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:It has been shown that Gushukang affects bone metabolism by regulating nucleotide and amino acid metabolism and immune mechanisms.Current research on the mechanism of Gushukang in the treatment of osteoporosis primarily focuses on osteoblast regulation and requires further improvement from the perspective of osteoclasts. OBJECTIVE:To investigate the mechanism by which Gushukang interferes with osteoclasts in the treatment of osteoporosis using RAW264.7 cells as the research model. METHODS:Twenty-four 8-week-old female Sprague-Dawley rats were randomly divided into four groups(n=6 per group):the three experimental groups were given 1,2 and 4 g/kg osteoporosis solution by gavage(2 times per day),and the control group was given an equal amount of distilled water by gavage(2 times per day).After 7 days of intragastric administration,aortic blood samples were extracted to collect serum samples using centrifugation,and serum samples from the same groups were combined to obtain the low-,medium-,and high-concentration Gushukang-containing and normal sera for the subsequent experiments.(1)RAW264.7 cells were cultured in six groups:normal serum was added to the control group;low,medium,and high concentration groups were added with low,medium,and high concentrations of Gushukang-containing serum,respectively;ML385,a nuclear factor erythroid 2-related factor 2(Nrf2)inhibitor was given in the Nrf2 inhibitor group;and t-BHQ,a Nrf2 activator,was added in the Nrf2 activator group.Cell viability was detected using the cell counting kit-8 assay.(2)The 3rd generation RAW 264.7 cells were cultured and divided into five groups:the blank control group was added with normal serum,the osteoclast group was added with receptor activator of nuclear factor κB ligand(RANKL),and the low-,medium-,and high-concentration groups were added with low-,medium-,and high-concentration Gushukang-containing serum based on the addition of RANKL.Tartrate-resistant acid phosphate staining was performed after 5 days of culture.(3)RAW264.7 cells were cultured and divided into five groups:blank control group was cultured with normal serum,osteoclast group cultured with normal serum and RANKL,high concentration+osteoclast group cultured with RANKL+high concentration Gushukang-containing serum,osteoclast+Nrf2 agonist group cultured with RANKL+t-BHQ,and high concentration+osteoclast+Nrf2 inhibitor group cultured with RANKL+high concentration Gushukang-containing serum+ML385.Western blot assay and determination of reactive oxygen content were performed after 5 days of culture. RESULTS AND CONCLUSION:The cell counting kit-8 results indicated that Gushukang-containing serum,NRF2 inhibitor or agonist had no significant effect on RAW264.7 cell viability.Tartrate-resistant acid phosphate staining results demonstrated that Gushukang-containing serum exhibited a concentration-dependent inhibitory effect on osteoclast differentiation.Western blot analysis and determination of reactive oxygen species revealed that compared with the blank control group,Nrf2 protein expression was decreased in the osteoclast group(P<0.05),while c-Fos and NFATc1 protein expression and reactive oxygen species content were elevated(P<0.05);compared with the osteoclast group,Nrf2 protein expression was elevated and reactive oxygen species content was decreased in the high-concentration+osteoclast group,osteoclast+Nrf2 agonist group,and high-concentration+osteoclast+Nrf2 inhibitor group(P<0.05),while c-Fos and NFATc1 protein expression was decreased in the high concentration+osteoclast group and osteoclast+Nrf2 agonist group(P<0.05);compared with the high concentration+osteoclast group,Nrf2 protein expression was decreased(P<0.05)and reactive oxygen species content was elevated(P<0.05)in the high concentration+osteoclast+Nrf2 inhibitor group.To conclude,Gushukang reduces reactive oxygen species production by activating Nrf2,thereby inhibiting downstream of the c-Fos/NFATc1 pathway and suppressing osteoclast differentiation.

Objective:To address the challenges in cultivating young medical researchers, including the lack of initial research funding, insufficient interdisciplinary collaboration, absence of academic exchange platforms, and inadequate talent incentives, this study analyzes the specific practical measures of the new model(Fund-Alliance-Academic activities-Award Model, hereinafter referred to as ″FAAA model″) of A certain medical college in enhancing the innovative capabilities and interdisciplinary research proficiency of young medical talents in initial stage, and evaluates the practical significance of these initiatives.Methods:Through literature review, the inevitability of interdisciplinary integration was examined in the context of China′s developmental needs and medical discipline advancement. Innovative practices under the FAAA model of A certain medical college were retrospectively analyzed, focusing on the construction of a medical youth scientific innovation and development platform.Results:The FAAA model had achieved effective outcomes in improving young researchers′ capabilities, fostering interdisciplinary achievements, expanding academic influence, and advancing talent echelon development, yet required further refinement.Conclusions:The FAAA model effectively addresses critical bottlenecks in the growth of young medical researchers through systematic support mechanisms, significantly enhancing their scientific competitiveness and interdisciplinary innovation capacity. Its practical measures offer referential value for peer institutions. Future efforts should optimize the ″early funding-achievement incubation-national project linkage″ chain, strengthen institutionalized interdisciplinary collaboration, and build a data-driven ecosystem to provide sustainable talent support for medical science and technology innovation.

Objective:To explore the key components and mechanism of Qufeng Ningfei Powder in treating asthma through qualitative analysis of its blood components, combined with network pharmacology and molecular docking techniques.Methods:The blood components of Qufeng Ningfei Powder were qualitatively analyzed using UPLC-QE-Orbitrap-MS technology. R language was employed to analyze chip data from the GEO database, obtaining a list of differentially expressed genes. SwissTargetPrediction was utilized to predict the targets of drug components. Asthma-related targets were searched through databases such as OMIM, GeneCards, and TTD. The intersection of drug and disease targets was identified using Venn online analysis tool, constructing a "drug-component-target-disease" network to screen potential core components. A protein-protein interaction network (PPI) of core targets was constructed using STRING platform and Cytoscape software. GO function enrichment and KEGG pathway analysis were conducted using DAVID database to validate potential mechanism. Molecular docking was performed to verify the interaction between key components and core targets.Results:A total of 64 components were identified, from which 53 active components were screened, corresponding to 609 targets. Further searching disease databases revealed 96 target genes related to asthma, with an intersection of 6 genes between drug and asthma differential genes. Core target gene IL6 and its corresponding core compound were determined through network topology analysis. Molecular docking confirmed the binding of the main active components of Qufeng Ningfei Powder with the core target protein IL6.Conclusion:The blood components of Qufeng Ningfei Powder may regulate IL-17 through IL6, counteract airway remodeling, oxidative stress, and airway hyperresponsiveness, and thus treat asthma.

To analyze the distribution of serotypes and antimicrobial resistance of clinical Salmonella isolates from multiple centers across China.

Clostridioides difficile infection(CDI)is the leading cause of hospital-acquired diarrhea and has be-come a major challenge in the global public health field.In recent years,it has been found that nutrients and gut mi-crobes play key roles in regulating growth,metabolic activity,and virulence expression of Clostridioides difficile.However,current research focuses on the independent effects of a single nutrient or gut microbe,systematic under-standing on the interactions between them is still lacking.This paper reviews the specific effect of different nutrients on Clostridioides difficile,explores how other gut microbes inhibit the growth of Clostridioides difficile by com-peting or metabolizing nutrients.In addition,this paper also discusses the application of emerging technologies in CDI research and their potentiality in clinical intervention strategies.Future research needs to integrate multi-omics data and artificial intelligence analysis,deeply analyze the complex interactive network of nutrient-microbe-host,and provide new ideas for precise prevention and treatment of CDI.