视黄酸和亚硒酸钠对肝癌细胞某些表型逆转的加和作用

 人肝癌细胞株SMMC-7721经1μmol/L视黄酸和或2.5μmol/L亚硒酸钠处理后,膜上纤维连接蛋白沉着量逐日上升,且较相应天数的对照组细胞增加,而甲胎蛋白分泌量和~3H-TdR参入率被明显抑制。视黄酸和亚硒酸钠同时处理的联合组作用强度接近于两者单独使用时作用强度的加和。对以上结果和视黄酸及亚硒酸钠使肝癌细胞接触抑制恢复及表型逆转的关系作了讨论。     

Effect of 6-thioguanine on Chlamydia trachomatis growth in wild-type and hypoxanthine-guanine phosphoribosyltransferase-deficient cells.

Chlamydiae have evolved a biphasic life cycle to facilitate their survival in two discontinuous habitats. The unique growth cycle is represented by two alternating forms of the organism, the elementary body and the reticulate body. Chlamydiae have an absolute nutritional dependency on the host cell to provide ribonucleoside triphosphates and other essential intermediates of metabolism. This report describes the pleiotropic effects of the purine antimetabolite 6-thioguanine on chlamydial replication. In order to display cytotoxicity, 6-thioguanine must first be converted to the nucleotide level by the host cell enzyme hypoxanthine-guanine phosphoribosyltransferase. Our results show that 6-thioguanine is an effective inhibitor of chlamydial growth with either wild-type or hypoxanthine-guanine phosphoribosyltransferase-deficient cell lines as the host. Interestingly, the mechanism of 6-thioguanine-induced inhibition of chlamydial growth is different depending on which cell line is used. With wild-type cells as the host, the cytotoxic effects of 6-thioguanine on chlamydial growth are relatively fast and irreversible. Under these circumstances, cytotoxicity likely results from the combined effect of starving chlamydiae for purine ribonucleotides and incorporation of host-derived 6-thioguanine-containing nucleotides into chlamydial nucleic acids. With hypoxanthine-guanine phosphoribosyltransferase-deficient cells as the host, 6-thioguanine must be present at the start of the chlamydial infection cycle to be effective and the growth inhibition is reversible upon removal of the antimetabolite. These findings suggest that in hypoxanthine-guanine phosphoribosyltransferase-deficient cells, the free base 6-thioguanine may inhibit the differentiation of elementary bodies to reticulate bodies. With hypoxanthine-guanine phosphoribosyltransferase-deficient cells as the host, 6-thioguanine was used as a selective agent in culture to isolate a Chlamydia trachomatis isolate resistant to the effects of the drug. This drug resistant C. trachomatis isolate was completely resistant to 6-thioguanine in hypoxanthine-guanine phosphoribosyltransferase-deficient cells; however, it displayed wildtype sensitivity to 6-thioguanine when cultured in wild-type host cells.     

LncRNA LEF1-AS1 regulates the migration and proliferation of vascular smooth muscle cells by targeting miR-544a/PTEN axis

Long noncoding RNAs (lncRNAs) play important roles in endothelium development. A lncRNA, LEF1-AS1, is recently emerging as a potent mediator of the proliferation and migration of a number of cells, including smooth muscle cells. However, the effects of LEF1-AS1 in atherosclerosis remains largely unknown. Specimens from patients with coronary artery atherosclerosis were collected. The quantitative real-time polymerase chain reaction was used to analyze levels of LEF1-AS1 and microRNA-544a (miR-544a). Western blot analysis was used to assess PTEN, P-Akt, and T-Akt protein expression. Proliferation, migration, and invasion of cells were analyzed by cell counting kit-8 assay, scratch wound assay, and transwell assay, respectively. The interaction between LEF1-AS1, miR-544a, and PTEN was probed using bioinformatical analysis and dual-luciferase assay. In plasma and tissue of patients with coronary artery atherosclerosis, LEF1-AS1 was upregulated and miR-544a was downregulated. A negative correlation was found between LEF1-AS1 and miR-544a. miR-544a overexpression reversed the inhibition of LEF1-AS1 in smooth muscle cell proliferation and invasion, which were mediated through the PTEN pathway. LEF1-AS1 regulates smooth muscle cell proliferation and migration through the miR-544a/PTEN axis, indicating that LEF1-AS1 may be a potential therapeutic target in atherosclerosis.     

Using LiDAR Data to Measure the 3D Green Biomass of Beijing Urban Forest in China

The purpose of the paper is to find a new approach to measure 3D green biomass of urban forest and to testify its precision. In this study, the 3D green biomass could be acquired on basis of a remote sensing inversion model in which each standing wood was first scanned by Terrestrial Laser Scanner to catch its point cloud data, then the point cloud picture was opened in a digital mapping data acquisition system to get the elevation in an independent coordinate, and at last the individual volume captured was associated with the remote sensing image in SPOT5(System Probatoired''Observation dela Tarre)by means of such tools as SPSS (Statistical Product and Service Solutions), GIS (Geographic Information System), RS (Remote Sensing) and spatial analysis software (FARO SCENE and Geomagic studio11). The results showed that the 3D green biomass of Beijing urban forest was 399.1295 million m³, of which coniferous was 28.7871 million m³ and broad-leaf was 370.3424 million m³. The accuracy of 3D green biomass was over 85%, comparison with the values from 235 field sample data in a typical sampling way. This suggested that the precision done by the 3D forest green biomass based on the image in SPOT5 could meet requirements. This represents an improvement over the conventional method because it not only provides a basis to evalue indices of Beijing urban greenings, but also introduces a new technique to assess 3D green biomass in other cities.     

中国小菇属十个新记录种

报道了小菇科小菇属真菌10个中国新记录种,香菌组：橙盖小菇Mycena aurantiidisca、黄白小菇Mycena flavoalba、粉黄小菇Mycena floridula;棘刺组：异刺小菇Mycena heteracantha;纤柄组：碱味小菇Mycena amygdalina;脆足组：粉被小菇Mycena zephirus;冬生组：绣线菊小菇Mycena speirea、冬生小菇Mycena hiemalis;小菇组：绒柄小菇Mycena flos-nivium,分别来自吉林等11个省份、自治区。提供了每个物种的形态描述和线条图,以及与相近种的讨论。共计90条自测及下载ITS序列,在采用贝叶斯法和最大似然法构建的小菇属系统发育树中,新记录种均得到分子数据支持。凭证标本存放于吉林农业大学菌物标本馆（HMJAU）。     

Intersected functional zone of transcriptional regulators patterns stemness within stem cell niche of root apical meristem

Root stem cell niche (SCN) consists of a quiescent center (QC) and surrounding stem cells. Disrupted symplastic communication leads to loss of stemness in the whole SCN. Several SCN regulators were reported to move between cells for SCN maintenance. However, single mutant of these regulators is insufficient to abolish QC stemness despite the high differentiation rate in surrounding stem cells. To dissect the mechanism behind such distinct stemness in SCN, we combined the mis‐expression strategy with pWOX5:icals3m system in which QC is symplastically isolated. We found the starch accumulation in QC could be synergistically repressed by WUSCHEL‐RELATED HOMEOBOX 5 (WOX5), SHORT‐ROOT (SHR), SCARCROW (SCR), and PLETHORA (PLT). Like PLTs, other core regulators also exhibited dimorphic functions by inhibiting differentiation at a higher dose while promoting cell division at a low protein level. Being located in the center of the intersected expression zones, QC cells receive the highest level of core regulators, forming the most robust stemness within SCN. WUSCHEL‐RELATED HOMEOBOX 5 was sufficient to activate PLT1/2 expression, contributing to the QC‐enriched PLTs. Our results provide experimental evidence supporting the long‐standing hypothesis that the combination of spatial expression, synergistic function and dosage effect of core regulators result in spatially distinct stemness in SCN.