Ming Cheng

Background: Sciatica is a common neuropathic pain condition associated with substantial functional disability. Emerging evidence suggests that diet-induced inflammation may play a role in chronic pain development. However, the association between dietary inflammatory potential and clinical outcomes in sciatica remains unclear. Methods: In this cross-sectional study, we enrolled 598 patients diagnosed with sciatica from two hospitals in Sichuan Province, China. The Dietary Inflammatory Index (DII) was calculated from food frequency questionnaires. Pain intensity and functional disability were assessed using the Visual Analog Scale (VAS) and Oswestry Disability Index (ODI), respectively. Serum C-reactive protein (CRP) was measured as an inflammatory biomarker. Correlation analysis, multivariable linear regression, mediation analysis, and restricted cubic spline models were applied. Results: In adjusted models ( n = 598; mean age 55.6 years, 47.5% male), higher DII scores were strongly associated with greater pain and disability. Each 1-unit increase in DII corresponded to a 0.48-point increase in VAS ( β = 0.48, 95% CI: 0.42–0.53, partial R ² ≈ 0.31) and a 4.75-point increase in ODI ( β = 4.75, 95% CI: 4.16–5.34, partial R ² ≈ 0.30; all p < 0.001). The magnitude of the association with VAS exceeded the commonly reported minimal clinically important difference (≈1.5 points) for leg pain, suggesting clinical relevance. DII was not significantly associated with CRP, and CRP did not mediate the DII–pain relationship. Nonlinear dose–response patterns were observed for both VAS and ODI. Conclusion: Pro-inflammatory dietary patterns, as reflected by higher DII scores, are independently associated with greater pain and disability in patients with sciatica, not mediated by CRP but likely involving broader inflammation-related pathways. These findings highlight the potential role of anti-inflammatory nutritional strategies in the integrative management of sciatica.

The ACL rupture is a prevalent and debilitating joint injury that has garnered significant clinical and scientific interest. Surgical reconstruction is often necessary for ACL rupture, yet numerous clinical cases indicate that the outcomes of such procedures are frequently suboptimal. Research has highlighted that the treatment of ACL rupture is particularly challenging due to factors such as the inflammatory response, the formation of vascular scar tissue, and the slow healing of tendon-bone interface attachment points. These complications result in poor integration of tendon grafts within bone tunnels. Recent advancements in stem cell research have introduced new possibilities for ACL rupture treatment. However, stem cell therapy is not without its limitations, including safety concerns such as the risk of aberrant differentiation leading to oncogenesis. Exosomes, a type of extracellular vesicle secreted by stem cells, have been found to modulate immune responses, promote neovascularization, influence scar formation, and regulate bone homeostasis in vivo . This review seeks to systematically evaluate the therapeutic potential of stem cell-derived exosomes in the context of ACL rupture repair.

Background: Body mass index (BMI) is a known risk factor for poor glycemic control in patients with Type 2 diabetes mellitus (T2DM). However, the extent to which BMI correlates with glycated hemoglobin (HbA1c) levels and its clinical implications require further investigation. Objective: This study aimed to assess the relationship between BMI and HbA1c levels in T2DM patients and to explore the clinical significance of BMI management in optimizing glycemic control. Methods: A cross-sectional study was conducted on 200 T2DM patients from Jinniu District Hospital between 2024/04/01 and 2024/10/03. BMI and HbA1c levels were recorded, and patients were categorized into normal weight (BMI < 25 kg/m²), overweight (25 ≤ BMI < 30 kg/m²), and obese (BMI ≥ 30 kg/m²). Pearson correlation analysis was used to assess the relationship between BMI and HbA1c. One-way ANOVA was employed to compare HbA1c levels across BMI categories. Results: A significant positive correlation between BMI and HbA1c was observed (r = 0.45, P < 0.001). Obese patients had significantly higher HbA1c levels (8.5 [7.8– 9.0]%) compared to overweight (7.7 [7.2– 8.1]%, P < 0.01) and normal-weight patients (6.9 [6.4– 7.5]%, P < 0.001). The graded relationship indicated worsening glycemic control with increasing BMI. Conclusion: Higher BMI is associated with poorer glycemic control in T2DM patients. Obese patients, in particular, may benefit from more intensive weight management strategies to reduce HbA1c levels and prevent diabetes-related complications. These findings underscore the importance of integrating BMI reduction into diabetes management plans to improve clinical outcomes.

探讨强直性脊柱炎（ankylosing spondylitis, AS）中组蛋白H3K27me3甲基化及其调节酶JMJD3和EZH2在Th17细胞分化中的作用，以揭示其在AS发病机制中的潜在作用。通过分析H3K27me3的甲基化状态及其与Th17相关因子之间的相互作用，为AS的临床治疗提供新的策略和靶点。 采集84名AS的患者（活跃期、稳定期各42例）和84名健康志愿者（对照组）血液样本，ELISA检测Th17细胞及相关细胞因子（IL-21、IL-22和IL-17），RT-PCR分析Th分化关键信号通路 RORc、 JAK2、 STAT3基因的表达，蛋白质印迹法检测RORc、JAK2/STAT3通路蛋白、H3K27me3及相关蛋白酶EZH2、JMJD3的表达。对活动期AS患者H3K27me3、EZH2、JMJD3与Th分化关键信号通路分子的关联性进行Pearson相关分析。 RORc、 JAK2、 STAT3 mRNA表达，活动期组>稳定期组，差异有统计学意义（ PP稳定期组>对照组，差异有统计学意义（ PPP<0.05）。 AS中H3K27me3的低表达受到基因位点JMJD3和EZH2的影响，可以调节Th17细胞的分化，从而在AS的发病和进展中发挥作用。

分析骨髓间充质干细胞（BMSCs）对骨质疏松（OP）性椎体骨折大鼠骨碱性磷酸酶（BALP）/Ⅰ型胶原交联C-末端肽（CTX-1）表达与力学动态的影响。 把60只SD雌性大鼠均等划入至假手术组（sham组）、OP性椎体骨折大鼠组（OP组）、行BMSCs处理的OP性椎体骨折大鼠组（BMSCs组），对比3组动物骨动力学改变、骨定量振幅衰减（BUA）状况、骨密度（BMD），经由HE染色查看椎体骨组织形态学与参数；ELISA测定血清内CTX-1、BALP水平。 力学对比表明，在L₅椎体与右侧股骨力学改变方面，对比3组实验动物发现存在显著区别（PPPPPP>0.05）。在骨小梁数量上，与sham组相比，OP组明显偏少，同时分布失调缺乏规则性；在此项指标上，与OP组相比，BMSCs组偏多，同时分布较为规则。相较于sham组，OP组椎体骨组织学形态参数出现大幅改变，MTPT与TBV这2项参数皆大幅下降，MAR与TRS参数皆大幅上调（PPPP<0.05）。 BMSCs对OP性椎体骨折大鼠力学改变具改善作用，可提升骨组织最大荷载与弹性模量，同时BMSCs可上调血清内BALP表达，使CTX-1表达下调，由此帮助OP性椎体骨折大鼠早日愈合。

OBJECTIVE: Our aim is to investigate the correlation between risk factors of postmenopausal osteoporotic fracture, BMD and Bone turnover markers, lipid metabolism and BMI. SUBJECTS AND METHODS: The Cox proportional hazard model was used to conduct univariate and multivariate analysis to screen the risk factors related to postmenopausal osteoporotic fractures. Blood samples were collected to detect biochemical markers of bone turnover, blood lipids content, and then measure the BMI of the survey subjects. BMD was measured and its correlation with biochemical markers of bone turnover, lipid metabolism and BMI was analyzed. RESULTS: Cox univariate analysis indicated that average age, menopause, years since menopause, number of deliveries, and limb spasm are associated covariates of postmenopausal osteoporotic fractures. Where, BMD severity, history of hysterectomy or ovariectomy, and years since menopause are significant covariates for the incidence of postmenopausal osteoporotic fractures. The correlation study with lipid metabolism found that the smaller the BMI value, the greater the BMD loss; the smaller the TG value, the greater the BMD loss, exhibiting a downward trend. No difference was observed between HDL-C and LDL-C content, and the difference was not statistically significant (p>0.05). Femoral neck BMD was negatively correlated with CatheK, serum osteocalcin, PINP, ss-crosslaps and TRAP, and lumbar spine BMD was also negatively correlated with CatheK, serum osteocalcin, PINP, ss-crosslaps and TRAP. CONCLUSIONS: Biochemical markers of bone turnover are highly expressed in postmenopausal women and increase with the decrease of bone density, which can be used as markers for disease prediction. Combined with BMI, triglyceride and other related indicators, and closely related factors such as the patient's age, the number of deliveries, it is possible to predict the incidence of PMOP fractures early.

Background: Enoxaparin is an anticoagulant that falls in the class of medications called low molecular weight heparins (LMWHs), and is used to prevent or treat patients with deep vein thrombosis (DVT) and pulmonary embolism. Enoxaparin is the most widely used LMWH for DVT prophylaxis following knee or hip replacement surgery. Common side effects of enoxaparin include bleeding, petechiae at the injection site, and thrombocytopenia. However, reactive thrombocytosis is a rarely reported adverse reaction. We managed a patient who developed enoxaparin-associated thrombocytosis, which was completely resolved after treatment cessation. Case presentation: A 78-year-old female was hospitalized for post-hip replacement rehabilitation. Low molecular weight heparin 40 mg/day was administered subcutaneously to prevent deep venous thrombosis (DVT). At admission, her platelet count was normal (228 × 10⁹/L) and her white blood cell count was slightly elevated (12.91 × 10⁹/L). Seven days after admission, the patient developed thrombocytosis, which peaked on the 14th day (836 × 10⁹/L), while her white blood cell count had returned to normal (8.86 × 10⁹/L). Her therapeutic regimen was reviewed, and enoxaparin was identified as a potentially reversible cause of reactive thrombocytosis. Switching from enoxaparin to rivaroxaban lead to a gradual decrease in the patient’s platelet count, which eventually returned to normal levels 16 days after enoxaparin was discontinued. No complications secondary to thrombocytosis was observed, and no conclusion was reached on the use of small doses of aspirin for antithrombotic therapy under these circumstances. Conclusion: Enoxaparin-induced reactive thrombocytosis should be suspected in patients with thrombocytosis following enoxaparin administration as an anticoagulant to prevent certain complications.