球形芽孢杆菌对淡色尖音库蚊的毒性及新分离株

1980年秋我们从Myers和Yousten博士处引入蚊虫病原菌球形芽孢杆菌(Bacillus sphaericus)1593及SSII-1菌株,与天津市卫生防疫站协作在筛选对淡色库蚊(Culex pipiens varpallens Coq.)高效菌的同时,对B.s-1593和苏云金杆菌以色列变种1897(Bacillus thuringiensis var.israelensis 1897)进行培养特性、热处理、冷藏、超声等对毒力影响的对比。发现B.s-1593和B.t-1897对上述处理稳定性相似,容易培养;对65℃下30分钟;80℃下12分钟;0°—4℃贮存15天均不丧失杀虫活性。1593对淡色库蚊3龄幼虫的LC_(50)为原液稀释349万倍(1.17×10~3菌/毫升),B.s-1593有别于B.t-1897的特点是:它毒杀蚊虫的死亡高峰比B·t-1897慢8—12小时,详细内容另文发表。     

中华按蚊在实验室内的自然交配习性

1973年我们在上海曾对宝山县中华按蚊(Anopheles sinensis)进行了室内饲养,通过自然交配繁殖了8代。1975年又对重庆郊区的中华按蚊同样地进行了室内累代饲育。近几年来文献上报道:未经驯化的中华按蚊,在实验室内常规饲养条件下,不易发生自然交配(Oguma和Kanda,1976;潘家复和韩罗珍,1979)。这一报道与我们的经验很不一致。为了弄清引起这种不一致的原因,以便改进饲养工作,我们特别对第一代中华按蚊在实验室内自然交配的某些规律,进行了观察。现将观察结果报告如下。     

温度对干旱、盐胁迫下两种黄芪属种子萌发和幼苗生长的影响

为探讨温度对干旱、盐胁迫下黄芪属种子萌发和幼苗生长特性的影响,以黄芪属蒙古黄芪和扁茎黄芪2种种子为研究对象,纯净水处理为对照组,NaCl、PEG处理为实验组,设置4个渗透势水平(0、-0.1、-0.3、-0.5 MPa),置于5种不同的温度(10、15、20、25、30 ℃)下,每日观察并记录两种种子萌发和幼苗生长情况。结果表明：旱盐胁迫下蒙古黄芪和扁茎黄芪种子萌发最适宜的温度分别为25和20 ℃左右;蒙古黄芪耐高温不耐低温,而扁茎黄芪恰恰相反;但25和20 ℃均适宜两种幼苗生长,包括胚根、胚轴和子叶的生长。蒙古黄芪各处理组(除未发芽的种子)的平均发芽时间都比扁茎黄芪长;NaCl胁迫程度的增加使得两种种子的最终发芽率降低,但蒙古黄芪的耐盐性高于扁茎黄芪;随着PEG胁迫程度的增加,二者的发芽均受到抑制,甚至会出现完全不萌发,但扁茎黄芪的耐旱性高于蒙古黄芪;在相同的渗透势时,尤其是-0.5 MPa,PEG比NaCl对两种种子的影响大;交互胁迫作用下,随着渗透势的增加两种幼苗的鲜重、干重以及胚根、胚轴、子叶的长和宽变化较大;利用Design Expert软件预测发现：温度25 ℃、NaCl渗透势为-0.1 MPa,温度24 ℃、PEG渗透势为-0.04 MPa的处理是蒙古黄芪种子萌发和幼苗生长达到最优化的组合;而扁茎黄芪最优化的组合则为23 ℃下NaCl渗透势为-0.07 MPa的处理,20 ℃下PEG渗透势为-0.13 MPa的处理。     

Analysis of larger than tetrameric poly(adenosine diphosphoribose) by a radioimmunoassay in nuclei separated in organic solvents.

Anitibodies were prepared against poly(adenosine diphosphoribose) of an average chain length of 40 adenosine diphosphoribose units by repeated injection of the polymer mixed with methylated albumin and adjuvants into rabbits. The antibody was present mainly in the 7 S fraction of the immunoglobulins. A membrane binding assay was developed, and its specificity determined for the detection of (adenosine diphosphoribose)ngreater than4 in organs. The method is suitable for the study of the variation of the polymer content of nuclei. The size recognition of the anti-poly(adenosine diphosphoribose) globulin fraction was the same for polymers composed of 4--40 adenosine diphosphoribose units, but smaller oligomers were not detectible. A quantitative extraction technique was developed and applied for radioimmunoassay of nuclear (adenosine diphosphoribose)n greater than 4. Organs were freeze-clamped, freeze dried, broken into subcellular fragments in a colloid mill, and the nuclear fraction was subsequently separated in organic solvents in order to preserve the polymer. Nicotinamide and nicotinic acid, when administered in vivo, augmented the (adenosine diphosphoribose)n greater than 4 content of rat liver and heart. Tissues of infant pigeons contained larger quantites of (adenosine diphosphoribose)ngreater than4 than tissues of adult rats.     

Comparative proteome analysis using amine-reactive isobaric tagging reagents coupled with 2D LC/MS/MS in 3T3-L1 adipocytes following hypoxia or normoxia

Hypoxia during the expansion of adipocytes is known to contribute both to the secretion of multiple inflammation-related adipokines as well as to obesity. We therefore investigated the nature of protein changes occurring in adipocytes during hypoxia by observation of the intracellular proteins that are expressed in 3T3-L1 adipocytes. Lysates were utilized for quantitative proteome analysis using isobaric tags for relative and absolute quantitation (iTRAQ) combined with peptide separation by multi-dimensional liquid chromatography. Antioxidants and elongation factors, as well as glycolytic enzymes were increased in hypoxic adipocytes. These changes were supported by similar changes suggested by real-time PCR. The proteins showing changes are all potential targets for revering the mechanism behind the phenomenon of induction of obese adipocytes by hypoxia. This study can therefore aid in defining the proteomic changes that occur in adipocytes in response to oxygen stress, and can further characterize adipocyte metabolism and adaptation to low oxygen conditions.     

Autophagy induction by xanthoangelol exhibits anti‐metastatic activities in hepatocellular carcinoma

Xanthoangelol (XAG), a prenylated chalcone isolated from the Japanese herb Angelica keiskei Koidzumi, has been reported to exhibit antineoplastic properties. However, the specific anti‐tumor activity of XAG in human hepatocellular carcinoma (HCC), and the relevant mechanisms are not known. Herein, we evaluated the effect of XAG against HCC in vitro and in vivo. Although XAG treatment did not significantly reduce the viability of the Hep3B and Huh7 cell lines, it suppressed cell migration, invasion, and EMT. This anti‐metastatic effect of XAG was due to induction of autophagy, because treatment with the autophagy inhibitor 3‐methyadenine (3‐MA) or knockdown of the pro‐autophagy Beclin‐1 effectively abrogated the XAG‐induced suppression of metastasis. Mechanistically, XAG induced autophagy via activation of the AMPK/mTOR signaling pathway, and XAG treatment dramatically increased the expression of p‐AMPK while decreasing p‐mTOR expression. In addition, blocking AMPK/mTOR axis with compound C abrogated the autophagy‐mediated inhibition of metastasis. The murine model of HCC metastasis also showed that XAG effectively reduced the number of metastatic pulmonary nodules. Taken together, our results revealed that autophagy via the activation of AMPK/mTOR pathway is essential for the anti‐metastatic effect of XAG against HCC. These findings not only contribute to our understanding of the anti‐tumor activity of XAG but also provide a basis for its clinical application in HCC. Before this study, evidence of XAG on HCC was purely anecdotal; present study provides the first comprehensive assessments of XAG on HCC metastasis and investigates its underlying mechanism. Results suggest that XAG exerts anti‐metastatic properties against HCC through inducing autophagy which is mediated by the activation of AMPK/mTOR signaling pathway. This research extends our knowledge about the antineoplastic properties of XAG and suggests that induction autophagy may represent future treatment strategies for metastatic HCC.     

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.     

Monophosphoryl lipid A alleviated radiation-induced testicular injury through TLR4-dependent exosomes

Radiation protection on male testis is an important task for ionizing radiation-related workers or people who receive radiotherapy for tumours near the testicle. In recent years, Toll-like receptors (TLRs), especially TLR4, have been widely studied as a radiation protection target. In this study, we detected that a low-toxicity TLR4 agonist monophosphoryl lipid A (MPLA) produced obvious radiation protection effects on mice testis. We found that MPLA effectively alleviated testis structure damage and cell apoptosis induced by ionizing radiation (IR). However, as the expression abundance differs a lot in distinct cells and tissues, MPLA seemed not to directly activate TLR4 singling pathway in mice testis. Here, we demonstrated a brand new mechanism for MPLA producing radiation protection effects on testis. We observed a significant activation of TLR4 pathway in macrophages after MPLA stimulation and identified significant changes in macrophage-derived exosomes protein expression. We proved that after MPLA treatment, macrophage-derived exosomes played an important role in testis radiation protection, and specially, G-CSF and MIP-2 in exosomes are the core molecules in this protection effect.