Active Suppression of the Allogeneic Histocompatibility Reactions During the Metamorphosis of the Clawed Toad Xenopus

Metamorphosis is a privileged period for the induction of tolerance to allografts. Transfers of lymphocytes from metamorphosing Xenopus into isogenic adults prevented the rejection of a skin graft differing from the adult host by minor histocompatibility antigens. This implies that active suppression is involved at one step of the induction of tolerance to the self-antigens that differentiate at the time of metamorphosis. The reciprocal experiments of preventing tolerance induction by transfer of normal adult cells into metamorphosing animals failed. However, passive transfer of anti-graft immunity in tolerant animals was partially observed, provided that a transfer of primed cells was done simultaneously with the challenging graft. Thus, memory cells are not as sensitive to the suppression as are the cells that respond in a first set reaction.     

MiR-186-5p对3T3-L1前脂肪细胞增殖分化的影响研究 *

目的 探究miR-186-5p对小鼠3T3-L1前脂肪细胞增殖,分化的影响及其潜在的分子机制.方法: qRT-PCR检测miR-186-5p在不同周龄小鼠白色脂肪组织及3T3-L1前脂肪细胞增殖分化过程中的表达变化;通过脂质体将miR-186-5p mimics,inhibitors转染入增殖液或分化液培养的3T3-L1细胞后,利用CCK-8,EdU和qRT-PCR检测3T3-L1前脂肪细胞增殖变化,油红O染色观察其脂滴形态;通过生物信息软件TargetScan和双荧光报告系统分别对miR-186-5p靶基因进行预测和确认.结果: (1)miR-186-5p在1~6周龄小鼠的白色脂肪组织及3T3-L1前脂肪细胞自然分化过程中表达量均逐渐上调.(2)与阴性对照相比,mimics或inhibitors转染分别显著地促进或抑制了miR-186-5p的表达.(3)过表达miR-186-5p后,3T3-L1前脂肪细胞的增殖速率减慢,脂滴增大增多;而抑制miR-186-5p后,3T3-L1前脂肪细胞增殖速率增快,脂滴数量减少,且粒径变小.其中过表达miR-186-5p显著地降低了野生型Wnt5a和Mapk1 3'-UTR活性,而突变相应的绑定位点可解除该抑制作用.结论: miR-186-5p可抑制3T3-L1前脂肪细胞增殖,且通过直接靶向Wnt5a和Mapk1以促进其分化为成熟脂肪细胞.     

干皮孔菌属的一个新种和三个组合种

本文报道了产自斯里兰卡的干皮孔菌属一个新种,该种的主要特征是具有平伏反卷或具菌盖的子实体,很小的孔口（每毫米8-10个）,菌丝系统二系,生殖菌丝覆盖有刺状结晶,骨架菌丝橙棕色,细腊肠状担孢子（2.7-3.4×0.5-0.8μm）。基于ITS和nLSU序列的系统发育分析表明该新种属于干皮孔菌属的一个明确的分支。此外,将毛孔菌属组合到干皮孔菌属中,并报道了3个组合种,白边干皮孔菌、印度干皮孔菌和萨彦干皮孔菌。     

Exosomes derived from umbilical cord mesenchymal stem cells alleviate viral myocarditis through activating AMPK/mTOR‐mediated autophagy flux pathway

Human umbilical cord mesenchymal stem cell‐derived exosomes (hucMSC‐exosomes) have been implicated as a novel therapeutic approach for tissue injury repair and regeneration, but the effects of hucMSC‐exosomes on coxsackievirus B3 (CVB3)‐induced myocarditis remain unknown. The object of the present study is to investigate whether hucMSC‐exosomes have therapeutic effects on CVB3‐induced myocarditis (VMC). HucMSC‐exosomes were identified using nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM) and Western blot. The purified hucMSC‐exosomes tagged with PKH26 were tail intravenously injected into VMC model mice in vivo and used to administrate CVB3‐infected human cardiomyocytes (HCMs) in vitro, respectively. The effects of hucMSC‐exosomes on myocardial pathology injury, proinflammatory cytokines and cardiac function were evaluated through haematoxylin and eosin (H&E) staining, quantitative polymerase chain reaction (qPCR) and Doppler echocardiography. The anti‐apoptosis role and potential mechanism of hucMSC‐exosomes were explored using TUNEL staining, flow cytometry, immunohistochemistry, Ad‐mRFP‐GFP‐LC3 transduction and Western blot. In vivo results showed that hucMSC‐exosomes (50 μg iv) significantly alleviated myocardium injury, shrank the production of proinflammatory cytokines and improved cardiac function. Moreover, in vitro data showed that hucMSC‐exosomes (50 μg/mL) inhibited the apoptosis of CVB3‐infected HCM through increasing pAMPK/AMPK ratio and up‐regulating autophagy proteins LC3II/I, BECLIN‐1 and anti‐apoptosis protein BCL‐2 as well as decreasing pmTOR/mTOR ratio, promoting the degradation of autophagy flux protein P62 and down‐regulating apoptosis protein BAX. In conclusion, hucMSC‐exosomes could alleviate CVB3‐induced myocarditis via activating AMPK/mTOR‐mediated autophagy flux pathway to attenuate cardiomyocyte apoptosis, which will be benefit for MSC‐exosome therapy of myocarditis in the future.     

脑缺血大鼠肺组织NGF/TrkA表达变化及其意义

目的:探讨大鼠脑缺血后肺组织神经生长因子(nerve growth factor,NGF)/酪氨酸蛋白激酶A(tropomyosin-related kinase A,TrkA)表达的变化。方法:成年雄性大鼠随机分为假手术组和脑缺血后6 h、24 h及48 h组,每组8只。建立大脑中动脉永久性局灶性缺血模型,术后于各时间点麻醉处死大鼠后,测定肺组织湿重/干重(W/D),光镜下观察HE染色肺组织病理学改变;Western blot法检测肺组织NGF、TrkA蛋白表达。结果:与假手术组相比,脑缺血后6 h肺组织W/D有增加,差异无统计学意义(P>0.05),而脑缺血后24 h及48 h肺组织W/D均有显著增高(P<0.05),其中以24 h组最明显(P<0.01);脑缺血后6 h肺组织出现轻度充血、水肿及炎性改变,24 h及48 h组肺泡结构破坏明显。病理学评分结果显示,脑缺血后24 h及48 h组大鼠肺组织病理评分较假手术组显著升高(P<0.05);Western blot法显示,脑缺血6 h肺组织中NGF表达增加(P<0.05),48 h时表达有下降趋势,但仍高于假手术组(P<0.05)。而肺组织中TrkA表达在脑缺血6h有下降(P>0.05),24 h下降明显(P<0.05),48 h时TrkA蛋白表达虽有上升,仍显著低于假手术组(P<0.05)。结论:大鼠肺组织NGF/TrkA的动态变化可能参与了脑缺血后肺损伤的病理生理过程。     

白蛋白静脉滴注联合茵栀黄颗粒治疗新生儿黄疸血清 AKP、TBA、 FFA、γ-GT、HS-CRP的影响

目的:研究白蛋白静脉滴注联合茵栀黄颗粒对新生儿黄疸血清碱性磷酸酶(alkaline phosphatase,AKP)、总胆汁酸(totalbileacids,TBA)、游离脂肪酸(free fatty acid,FFA)、γ-谷氨酰基转移酶(γ-glutamyltransferase,γ-GT)、超敏C-反应蛋白(hypersensitive C-reactive protein, HS-CRP)的影响。方法:选择2016年1月～2019年1月我院收治的95例新生儿病理性黄疸患儿,随机分为两组。对照组服用茵栀黄颗粒治疗,观察组在服用茵栀黄的基础上静脉滴注白蛋白治疗。检测两组的血清间接胆红素(indirectreacting bilirubin,,IBIL)、总胆红素(total bilirubin,TBIL)和AKP、TBA、FFA、y-GT、HS-CRP水平。结果:观察组的有效率明显高于对照组(P0.05);两组治疗后的血清IBIL、TBIL水平明显降低(P0.05),观察组的IBIL、TBIL水平明显低于对照组(P0.05);两组治疗后的血清AKP、TBA、FFA、γ-GT、HS-CRP水平明显降低(P0.05),观察组的血清AKP、TBA、FFA、γ-GT、HS-CRP水平明显低于对照组(P0.05)。结论:白蛋白静脉滴注联合茵栀黄颗粒对新生儿黄疸的治疗效果良好,有助于促进血清胆红素和其他血清学相关指标恢复正常,且安全性好。     

门冬胰岛素联合甘精胰岛素对新诊断2型糖尿病患者炎性因子、血糖及血脂水平的影响

目的:探讨门冬胰岛素联合甘精胰岛素对新诊断2型糖尿病患者血清炎性因子、血糖及血脂水平的影响。方法:选取我院2017年3月～2019年3月收治的100例新诊断2型糖尿病患者,将其随机分为研究组和对照组,每组50例患者。对照组患者给予门冬胰岛素治疗,研究组患者给予门冬胰岛素联合甘精胰岛素治疗,对比两组患者治疗前后血清炎性因子、血糖及血脂水平的变化。结果:治疗后,两组患者糖化血红蛋白(hemoglobin A1c,HbA1c)、空腹血糖(fasting plasma glucose,FPG)、餐后2h血糖(2h postprandial blod glucose,2hPBG)、血清肿瘤坏死因子(Tumor necrosis factor,TNF-α)、高敏C反应蛋白(high-sensitive C-reactive protein,hs-CRP)水平均较治疗前明显降低(P0.05),且研究组患者以上指标均显著低于对照组(P0.05);两组患者治疗后总胆固醇(Total Cholesterol,TC)、甘油三酯(Triglyceride,TG)、低密度脂蛋白胆固醇(Low-density lipoprotein cholesterol,LDL-C)水平均较治疗前明显降低,高密度脂蛋白胆固醇(High-density lipoprotein cholesterol,HDL-C)明显升高(P0.05),且研究组以上指标的改善程度均优于对照组(P0.05)。研究组患者的胰岛素用量明显少于对照组(P0.05),患者血糖首次达标时间明显短于对照组(P0.05)。结论:门冬胰岛素联合甘精胰岛素适用于新诊断2型糖尿病患者,可有效降低血糖、血脂、血清TNF-α和hs-CRP水平。     

不同温度下稻螟赤眼蜂在黏虫卵上的种群生命表

稻螟赤眼蜂Trichogramma japonicum Ashmead是水稻二化螟Chilo suppressalis(Walker)的优势卵寄生蜂。本文构建了以黏虫卵为中间寄主,稻螟赤眼蜂在20℃、25℃、30℃、33℃四个温度条件下的生命表。研究结果表明利用黏虫卵繁育稻螟赤眼蜂时,不同温度下其生长发育和繁殖均存在显著差异,雌蜂平均寿命随温度的升高呈下降趋势,在20℃条件下,雌蜂平均寿命为1.44 d,显著长于其它温度,当温度为30~33℃时,雌蜂寿命最短,平均为0.59 d。在温度为20℃和25℃时,稻螟赤眼蜂的羽化率显著高于温度较高的30℃和33℃,平均为94.73%。在25℃条件下,黏虫卵繁育的稻螟赤眼蜂的净生殖力(R 0)最大,达到31.9176,单雌寄生卵数最多,为32.88个,表现出最强的繁殖能力,而在30℃条件下,瞬时增长率r m和周限增长率λ达到最大值。综合生命表参数、单雌寄生黏虫卵数、寿命、羽化率等指标,利用黏虫卵工厂化繁殖稻螟赤眼蜂的最佳温度为25℃。本研究为利用黏虫卵大量繁殖稻螟赤眼蜂提供了有价值的参考。