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简介：摘要总结深圳市儿童医院诊断的1例胎儿酒精综合征(FAS)患儿的临床特点。患儿，女，6岁4个月，因"身高增长缓慢6年余"入院。患儿胎儿期存在明确的酒精暴露史，出生时为低体质量儿，出生后身高、体质量增长缓慢，存在典型的FAS面部特征，有小头畸形，记忆及叙述能力低下，可诊断为FAS。孕期酒精暴露对胎儿造成的影响是永久性的，而戒酒则是唯一也是彻底预防FAS的办法。现总结FAS临床特点并复习文献，旨在提高临床对该病的认识。

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简介：摘 要： 屈辱百年之后的中国，唯有今天离实现“国家富强、民族振兴、人民幸福”目标如此接近。那么实现“中国梦”需要哪些现实基础呢？一是勿忘过往百年的屈辱，在“民族独立”的基础上追梦；二是牢记贫穷不是社会主义，在殷实的物质基础上追梦；三是警惕木桶定律的短板效应，在“四位一体”的基础上追梦；四是避免闭关锁国重现，在“开放包容”的姿态下追梦；五是打造中华民族品格，在民族文化传承与创新中追梦；六是反腐倡廉抓实效和讲机制，在创新反腐制度中追梦。

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简介：摘要目的探讨SMARCB1（INI1）缺失的鼻腔鼻窦癌临床病理特征及其诊断和鉴别诊断。方法收集2016至2018年复旦大学附属眼耳鼻喉科医院手术切除SMARCB1（INI1）缺失的鼻腔鼻窦癌标本/活检病例6例，观察其临床特点、影像学特征、组织形态、免疫组织化学特征以及预后，并结合文献进行复习。结果5例男性，1例女性；年龄37~75岁（平均约56岁）。1例患者属于T2期，5例患者属于T4期，CT及MRI示鼻腔鼻窦占位伴骨质破坏。镜下观察：肿瘤境界不清，基底样细胞型4例，肿瘤细胞形态较单一，高核质比，细胞质稀少，呈巢状或片状分布于间质中；横纹肌样细胞型2例，肿瘤细胞呈巢状或条索状排列，细胞胞质丰富，嗜酸性，核偏位。免疫组织化学染色示6/6 INI1完全缺失，6/6弥漫强阳性表达广谱细胞角蛋白（CKpan），6/6均不表达S-100蛋白，6/6 EB病毒编码的小RNA（EBER）原位杂交阴性，4/6部分表达p63，1/5部分表达突触素，1/5部分表达p16，Ki-67阳性指数范围30%~70%。5例患者随访1~26个月，其中1例因广泛转移死亡，1例复发，2例淋巴结转移，1例无复发和转移。1例失访。结论SMARCB1（INI1）缺失的鼻腔鼻窦癌恶性程度高，病程进展快，预后差，组织形态主要为基底样细胞型和横纹肌样细胞型，细胞核INI1完全缺失有助于诊断及鉴别诊断。

简介：摘要：目的 因此本研究通过建立骨关节炎模型，主要探讨整合素 pI和 GIT 1对软骨细胞的影响，及二者之间的调控关系。以便对临床上骨性关节炎的治疗起指导作用。 方法本次研究，我们采用约一周龄的年乳大鼠 20只，雌雄不限。分别采用定量 PCR和 Western Blotting检测对照组、 pcDNA3.1空载体转染组、 pcDNA3.1-GIT 1过表达组、 pcDNA3 . I -integrin-p1过表达组、 integrin-p 1 siRNA组和 NC siRNA组中， integrin-p1和 GIT1的 mRNA和蛋白质的表达水平，来判断 integrin-p1和 GIT1之间的调控关系。结论 在体外骨关节炎关节软骨细胞模型中发现， integrin-pl和 GIT1均能促进软骨细胞的增殖，并抑制其凋亡发生。 integrin-印的过表达可以提高 GIT1的表达，反过来， GITI的高表达对 integrin-pI没有影响，说明 integrin-p1可以调控 GIT1的表达， GTI1可能是位于 integrin-pI下游的一个关键分子。

简介：摘要：目的 通过建立骨关节炎模型探讨整合素pI和GIT 1对软骨细胞的影响，及二者之间的调控关系。对临床上骨性关节炎的治疗起指导作用。 方法 采用约一周龄的年乳大鼠20只，用定量PCR和Western Blotting检测对照组、pcDNA3.1空载体转染组、pcDNA3.1-GIT 1过表达组、pcDNA3 . I -integrin-p1过表达组、integrin-p 1 siRNA组和NC siRNA组中，integrin-p1和GIT1的mRNA和蛋白质的表达水平，来判断integrin-p1和GIT1之间的调控关系。结论 integrin-p1可以调控GIT1的表达，GTI1可能是位于integrin-pI下游的一个关键分子。

简介：摘要目的探讨过表达趋化因子CXCL1促进胃癌细胞迁移及相关分子机制。方法应用胃癌细胞株（SGC-7901、BGC-823），重组慢病毒方法构建过表达CXCL1细胞株，siRNA敲低胃癌细胞表达整合素β1（integrin β1）。Western blotting法检测CXCL1、integrin β1、基质金属蛋白酶（MMP）-2、MMP-9、FAK、SRC和ERK的表达，Transwell实验评估胃癌细胞的迁移能力。结果过表达CXCL1的SGC-7901和BGC-823细胞中integrin β1表达水平高于对照细胞，siRNA干扰CXCL1表达后，胃癌细胞integrin β1表达水平下降。外源性CXCL1分别增强SGC-7901和BGC-823细胞迁移能力（2.40±0.44）倍（P=0.002）和（2.08±0.30）倍（P=0.001）。此外，CXCL1还增强FAK、SRC和ERK的磷酸化水平。integrin β1-siRNA可以阻断CXCL1所引起的SGC-7901和BGC-823细胞迁移能力增强（P<0.05）及FAK、SRC和ERK的磷酸化水平。CXCL1调控SGC-7901和BGC-823细胞的MMP-2、MMP-9表达，而敲低integrin β1后MMP-2、MMP-9表达随之下调。MMP抑制剂GM6001抑制7901-CXCL1和823-CXCL1细胞的迁移能力（P<0.05）。结论CXCL1通过integrin β1激活FAK-SRC-ERK通路和调控MMP-2、MMP-9的表达，最终调控胃癌细胞迁移。

简介：【摘要】：2020年春，新冠肺炎肆虐全国，线上课堂全面开启。然而在网课期间，问题频频。基于网课中的“云”学生、“云”氛围、“云”质量、“云”视力，在后疫情下，本文通过主题系列作业方式链接手账、链接素描、链接工艺品改善这些问题。探究如何将线上“云”课堂和线下课堂之间巧妙融合，从而提升学生基于问题、讨论问题、解决问题、应用问题的综合美术操作能力，产生

简介：AbstractBackground:Gastric cancer (GC) is one of the most common malignancies, and intestinal-type GC is the main histopathologic type of GC in China. We previously reported that casein kinase 2 interacting protein 1 (CKIP-1) acts as a candidate tumor suppressor in intestinal-type GC. CKIP-1 participates in the regulation of multiple signaling pathways, including the Wnt/β-catenin pathway, of which caudal-related homeobox 1 (CDX1) may be a downstream target gene. The purpose of this study was to investigate the relationship between CKIP-1 and CDX1 in intestinal-type GC.Methods:Sixty-seven gastroscopy biopsy specimens and surgically resected gastric specimens were divided into four groups: gastric mucosa group, intestinal metaplasia (IM) group, dysplasia group, and intestinal-type GC group. The expression levels of CKIP-1 and CDX1 were detected in these groups and GC cell lines, and the correlations between these expression levels were analyzed. SGC7901 and BGC823 cells were divided into CKIP-1 shRNA groups and CKIP-1 over-expression groups, and CDX1 expression was detected. β-Catenin expression was detected in intestinal-type GC tissue samples and CKIP-1 shRNA and CKIP-1 over-expression SGC7901 cells, and its correlation with CKIP-1 expression in intestinal-type GC tissue was analyzed. The Wnt/β-catenin pathway inhibitor DKK-1 and activator LiCl were incubated with SGC7901 cells, BGC823 cells, and CKIP-1 shRNA and CKIP-1 over-expression SGC7901 and BGC823 cells, following which CDX1 and Ki-67 expression were detected.Results:The expression levels of CKIP-1 and CDX1 were lower in patients with intestinal-type GC than in patients with IM and dysplasia (both P < 0.05). CKIP-1 and CDX1 expression levels were positively correlated in IM, dysplasia, and intestinal-type GC tissue and cell lines (r = 0.771, P < 0.01; r = 0.597, P < 0.01; r = 0.654, P < 0.01; r = 0.811, P < 0.01, respectively). CDX1 expression was decreased in the CKIP-1 shRNA groups and increased in the CKIP-1 over-expression groups of SGC7901 and BGC823 cells compared to that in the corresponding control groups (both P < 0.05). CKIP-1 expression was negatively correlated with β-catenin expression in intestinal-type GC patients (r = -0.458, P < 0.01). Compared to the control group, β-catenin expression was increased in the CKIP-1 shRNA SGC7901 cell group and decreased in the CKIP-1 over-expression SGC7901 cell group (P < 0.05). CDX1 expression was increased in SGC7901 and BGC823 cells treated with DKK-1, DKK-1 increased CDX1 expression and decreased Ki-67 expression in the CKIP-1 shRNA group; the opposite result was observed in SGC7901 and BGC823 cells treated with LiCl, and LiCl decreased CDX1 expression and increased Ki-67 expression in the CKIP-1 over-expression group (both P < 0.05).Conclusions:Through the Wnt/β-catenin signaling pathway, CKIP-1 may positively regulate CDX1 in intestinal-type GC.

简介：AbstractHistorically, breast cancer has been regarded as an immunogenic "cold" tumor. However, the discovery of immune checkpoint inhibitors has made immunotherapy becoming an emerging new treatment modality for breast cancer. This review discusses the immune system, immune features of breast cancer, and the programmed cell death protein-1/programmed cell death protein ligand-1 (PD-1/PD-L1) inhibitors used in the treatment of breast cancer. High T lymphocyte infiltration and mutation burden were observed in triple-negative breast cancer and human epidermal growth factor receptor 2 positive breast cancer. Increasing breast cancer immunogenicity and modulating the tumor microenvironment has been reported to improve the therapeutic efficacy of immunotherapy. Recent clinical trials involving PD-1/PD-L1 inhibitors monotherapy in breast cancer has revealed little efficacy, which highlights the need to develop combinations of PD-1/PD-L1 inhibitors with chemotherapy, molecularly targeted therapies, and other immunotherapies to maximize the clinical efficacy. Collectively, the immunotherapy might be a promising therapeutic strategy for breast cancer and several clinical trials are still on-going.

简介：摘要细胞程序性死亡蛋白1及其配体1（PD-1/PD-L1）通路已经成为研究热点，无论在抗肿瘤还是在抗炎方面均取得了一定的成果，但具体的机制目前尚不完全清楚。本文介绍了PD-1及PD-L1的分子结构、功能以及与其他通路之间的关系。PD-1蛋白是免疫抑制分子，与其配体PD-L1结合起促进细胞凋亡的作用。在肿瘤或炎症中，JAK/STAT、NF-κB、MAPK、PI3K以及TIM-3/Gal-9等其他信号通路被激活，诱导免疫细胞及肿瘤细胞高表达PD-1及PD-L1，使免疫细胞活性降低，消耗增加，募集减少，从而使机体抗肿瘤、抗炎能力下降。PD-1/PD-L1与JAK/STAT、NF-κB、MAPK、PI3K以及TIM-3/Gal-9等其他信号通路也起相互调控作用。PD-1/PD-L1抑制剂与JAK/STAT、NF-κB、MAPK、PI3K以及TIM-3/Gal-9等通路抑制剂联合应用，在抗肿瘤以及肿瘤耐药性方面取得了突破性进展。然而，相对于PD-1/PD-L1对肿瘤作用的研究而言，PD-1/PD-L1在炎症方面的研究相对较少，无相应的药物应用于临床，需要大量的基础研究支持。