雌雄子午沙鼠的认知行为及其神经内分泌水平的差异

本研究通过对雌雄子午沙鼠进行新物体识别和社会认知实验,运用免疫组化方法检测其相关脑区合成催产素（OT）、加压素（AVP）和多巴胺（DA）能的神经元数量,采用酶联免疫试验（ELISA）方法检测了其血清中OT、AVP的水平,探究了雌雄子午沙鼠的两性认知差异及其神经内分泌水平的差异。结果表明,雌雄子午沙鼠对新物体的探究时间均要显著高于旧物体,雌雄子午沙鼠的辨别指数无显著差异（P＞0.05）;雄性子午沙鼠随着探究次数的增加对重复刺激鼠a的探究时间不断减少,对陌生刺激鼠b的探究时间显著高于刺激鼠a（P＜0.05）;雌性子午沙鼠没有此趋势。雄性子午沙鼠OT能神经元数量在下丘脑室旁核(PVN)和视上核(SON)均要显著少于雌性（P＜0.05）;雄性个体DA能神经元数量在黑质显著高于雌性（P＜0.01）;然而雄性个体DA能神经元数量在腹侧被盖区显著少于雌性（P＜0.01）;雌雄子午沙鼠血清OT、AVP水平均无显著差异。综上所述,雌雄子午沙鼠对新物体的识别能力无显著差异,然而雄性子午沙鼠的社会认知能力强于雌性。在神经内分泌水平上,雌雄子午沙鼠PVN和SON中OT能神经元数量、黑质和腹侧背盖区的DA能神经元数量均呈现出了两性差异。     

IgA1 isolated from Henoch‐Schönlein purpura children promotes proliferation of human mesangial cells in vitro

Previous studies show that the proliferation of human mesangial cells (HMCs) played a significant part in the pathogenesis of Henoch‐Schönlein purpura nephritis (HSPN). The aim of this study was to explore the proliferation of HMCs induced by IgA1 isolated from the sera of HSP patients. HMCs were cultured in three different types of media, including IgA1 from patients with HSP (HSP IgA1 group), healthy children (healthy IgA1 group) and medium (control group). The proliferation of HMCs incubated with IgA1 was determined by cell counting kit‐8 assay and bromodeoxyuridine incorporation. The expression of ERK1/2 and phosphatidylinositol 3 kinase/protein kinase B/mammalian targets of the rapamycin (PI3K/AKt/mTOR) signals and transferrin receptor (TfR/CD71) was detected with the methods of immunoblotting. The results indicated that the proliferation of HMCs significantly increased in the HSP IgA1 group compared with that in the control group or the healthy IgA1 group (P < 0.001). Moreover, we found that IgA1 isolated from HSP patients activated ERK and PI3K/AKt/mTOR signals, and markedly increased TfR/CD71 expression in HMCs. These effects induced by IgA1 isolated from patients with HSP were inhibited by human TfR polyclonal antibody (hTfR pAb) and soluble human transferrin receptor (sTfR), indicating that IgA1‐induced HMC proliferation and ERK1/2 and PI3K/AKt/mTOR activation were dependent on TfR/CD71 engagement. Altogether, these data suggested that TfR/CD71 overexpression and ERK1/2 and PI3K/AKt/mTOR activation were engaged in HMC proliferation induced by IgA1 from HSP patients, which might be related to the mesangial injury of HSPN.     

Long non‐coding RNA cardiac hypertrophy‐associated regulator governs cardiac hypertrophy via regulating miR‐20b and the downstream PTEN/AKT pathway

Pathological cardiac hypertrophy (CH) is a key factor leading to heart failure and ultimately sudden death. Long non‐coding RNAs (lncRNAs) are emerging as a new player in gene regulation relevant to a wide spectrum of human disease including cardiac disorders. Here, we characterize the role of a specific lncRNA named cardiac hypertrophy‐associated regulator (CHAR) in CH and delineate the underlying signalling pathway. CHAR was found markedly down‐regulated in both in vivo mouse model of cardiac hypertrophy induced by pressure overload and in vitro cellular model of cardiomyocyte hypertrophy induced by angiotensin II (AngII) insult. CHAR down‐regulation alone was sufficient to induce hypertrophic phenotypes in healthy mice and neonatal rat ventricular cells (NRVCs). Overexpression of CHAR reduced the hypertrophic responses. CHAR was found to act as a competitive endogenous RNA (ceRNA) to down‐regulate miR‐20b that we established as a pro‐hypertrophic miRNA. We experimentally established phosphatase and tensin homolog (PTEN), an anti‐hypertrophic signalling molecule, as a target gene for miR‐20b. We found that miR‐20b induced CH by directly repressing PTEN expression and indirectly increasing AKT activity. Moreover, CHAR overexpression mitigated the repression of PTEN and activation of AKT by miR‐20b, and as such, it abrogated the deleterious effects of miR‐20b on CH. Collectively, this study characterized a new lncRNA CHAR and unravelled a new pro‐hypertrophic signalling pathway: lncRNA‐CHAR/miR‐20b/PTEN/AKT. The findings therefore should improve our understanding of the cellular functionality and pathophysiological role of lncRNAs in the heart.     

Genome-wide identification and expression profiling analysis of brassinolide signal transduction genes regulating apple tree architecture

Brassinolide (BR) is crucial for regulating plant architecture. Apple dwarfing rootstocks are used to control apple tree size. However, information regarding the effects of BR on apple trees is limited. In addition, the molecular mechanism underlying the dwarfing of apple rootstocks is poorly understood. To elucidate the role of BR signal transduction genes in controlling apple tree architecture, five BR receptor kinase 1 (BRI1), nine BR-signaling kinase 1 (BSK1), two BRI1 KINASE INHIBITOR 1 (BKI1), and seven BR-insensitive 2 (BIN2) genes were analyzed. Bioinformatic analyses revealed that gene duplication events likely contributed to the expansion and evolution of the identified genes. Nine homologs between apple and Arabidopsis thaliana were also identified, and their expression patterns in different tissues were characterized. Exogenous BR treatments increased the primary shoot length and altered the expression of BR signal transduction genes (MdBRI1-5, MdBSK3-8, MdBKI1–2, MdBIN1–4, and MdBIN6/7). The scion of Fuji/Malling 9 (M.9) trees exhibited inhibited growth compared with that of Fuji/Fuji trees. The Fuji/M.9 trees had lower levels of the positive regulators of BR signaling (MdBRI1-5,MdBSK1, MdBSK4/7, and MdBSK6) and higher levels of the negative regulators (MdBIN5-7) compared with the Fuji/Fuji trees. Thus, the above-mentioned genes may help to regulate apple tree size in response to BR. In addition, MdBRI1–5, MdBSK1, MdBSK4/7, MdBSK6, and MdBIN5–7 have important roles in different grafting combinations. Our results may provide the basis for future analyses of BR signal transduction genes regarding their potential involvement in the regulation of plant architecture.     

京沪穗三地近十年夜间热力景观格局演变对比研究

城市热环境是城市生态环境的重要方面,它与城市气候、城市生态、城市灾害有着重要的联系.以北京、上海、广州三地为研究区,选取近10年MODIS的夜晚地表温度(LST)产品MOD11A2,分别采用质心迁移、景观格局指数、空间自相关方法研究京沪穗三地近10年的不同等级热力景观质心迁移演变、格局变迁和空间集聚特征.主要结论为:三地热力景观随郊区向市中心趋近,体现了由低温区、次中温区向中温区、次高温区、高温区过渡的趋势;三地的中温区所占比例最大,城市热力景观破碎度三地中上海市最高,5种热力景观比较,次中温区和高温区的破碎度最高;城市热力景观离散度三地中北京市最高,低温区和高温区的离散度较高.热环境空间自相关分析表明三地均以高温-高温区,低温-低温区集聚为主,北京、广州高温-高温区分布于南部,且集中成片分布,而上海市高温-高温区分布比较离散,相对较为复杂.从分布面积来说,10a中北京、上海表现为先减少后增加,而广州则持续减少.总体而言北京热环境恶化,而广州、上海热环境有所好转.     

连作杨树人工林细根寿命的代际差异及其影响因素

细根寿命是调控森林生产力形成的关键。通过在连作Ⅰ、Ⅱ代杨树人工林固定样地内埋设微根管,对杨树不同根序细根年度生长动态开展连续观测并进行生存分析。结果表明,杨树不同根序细根累积生存率存在显著差异,高级根(3—5级)寿命较长,其累积生存率显著高于1级和2级细根。杨树细根寿命存在显著的代际差异,连作Ⅱ代人工林活根量、死根量和细根总量均高于Ⅰ代林。连作Ⅱ代人工林细根中位值寿命为(90±16)d,显著低于Ⅰ代人工林((102±22)d)。连作Ⅱ代林各根序细根数量、分布比例均高于Ⅰ代林,低级细根累积生存率低于Ⅰ代林而高级细根累积生存率显著高于Ⅰ代林。连作杨树人工林细根寿命显著受制于土壤环境,1级细根寿命与土壤速效氮相关性极显著(r=-0.861),2级细根寿命与土壤物理性状相关性较强且与土壤酚酸含量呈现极显著相关(r=0.870),高级根序细根寿命与土壤物理性质和养分状况等也具有一定相关性。连作杨树人工林土壤酚酸累积和养分有效性下降影响了细根寿命和周转,并进而造成净初级生产力损耗,相关结论为连作杨树人工林生产力衰退机理模型的建立提供了科学依据。