准噶尔荒漠土壤多功能性的空间变异特征及其驱动因素

荒漠是重要的陆地生态系统之一, 其生态系统极其脆弱, 极易发生荒漠化。荒漠土壤的稳定和功能对于荒漠生态系统结构和功能的维持至关重要。但在荒漠地区, 大多数土壤功能的研究还主要集中在单一的土壤功能性。本研究基于准噶尔荒漠79个样点的土壤有机碳(SOC)、氮(N)、磷(P)、有效氮(AN)和有效磷(AP)等指标, 通过平均值法和因子分析法计算土壤多功能(soil multifunctionality, SMF)指数, 研究SMF空间变异特征及驱动因素。空间分析所示从整体来看, 荒漠SMF在空间分布上具有较大的异质性, 自西向东, SMF总体呈现逐渐增加的趋势, 而从南向北, SMF呈现先增加后降低的趋势。最优拟合显示, SMF与年均降雨量(MAP)和年均温(MAT)呈显著二次函数关系, 随着MAP和MAT的增加表现出先降低后升高的趋势; SMF与pH和植被增强指数(EVI)呈显著线性关系, SMF随着pH的增加表现出显著降低趋势, 而随着EVI的增加表现为显著上升的趋势; SMF与Aridity (干旱度)之间既符合二次函数关系也呈现线性关系(二者R²相同), 随Aridity增加而减少。结构方程模型结果表明, 土壤含水率(SWC)是SMF变化的最重要的驱动因素, 其次为EVI。土壤pH、SWC、MAT、Aridity和EVI对荒漠SMF具有显著的直接效应, 其中SWC和EVI为显著正效应, 其他为负效应。MAP、经度(Lon)、纬度(Lat)和海拔(Alt)可通过影响MAT等指标对SMF产生间接效应。研究结果对深入理解准噶尔荒漠SMF的空间变异特征及驱动因素具有重要意义, 将有助于预测环境变化对荒漠生态系统多功能性的影响, 为生态系统科学管理服务。     

微生物相互作用中的空间自组织

微生物在全球生态系统中占据着重要地位, 其中一个重要的研究领域是微生物与环境(包括无机环境与生物环境)之间的相互作用。在生态相互作用过程中, 微生物常常通过自组织形成特定的空间模式。微生物的空间模式在种群稳定性、群落动态变化以及维持合作行为方面具有重要作用。本文中, 我们梳理了当下对微生物空间自组织及其所形成的空间模式的研究内容, 首先介绍什么是空间自组织, 再根据生态相互作用类型对自组织的空间模式进行描述, 其中重点讨论合作与竞争中的空间模式, 接着关注微生物空间自组织的过程, 最后我们指出空间自组织对整个群体的结构和功能稳定具有重要意义。研究微生物种群间相互作用中的空间模式, 有助于探索维持合作行为的新机制, 进而为微生物共生系统的构建提供新的理解。     

土壤原生生物多样性及其生态功能研究进展

原生生物广泛分布在土壤和不同生境中, 其数量庞大、种类繁多, 在生态系统物质循环和能量流动以及维持土壤和植物健康中起着举足轻重的作用。与土壤其他生物类群相比, 原生生物分类体系和生态类型复杂, 分类鉴定困难且分子检测技术不够成熟, 目前对原生生物的认识相对不足。本文对当前原生生物的相关研究进展进行了总结和梳理, 系统阐述了原生生物的分类系统和营养功能群特征、土壤原生生物的多样性分布特征及影响因子, 重点介绍了原生生物群落在参与土壤养分循环、维持土壤和植物健康等中的功能作用, 并对未来的研究方向与应用前景进行了展望。对土壤原生生物的研究有助于我们深入认识土壤生物多样性资源, 并进行保护性地开发和利用, 维护土壤和生态系统健康。     

综述与专论: 白质消融性白质脑病研究进展

白质消融性白质脑病（leukoencephalopathy with vanishing white matter,VWM）是一种常染色体隐性遗传性脑白质病,其致病基因EIF2B 1~5分别编码真核细胞蛋白质翻译起始因子2B（eukaryotic initiation factor 2B,eIF2B）的5个亚基α~ε,其中任一编码基因突变均可引起发病。起病多见于婴幼儿及儿童期,临床表型差异大,典型表现为进行性运动功能退行,可伴共济失调和癫痫。应激（发热、外伤等）可导致发作性加重。影像学显示大脑白质进行性液化。尸解神经病理学特征主要表现为广泛性白质稀疏和囊性变性,无神经胶质细胞反应性增生,星形胶质细胞形态异常,过表达祖细胞标志物巢蛋白（Nestin）和胶质纤维酸性蛋白δ（GFAPδ）,少突前体细胞数量增加和成熟少突胶质细胞减少、泡沫化且凋亡增加。VWM致病基因EIF2B 1~5是管家基因,但多数患者通常仅脑白质受累。少数胎儿期及婴儿早期发病的患者可出现多系统受累,成年女性患者可有卵巢功能障碍。目前认为,星形胶质细胞在其致病机制中起着核心作用,病理性星形胶质细胞继发性引起少突胶质细胞成熟障碍和髓鞘形成异常,进而导致脑白质病变。其他疾病机制包括内质网应激后未折叠蛋白反应（UPR）过度激活、线粒体功能障碍、自噬抑制等,尚不完全明确。     

The structure of Crimean-Congo hemorrhagic fever virus Gc is revealed; many more still need an answer

Highlights
1. The structure of glycoprotein Gc, responsible for mediating membrane fusion between cell and CCHFV, is revealed, but many more mysteries remain.
2. Why do only antibodies against Gc have neutralizing effect, but not the one against Gn?
3. Why can NAbs against Gc only be protective in the animals in preventive settings, but not in the therapeutic administration?     

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.     

Infection and pathogenesis of the Delta variant of SARS-CoV-2 in Rhesus macaque

Highlights
1. Delta variant of SARS-CoV-2 can effectively infect the Rhesus macaque.
2. The Delta variant grows faster than the early strain isolated from Wuhan in late 2019.
3. The shedding pattern, viral load and disease severity of Delta variant are similar with the early strain isolated from Wuhan in late 2019.
4. This study supports the attributed rapid disease spread of the Delta variant.     

Aggregation of human dental pulp cells into 3D spheroids enhances their migration ability after reseeding

Multicellular three-dimensional (3D) spheroids allow intimate cell–cell communication and cell–extracellular matrix interaction. Thus, 3D cell spheroids better mimic microenvironment in vivo than two-dimensional (2D) monolayer cultures. The purpose of this study was to evaluate the behaviors of human dental pulp cells (DPCs) cultured on chitosan and polyvinyl alcohol (PVA) membranes. The protein expression of hypoxia-inducible factor 1-α (HIF-1α) and vascular endothelial growth factor (VEGF), and the migration ability of the DPCs from 2D versus 3D environments were investigated. The results showed that both chitosan and PVA membranes support DPCs aggregation to form multicellular spheroids. In comparison to 2D cultures on tissue culture polystyrene, DPC spheroids exhibited higher protein expression of HIF-1α and VEGF. The treatment with YC-1 (inhibitor to HIF-1α) blocked the upregulation of VEGF, indicating a downstream event to HIF-1α expression. When DPC spheroids were collected and subjected to the transwell assay, the cells growing outward from 3D spheroids showed greater migration ability than those from 2D cultures. Moreover, DPCs aggregation and spheroid formation on chitosan membrane were abolished by Y-27632 (inhibitor to Rho-associated kinases), whereas the inhibitory effect did not exist on PVA membrane. This suggests that the mechanism regulating DPCs aggregation and spheroid formation on chitosan membrane is involved with the Rho-associated kinase signaling pathway. In summary, the multicellular spheroid structure was beneficial to the protein expression of HIF-1α and VEGF in DPCs and enhanced the migration ability of the cells climbing from spheroids. This study showed a new perspective in exploring novel strategies for DPC-based research and application.     

MicroRNA-638 inhibits human airway smooth muscle cell proliferation and migration through targeting cyclin D1 and NOR1

Abnormal airway smooth muscle cell (ASMC) proliferation and migration contribute significantly to increased ASM mass associated with asthma. MicroRNA (miR)-638 is a primate-specific miRNA that plays important roles in development, DNA damage repair, hematopoiesis, and tumorigenesis. Although it is highly expressed in ASMCs, its function in ASM remodeling remains unknown. In the current study, we found that in response to various mitogenic stimuli, including platelet-derived growth factor-two B chains (PDGF-BB), transforming growth factor β1, and fetal bovine serum, the expression of miR-638, as determined by quantitative real-time polymerase chain reaction (qRT-PCR), was significantly downregulated in the proliferative human ASMCs. Both gain- and loss-of-function studies were performed to study the role of miR-638 in ASMC proliferation and migration. We found that adenovirus-mediated miR-638 overexpression markedly inhibits ASMC proliferation and migration, while ablation of miR-638 by anti-miR-638 markedly increases cell proliferation and migration, as determined by WST-8 proliferation and scratch wound assays. Dual-luciferase reporter assay, qRT-PCR, and immunoblot analysis were used to investigate the effects of miR-638 on the expression of the downstream target genes in ASMCs. Our results demonstrated that miR-638 overexpression significantly reduced the expression of downstream target cyclin D1 and NOR1, both of which have been shown to be essential for cell proliferation and migration. Together, our study provides the first in vitro evidence highlighting the antiproliferative and antimigratory roles of miR-638 in human ASMC remodeling and suggests that targeted overexpression of miR-638 in ASMCs may provide a novel therapeutic strategy for preventing ASM hyperplasia associated with asthma.     

Hypoxic conditioned medium derived from bone marrow mesenchymal stromal cells protects against ischemic stroke in rats

In recent years, studies have shown that the secretome of bone marrow mesenchymal stromal cells (BMSCs) contains many growth factors, cytokines, and antioxidants, which may provide novel approaches to treat ischemic diseases. Furthermore, the secretome may be modulated by hypoxic preconditioning. We hypothesized that conditioned medium (CM) derived from BMSCs plays a crucial role in reducing tissue damage and improving neurological recovery after ischemic stroke and that hypoxic preconditioning of BMSCs robustly improves these activities. Rats were subjected to ischemic stroke by middle cerebral artery occlusion and then intravenously administered hypoxic CM, normoxic CM, or Dulbecco modified Eagle medium (DMEM, control). Cytokine antibody arrays and label-free quantitative proteomics analysis were used to compare the differences between hypoxic CM and normoxic CM. Injection of normoxic CM significantly reduced the infarct area and improved neurological recovery after stroke compared with administering DMEM. These outcomes may be associated with the attenuation of apoptosis and promotion of angiogenesis. Hypoxic preconditioning significantly enhanced these therapeutic effects. Fourteen proteins were significantly increased in hypoxic CM compared with normoxic CM as measured by cytokine arrays. The label-free quantitative proteomics analysis revealed 163 proteins that were differentially expressed between the two groups, including 107 upregulated proteins and 56 downregulated proteins. Collectively, our results demonstrate that hypoxic CM protected brain tissue from ischemic injury and promoted functional recovery after stroke in rats and that hypoxic CM may be the basis of a potential therapy for stroke patients.