利用耳甲腔型小耳畸形残耳皮瓣及软骨改善再造耳颅耳沟效果观察

目的探讨对先天性耳甲腔型小耳畸形患者行全扩张法全耳再造术后，利用残耳皮瓣改善再造耳颅耳沟的效果。方法回顾分析 2012 年 1 月—2017 年 1 月收治的 150 例先天性耳甲腔型小耳畸形患者。其中男 92 例，女 58 例；年龄 6.5～35.0 岁，平均 11.1 岁。采用一期扩张器埋置、二期全扩张法全耳再造术后发现上部颅耳沟浅显；于 6～12 个月后行三期再造耳修整。将残耳垂通过“Z”字改型转移以再造耳垂。在残耳上部作蒂在轮屏切迹的残耳上部皮瓣，弧形切开松解并加深上部颅耳沟，将上部残耳皮瓣向颅耳沟创面旋转推进缝合以覆盖创面；将带皮下组织蒂的残耳软骨组织瓣插入支架底部形成的腔隙内，并缝合固定，以增加支架的高度；耳甲腔区其余残耳皮瓣用以覆盖耳甲腔创面。结果术后拆线时 1 例患儿皮瓣远端出现直径约 0.5 cm 的表皮水疱，经换药 2 周后愈合；其余患者皮瓣成活良好。患者均获随访，随访时间 6～12 个月，平均 9.6 个月。再造耳上部颅耳沟均明显加深，再造耳支架高度不同程度增加，双耳对称性佳，耳甲腔无明显挛缩变小，再造耳外观满意。再造耳上部表面毛发明显减少，耳周发际线上移。结论采用耳甲腔型小耳畸形的残耳皮瓣及残耳软骨瓣转移，不仅可加深颅耳沟，而且可增加上部支架的高度，术后颅耳沟变形较轻，再造耳与正常耳廓的对称性更佳。     

藿香正气汤抑制新型冠状病毒复制过程的有效成分及机制初探＊

目的 收集藿香正气汤的主要活性成分，通过分子对接及网络药理学探讨其防控新型冠状病毒肺炎（COVID-19）的有效成分及治疗机制。方法 通过基于配体-蛋白质相互作用的计算方法，以瑞德西韦为对照，探索藿香正气汤潜在治疗COVID-19的成分，并选出对接较好成分进行药理学机制预测，初探其药理学机制。结果 本研究筛选出5种与新冠病毒3CLpro结合能力强于瑞德西韦的小分子成分。网络药理学初步预测抗病毒途径可能是通过PI3K-Akt 信号通路影响病毒复制。结论 成分C1-C5与3CLpro结合良好，推测其可能是潜在的3CLpro的抑制剂，为抗病毒天然药物的开发提供了理论依据。     

Lack of ceramide synthase 2 suppresses the development of experimental autoimmune encephalomyelitis by impairing the migratory capacity of neutrophils

Ceramide synthases (CerS) synthesise ceramides of defined acyl chain lengths, which are thought to mediate cellular processes in a chain length-dependent manner. In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), we observed a significant elevation of CerS2 and its products, C24-ceramides, in CD11b⁺ cells (monocytes and neutrophils) isolated from blood. This result correlates with the clinical finding that CerS2 mRNA expression and C24-ceramide levels were significantly increased by 2.2- and 1.5-fold, respectively, in white blood cells of MS patients. The increased CerS2 mRNA/C24-ceramide expression in neutrophils/monocytes seems to mediate pro-inflammatory effects, since a specific genetic deletion of CerS2 in blood cells or a total genetic deletion of CerS2 significantly delayed the onset of clinical symptoms, due to a reduced infiltration of immune cells, in particular neutrophils, into the central nervous system. CXCR2 chemokine receptors, expressed on neutrophils, promote the migration of neutrophils into the central nervous system, which is a prerequisite for the recruitment of further immune cells and the inflammatory process that leads to the development of MS. Interestingly, neutrophils isolated from CerS2 null EAE mice, as opposed to WT EAE mice, were characterised by significantly lower CXCR2 receptor mRNA expression resulting in their reduced migratory capacity towards CXCL2. Most importantly, G-CSF-induced CXCR2 expression was significantly reduced in CerS2 null neutrophils and their migratory capacity was significantly impaired. In conclusion, our data strongly indicate that G-CSF-induced CXCR2 expression is regulated in a CerS2-dependent manner and that CerS2 thereby promotes the migration of neutrophils, thus, contributing to inflammation and the development of EAE and MS.     

Retinal disease in the C3 glomerulopathies and the risk of impaired vision

Background: Dense deposit disease and atypical hemolytic uremic syndrome are often caused by Complement Factor H (CFH) mutations. This study describes the retinal abnormalities in dense deposit disease and, for the first time, atypical haemolytic uremic syndrome. It also reviews our understanding of drusen pathogenesis and their relevance for glomerular disease. Methods: Six individuals with dense deposit disease and one with atypical haemolytic uremic syndrome were studied from 2 to 40 years after presentation. Five had renal transplants. All four who had genetic testing had CFH mutations. Individuals underwent ophthalmological review and retinal photography, and in some cases, optical coherence tomography, and further tests of retinal function. Results: All subjects with dense deposit disease had impaired night vision and retinal drusen or whitish-yellow deposits. Retinal atrophy, pigmentation, and hemorrhage were common. In late disease, peripheral vision was restricted, central vision was distorted, and there were scotoma from sub-retinal choroidal neovascular membranes and atypical serous retinopathy. Drusen were present but less prominent in the young person with atypical uremic syndrome due to a heterozygous CFH mutation. Conclusions: Drusen are common in forms of C3 glomerulopathy caused by compound heterozygous or heterozygous CFH mutations. They are useful diagnostically but also impair vision. Drusen have an identical composition to glomerular deposits. They are also identical to the drusen of age-related macular degeneration, and may respond to the same treatments. Individuals with a C3 glomerulopathy should be assessed ophthalmologically at diagnosis, and monitored regularly for vision-threatening complications.     

单孔胸腔镜下肺癌术后胸腔引流时间的影响因素分析北大核心

目的:探讨单孔胸腔镜下肺癌手术术后胸腔引流时间的影响因素。方法:本研究采用回顾性分析方法,回顾我院2018年01月至2019年12月原发性肺癌患者经单孔胸腔镜手术治疗的病例199例。按照术后胸腔引流时间分为两组,Ⅰ组(术后胸腔引流时间<5天)和Ⅱ组(术后胸腔引流时间≥5天)。对于影响术后胸腔引流时间的可能因素在两组间先采用单因素分析的方法筛选,再将筛选出来的对术后胸腔引流时间可能有意义的影响因素进行二项Logistic多因素回归分析。结果:经单因素分析及二项Logistic多因素回归分析结果显示:年龄≥60岁、手术部位、肺段切除术、胸膜粘连、手术时间≥180 min、术后早期下床活动是术后胸腔引流时间的独立影响因素(P<0.05)。结论:对于具有多个延长术后胸腔引流时间的独立影响因素的患者,应制定个体化管理方案,尽可能减少术后胸腔引流时间,减少住院天数,加快患者康复。     

丹青胶囊联合他扎罗汀倍他米松治疗银屑病的临床研究

目的 探讨丹青胶囊联合他扎罗汀倍他米松治疗银屑病的临床疗效.方法 选取2019年6月—2021年6月在天津市职业病防治院门诊皮肤科就诊治疗的114例银屑病患者,根据随机数字法分为对照组和治疗组,每组各57例.对照组患者给予他扎罗汀倍他米松乳膏,洗净患处,待皮肤干爽后,将适量本品均匀涂抹于患处,1次/d.治疗组患者在对照组治疗基础上口服丹青胶囊,4粒/次,3次/d.两组患者均连续治疗7 d.观察两组患者的临床疗效和临床症状好转时间,比较两组治疗前与治疗1、4、8周的皮损面积和严重程度指数(PASI)评分和血清炎性因子水平.结果 治疗后,治疗组总有效率是98.25％,显著高于对照组的82.46％(P<0.05).治疗后,治疗组患者皮损暗红、皮损肥厚、皮肤瘙痒、皮肤疼痛等症状好转时间均显著短于对照组(P<0.05).治疗后,两组PASI评分均较治疗前显著降低(P<0.05);治疗1、4、8周治疗组PASI评分显著低于对照组(P<0.05).治疗后,两组患者血清炎性因子白细胞介素6(IL-6)、白细胞介素17(IL-17)、肿瘤坏死因子α(TNF-α)、干扰素-γ(IFN-γ)水平均较治疗前显著降低(P<0.05);治疗后,治疗组血清炎性因子水平显著低于对照组(P<0.05).结论 丹青胶囊联合他扎罗汀倍他米松治疗银屑病效果明显,能显著降低炎性因子水平,并有助于改善皮损情况,值得临床推广应用.     

Proteases and their inhibitors as prognostic factors for high-grade serous ovarian cancer

Ovarian carcinoma is one of the most lethal malignancies, but only very few prognostic biomarkers are known. The degradome, comprising proteases, protease non-proteolytic homologues and inhibitors, have been involved in the prognosis of many cancer types, including ovarian carcinoma. The prognostic significance of the whole degradome family has not been specifically studied in high-grade serous ovarian cancer. A targeted DNA microarray known as the CLIP-CHIP microarray was used to identify potential prognostic factors in ten high-grade serous ovarian cancer women who had early recurrence (<1.6 years) or late/no recurrence after first line surgery and chemotherapy. In women with early recurrence, we identified seven upregulated genes (TMPRSS4, MASP1/3, SPC18, PSMB1, IGFBP2, CFI – encoding Complement Factor I – and MMP9) and one down-regulated gene (ADAM-10). Using immunohistochemistry, we evaluated the prognostic effect of these 8 candidate genes in an independent cohort of 112 high-grade serous ovarian cancer women. Outcomes were progression, defined according to CA-125 criteria, and death. Multivariate Cox proportional hazard regression models were done to estimate the associations between each protein and each outcome. High ADAM-10 expression (intensity of 2–3) was associated with a lower risk of progression (adjusted hazard ratio (HR): 0.51; 95% confidence interval (CI): 0.29-0.87). High complement factor I expression (intensity 2–3) was associated with a higher risk of progression (adjusted HR: 2.30, 95% CI: 1.17–4.53) and death (adjusted HR: 3.42; 95% CI: 1.72–6.79). Overall, we identified the prognostic value of two proteases, ADAM-10 and complement factor I, for high-grade serous ovarian cancer which could have clinical significance.