Serologic Response to SARS-CoV-2 in COVID-19 Patients with Different Severity

Virologica Sinica - The immense patient number caused by coronavirus disease 2019 (COVID-19) global pandemic brings the urge for more knowledge about its immunological features, including the...     

Model Compounds of the Mn Cluster in Oxygen-evolving Complex of PS￠ò

Six model compounds have been synthesized and used for probing the structural features of the Mn cluster in oxygen-evolving complex (OEC) of photosystem Ⅱ (PSⅡ). The model compounds contain Mn2(μ-O) 2 and μ-O-μ-carboxylato di-manganese structural units, which offer Mn—Mn, Mn……Mn, and Mn—O(N) structural parameters consistent with the corresponding data of the OEC in PSⅡ, implying that the Mn cluster in OEC may possess similar structural features. Two model compounds containing halide anion have been used for discussing the binding of Cl- to Mn in PSⅡ. It is suggested that in the five S states, ligand exchange would lead to the ligation of chloride to Mn in the S states with Mn of higher valence.     

microRNA-665 silencing improves cardiac function in rats with heart failure through activation of the cAMP signaling pathway

Heart failure (HF) is a disease with high mortality and morbidity rate. Previous studies have shown that microRNAs (miRNAs) may be implicated in the pathogenesis of HF, potentially being able to improve the cardiac function in an HF rat model. The present study was designed to define the role of miR-665 in the cardiac function of the HF rats. Following the establishm;ent of the rat models of HF, the functional role miR-665 in HF was determined using an ectopic expression and knockdown experiments. The cardiac function was evaluated with the determination of ventricular mass index and hemodynamic parameters. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining was performed, with the apoptosis of cardiac cells detected in the process. The expression of miR-665, glucagon-like peptide 1 receptor (GLP1R), cyclic adenosine monophosphate (cAMP) signaling pathway-related, and apoptosis-related genes was examined. Enzyme-linked immunosorbent assay was conducted to determine the levels of inflammation-related genes. Initially, the upregulation of miR-665, downregulation of GLP1R, and inactivation of cAMP signaling pathway were observed in HF rats. GLP1R was a target of miR-665. Forced expression of miR-665 promoted cell apoptosis and inhibited GLP1R and the cAMP signaling pathway. In addition, miR-665 overexpression has been known to impair cardiac function, promote inflammatory response while elevating malondialdehyde and superoxide dismutase levels, and decreasing mitochondrial respiratory chain enzyme activities. Furthermore, we also observed that the effects of miR-665 inhibition had been reversed when the cAMP signaling pathway was also inhibited. This study demonstrates that miR-665 inhibition can stabilize the cardiac function of HF rats via the cAMP signaling pathway via upregulation of the GLP1R.     

Targeting IL-10 in Auto-immune Diseases

IL-10 is a multifunctional cytokine secreted by a variety of cells. It not only inhibits activation of monocyte/macrophage system and synthesis of monocyte cytokine and inflammatory cytokine but also promotes the proliferation and maturation of non-monocyte-dependent T cell, stimulating proliferation of antigen-specific B cell. Increasing evidence indicates that IL-10 plays an important role in both the onset and development of auto-immune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjogren’s syndrome (SS), multiple sclerosis (MS), Crohn’s disease (CD), and psoriasis. However, the exact mechanisms of IL-10 in auto-immune diseases remain unclear. In the present review, we will summarize the biological effects of IL-10, as well as its role and therapeutic potential in auto-immune diseases.     

主养草鱼高密度池塘溶氧收支平衡的研究

采用原位生态学的方法测定广东省中山市9口主养草鱼高密度池塘中浮游植物光合作用产氧量、水柱呼吸耗氧量、底泥呼吸耗氧量和鱼呼吸耗氧量, 并用数学模型计算增氧机增氧量及用差减法计算大气扩散作用引起的得氧或失氧, 对高密度养殖池塘中溶氧收支平衡状况进行了研究。结果显示: 在水深为1.5-2.0 m的主养草鱼高密度池塘中, 光合作用产氧量随着水深的增加而显著降低(P0.05), 底层出现负值呈现氧债现象。水呼吸耗氧量在表层、中层和底层之间没有显著差异(P0.05)。表层水光合作用产氧量显著大于水呼吸耗氧量(P0.05), 而中层和底层水光合作用产氧量却显著小于水呼吸耗氧量(P0.05)。在主养草鱼高密度池塘溶氧的收入中, 浮游植物光合作用产氧量、增氧机增氧量和大气扩散溶入氧量分别占总溶氧来源的44.7%、42.3%和13.0%, 机械增氧作用已接近光合作用, 成为溶氧来源的主要贡献者; 在池塘溶氧的支出中, 水呼吸、鱼呼吸和底泥呼吸耗氧量分别占总耗氧量的45.9%、45.0%和9.1%, 鱼呼吸耗氧与水呼吸耗氧相当, 成为水体中氧气的主要消耗者。结果表明在草鱼高密度养殖过程中, 合理使用机械增氧是池塘溶氧管理的有效措施。       

珠三角高产养殖池塘浮游动物群落结构及水质评价

为进一步了解珠三角高产池塘养殖环境状况, 分析珠三角高产池塘浮游动物群落特征及与池塘水质的相关性, 研究于2016年7—8月对珠三角地区6种主要高产养殖模式30口池塘的浮游动物和环境因子进行了调查。研究结果表明: (1)共采集浮游动物55种, 其中原生动物17种、轮虫29种、枝角类4种、桡足类5种。6种养殖模式池塘中, 大口黑鲈S池塘浮游动物种类数最多, 为34种; 草鱼池塘最少, 为18种。(2)30口池塘共记录优势种8种, 其中原生动物和轮虫各4种, 枝角类和桡足类均不占优势。在6种养殖模式池塘中, 优势种也仅包括原生动物和轮虫, 优势种种类数变化范围为5—8种。(3)30口池塘浮游动物平均密度和生物量均较高, 分别为21354 ind./L和9.36 mg/L。方差分析结果表明6种养殖模式池塘浮游动物密度和生物量均不存在显著差异。(4)RDA分析结果表明, TP和pH是影响珠三角池塘浮游动物分布的主要因素。采用浮游动物丰度和生物量对水质的评价结果显示, 6种养殖模式池塘均处于富营养化状态; 运用Shannon-Wiener多样性指数和Margalef多样性指数对水质的评价结果表明, 6种模式养殖池塘均处于α-中污状态, 且以草鱼池塘的污染最为严重。本研究首次利用浮游动物对珠三角高产池塘进行水质评价, 研究结果可为池塘生态修复和管理提供一定的指导意见。     

珠江水系倒刺鲃生长的初步研究

对采集于珠江水系西江及北江流域的倒刺(Spinibarbus denticulatus denticulatus)样本进行了年龄鉴定和性腺组织学观察,并对鳞长、卵径等进行了测定。结果表明,倒刺鳞片的年轮特征为疏密切割型,新年轮出现时期主要在4~6月。体长和体重呈幂函数关系,西江和北江可分别用公式WX=2.498 4×10-2L2.999 6(r=0.956 1)和WB=1.373 3×10-2L2.815 9(r=0.925 3)表示。根据生长阶段分析,雌性倒刺的性成熟年龄为5龄,5龄以前为幼鱼生长阶段,5~10龄为成鱼生长阶段。雄性倒刺的性成熟年龄为3龄。3龄以前为幼鱼生长阶段,3龄以上为成鱼生长阶段。倒刺的繁殖季节为4~6月份。     

IL-1023-57-PE40分泌表达的初步研究

将IL-1023-57-PE40基因与pelB信号肽融合置于pET-20b构建分泌表达质粒pET-20b-IL-1023-57-PE40,然后将pET-20b-IL-1023-57-PE40分别转化至BL21(DE3),BL21(DE3)pLysS,Rosetta(DE3),E·coliK12TB1,ER2566中。无论是在37℃或是在26℃,亦或在培养基中添加葡萄糖的情况下,IPTG诱导后,IL-1023-57-PE40蛋白只在BL21(DE3)pLysS菌中以可溶分泌形式表达,其中以37℃时培养基中不添加葡萄糖表达量为最高,占菌体蛋白总量的15%,说明蛋白的分泌表达与菌种的选择有关。表达产物经免疫印记检测可被抗PE40的特异抗体识别。通过质粒稳定性实验证明,pET-20b-IL-1023-57-PE40在BL21(DE3)中不稳定,导致蛋白的不表达,在Rosetta(DE3)BL21,E·coliK12TB1,ER2566中稳定但不表达,因此,以Rosetta(DE3)BL21为例,通过SDS-PAGE、DNAStar和ANThewin蛋白分析软件对本室构建的几种PE重组毒素进行比较分析,我们发现:并不是所有PE重组毒素融合信号肽序列后,就能分泌表达,PE重组毒素分泌表达还可能与导向部分的性质有关。     

Coupling between NMDA receptor and acid-sensing ion channel contributes to ischemic neuronal death

Acid-sensing ion channels (ASICs) composed of ASIC1a subunit exhibit a high Ca(2+) permeability and play important roles in synaptic plasticity and acid-induced cell death. Here, we show that ischemia enhances ASIC currents through the phosphorylation at Ser478 and Ser479 of ASIC1a, leading to exacerbated ischemic cell death. The phosphorylation is catalyzed by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity, as a result of activation of NR2B-containing N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) during ischemia. Furthermore, NR2B-specific antagonist, CaMKII inhibitor, or overexpression of mutated form of ASIC1a with Ser478 or Ser479 replaced by alanine (ASIC1a-S478A, ASIC1a-S479A) in cultured hippocampal neurons prevented ischemia-induced enhancement of ASIC currents, cytoplasmic Ca(2+) elevation, as well as neuronal death. Thus, NMDAR-CaMKII cascade is functionally coupled to ASICs and contributes to acidotoxicity during ischemia. Specific blockade of NMDAR/CaMKII-ASIC coupling may reduce neuronal death after ischemia and other pathological conditions involving excessive glutamate release and acidosis.