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.

Bone defect is the loss of bone tissue due to trauma, fracture, infection, etc. This loss may lead to non-union of fracture, bone defect or bone deficiency, which seriously affects the patient's quality of life and even leads to dysfunction and disability. Although surgical repair is a common treatment modality, the surgical procedure is complicated, with a long postoperative recovery period and certain surgical risks, such as infection and bleeding. Platelet-rich plasma (PRP), as a novel therapeutic approach, has demonstrated remarkable potential in bone defect repair. PRP is rich in growth factors, such as platelet-derived growth factor (PDGF), transforming growth factor-β (TGF-β), vascular endothelial growth factor (VEGF), etc., and can have a beneficial effect on bone defect repair through various mechanisms, such as the release of growth factors, the promotion of angiogenesis, the inhibition of inflammatory response, and the recruitment of activated cells and other mechanisms, which play a positive role in the repair of bone defects and provide strong support for the regeneration and repair of bone tissue.

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.

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.