浅谈如何提高医疗质量

为提高医疗质量，论述以下三点：①强调“以病人为中心”，坚持服务方向、整合优化流程、收集反馈信息；②加强医务人员思想道道修养，在加大教育、监督、管理力度三个方面下功夫；③强化引导管理模式，采取开展质量分析、狠抓环节质控、进行法律法规引导等方法收到较好效果。     

进展性脑卒中危险因素临床探讨

目的探讨缺血性进展性脑卒中(SIP)的危险因素。方法回顾性总结104例缺血性脑卒中患者的临床资料,其中进展组、非进展组各52例,对其体温、血压、血糖及头颅CT、TCD等项目结果进行分析。结果 (1)进展组24 h内体温增高者18例,非进展组9例,两组比较差异有统计学意义。(2)进展组有糖尿病史者高于非进展组(P<0．01),且进展组收缩压≥140 mm Hg(1 mm Hg=0．133 kPa)者占75％,非进展组者占52％,两组相比差异有统计学意义(P<0．01)。(3)缺血性进展性卒中(SIP)组TCD检查颅内外大血管狭窄率85％,明显高于非进展组(24．2％)。(4)头颅CT 示分水岭脑梗死或侧脑室体旁梗死多提示大血管病变,常预示进展性脑卒中。结论 SIP危险因素与发热、卒中后收缩压水平、糖尿病及是否并发颅内外大血管狭窄或闭塞有关,且患者收缩压下降易引起SIP,故禁止盲目应用降血压药。     

浅谈胃肠外科进展

近年来，经济以及科技环境的变化对胃肠外科的进展产生的重要影响。这些影响不仅表现在对病因、发病机制的研究上，更表现在研究成果在临床的应用和改进上。本文主要从流行病学、新器械新技术以及观念变革三个方面归纳了胃肠外科的最新进展。     

以弥漫性脑白质病变为表现的原发中枢神经系统弥漫性大B细胞淋巴瘤临床病理学特征

目的分析以弥漫性脑白质病变为表现的原发中枢神经系统弥漫性大B细胞淋巴瘤(又称大脑淋巴瘤病)的临床及病理学特征, 探讨其鉴别诊断、治疗及预后。方法选取2020年6月至2022年6月首都医科大学附属北京天坛医院病理科诊断的2例大脑淋巴瘤病患者资料, 分析临床、磁共振成像(MRI)及病理学表现。结果 2例患者均为男性, 年龄分别53岁(例1)、69岁(例2), 临床表现为头晕乏力、记忆力减退, 均伴有言语错乱;MRI均未见肿块形成, 表现为弥漫性脑白质病变, 呈T1稍低信号、T2及T2-FLAIR高信号、增强病灶未见明显强化, 其中例2患者于2个月后复查MRI, 病变范围较前扩大, 病灶出现部分强化;送检穿刺组织镜下白质结构基本完整, 可见弥漫浸润的异型淋巴细胞, 核分裂象可见, 核仁明显, 免疫组织化学染色CD20、CD79α及PAX5强阳性, CD3弱阳性, Ki-67阳性指数高;例1进行以甲氨蝶呤为基础的化疗, 就诊后5个月存活;例2未行特殊治疗, 就诊后13个月死亡。结论大脑淋巴瘤病临床罕见、预后不佳, 临床表现为快速进展的认知功能障碍、影像学表现为弥漫性脑白质病变, 没有明确肿块形...     

Hyperoxia-induced apoptosis of AEC Ⅱ in premature rats by inhibiting expression of focal adhesion kinase

Objective To explore the role of focal adhesion kinase (FAK) in hyperoxia-apopto- sis of type Ⅱ alveolar epithelial cells (AEC Ⅱ s) of premature rats. Methods AEC Ⅱ from prema- ture rat lungs were cultured and randomly assigned to air group and hyperoxia group. After exposed to hyperoxia for 6, 12, 24 and 48 h, apoptosis rate of AEC Ⅱ were analyzed by flow cytometry with an- nexin-Ⅴ/propidium iodine (PI) double staining. FAK mRNA and FAK and fAK-Tyr397 peptide were detected by RT-PCR and Western blot, respectively. Results Positive cells of Annexin-Ⅴ+ / PI- in AEC Ⅱ after 6,12,24 and 48 h of hyperoxia exposure were significantly decreased, and the maximal apoptosis rate of AEC Ⅱ (stained of Annexin-Ⅴ+ / PI- ) was found in the hyperoxia group at 12 h (23.83%±4.43%). Compared to the air group, the expression of FAK mRNA and of FAK de- creased markedly and progressively in hyperoxia groups at 12, 24 and 48 h(P<0. 05). Conclusions Decreased expression of FAK induced by hyperoxia is likely to contribute to the apoptosis and neco-z sis of AEC Ⅱ.     

早产儿高氧肺损伤的基础研究与临床

自1976年Northway等首次报道并命名支气管肺发育不良(bronchopulmonary dysplasia,BPD)以来,新生儿、尤其早产儿长期吸入高浓度氧可导致肺部出现以炎症和纤维化为主要特征的急慢性损伤已为国内、外广大学者所接受.目前对于BPD已有了更深入的认识,即其本质是在遗传易感性的基础上,由氧中毒、气压伤或容量伤以及感染或炎症等多种不利因素对发育不成熟的肺造成的损伤,以及损伤后肺组织异常修复,但其中高浓度氧所致的氧化应激损伤在BPD的发生和发展中仍起着至关重要的作用.     

早产大鼠肺泡Ⅱ型上皮细胞与成纤维细胞共培养模型的建立

目的建立早产大鼠肺泡Ⅱ型上皮细胞(AECⅡ)与肺成纤维细胞(LF)共培养模型,为研究肺发育和肺损伤时AECⅡ和LF的相互作用提供实验基础。方法分离、纯化胎鼠AECⅡ和LF,通过插入式培养皿和培养板来构建AECⅡ-LF共培养模型。AECⅡ以5×105／mL的密度接种到6孔板中,LF以1×106／mL的密度接种到PCF插入式Millicell培养皿中,以6孔板中不放入套皿单独培养的AECⅡ为对照。用倒置显微镜观察AECⅡ形态和基本生长情况,台盼蓝染色了解细胞成活情况,免疫细胞化学染色法检测AECⅡ Ki67表达。结果早产大鼠AECⅡ和LF共培养模型成功构建。共培养2 d与单独培养2 d相比,AECⅡ的形态、活力和增殖无明显差异。共培养4 d,AECⅡ仍可保持其细胞形态,细胞数目、细胞活力;AECⅡ Ki67表达较单独培养4d 明显增加。结论体外构建的早产大鼠AECⅡ与LF共培养模型,部分模拟了体内微环境。AECⅡ和LF共培养体系有利于保持 AECⅡ的增殖和分化功能,可用于体外研究肺发育和肺损伤时AECⅡ和LF的相互作用。     

槟榔多酚对大鼠肺微血管内皮细胞低氧损伤的保护作用

目的：探究槟榔多酚对大鼠肺微血管内皮细胞（PMVEC）低氧损伤的保护作用。方法：采用氧化应激指标丙二醛和超氧化物歧化酶筛选肺部缺氧损伤细胞模型最适条件;采用细胞计数试剂盒法筛选槟榔多酚最适给药剂量。将PMVEC分为常氧对照组、模型对照组和槟榔多酚组,采用BCA法检测蛋白浓度并测定PMVEC中的氧化应激水平,蛋白质印迹法检测炎症和凋亡相关蛋白的表达,免疫荧光染色法检测闭合蛋白和闭锁小带1等紧密连接蛋白的表达,Transwell小室实验检测跨内皮细胞膜电阻,罗丹明荧光染料检测PMVEC屏障的通透性。结果：1%氧浓度培养PMVEC细胞48 h后成功构建肺部缺氧损伤细胞模型;20μg/mL的槟榔多酚可以显著逆转缺氧损伤细胞模型中PMVEC的存活率下降以及氧化应激水平的升高（均P<0.05）;槟榔多酚对于低氧诱导下PMVEC中炎症相关蛋白核因子κB(NF-κB)和核因子E2相关因子（Nrf）2的上调有显著抑制作用（均P<0.05）;槟榔多酚可以下调低氧诱导下PMVEC中凋亡相关蛋白胱天蛋白酶（caspase）3、Bcl-2相关X蛋白（Bax）的表达（均P<0.05）,从而减轻低...     

北京市平谷区中药资源普查的实践与思考

目的摸清平谷区野生中药资源家底,掌握平谷区中药材栽培基本状况。方法依据《国家中药资源普查技术规范》和北京市中药资源普查方案,采用3S技术,实地考察平谷区37个样地的野生中药资源和2个中药材种植基地。结果发现68科186种药用植物,其中濒危植物2种,采集并加工制作蜡叶标本980份,中药材标本31种,拍摄照片15 000多张。结论基本摸清了平谷区野生中药资源的种类与分布,初步掌握了平谷区中药材种植基地现存的主要问题,并提出产业发展建议。     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.