the model group， the sucrose preference rate in each treatment group increased （P<0.01）. The open field test revealed that compared with the normal group， the model group exhibited decreased movement distance， average speed， frequency of visits to the central area， and time spent in the central area （P<0.01）， and compared with those in the model group， these parameters in each treatment group increased （P<0.05， P<0.01）. HE staining showed that compared with the normal group， the model group exhibited disarrangement of neurons in the hypothalamus， enlarged intercellular space， and severe nuclear condensation， while the degree of hypothalamic neuronal damage in each treatment group was alleviated. Nissl staining indicated that compared with the normal group， the model group demonstrated aggravated neuronal damage and increased damaged cells （P<0.01）. Compared with that in the model group， the number of damaged cells in each treatment group decreased （P<0.01）. Transmission electron microscopy showed that compared with the normal group， the model group exhibited mitochondrial swelling and rupture in the hypothalamus， with visible autophagic lysosomes in the cytoplasm. Compared with those in the model group， only a few autophagic lysosomes were observed in the BZ-L group， and the degree of mitochondrial swelling and rupture was alleviated in the other treatment groups. ROS immunofluorescence assay showed that compared with the normal group， the model group displayed enhanced red fluorescence intensity of mitochondrial ROS （P<0.01）， which was attenuated in each treatment group （P<0.01）. Mitochondrial membrane potential assay showed that compared with the normal group， the model group had declined mitochondrial membrane potential （P<0.01）， which was recovered in each treatment group （P<0.05， P<0.01）. The biochemical assay of ATP levels indicated that compared with the normal group， the model group exhibited decreased ATP content （P<0.01）， which rebound in each treatment group （P<0.05， P<0.01）. ELISA showed that compared with the normal group， the model group exhibited decreased 5-HT content and increased NE and CORT content （P<0.01）. Compared with the model group， each treatment group showed increased 5-HT content （P<0.01） and reduced NE content （P<0.01） and CORT content （P<0.05， P<0.01）. Western blot of the hypothalamus showed that compared with the normal group， the model group exhibited downregulated protein levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated protein level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated protein levels of PINK1， Parkin， and LC3 （P<0.05， P<0.01） and downregulated protein level of p62 （P<0.05， P<0.01）. Real-time PCR showed that compared with the normal group， the model group exhibited downregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated mRNA level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and downregulated mRNA level of p62 （P<0.01）. ConclusionBZ can ameliorate the insomnia and anxiety state of mice by regulating PINK1/Parkin signaling pathway to improve the mitochondrial function， enhance mitochondrial autophagy， protect neurons， and repair damaged nerve cells.

ObjectiveTo investigate the effect and mechanism of Banxia Shumitang plus Zhizichi Tang （BZ） on PTEN-induced kinase 1 （PINK1）/Parkin signaling pathway in regulating mitochondrial autophagy in preventing insomnia with depression. MethodsSeventy-two 6-week-old male Kunming mice were randomized into a normal group， a model group， low-dose， medium-dose， and high-dose BZ groups （BZ-L， BZ-M， BZ-H， 2.92， 5.85， 11.7 g·kg^-1）， and an estazolam （0.21 mg·kg^-1） group. Insomnia model was established on days 1 to 3. p-Chlorophenylalanine （PCPA） was injected intraperitoneally at a dose of 400 mg·kg^-1 into mice of the model group and administration groups for 3 consecutive days. Then， the classic depression model was established with chronic unpredictable mild stress （CUMS） for 28 consecutive days. Administration and modeling were performed simultaneously. After gavage， 24 h spontaneous activity test was performed to test sleep state， and sugar preference test and open field test were performed to evaluate anxiety-like state. The morphological changes of the hypothalamus were observed by hematoxylin-eosin （HE） staining， and the number of Nissl bodies was observed by Nissl staining. The ultrastructure of mitochondria was observed by transmission electron microscopy. The mitochondrial membrane potential assay kit （JC-1） was used to examine the mitochondrial function， and a biochemical assay kit was used to measure the ATP content in the hypothalamus. The level of reactive oxygen species （ROS） was determined by the immunofluorescence assay， and the serum levels of 5-hydroxytryptamine （5-HT）， noradrenalin （NE）， and cortisol （CORT） were determined by enzyme-linked immunosorbent assay （ELISA）. Western blot and Real-time quantitative polymerase chain reaction （Real-time PCR） were employed to determine the expression of PINK1， Parkin， microtubule-associated protein 1 light chain 3 （LC3）， and isolator protein 1 （p62） at protein and mRNA levels， respectively. ResultsThe 24 h spontaneous activity test showed that compared with the normal group， the model group did not exhibit circadian rhythm characteristics in their spontaneous activity time， while the circadian rhythm characteristics were restored in each treatment group （P<0.05）. The sucrose preference test indicated that compared with that in the normal group， the sucrose preference rate in the model group reduced （P<0.01）， and compared with that in the model group， the sucrose preference rate in each treatment group increased （P<0.01）. The open field test revealed that compared with the normal group， the model group exhibited decreased movement distance， average speed， frequency of visits to the central area， and time spent in the central area （P<0.01）， and compared with those in the model group， these parameters in each treatment group increased （P<0.05， P<0.01）. HE staining showed that compared with the normal group， the model group exhibited disarrangement of neurons in the hypothalamus， enlarged intercellular space， and severe nuclear condensation， while the degree of hypothalamic neuronal damage in each treatment group was alleviated. Nissl staining indicated that compared with the normal group， the model group demonstrated aggravated neuronal damage and increased damaged cells （P<0.01）. Compared with that in the model group， the number of damaged cells in each treatment group decreased （P<0.01）. Transmission electron microscopy showed that compared with the normal group， the model group exhibited mitochondrial swelling and rupture in the hypothalamus， with visible autophagic lysosomes in the cytoplasm. Compared with those in the model group， only a few autophagic lysosomes were observed in the BZ-L group， and the degree of mitochondrial swelling and rupture was alleviated in the other treatment groups. ROS immunofluorescence assay showed that compared with the normal group， the model group displayed enhanced red fluorescence intensity of mitochondrial ROS （P<0.01）， which was attenuated in each treatment group （P<0.01）. Mitochondrial membrane potential assay showed that compared with the normal group， the model group had declined mitochondrial membrane potential （P<0.01）， which was recovered in each treatment group （P<0.05， P<0.01）. The biochemical assay of ATP levels indicated that compared with the normal group， the model group exhibited decreased ATP content （P<0.01）， which rebound in each treatment group （P<0.05， P<0.01）. ELISA showed that compared with the normal group， the model group exhibited decreased 5-HT content and increased NE and CORT content （P<0.01）. Compared with the model group， each treatment group showed increased 5-HT content （P<0.01） and reduced NE content （P<0.01） and CORT content （P<0.05， P<0.01）. Western blot of the hypothalamus showed that compared with the normal group， the model group exhibited downregulated protein levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated protein level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated protein levels of PINK1， Parkin， and LC3 （P<0.05， P<0.01） and downregulated protein level of p62 （P<0.05， P<0.01）. Real-time PCR showed that compared with the normal group， the model group exhibited downregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated mRNA level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and downregulated mRNA level of p62 （P<0.01）. ConclusionBZ can ameliorate the insomnia and anxiety state of mice by regulating PINK1/Parkin signaling pathway to improve the mitochondrial function， enhance mitochondrial autophagy， protect neurons， and repair damaged nerve cells.

ObjectiveTo explore psychological experiences and care needs of elderly patients with chronic obstructive pulmonary disease (COPD) following dysphagia. MethodsFrom April to June, 2024, 13 elderly patients with COPD and dysphagia received treatment in Yixing No. 2 People's Hospital (Yixing Occupational Disease Institute) and Northern Jiangsu People's Hospital were interviewed. Nvivo 11.0 and content analysis were employed to analyze and summarize themes. ResultsTwo main themes were identified. The psychological experiences included fear of eating due to swallowing and choking, swallowing anxiety in social situations, concerns about malnutrition, and emotional loss related to family. The care needs included improvement in swallowing function, adjustment of food texture, assistance with disease adaptation and effective access to health education information. ConclusionHealthcare professionals should thoroughly understand the psychological and needs of elderly patients with COPD-related dysphagia, and comprehensive nursing strategies should be developed and implemented to improve swallowing function and overall quality of life.