中医药治疗慢性前列腺炎研究概况

综述近年中医药治疗慢性前列腺炎的临床研究,认为本病病因病机之核心在于脾肾亏虚为本,湿热、痰浊、瘀毒为标,病久则伤及脾肾,由实转虚。中医内治法主要以辨证论治、辨病论治或单方验方为主,外治法以中药洗浴、中药灌肠、肛门给药、针灸为主。中医药治疗本病优势明显。应继续完善对中医药作用机制的认识,制订统一的辨证论治及疗效评价标准,针对效果显著的名方开展研究。     

Human breast milk oligosaccharides attenuate necrotizing enterocolitis in rats by suppressing mast cell accumulation,DPPI activity and TLR4 expression in ileum tissue,and regulating mitochondrial damage of Caco-2 cells

Necrotizing enterocolitis (NEC), a devastating infant disease characterized by severe intestinal necrosis, its pathogenesis is poorly understood, but appears to be multifactorial and highly associated with immaturity of gastrointestinal tract and immature innate-immune system. Breast-milk is effective strategy to protect infants against NEC. This study is using a NEC rat model to investigate the pathological mechanism of NEC involved intestinal-damages, and the therapeutic mechanism of sialylated human milk oligosaccharides (SHMOs) on NEC rats; also using cell model to investigate the effects of SHMOs on colon-epithelial cells (Caco-2) in-vitro.Extraction and characterization of SHMOs from breast milk, establishment of a NEC rat model, histopathological analysis and mast cell accounting of the terminal ileum were taken; The levels of DPPI, TLR4, IL-6, TNF-α, MMP-2/9 and glutathione were measured using various methods. Caco-2 cells were pre-treated with SHMOs and cultured with LPS, histamine, chymase or DPPI, cell viabilities and mitochondrial membrane potential were examined; flow cytometry was used to detect cell cycle.The accumulation of mast cells was found in the ileum of NEC rats, but prohibited by SHMOs treatment; the increased levels of TLR4, DPPI, IL-6, TNF-α, MMP-2/9 in NEC ileum were suppressed by SHMOs in-vivo. SHMOs prevented Caco-2 cells from LPS, histamine, chymase induced damages by surviving cell viability, regulating G0/G1 and S phase in cell cycles, and increasing mitochondrial membrane potential. These findings provide a new insight into the pharmacological mechanism of SHMOs treatment for NEC and suggest that SHMOs needs well attention for therapeutic aims.     

Primary Conservative Therapy for Symptomatic Isolated Mesenteric Artery Dissection with Severely Compressed True Lumen or Large Dissecting Aneurysm

PurposeTo investigate the safety and effectiveness of primary conservative therapy for patients with symptomatic isolated mesenteric artery dissection (IMAD) with a severely compressed true lumen and/or a large dissecting aneurysm.Materials and MethodsA total of 35 consecutive patients (all men; median age, 53 y) with symptomatic IMAD with a severely compressed true lumen and/or a large dissecting aneurysm but without intestinal necrosis or arterial rupture who were treated with primary conservative therapy between November 2018 and February 2020 were assessed. A severely compressed true lumen was defined as luminal stenosis > 70%. A large dissecting aneurysm was defined as dissecting aneurysm diameter ≥ 1.5 times larger than the normal mesenteric artery diameter.ResultsThere was a strong positive relationship among abdominal pain, degree of luminal stenosis, and length of dissection (R = 0.811; P < .001). Conservative treatment was successful in all patients. Abdominal pain was eliminated within 4.7 d ± 4.8 (range, 2–31 d) in all patients, within 3.6 d ± 1.2 (range, 2–6) in the 31 patients with minor or moderate abdominal pain, and within 13.3 d ± 11.9 (range, 6–31 d) in the 4 patients with severe abdominal pain. Complete or partial remodeling of the mesenteric artery was achieved in 6 (17.1%) and 29 (82.9%) patients, respectively, during 8.6 mo ± 4.3 of follow-up.ConclusionsPrimary conservative therapy can be used safely and effectively in patients with symptomatic IMAD with a severely compressed true lumen and/or a large dissecting aneurysm but without intestinal necrosis or arterial rupture.     

聚腺苷二磷酸核糖聚合酶抑制剂在肿瘤放射治疗中的应用研究进展

聚腺苷二磷酸核糖聚合酶（PARP）是一类在真核细胞中高表达的核酶，在DNA损伤修复中起关键作用。近年来，PARP抑制剂在肿瘤治疗中显示出巨大的潜力，几种小分子PARP抑制剂已被美国食品药品管理局（FDA）批准用于多种肿瘤的维持治疗。PARP抑制剂主要通过抑制PARP酶促作用和PARP捕获作用，导致DNA单链断裂的持续存在，在DNA复制的过程中，转变为双链断裂。研究证明，PARP抑制剂不仅具有显著的抗肿瘤效应，而且与放射治疗联合具有一定的协同作用。本文将阐述PARP抑制剂联合放疗的潜在理论基础，总结近年来PARP抑制剂在肿瘤放射治疗中的临床前和临床研究进展，梳理该领域目前亟待解决的问题，并对其在抗肿瘤治疗中的应用前景进行展望。     

外周血miR-150-5p、SOCS1 mRNA对类风湿关节炎“病”“证”诊断意义的初步探讨＊

目的 探讨类风湿关节炎患者外周血miR-150-5p、细胞因子信号抑制因子1（suppressor of cytokine signaling 1，SOCS1）mRNA的表达及对类风湿关节炎（Rheumatoid Arthritis，RA）疾病诊断、中医证型判断的意义。方法 纳入符合诊断标准的RA患者57例及健康对照组19例，根据《22个专业95个病种中医诊疗方案》有关RA的中医证候诊断标准，判断RA的中医证型。qPCR检测RA患者及健康对照组miR-150-5p、SOCS1mRNA的相对表达水平，同时检测血常规、肝功能、肾功能等常规指标。双荧光素酶分析方法判断两者是否存在靶向关系。统计分析miR-150-5p、SOCS1 mRNA对RA疾病的诊断意义及其与中医证型的相关性。结果 RA患者外周血miR-150-5p的相对表达水平下调，低于正常人群（t = -19.019，P < 0.05）；其表达水平随疾病活动度升高，有下降趋势；患者外周血SOCS1 mRNA的相对表达水平上调，低于正常人群（t = 5.333，P < 0.05）；其表达水平随疾病活动度升高，有上升趋势。MiR-150-5p与SOCS1 mRNA有靶向结合关系（P < 0.05）。通过AUC曲线比较，miR-150-5p的相对表达水平区分RA的敏感性及特异性分别为98.1%、92.1%（AUC = 0.972，P < 0.05）；SOCS1 mRNA的相对表达水平无法区分RA（AUC = 0.472，P > 0.05）。RA患者中miR-150-5p的相对表达水平低于3.06，RA患者风湿痹阻证、寒湿痹阻证的相对风险分别为8.33、250.00（P < 0.05）。结论 miR-150-5p、SOCS1 mRNA在RA患者中有差异性表达，且有靶向结合关系。miR-150-5p可能是RA的疾病诊断及中医风湿痹阻证、寒湿痹阻证证型诊断的潜在生物标志物。     

重症监护病房患者导尿管相关尿路感染风险评分系统的建立与验证

目的建立并验证重症监护病房(ICU)患者导尿管相关尿路感染(CAUTI)风险评分系统,为ICU降低CAUTI的发生率提供依据。方法对常州市第一人民医院ICU在2017年1月-2018年12月期间1026例留置导尿管患者进行CAUTI目标性监测,利用1∶1简单化随机方法分为模型组和验证组,各513例。根据模型组数据筛选出CAUTI影响因素,建立风险评分系统应用于验证组,计算验证组中每例患者的风险评分。采用模型组和验证组数据建立受试者工作特征曲线图(ROC),根据ROC曲线下面积判断该风险评分系统建立的有效性。结果本研究期间患者发生CAUTI 44例,千日感染率为3.99‰。ICU住院时间、插管日数、未正确固定尿管、未规范执行手卫生是模型组导尿管插管患者CAUTI发生的影响因素(P<0.05)。利用此结果建立CAUTI风险评分系统,发现验证组中的高、中、低风险得分患者CAUTI发生率的差异有统计学意义,得分越高者患CAUTI的风险更高。最终利用该评分系统对模型组及验证组患者绘制ROC曲线,发现二者ROC曲线下面积均接近1,且差异无统计学意义,再次说明该评分系统具有较好的预测效果。结论建立CAUTI风险评分系统,采取针对性的早期干预可降低CAUTI的发生率,为患者提供最优经验治疗。     

The RNA m6A methyltransferase METTL3 promotes pancreatic cancer cell proliferation and invasion

Epigenetic modifications are involved in carcinogenesis and METTL3 is involved in RNA methylation. This study aimed to explore the role of the RNA m6A methyltransferase METTL3 in pancreatic cancer cells. The m6A modification was analyzed in human pancreatic cancer and paracancerous specimens, as well as in the normal HPDE6-C7 pancreatic cell line and the MIA-PaCa-2 and BxPC-3 pancreatic cancer cell lines. Immunohistochemistry (IHC), western blotting, and RT-qPCR were used to detect the expression of METTL3. Cell lines were transfected with siRNAs against METLL3. Proliferation, invasion, and migration were examined. The functions of METTL3 were predicted by bioinformatics analysis. In the 40 patients included, high METTL3 expression was associated with high pathological stage (P = 0.02) and high N stage (P = 0.02). Survival was better in patients with low METTL3 expression compared with those with high MTTL3 expression (P < 0.01). METTL3 and CIITA expression levels were inversely correlated (r = ?0.71, P < 0.01). RNA m6A content in tumor specimens was significantly higher than that in paracancerous specimens. METTL3 protein and mRNA levels were significantly higher in tumor specimens compared with paracancerous specimens, as well as in cancerous cell lines vs. normal cells. METTL3 knockdown in MIA PaCa-2 and BxPC-3 cells decreased RNA m6A modifications. Cell proliferation, invasion, and migration were decreased by METTL3 knockdown in cancerous cell lines. A total of 673 differentially expressed genes were identified by bioinformatics: 659 were upregulated and 14 were downregulated. In conclusion, METTL3 is probably involved in pancreatic carcinogenesis. It could eventually be a prognostic marker or a treatment target.