Molecular Characterization of Segments S7 to S10 of a Southern Rice Black-streaked Dwarf Virus Isolate from Maize in Northern China

Southern rice black-streaked dwarf virus (SRBSDV) is a novel Fijivirus prevalent in rice in southern and central China,and northern Vietnam. Its genome has 10 segments of double-stranded RNA named S1 to S10 according to their size. An isolate of SRBSDV,JNi4,was obtained from naturally infected maize plants from Ji'ning,Shandong province,in the 2008 maize season. Segments S7 to S10 of JNi4 share nucleotide identities of 72.6%-73.1%,72.3%-73%,73.9%-74.5% and 77.3%-79%,respectively,with corresponding segments of Rice black-streaked dwarf virus isolates,and identities of 99.7%,99.1%-99.7%,98.9%-99.5%,and 98.6%-99.2% with those of SRBSDV isolates HN and GD. JNi4 forms a separate branch with GD and HN in the phylogenetic trees constructed with genomic sequences of S7 to S10. These results confirm the proposed taxonomic status of SRBSDV as a distinct species of the genus Fijivirus and indicate that JNi4 is an isolate of SRBSDV. Shandong is so far the northernmost region where SRBSDV is found in China.

Panax quinquefolium saponin attenuates cardiomyocyte apoptosis induced by thapsigargin through inhibition of endoplasmic reticulum stress

BackgroundEndoplasmic 蜂窝胃(嗯) 压力相关的 apoptosis 涉及许多心血管的疾病的 pathophysiology，并且人参属 quinquefolium saponin (PQS ) 能禁止过多嗯 cardiomyocytes 追随者 hypoxia/reoxygenation 和心肌的梗塞的压力相关的 apoptosis。然而， PQS 由禁止压力相关的 apoptosis 不是的 ER 很好的小径理解。进一步调查 PQS 的保护的效果对嗯压力相关的 apoptosis ，主要有教养的 cardiomyocytes 与 thapsigargin ( TG )被刺激，它广泛地被用来当模特儿细胞嗯应力，并且它能在足够的 concentration.MethodsPrimary 导致 apoptotic 房间死亡从新生的老鼠的有教养的 cardiomyocytes 暴露于 TG ( 1 &#x000b5 ； mol/L )为 24 h 的处理，后面的 PQS 预告的处理( 160 &#x000b5 ； g/mL )为有小介入的 24 h 或预告的处理， RNA 指导了 agai 生存能力和 cardiomyocytes 的 apoptosis 率被分别地数 kit-8 和流动 cytometry 的房间检测。嗯压力相关的蛋白质表示，例如调整葡萄糖的蛋白质 78 (GRP78 ) ， calreticulin，津贴，真核细胞的翻译开始因素 2 &#x003b1；( eIF2&#x003b1 ；)，激活抄写因素 4 ( ATF4 )，并且 C/EBP 相应蛋白质(砍)是由西方的 blotting.ResultsBoth PQS 预告的处理和津贴的 assayed 击倒显著地禁止了 TG 导致的 cardiomyocyte apoptosis ，增加的房间生存能力，津贴和 eIF2&#x003b1 的减少的 phosphorylation ；，并且减少 ATF4 和砍的蛋白质层次。PQS 预告的处理和在 cardioprotective effect.ConclusionsOur 数据击倒的津贴之间没有统计上重要的差别显示 PERK-eIF2&#x003b1； -ATF4-CHOP 小径嗯应力涉及 TG 导致的 apoptosis，并且 PQS 可能通过包含这条小径的抑制的机制阻止导致 TG 的 cardiomyocyte apoptosis。这些调查结果关于 PQS 由禁止 cardiomyocyte apoptosis 的分子的机制提供新奇数据。

Calreticulin Translocation Aggravates Endoplasmic Reticulum Stress-associated Apoptosis during Cardiomyocyte Hypoxia/Reoxygenation

Background： Calreticulin （CRT） is major Ca^2＋-binding chaperone mainly resident in the endoplasmic reticulum （ER） lumen. Recently, it has been shown that non-ER CRT regulates a wide array of cellular responses. We previously found that CRT was up-regulated during hypoxia/ reoxygenation （H/R） and this study was aimed to investigate whether CRT nuclear translocation aggravates ER stress （ERS）-associated apoptosis during H/R injury in neonatal rat cardiomyocytes. Methods： Apoptosis rate and lactate dehydrogenase （LDH） leakage in culture medium were measured as indices of cell injury. lmmunofluorescence staining showed the morphological changes of ER and intracellular translocation of CRT. Western blotting or reverse transcription polymerase chain reaction was used to detect the expression of target molecules. Results： Compared with control, H/R increased apoptosis rate and LDH activity. The ER became condensed and bubbled, and CRT translocated to the nucleus. Western blotting showed up-regulation of CRT, Nrf2, activating transcription factor 4 （ATF4）, CHOP and caspase-12 expression after H/R. Exogenous CRT overexpression induced by plasmid transfection before H/R increased cell apoptosis, LDH leakage, ER disorder, CRT nuclear translocation and the expression of ERS-associated molecules. However, administration of the ERS inhibitor, taurine, or CRT siRNA alleviated cell injury, ER disorder, and inhibited ERS-associated apoptosis. Conclusions： Our results indicated that during H/R stress, CRT translocation increases cell apoptosis and LDH leakage, aggravates ER disorder, up-regulates expression of nuclear transcription factors, Nrf2 and ATF4, and activates ERS-associated apoptosis.

Brain-Derived Glia Maturation Factor b Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia(ACI), we established a middle cerebral artery occlusion(MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor b(GMFB) based on quantitative analysis of the global rat serum proteome.Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was overexpressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation(OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium(CM) after OGD.We then used the CM to culture pulmonary microvascular endothelial cells(PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover,ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells.In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.

Molecular dynamics study on surface formation and phase transformation in nanometric cutting of β-Sn

Atomic motion and surface formation in the nanometric cutting process ofβ-Sn are investigated using molecular dynamics(MD).A stagnation region is observed that changes the shape of the tool edge involved in nanometric cutting,resulting in a fluctuation in the cutting forces.It is found that single-crystal tin releases the high compressive stress generated under the tool pressure through slip and phase transformation.The tin transformation proceeds from aβ-Sn structure to a bct-Sn structure.The effects of the cutting speed,undeformed chip thickness(UCT)and tool edge radius on material removal are also explored.A better surface is obtained through material embrittlement caused by a higher speed.In addition,a smaller UCT and sharper tool edge help reduce subsurface damage.