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简介：AbstractThe human gastrointestinal tract accommodates an entire micro-environment for divergent physiologic processes, the dysbiosis of this micro-ecology has a strong inter-action with the pathogenesis of inflammatory bowel disease (IBD). In the past few years, with the advances in the understanding of microbiome, its metabolites and further application of next generation sequencing, analysis of dynamic alteration of gut micro-environment was realized, which provides numerous information beyond simple microbiota structure or metabolites differences under chronic colitis status. The subsequent intervention strategies targeting the modulation of intestinal micro-environment have been explored as a potential therapy. In this review, we will summarize the recent knowledge about multi-dimensional dysbiosis, the inter-action between fungus and bacteria under inflamed mucosa, and the clinical application of probiotics and fecal microbiota transplantation as a promising therapeutic approach in IBD.

简介：摘要：文章以“篮球计数器”作品的设计和制作为例，详细介绍了项目提出的背景以及项目的具体实施过程，从而为基于 Micro:bit开源板的大班额普惠式创客教育项目的开展引出了框架，保证了大班额普惠式创客教育较好的课堂的效果。

简介：摘要目的研究舟月骨间韧带（SLIL）的形态和血供分布,并从解剖学角度探讨临床上SLIL损伤对其血供的影响及重建的方法。方法2018年10月至2018年12月,选取12例新鲜成人前臂标本,从尺动脉或桡动脉灌注明胶-氧化铅溶液,于Micro-CT下扫描,通过Mimics软件三维重建图像,观察SLIL在中立位的形态和韧带内滋养血管分布,测量韧带掌侧、背侧和近端的宽度、长度、厚度,测量SLIL内滋养血管入口处的解剖参数,并分析其与舟、月骨的血供关系。结果①数字化技术三维重建SLIL的大体形态并测量其解剖参数,近端长度均值最大,掌侧、背侧长度相近；韧带掌侧最宽,厚度最小,而背侧与近端在厚度与宽度上相近。②SLIL的近端无滋养血管分布,掌侧与背侧均有丰富的滋养血管分布,其血供分布差异无统计学意义（P>0.05）。③SLIL的掌侧与背侧内滋养血管从SLIL附着处进入舟、月骨内形成吻合。结论SLIL掌侧较宽且厚度小,从解剖学角度分析其较其它亚区更易损伤；其掌侧与背侧亚区均有丰富的血供且与舟、月骨内相吻合,而近端无血管分布,因此,掌、背侧韧带早期轻度损伤有一定的自我修复能力,而近端损伤则较难修复,韧带掌侧与背侧损伤对舟、月骨血供会产生一定影响。

简介：摘要目的应用Micro-CT扫描技术分析尿道下裂大鼠包皮血管的分布规律，阐述不同类型尿道下裂血管的分布特点，为尿道下裂皮瓣的选择提供理论基础。方法选取孕鼠6只，应用非那雄胺溶液(40 mg·kg-1·d-1)于孕12～17 d连续6 d经腹部皮下注射，分娩28 d后对幼鼠进行计数，根据幼鼠尿道外口位置分为正常组和轻度、重度尿道下裂组。幼鼠6个月龄时于腹主动脉插管并行硅酮橡胶(Microfil)灌注后行Micro-CT扫描，CTAn软件收集扫描数据后对整个阴茎组织行三维重建，得到完整包皮血管影像，观察不同程度尿道下裂包皮血管的分布特点并计算包皮血管分数。结果共产幼鼠41只，雄性24只，阴茎正常的有8只，尿道下裂的有16只，轻度尿道下裂的有3只，重度尿道下裂的有13只。Micro-CT扫描包皮血管情况：①正常组及轻度下裂组，二者包皮血管形态相似，两侧阴茎背浅动脉的深层血管分别走行于阴茎体的背外侧，于包皮内外板交界处形成环绕阴茎头的血管环结构后向内板发出细小分支；②重度下裂组，根据血管形态分为血供良好(6只)和血供不良(7只)两种类型，血供良好型内外板交界处可形成类似正常组和轻度尿道下裂组的血管环；血供不良型则不能形成血管环结构，其血管分支不发达，部分血管呈网状分布。结论大鼠孕期应用非那雄胺可产生稳定尿道下裂后代。包皮内外板交界处血运丰富，适合作尿道皮瓣材料；内外板交界处的血管环结构与横裁岛状皮瓣法裁剪方向一致，最大程度地保存了皮瓣血运。包皮血供不良的重度尿道下裂内外板的血管环结构消失，而管径细小的网状血管增多，这可能是重度尿道下裂患者术后并发症发生率较高的原因之一。

简介：摘要目的探讨1例发育落后患儿的临床及遗传学特征。方法对患儿进行全外显子组测序分析，并用Sanger测序对变异位点进行验证。结果全外显子组测序显示患儿携带两个RAB3GAP1基因的杂合性剪接变异：c.2607-1G>C和c.899＋2dupT，分别遗传自其表型正常的母亲和父亲。结论确诊了1例罕见的Warburg micro综合征1型。患儿的表型与文献报道一致，并存在腭弓发育不良、显著的高腭弓及牙齿发育不良等罕见表现。

简介：摘要目的研究大鼠放射性脑损伤模型中葡萄糖代谢与神经元活性的相关性，探讨2-18F-2-脱氧-D-葡萄糖(18F-FDG)micro-PET用于放射性认知功能障碍评估的潜在价值。方法将3周龄雄性SD大鼠按照随机数表法分成对照组以及全脑照射组，每组10只，脑照射组利用小动物精确放疗仪给予10 Gy X射线照射，对照组不予照射。通过Morris水迷宫(MWM)实验评估大鼠认知功能，对两组大鼠脑部micro-PET图像数据进行对比分析，免疫组织化学染色检测神经元活性标记物c-Fos蛋白在脑内的表达变化，免疫荧光染色检测幼稚神经元标志物DCX及新生成熟神经元标志物BrdU/NeuN阳性细胞数的变化。结果照射3个月后，与对照组相比，全脑照射的大鼠在MWM定向航行实验中第2至4天的潜伏期均显著延长(t＝2.179、3.393、3.219，P<0.05)，MWM空间探索实验中的目标象限的探索时间百分比减少(t＝3.857, P<0.01)，提示全脑照射可引起海马依赖性认知能力下降；SPM分析micro-PET图像显示全脑照射组海马区域葡萄糖代谢显著降低(t＝5.12, P<0.05)；此外，全脑照射组海马区域神经元活性标记蛋白c-Fos的表达显著减少(t＝14.22, P<0.01)，幼稚神经元标志物DCX及新生成熟神经元标志物BrdU/NeuN阳性细胞数均较对照组减少(t＝18.77、9.304, P<0.01)。结论全脑放疗后海马区域的葡萄糖代谢减低，与海马神经元活性下降及神经发生减少相一致，表明18F-FDG micro-PET可以作为评估放射性认知功能障碍的有效方法。

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.