45例嗜酸性筋膜炎的临床特征、超声诊断及治疗随访的单中心回顾性研究

目的回顾嗜酸性筋膜炎（EF）的临床症状、化验、检查、治疗及预后，并探讨超声在EF中的应用价值。方法回顾2006年1月1日~2022年2月28日在我中心就诊的EF患者的临床资料，并进行统计描述、分析，评估超声及磁共振成像（MRI）结果间的一致性。结果45例EF患者，男女比例3.5:1，发病年龄16~64岁，平均病程22.6个月，从出现症状到确诊的平均时间为16个月。最常见的诱因是剧烈运动诱发，占22%（10/45例）。EF以对称性四肢受累为主，前臂（86.7%）及小腿（80%）最常见。临床表现包括：皮下肿胀/紧硬（95.6%）、关节痛/炎（55.6%）、沟征（42.2%）、手关节屈曲挛缩（42.2%）、色素沉着（37.8%）、橘皮样皮肤病变（13.3%）等。31例（68.9%）患者嗜酸性|92;细胞升高，52.3%（23/44例）的患者IgG升高，9例（20%）抗核抗体阳性。21例患者接受了≥200 mg/d（3~5 d）的927;剂量激素治疗，与未接受927;剂量激素治疗的患者相比，虽未达到统计学差异，但患者入院前曾复发的比例更高、受累部位更广、IgG升高的比例更多，且没有发热。共有31例（68.9%）患者完成了随访，12/31例（38.7%）患者完全缓解，随访的中位时间为3.2年（0.2~15.9年），5.5年时完全缓解的累积发生率为44.1%。未发现与治疗反应相关的特殊基线特征及免疫抑制剂种类。共26例患者同时进行了超声及MRI检查，超声与MRI在确定筋膜增厚/炎症方面一致性很好（Kappa=0.91）。结论EF的临床特征为对称性四肢皮下肿胀、紧硬，伴嗜酸性|92;细胞、IgG升高，激素治疗效果好。超声识别皮下筋膜增厚是诊断EF的一个早期最有效的工具。     

经鼻高流量预充氧可保障老年患者全麻气管插管诱导期的安全

目的评估经鼻高流量预充氧在老年患者全麻气管插管诱导期的安全性研究。方法56例非困难气道老年患者，采用随机数字表法分为经鼻高流量吸氧组（HF组）和传统面罩经口鼻吸氧组（M组），28例/组。全麻气管插管诱导给药前预充氧5 min，HF组喉镜检查期间维持给氧，M组通气持续到喉镜检查。观察并记录两组患者基本资料，预充氧前（T1）、预充氧5 min（T2）及插管成功即刻（T3）的超声下胃窦横截面积（CSA）和动脉血气分析指标：PaO₂、PaCO₂、cSO₂，z92;息安全时间，插管时间，面罩通气的次数及术后并发症。结果两组患者的基本资料差异无统计学意义。预充氧5 min，两组患者的PaO₂和cSO₂均明显升高，且HF组PaO₂较M组明显（F=118.108vs 9.511，P < 0.05），插管成功后PaO₂和cSO₂均下降，HF组的PaO₂值较M组下降缓慢，且仍高于其T1时点，而M组的cSO₂值下降显著，低于其T1时点值。HF组z92;息安全时间显著高于M组（t=5.305，P < 0.05），且HF组面罩通气次数少于M组（χ²=6.720，P < 0.05）。两组插管后的PaCO₂值均增高，但两组比较差异无统计学意义（F=3.138，P > 0.05），其余结果差异也无统计学意义（P > 0.05）。结论经鼻高流量吸氧是一种安全简单有效的预充氧方式，与传统的面罩预充氧相比，能提高老年患者的动脉氧分压，延长患者z92;息安全时间，可保障老年患者全麻诱导插管时气道管理的安全。     

术前外周血炎症指标对舌鳞状细胞癌预后预测价值的分析

目的探讨术前外周血炎症指标对舌鳞状细胞癌（TSCC）患者预后的预测价值。方法回顾性分析2010年1月至2017年12月于郑州927;学第一附属医院因TSCC行根治性切除术的210例患者的临床病理资料，应用临床诊断性能曲线确定血小板/淋巴细胞比值（PLR）、中性|92;细胞/淋巴细胞比值（NLR）的最佳截断值。生存单因素分析应用Kaplan-Meier法和Log-rank检验，多因素分析应用Cox比例风险回归模型，基于Cox回归模型筛选的独立危险因素构建Nomogram模型。结果单因素分析显示，PLR、NLR、肿瘤分化程度、T分期、N分期和TNM分期为影响TSCC预后的危险因素（P<0.05）；多因素分析显示，PLR、N分期和TNM分期为独立危险因素（P<0.05）。Nomogram模型的C指数为0.701（95%CI：0.651~0.752），校准曲线表明Nomogram模型预测无进展生存率与实际无进展生存率具有较好的一致性。结论术前外周血炎症指标对TSCC术后患者的预后可能有一定的预测作用。     

Construction of the Eukaryotic Expression Vector for Outer Membrane Protein Tp92 from Treponema pallidum and Its Preliminary Study on the Immune Responses in New Zealand Rabbits

Treponema pallidum subsp. pallidum is the causative a gents of syphilis. Presently, the annual infection rate ofdomestic and international syphilis remains rather high [1,2]. Apart from the serious nature of the disease itself, anumber of studies sugg…     

The Treponema pallidum outer membrane protein Tp92 activates endothelial cells via the chemerin/CMKLR1 pathway

Endothelium damage caused by Treponema pallidum is the key step in the systemic dissemination and pathophysiology of syphilis, particularly cardiovascular syphilis and neurosyphilis. However, the molecular mechanisms supporting endothelium damage of syphilis are undefined. The outer membrane proteins were thought to be involved. Tp92 was first identified as an outer membrane protein of T. pallidum. Homologous proteins to Tp92 play important roles in cell attachment, inflammation, and tissue destruction in other bacterial species. In this study, we investigated the effect of Tp92 on endothelial cells activation. The data showed that Tp92 induced chemerin production in activated endothelial cells. Endothelial cell-derived chemerin upregulated the expression of TNF-α and ICAM-1 in endothelial cells via CMKLR1. In addition, endothelial cell-derived chemerin promoted THP-1-derived macrophage migration towards endothelial cells. These findings suggest that Tp92 may play an important role in mediating endothelial cell activation by inducing the secretion of chemerin.     

Intracellular and extracellular adenosine triphosphate in regulation of insulin secretion from pancreatic β cells (细胞内外三磷酸腺苷对胰岛β细胞胰岛素分泌的调控作用)

Adenosine triphosphate (ATP) synthesis and release in mitochondria play critical roles in regulating insulin secretion in pancreatic β cells. Mitochondrial dysfunction is mainly characterized by a decrease in ATP production, which is a central event in the progression of pancreatic β cell dysfunction and diabetes. ATP has been demonstrated to regulate insulin secretion via several pathways: (i) Intracellular ATP directly closes ATP‐sensitive potassium channel to open L‐type calcium channel, leading to an increase in free cytosolic calcium levels and exocytosis of insulin granules; (ii) A decrease in ATP production is always associated with an increase in production of reactive oxygen species, which exerts deleterious effects on pancreatic β cell survival and insulin secretion; and (iii) ATP can be co‐secreted with insulin from pancreatic β cells, and the released ATP functions as an autocrine signal to modulate insulin secretory process via P2 receptors on the cell membrane. In this review, the recent findings regarding the role and mechanism of ATP synthesis and release in regulation of insulin secretion from pancreatic β cells will be summarized and discussed.