Reconstruction of the Hypothalamo-Neurohypophysial System and Functional Dissection of Magnocellular Oxytocin Neurons in the Brain

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20个赤苍藤种质资源表型性状的遗传多样性分析及综合评价

分析木本蔬菜赤苍藤不同种质资源的表型性状特点,为筛选出叶大、枝条生长旺盛的赤苍藤优良种源奠定基础,该研究以来自越南及中国3省(区)(广西、广东、福建)的20个赤苍藤种源为对象,对12个叶性状及4个枝条性状进行测定及计算,对各性状进行描述统计、方差分析及性状相关性分析,采用主成分分析法计算各种源主成分得分并对各种源进行聚类,对不同赤苍藤种源表型性状进行统计、分类及评价。结果表明:(1)各赤苍藤种源间大多数叶、枝条性状存在显著或极显著差异。种源内各性状变异系数变化幅度不尽相同。种源间各性状变异系数变化幅度依次为叶功能性状(15.42%～70.01%)>枝条性状(20.57%～71.71%)>叶形态性状(3.39%～20.01%); 种源内表型变异更突出。(2)就性状间相关性而言,叶形态性状及叶功能性状指标间多为极显著相关,新枝数量与节间数、新叶数极显著相关,但与叶形态性状的相关关系不明显。(3)16个表型性状共可提取4个主成分,累计贡献率达85.528%。4个主成分分别体现出叶的形态、枝叶萌发生长、叶形状及叶干物质积累及枝条增粗状况。(4)对20个种源进行聚类分析可分为三大类,一类为叶大、生长良好的种源,一类为叶较小、枝条生长旺盛的种源,还有一类种源综合表现不突出。各大类种源中的小类在地理分布上较为接近。(5)福建安溪及福清的种源可选择为大叶种源; 广西大新、上思和桂平的种源可选择为枝条生长旺盛种源。综合来看,中国福建安溪种源综合表现最佳,其次为中国福建福清、中国广东海丰、中国广西南宁、越南茶陵。广西昭平、宜州的两种源综合表现最差,不适宜广西南宁地区引种栽培。部分种源中存在生长表现突出的优良单株,可将此类植株开发为无性系,进行更深入的种源试验。该研究结果为赤苍藤种源表型性状分析及广西南宁引种初步表现提供了科学依据,为筛选、培育高产赤苍藤品种奠定了基础。     

青海省南部治多-杂多一带早石炭世有孔虫动物群

在青海省南部的治多—杂多一带1／25万地质填图中，于杂多群中首次发现非筵有孔虫，建立2个组合，即Endothyra-Mediocris—Archaediscus组合和Bradyina-Endothyranopsis组合，地质时代为早石炭世大塘期德坞期，与华南、塔里木盆地、西秦岭、前苏联等地同期生物群可很好地对比，同时结合大冢相似系数的计算表明，青海南部地区在早石炭世属于特提斯大区华夏生物区华南省。     

Calcium ameliorates obesity induced by high-fat diet and its potential correlation with p38 MAPK pathway

To investigate whether and on which pathway dietary calcium influence the obesity induced by high-fat diet, thirty male Kunming mice were fed in six groups for 4 weeks and mouse preadipocytes were divided into eight groups for different treatment. Body weight gain was measured each week. Calcium in serum and tissues, intracellular free Ca²⁺ concentration ([Ca²⁺]i), blood fat and intracellular lipid content were also measured. The expression of Lipid metabolism-related genes were measured by q RT-PCR. Compared with control group, body weight gain (P < 0.05) and fat pad weight (P < 0.01) in Low calcium group decreased. Triglycerides (TG) and total Cholesterol (TC) level decreased (P < 0.01), while HDL-Cholesterol (HDL) level increased (P < 0.01). And calcium supply increased calcium content in blood serum and tissues. In tissues, adipogenesis and vitamin D receptor (VDR) genes expression decreased but lipoclasis genes expression increased. These anti-obesity effects were more obvious when supplying with 2.8% calcium, but the effects were reduced while supplying Nifedipine at the same time. The results in preadipocytes indicated that calcium-treated can reduce intracellular lipid content, along with adipogenesis and lipoclasis genes expression decrease, promoted the expression levels of p38 MAPK pathway upstream gene MKK6 (P < 0.01) and downstream gene MAPKAPK2 (P < 0.01). Treated with SB203580 could increase adipogenesis genes expression, decrease lipoclasis genes expression and ([Ca²⁺]i) (P < 0.01). These results implied that dietary calcium had remarkable effect on anti-obesity effect and p38 MAPK pathway potentially participated in calcium-mediated lipid accumulation and lipolysis in mouse preadipocytes.     

SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

Our previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.Subject terms: Macroautophagy, Acetylation     

异染色质相关蛋白TRIM28调控锌指蛋白和原钙黏蛋白家族基因的转录

目的 TRIM28是一种异染色质相关蛋白,通过和SETDB1、HP1相互作用参与H3K9me3修饰的建立,本文旨在更深入地研究TRIM28的相关功能。方法 本文利用CRISPR/Cas9技术、染色质免疫共沉淀技术、免疫印迹技术和实时荧光定量PCR技术,建立HEK293F Trim28基因敲除细胞系,分析一系列实验数据结果。结果 Trim28主要抑制内源表达水平较低的基因转录,进一步分析发现Trim28调控锌指蛋白家族基因和原钙黏蛋白β家族基因的转录。在Trim28敲除细胞系中,锌指蛋白家族基因H3K27ac修饰、H3K4me1修饰和H3K4me3修饰都显著上升,H3K9me3修饰下降。原钙黏蛋白β家族基因的H3K4me3修饰显著上升,H3K9me3修饰下降。结论 这些结果提示TRIM28通过改变染色质的开放程度调控锌指蛋白和原钙黏蛋白β家族基因的转录,为更深入研究TRIM28的功能提供了新的思路。     

单克隆抗体及其抗感染作用的研究进展

骨髓瘤细胞和单个B细胞可融合形成杂交瘤细胞,这种细胞分离并克隆后可产生针对单一表位,且结构和功能相同的抗体,即单克隆抗体(monoclonal antibody, mAb)。单克隆抗体发展历程经历了四个阶段。其制备技术也在不断革新与发展。目前单克隆抗体技术发展日益成熟,在疾病治疗与诊断中发挥着关键的作用。单克隆抗体与天然抗体不同,具有效价高、特异性强、交叉反应少、可大量制备,靶向性高等特点。mAb可用于诊断及治疗感染性疾病、自身免疫病以及癌症等。对mAb的发展历程及mAb在抗感染性疾病中的应用进行简要阐述。     

Uncovering the mysterious identity of Taisui—an old Chinese folk legend

Science China Life Sciences -     

Targeting CD276 by CAR-T cells induces regression of esophagus squamous cell carcinoma in xenograft mouse models

Esophageal cancer, including esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), has a poor prognosis and limited therapeutic options. Chimeric antigen receptor (CAR)-T cells represent a potential ESCC treatment. In this study, we examined CD276 expression in healthy and esophageal tumor tissues and explored the tumoricidal potential of CD276-targeting CAR-T cells in ESCC. CD276 was strongly and homogenously expressed in ESCC and EAC tumor lesions but mildly in healthy tissues, representing a good target for CAR-T cell therapy. We generated CD276-directed CAR-T cells with a humanized antigen-recognizing domain and CD28 or 4–1BB co-stimulation. CD276-specific CAR-T cells efficiently killed ESCC tumor cells in an antigen-dependent manner both in vitro and in vivo. In patient-derived xenograft models, CAR-T cells induced tumor regression and extended mouse survival. In addition, CAR-T cells generated from patient T cells demonstrated potent cytotoxicity against autologous tumor cells. Our study indicates that CD276 is an attractive target for ESCC therapy, and CD276-targeting CAR-T cells are worth testing in ESCC clinical trials.