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关键词： Atherosclerosis   Calcium score   Free fatty acid receptors (FFARs)   IL-1β   Total antioxidant capacity (TAC)  

摘要： Background and Aims Cardiovascular diseases pose a major health threat, with atherosclerosis being the leading cause. Free fatty acids (FFAs) can act as signaling molecules, influencing inflammation and oxidative stress, thereby potentially impacting atherosclerosis risk. This study examined the expression of FFAR2 and FFAR3 and their relationship with serum IL-1β, total antioxidant capacity (TAC), and malondialdehyde (MDA) levels in patients undergoing CT angiography. Methods and Results Fasting blood samples from 113 patients were collected, dividing them into a high coronary artery disease risk group (n=52), Low Risk of CAD (n=37) and a control group (n=24) based on calcium scores. FFAR2 expression was significantly lower in the case group, while FFAR3 levels showed no difference. Increased interleukine-1 beta (IL-1β) and MDA levels, alongside decreased total antioxidant capacity (TAC), were noted in the case group. Conclusion The study identified a negative correlation between FFAR2 expression and atherosclerotic indices, while serum IL-1β and MDA exhibited positive correlations. Thus, FFAR2 and IL-1β may be potential biomarkers for coronary artery disease risk.

关键词： 急性淋巴细胞白血病   大剂量甲氨蝶呤   化疗   护理  

摘要： 探究急性淋巴细胞白血病患者采取大剂量甲氨蝶呤、化疗治疗时的护理内容、应用价值。方法 按照电脑随机法将2024年1月至2025年3月我院急性淋巴细胞白血病患者分组,即:对照组(n=43例,常规护理)、实验组(n=43例,综合护理),两组治疗时,均接受大剂量甲氨蝶呤+化疗方案,比较护理效果。结果 实验组在护理总有效率方面较对照组优势显著(P<0.05);实验组不良反应发生率低于对照组(P<0.05);实验组护理满意度比对照组更高(P<0.05)。结论 大剂量甲氨蝶呤、化疗治疗时,综合护理的开展在多个层面均展现出了明显优势,对于急性淋巴细胞白血病患者来说,在疾病症状方面能够较好地控制,可提高总有效率,保障满意度,值得注意的是,上述护理安全系数高,具体表现在:降低患者不良反应发生率方面,推广价值显著。

关键词： 右美托咪定   全膝关节置换术   肢体缺血再灌注损伤   肿瘤坏死因子-a   血清丙二醛   临床疗效  

摘要： 分析右美托咪定(Dexmedetomidine,Dex)在全膝关节置换术(totalkneearthroplasty,TKA)中减轻肢体缺血再灌注损伤(ischemia-reperfusioninjury,IRI)的效果及对肿瘤坏死因子-a(tumornecrosisfactor,TNF-α)、血清丙二醛(maleicdialdehyde,MDA)水平的影响。方法 选取时间为:2023年1月-2024年1月于期间,于新疆医科大学第六附属医院接受TKA治疗的90例患者为研究对象,所有患者均在腰—硬联合阻滞麻醉下实施手术,研究组(n=45)在采用止血带前20min应用Dex,对照组(n=45)采用予等量0.9%氯化钠溶液应用,比较两组具体效果。结果 术后两组患者的患肢周径均增长,但研究组肿胀周径小于对照组,且周径增长率也低于对照组;研究组患者在停用止血带后TNF-α水平浓度[(1.72±0.52)VS(2.20±0.49)]与MDA水平浓度[(4.84±0.37)VS(6.82±1.11)]均低于对照组,停用止血带30分钟后,两组炎症指标水平浓度均显示下降,且研究组TNF-α[(1.42±0.44)VS(2.04±0.71)]与MDA水平浓度[(4.58±0.26)VS(5.97±0.34)]仍然较对照组相比水平更低,以上对比,差异均具有统计学意义,(P<0.05)。结论 Dex运用于TKA中减轻肢体IRI情况有显著效果,且安全性较高。

关键词： 肺炎支原体肺炎   T淋巴细胞亚群   细胞因子   血小板  

摘要： 分析儿童肺炎支原体肺炎外周血T淋巴细胞亚群与细胞因子以及血小板的特征。方法 纳入医院接诊支原体肺炎患儿(肺炎组86例),同期入院健康体检儿童(健康组86例)进行回顾性分析(2022.03-2024.3)。两组均采集外周静脉血样本,比较支原体肺炎患儿、健康儿童外周血T淋巴细胞亚群差异;比较两组细胞因子差异及血小板计数差异。结果 较健康者,支原体肺炎患儿CD3+、CD4+、CD4+/CD8+较低,CD8+较高(P<0.05);较健康者比较,支原体肺炎患儿IL-2较低,IL-4、IL-6较高(P<0.05);较健康者比较,肺炎组血小板计数更高(P<0.05)。结论 肺炎支原体肺炎发生后,会引起患儿外周血T淋巴细胞亚群与细胞因子以及血小板改变,可为该病的临床筛查提供有效依据。

关键词： NPAR   SII   ELR   急性淋巴细胞白血病   临床意义  

摘要： 目的：探讨急性淋巴细胞白血病（ALL）患者外周血中性粒细胞百分比/白蛋白比值（NPAR）、系统免疫炎症指数（SII）和嗜酸性粒细胞与淋巴细胞比值（ELR）水平变化及临床意义。方法：本研究回顾性选择2019年6月至2021年6月廊坊市人民医院和廊坊市中医医院收治的133例ALL患者作为观察组。同时选择同期119例健康体检者作为对照组。采用受试者工作特征（ROC）曲线评估外周血NPAR、SII和ELR水平对ALL发生的预测价值。采用Kaplan-Meier分析、多因素Cox回归分析外周血NPAR、SII和ELR水平变化与ALL患者预后的关系。结果：与对照组相比，观察组患者、、骨髓原幼细胞比例、NPAR、SII和ELR水平明显升高（P＜0.05）。Kaplan-Meier生存分析结果显示，外周血NPAR、SII和ELR高表达患者的明显低于低表达患者（P＜0.05）。Cox回归分析结果显示，WBC、LDH、骨髓原幼细胞比例、NPAR、SII和ELR水平均为ALL患者预后不良的独立危险因素（P＜0.05）。ROC结果显示，外周血NPAR、SII和ELR水平联合预测的AUC明显高于NPAR、SII、ELR单独使用时的AUC（P<0.05）。结论：外周血NPAR、SII和ELR在ALL患者中呈高表达状态，且联合检测外周血NPAR、SII和ELR水平对ALL的诊断、疗效观察、预后评估具有重要的临床意义。

关键词： 中药扶正抗癌方   PD-1抗体治疗   T细胞功能   细胞因子水平  

摘要： 观察晚期肺癌治疗中,应用中药扶正抗癌方+PD-1抗体治疗对机体T细胞功能与细胞因子水平的相关性影响。方法 2023年6月至2025年2月期间,我院从中抽取80例晚期肺癌患者,随机分为两组,每组40例。对照组只给予PD-1抗体干预,治疗组在此基础上联合应用 中药扶正抗癌方,比对临床疗效。结果 治疗组临床疗效(65.50%)高于对照组(57.50%),但无统计学意义,P>0.05。治疗组不良反应发生率为5.00%,低于对照组的20.00%,P<0.05;干预后,治疗组T细胞亚群改善情况较对照组更优,且身体功能也优于对照组,P<0.05。结论 在晚期肺癌患者的PD-1抗体治疗基础上,给予其中药扶正抗癌方干预,不良反应少,能够实现对T细胞功能与细胞因子水平的有效调节,改善机体的免疫细胞抑制情况,抑制病情的进展,进而改善患者的预后。

关键词： CircVAMP3   Macrophages   Lipopolysaccharide   Acute respiratory distress syndrome   Interferon-beta  

摘要： Circular RNA (circRNA) is a prominent group of non-coding RNA (ncRNA) that regulates gene expression at the post-transcriptional level in various diseases including acute respiratory distress syndrome (ARDS). In our study, circVAMP3 was a novel circRNA significantly increased in macrophages in an acute lung injury (ALI) model. Through knockdown and overexpression of circVAMP3, we found circVAMP3 promoted the expression of IFN-beta in macrophages, which was vital in the pathophysiological process of ARDS. Moreover, we showed that circVAMP3 targeted Stimulator of Interferon Genes (STING) through miR-580-3p by bioinformatics analysis and intervene of miR-580-3p. CircVAMP3 acts as a pro-inflammation ncRNA by regulating the miR-580-3p/STING/IFN-beta axis and could be a potential biomarker and therapeutic target for ARDS.

关键词： BMSCs   IFN-gamma   JAK/STAT   UHPLC-HRMS   lung adenocarcinoma   network pharmacology  

摘要： Background Lung cancer is a significant public health concern in China, posing a serious threat to the population. The QiShenFuZhengYiLiu (QSFZYL) is commonly prescribed as a complementary treatment for cancer patients, although its anticancer mechanism remains unclear. The purpose of this study was to explore the therapeutic mechanisms of QSFZYL in lung adenocarcinoma (LUAD).Methods The mechanism of QSFZYL for treating LUAD was analyzed using comprehensive network pharmacology and UHPLC-HRMS, combined with experimental validation (in vivo).Results Network pharmacology analysis suggested that the therapeutic effects of QSFZYL on LUAD may involve the JAK/STAT signaling pathway. UHPLC-HRMS identified 26 differential components, with representative compounds including astragalus lysine alkaloids, monoterpenoids, isoflavonoids, and flavonoids. In vivo experiments demonstrated that QSFZYL combined with IFN-gamma significantly inhibited LUAD growth and promoted infiltration of CD3 and CD8 T cell, and downregulated JAK2, STAT3, and PD-L1 expression, promoted *** QSFZY combined with IFN-gamma overexpressing BMSCs effectively inhibit LUAD progression. The primary mechanisms include the suppression of cancer cell growth, promotion of apoptosis and infiltration of CD3 and CD8 T cells, and inhibition of the JAK2/STAT3 signaling pathway, and downregulated PD-L1 expression.

摘要： Herpes simplex keratitis (HSK) is a leading cause of corneal blindness globally, primarily resulting from herpes simplex virus type 1 (HSV-1) infection. HSK can cause pervasive and irreversible corneal nerve damage, leading to decreased corneal sensitivity and vision loss. Interleukin (IL)-33, a multifunctional cytokine, plays an important role in immune and inflammatory responses. However, the effects of IL-33 on nerve damage associated with HSK and the underlying mechanisms remain poorly understood. In this study, we first evaluated the effects of IL-33 on the severity of HSK and corneal nerve damage in a mouse model of HSK. The mechanisms of IL-33 on the production of neuroprotective factors by corneal epithelial cells (HCE-Ts) were investigated in an HSV-1 infection model in vitro. Additionally, the role and mechanism of IL-33 in regulating macrophage polarization for neuroprotection were investigated through in vitro co-culture experiments. The results indicated that IL-33 reduced the severity of HSK and protected corneal nerves in HSK mouse model. Mechanistically, IL-33 promoted the production of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) via activation of the GSK3 beta/beta-catenin signaling pathway in corneal epithelial cells. Furthermore, IL-33 promoted M2 macrophage polarization through activation of the JAK2/STAT6 pathway, which in turn attenuated inflammatory responses and reduced neuronal apoptosis. These findings reveal the neuroprotective mechanisms of IL-33 in HSK and offer new insights for further research and treatment of HSK.