BackgroundAnxiety exhibits a rising prevalence among college students. Investigating the mechanisms through which family function relates to anxiety and examining the moderating role of emotion regulation strategies within this context hold substantial implications for promoting mental health among college students. However， existing research has not sufficiently elucidated the complex interplay among family function， emotion regulation， and anxiety among college students. Further research is warranted to clarify the underlying mechanisms linking family function to anxiety outcomes and to examine the potential moderating role of emotion regulation strategies in this causal pathway. ObjectiveTo explore the relationship between family function and anxiety among lower-grade college students， and to validate the moderating role of emotion regulation strategies in this relationship， thereby offering evidence-based insights for anxiety reduction interventions in this population. MethodsIn March 2023， a total of 1 980 first- and second-year students from a comprehensive university in Shanghai were selected using the cluster sampling method. A self-designed demographic questionnaire， the Emotion Regulation Questionnaire （ERQ）， the Family Adaptability and Cohesion Evaluation Scale Ⅱ-Chinese Version （FACES Ⅱ-CV）， and the Symptom Checklist-90 （SCL-90） were utilized for assessment. Pearson correlation analysis and Spearman correlation analysis were employed to test the correlations of each variable. Hierarchical linear regression analysis was conducted to certify the moderating role of emotion regulation strategies in the relationship between family function and anxiety. ResultsCompared with female students， male students scored significantly lower on ERQ cognitive reappraisal （t=-5.793， P<0.01） but significantly higher on ERQ expressive suppression （t=8.359， P<0.01）. For lower-grade college students， scores on adaptability and cohesion subscales of FACES Ⅱ-CV showed a positive association with cognitive reappraisal in ERQ （r=0.251， 0.302， P<0.01）， while simultaneously displaying negative correlations with both expressive suppression in ERQ （r=-0.113， -0.154， P<0.01） and anxiety in SCL-90 （r=-0.243， -0.202， P<0.01）. Notably， anxiety scores in SCL-90 were inversely related to cognitive reappraisal scores in ERQ （r=-0.159， P<0.01） but directly associated with expressive suppression scores in ERQ （r=0.171， P<0.01）. Hierarchical regression analysis indicated that cognitive reappraisal significantly moderated the relationship between family cohesion and anxiety （β=-0.421， P<0.01）. ConclusionThe cognitive reappraisal strategy serves as a moderator in the relationship between family cohesion and anxiety， potentially mitigating the escalation of anxiety levels associated with family dysfunction. ［Funded by Science and Technology Development Fund of Shanghai Pudong New Area （number， PKJ2023-Y21）］

ObjectiveTo verify the therapeutic effect of Yinqi Sanhuang Jiedu decoction （YQSH） on carbon tetrachloride （CCl₄）-induced hepatic fibrosis in mice， and to explore whether its effect was related to the inhibition of neutrophil infiltration and the formation of neutrophil extracellular traps （NETs）. MethodsThe 36 C57BL/6J mice were randomly divided into control group， model group， positive drug silybin （SF） group （55 mg·kg^-1·d^-1）， YQSH-L group， YQSH-M group， and YQSH-H group （8.325， 16.65， 33.3 g·kg^-1·d^-1， respectively），n=6 in each group. Except for the control group， mice in all other groups were intraperitoneally injected with CCl₄ to induce hepatic fibrosis. After successful modeling， each drug administration group was given the corresponding drugs by gavage for eight weeks. Hematoxylin-eosin （HE） staining， Sirius red staining and Masson staining were used to observe the pathological changes of liver tissue. Liver elasticity was detected by a color Doppler ultrasound system. Immunohistochemistry and real-time fluorescent quantitative polymerase chain reaction （Real-time PCR） were performed to detect the protein expression and mRNA levels of C-X-C motif chemokine ligand 1 （CXCL1）， CXCL2 and CXCL5. Neutrophil levels were detected by flow cytometry. The expression of neutrophil elastase （NE） and myeloperoxidase （MPO） positive protein was observed by immunofluorescence. The contents of MPO， NE and CitH3 were detected by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the control group， the liver of the model group showed obvious inflammatory cell infiltration and collagen deposition， and the liver elasticity， CXCL1， CXCL2， CXCL5 expression， neutrophil level， and MPO， NE and CitH3 levels were significantly increased （P<0.05， P<0.01）. Compared with the model group， inflammatory cell infiltration and collagen deposition in the liver tissue of mice were reduced after YQSH treatment. Moreover， the liver elasticity was reduced （P<0.01）. The protein expression （P<0.01） and mRNA level of CXCL1， CXCL2 and CXCL5 were decreased（P<0.05，P<0.01）. The neutrophil level was decreased （P<0.01）， the expression of MPO and NE positive protein was significantly decreased（P<0.05，P<0.01）， and the levels of MPO， NE and CitH3 were decreased （P<0.05， P<0.01）. ConclusionThe anti-hepatic fibrosis effect of YQSH may be related to its inhibition of chemokines （CXCL1， CXCL2， CXCL5）， reduction of neutrophil infiltration， and inhibition of NETs generation.

ObjectiveTo verify the therapeutic effect of Yinqi Sanhuang Jiedu decoction （YQSH） on carbon tetrachloride （CCl₄）-induced hepatic fibrosis in mice， and to explore whether its effect was related to the inhibition of neutrophil infiltration and the formation of neutrophil extracellular traps （NETs）. MethodsThe 36 C57BL/6J mice were randomly divided into control group， model group， positive drug silybin （SF） group （55 mg·kg^-1·d^-1）， YQSH-L group， YQSH-M group， and YQSH-H group （8.325， 16.65， 33.3 g·kg^-1·d^-1， respectively），n=6 in each group. Except for the control group， mice in all other groups were intraperitoneally injected with CCl₄ to induce hepatic fibrosis. After successful modeling， each drug administration group was given the corresponding drugs by gavage for eight weeks. Hematoxylin-eosin （HE） staining， Sirius red staining and Masson staining were used to observe the pathological changes of liver tissue. Liver elasticity was detected by a color Doppler ultrasound system. Immunohistochemistry and real-time fluorescent quantitative polymerase chain reaction （Real-time PCR） were performed to detect the protein expression and mRNA levels of C-X-C motif chemokine ligand 1 （CXCL1）， CXCL2 and CXCL5. Neutrophil levels were detected by flow cytometry. The expression of neutrophil elastase （NE） and myeloperoxidase （MPO） positive protein was observed by immunofluorescence. The contents of MPO， NE and CitH3 were detected by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the control group， the liver of the model group showed obvious inflammatory cell infiltration and collagen deposition， and the liver elasticity， CXCL1， CXCL2， CXCL5 expression， neutrophil level， and MPO， NE and CitH3 levels were significantly increased （P<0.05， P<0.01）. Compared with the model group， inflammatory cell infiltration and collagen deposition in the liver tissue of mice were reduced after YQSH treatment. Moreover， the liver elasticity was reduced （P<0.01）. The protein expression （P<0.01） and mRNA level of CXCL1， CXCL2 and CXCL5 were decreased（P<0.05，P<0.01）. The neutrophil level was decreased （P<0.01）， the expression of MPO and NE positive protein was significantly decreased（P<0.05，P<0.01）， and the levels of MPO， NE and CitH3 were decreased （P<0.05， P<0.01）. ConclusionThe anti-hepatic fibrosis effect of YQSH may be related to its inhibition of chemokines （CXCL1， CXCL2， CXCL5）， reduction of neutrophil infiltration， and inhibition of NETs generation.

AIM:To investigate the effect of peripheral defocus design rigid gas permeable contact lenses(defocus RGPCL)in controlling myopia progression in children aged 6-12 y with high myopia, and to compare the outcomes with traditional single-vision RGPCL and single-vision spectacles.METHODS:This prospective cohort study enrolled children aged 6-12 y with high myopia who visited the Ophthalmology and Optometry Center of Xi'an No.1 Hospital between January 2022 and January 2023. Based on parental preference, participants were divided into three groups: defocused RGPCL group, single-vision RGPCL group, and single-vision spectacles group. The axial length(AL)and cycloplegic spherical equivalent(SE)refraction were compared at baseline, 0.5, 1, 1.5, and 2 y after lens wear. Additionally, AL and SE delay rates were calculated for each group.RESULTS: This study enrolled a total of 90 children with high myopia(180 eyes), with no participants lost to follow-up. Participants were allocated into three groups based on parental preference. Thirty children(60 eyes)were assigned to the peripheral defocus RGPCL group, consisting of 12 boys and 18 girls with a mean age of 9.96±1.56 y; 30 children(60 eyes)to the single-vision RGPCL group, including 15 boys and 15 girls with a mean age of 9.40±1.52 y; and 30 children(60 eyes)to the single-vision spectacles group, with 14 boys and 16 girls and a mean age of 9.80±1.37 y. At 0.5, 1, 1.5, and 2 y lens fitting, AL and SE increased significantly in all three groups(all P<0.05), with the growth rates in the defocused RGPCL group being significantly lower than those in the single-vision RGPCL and single-vision spectacles groups(all P<0.05). At 2 y lens fitting, the AL elongation was 0.22±0.24 mm and the mean SE progression was 0.70±0.70 D in the peripheral defocus RGPCL group; 0.49±0.38 mm and 1.34±0.60 D in the single-vision RGPCL group; and 0.50±0.21 mm and 1.72±0.47 D in the single-vision spectacles group. Using the single-vision spectacles group as the control, the AL delay rate and SE delay rate at 2 y lens fitting were 56.0% and 59.3%, respectively, in the defocused RGPCL group.CONCLUSION:For children with high myopia aged 6-12 y, defocus RGPCLs can effectively and significantly delay AL elongation and SE progression, demonstrating markedly superior control efficacy compared to single-vision RGPCL or single-vision spectacles. Defocused RGPCL can serve as an effective optical intervention for high myopia children.

ObjectiveTo validate the therapeutic effect of Yinqi Sanhuang Jiedu decoction （YQSH） on a mouse model of carbon tetrachloride （CCl₄）-induced liver fibrosis and to investigate its correlations with the Piezo-type mechanosensitive ion channel component 1 （Piezo1）-Yes-associated protein （YAP） mechanical signaling axis and macrophage polarization. MethodsFifty-four C57BL/6J mice were randomized into a blank control group， a 4-week model group， a 6-week model group， a 8-week model group， a positive drug （silymarin， 55 mg·kg^-1·d^-1） group， and low-， medium-， and high-dose （8.325， 16.65， 33.3 g·kg^-1·d^-1， respectively） YQSH groups. Except the 6-week model group （n=12）， each of the other groups had 6 mice. Mice in other groups except the blank control group received intraperitoneal injections of 10% CCl₄ twice weekly for the modeling of liver fibrosis. Drug interventions began one week after the initial modeling through gavage， and the blank control and model groups received 0.2 mL of normal saline via gavage. The histopathological changes and collagen deposition in the liver were observed via hematoxylin-eosin （HE）， Masson's trichrome， and Sirius red staining. Serum activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST）， as well as serum levels of total protein （TP）， albumin （ALB）， total bilirubin （TBIL）， hyaluronic acid （HA）， laminin （LN）， procollagen type Ⅲ （PCⅢ）， and collagen type Ⅳ （Ⅳ-C）， were measured. The levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the liver tissue were determined by enzyme-linked immunosorbent assay （ELISA）. The protein and mRNA levels of Piezo1 and YAP1 in the liver tissue were determined by immunohistochemistry （IHC） and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. Co-localization of Piezo1 with YAP1， and YAP1 with inducible nitric oxide synthase （iNOS） was observed by the immunofluorescence （IF） assay. The proportions of M1-type （F4/80⁺CD80⁺） and M2-type （F4/80⁺CD206⁺） macrophages in the liver tissue were examined by flow cytometry. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses and gene set enrichment analysis （GSEA） were performed through transcriptomic sequencing. ResultsCompared with the blank control group， the model group exhibited gradually worsened liver fibrosis at the 4^th， 6^th， and 8^th weeks. The 6- and 8-week model groups showcased inflammatory cell infiltration and collagen deposition in the liver （P<0.01） and upregulated protein levels of both Piezo1 and YAP1 （P<0.01）. Compared with the model groups， treatment with YQSH improved the liver function （P<0.05， P<0.01）， alleviated liver fibrosis （P<0.05， P<0.01）， and reduced intrahepatic inflammatory cell infiltration and collagen deposition （P<0.01）. Furthermore， the treatment downregulated the protein and mRNA levels of Piezo1 and YAP1 （P<0.05， P<0.01）， lowered the levels of inflammatory factors TNF-α and IL-1β （P<0.05， P<0.01）， and decreased the ratio of CD80 （M1-type）/CD206 （M2-type） macrophage proteins （P<0.01）. The IF assay showed co-localization of YAP1 with Piezo1 and iNOS. Compared with the model groups， YQSH treatment downregulated the expression of Piezo1， YAP1， and iNOS （P<0.05， P<0.01）. Transcriptomic analysis suggested that the anti-liver fibrosis effect of YQSH may be related to the Hippo signaling pathway （P<0.05）. ConclusionThe anti-liver fibrosis effect of YQSH may be related to its inhibition of the Piezo1-YAP signaling axis and regulation of macrophage polarization.

ObjectiveTo validate the therapeutic effect of Yinqi Sanhuang Jiedu decoction （YQSH） on a mouse model of carbon tetrachloride （CCl₄）-induced liver fibrosis and to investigate its correlations with the Piezo-type mechanosensitive ion channel component 1 （Piezo1）-Yes-associated protein （YAP） mechanical signaling axis and macrophage polarization. MethodsFifty-four C57BL/6J mice were randomized into a blank control group， a 4-week model group， a 6-week model group， a 8-week model group， a positive drug （silymarin， 55 mg·kg^-1·d^-1） group， and low-， medium-， and high-dose （8.325， 16.65， 33.3 g·kg^-1·d^-1， respectively） YQSH groups. Except the 6-week model group （n=12）， each of the other groups had 6 mice. Mice in other groups except the blank control group received intraperitoneal injections of 10% CCl₄ twice weekly for the modeling of liver fibrosis. Drug interventions began one week after the initial modeling through gavage， and the blank control and model groups received 0.2 mL of normal saline via gavage. The histopathological changes and collagen deposition in the liver were observed via hematoxylin-eosin （HE）， Masson's trichrome， and Sirius red staining. Serum activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST）， as well as serum levels of total protein （TP）， albumin （ALB）， total bilirubin （TBIL）， hyaluronic acid （HA）， laminin （LN）， procollagen type Ⅲ （PCⅢ）， and collagen type Ⅳ （Ⅳ-C）， were measured. The levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the liver tissue were determined by enzyme-linked immunosorbent assay （ELISA）. The protein and mRNA levels of Piezo1 and YAP1 in the liver tissue were determined by immunohistochemistry （IHC） and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. Co-localization of Piezo1 with YAP1， and YAP1 with inducible nitric oxide synthase （iNOS） was observed by the immunofluorescence （IF） assay. The proportions of M1-type （F4/80⁺CD80⁺） and M2-type （F4/80⁺CD206⁺） macrophages in the liver tissue were examined by flow cytometry. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses and gene set enrichment analysis （GSEA） were performed through transcriptomic sequencing. ResultsCompared with the blank control group， the model group exhibited gradually worsened liver fibrosis at the 4^th， 6^th， and 8^th weeks. The 6- and 8-week model groups showcased inflammatory cell infiltration and collagen deposition in the liver （P<0.01） and upregulated protein levels of both Piezo1 and YAP1 （P<0.01）. Compared with the model groups， treatment with YQSH improved the liver function （P<0.05， P<0.01）， alleviated liver fibrosis （P<0.05， P<0.01）， and reduced intrahepatic inflammatory cell infiltration and collagen deposition （P<0.01）. Furthermore， the treatment downregulated the protein and mRNA levels of Piezo1 and YAP1 （P<0.05， P<0.01）， lowered the levels of inflammatory factors TNF-α and IL-1β （P<0.05， P<0.01）， and decreased the ratio of CD80 （M1-type）/CD206 （M2-type） macrophage proteins （P<0.01）. The IF assay showed co-localization of YAP1 with Piezo1 and iNOS. Compared with the model groups， YQSH treatment downregulated the expression of Piezo1， YAP1， and iNOS （P<0.05， P<0.01）. Transcriptomic analysis suggested that the anti-liver fibrosis effect of YQSH may be related to the Hippo signaling pathway （P<0.05）. ConclusionThe anti-liver fibrosis effect of YQSH may be related to its inhibition of the Piezo1-YAP signaling axis and regulation of macrophage polarization.

Objective To evaluate the anticoagulation efficacy of non-vitamin K antagonist oral anticoagulants (NOACs) and vitamin K antagonists (VKAs) in patients with high-risk atrial fibrillation (AF) undergoing transcatheter aortic valve implantation (TAVI). Methods A computer-based search was conducted on PubMed, EMbase, The Cochrane Library, CNKI, SinoMed, and VIP databases to identify studies on the application of NOACs and VKAs in high-risk AF patients after TAVI. The search period was from database inception to January 2023. The quality of the included studies was assessed using the Cochrane risk assessment tool and the Newcastle-Ottawa Scale (NOS). Meta-analysis was performed using RevMan 5.4 software. Results A total of 7 studies involving 24 592 patients were included. The meta-analysis results showed that compared to patients using VKAs, those treated with NOACs had a significantly lower risk of all-cause mortality [RR=0.74, 95%CI (0.58, 0.94), P=0.01]. Subgroup analysis indicated that when the follow-up period was less than 1 year, there was no significant difference in all-cause mortality between the NOAC and VKA groups [RR=0.57, 95%CI (0.17, 1.88), P=0.35]; however, when the follow-up period was ≥1 year, the VKA group had a higher all-cause mortality rate than the NOAC group, with a statistically significant difference [RR=0.73, 95%CI (0.57, 0.95), P=0.02]. No significant differences were found between the two groups regarding early stroke [RR=0.50, 95%CI (0.19, 1.28), P=0.15], stroke during follow-up [RR=1.04, 95%CI (0.88, 1.22), P=0.64], bleeding [RR=0.94, 95%CI (0.73, 1.21), P=0.61], major or life-threatening bleeding [RR=0.80, 95%CI (0.49, 1.31), P=0.38], or acute kidney injury [RR=0.51, 95%CI (0.16, 1.59), P=0.24]. Conclusion Compared to VKAs, the use of NOACs in patients with high-risk AF undergoing TAVI may reduce the risk of all-cause mortality, especially during long-term anticoagulation therapy, potentially offering greater benefits. However, further evidence from randomized controlled trials is needed to confirm these findings.

Mesenchymal stem cells (MSCs) have been widely used in the treatment of various autoimmune and inflammation-related diseases due to their potent immunomodulatory properties. Several studies have demonstrated that MSC-mediated immunomodulation is complex and bidirectional, with the in vivo microenvironment influencing the direction of this modulation. Indoleamine-2,3-dioxygenase (IDO), an immunosuppressive factor, has been identified as a key "switch" in the immunomodulatory role of MSCs. In this review, we explore how IDO functions as a critical regulator of MSC immunoregulatory plasticity. We delve into the mechanisms by which changes in IDO expression affect the function of various immune cells, summarize relevant research and clinical advances regarding the role of IDO expression in MSC-based therapies for various diseases, and discuss potential therapeutic strategies that target IDO to enhance the stability of MSC therapeutic effects. This provides a theoretical foundation for optimizing MSCs as safer and more effective clinical therapeutic agents.

Objective:To predict the monthly incidence of hemorrhagic fever with renal syndrome (HFRS) in Hebei Province by using the generalized additive model (GAM).Methods:The incidence data of HFRS in Hebei from 2006 to 2020 were collected, and the correlation coefficients between meteorological factors and the monthly incidence of HFRS in Hebei were analyzed by Spearman's correlation, and the meteorological factors were lagged by 0-6 orders, and those with the largest absolute values of the correlation coefficients were screened to be included in the multifactorial GAM to evaluate the effects of meteorological factors.Results:The monthly incidence of HFRS had the strongest correlation with monthly mean air temperature at lag order 2, monthly mean wind speed at lag order 0, monthly mean sunshine at lag order 4, monthly mean precipitation at lag order 2 and monthly mean humidity at lag order 1, which were diagnosed by the variance inflation factor and included in the multifactorial GAM, and the results showed significant differences among the factors (all P<0.001), and they showed non-linear relationships with the monthly incidence of HFRS. Mean monthly temperature was an important factor influencing HFRS incidence. Mean monthly air temperature, mean monthly sunshine and mean monthly wind speed were negatively associated with HFRS incidence, whereas mean monthly precipitation and mean monthly humidity were positively associated with HFRS incidence. Conclusions:There was a complex non-linear relationship between meteorological factors and the incidence of HFRS. GAM incorporated with lagged meteorological factors can be used to predict the incidence of HFRS in Hebei.

OBJECTIVE: Cassiae Semen (CS, Juemingzi in Chinese) is a widely used traditional Chinese medicine with a variety of pharmacological effects. This study aimed to investigate the potential therapeutic effects and molecular mechanisms of anthraquinones of CS (AQS) for adiposity. METHODS: The chemical components of the AQS were determined using high-performance liquid chromatography (HPLC). Network pharmacology analysis was used to predict potential anti-obesity targets of action for AQS. We constructed high fat with high sugar water diet-induced obese mice and observed their body weight and whole-body lipid metabolism to evaluate the efficacy of AQS in promoting lipid metabolism. Subsequently, the epidermal temperature at the brown adipose tissue (BAT) before and after cold stimulation was observed and the expression of lipid metabolism-related genes in the liver and BAT tissues was detected to clarify the mechanism of action of AQS. RESULTS: Network pharmacology analysis showed that AQS was involved in the regulation of liver and adipose tissue function under obesity. Pathological and biochemical results showed that AQS reduced lipid accumulation in the liver and adipose tissue induced by an unhealthy diet. With the increase of cold tolerance, the volume and weight of BAT were increased by AQS, suggesting that it regulated the body heat production dominated by BAT. After AQS treatment, the levels of genes related to uncoupling protein1 (UCP1)-mediated adaptive thermogenesis in BAT tissues and lipid metabolism in the liver were also increased, which further proved that AQS activated BAT function to promote lipid metabolism in the whole body. CONCLUSION This study revealed the pharmacological effects of AQS, thereby providing a scientific basis for regulating BAT thermogenesis and liver lipid metabolism to alleviate obesity and providing clues for further exploring the application of natural active ingredients in the treatment of metabolism-related diseases.