Flap transplantation is a critical surgical strategy for the reconstruction of tissue defects caused by trauma, tumor resection, and congenital malformations, and its survival rate directly determines surgical efficacy and patient prognosis. Following transplantation, flaps inevitably undergo ischemia-reperfusion (I/R) injury, during which oxidative stress, inflammatory responses, and metabolic disturbances are intricately intertwined, ultimately leading to cellular injury and tissue necrosis. Recent studies have demonstrated that multiple forms of programmed cell death—including apoptosis, pyroptosis, ferroptosis, necroptosis, and PANoptosis—play central roles in flap I/R injury. The extensive crosstalk and molecular interactions among these pathways form a highly complex cell death network. Specifically, apoptosis is mediated by the imbalance of Bcl-2 family proteins and the activation of cysteine-dependent aspartate-specific protease (caspase) cascades; pyroptosis is driven by the NLRP3-caspase-1-GSDMD axis, resulting in membrane pore formation and the release of pro-inflammatory cytokines; ferroptosis is characterized by iron-dependent lipid peroxidation and dysfunction of glutathione peroxidase 4 (GPX4); necroptosis is triggered by the receptor-interacting serine/threonine-protein kinase 1 (RIPK1)-RIPK3-MLKL signaling complex, leading to membrane rupture; and PANoptosis represents an integrated form of inflammatory cell death that coordinates multiple death pathways. Importantly, these forms of programmed cell death are not independent but are interconnected through extensive signaling crosstalk. Key regulatory molecules, including caspase-8, reactive oxygen species (ROS), nuclear factor-κB (NF-κB), and nuclear factor erythroid 2-related factor 2 (Nrf2), collectively modulate the dynamic balance among these pathways. Therefore, the multidimensional interplay and spatiotemporal dynamics of programmed cell death constitute a fundamental pathological basis of flap I/R injury. This review systematically summarizes the latest advances in the mechanisms and interactions of various programmed cell death pathways in flap I/R injury, aiming to elucidate the underlying regulatory network. These insights may provide novel theoretical foundations for optimizing flap protection strategies, improving flap survival, and promoting tissue repair.

BACKGROUND:Persistent hyperglycemia has been identified as promoting neurovascular dysfunction,leading to irreversible endothelial dysfunction,increased neuronal apoptosis,oxidative stress and inflammation.These changes in combination or alone lead to microvascular and macrovascular lesions as well as progressive neuropathy.Noncoding RNAs may provide a new strategy for understanding the etiology,pathogenesis and treatment of the disease. OBJECTIVE:To review the role and mechanism of noncoding RNAs in the occurrence and development of diabetic peripheral neuropathy by reviewing relevant literature at home and abroad,in order to provide new ideas and approaches for noncoding RNAs in the prevention,diagnosis and treatment of diabetes neuropathy. METHODS:CNKI and PubMed were retrieved for relevant literature published from database inception to 2022.The key words were"noncoding RNA;lncRNA;miRNA;diabetes peripheral neuropathy;expression profile"in Chinese and English,respectively.The retrieved documents were summarized and analyzed,and 61 articles were finally selected for further review. RESULTS AND CONCLUSION:(1)Noncoding RNA plays a key role in the pathophysiological process of diabetic peripheral neuropathy.Among the most widely studied regulatory noncoding RNA species,there are long noncoding RNAs,circular RNAs and microRNAs.(2)Through the regulation of noncoding RNAs,the activation or inhibition of related cell pathways,inflammatory genes and downstream-related cytokines will inhibit cell apoptosis,improve inflammation,and thus change the expression of target genes to participate in the process of diabetic neuralgia.(3)Although many microRNAs and long noncoding RNAs have been found to participate in diabetic peripheral neuropathy,the mechanisms of many noncoding RNAs are unclear,and the same noncoding RNAs may play different roles in different modes.Therefore,it is necessary to further study their action modes in disease etiology and pathology,thereby clarifying their role in the pathogenesis of diabetic peripheral neuropathy.However,the criteria for evaluating noncoding RNA activity have not yet been established,and further research is needed on which specific noncoding RNAs play a dominant regulatory role.(4)MicroRNAs,long noncoding RNAs and their target genes can regulate progressive neuropathy,which are expected to become new targets for the clinical prevention and treatment of diabetic peripheral neuropathy and new biomarkers for the development and prognosis of diabetic peripheral neuropathy.

Objective To investigate the clinical efficacy of percutaneous minimally invasive anchorage in the treatment of acute closed rupture of Achilles tendon. Methods A retrospective casecontrol study was conducted on the clinical data of 32 patients (16 cases on the left side and 16 cases on the right side) with acute closed Achilles tendon rupture treated from January 2015 to January 2017. There were 27 males and five females, aged 24-67 years (mean, 40.8 years). The patients were divided into treatment group which adopted percutaneous minimally invasive combined with anchor suture and control group which used simple minimally invasive suture, with 16 cases in each group. The operation time, hospitalization time, sural nerve injury, single foot heel raise at 3 months and 6 months, difference of calf circumference on the rupture surface between the affected side and healthy side at 6 months, ankle back foot score scale (AOFAS), and infection at 6 months were recorded. Results All patients were followed up for average 8.9 months (range, 6-12 months). In treatment group, the operation time was (35.75 ±3.10) minutes and hospitalization time was (8.38±1.62) days. The AOFAS score was(92.12 ±5.86)points. The result of single foot heel raise was positive in one case at 3 months and in 0 case at 6 months. The difference of calf circumference on the rupture surface between the affected side and healthy side at 6 months was (2.23 ±0.97)cm. In the control group, the operation time was (33.43± 3.89)minutes and hospitalization time was (8.50±1.75)days. The AOFAS score was (91.00 ±7.15) points at 6 months. The result of single foot heel raise was positive in eight cases at 3 months and in 0 case at 6 months. The difference of calf circumference on the rupture surface between the affected side and healthy side at 6 months was (1.64 ±2.34) cm. There were no significant differences between the two groups in operation time, hospitalization time, the AOFAS score at 6 months, and the results of single foot heel raise at 6 months(P ＞0.05). Treatment group had better results than control group in terms of the difference of calf circumference on the rupture surface between the affected side and healthy side at 6 months as well as the result of single foot heel raise at 3 months (P ＜ 0.05). No infection and sural nerve injury were found in either group. Conclusion The repair of Achilles tendon rupture by percutaneous minimally invasive anchor technique can help patients achieve heel raise early, obtain better muscle capacity, and return to work earlier.