Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Objective To investigate the changes of macrophages and hemophagocytes in bone marrow smears of patients with multiple myeloma(MM)before and after chemotherapy and their correlation with clinical prognostic value.Methods A total of 300 MM patients treated in Liaocheng Second People's Hospital Affiliated to Shandong First Medical University from June 2018 to June 2023 were selected as the study objects.All patients received at least 3 courses of chemotherapy and were divided into the remission group(n=214)and the non-remission group(n=86)according to the clinical effect.Immunoglobulin(Ig)A,IgG,CD3+,CD4+,CD8+,interleukin(IL-2),IL-4,IL-6,IL-17,tumor necrosis factor(TNF)-α,transforming growth factor(TGF)-β,macrophages and hemophagocytes were detected in the two groups and compared between the two groups.COX regression was used to analyze the relationship between immunological indexes and non-remission of chemotherapy.The relationship between macrophages and hemophagocytes and non-remission of chemotherapy was analyzed by restricted cubic spline.The multiplicative interaction of macrophages and hemophagocytes on non-remission of chemotherapy was analyzed using an unconditioned Logistic regression model,and the additive interaction was analyzed using the interaction calculation table.Receiver operating characteristic(ROC)curve analysis of macrophages and hemophagocytes alone or in combination to determine the value of chemotherapy non-remission.Results The overall response rate(ORR)and non-response rate(NRR)of MM patients were 71.33%and 28.67%respectively.Compared with before treatment,IgA,IgG,CD8+,IL-6,IL-17,TNF-α,TGF-β,macrophages and hemophagocytes were significantly decreased in both groups after treatment(tslow=9.252～61.177,tnot slow=4.057～35.797).CD3+,CD4+,CD4+/CD8+,IL-2 and IL-4 were significantly increased(tslow=9.706～33.940,tnot slow=4.227～16.167),and the differences were statistically significant(all P<0.05).After treatment,compared with the remission group,IgA,IgG,CD8+,IL-6,IL-17,TNF-α,TGF-β,macrophages and hemophagocytes in the non-remission group were significantly higher than those in remission group(t=3.362～30.028),CD3+,CD4+,CD4+/CD8+,IL-2 and IL-4 were significantly lower than those in remission group(t=3.736～13.998).and the differences were statistically significant(all P＜0.05).After adjusting the influence of other factors by COX regression,the trend test of macrophages and hemophagocytes was still statistically significant the trend test of macrophages and hemophagocytes was still statistically significant(P<0.05).Patients with≥5 macrophages/tablet and≥3 hemophagocytes/tablet had a significantly increased risk of non-remission from chemotherapy(P<0.05).There were additive(OR=6.157,95%CI:3.768～12.978)and multiplicative(OR=5.648,95%CI:1.035～17.492)interactions between macrophages and hemophagocytes in the non-remission of chemotherapy.Compared with the single judgment of macrophages and hemophagocytes,the combination of the two has the highest accuracy in determining chemotherapy non-remission(P＜0.05).Conclusion Macrophages and hemophagocytic cells in MM patients after chemotherapy are significantly lower than those before chemotherapy,with≥5 macrophages/tablet and≥3 hemocyte phages/tablet,indicating that the risk of non-remission in patients with chemotherapy increased significantly,and the combination of the two can accurately judge the clinical efficacy.

Objective To establish a rat model of ovarian endometriosis(EMS)using the horn reversion method,to provide an ideal animal model for exploring the pathogenesis and treatment of EMS.Methods Fifty SPF-grade female SD rats were divided randomly into five groups:a sham group,and 1,2,3,and 4 weeks after surgery groups,respectively(n=10 rats per group).Apart from the sham group,an ovarian-type EMS model was established in the other groups by the uterine horn refracture method,and the modeling success rate,and ectopic foci volume and mass were observed in each group.The morphology of ectopic foci was observed by hematoxylin-eosin(HE),and expression of proliferating cell nuclear antigen(PCNA),Ki67,epithelial cadherin(E-cadherin),and neural cadherin(N-cadherin)in the uterus and ectopic foci tissues were detected by immunohistochemistry.The model was further evaluated and the degree of cell proliferation and epithelial mesenchymal transformation at different times after modeling were analyzed.Results The modeling success rates in the 1,2,3,and 4 weeks after surgery groups were 80%,90%,100%,and 100%,respectively(P＞0.05).The volume and mass of the ectopic foci were significantly greater in the 3 and 4 weeks after surgery groups compared with the 1 and 2 weeks after surgery groups(P＜0.01).HE staining showed endometrial epithelial cells,mesenchymal cells and a few glands in the ectopic foci tissues.Immunohistochemical staining showed that expression levels of Ki67,PCNA,and N-cadherin in uterus tissues were significantly higher(P＜0.05,P＜0.01)in all the model groups compared with the sham group,while expression levels of E-cadherin were significantly lower(P＜0.05,P＜0.01).Expression levels of Ki67,PCNA,and N-cadherin in the uterus and ectopic foci tissues were significantly higher(P＜0.05,P＜0.01)in the 2,3,and 4 weeks after surgery groups compared with the 1 week after surgery group,while expression levels of E-cadherin were significantly lower(P＜0.05,P＜0.01).Conclusion The uterine horn reversion method can be used to establish an ovarian EMS model in rats.Ectopic lesions can be observed 1 week after surgery.The success rate of modeling increases with modeling time,stabilizing at 3 weeks postoperatively.Ki67,PCNA,and N-cadherin were significantly expressed in the uterus and ectopic foci tissues,and their expression levels increased with modeling time,while E-cadherin expression in the uterus and ectopic foci tissues decreased with modeling time.These results showed good modeling success of the EMS rat model,suggesting that it could be used as a stable EMS modeling method.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Objective:To investigate the efficacy and potential mechanism of sulfasalazine (SASP) therapy for intrahepatic cholestasis.Methods:Forty SD rats were randomly divided into a normal group (carboxymethylcellulose sodium 0.5%), a model group (carboxymethylcellulose sodium 0.5%), a SASP group (sulfasalazine 150 mg/kg), and an ursodeoxycholic acid (UDCA 100 mg/kg) group, with ten rats in each group. The cholestatic liver injury model was induced using α-naphthylisothiocyanate. Blood samples were collected to detect liver biochemistry and cholestasis indexes. Rat liver tissue was collected for hematoxylin-eosin staining and Mason staining. Liver tissue was analyzed using transcriptome sequencing, real-time reverse transcription quantitative polymerase chain reaction, Western blotting and flow cytometry. Simultaneously, the level of inflammatory factors, total cholesterol, and total bile acids were measured in liver tissue. A t-test or a nonparametric test was selected based on the distribution and variance characteristics of the data. Results:The serum levels of alanine aminotransferase [(386.88±155.77) U/L], aspartate aminotransferase [(593.13±251.44) U/L], alkaline phosphatase [(561.25±167.54) U/L], total bilirubin [(38.00±29.75) mol/L] and total bile acids [(191.31±91.48) mol/L] were significantly lower in the SASP than the model groups [(778.75±313.59) U/L, (1 159.38±274.62) U/L, (801.25±161.28) U/L, (86.63±27.83) mol/L, (432.63±151.54) mol/L, P<0.05]. Liver histopathology showed that the inflammatory cells in the manifold area, the bile duct proliferation and dilation, and the collagen deposition in the manifold area were significantly improved under the pathological state of cholestasis in the SASP group. The results of transcriptome sequencing demonstrated that SASP activated the peroxisome proliferator actived receptor α (PPAR α) and inhibited Th17 cell differentiation. The PPARα mRNA level in the liver tissue of rats was significantly increased in the SASP group compared with that in the model group [(0.41±0.28) vs. (0.16±0.04), P<0.05], and the expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase was decreased compared with that in the model group [(3.09±1.16) vs. (8.19±2.19), P<0.05], which was also verified at the protein level. The concentrations of total cholesterol [(0.31±0.34) mmol/g] and total bile acids [(2.58±0.99) μmol/g] were lower than the model group [(0.83±0.62) mmol/g and (4.07±0.91) μmol/g] ( P<0.05), and at the same time it was accompanied by lower levels of inflammatory factors ( P<0.05). SASP treatment decreased the expression of retinoic acid receptor-related orphan receptor γt gene ( P<0.05) and the proportion of Th17 ( P<0.05). Conclusion:SASP can improve cholestatic liver injury, and its mechanism is related to the activation of peroxisome proliferator-activated receptor α and the inhibition of Th17 cell differentiation.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Objective To systematically review and quantify the content and structure of the non-accompanied wards policy texts at the provincial level in China from the perspective of policy tools,providing references and insights for optimizing and implementing future policies.Methods Using the policy analysis tools as framework,it applies content ana lysis to construct a two-dimensional analytical framework with the X-dimension and Y-dimension.A total of 19 policy texts related to non-accompanied ward issued by provincial governments in China from January 2000 to August 2024 were coded and analyzed.Results A total of 141 entries were coded.In the X-dimension,supply-oriented,demand-oriented,and environment-oriented policy tools accounted for 21.28%,19.86%,and 58.86%,respectively,indicating a greater reliance on environmental-oriented policy tools;In the Y-dimension,policies from the"12th Five-Year Plan"(16.31%),"13th Five-Year Plan"(14.89%),and"14th Five-Year Plan"(68.80%)phases were analyzed.The number of policies in the"14th Five-Year Plan"phase was the highest among the three periods.Conclusion The policy framework for non-accompanied wards in China is still in its initial exploration phase and has room for improvement.It is recommended that future policies optimize the use of policy tools,strengthen coordination among them,and support the development of non-accompanied wards.

Objective:To explore and practice the construction of an innovative ecosystem that integrates innovation in the National Clinical Research Center for Orthopedics and Sports Rehabilitation, providing references and insights for driving high-quality development of medical care.Methods:Guided by a national policy framework and Industry-Academia-Research-Government-Enterprise Collaborative Innovation, the Center had established six innovation platforms and three systemic pillars. The study analyzed its integrated strategy, which encompassed ecosystem design, platform-enabled empowerment, comprehensive system support, end-to-end coverage, a folded innovation approach, and a standardization-driven mechanism.Results:The Center had built a highly integrated innovation ecosystem, creating a powerful driver for technological advancement and commercialization in orthopedics and sports rehabilitation, accelerating the industrialization of key technologies like surgical robots and 3D-printed implants.Conclusions:Guided by the principle of ″simplifying complex surgeries and standardizing common procedures″, the Center will leverage digital intelligence throughout clinical care, aiming to bridge gaps in healthcare quality so that patients can receive top-tier treatment for major diseases within their home provinces. This commitment to homogenized, high-quality care presents a ″China Model″ for global health and advance the national ″Healthy China″ initiative.