生物复苏——大绝灭后生物演化历史的第一幕

生命史是一部生物界短期,快速剧变与长期,慢速稳定相互交替的历史。大绝灭（即集群绝灭）事件反映了全球环境的大突变,点断了地质历史中的生命记录及其发展历程,预示着生物界的演化出现了最有意义的飞跃,近年来尝试研究大绝灭后全球生物界的残存－复苏及其基本型式,并探索复苏的控制因素,标志着地质科学中一个重心的转移（即从大绝灭转向其后的生物残存与复苏的研究）。生物复苏揭示了大绝灭后生物演化历史的第一幕,其研究的     

病毒基因组启动子识别的人工神经网络方法

本文运用神经网络方法,并结合病毒基因分子生物学有关理论与统计事实,对病毒基因启动子区域进行了识别,文中选择了共35个基因组,作为研究对象．学习组选择了28个基因组,预测组选择了7个基因组,结果表明,将神经网络模型与病毒基因有关理论相结合,能够运用计算方法,以大量的可能启动子组合中排列出唯一的启动子区域．     

鼠肺支原体单克隆抗体的研究

通过杂交瘤技术建立了３株抗鼠肺支原体单克隆抗体细胞株,它们分别是ＢＡ１１,ＢＤ７和Ｂ６１２．试验表明：３株细胞所分泌的抗体均属ＩｇＧ１亚类,都是鼠肺支原体的特异性抗体,与多种其它支原体无交叉反应。     

ATPR triggers acute myeloid leukaemia cells differentiation and cycle arrest via the RARα/LDHB/ERK‐glycolysis signalling axis

Acute myeloid leukaemia (AML) remains a therapeutic challenge and improvements in chemotherapy are needed. 4‐Amino‐2‐trifluoromethyl‐phenyl retinate (ATPR), a novel all‐trans retinoic acid (ATRA) derivative designed and synthesized by our team, has been proven to show superior anticancer effect compared with ATRA on various cancers. However, its potential effect on AML remains largely unknown. Lactate dehydrogenase B (LDHB) is the key glycolytic enzyme that catalyses the interconversion between pyruvate and lactate. Currently, little is known about the role of LDHB in AML. In this study, we found that ATPR showed antileukaemic effects with RARα dependent in AML cells. LDHB was aberrantly overexpressed in human AML peripheral blood mononuclear cell (PBMC) and AML cell lines. A lentiviral vector expressing LDHB‐targeting shRNA was constructed to generate a stable AML cells with low expression of LDHB. The effect of LDHB knockdown on differentiation and cycle arrest of AML cells was assessed in vitro and vivo, including involvement of Raf/MEK/ERK signalling. Finally, these data suggested that ATPR showed antileukaemic effects by RARα/LDHB/ ERK‐glycolysis signalling axis. Further studies should focus on the underlying leukaemia‐promoting mechanisms and investigate LDHB as a therapeutic target.     

Mutation of the chloroplast‐localized phosphate transporter OsPHT2;1 reduces flavonoid accumulation and UV tolerance in rice

Phosphorus (P) is an essential macronutrient required for plant development and production. The mechanisms regulating phosphate (Pi) uptake are well established, but the function of chloroplast Pi homeostasis is poorly understood in Oryza sativa (rice). PHT2;1 is one of the transporters/translocators mediating Pi import into chloroplasts. In this study, to gain insight into the role of OsPHT2;1‐mediated stroma Pi, we analyzed OsPHT2;1 function in Pi utilization and photoprotection. Our results showed that OsPHT2;1 was induced by Pi starvation and light exposure. Cell‐based assays showed that OsPHT2;1 localized to the chloroplast envelope and functioned as a low‐affinity Pi transporter. The ospht2;1 had reduced Pi accumulation, plant growth and photosynthetic rates. Metabolite profiling revealed that 52.6% of the decreased metabolites in ospht2;1 plants were flavonoids, which was further confirmed by 40% lower content of total flavonoids compared with the wild type. As a consequence, ospht2;1 plants were more sensitive to UV‐B irradiation. Moreover, the content of phenylalanine, the precursor of flavonoids, was also reduced, and was largely associated with the repressed expression of ADT1/MTR1. Furthermore, the ospht2;1 plants showed decreased grain yields at relatively high levels of UV‐B irradiance. In summary, OsPHT2;1 functions as a chloroplast‐localized low‐affinity Pi transporter that mediates UV tolerance and rice yields at different latitudes.     

益生菌在结直肠癌患者中的应用

结直肠癌(colorectal cancer,CRC)的发病率及病死率在多国多年居高不下,肠道微生态的失衡在CRC的发生发展中所起的作用被许多学者所证实。专家一致认为,积极纠正肠道微生态失衡是可取的。CRC患者术前肠道菌群已经出现改变,术后肠道菌群失衡加重,化疗会进一步加重这种失衡状态。肠道微生态的稳态对机体肠道功能和免疫功能等起着重要作用。益生菌作为一种可调节肠道菌群的微生态制剂,已显现出在CRC患者治疗中的应用价值,现对益生菌在CRC患者中的应用进展作一综述。     

Periostin Mediates the Increased Pro‐Angiogenic Activity of Gastric Cancer Cells under Hypoxic Conditions

This study was conducted to investigate the biological role of periostin in gastric cancer (GC) under hypoxia. Western blot analysis revealed that along with an upregulation of hypoxia‐inducible factor‐1alpha, there was a time‐dependent induction of periostin in MKN‐45 cells under hypoxia (2% O₂), increasing by eightfold as compared to normoxic cells. Pretreatment with 30 µM PD98059, an inhibitor of ERK1/2, significantly reduced hypoxia‐stimulated periostin expression (P < 0.01). Periostin knockdown in MKN‐45 cells was achieved by specific small interfering RNA (siRNA). The conditioned medium from periostin siRNA‐transfected MKN‐45 cells induced significantly less (P < 0.01) endothelial tube formation than control siRNA‐transfected cells. Additionally, periostin silencing markedly decreased the mRNA expression and secretion of vascular endothelial growth factor (VEGF) in hypoxic MKN‐45 cells. Thus, our data suggest that periostin is a hypoxia‐response gene and mediates a cross talk between GC and endothelial cells under hypoxia, partially through regulation of the VEGF expression. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:364‐369, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21498     

Tumor Necrosis Factor -α, Interleukin-10, Intercellular and Vascular Adhesion Molecules Are Possible Biomarkers of Disease Severity in Complicated Plasmodium vivax Isolates from Pakistan

Background

Cytokine-mediated endothelial activation pathway is a known mechanism of pathogenesis employed by Plasmodium falciparum to induce severe disease symptoms in human host. Though considered benign, complicated cases of Plasmodium vivax are being reported worldwide and from Pakistan. It has been hypothesized that P.vivax utilizes similar mechanism of pathogenesis, as that of P.falciparum for manifestations of severe malaria. Therefore, the main objective of this study was to characterize the role of cytokines and endothelial activation markers in complicated Plasmodium vivax isolates from Pakistan.

Methods and Principle Findings

A case control study using plasma samples from well-characterized groups suffering from P.vivax infection including uncomplicated cases (n=100), complicated cases (n=82) and healthy controls (n=100) were investigated. Base line levels of Tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), Interleukin-10 (IL-10), Intercellular adhesion molecule-1 (ICAM-1), Vascular adhesion molecule-1(VCAM-1) and E-selectin were measured by ELISA. Correlation of cytokines and endothelial activation markers was done using Spearman’s correlation analysis. Furthermore, significance of these biomarkers as indicators of disease severity was also analyzed. The results showed that TNF-α, IL-10, ICAM-1and VCAM-1 were 3-fold, 3.7 fold and 2 fold increased between uncomplicated and complicated cases. Comparison of healthy controls with uncomplicated cases showed no significant difference in TNF-α concentrations while IL-6, IL-10, ICAM-1, VCAM-1 and E-selectin were found to be elevated respectively. In addition, significant positive correlation was observed between TNF-α and IL-10/ ICAM-1, IL-6 and IL-10, ICAM-1 and VCAM-1.A Receiver operating curve (ROC) was generated which showed that TNF-α, IL-10, ICAM-1 and VCAM-1 were the best individual predictors of complicated P.vivax malaria.

Conclusion

The results suggest that though endothelial adhesion molecules are inducible by pro-inflammatory cytokine TNF-α, however, cytokine-mediated endothelial activation pathway is not clearly demonstrated as a mechanism of pathogenesis in complicated P.vivax malaria cases from Pakistan.