目的 构建基于医疗机构的突发呼吸道传染病症状监测预警机制,实现突发呼吸道传染病目标症状的实时监测、快速预警、迅速鉴别以及闭环管理.方法 通过文献查阅和专家咨询确认目标疾病和症状,采用统计学方法建立基于时间序列数学模型的症状预测预警模型,通过大数据等信息技术搭建症状监测预警信息综合管理平台.结果 以突发呼吸道传染病为目标,通过科学选取目标疾病和症状,以复旦大学附属华山医院各院区2013—2019年的门急诊患者就诊信息为数据来源,构建了基于医疗机构的突发呼吸道传染病症状监测预警模型和信息综合管理平台,可实现目标症状的实时监测预警、可视化展示和患者核心数据快速获取和异常数据的及时甄别.结论 华山医院突发呼吸道传染病症状监测预警系统及闭环管理机制的建立是一次成功的探索和实践,为未来症状监测系统在传染病等突发公共卫生事件早期预警方面的进一步推广应用奠定了一定基础.

目的 探讨中性粒细胞/淋巴细胞比值(NLR)和血小板/淋巴细胞比值(PLR)与高脂血症(HLP)的相关性.方法 回顾性分析495例HLP患者(HLP组)和500名健康体检者(对照组)的实验室检测结果 .结果HLP组NLR和PLR明显高于对照组(P=0.007).单因素分析结果显示,白细胞、血红蛋白水平、NLR、PLR与HLP呈中度相关.受试者工作特征(ROC)曲线分析发现,NLR的最佳临界值为1.71(P<0.001),敏感性为68.0％,特异性为78.5％,NLR的预测强度优于其他指标,且HLP的严重程度与NLR呈高度正相关.结论 HLP患者的NLR和PLR明显高于健康体检者,NLR随HLP严重程度相应上升.

多发性内分泌腺瘤病(multiple endocrine neoplasia,MEN)是一组有明显家族倾向的常染色体显性遗传性疾病,表现为在同一患者身上同时或先后出现2个及以上的内分泌腺肿瘤或因增生而产生的一种以受累腺体功能亢进为表现的临床综合征.MEN可分为MEN 1型及MEN 2型,后者又可分为MEN 2A型、MEN 2B型.此外,还有不能归属于MEN 1或MEN 2的混合型MEN[1],此类疾病临床少见.复旦大学附属华山医院因降钙素异常增高发现多发性内分泌腺瘤病2A型1例.

目的 分析M蛋白阳性患者疾病谱的构成,比较不同疾病之间血清免疫学特征的差异.方法 选取M蛋白阳性住院患者211例,分析病种分布并比较不同疾病免疫球蛋白(Ig)及轻链检测结果的差异.结果 在M蛋白阳性患者中,发病率居前3位的依次为多发性骨髓瘤(MM)(53.0％)、意义未明丙种球蛋白血症(MGUS)(25.6％)、POEMS综合征(7.6％).MM患者M蛋白对应的Ig和轻链检测结果均高于MGUS和POEMS综合征患者(P<0.05),非对应的Ig和轻链检测结果均低于MGUS和POEMS综合征患者(P<0.05),而MGUS患者与POEMS综合征患者之间不同类型的Ig和轻链检测结果差异均无统计学意义(P>0.05).结论 M蛋白阳性患者中不同类型的M蛋白对应的疾病谱不同,且不同疾病之间Ig和轻链水平存在差异.

Objective To establish a human lymphoma cell line that stably expresses deleted in human liver cancer-1 gene(DLC-1).Methods The reconstructed plasmid,pcDNA3.1-DLC-1,was transfected to the human lymphoma cell line of Raji.Then the transfected Raji cells were selected by G418.The stable overexpression of DLC-1 was identified by Western blot assay.Results The recombined plasmid,pcDNA3.1-DLC-1,was confirmed by restriction endonuclease examination and sequencing.Western-blot showed that DLC-1 protein expression was increased in the transfected Raji cells.Conclusion A human lymphoma cell line with stable expression of DLC-1 is established.

Objective To investigate the modulation for multidrug resistance cell line K562/A02 us- ing a specific siRNA against mdrl,GSTπ.Methods siRNA were synthesized targeting the coding region se- quences of mdrl(79～99 nt)and GSTπ(308～327nt)respectively,and cloned to plasmid pSilence2.1-U6.The cloned products pSilenee-mdr1 and pSilence-GSTπ were transfected into K562/A02 cells.Expression of mdr1 and GSTπ mRNA were assayed by SYBR Green Ⅰ real-time PCR.The apoptosis of cell line K562/A02 was examined by Flow cytometry,50% inhibition concentration(IC_(50))of doxorubicin on K562/A02 cell was deter- mined by MTT method.Results The siRNA expression vector against mdr1,GSTπ mRNA was constructed successfully.After transfected with pSilenee-mdr1,the expression of mdr1 mRNA in K562/A02 in was re- duced 71.5 % compared to the mock transfeetion,from(2.8±1.65)×10~8 copy/μg RNA to(3.9±2.37)×10~7 copy/μg RNA(P0.01);While the expression of GSTπ mRNA in K562/A02 cell transfeeted with pSilenee-GSTπ was reduced 39.8% compared to the mock transfection,from(2.3±1.14)×10~5 copy/μg RNA to(5.4±2.45)×10~4 copy/μg RNA(P0.01).The apoptosis rate of K562/A02 cell line transfected with pSilence2.1-U6 was(11.65±4.06)%, the apoptosis rate of K562/A02 cell line transfected with pSilence-mdr1 and GSTπ were(44.98±11.27)%(P 0.01).After transfected with pSilence-mdr1 and GSTπ,the resistance index(RI)of cell line K562/A02 trans- fected with pSilence2.1-U6 was 23,and RI of cell line K562/A02 transfected with pSilence-mdr1 and GSTπ was 7.IC_(50)of doxorubicin(ADR)on K562/A02 cell was decreased from(1.16±0.38)mmol/ml to(0.33±0.04) mmol/ml(P0.01).Conclusion pSilence-mdr1 and pSilenee-GSTπ can effectively reverse the multidrug resistance of cell line K562/A02.

Objective To explore the apoptosis of multidrug resistance human leukemia cell line K562/ADR induced by siRNA expression vector pSilence MDR-1 and GSTπ. Methods pSilence MDR-1 and GSTπ were transfected into K562/ADR. pSilencer2.1-U6,as a control group(mock), was also transfected into K562/ADR. The apoptosis of cell line K562/ADR was examined by flow cytometry, 50% inhibition concentration (IC50)of doxorubicin(ADM) on K562/ADR cell was determined by MTT method. Results The apoptosis rate of cell line K562/ADR transfected with pSilence-2.1-U6 was (11.65±4.06%), the apoptosis rate of cell line K562/ADR transfected with pSilence MDR-1 and GSTπ were 44.98±11.27, P<0.01. The resistance index (RI) of cell line K562/ADR was 24. RI of cell line K562/ADR transfected with pSilence2.1-U6 and transfected with pSilence MDR-1 and GSTπ was respectively 7 and 23. IC50 of doxorubicin (ADM) on K562/ADR cell transfected with pSilence MDR-1 and GSTπ was decreased from(1.16±0.38)mol/ml to(0.33±0.04)mol/ml, P<0.01.Conclusion pSilence MDR-1 and GSTπ can induce cell line K562/ADR apoptosis and effectively modulate the multidrug resistance of K562/ADR cell line.

Objective To study the apoptosis mechanism of cell lines K562/Adr induced by siRNA.Methods pSilence MDR-1 and psilence neo-GST π were transfected into K562/Adr,the ultrastructural changes of K562/Adr cell line were observed by transmission electron microscope,the amount of bcl-2 was examined by Western blot.Results Under the electron microscope,the cell's nucleus transfected by pSilence MDR-1 and pSilence neo-GSTπ became shrinking,the crescent and apoptotic carpuscle were found in chromatin,and there were more vacuolas in the concentrated cytoplasm.After transfected with pSilence-MDRI and neo-GSTπ,the amount of bcl-2 was decreased from 0.75±0.03 to 0.52±0.12,which was significantly different from control group(P<0.05).Conclusion pSilence-MDR1 and pSilence-GSTπ can induce cell line K562/Adr apoptosis by decreasing bcl-2,reverse the multidrug resistance of K562/Adr cell line,and provide the theoretic evidence for reversing multidrug resistance of leukemia cell by siRNA.