Ovine Iliac Vein Model for Endovascular Thrombectomy of Acute Deep Venous Thrombosis

An ovine iliac vein thrombosis model was devised to test a wall-contacting rotational thrombectomy device. Thrombosis was successfully induced in 9 sheep with an average clot length of 31 mm ± 12 and >60% vessel occlusion on angiography. The thrombus was subsequently removed, maintaining normal intraoperative pulmonary arterial pressure (5.9 mm Hg ± 3.6) and complete distal reperfusion after thrombectomy. Additionally, the sheep were without signs of vascular trauma or embolic complications on gross necropsy and histopathologic analysis. The findings from this study support the use of an ovine iliac deep vein thrombosis model for testing of a lower extremity thrombectomy device.     

艾拉莫德联合甲氨蝶呤治疗类风湿性关节炎的临床疗效及对患者骨代谢的影响

目的 探讨艾拉莫德联合甲氨蝶呤治疗类风湿性关节炎(RA)的临床效果及对患者骨代谢的影响。方法 将我院收治的86例RA患者随机分为两组各43例。对照组采用甲氨蝶呤治疗,观察组采用艾拉莫德联合甲氨蝶呤治疗。比较两组的临床疗效、骨代谢指标(β-CTX、 TPINP、 N-MID)及不良反应发生情况。结果 观察组治疗总有效率为95.35%,明显高于对照组的81.40%(P<0.05)。治疗后,两组的β-CTX水平降低, TPINP、 N-MID水平升高(P<0.05);观察组的β-CTX水平明显低于对照组, TPINP、 N-MID水平高于对照组(P<0.05)。两组的不良反应发生率(9.30%vs. 6.98%)比较差异无统计学意义(P>0.05)。结论 艾拉莫德联合甲氨蝶呤治疗RA效果显著,可有效改善患者的骨代谢,且安全性较高。     

脑出血继发损伤中沉默信息调节因子2的表达和炎症反应*

目的：探讨脑出血对酵母沉默信息调节因子2（Sirt2）和炎症的影响。方法：将胶原酶Ⅳ注入SD大鼠右侧 纹状体中建立脑出血模型，通过免疫印迹和ELISA 等方法测定大鼠脑出血后48 h 的Sirt2 的表达及炎症变化。利 用Hemin 诱导PC12 细胞损伤模拟体外脑出血模型，并检测Sirt2 及炎症变化；采用短发夹RNA（shRNA）-Sirt2 沉 默Sirt2 在PC12 细胞中的表达及对炎症的影响。结果：手术后48 h 脑出血行为学评分最低。脑出血组Sirt2 的表达 显著高于假手术组。脑出血组IL-6、IL-1β 表达显著升高。结论：脑出血可以促进Sirt2 的表达和炎症反应，降低 Sirt2 的表达可减缓炎症反应。 关键词 脑出血；沉默信息调节     

Overview of CF lung pathophysiology

Defects of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) protein affect the homeostasis of chloride, bicarbonate, sodium, and water in the airway surface liquid, influencing the mucus composition and viscosity, which induces a severe condition of infection and inflammation along the whole life of CF patients. The introduction of CFTR modulators, novel drugs directly intervening to rescue the function of CFTR protein, opens a new era of experimental research. The review summarizes the most recent advancements to understand the characteristics of the infective and inflammatory pathology of CF lungs.     

基于罗森塔尔效应的护理干预对脑出血后遗症病人的心理状况和生活质量的影响

目的:探讨基于罗森塔尔效应的护理干预对脑出血后遗症病人的心理状况和生活质量的影响。方法:按照随机数字表法将2019年1月—2021年1月收治的98例脑出血后遗症病人分为对照组和观察组各49例,对照组实施常规护理,观察组在常规护理基础上给予基于罗森塔尔效应的护理干预。干预前后采用卒中量表(NIHSS)、功能独立性评定量表(FIM)、生活活动功能测量量表Barthel指数(BADL)评定两组病人康复情况,采用非精神病性焦虑量表(HADS-A)、非精神病性抑郁量表(HADS-D)、自我效能量表(GSES)评定两组病人心理状态,采用生活质量简明调查表(SF-36)评定两组病人生活质量。结果:观察组病人干预后NIHSS评分低于对照组,FIM和BADL评分高于对照组(P<0.05);观察组病人干预后HADS-A和HADS-D评分低于对照组,GSES评分高于对照组(P<0.05);观察组病人干预后生活质量各维度(躯体功能、躯体角色、肌体疼痛、总体健康、活力、社会功能、情绪角色、心理卫生)评分均明显高于对照组(P<0.05)。结论:基于罗森塔尔效应的护理干预应用于脑出血后遗症病人能有效促进病人康复,改善病人心理状态,提高病人生活质量。     

肥胖型PCOS患者的生物学特征和临床特征

多囊卵巢综合征（polycystic ovary syndrome,PCOS）是一种内分泌代谢紊乱综合征,临床表现高度异质性。肥胖是PCOS异质性临床表现之一,超过50%的PCOS患者超重或肥胖。肥胖型PCOS主要表现为高雄激素血症、中心型肥胖和糖脂代谢紊乱,非肥胖型PCOS主要表现为黄体生成激素（luteinizing hormone,LH）水平异常升高。尽管肥胖型和非肥胖型PCOS均存在内分泌代谢异常,然而肥胖可加重PCOS糖脂代谢紊乱;肥胖型PCOS还表现脂肪代谢的异常。综述肥胖型PCOS患者的临床特征、性激素水平、糖脂代谢特征,旨在为肥胖型和非肥胖型PCOS患者新的分型诊治提供参考。     

Sinensetin attenuates oxygen–glucose deprivation/reperfusion-induced neurotoxicity by MAPK pathway in human cerebral microvascular endothelial cells

Sinensetin is a polymethoxylated flavone with anti-inflammatory and anti-oxidative activities. This work aimed to explore the function and mechanism of sinensetin in oxygen and glucose deprivation/reperfusion (OGD/R)-induced neurotoxicity. The overlapping target genes of cerebral stroke and sinensetin were determined according to GeneCards and ParmMapper tools and were subjected to Gene Ontology (GO) annotations and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Human cerebral microvascular endothelial cells (HCMECs) were stimulated with OGD/R. Neurotoxicity was investigated by Cell Counting Kit-8, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) level, qRT-PCR, and TUNEL analysis. The proteins (p38, JNK, and ERK) in mitogen-activated protein kinase (MAPK) signaling were measured using Western blotting. Total of 50 overlapping target genes of cerebral stroke and sinensetin were predicted. Pathway analysis showed they might be involved in the MAPK pathway. Sinensetin attenuated OGD/R-induced neurotoxicity by mitigating viability reduction, LDH release, ROS generation, inflammatory response, and apoptosis in HCMECs. Sinensetin weakened OGD/R-induced activation of the MAPK pathway via decreasing the phosphorylation of p38, JNK, and ERK. The pathway inhibitors mitigated the activation of the MAPK signaling, and sinensetin exacerbated this effect. The inhibitors reversed OGD/R-induced neurotoxicity in HCMECs, and sinensetin contributed to this role. Overall, sinensetin prevents OGD/R-induced neurotoxicity through decreasing the activation of MAPK pathway.