中国对虾（Penaeus chinensis）4个种群的同工酶遗传变异

采用水平淀粉凝胶电泳技术分析了中国对虾（Penaeuschinensis）黄渤海沿岸种群（YP）、朝鲜半岛西海岸种群（KP）和2个养殖种群（CP1和CP2）的同工酶遗传变异水平。每个种群随机选取50尾中国对虾进行同工酶检测。在所分析的12种同工酶编码的20个基因位点中,有4个是多态位点。4个种群的多态位点比例（P0.99）分别为15%、20%、10%和20%。种群平均杂合度（观测值）（Ho）分别为0.014±0.007、0.020±0.010、0.010±0.007和0.033±0.017。4个种群的位点有效等位基因数（Ne）分别为1.015±0.008、1.023±0.011、1.011±0.007和1.042±0.022。杂合子平衡偏离指数（D）分别为+0.037、-0.030、-0.098和-0.030。2个地理种群（YP和KP）的遗传相似性系数（I）和遗传距离（D     

马齿苋的栽培及开发利用

马齿苋Portulaca oleracea是常用的药食兼用植物。本文对其药、食用价值及开发前景作了综述,并对其栽培条件作了初步的研究。     

A miRNA-HERC4 pathway promotes breast tumorigenesis by inactivating tumor suppressor LATS1

The E3 ligase HERC4 is overexpressed in human breast cancer and its expression levels correlated with the prognosis of breast cancer patients. However, the roles of HERC4 in mammary tumorigenesis remain unclear. Here we demonstrate that the knockdown of HERC4 in human breast cancer cells dramatically suppressed their proliferation, survival, migration, and tumor growth in vivo, while the overexpression of HERC4 promoted their aggressive tumorigenic activities. HERC4 is a new E3 ligase for the tumor suppressor LATS1 and destabilizes LATS1 by promoting the ubiquitination of LATS1. miRNA-136-5p and miRNA-1285-5p, expression of which is decreased in human breast cancers and is inversely correlated with the prognosis of breast cancer patients, are directly involved in suppressing the expression of HERC4. In summary, we discover a miRNA-HERC4-LATS1 pathway that plays important roles in the pathogenesis of breast cancer and represents new therapeutic targets for human breast cancer.     

安徽两种蜜蜂种群的春季繁殖及数量动态特征

1997～ 1999年在皖中和皖西、皖南山区对意大利蜜蜂 (ApismelliferaLigusticaSpi.)和中华蜜蜂(ApisceranaceranaFeb .)种群数量动态进行系统观察研究 .结果表明 ,蜜蜂种群数量明显受气候和蜜粉源植物的影响 ,周年呈现“两高”(春、秋 )和两低 (夏、冬 )的变化模式曲线 ;意大利蜜蜂春繁及秋季更新速度明显快于中华蜜蜂 ,但越夏效果不及中华蜜蜂 .意大利蜜蜂的性比值为 (314.4± 2 89.9)∶1～ (32 9.4± 30 5 .8)∶1,中华蜜蜂为 (334.2± 2 35 .5 )∶1～ (413 .1± 377.2 )∶1,雄蜂呈季节性出现 .蜜蜂种群内年龄组配在不断变化 .     

Regulation of the mitogen-activated protein kinase signaling pathway by SHP2.

Gab1-SHP2 association is required for Erk mitogen-activated protein kinase activation by several growth factors. Gab1-SHP2 interaction activates SHP2. However, an activated SHP2 still needs to associate with Gab1 to mediate Erk activation. It was unclear whether SHP2 is required to dephosphorylate a negative phosphorylation site on Gab1 or whether SHP2 needs the Gab1 pleckstrin homology (PH) domain to target it to the plasma membrane. We found that expression of a fusion protein consisting of the Gab1 PH domain and an active SHP2 (Gab1PH-SHP2DeltaN) induced constitutive Mek1 and Erk2 activation. Linking the active SHP2DeltaN to the PDK1 PH domain or the FRS2beta myristoylation sequence also induced Mek1 activation. Mek1 activation by Gab1PH-SHP2DeltaN was inhibited by an Src inhibitor and by Csk. Significantly, Gab1PH-SHP2DeltaN induced Src activation. Gab1PH-SHP2DeltaN expression activated Ras, and the Gab1PH-SHP2DeltaN-induced Mek1 activation was blocked by RasN17. These findings suggest that Gab1PH-SHP2DeltaN activated a signaling step upstream of Src and Ras. The SHP2 tyrosine phosphatase activity is essential for the function of the fusion protein. Together, these data show that the Gab1 sequence, besides the PH domain and SHP2 binding sites, is dispensable for Erk activation, suggesting that the primary role of Gab1 association with an activated SHP2 is to target it to the membrane.     

Pancreatic cancer-derived exosomal microRNA-19a induces β-cell dysfunction by targeting ADCY1 and EPAC2

New-onset diabetes mellitus has a rough correlation with pancreatic cancer (PaC), but the underlying mechanism remains unclear. This study aimed to explore the exosomal microRNAs and their potential role in PaC-induced β-cell dysfunction. The pancreatic β cells were treated with isolated exosomes from PaC cell lines, SW1990 and BxPC-3, before measuring the glucose-stimulated insulin secretion (GSIS), validating that SW1990 and BxPC-3 might disrupt GSIS of both β cell line MIN6 and primary mouse pancreatic islets. The difference in expression profiles between exosomes and exosome-free medium of PaC cell lines was further defined, revealing that miR-19a secreted by PaC cells might be an important signaling molecule in this process. Furthermore, adenylyl cyclase 1 (Adcy1) and exchange protein directly activated by cAMP 2 (Epac2) were verified as the direct targets of exogenous miR-19a, which was involved in insulin secretion. These results indicated that exosomes might be an important mediator in the pathogenesis of PaC-DM, and miR-19a might be the effector molecule. The findings shed light on the pathogenesis of PaC-DM.     

Cutting edge: membrane lymphotoxin regulates CD8(+) T cell-mediated intestinal allograft rejection.

Blocking the CD28/B7 and/or CD154/CD40 costimulatory pathways promotes long-term allograft survival in many transplant models where CD4(+) T cells are necessary for rejection. When CD8(+) T cells are sufficient to mediate rejection, these approaches fail, resulting in costimulation blockade-resistant rejection. To address this problem we examined the role of lymphotoxin-related molecules in CD8(+) T cell-mediated rejection of murine intestinal allografts. Targeting membrane lymphotoxin by means of a fusion protein, mAb, or genetic mutation inhibited rejection of intestinal allografts by CD8(+) T cells. This effect was associated with decreased monokine induced by IFN-gamma (Mig) and secondary lymphoid chemokine (SLC) gene expression within allografts and spleens respectively. Blocking membrane lymphotoxin did not inhibit rejection mediated by CD4(+) T cells. Combining disruption of membrane lymphotoxin and treatment with CTLA4-Ig inhibited rejection in wild-type mice. These data demonstrate that membrane lymphotoxin is an important regulatory molecule for CD8(+) T cells mediating rejection and suggest a strategy to avoid costimulation blockade-resistant rejection.     

钙信号转导途径介导肺炎链球菌侵袭人肺Ⅱ型上皮细胞

用Factin 特异性FITCphalloidin荧光染料,观察肺炎链球菌（Streptococcus pneumoniae）作用A549细胞前后的Factin细胞骨架重排情况;用细胞松弛素D预处理A49细胞,观察肺炎链球菌对A549细胞的侵袭率;使用Datrolene预处理A549细胞,观察其与Factin细胞骨架重排百分率间是否存在剂量依赖关系;用Fura2/AM荧光探针负载A549细胞后测定肺炎链球菌粘附A549细胞后的胞内Ca2+浓度。结果发现肺炎链球菌作用A549细胞后,Factin细胞骨架呈块状、丝状聚集;而松弛素D可明显降低肺炎链球菌对A549细胞的侵袭率;肺炎链球菌粘附A549细胞后胞内Ca2+高于对照;Datrolene可部分抑制A549细胞Factin细胞骨架重排,且与Factin细胞骨架重排百分率间存在量效关系。以上结果提示肺炎链球菌可通过Ca2+细胞信号转导途径触发A549细胞Factin细胞骨架重排,进而导致肺炎链球菌侵袭A549细胞。     

Nitrobenzene compounds inhibit expression of VCAM-1.

A series of nitrobenzene compounds has been discovered as potent inhibitors of VCAM-1 expression and, therefore, potential drug candidates for autoimmune and allergic inflammatory diseases. Structure-activity relationship (SAR) studies showed that a nitro group and two other electron-withdrawing groups are essential for these compounds to be potent inhibitors of VCAM-1 expression.