黏附分子在肿瘤发生及发展中的作用

细胞黏附分子是以配体和受体相结合的形式,介导细胞与细胞间或细胞与基质间相互作用的一类分子,参与机体的多种重要生理和病理过程.近年来,在对肿瘤发生和发展的研究中发现,黏附分子可通过多种途径影响肿瘤的生长、浸润及转移过程.因此.对黏附分子在肿瘤发生和发展中作用及机制的深入研究,可为肿瘤早期诊断提供重要的分子指标和发现新的治疗靶标.并为进而形成临床诊疗新策略提供重要理论支持.现就几种重要黏附分子在肿瘤生长与转移中的作用进行综述.     

LncRNA TUG1 alleviates cardiac hypertrophy by targeting miR-34a/DKK1/Wnt-β-catenin signalling

The current study was designed to explore the role and underlying mechanism of lncRNA taurine up-regulated gene 1 (TUG1) in cardiac hypertrophy. Mice were treated by transverse aortic constriction (TAC) surgery to induce cardiac hypertrophy, and cardiomyocytes were treated by phenylephrine (PE) to induce hypertrophic phenotype. Haematoxylin-eosin (HE), wheat germ agglutinin (WGA) and immunofluorescence (IF) were used to examine morphological alterations. Real-time PCR, Western blots and IF staining were used to detect the expression of RNAs and proteins. Luciferase assay and RNA pull-down assay were used to verify the interaction. It is revealed that TUG1 was up-regulated in the hearts of mice treated by TAC surgery and in PE-induced cardiomyocytes. Functionally, overexpression of TUG1 alleviated cardiac hypertrophy both in vivo and in vitro. Mechanically, TUG1 sponged and sequestered miR-34a to increase the Dickkopf 1 (DKK1) level, which eventually inhibited the activation of Wnt/β-catenin signalling. In conclusion, the current study reported the protective role and regulatory mechanism of TUG1 in cardiac hypertrophy and suggested that TUG1 may serve as a novel molecular target for treating cardiac hypertrophy.     

The detrimental effect of iron on OA chondrocytes: Importance of pro-inflammatory cytokines induced iron influx and oxidative stress

Iron overload is common in elderly people which is implicated in the disease progression of osteoarthritis (OA), however, how iron homeostasis is regulated during the onset and progression of OA and how it contributes to the pathological transition of articular chondrocytes remain unknown. In the present study, we developed an in vitro approach to investigate the roles of iron homeostasis and iron overload mediated oxidative stress in chondrocytes under an inflammatory environment. We found that pro-inflammatory cytokines could disrupt chondrocytes iron homeostasis via upregulating iron influx transporter TfR1 and downregulating iron efflux transporter FPN, thus leading to chondrocytes iron overload. Iron overload would promote the expression of chondrocytes catabolic markers, MMP3 and MMP13 expression. In addition, we found that oxidative stress and mitochondrial dysfunction played important roles in iron overload-induced cartilage degeneration, reducing iron concentration using iron chelator or antioxidant drugs could inhibit iron overload-induced OA-related catabolic markers and mitochondrial dysfunction. Our results suggest that pro-inflammatory cytokines could disrupt chondrocytes iron homeostasis and promote iron influx, iron overload-induced oxidative stress and mitochondrial dysfunction play important roles in iron overload-induced cartilage degeneration.     

腐食酪螨在不同温度和营养条件下生长发育的比较研究

在12.5℃、15℃、20℃、25℃和30℃恒温下,用啤酒酵母粉和玉米粉为饲料,测定了不同温度和饲料条件下腐食酪螨Tyrophagus putrescentiae各个发育阶段和世代的发育历期,获得其在各条件下的发育起点温度和有效积温。结果表明,在本文的实验温度范围内,该螨的发育历期与温度呈负相关,即随着温度的升高发育历期缩短。在各发育阶段不同饲料条件下发育起点温度和有效积温都有所差异。用啤酒酵母粉作饲料时,腐食酪螨的全世代历期为48.04天（12.5℃下）和8.41天（30℃下）,发育起点温度为10.18℃,有效积温为155.44 d·℃; 用玉米粉作饲料时,全世代历期为78.79天（12.5℃下）和10.77天（30℃下）,发育起点温度为10.52℃,有效积温为208.33 d·℃。以成螨体长和体宽为指标,比较了在各温度条件及不同饲料条件对其生长的影响,结果表明不同饲料对螨体大小有显著影响,温度的影响不明显。     

蝉虫草样品的分级萃取与化学成分分析

利用索氏萃取技术,依次采用石油醚、乙酸乙酯、丙酮、无水乙醇和甲醇等5种溶剂对蝉虫草纯粉进行分级萃取,运用傅里叶变换红外光谱分析法和气相色谱-质谱联用技术对5级萃取物进行分析鉴定。傅里叶变换红外光谱分析显示萃取物中含有与烯烃类、羧酸类、酯类、醇类和酮类等化合物相关的C-H、C=O、C-O和C=C等官能团。气相色谱-质谱联用技术共鉴定出有机小分子化合物34种,以酯类和脂肪酸类为主,多为碳链长度为15-20的长链脂肪酸及对应的酯,其中十八碳不饱和脂肪酸相对含量高达28.95%;分别存在于两种或以上萃取物中的有机化合物共有11种;仅存于石油醚萃取物中的化合物6种,乙酸乙酯萃取物中3种,丙酮萃取物中2种,无水乙醇萃取物中6种,甲醇萃取物中6种。在一定极性范围内,利用溶剂的极性梯度变化,可实现蝉虫草中活性物质的按极性梯度分离;采用分级萃取技术可有效分离蝉虫草中部分化学成分。鉴定结果充实了蝉虫草中化合物的种类资源,为蝉虫草中活性物质谱图库的完善、构效关系的建立及蝉虫草产品的利用开发提供支撑。     

Clopidogrel reduces lipopolysaccharide‐induced inflammation and neutrophil‐platelet aggregates in an experimental endotoxemic model

Platelet activation contributes to organs failure in inflammation and plays an important role in endotoxemia. Clopidogrel inhibits platelet aggregation and activation. However, the role of clopidogrel in modulating inflammatory progression of endotoxemia remains largely unexplored. Therefore, we investigated the role of clopidogrel on the activation of platelet and leukocytes in lipopolysaccharide (LPS)‐induced inflammation in mice. Animals were treated with clopidogrel or vehicle before LPS induction. The expression of neutrophil‐platelet aggregates and platelet activation and tissue factor was determined. Immunofluorescence was used to analyze platelet‐leukocyte interactions and tissue factor (TF) expression on leukocytes. Clopidogrel pretreatment markedly decreased lung damage, inhibited platelet‐neutrophil aggregates and TF expression. In addition, clopidogrel reduced thrombocytopenia and affected the number of circulating white blood cell in endotoxemia mice. Moreover, clopidogrel also reduced platelet shedding of CD40L and CD62P in endotoxemic mice. Taken together, clopidogrel played an important role through reducing platelet activation and inflammatory process in endotoxemia.     

High-Efficiency Rescue of Equine Infectious Anemia Virus from a CMV-Driven Infectious Clone

<正>Dear Editor,Equine infectious anemia virus (EIAV) belongs to the macrophage-tropic lentiviruses family and infects mainly equines, including horses, donkeys and mules. EIAV shares many similar characteristics in its viral biology and hostvirus immune regulation with other lentiviruses, such as human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV), and has been accepted as a     

NaCl胁迫对甘薯叶片叶绿体超微结构及一些酶活性的影响

随ＮａＣｌ 胁迫浓度的提高,甘薯叶片叶绿体数目逐渐减少, 类囊体膜片层松散、扭曲、破裂并逐渐解体, 叶绿素含量下降。与此同时,Ｈ２Ｏ２ 、ＭＤＡ 含量增加, ＡＳＰ、ＳＯＤ 活性表现出先上升后下降的趋势。耐盐品种在ＮａＣｌ 胁迫下能维持较强的Ｈ２Ｏ２ 清除能力和较低的ＭＤＡ 水平