人中鼻甲来源嗅鞘细胞培养与鉴定的初步研究

目的探索一种从人中鼻甲分离培养嗅鞘细胞的方法并鉴定所获得的细胞。 方法通过手术获取人中鼻甲黏膜组织,随后进行两步消化并剥离黏膜上皮组织,得到体积较小的组织块,再进行组织块原代（传代）培养并加压筛选,最终得到双极或多极样细胞并对获得的细胞进行免疫荧光鉴定。上皮样细胞比例、S100β和p75阳性细胞比例用 ±s表示,组间比较采用独立样本t检验。 结果将不剥离上皮层与剥离上皮层培养的原代细胞中上皮样细胞的比例进行对比,发现上皮层组上皮样细胞比例为（92.23±3.93）%高于剥离上皮层组上皮样细胞的比例（77.63±2.97）%,差异具有统计学意义（t = 5.129,P = 0.007）。采用剥离上皮层法培养原代细胞,经过加压筛选的细胞呈现双极或多极样,符合嗅鞘细胞形态学特点。免疫荧光染色发现,S100β阳性细胞占总细胞量的（8.1±1.7）%,而p75阳性细胞占总细胞量的5%以下,达到国内外研究同等水平。 结论通过使用两步消化法和加压筛选联合的方法从人中鼻甲粘膜组织中成功获得了人中鼻甲嗅鞘细胞,相比较传统方法,细胞分离培养周期明显缩短。     

OsRLCK160 contributes to flavonoid accumulation and UV-B tolerance by regulating OsbZIP48 in rice

Science China Life Sciences - Plants produce specialized metabolites to adapt to the ever-changing environments. Flavonoids are antioxidants essential for growth, development, and breeding with...     

Spectroscopic and molecular modeling studies of the interaction between cytidine and human serum albumin and its analytical application

In this study, the interaction between cytidine and human serum albumin (HSA) was investigated for the first time by fluorescence spectroscopy in combination with UV absorption spectrum and molecular modeling under simulative physiological conditions. Experimental results indicated that cytidine had a strong ability to quench the intrinsic fluorescence of human serum albumin. The binding constants (K) at different temperatures, thermodynamic parameter enthalpy changes (DeltaH) and entropy changes (DeltaS) of HSA-cytidine had been calculated according to the relevant fluorescence data, which indicated that the hydrophobic and electrostatic interactions played a major role, which was in agreement with the results of molecular modeling study. In addition, the effects of other ions on the binding constants were also studied. Furthermore, synchronous fluorescence technology was successfully applied to the determination of human serum albumin added into the cytidine solution.     

Nitric oxide destabilizes Pias3 and regulates sumoylation

Small ubiquitin-related protein modifiers (SUMO) modification is an important mechanism for posttranslational regulation of protein function. However, it is largely unknown how the sumoylation pathway is regulated. Here, we report that nitric oxide (NO) causes global hyposumoylation in mammalian cells. Both SUMO E2 conjugating enzyme Ubc9 and E3 ligase protein inhibitor of activated STAT3 (Pias3) were targets for S-nitrosation. S-nitrosation did not interfere with the SUMO conjugating activity of Ubc9, but promoted Pias3 degradation by facilitating its interaction with tripartite motif-containing 32 (Trim32), a ubiquitin E3 ligase. On the one hand, NO promoted Trim32-mediated Pias3 ubiquitination. On the other hand, NO enhanced the stimulatory effect of Pias3 on Trim32 autoubiquitination. The residue Cys459 of Pias3 was identified as a target site for S-nitrosation. Mutation of Cys459 abolished the stimulatory effect of NO on the Pias3-Trim32 interaction, indicating a requirement of S-nitrosation at Cys459 for positive regulation of the Pias3-Trim32 interplay. This study reveals a novel crosstalk between S-nitrosation, ubiquitination, and sumoylation, which may be crucial for NO-related physiological and pathological processes.     

Targeting autophagic regulation of NFkappaB in HTLV-I transformed cells by geldanamycin: implications for therapeutic interventions

The IkappaB kinase (IKK)/NFkappaB signaling pathway plays an essential role in the development and survival of many types of cancers including adult T-cell leukemia (ATL) caused by the human T-cell leukemia virus type I (HTLV-I) infection. Accordingly, targeting NFkappaB provides an attractive strategy for cancer therapy. We recently found that specific inhibition of Hsp90 by geldanamycin (GA) results in autophagic degradation of IKK and NFkappaB-inducing kinase (NIK), an upstream kinase of IKK, and inactivation of NFkappaB in various cell lines. Here, we further report that GA inhibition of Hsp90 also led to IKK autophagic degradation and NFkappaB inhibition in both HTLV-transformed T cells and ATL-derived cell lines. Importantly, GA treatment led to efficient apoptosis of these malignant cells, whereas inhibition of autophagic degradation of IKK significantly ameliorated the cytotoxic effect of GA. These findings thus not only provide mechanistic insights into the tumor suppression function of autophagy and the anti-tumor activity of GA, but also suggest an immediate therapeutic strategy for ATL and other diseases associated with NFkappaB activation by targeting autophagic degradation of the central NFkappaB activating kinases.     

Community response grids: using information technology to help communities respond to bioterror emergencies

Access to accurate and trusted information is vital in preparing for, responding to, and recovering from an emergency. To facilitate response in large-scale emergency situations, Community Response Grids (CRGs) integrate Internet and mobile technologies to enable residents to report information, professional emergency responders to disseminate instructions, and residents to assist one another. CRGs use technology to help residents and professional emergency responders to work together in community response to emergencies, including bioterrorism events. In a time of increased danger from bioterrorist threats, the application of advanced information and communication technologies to community response is vital in confronting such threats. This article describes CRGs, their underlying concepts, development efforts, their relevance to biosecurity and bioterrorism, and future research issues in the use of technology to facilitate community response.     

Dissecting multiple steps of GLUT4 trafficking and identifying the sites of insulin action

Insulin-stimulated GLUT4 translocation is central to glucose homeostasis. Functional assays to distinguish individual steps in the GLUT4 translocation process are lacking, thus limiting progress toward elucidation of the underlying molecular mechanism. Here we have developed a robust method, which relies on dynamic tracking of single GLUT4 storage vesicles (GSVs) in real time, for dissecting and systematically analyzing the docking, priming, and fusion steps of GSVs with the cell surface in vivo. Using this method, we have shown that the preparation of GSVs for fusion competence after docking at the surface is a key step regulated by insulin, whereas the docking step is regulated by PI3K and its downstream effector, the Rab GAP AS160. These data show that Akt-dependent phosphorylation of AS160 is not the major regulated step in GLUT4 trafficking, implicating alternative Akt substrates or alternative signaling pathways downstream of GSV docking at the cell surface as the major regulatory node.     

楸树CbuATX1，CbuATX1-like和CbuATX2基因克隆及生物信息学分析

开花是高等植物内部遗传因素和外界环境因素共同调节完成的复杂生命过程,是植物进入生殖生长从而具备遗传能力和繁殖能力的象征。使用PCR技术,以楸树（Catalpa bungei）混合芽cDNA为模板分别克隆CbuATX1,CbuATX1-like和CbuATX2 3个基因,并利用相关生物信息学软件对这3个基因编码的蛋白质结构进行预测,同时对基因的启动子序列进行顺式作用元件分析,通过qRT-PCR技术检测3个基因在楸树混合芽不同发育时期的表达量。结果表明：CbuATX1的CDS全长为726 bp,编码241个氨基酸,存在跨膜运输结构,属于HMA蛋白家族,与芝麻（Sesamum indicum）、甜菜（Beta vulgaris）亲缘关系较近。CbuATX1-like的CDS全长为801 bp,编码266个氨基酸,存在跨膜运输结构,属于HMA蛋白家族,与胡萝卜（Daucus carota）、欧洲橄榄（Olea europaea）亲缘关系较近。CbuATX2的CDS全长为1 554 bp,编码517个氨基酸,不存在跨膜运输结构,属于PWWP蛋白家族,与马尾草（Erythranthe guttatus）亲缘关系较近。这3个基因启动子均含有多个真核生物启动子的基本元件,如CAAT-box和TATA-box等,此外,还含有光响应、低温响应、生长素响应,以及与干旱诱导相关的MYB结合位点等3个基因与光响应密切相关,还可能参与外界环境胁迫响应等过程。qRT-PCR结果显示,上述3个基因在1年生普通楸树无性系9-1和突变株系-百日花楸树不同发育时期的表达量呈现显著差异。通过以上研究以期能够进一步阐述百日花楸树开花的性状,为楸树开花机制的研究和楸树的定向遗传改良提供理论支持。     

Characteristics of replication and pathogenicity of SARS-CoV-2 Alpha and Delta isolates

The continuously arising of SARS-CoV-2 variants has been posting a great threat to public health safety globally, from B.1.17 (Alpha), B.1.351 (Beta), P.1 (Gamma), B.1.617.2 (Delta) to B.1.1.529 (Omicron). The emerging or reemerging of the SARS-CoV-2 variants of concern is calling for the constant monitoring of their epidemics, pathogenicity and immune escape. In this study, we aimed to characterize replication and pathogenicity of the Alpha and Delta variant strains isolated from patients infected in Laos. The amino acid mutations within the spike fragment of the isolates were determined via sequencing. The more efficient replication of the Alpha and Delta isolates was documented than the prototyped SARS-CoV-2 in Calu-3 and Caco-2 cells, while such features were not observed in Huh-7, Vero E6 and HPA-3 cells. We utilized both animal models of human ACE2 (hACE2) transgenic mice and hamsters to evaluate the pathogenesis of the isolates. The Alpha and Delta can replicate well in multiple organs and cause moderate to severe lung pathology in these animals. In conclusion, the spike protein of the isolated Alpha and Delta variant strains was characterized, and the replication and pathogenicity of the strains in the cells and animal models were also evaluated.