BACKGROUND:Currently,miR-196b-5p has been found to play a role in cell proliferation,migration and inhibition of scar hyperplasia,but there is a lack of relevant studies on whether it plays a role in the process of wound healing.OBJECTIVE:To investigate the effect of miR-196b-5p in adipose stem cell-derived exosomes on burn wound healing.METHODS:The models of deep second degree skin burn in SD rats were established and randomly divided into four groups:blank control group,exosome group,agomiR-196b-5p group,and exosome+antagomiR-196b-5p group,with 10 rats in each group.PBS,adipose-derived stem cell-derived exosomes,miR-196b-5p agonist,and miR-196b-5p inhibitor were injected around the wound according to different groups.Wound healing was observed immediately after injury and on days 7,14,and 21 after injury.On day 7 after surgery,hematoxylin-eosin staining was used to observe the expression of inflammation in the wound surface.On day 14 after suregery,Masson staining was used to observe the expression of collagen and immunohistochemical staining was used to observe the expression of CD31 in the wound surface.On day 7 after surgery,western blot assay was performed to detect the expression of α-smooth muscle actin and type Ⅰ collagen in the wound surface.RESULTS AND CONCLUSION:(1)The wound healing was faster in the agomiR-196b-5p group,while it was slower in the blank control group and the exosome+antagomiR-196b-5p group.(2)Compared with the blank control group and the exosome+antagomiR-196b-5p group,the wound infiltration of inflammatory cells was less in the exosome group and the agomiR-196b-5p group,and the expression of CD31 was significantly increased(P＜0.01).(3)Compared with the blank control group and the exosome+antagomiR-196b-5p group,the expression levels of α-smooth muscle actin and type Ⅰ collagen were increased in the exosome group and the agomiR-196b-5p group(P＜0.05).These findings indicate that miR-196b-5p in adipose stem cell-derived exosomes can promote burn wound healing in rats.

BACKGROUND:Currently,miR-196b-5p has been found to play a role in cell proliferation,migration and inhibition of scar hyperplasia,but there is a lack of relevant studies on whether it plays a role in the process of wound healing.OBJECTIVE:To investigate the effect of miR-196b-5p in adipose stem cell-derived exosomes on burn wound healing.METHODS:The models of deep second degree skin burn in SD rats were established and randomly divided into four groups:blank control group,exosome group,agomiR-196b-5p group,and exosome+antagomiR-196b-5p group,with 10 rats in each group.PBS,adipose-derived stem cell-derived exosomes,miR-196b-5p agonist,and miR-196b-5p inhibitor were injected around the wound according to different groups.Wound healing was observed immediately after injury and on days 7,14,and 21 after injury.On day 7 after surgery,hematoxylin-eosin staining was used to observe the expression of inflammation in the wound surface.On day 14 after suregery,Masson staining was used to observe the expression of collagen and immunohistochemical staining was used to observe the expression of CD31 in the wound surface.On day 7 after surgery,western blot assay was performed to detect the expression of α-smooth muscle actin and type Ⅰ collagen in the wound surface.RESULTS AND CONCLUSION:(1)The wound healing was faster in the agomiR-196b-5p group,while it was slower in the blank control group and the exosome+antagomiR-196b-5p group.(2)Compared with the blank control group and the exosome+antagomiR-196b-5p group,the wound infiltration of inflammatory cells was less in the exosome group and the agomiR-196b-5p group,and the expression of CD31 was significantly increased(P＜0.01).(3)Compared with the blank control group and the exosome+antagomiR-196b-5p group,the expression levels of α-smooth muscle actin and type Ⅰ collagen were increased in the exosome group and the agomiR-196b-5p group(P＜0.05).These findings indicate that miR-196b-5p in adipose stem cell-derived exosomes can promote burn wound healing in rats.

Background Long working hours, as a common risk factor for occupational stress, is closely related to the occurrence of depressive symptoms. Understanding how long working hours affect occupational stress and depressive symptoms will inform occupational health interventions. Objective To quantify the impact of long working hours exposure on occupational stress and depressive symptoms among Internet industry employees, translate black-box outputs into actionable insights, and demonstrate the value of interpretable machine learning for early-warning occupational-health surveillance. Methods A dataset was derived from a cross-sectional survey involving 2866 internet industry employees in China. This survey was part of the project Risk Assessment Of Long Working Hour Exposure And Its Adverse Health Effects, conducted by the National Institute for Occupational Health and Poisoning Control, Chinese Center for Disease Control and Prevention, from 2021 to 2023. Working hours, occupational stress and depressive symptoms were quantified with a set of structured questionnaires including the Core Occupational Stress Scale and the Patient Health Questionnaire. Pairwise associations were screened by Mantel tests and variance-inflation factors. Key predictors identified through feature selection were fed into six machine-learning risk-prediction models. Visual interpretation was provided by feature importance, Shapley additive explanations (SHAP) and local interpretable model-agnostic explanations (LIME), while directed causal effects and intervention impacts of prolonged working hours exposure on occupational stress and depressive symptoms were dissected with causal explanation of features techniques. Results The positive rates of occupational stress and depressive symptoms among internet employees were 12.9% and 77.8% respectively. Twelve core features for occupational stress and nine for depressive symptoms were retained after selection. After these features were supplied to six predictive algorithms and evaluated on five metrics, the Light Gradient Boosting Machine (LGBM) achieved the highest accuracy—0.89 for occupational stress and 0.79 for depressive symptoms on the hold-out test set. The feature-importance rankings converged on fatigue accumulation and life satisfaction as dominant drivers for both outcomes, whereas weekly working hours and daily overtime emerged as the principal exposure-related predictors. The SHAP summary plots revealed that longer weekly hours and daily overtime systematically elevated the probability of occupational stress. The causal feature explanation further quantified that ascending one category in weekly working hours increased the probability of occupational stress by 7.04%. Conclusion Exposure to long working hours is associated with both occupational stress and depressive symptoms among internet industry employees. Interpretable machine-learning frameworks translate these associations into transparent, defensible drivers, enabling precise identification of the pivotal factors and their interplay. This evidence base equips occupational-health practitioners with actionable insights for designing targeted prevention and intervention strategies.

Lung cancer remains the most prevalent malignancy worldwide, with the highest incidence and mortality rates. Its complex tumor microenvironment (TME) poses major challenges for conventional two-dimensional (2D) culture systems and animal models, which fail to accurately reproduce in vivo pathological conditions. In recent years, three-dimensional (3D) bioprinting technology—featuring controllable spatial resolution, multi-cell co-printing capability, and structural reproducibility—has emerged as a powerful tool for reconstructing the lung cancer TME. This review systematically summarizes recent progress in 3D bioprinted lung cancer models, encompassing printing techniques, optimization of bio-ink systems, model construction strategies, and the clinical relevance of drug sensitivity testing. Particular attention is given to vascularization and immune co-culture approaches that recapitulate tumor heterogeneity, metabolic gradients, and immune interactions. The advantages of 3D bioprinted models over traditional 2D cultures in predicting therapeutic responses and enabling precision drug screening and personalized treatment are also highlighted. Future research should focus on standardizing bio-ink formulations, integrating patient-derived organoids with microfluidic platforms, and establishing robust evaluation systems to facilitate the clinical translation and application of 3D bioprinting in precision lung cancer diagnosis and therapy.

AIM: To analysis the correlation between extraocular muscle thickness measured by quantitative CT analysis of orbital structures and clinical activity score(CAS)of thyroid-associated ophthalmopathy(TAO).METHODS:This was a retrospective analysis, selecting clinical data of TAO patients admitted to the hospital from October 2020 to February 2025. Healthy individuals were chosen from hospital's physical examination as the control group. All participants underwent CT examination, the superior rectus muscle, inferior rectus muscle, medial rectus muscle, lateral rectus muscle, orbital area, protrusion degree, and total cross-sectional area of extraocular muscles/total orbital area ratio(OM/TOA)from the two groups of participants were compared. CAS was used to evaluate TAO patients, and the correlation between CAS score and quantitative analysis indicators of CT orbital structure was analyzed. Quantitative analysis indicators for CT orbital structure in TAO patients at different stages of activity were compared, and the predictive value of these indicators for TAO patients at different activity stages was investigated.RESULTS:A total of 77 TAO patients were enrolled in this study, including 38 males and 39 females, with ages ranging from 28 to 70 y(mean age 49.5±6.9 y). There were 77 cases in the control group, including 40 males and 37 females, with ages ranging from 26 to 70 y(mean age 49.0±7.3 y). There was no significant difference in gender and age between the two groups(both P>0.05). The quantitative analysis of left eye, right eye, and binocular CT orbital structure in TAO group patients showed significantly higher indicators than the control group(all P<0.001), and the CAS score of TAO group was 3.94±1.51 points. The CAS score was positively correlated with various indicators of CT orbital structure quantitative analysis(all P<0.05). According to the CAS score results, 14 cases(28 eyes)of TAO patients with a CAS score<3 were classified as inactive phase, including 8 males and 6 females, with an average age of 43.79±9.58 y. A total of 63 cases(126 eyes)with a CAS score of ≥3 was classified as active phase, including 30 males and 33 females, with an average age of 50.78±5.47 y. There was no significant difference in gender among TAO patients with different active phases(P=0.519), but there was a significant difference in age(P<0.001). The quantitative indicators of CT orbital structure in inactive patients were significantly lower than those in active patients(P<0.05). Finally, the superior rectus muscle, age, and degree of protrusion were selected to be included in the Logistic regression model. The analysis results showed that there was a correlation between the superior rectus muscle index, degree of protrusion and TAO activity phase(P<0.05), while age, and TAO activity phase showed no significant correlation(P>0.05). The ROC curve analysis results showed that the area under the curve(AUC)was 0.863, the standard error was 0.063, P<0.001, and the 95% confidence interval(95% CI)of AUC was 0.740-0.985. The sensitivity of the model prediction was 73.0%, the specificity was 92.9%, and the Youden index was 0.659. The prediction accuracy was 97.9%, the recall rate was 73.0%, and the F1 value was 0.836. The predicted optimal critical value was 0.857. The predicted probability was 0.74.CONCLUSION:Quantitative CT analysis of orbital structures can be used to assess disease severity in TAO patients.

Hypercoagulable state (HCS) after kidney transplantation is one of the common and serious complications in kidney transplant recipients, which has attracted increasing attention in recent years. HCS refers to the abnormal and excessive activation of blood coagulation function, leading to the increased risk of thrombosis. After kidney transplantation, the combined effects of hemodynamic changes, surgical trauma and severe rejection increase the incidence of HCS, not only raising the risk of thrombosis but also potentially causing graft failure and affecting the postoperative survival rate of patients. This article reviews the influencing factors, clinical manifestations, diagnostic methods and preventive strategies of HCS after kidney transplantation, aiming to provide a theoretical basis for optimizing perioperative management and improving the prognosis of patients.

ObjectiveTo investigate the effect of Danggui Shaoyaosan on ferroptosis in the rat model of non-alcoholic fatty liver disease （NAFLD） and explore the underlying mechanism based on the nuclear factor E₂-related factor 2 （Nrf2）/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） signaling pathway. MethodsThe sixty SD rats were randomly grouped as follows： control， model， Yishanfu （0.144 g·kg^-1）， and low-， medium-， and high-dose （2.44， 4.88， and 9.76 g·kg^-1， respectively） Danggui Shaoyaosan. A high-fat diet was used to establish the rat model of NAFLD. After 12 weeks of modeling， rats were treated with corresponding agents for 4 weeks. Then， the body weight and liver weight were measured， and the liver index was calculated. At the same time， serum and liver samples were collected. The levels or activities of total cholesterol （TC）， triglycerides （TG）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， and Fe²⁺ in the serum and TC， TG， free fatty acids （FFA）， malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione peroxidase （GPX）， and Fe²⁺ in the liver were measured. Hematoxylin-eosin staining and oil red O staining were employed to observe the pathological changes in the liver. Immunofluorescence was used to assess the reactive oxygen species （ROS） content in the liver. Mitochondrial morphology was observed by transmission electron microscopy. The protein levels of Nrf2， SLC7A11， GPX4， transferrin receptor 1 （TFR1）， and divalent metal transporter 1 （DMT1） in the liver were determined by Western blot. ResultsCompared with the control group， the model group showed increases in the body weight， liver weight， liver index， levels or activities of TC， TG， ALT， AST， and Fe²⁺ in the serum， levels of TC， TG， FFA， MDA， Fe²⁺， and ROS in the liver， and protein levels of TFR1 and DMT1 in the liver （P<0.01）， and decreases in the activities of SOD， GPX and the protein levels of Nrf2， SLC7A11， and GPX4 in the liver （P<0.05， P<0.01）. Meanwhile， the liver tissue in the model group presented steatosis， iron deposition， mitochondrial shrinkage， and blurred or swollen mitochondrial cristae. Compared with the model group， all doses of Danggui Shaoyaosan reduced the body weight， liver weight， liver index， levels or activities of TC， TG， ALT， AST， and Fe²⁺ in the serum， levels of TC， TG， FFA， MDA， Fe²⁺， and ROS in the liver， and protein levels of TFR1 and DMT1 in the liver （P<0.01）， while increasing the activities of SOD and GPX and the protein levels of Nrf2， SLC7A11， and GPX4 in the liver （P<0.01）. Furthermore， Danggui Shaoyaosan alleviated steatosis， iron deposition， and mitochondrial damage in the liver. ConclusionDanggui Shaoyaosan may inhibit lipid peroxidation and ferroptosis by activating the Nrf2/SLC7A11/GPX4 signaling pathway to treat NAFLD.

ObjectiveTo observe and analyze the plasma metabolite differences among colorectal cancer patients with spleen-qi deficiency， damp-heat stasis-toxin syndrome（SRYD）， non-spleen-qi deficiency， damp-heat stasis-toxin syndrome（non-SRYD）， and normal human beings（Normal）， aiming to identify unique metabolites specific to SRYD colorectal cancer patients and their potential biomarkers. MethodsBased on the diagnostic criteria of SRYD and non-SRYD colorectal cancer， 30 patients were included， including 10 patients with SRYD colorectal cancer and 20 patients with non-SRYD colorectal cancer， while 10 individuals were recruited for the Normal group. Metabolome sequencing of plasma from the three groups was performed by ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap mass spectrometry（UPLC-Q-Exactive-Orbitrap-MS）. Multivariate statistical analysis were performed by principal component analysis（PCA） and partial least squares-discriminant analysis（PLS-DA）， and the intergroup differential metabolites were identified based on variable importance in the projection（VIP） value>1 and t-test P<0.05. And pathway enrichment analysis based on Kyoto Encyclopedia of Genes and Genomes（KEGG） was performed to explore the metabolites and metabolic pathways specific to SRYD colorectal cancer patients. ResultsMetabolome sequencing results showed some differences in metabolic profiles between the groups. A total of 111 plasma differential metabolites were found in the SRYD group and the Normal group， of which 31 were up-regulated and 80 were down-regulated， mainly including stearoyl lysophosphatidylcholine， indole-3-acrylic acid， and dehydroepiandrosterone sulfate（P<0.05）. The non-SRYD group exhibited 97 differentially expressed metabolites compared to the Normal group， with 36 up-regulated and 61 down-regulated， mainly including stearoyl lysophosphatidylcholine， sphingosine， and palmitoyl lysophosphatidylcholine（P<0.05）. And the SRYD group exhibited 19 differentially expressed metabolites compared to the non-SRYD group， of which 5 were up-regulated and 14 were down-regulated， mainly including dihydrosphingosine， palmitic acid， and linoleoylethanolamide（P<0.05）. The significant differential metabolites were subjected to KEGG analysis to obtain significantly enriched metabolic pathways in each group， and the results showed that 11 metabolic pathways such as primary bile acid synthesis， cholesterol metabolism and bile secretion were differential signaling pathways specific to SRYD colorectal cancer. Further retrieval of the above key signaling pathways showed that bile acids were up-regulated in both bile secretion and primary bile acid synthesis pathways， and there was a trend of up-regulation of glycochenodeoxycholic acid， taurochenodeoxycholic acid， and chenodeoxycholic acid. ConclusionPrimary bile acid synthesis， cholesterol metabolism， and bile secretion-related pathways may be differential signaling pathways specific to SRYD colorectal cancer， and bile acid is a core molecule in the metabolic pathway， which can serve as potential biomarkers closely related to the development and progression of SRYD colorectal cancer.

ObjectiveTo observe and analyze the plasma metabolite differences among colorectal cancer patients with spleen-qi deficiency， damp-heat stasis-toxin syndrome（SRYD）， non-spleen-qi deficiency， damp-heat stasis-toxin syndrome（non-SRYD）， and normal human beings（Normal）， aiming to identify unique metabolites specific to SRYD colorectal cancer patients and their potential biomarkers. MethodsBased on the diagnostic criteria of SRYD and non-SRYD colorectal cancer， 30 patients were included， including 10 patients with SRYD colorectal cancer and 20 patients with non-SRYD colorectal cancer， while 10 individuals were recruited for the Normal group. Metabolome sequencing of plasma from the three groups was performed by ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap mass spectrometry（UPLC-Q-Exactive-Orbitrap-MS）. Multivariate statistical analysis were performed by principal component analysis（PCA） and partial least squares-discriminant analysis（PLS-DA）， and the intergroup differential metabolites were identified based on variable importance in the projection（VIP） value>1 and t-test P<0.05. And pathway enrichment analysis based on Kyoto Encyclopedia of Genes and Genomes（KEGG） was performed to explore the metabolites and metabolic pathways specific to SRYD colorectal cancer patients. ResultsMetabolome sequencing results showed some differences in metabolic profiles between the groups. A total of 111 plasma differential metabolites were found in the SRYD group and the Normal group， of which 31 were up-regulated and 80 were down-regulated， mainly including stearoyl lysophosphatidylcholine， indole-3-acrylic acid， and dehydroepiandrosterone sulfate（P<0.05）. The non-SRYD group exhibited 97 differentially expressed metabolites compared to the Normal group， with 36 up-regulated and 61 down-regulated， mainly including stearoyl lysophosphatidylcholine， sphingosine， and palmitoyl lysophosphatidylcholine（P<0.05）. And the SRYD group exhibited 19 differentially expressed metabolites compared to the non-SRYD group， of which 5 were up-regulated and 14 were down-regulated， mainly including dihydrosphingosine， palmitic acid， and linoleoylethanolamide（P<0.05）. The significant differential metabolites were subjected to KEGG analysis to obtain significantly enriched metabolic pathways in each group， and the results showed that 11 metabolic pathways such as primary bile acid synthesis， cholesterol metabolism and bile secretion were differential signaling pathways specific to SRYD colorectal cancer. Further retrieval of the above key signaling pathways showed that bile acids were up-regulated in both bile secretion and primary bile acid synthesis pathways， and there was a trend of up-regulation of glycochenodeoxycholic acid， taurochenodeoxycholic acid， and chenodeoxycholic acid. ConclusionPrimary bile acid synthesis， cholesterol metabolism， and bile secretion-related pathways may be differential signaling pathways specific to SRYD colorectal cancer， and bile acid is a core molecule in the metabolic pathway， which can serve as potential biomarkers closely related to the development and progression of SRYD colorectal cancer.

The prevalence rate of metabolic associated fatty liver disease （MAFLD） is steadily increasing worldwide， and MAFLD is now considered a significant risk factor for a wide range of metabolic comorbidities. However， current clinical management strategies often address MAFLD from a single-disease perspective， lacking a comprehensive understanding of the central role and systemic impact of MAFLD in the prevention and control of metabolic comorbidities. This article reviews the current evidence supporting MASLD as both a trigger and a key node in systemic metabolic dysfunction and elaborates on how hepatic insulin resistance， lipotoxic injury， inflammatory responses， and dysregulation of hepatokines mediate organ-specific metabolic disorders including cardiovascular disease， chronic kidney disease， and diabetes. With reference to the latest national and international guidelines， this article proposes an integrated multidisciplinary management strategy， including liver-glucose joint intervention and a cross-organ “cardio-renal-hepatic” strategy， and it also advocates for a paradigm shift from conventional liver-focused management toward liver-centered systemic metabolic control， in order to effectively delay the progression of MAFLD and its related multisystem complications.