Overexpression of miR-26b-5p regulates the cell cycle by targeting CCND2 in GC-2 cells under exposure to extremely low frequency electromagnetic fields

The increasing prevalence of extremely low frequency electromagnetic fields (ELF-EMFs) exposure has raised considerable public concern regarding the potential hazardous effects of ELF-EMFs on male reproductive function. Increasing evidence indicates that miRNAs are necessary for spermatogenesis and male fertility. However, the regulation of miRNA expression and the roles of miRNAs in response to ELF-EMFs remain unclear. In our study, mouse spermatocyte-derived GC-2 cells were intermittently exposed to a 50 Hz ELF-EMF for 72 h (5 min on/10 min off) at magnetic field intensities of 1 mT, 2 mT and 3 mT. MiR-26b-5p was differentially expressed in response to different magnetic field intensities of ELF-EMFs. The host gene CTDSP1 showed an unmethylation status in GC-2 cells at different magnetic field intensities of ELF-EMF exposure. MiR-26b-5p had no significant, obvious influence on the cell viability, apoptosis or cell cycle of GC-2 cells. However, the overexpression of miR-26b-5p significantly decreased the percentage of G0/G1 phase cells and slightly increased the percentage of S phase cells compared to the sham group that was exposed to a 50 Hz ELF-EMF. Computational algorithms identified Cyclin D2 (CCND2) as a direct target of miR-26b-5p. MiR-26b-5p and a 50 Hz ELF-EMF altered the expression of CCND2 at both the mRNA and protein levels. Overexpressed miR-26b-5p in GC-2 cells can change the mRNA expression of CCND2 following 50 Hz ELF-EMF at 3 mT. These findings demonstrate that miR-26b-5p could serve as a potential biomarker following 50 Hz ELF-EMF exposure, and miR-26b-5p-CCND2-mediated cell cycle regulation might play a pivotal role in the biological effects of ELF-EMFs.     

Synthesis and amine transporter affinities of novel phenyltropane derivatives as potential positron emission tomography (PET) imaging agents

A series of novel fluoroalkyl-containing tropane derivatives (6-8, 10-14, 17, and 18) were synthesized from cocaine. Novel compounds were evaluated for affinity and selectivity in competitive radioligand binding assays selective for cerebral serotonin (5-HT), dopamine (DA), and norepinephrine (NE) transporters (SERT, DAT, and NET). The nortropane-fluoroalkyl esters (7, 10, 11) were most potent for SERT (K(i): 0.18, 0.24, and 0.30 nM, respectively). Tosylate esters 17 and 18, synthesized as precursors for [(18)F]-labeled, Positron Emission Tomography (PET) imaging agents, also showed high affinity for DAT.     

贵州猴耳天坑地下森林苔藓植物多样性特征研究

为了探索苔藓在地下森林中的多样性特征,采用梯度划分法,对贵州猴耳天坑（深度280 m,坑口直径300 m）地下森林进行实地调查研究。结果表明：（1）猴耳天坑地下森林共有苔藓植物71种,包含5种不同生长基质苔藓,其中树附生苔藓物种最为丰富有41种,其余基质苔藓物种数量依次为：土附生>石面生>腐木生>叶附生。（2）地下森林苔藓生活型共计10种,喜阴暗潮湿环境的生活型种类达88%,而适应于强光干旱环境的生活型种类仅12%。（3）对地下森林不同梯度苔藓植物物种丰富度指数分析表明,坡中最高（8.461 7）,依次是坡底（7.502 0）和坡顶（6.978 5）,而苔藓植物Pielou均匀度指数的大小依次为：坡顶（0.945 4）>坡底（0.907 2）>坡中（0.844 5）。（4）β多样性指数分析表明,地下森林不同梯度群落间的相异性都介于（0.75~1.00）之间,底部与顶部的相异系数高达0.960 8。（5）地下森林因其独特的地形地貌和水热条件,不仅各个梯度群落间异质性较高,而且各个群落间相异性也都较高,结构分异明显,生境复杂。（6）RDA分析表明,光照、湿度和温度是影响天坑地下森林苔藓物种分布的主要因子,其中光照度影响最大。（7）坑内与坑外物种多样性的对比研究表明,天坑地下森林苔藓植物物种多样性高,是喀斯特石漠化地区物种的天然避难所。     

中国自然保护地体系分类研究

建设自然保护地体系是为子孙后代保留生物多样性资源与自然遗产最有效的途径。自1956年我国建立第一个自然保护区以来,已建设形成覆盖森林、草地、湿地、海洋、荒漠各类生态系统,珍稀濒危动植物物种和种质资源,自然遗迹和自然景观,以及水源保护等各类自然保护地。但由于缺乏自然保护地体系的顶层设计,各类保护地面临功能区分不清晰、空间重叠、管理成效不高等问题。建设以国家公园为主体的自然保护地体系的部署,为理顺我国保护地体系,明确各类保护地的功能定位提供了难得的机会。在分析我国现有自然保护地类型,并参考国际自然保护地体系分类经验的基础上,探讨了我国保护地体系分类,建议将我国自然保护地分为5大类,第I类为自然保护区,第Ⅱ类为国家公园,第Ⅲ类为自然公园,第Ⅳ类为物种与种质资源保护区,第Ⅴ类为生态功能保护区,并分析了各类自然保护地的功能定位和管理目标,以期为自然保护地体系规划建设提供参考。完善我国自然保护地体系分类,根据各类保护地的特点,创新保护地建设政策与机制,加大政府对自然保护地建设力度的同时,发挥全社会力量建设自然保护地,我国自然保护地建设将大有可为。     

Preferential carcinogen-DNA adduct formation at codons 12 and 14 in the human K-ras gene and their possible mechanisms

In the ras gene superfamily, codon 12 (-TGGTG-) of the K-ras gene is the most frequently mutated codon in human cancers. Recently, we have found that bulky chemical carcinogens preferentially form DNA adducts at codons 12 and 14 (-CGTAG-) in the K-ras gene in normal human bronchial epithelial (NHBE) cells. Furthermore, DNA adducts formed at codon 12 of the K-ras gene are poorly repaired compared with those at other codons including codon 14. These results suggest that targeted carcinogen-DNA adduct formation is a major reason for the observed high mutation frequency at codon 12 of the K-ras gene in human cancers. This preferential carcinogen-DNA adduct formation at codons 12 and 14 could result from effects of (1) primary sequences of these codons and their surrounding codons in the K-ras gene, (2) the chromatin structure, and/or (3) epigenetic factors such as C5 cytosine methylation or other DNA modifications at these codons and their surrounding codons. To distinguish these possibilities, we have introduced modifications with benzo[a]pyrene diol epoxide, N-hydroxy-2-aminofluorene, and aflatoxin B1 8,9-epoxide in (1) naked intact genomic DNA isolated from NHBE cells, (2) fragmented genomic DNA digested by restriction enzymes, and (3) in vitro synthesized DNA fragments containing the K-ras gene exon 1 sequence with or without methylation of the cytosines at CpG sites and the cytosines pairing with the guanines of codons 12 and 14. The distribution of carcinogen-DNA adducts in the K-ras gene was mapped at the nucleotide sequence level using the UvrABC nuclease incision method with or without the ligation-mediated polymerase chain reaction technique. We have found that carcinogens preferentially form adducts at codons 12 and 14 in the K-ras gene exon 1 in intact as well as in fragmented genomic DNA. In contrast, this preferential DNA adduct formation at codons 12 and 14 was not observed in PCR-amplified DNA fragments containing the K-ras gene exon 1 sequence. Methylation of the cytosine at the CpG site of codon 14, or the cytosine pairing with guanine of codon 14, greatly enhanced carcinogen-DNA adduct formation at codon 14 but did not affect carcinogen-DNA adduct formation at codon 12. Methylation of the cytosine pairing with the guanine of codon 12 also did not enhance carcinogen-DNA adduct formation at codon 12. Furthermore, we found that the cytosine at the CpG site of codon 14 is highly methylated in NHBE cells. These results suggest that cytosine methylation at the CpG site is the major reason for the preferential DNA damage at codon 14 and that epigenetic modification(s) other than cytosine methylation may contribute to the preferential DNA damage at codon 12 of the K-ras gene.     

甲藻孢囊在长江口海域表层沉积物中的分布

为了了解长江口海域赤潮爆发潜势,于2002年4月至5月用采泥器采集了位于122°～123．5°E、29°～32°N之间12个站位的表层沉积物,分析沉积物中甲藻孢囊的分布．共分析鉴定出孢囊类型29种,其中自养型11种,异养型18种．每个站位的孢囊种类在10～21之间,孢囊密度为11．7～587孢囊·g-1干泥之间．远岸海域孢囊种类较为丰富,密度也较高．在调查区域内,孢囊密度及种类自西向东、自北向南逐渐增加．亚历山大藻孢囊分布广泛,最高密度为40．4孢囊·g-1干泥,其他赤潮种类的孢囊如链状裸甲藻、多边舌甲藻、锥状斯氏藻、科夫多沟藻和无纹多沟藻等都在长江口海域有分布．     

How myosin VI coordinates its heads during processive movement

A processive molecular motor must coordinate the enzymatic state of its two catalytic domains in order to prevent premature detachment from its track. For myosin V, internal strain produced when both heads of are attached to an actin track prevents completion of the lever arm swing of the lead head and blocks ADP release. However, this mechanism cannot work for myosin VI, since its lever arm positions are reversed. Here, we demonstrate that myosin VI gating is achieved instead by blocking ATP binding to the lead head once it has released its ADP. The structural basis for this unique gating mechanism involves an insert near the nucleotide binding pocket that is found only in class VI myosin. Reverse strain greatly favors binding of ADP to the lead head, which makes it possible for myosin VI to function as a processive transporter as well as an actin-based anchor. While this mechanism is unlike that of any other myosin superfamily member, it bears remarkable similarities to that of another processive motor from a different superfamily--kinesin I.     

Role of dephosphorylation of FOXO1 on apoptosis induced by wortmannin for non-Hodgkin’s lymphoma cells

The aim of this study was to ascertain the relationship between the phosphorylation of FOXO1 and the apoptosis and the proliferation of lymphoma cells so as to further clarify the cellular biology and pathogenesis of the disease. The lymphoma cells Namalwa and Jurkat were treated with PI3K inhibitor wortmannin or etoposide alone or wortmannin plus etoposide with different schedule. The inhibition rates of lymphoma cell growth were examined by XTT assay. Apoptosis were detected by flow cytometry. The expression of p-Akt, p-FOXO1, FOXO1, bim were determined by western blot analysis. Wortmannin induced apoptosis of Jurkat cells and Namalwa cells and inhibited their survival effectively. The rate of growth inhibition and apoptosis of lymphoma cells induced by wortmannin plus etoposide were higher than those induced by etoposide alone. After treated with wortmannin, phosphorylation of FOXO1 remarkably reduced and bim increased. The dephosphorylation of FOXO1 inhibited proliferation of Jurkat cells and Namalwa cells, promoted their apoptosis and sensitized Non-Hodgkin lymphoma cells to etoposide. Bim activated by FOXO1 promoted cells apoptosis.     

解淀粉芽孢杆菌诱变育种及其突变株在降低酱油中氨基甲酸乙酯的应用

【目的】通过诱变育种提高解淀粉芽孢杆菌JY06利用精氨酸的能力,并将其用于降低酱油中的氨基甲酸乙酯及前体,从而提高酿造酱油的安全性。【方法】采用等离子诱变和紫外诱变两种诱变育种方法对解淀粉芽孢杆菌JY06进行突变,应用高通量筛选手段获得具有高精氨酸利用能力的突变株,验证突变株降低酱油中氨基甲酸乙酯的能力。【结果】获得了12株精氨酸利用能力提高的突变株,与出发菌株JY06相比,突变株C12和E6可使酱油中瓜氨酸含量分别降低了15.6%和14.7%,EC的含量分别降低了19.3%和13.1%。【结论】通过等离子诱变和紫外诱变进一步提高了解淀粉芽孢杆菌JY06降低酱油中EC及其前体瓜氨酸的能力,具有控制或减少酱油中生物危害物的应用潜力。