Objective To search for potential prognostic markers for severe community-acquired pneumonia（SCAP）using non-targeted metabolomics. Methods Testing plasma samples from 30 healthy people and 68 SCAP patients (all collected from January 2015 to June 2019 at Peking Union Medical College Hospital) by liquid chromatography mass spectrometry(LC-MS ).According to clinical prognosis，patients were divided into survive group (n=49)and non-survive group(n=19).OPLS-DA(multivariate statistical analysis)and Kruskal Wallis Test (single variable statistical analysis) were used to identify differential metabolites. Correlation analysis of clinical indicators and prognostic analysis were also used for differential metabolites. Results Totally 3463 metabolites were detected in healthy people and SCAP patients by LC-MS. Among them, 126 metabolites were screened out by OPLS-DA andKruskal Wallis Test analysis methods. Prognostic analysis showed that the quantity of 5-hydroxytryptamine(5-HT) was significantly different between survive group and non-survive group(P<0.05，AUC>0.75).Correlation analysis of clinical indicators showed that 5-HT was positively correlated with oxygenation index (OI) and negatively cor-related with acute physiology and chronic health evaluation(APACHE II)score. Conclusions The 5-HT as a potential prognostic marker for SCAP，may predict the prognosis of SCAP patients.

[摘 要] 目的：探讨多能蛋白聚糖（VCAN）和基质金属蛋白酶9（MMP9）在肺腺癌（LUAD）侵袭与转移中的作用及其调控机制。方法：收集30例LUAD及配对癌旁组织，采用免疫组织化学（IHC）法检测VCAN和MMP9表达；另以人LUAD细胞NCI-H1975和A549为模型，运用siRNA干扰和质粒过表达技术，结合挽救实验，采用CCK-8、划痕愈合实验及Transwell实验评估细胞增殖、迁移与侵袭能力，RT-qPCR及WB法检测基因和蛋白表达。结果：VCAN和MMP9在LUAD组织中的表达均显著高于癌旁组织（均P < 0.001），且H-score随肿瘤分期的进展呈递增趋势（均P < 0.01）。体外实验表明，si-VCAN显著降低VCAN和MMP9的mRNA及蛋白水平，抑制细胞活力、迁移和侵袭（均P < 0.01）；过表达MMP9则显著增强上述恶性表型（均P < 0.001），并可被si-VCAN逆转（均P < 0.01），而MMP9沉默对VCAN蛋白表达无显著影响（P > 0.05）。结论：VCAN通过上调MMP9表达促进LUAD细胞的增殖、迁移和侵袭，VCAN/MMP9轴可能成为LUAD治疗的潜在靶点。

[摘 要] 目的：探讨NOD样受体蛋白3（NLRP3）炎症小体的活化在子宫内膜异位症（EMT）进展为EMT相关性卵巢癌（EAOC）过程中的作用及其机制。方法：选取2018年4月至2019年6月上海市长宁区幼保健院收治的EAOC、EMT、正常子宫内膜（CON组）组织标本各15例及患者的临床资料，利用免疫组织化学染色法、WB法检测EAOC、EMT和CON组织中NLRP3、caspase-1和IL-1β及含BRCA1/BRCA2的复杂亚基3（BRCC3）的表达水平。构建过表达BRCC3质粒和si-NLRP3质粒并转染EMT细胞CRL-7566，通过WB法检测转染后细胞中BRCC3蛋白的表达水平，利用MTT法、流式细胞术及Transwell实验分别检测转染后细胞增殖、凋亡、迁移与侵袭能力的变化。对过表达BRCC3组细胞进行干扰NLRP3实验，通过WB法检测干扰后BRCC3和NLRP3蛋白的表达水平，检测干扰后细胞增殖、凋亡、迁移与侵袭能力的变化。结果：EAOC和EMT组织中NLRP3、caspase-1、IL-1β和BRCC3的表达水平较CON组均呈明显升高（均P<0.01），且EAOC组织中NLRP3与BRCC3的表达呈正相关（r=0.65，P<0.01）。在CRL-7566细胞中过表达BRCC3显著促进细胞的增殖、迁移和侵袭并抑制细胞凋亡（均P<0.01），敲减NLRP3则抑制CRL-7566细胞的上述表型（均P<0.01），过表达BRCC3增强NLRP3的表达水平（P<0.01），而干扰BRCC3则抑制NLRP3表达（P<0.01）；干扰NLRP3可以部分逆转BRCC3对细胞凋亡的抑制作用（P<0.01）、对细胞迁移（P<0.05）和侵袭（P<0.01）的促进作用。结论：EAOC和EMT组织中NLRP3和BRCC3均呈高表达，过表达BRCC3可促进CRL-7566细胞的增殖、迁移和侵袭并抑制细胞凋亡，与EMT向EAOC转化有关，BRCC3/NLRP3是潜在的EAOC炎癌转化预测标志物及治疗靶点。