Downregulation of lysyl oxidase-like 4 LOXL4 by miR-135a-5p promotes lung cancer progression in vitro and in vivo

Aberrant microRNAs are widely identified in multiple cancers, including lung cancer. miR-135a-5p can function as a significant tumor regulator in diverse cancers via impacting multiple genes in oncogenic pathways. Nevertheless, the biological role of miR-135a-5p in lung cancer is poorly known. Here, we investigated its function in lung cancer. As exhibited, miR-135a-5p was elevated in lung cancer cells in contrast to BEAS-2B cells. Then, we inhibited miR-135a-5p expression by transfecting LV-anti-miR-135a-5p into lung cancer cells. As displayed, miR-135a-5p was obviously reduced in A549 and H1299 cells. Knockdown of miR-135a-5p repressed lung cancer cell growth and cell proliferation. Meanwhile, cell colony formation capacity was depressed, cell apoptosis was enhanced and cell cycle progression was blocked in G1 phase by inhibition of miR-135a-5p in vitro. Additionally, the migration and invasion of A549 and H1299 cells was strongly depressed by LV-anti-miR-135a-5p. For another, by using informatics analysis, lysyl oxidase-like 4 (LOXL4) was speculated as the downstream target of miR-135a-5p. We validated their direct correlation and moreover, overexpression of miR-135a-5p restrained LOXL4 levels in lung cancer cells. Subsequently, we proved that miR-135a-5p promoted lung cancer development via targeting LOXL4 by carrying out the in vivo assays. Taken these together, our study revealed miR-135a-5p might be indicated as a perspective for lung cancer via targeting LOXL4.     

Cell origins and diagnostic accuracy of interleukin 27 in pleural effusions

The objective of the present study was to investigate the presence of interleukin (IL)-27 in pleural effusions and to evaluate the diagnostic significance of pleural IL-27. The concentrations of IL-27 were determined in pleural fluids and sera from 68 patients with tuberculous pleural effusion, 63 malignant pleural effusion, 22 infectious pleural effusion, and 21 transudative pleural effusion. Flow cytometry was used to identify which pleural cell types expressed IL-27. It was found that the concentrations of pleural IL-27 in tuberculous group were significantly higher than those in malignant, infectious, and transudative groups, respectively. Pleural CD4(+) T cells, CD8(+) T cells, NK cells, NKT cells, B cells, monocytes, macrophages, and mesothelial cells might be the cell sources for IL-27. IL-27 levels could be used for diagnostic purpose for tuberculous pleural effusion, with the cut off value of 1,007 ng/L, IL-27 had a sensitivity of 92.7% and specificity of 99.1% for differential diagnosing tuberculous pleural effusion from non-tuberculous pleural effusions. Therefore, compared to non-tuberculous pleural effusions, IL-27 appeared to be increased in tuberculous pleural effusion. IL-27 in pleural fluid is a sensitive and specific biomarker for the differential diagnosing tuberculous pleural effusion from pleural effusions with the other causes.     

皖南汉族的趾纹研究

本文对皖南地区520例汉族大学生的趾纹进行了调查分析,计算出了各型趾纹频率、趾纹组合、趾嵴纹计数等项参数。比较了不同性别、不同侧别和不同人种间的差异,分析了趾纹类型和趾嵴纹计数在各趾的分布特点,并对差异的原因进行了讨论。Abstract: The authors inverstigated and analysed the toe prints of 520 cases of good healthy students in Wannan area of Aahui, and calculated the frequency of various toe patterns, combinations of toe patterns, toe ridge counts (TRC) and so on. The differences between sexes, sides and reces were compared. The distributive character of toe patterns and toe ridge count on every toe were analysed. The different cause were discussed.     

Bcl-2和Bax在吗啡依赖雄性大鼠生殖细胞中的表达

目的：探讨B细胞淋巴瘤/白血病-2和人Bcl-2相关x蛋白（Bcl-2、Bax）在吗啡依赖大鼠睾丸生殖细胞中的表达及细胞凋亡可能机制,为治疗阿片类毒品造成的男性性功能减退提供理论依据。方法：以递增法每日给予雄性大鼠皮下注射盐酸吗啡针剂,建立吗啡依赖组。空白对照组注射等量生理盐水。实验成功后将两组大鼠睾丸组织作常规HE染色和免疫组化染色。结果：吗啡依赖组大鼠生精管壁细胞明显地出现上皮层次减少,仅有2~3层,细胞排列疏松,界限模糊,精子细胞和精子数目减少,并发现曲细精管腔内有脱落的生精细胞;免疫组化结果：吗啡依赖组大鼠生殖细胞中bcl-2的阳性表达率明显低于对照组（P〈0.01）,而生殖细胞中bax蛋白的阳性表达率明显高于对照组（P〈0.01）。结论：吗啡依赖可造成雄性大鼠生殖细胞凋亡数量显著增加,其机制可能是通过下调抑凋亡因子Bcl-2,上调促凋亡因子Bax,促进生殖细胞凋亡来实现的。     

葡萄酒酿酒酵母嗜果糖特性的评价方法

[目的]酿酒酵母的嗜果糖性是葡萄酒酵母选育工作的一项重要内容.建立评价菌体发酵果糖能力的方法,是葡萄酒酿酒酵母嗜果糖性研究的基础.[方法]以3株不同果糖发酵能力的酵母菌为研究对象,考察菌体在模拟葡萄汁培养基条件下,发酵情况与单糖利用之间的关系;并通过数学方程拟合单糖动力发酵曲线,得到发酵持续时间、葡萄糖浓度拟为0时的果糖浓度、果糖与葡萄糖曲线面积的差值等参数.[结果]这些参数可以反应出菌体的发酵速率和嗜果糖性.其中后两个参数能显著将3个菌株的嗜果糖特性区分开.[结论]为高果糖利周优良葡萄酒酿酒酵母菌株的筛选和构建,提供了较为全面、客观和有效的评价方法.     

Green synthesis of silver nanoparticles using Rhodobacter Sphaeroides

The use of microorganisms in the synthesis of nanoparticles emerges as an eco-friendly and exciting approach. In this study, silver nanoparticles were successfully synthesized from AgNO₃ by reduction of aqueous Ag⁺ ions with the cell filtrate of Rhodobacter sphaeroides. Nanoparticles were characterized by means of UV–vis absorption spectroscopy, X-Ray Diffraction (XRD), transmission electron microscopy (TEM) and high-resolution transmission electron microscopy (HRTEM). Crystalline nature of the nanoparticles in the fcc structure are confirmed by the peaks in the XRD pattern corresponding to (111), (200), (220) and (311) planes, bright circular spots in the selected are a electron diffraction (SAED) and clear lattice fringes in the high-resolution TEM image. Also, the size of silver nanoparticles was controlled by the specific activity of nitrate reductase in the cell filtrate.     

影响武夷山景区松墨天牛种群动态变化的因素分析

为了监测武夷山景区松墨天牛Monochamus alternatus Hope的发生,防范松材松材线虫Bursaphelonchus xylophilus病的入侵,于2005-2007年每年4-9月,在武夷山景区10个地点进行了调查,研究了气象因素和环境因素对松墨天牛数量变化的综合影响规律及其程度,对调查结果进行了矢量递进因子分析。结果表明：环境因子和气象因子是松墨天牛羽化孔数和诱集成虫数变化的主要因素,影响松墨天牛成虫诱集数的环境因子按重要性排列依次为：郁闭度、地被物覆盖率、海拔、林龄、坡位、坡向和树高;影响羽化孔数的环境因子按重要性排列依次为：郁闭度、地被物覆盖率、树高、林龄、海拔、坡位和坡向。影响松墨天牛诱集成虫数和羽化孔数的气象因子按重要性排列依次为：月平均温度、最高与最低温差、总降雨量（mm）、气压（hpa）和平均湿度（%）。单从环境因子和气象因子的统计数据分析,环境因子的重要性次序是：坡位、郁闭度、地被物覆盖率、海拔（m）、 林龄（a）、树高（m）、坡向;气象因子的重要性次序是：气压（hpa）、 平均温度 （℃）、最高与最低温差（℃）、 总降雨量（mm）、平均湿度（%）。按月分析和按年度分析时其相对重要性基本上是一致的。结论认为,环境因子和气象因子对松墨天牛的数量变化有重要影响。     

Activation of Class I histone deacetylases contributes to mitochondrial dysfunction in cardiomyocytes with altered complex activities

Histone deacetylases (HDACs) play vital roles in the pathophysiology of heart failure, which is associated with mitochondrial dysfunction. Tumor necrosis factor-α (TNF-α) contributes to the genesis of heart failure and impairs mitochondria. This study evaluated the role of HDACs in TNF-α-induced mitochondrial dysfunction and investigated their therapeutic potential and underlying mechanisms. We measured mitochondrial oxygen consumption rate (OCR) and ATP production using Seahorse XF24 extracellular flux analyzer and bioluminescent assay in control and TNF-α (10 ng/ml, 24 h)-treated HL-1 cells with or without HDAC inhibition. TNF-α increased Class I and II (but not Class IIa) HDAC activities (assessed by Luminescent) with enhanced expressions of Class I (HDAC1, HDAC2, HDAC3, and HDAC8) but not Class IIb HDAC (HDAC6 and HDAC10) proteins in HL-1 cells. TNF-α induced mitochondrial dysfunction with impaired basal, ATP-linked, and maximal respiration, decreased cellular ATP synthesis, and increased mitochondrial superoxide production (measured by MitoSOX red fluorescence), which were rescued by inhibiting HDACs with MPT0E014 (1 μM, a Class I and IIb inhibitor), or MS-275 (1 μM, a Class I inhibitor). MPT0E014 reduced TNF-α-decreased complex I and II enzyme (but not III or IV) activities (by enzyme activity microplate assays). Our results suggest that Class I HDAC actions contribute to TNF-α-induced mitochondrial dysfunction in cardiomyocytes with altered complex I and II enzyme regulation. HDAC inhibition improves dysfunctional mitochondrial bioenergetics with attenuation of TNF-α-induced oxidative stress, suggesting the therapeutic potential of HDAC inhibition in cardiac dysfunction.     

长白山林区核桃楸种群数量动态变化的研究

运用种群年龄结构、存活曲线统计和Leslie模型对长白山核桃楸种群在水胡林、针阔混交林、核桃楸占优杂木林和杂木林4种不同群落类型中种群数量动态变化进行了研究和预测。结果表明,核桃楸种群表现出衰退型的年龄结构特点,幼苗和幼树比例较小,种群在幼年期死亡率较高,反映出核桃楸种群15~20龄在个体经历了比较强烈的环境筛作用;Leslie模型预测显示,核桃楸幼苗数量和种群总数量在今后35年基本呈下降趋势,除在核桃楸占优的林分中种群维持增长外,在其它3中森林类型都表现出衰退趋势。因此,促进核桃楸的天然更新、加强幼苗幼树的抚育工作对长白山地区核桃楸种群的发展至关重要。     

Lethal (2) giant larvae regulates pleural mesothelial cell polarity in pleural fibrosis

Pleural fibrosis is barely reversible and the underlying mechanisms are poorly understood. Pleural mesothelial cells (PMCs) which have apical-basal polarity play a key role in pleural fibrosis. Loss of cell polarity is involved in the development of fibrotic diseases. Partition defective protein (PAR) complex is a key regulator of cell polarity. However, changes of PMC polarity and PAR complex in pleural fibrosis are still unknown. In this study, we observed that PMC polarity was lost in fibrotic pleura. Next we found increased Lethal (2) giant larvae (Lgl) bound with aPKC and PAR-6B competing against PAR-3A in PAR complex, which led to cell polarity loss. Then we demonstrated that Lgl1 siRNA prevented cell polarity loss in PMCs, and Lgl1 conditional knockout (ER-Cre^+/?Lgl1^flox/flox) attenuated pleural fibrosis in a mouse model. Our data indicated that Lgl1 regulates cell polarity of PMCs, inhibition of Lgl1 and maintenance of cell polarity in PMCs could be a potential therapeutic treatment approach for pleural fibrosis.