全息影像术中导航在泌尿外科腹腔镜和机器人手术中的应用价值

目的探讨全息影像术中导航在泌尿外科腹腔镜和机器人手术中的应用价值。方法回顾性分析2019年1—12月北京和睦家医院等19家医疗中心收治的86例患者的病例资料,临床诊断包括肾肿瘤78例,膀胱癌2例,肾上腺肿瘤2例,肾囊肿1例,前列腺癌1例,汗腺癌淋巴结转移1例,根治性膀胱切除术后盆腔转移瘤1例。其中,32例接受标准腹腔镜手术,分别为肾部分切除术(LPN)27例,根治性前列腺切除术1例,根治性膀胱切除术2例,肾上腺肿瘤切除术2例;54例接受达芬奇机器人手术,分别为肾部分切除术(RAPN)51例,腹膜后淋巴结清扫术1例,双侧肾囊肿去顶减压术1例,盆腔转移肿瘤切除术1例。两种术式的肾部分切除术患者中41例有可统计的临床数据,其中RAPN 23例,LPN 18例。男26例,女15例;中位年龄53.5(24~76)岁;中位R.E.N.A.L评分7.8(4~11)分。专业工程师根据86例术前增强CT检查图像和诊断报告重建全息影像。术前,全息影像可帮助术者对供应肿瘤或手术切除部位的动静脉血管、淋巴结和神经的立体空间结构及相互关系有更直观的认识,协助术前手术规划。在术中将全息影像与腹腔镜监视器中的术野图像进行实时追踪和融合,实现术中导航。结果本组86例手术均顺利完成。术中通过人工调整全息影像,可提示重要血管如肾动脉和肾静脉在体内的投影位置,帮助术者定位血管、淋巴结和其他重要解剖结构的位置,便于精准分离。本研究采用标准腹腔镜手术和达芬奇机器人手术的肾部分切除术患者中共41例有可统计的临床数据。41例中位手术时间140(50~225)min,其中RAPN为140(50~215)min,LPN为160(80~225)min;中位热缺血时间23(14~60)min,其中RAPN为21(17~40)min,LPN为25(14~60)min;中位出血量80(5~1200)ml,其中RAPN为150(30~1200)ml,LPN为50(5~1200)ml。术中无周围重要脏器损伤。2例LPN患者出现ClavienⅡ级并发症,1例出血1200 ml给予输血,另一例血肿未予处理,自行吸收。此2例分别为前、后肾门肿瘤,R.E.N.A.L评分均为11分。结论全息影像术中导航可协助术者在腹腔镜和机器人手术中对重要的解剖结构进行定位、识别,在减少术中组织和器官损伤、降低手术并发症和提高手术成功率方面有重要的应用价值。     

PFKFB3参与脂多糖诱导肺成纤维细胞及肺组织有氧糖酵解的观察性研究

目的:观察脂多糖(lipopolysaccharide,LPS)诱导肺成纤维细胞及肺组织有氧糖酵解关键酶6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶3(6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3,PFKFB3)表达及其与有氧糖酵解的关系,探讨在LPS诱导肺纤维化过程中肺成纤维细胞和肺组织有氧糖酵解的潜在机制。方法:将人胚肺成纤维细胞MRC-5细胞系采用随机数字表法分为PBS对照组(PBS组)和LPS组(每组3孔),Western blot检测LPS刺激细胞6h后PFKFB3表达情况,同时免疫荧光显示PFKFB3在细胞内的定位情况;于LPS刺激后48 h采用海马细胞能量代谢仪检测细胞耗氧率(oxygen consumption rate,OCR)和产酸率(extracellular acidification rate,ECAR),并采用比色法检测有氧糖酵解产物乳酸产生情况,同时Western blot检测LPS刺激48 h后Ⅰ型胶原蛋白合成情况。将24只C57BL/6小鼠按随机数字表法分为生理盐水对照组(C组)、LPS组(L组),每组12只,L组、C组连续5d分别腹腔注射5 mg/kg LPS、等容量生理盐水;每组各6只于造模后第7天无痛处死小鼠,取血浆和肺组织,Western blot和免疫荧光检测各组肺组织中PFKFB3表达情况,比色法检测各组小鼠血浆中乳酸的含量;剩余小鼠于造模后第28天取肺组织,一侧肺通过Western blot检测肺组织Ⅰ型胶原蛋白合成情况,另一侧肺做石蜡切片进行病理学检测。结果:与PBS组比较,LPS刺激细胞6h后PFKFB3表达明显升高(P<0.05);LPS刺激细胞48 h后,与PBS组比较,LPS组细胞耗氧率降低、产酸率增加,代谢产物乳酸含量明显升高(P<0.05),同时细胞Ⅰ型胶原蛋白合成显著增加(P<0.05)。与C组比较,L组小鼠腹腔注射LPS 7 d后肺组织中PFKFB3表达明显升高(P<0.05),血浆乳酸含量明显升高(P<0.05);LPS注射28 d后,L组小鼠Ⅰ型胶原蛋白表达明显升高(P<0.05),肺组织出现明显纤维化。结论:在LPS诱导的肺纤维化过程中,LPS可诱导肺成纤维细胞和肺组织中PFKFB3蛋白表达,该过程与其有氧糖酵解过程相关,PFKFB3的表达上调可能是LPS诱导肺成纤维细胞和肺组织有氧糖酵解和肺纤维化的关键环节。     

新型冠状病毒肺炎定点医院护理质量和安全管理

目的总结新型冠状病毒肺炎定点医院护理质量与安全管理经验,为应对突发公共卫生事件提供借鉴。方法将肿瘤中心改建为符合收治新型冠状病毒肺炎患者标准的定点医院,设14个病区850张床位;与援鄂医疗队共同成立联合护理部,制定护理工作制度和规范,建立护理安全事件处理流程,构建护理质量评价指标;严格督导与质控。结果累计收治患者1 022例,治愈出院763例;三级护理质量控制检查合格率为100%;隔离病区医护人员零感染。结论构建统一的制度、工作流程及质量与安全管理标准,有利于多团队协作工作及同质化管理,从而提高工作效率和质量,确保患者安全。     

氯胺酮和氯诺昔康对慢性关节炎疼痛治疗的实验研究

目的研究氯胺酮、氯诺昔康及两药联合关节内注射对慢性关节炎疼痛的疗效．方法大鼠右踝关节注射完全弗氏佐剂建立单发性关节炎模型，4周后，关节内注射氯胺酮、氯诺昔康及两药联用，每周3次，共用药2周．踝关节X线照片、关节病理切片、关节直径值、屈关节疼痛试验评分和血浆谷氨酸含量为指标．结果踝关节X线照片和病理切片结果提示慢性炎症存在．用药前实验组右踝关节直径值、屈关节疼痛试验评分、血浆谷氨酸含量显著高于对照组（P〈0．05）；用药2周3个用药组疼痛评分、血浆谷氨酸含量显著低于非用药组，其中氯诺昔康组和联合组右踝关节直径显著低于非用药组（P〈0．05），且2组关节病理切片均见到有新生关节软骨的形成．结论关节内注射氯胺酮和氯诺昔康均可缓解慢性关节炎疼痛，氯诺昔康较氯胺酮抗炎作用明显，还可促进受损关节的修复，联合注射氯胺酮和氯诺昔康，可大大减少两药的用量．     

性别特异性高胆固醇血症与Syndecan-3(SDC3)基因C1330T多态性的关联研究

目的研究syndecan-3(SDC3)基因的单核苷酸多态性(single-nucleotide polymorphism,SNP)C1330T在中国汉族农村人群中与高胆固醇血症,血脂水平的相关性。方法高胆固醇血症(HTC)定义为血清中总胆固醇水平≥200 mg/dL。本研究中男性336人(其中HTC161人,胆固醇正常者(NTC)175人),女性1491人(其中HTC935人,NTC556人)。研究对象中应用多聚酶链反应(PCR),限制性内切酶酶切进行基因分型,测定血清高密度脂蛋白(HDL-C),低密度脂蛋白(LDL-C),总胆固醇(TC),甘油三脂(TG),葡萄糖(GLU)。结果在男性研究对象中SDC3基因C1330T基因型及等位基因频率在HTC组和NTC组的分布有显著性差异(P<0.05),1330C与高胆固醇血症相关(OR=1.42,95%CI=1.040-1.926,P<0.03),在校正年龄,BMI和其他危险因素(吸烟饮酒等)后仍保持显著相关(OR=1.51,95%CI=1.06-2.14,P<0.03),而在女性研究对象中未发现明显相关(OR=1.06,95%CI=0.92-1.24,P=0.41),1330C与性别的交互作用呈临界统计学显著性(borderline statistically significant)(P=0.0742)。进一步应用显性模型分析C1330T与男性血脂水平(HDL-C,LDL-C)相关。结论SDC3基因C1330T多态性与男性高胆固醇血症及血脂水平有关。     

中药酚性化合物的抗肿瘤机制及制备方法

酚性化合物是许多中药的有效成分,具有抗肿瘤作用。其作用机理为抗氧化作用,抗细胞增殖,诱导细胞调亡,干预细胞转导和增强抑癌基因表达,干预细胞周期等。利用现代分离技术可将其提取并纯化。就酚性化合物抗肿瘤机理和提取纯化方法进行综述。     

2006年珠海市围产儿出生缺陷监测及干预研究

目的了解珠海市围产儿出生缺陷现状,探讨出生缺陷发生的相关因素,降低出生缺陷和残疾发生率,提高出生人口素质。方法根据珠海市出生缺陷监测方案,对全市35家医疗机构围产儿进行监测。结果出生缺陷发生率男性高于女性(X2=15.64,P<0.001),城市高于农村(X2=6.39,P=0.01),年龄<20岁的孕妇出生缺陷发生率明显高于其它人群,妇女最佳受孕年龄是20∽25岁。珠海市发生率最高的前5种疾病排序依次是:骨关节畸形、先心病、泌尿生殖系统畸形、唇腭裂、外耳畸形。结论珠海市围产儿出生缺陷发生率呈上升趋势。孕前期及孕妇早期口服小剂量叶酸预防神经管畸形,提高产前筛查和产前诊断技术,加强孕期保健,提高环保意识,这些是降低出生缺陷发生的有力措施。     

Primary Culture of Alveolar Epithelial Type Ⅱ Cells and Its Bionomic Study

To establish a better method of primary culture for alveolar epithelial type Ⅱ cells (AEC Ⅱ) and to study its bionomics, alveolar epithelial type Ⅱ cells were isolated by digestion with tryp- sin and collagenase, which were then purified by plated into culture flask coated with rat immu- noglobulin G. The purified AEC Ⅱ were identified by alkaline phosphatase staining, electron mi- croscopy, immunocytochemical staining of pulmonary surfactant protein A (SPA). The SPA expres- sion and transfection characteristics were compared with those of A549 cell line. The results showed that AEC Ⅱ could be isolated by digestion with trysin and collagenase and purified by adhesive pu- rification by using IgG, with a yield of about 2–3×107, and a purity of about 75%–84 %. Cells could be quickly identified with AKP staining. AECⅡ were different from A549 cell line in terms of SPA expression and transfection characteristics. It is concluded that adhesive purification with IgG can improve the purity of AECⅡ, and AKP staining is simple in cell identification. AECⅡ can not be completely replaced by A549 cells in some studies because the differences between them, such as SPA expression.     

Determination of Carboplatin Dose by Area Under the Curve in Combination Chemotherapy for Senile Non-small Cell Lung Cancer

To preliminarily determine the appropriate dosage of carboplatin (CBP) at AUC of 5 mg·Ml-1·min-1 in the combination chemotherapy for Chinese senile patients with non-small cell lung cancer (NSCLC). Thirty-five Chinese senile patients with NSCLC in advanced stage (Ⅲ/Ⅳ) were given 96 cycles of combination chemotherapy. Chemotherapy schedules included Taxol CBP, Gemzar CBP and NVB CBP. The dose of CBP was at 5 mg·mL-1·min-1 of area under the concen- tration-time curve (AUC). Side effects and quality of life were observed before and after the chemo- therapy. Myelosuppression was severe and commonly observed. Grade 3/4 of granulocytopenia was found in 47.9% (46/96) of the patients and grade 3/4 of thrombocytopenia was noted in 28.1% (27/96) of the subjects. However, other side effects were slight. The mean score of quality of life (QOL), ac- cording to the criteria of QOL for Chinese cancer patients had reduced 6.8. At 5 mg·mL-1·min-1 by AUC, the hematological toxicity of CBP was severe and it had some negative effects on the QOL. The administration of CBP at 5 mg·mL-1·min-1 by AUC may be too high for Chinese senile patients with non-small cell lung cancer.     

MDR1 and MDR3 Genes and Drug Resistance to Cisplatin of Ovarian Cancer Cells

To investigate the relationship between MDR1 and MDR3 gene and drug resistance to cisplatin of ovarian cancer cells. Two siRNAs (MDR1, MDR3) which specifically targeted MDR1 and MDR3 genes were transfered into A2780/DDP cells. Then double staining with Annexin- V-FITC/PI was used to detect cell apoptosis by the flow cytometry (FCM). A2780/DDP cell viability was determined by MTT. MDR1 and MDR3 mRNA were assessed by RT-PCR. Caspase-3 protein was detected by Western blotting. Transfection of MDR1 and MDR3 siRNA into A2780/DDP cells failed to reverse the drug-resistance of A2780/DDP cells to cisplatin (P>0.05). No significant differ- ence in the apoptosis efficiency was observed between the MDR1 and MDR3 siRNA, pSuppressor- Neo vector transfection cells and untreated cells (P>0.05). In the presence of cisplatin of different concentrations, the viability of A2780/DDP cells was not significantly decreased after the transfection. No changes in MDR1 and MDR3 mRNA were found in MDR1 and MDR3 siRNA-transfected A2780/DDP cells. As compared with pSuppressorNeo and untreated groups, no significant difference existed in the expression of MDR1 and MDR3 mRNA (P>0.05). The expression of caspase-3 protein in MDR1 and MDR3 siRNA transfected A2780/DDP cells was not significantly increased. It is con- cluded that multidrug resistance induced by cisplatin in ovarian carcinoma cell lines is not due to overexpression of MDR1 and MDR3 gene. The drug resistance of ovarian carcinoma cells to cisplatin is not mediated by P-glycoprotein.