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关键词： Wound healing   FOSL1   Keratinocytes   IL-17  

摘要： Keratinocytes, the most important cell type constituting the epidermis, migrate to restore the epithelial barrier during wound healing and are a crucial step in wound healing. This study utilized bioinformatics analysis of comprehensive expression datasets of aberrantly expressed genes in wound healing to identify the abnormal expression of the critical transcription factor Fos-like antigen-1 (FOSL1), which is involved in various diseases. Currently, there is limited research on the role of FOSL1 in wound healing, and its molecular mechanisms remain unclear. This study explores the role and regulatory mechanisms of FOSL1 in the wound-healing process. A comprehensive expression dataset of abnormal genes in wound repair was constructed by bioinformatics analysis. Mouse trauma models and mouse wound splint models were constructed to verify the role of FOSL1 in vivo. Real-time quantitative polymerase chain reaction (qRT-PCR), immunoblot, immunofluorescence staining, and HE staining were used to confirm the analysis, and FOSL1 was used as the target in the wound healing process. At the cellular level, using 5(y)-ethynyl-2(y)-deoxyuridine (EdU) assay, Transwell assay, Migration assay, western blotting and immunofluorescence, FOSL1 promoted the molecular mechanism of wound repair by regulating the proliferation and migration of keratinocytes through IL-17 signaling pathway. Bioinformatics analysis revealed differential expression of FOSL1 during wound healing. In the mouse back wound model, qRT-PCR, western blotting (WB), and immunofluorescence staining showed significant upregulation of FOSL1 and IL-17 expression during wound tissue healing, indicating a close association between FOSL1 and mouse wound healing. In the mouse wound splinting model, subcutaneous injection of recombinant FOSL1 protein contributed to wound surface healing. Overexpression of FOSL1 in HaCaT cells promoted their proliferation and migration abilities. When IL-17 inhibitor was added to HaCaT cells,

关键词： 急性淋巴细胞白血病   异基因造血干细胞移植   髓外复发   乳腺   肝脏  

摘要： 髓外浸润是急性淋巴细胞白血病的表现之一，预后极差。常见髓外浸润部位为中枢神经系统及睾丸，乳腺、肝脏浸润并不常见。同种异体移植后急性淋巴细胞白血病在乳房复发非常罕见，目前可查阅到的文献报道例数仅百例，缺少系统性分析与数据。我们的第一例便报道了移植后2月乳腺浸润，后出现中枢、双侧肾上腺、腹膜淋巴结等多处转移的病例。第二例于异体移植后43月肝脏复发。髓外复发时检测完全供体嵌合。表明骨髓及髓外复发机制并不相同。

关键词： 新生儿   ABO   溶血病   用药剂量   免疫球蛋白   总胆红素  

摘要： 探讨免疫球蛋白不同剂量治疗新生儿ABO溶血病的疗效及安全性。方法 选取我院收治的120例新生儿ABO溶血病患者,分为对照组和观察组。对照组采用常规剂量人免疫球蛋白分三天注射法,观察组则实施单次给予高剂量免疫球蛋白的注射方案。对比分析不同剂量下的临床应用效果。结果 相较于对照组,观察组在黄疸消退时长、光疗时长、住院天数以及换血治疗的应用比例上均有显著降低(P<0.05)。观察组的HCT、Hb以及RBC的水平均显示出低于对照组的趋势(P<0.05)。观察组患者的IgG1与IgG3水平相较于治疗前及对照组均有显著提升(P<0.05)。比较两组间的不良反应发生率无显著差异(P>0.05)。结论 单次给予大剂量免疫球蛋白的注射策略,通过调节IgG1和IgG3水平能显著提高ABO溶血病新生儿的疗效,展现出较高的临床应用价值。

关键词： 碳酸镧   左卡尼汀   肾功能衰竭   血清细胞因子   肾功能  

摘要： 探讨碳酸镧联合左卡尼汀对肾衰竭患者血清细胞因子及肾功能的改善作用。方法 98例肾衰竭患者随机分为观察组和对照组,各49例。对照组接受常规治疗联合左卡尼汀,观察组加用碳酸镧。对比两组治疗前后血清TNF-α、IL-6水平,肾功能(Scr、BUN、Ccr)及不良反应发生率。结果 观察组治疗后TNF-α、IL-6、Scr、BUN水平低于对照组,Ccr水平高于对照组(P<0.05);不良反应发生率无显著差异(P>0.05)。结论 碳酸镧联合左卡尼汀可有效调节肾衰竭患者血清细胞因子,改善肾功能,安全性良好。

关键词： glioblastoma   MHC   riskscore   immune microenvironment  

摘要： Glioma is the most common primary malignant intracranial tumor with limited treatment options and a dismal prognosis. This study aimed to develop a robust gene expression-based prognostic signature for GBM using the Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) datasets. Using WGCNA and LASSO algorithms, we identified four MHC-related genes (TNFSF14, MXRA5, FCGR2B, and TNFRSF9) as prognostic biomarkers for glioma. A risk model based on these genes effectively stratified patients into high- and low-risk groups with distinct survival outcomes across TCGA and CGGA cohorts. This signature correlated with immune pathways and glioma progression mechanisms, showing strong associations with immune function and tumor microenvironment infiltration patterns. The risk score reflected tumor microenvironment remodeling, suggesting its prognostic relevance. We further propose I-BET-762 and Enzastaurin as potential therapeutic candidates for glioma. In conclusion, the four-gene signature we identified and the corresponding risk score model constructed from it provide valuable tools for the prognosis prediction of glioblastoma multiforme (GBM) and may guide personalized treatment strategies. The least absolute shrinkage and selection operator (LASSO) risk score has demonstrated significant prognostic evaluation utility in clinical GBM patients, bringing potential implications for patient stratification and the optimization of treatment regimens.

关键词： C-reactive protein (CRP)   interleukin-1 beta (IL-1 beta)   interleukin-6 (IL-6)   ocular inflammation   uveitis   diabetic macular edema  

摘要： Introduction: C-reactive protein (CRP) plays a critical role in the innate immune system and serves as a biomarker for various inflammatory conditions. CRP is a dynamic protein undergoing conformational changes between pentameric (pCRP) and monomeric (mCRP) conformations. pCRP is the well-established systemic marker of inflammation, while mCRP is associated with localized tissue inflammation. Methods: This study aimed to evaluate systemic levels of pCRP, mCRP, interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta) in patients with a variety of intraocular inflammatory conditions, including diabetic macular edema (DME) and non-infectious uveitis such as Behcet's disease (BD), Birdshot retinochoroidopathy (BSRC), HLA-B27-associated uveitis, and undifferentiated uveitis (UU). Results: A total of 77 subjects were included. mCRP levels were significantly elevated in BD, DME, and UU compared to controls (p = 0.014, p = 0.036, and p = 0.031, respectively). The mCRP/pCRP ratio was also significantly higher in DME and UU (p = 0.035 and p = 0.011, respectively). In addition, a strong positive correlation was observed between IL-6 and IL-1 beta (rho = 0.638, p <0.0001). No significant differences in serum levels of pCRP, IL-6, or IL-1 beta were observed among the groups. Conclusions: These findings suggest that mCRP, rather than pCRP, may be a more specific systemic biomarker for certain intraocular inflammatory conditions. The involvement of the CRP axis and the strong correlation between IL-6 and IL-1 beta underscore the interaction of these key inflammatory mediators, providing further insight into the targeting of CRP axis for therapeutic purposes.

关键词： 猪源BVDV   分离鉴定   进化分析   淋巴细胞   致病性  

摘要： 为了解致猪腹泻的病原及其分子特征、致病性，本研究基于疑似猪瘟仔猪病料样品进行病毒的MDBK细胞分离培养、牛病毒性腹泻病毒（BVDV）RT-qPCR与IFA检测、5'-UTR和E0基因扩增测序与遗传进化分析，在分离病毒细胞培养物纯净性检测后将其以肌肉注射和滴鼻方式接种实验组仔猪，采用流式细胞术、RT-qPCR、ELISA分别检测感染猪淋巴细胞数量、外周血和主要脏器中BVDV 5'-UTR基因转录、抗体水平。结果显示，分离病毒经细胞盲传15代均未引起细胞病变，RT-qPCR检测出现扩增曲线，IFA检测出现典型的特异性胞浆内黄绿色荧光，与BVDV-1在同一进化分支，其5'-UTR、E0基因与牛源BVDV-1 VEDEVAC疫苗株同源性最高（98.2%、98.7%），命名为BVDV FQ株。FQ株第15代细胞培养物纯净性较好，将其感染猪后，第7 d实验组猪淋巴细胞数量下降至最低值并极显著低于对照组（P<0.01），此时4/5猪外周血检测到FQ株5'-UTR mRNA,3/5猪出现腹泻等临床症状，21 d后可检出BVDV抗体，主要脏器均可检出FQ株5'-UTR mRNA。本研究上述结果表明猪源BVDV FQ株属于BVDV-1基因型，可能起源于牛源BVDV，可明显降低感染猪淋巴细胞数量，对猪具有一定致病性。本研究为深入开展猪源BVDV病原学研究提供了参考。

关键词： TNF-alpha   EBV reactivation   Ferroptosis   GPX4  

摘要： Epstein-Barr virus (EBV) is a carcinogenic gamma-herpesvirus that remains latent in more than 95% of adults. The virus can undergo lytic activation when immune function is suppressed or when stimulated by drugs or pathogens. EBV reactivation poses a significant threat to human health and is closely associated with various cancers, such as Burkitt's lymphoma and nasopharyngeal carcinoma. Inhibiting EBV reactivation is a current clinical challenge. Tumour necrosis factor-alpha (TNF-alpha), an important cytokine, has different effects on various viruses. It also exerts varying effects on the same virus depending on the type of infected cell. This study aimed to investigate the impact of TNF-alpha on EBV reactivation and its underlying mechanisms. Our experimental research revealed that TNF-alpha significantly inhibits EBV reactivation and that this inhibitory effect is mediated primarily through its receptor TNFR1. Furthermore, TNF-alpha affects the expression of the GPX4 protein and regulates the potential ferroptosis state of cells. Using transmission electron microscopy and other methods, we observed typical characteristics of ferroptosis, such as changes in mitochondrial morphology and Fe2 + accumulation. Additionally, we established stable GPX4-knockdown cell lines, which demonstrated the crucial role of GPX4 in the process of TNF-alpha-mediated inhibition of EBV reactivation. Overall, TNF-alpha acts on the TNFR1 receptor, thereby affecting the GPX4 protein and the ferroptosis pathway to achieve its inhibitory effect on EBV reactivation. These findings provide new insights into the mechanisms of EBV reactivation and may offer new perspectives for the early treatment of EBV-related diseases.