简介：由endoparasitic黄蜂Pteromaluspuparum的寄生状态(Hymenoptera：Pteromalidae)由使用仅仅它的联系毒液，能压制Pierisrapae的immunal回答(鳞翅目：Pieridae)。直到现在，然而，机制的当前的知识被限制了。到寄生状态的主人血球的反应用光和传播电子显微镜学(TEM)的联合被调查。五种血球类型，prohemocytes(PR)，granulocytes(GR)，plasmatocytes(请)，oenocytoids(OE)和coagulocytes(公司)，从unparasitized被观察并且描绘并且寄生于Pierisrapae蛹。轻显微镜学显示出那GR并且请周围成为了更多并且在寄生状态以后反常地传播了，而血球的另外的类型的形状仍然保持未受影响。另外，当OE变得更小时，PR并且请的尺寸变得更大。PR的比例显著地在寄生状态和的以后增加了请在43.9%减少了，但是没有GR和OE的重要增加。TEM证明除了公司的血球的所有类型在寄生状态以后被损坏到各种各样的度，特别导致电子不透明的细胞质和原子核，不平的endoplasmic蜂窝胃的更少房间细胞器，线粒体和泡。我们的结果由P显示那个寄生状态。puparum影响微分血球计数和主人血球的结构，特别地为GR并且请，它可以是压制主人的parasitoid的主要原因细胞的有免疫力的回答。

简介：患儿,男,23个月,因抽搐6个月就诊。患儿于17个月时出现抽搐发作,表现为＂双眼向左凝视,左上肢抖动＂,每次持续1-2min,视频脑电图示右侧Rolandic区及前颞区棘波、棘慢波,诊断为癫癎,给予左乙拉西坦口服（目前30mg/kg/d）,仍1-2个月发作一次。

简介：AbstractBackground:The use of microRNAs in the therapy of kidney disease is hampered by the difficulties in their effective delivery. Microvesicles (MVs) are known as natural carriers of small RNAs. Our prior research has demonstrated that MVs isolated from mesenchymal stem cells (MSCs) are capable of attenuating kidney injuries induced by unilateral ureteral obstruction and 5/6 sub-total nephrectomy in mice. The present study aimed to evaluate the effects of miR-34a-5p (miR-34a)-modified MSC-MVs on transforming growth factor (TGF)-β1-induced fibrosis and apoptosis in vitro.Methods:Bone marrow MSCs were modified by lentiviruses over-expressing miR-34a, from which MVs were collected for the treatment of human Kidney-2 (HK-2) renal tubular cells exposed to TGF-β1 (6 ng/mL). The survival of HK-2 cells was determined using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) and Annexin V-Light 650/propidium iodide (PI) assays. The expression levels of epithelial markers (tight junction protein 1 [TJP1] and E-cadherin) and mesenchymal markers (smooth muscle actin alpha (α-SMA) and fibronectin) in HK-2 cells were measured using Western blot analysis and an immunofluorescence assay. In addition, changes in Notch-1/Jagged-1 signaling were analyzed using Western blotting. Data were analyzed using a Student’s t test or one-way analysis of variance.Results:MiR-34a expression increased three-fold in MVs generated by miR-34a-modified MSCs compared with that expressed in control MVs (P < 0.01, t= 16.55). In HK-2 cells, TJP1 and E-cadherin levels decreased to 31% and 37% after treatment with TGF-β1, respectively, and were restored to 62% and 70% by miR-34a-enriched MSC-MVs, respectively. The expression of α-SMA and fibronectin increased by 3.9- and 5.0-fold following TGF-β1 treatment, and decreased to 2.0- and 1.7-fold after treatment of HK-2 cells with miR-34a-enriched MSC-MVs. The effects of miR-34a-enriched MSC-MVs on epithelial-mesenchymal transition (EMT) markers were stronger than control MSC-MVs. The effects of miR-34a-enriched MSC-MVs on these EMT markers were stronger than control MSC-MVs. Notch-1 receptor and Jagged-1 ligand, two major molecules of Notch signaling pathway, are predicted targets of miR-34a. It was further observed that elevation of Notch-1 and Jagged-1 induced by TGF-β1 was inhibited by miR-34a-enriched MSC-MVs. In addition, TGF-β1 exposure also induced apoptosis in HK-2 cells. Although miR-34a-mofidied MSC-MVs were able to inhibit TGF-β1-triggered apoptosis in HK-2 cells, the effects were less significant than control MSC-MVs (control:TGF-β1 :miR-nc-MV:miR-34a-MV = 1.3:0.6:1.1:0.9 for MTT assay, 1.8%:23.3%:9.4%:17.4% for apoptosis assay). This phenomenon may be the result of the pro-apoptotic effects of miR-34a.Conclusions:The present study demonstrated that miR-34a-over-expressing MSC-MVs inhibit EMT induced by pro-fibrotic TGF-β1 in renal tubular epithelial cells, possibly through inhibition of the Jagged-1/Notch-1 pathway. Genetic modification of MSC-MVs with an anti-fibrotic molecule may represent a novel strategy for the treatment of renal injuries.