急性白血病RAD50基因多态性研究

目的研究温州地区急性白血病与RAD50基因多态性的关系。方法选取2018年6月～2019年6月来我院血液科就诊治疗的温州地区急性白血病100例患者为研究对象,并将其纳入急性白血病组(n=100)。100名体检正常者为对照组。采用PCR技术确定两组RAD50第4号内含子(rs17166050)基因分型(GA型、GG型),比较健康对照组与急性白血病组基因型频率。结果健康对照组与急性白血病组的RAD50(rs17166050)基因型GA型和GG型出现的频率比较差异有统计学意义(P0.05)。结论温州地区急性白血病与RAD50第4号内含子(rs17166050)的G等位基因的易感性相关。     

布地奈德联合博利康尼治疗慢性阻塞性肺疾病急性加重期疗效分析

目的观察布地奈德联合博利康尼治疗慢性阻塞性肺疾病急性加重期的临床疗效。方法选择2017年12月~2018年12月我院住院治疗的慢性阻塞性肺疾病患者80例,随机分为观察组和对照组,各40例,对照组予布地奈德雾化液1 mg+生理盐水3 m L,每天2次雾化吸入;观察组在对照组基础上加用博利康尼雾化液l mg联合布地奈德雾化液1 mg+生理盐水3 m L雾化吸入,每天2次,6 d为一个疗程。治疗后对比分析两组的临床疗效及肺功能各项指标的变化情况。结果观察组患者治疗后的总有效率达97.2%,显著高于对照组的75.0%,两组比较差异具有显著性(P0.05)。观察组患者治疗后的FEV1、PEF及FEV1/FVC分别为(1.93±0.27)L,(3.81±1.16)L/s、(90.43±12.65),均较治疗前明显提高,且观察组患者治疗后的FEV1、PEF及FEV1/FVC水平分别显著高于对照组,两组比较差异具有显著性(P0.05)。结论布地奈德联合博利康尼治疗慢性阻塞性肺疾病急性加重期疗效确切,能明显改善患者的肺功能,从而缓解患者的临床症状,提高生活质量,改善预后。     

Colchicine as a Novel Therapy for Suppressing Chemokine Production in Patients With an Acute Coronary Syndrome: A Pilot Study

PurposeExisting literature reports that colchicine inhibits inflammasome activation and downstream inflammatory cytokine production and stabilizes coronary plaque. However, colchicine's effect on chemokines, which orchestrate multiple atheroinflammatory pathways, is unknown.MethodsPatients with acute coronary syndrome (ACS) were randomly assigned to colchicine (1.5 mg PO) (n = 12; mean age, 65.2 years) or no treatment (n = 13; mean age, 62.2 years). Blood samples were collected during cardiac catheterization within 24 hours of colchicine administration from the coronary sinus, aortic root, and right atrium. Patients with colchicine-naive stable angina (SAP) (n = 13; mean age, 66.8 years) were additionally sampled. Serum chemokine levels were analyzed with ELISA. In parallel, monocytes from healthy donors were isolated and subjected to colchicine treatment.FindingsTranscoronary (TC) levels of chemokine ligand 2 (CCL2) and C-X3-C motif chemokine ligand 1 (CX3CL1) were significantly elevated in patients with ACS versus patients with SAP (P < 0.01). TC chemokine ligand 5 (CCL5) levels were not significantly (P = 0.084) elevated in patients with ACS versus patients with SAP. Colchicine treatment markedly reduced TC levels of CCL2, CCL5, and CX3CL1 in patients with ACS (P < 0.05). In vitro colchicine suppressed CCL2 gene expression in stimulated monocytes (P < 0.05). Colchicine treatment reduced the intracellular concentration of all 3 chemokines (P < 0.01) and impaired monocyte chemotaxis (P < 0.05).ImplicationsHere, we report for the first time that short-term colchicine therapy significantly reduces the local production of coronary chemokines, in part by attenuating production of these mediators by monocytes. These data provide further evidence of colchicine's beneficial role in patients with ACS.     

Hepcidin – Potential biomarker of contrast-induced acute kidney injury in patients undergoing percutaneous coronary interventions

PurposeContrast-induced acute kidney injury (CI-AKI) is a common and potentially serious complication of percutaneous coronary interventions (PCI). In this study, we tested the hypothesis whether serum and urinary hepcidin could represent early biomarkers of CI-AKI in patients with normal serum creatinine undergoing PCI. In addition, we assessed serum and urinary neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, eGFR and serum creatinine in these patients.MethodsSerum and urinary hepcidin and NGAL, serum cystatin C, were evaluated before, and after 2, 4, 8, 24 and 48 h after PCI using commercially available kits. Serum creatinine was assessed before, 24 and 48 h after PCI.ResultsWe found a significant rise in serum hepcidin as early as after 4 and 8 h when compared to the baseline values. Serum NGAL increased after 2, 4 and 8 h, and in urinary NGAL after 4, 8 and 24 h after PCI. We found a significant fall in urinary hepcidin after 8 and 24 h after PCI. Serum cystatin C increased significantly 8 h after PCI, reaching peak 24 h after PCI and then decreased after 48 h. The prevalence of CI-AKI was 8%. Urine hepcidin was significantly lower 8 and 24 h after PCI in patients with CI-AKI, while serum and urine NGAL were significantly higher in patients with CI-AKI.ConclusionsOur findings suggest that serum hepcidin might be an early predictive biomarker of ruling out CI-AKI after PCI, thereby contributing to early patient risk stratification. However, our data needs to be validated in large cohorts with various stages of CKD.     

2013~2017年北京地区儿童急性喉炎就诊特点及其与气象因素和空气污染物的相关性研究

目的 探讨北京地区儿童急性喉炎的发病特点及其与气象和环境等影响因素的相关性。 方法 收集2013~2017年在首都儿科研究所耳鼻喉科门诊就诊的急性喉炎患儿的年龄、性别以及诊断用药等相关信息,分析5年间北京市儿童急性喉炎就诊特点,并与同期北京市气象数据(平均气温、平均气压、平均相对湿度、平均风速)及主要环境污染物数据(PM_2.5、PM₁₀、SO₂、NO₂、CO、O₃)进行对比,应用SPSS 20.0统计软件进行分析。 结果 2013~2017年于我院耳鼻喉科门诊就诊的急性喉炎患儿共计3 286例次,男女性别比例约为2∶1;好发于4岁(含4岁)以下儿童(占69.42%),其中,1岁至2岁患儿就诊例次最多,8岁后趋于稳定,且性别差异不再明显。5年门诊就诊量分别是854、662、790、574及406例次,总体呈逐年下降趋势,与PM_2.5、PM₁₀逐年下降趋势相似;但5年的季节特点、就诊的高峰季和低谷季、高峰月和低谷月均不统一;急性喉炎季节就诊量与每季PM_2.5、CO有显著正相关关系(r值分别为0.490,0.547, P<0.05),与平均气温、平均气压、平均相对湿度、平均风速及PM₁₀、SO₂、NO₂、O₃值无显著相关关系。 结论 北京地区儿童急性喉炎发病有着明显的年龄规律和性别差异,并呈逐年下降趋势,季就诊量与平均PM_2.5、CO有显著正相关性。     

大气污染中气态污染物致大鼠喉黏膜急性损伤的研究

目的 探讨大气污染中气态污染物对大鼠喉黏膜的急性损伤及可能机制。 方法 采用200 g左右健康SPF级SD大鼠12只,随机分为对照组和气态污染物暴露组,每组6只。对照组大鼠饲养于SPF环境中,气态污染物暴露组大鼠呼吸的气体为2016年北京市红色预警期间外界大气经HEPA滤膜过滤颗粒物后的空气,暴露时间为6 d。暴露后处死大鼠,取喉黏膜,检测大鼠喉黏膜的病理学改变及喉黏膜组织细胞因子IL-1β、IL-4、IL-5、IL-6、IL-10、IL-12、IL-13、IL-17a、IFN-γ、TNF-α的表达情况。 结果 与对照组相比,气态污染物暴露组大鼠喉黏膜上皮有不同程度的过度角化、基底细胞排列紊乱;IL-1β、IL-10、IL-13、IL-17a、TNF-α的表达增强(P<0.05);IL-12、IFN-γ的表达减少(P<0.05)。 结论 大气污染中的气态污染物可以引起大鼠喉黏膜损伤,其机制可能与Th1/Th2失衡,呈Th2优势应答有关。     

Period prevalence of chronic pancreatitis diagnosis from 2001–2013 in the commercially insured population of the United States

BackgroundPrevalence estimates of chronic pancreatitis (CP) in the US are scarce. We aimed to determine the prevalence of CP in the commercially insured population of the US.MethodsWe analyzed the IQVIA Legacy PharMetrics database to calculate the period prevalence of CP from 2001 to 2013 among individuals with ≥1 year of enrollment. CP was defined as ≥1 healthcare contacts associated with a non-ancillary claim for a primary diagnosis of CP (ICD-9-CM 577.1). Prevalence estimates were age- and sex- adjusted to the 2010 US population. Sensitivity analysis was performed by using more stringent criteria: a) 1 claim of CP + [≥1 claims of acute pancreatitis (AP), CP or pancreatic cyst/pseudocyst]; b) 1 claim of CP + [≥1 claims for AP, CP or pancreatic cyst/pseudocyst in ≥3 months before or after the index CP claim]; c) ≥2 claims for CP; and d) ≥2 claims for CP separated by ≥ 6 months.ResultsOf 48.67 million eligible enrollees, 37,061 received the diagnosis of CP (mean age, 51.2 ± 15.2 years; 49% male). The age- and sex- adjusted period prevalence of CP per 100,000 was 73.4 (95% CI, 72.6–74.1), 98.7 (95% CI, 97.7–99.7) for adults and 8.3 (95% CI, 7.8–8.8) for children. Prevalence of CP was slightly higher in males (sex ratio, 1.05) and highest in the age group of 46–55 years (135/100,000). On sensitivity analysis, the prevalence of CP per 100,000 decreased to 60.2, 39.7, 38.8, and 18.8 with each of the alternative definitions.ConclusionPrevalence estimates reported in our study provide an insight into the population burden of CP in the US.