The role of exosomal microRNAs in central nervous system diseases

Molecular and Cellular Biochemistry - MicroRNAs (miRNA), endogenous non-coding RNAs approximately 22 nucleotides long, regulate gene expression by mediating translational inhibition or mRNA...     

林下植被和凋落物对寒温带森林生长季土壤CH4通量的影响

为进一步探究林下植被和凋落物管理对我国寒温带森林生长季土壤CH₄通量的影响,采用静态箱-气相色谱法对大兴安岭北部4种林型（白桦林、山杨林、樟子松林和兴安落叶松林）4种处理（自然状态、去除凋落物、去除林下植被以及去除林下植被和凋落物）的土壤CH₄通量排放特征进行观测研究。结果表明：该地区森林生长季土壤均表现为CH₄的汇,4种林型不同处理后土壤CH₄通量表现为单峰变化趋势,吸收峰值出现在7月或8月。自然状态4种林型土壤CH₄平均吸收通量表现为白桦林（-79.23±14.92）μg m^-2 h^-1>山杨林（-64.27±9.60）μg m^-2 h^-1>樟子松林（-62.54±15.48）μg m^-2 h^-1>兴安落叶松林（-48.73±12.26）μg m^-2 h^-1,兴安落叶松土壤CH₄平均吸收通量显著小于其他三种林型（P<0.05）。相比于自然状态,4种林型在去除凋落物后土壤CH₄吸收通量提高了2.12%-12.15%,但变化幅度均没有达到显著水平（P>0.05）。去除林下植被后4种林型CH₄吸收通量提高了0.84%-20.55%,且只有山杨林吸收增加达到显著水平（P<0.05）。同时去除林下植被和凋落物后,对白桦林和樟子松土壤CH₄通量影响不显著（P>0.05）,但对山杨林和兴安落叶松林影响显著（P<0.05）。总之,去除凋落物或林下植被均会提高土壤对CH₄吸收,去除林下植被对土壤CH₄通量的影响要大于去除凋落物的影响,但不同林型不同处理之间还存在差异。     

改变碳输入对沂蒙山区典型次生林土壤微生物碳源代谢功能的影响

凋落物和根系向土壤的碳输入是森林生态系统的关键过程,输入量及组分的变化直接影响森林土壤碳汇功能和生产力。在沂蒙山区栎类天然次生林中,开展添加/去除凋落物及去除根系的定位控制试验。于控制试验开展21个月后,采用Biolog Eco微平板培养法,研究凋落物和根系对土壤微生物碳源代谢功能的影响。结果表明,凋落物倍增处理增加了土壤微生物碳源代谢功能,增加了对糖类和胺类的代谢能力。去除凋落物处理、去除根系处理和无输入处理都降低了土壤微生物碳源代谢功能。去除凋落物处理降低土壤微生物碳源代谢功能的幅度大于去除根系处理,表明当前条件下凋落物对土壤微生物碳源代谢功能的影响大于根系,但如果抛除掉去除根系处理中残留根系的影响,凋落物和根系对土壤微生物碳源代谢功能的相对大小可能会发生变化。土壤有机碳含量、铵态氮含量显著影响微生物碳源代谢多样性（P<0.05）,并与碳源代谢功能正相关。凋落物倍增处理通过增加土壤铵态氮和有机碳含量,增加微生物碳源代谢功能,去除凋落物处理和无输入处理通过降低土壤铵态氮和有机碳含量,降低微生物碳源代谢功能。结果深化了碳输入途径（地上凋落物与地下根系）和数量（凋落物倍增、凋落物去除与对照）对温带栎类天然次生林土壤碳代谢过程的认识。     

强化产电微生物与电极间电子传递速率的研究进展

产电微生物是微生物燃料电池、电解池和电合成等微生物电化学技术(Microbial electrochemical technologies,METs)的研究基础。产电微生物与电极界面间的胞外电子传递(Extracellular electron transfer,EET)效率低以及生物被膜形成能力弱限制了METs在有机物降解、电能生产、海水淡化、生物修复和生物传感等方面的应用。因此,强化产电微生物与电极界面间的相互作用是过去几年的主要研究热点。针对近年的研究,本文系统概述了通过改造产电微生物来增强微生物-电极间相互作用的各种策略,重点分析了这些策略的适用性和局限性,并展望了强化产电微生物-电极界面作用在微生物电化学技术利用方面的研究前景。     

An inducible constitutive expression system in Bombyx mori mediated by phiC31 integrase

Inducible gene-expression systems play important roles in gene functional assays in the post-genome era. Streptomyces phage-derived phiC31 integrase, which mediates an irreversible site-specific cassette exchange between the phage attachment site (attP) and the bacterial attachment site (attB), provides a promising option for the construction of a controllable gene-expression system. Here, we report a phiC31 integrase-mediated promoter flip system (FLIP) for the inducible expression of target genes in silkworm (Bombyx mori). First, we constructed a FLIP reporter system, in which a BmAct4 promoter with enhanced translational efficiency was flanked by the attB and attP sites in a head-to-head orientation and further linked in a reverse orientation to a DsRed reporter gene. The coexpression of a C-terminal modified phiC31-NLS integrase carrying a simian virus 40 (SV40) nuclear localization signal (NLS) effectively flipped the BmAct4 promoter through an attB/attP exchange, thereby activating the downstream expression of DsRed in a silkworm embryo-derived cell line, BmE. Subsequently, the FLIP system, together with a system continuously expressing the phiC31-NLS integrase, was used to construct binary transgenic silkworm lines. Hybridization between FLIP and phiC31-NLS transgenic silkworm lines resulted in the successful flipping of the BmAct4 promoter, with an approximately 39% heritable transformation efficiency in silkworm offspring, leading to the constitutive and high-level expression of DsRed in silkworms, which accounted for approximately 0.81% of the silkworm pupal weight. Our successful development of the FLIP system offers an effective alternative for manipulating gene expression in silkworms and other lepidopteran species.     

LncRNA-HOTAIR promotes endothelial cell pyroptosis by regulating the miR-22/NLRP3 axis in hyperuricaemia

Long non-coding RNA (lncRNA) plays an important role in the renal inflammatory response caused by hyperuricaemia. However, the underlying molecular mechanisms through which lncRNA is involved in endothelial injury induced by hyperuricaemia remain unclear. In this study, we investigated the regulatory role of lncRNA-HOTAIR in high concentration of uric acid (HUA)–induced renal injury. We established hyperuricaemia mouse model and an in vitro uric acid (UA)–induced human umbilical vein endothelial cell (HUVEC) injury model. In HUA-treated HUVECs and hyperuricaemia mice, we observed increased HOTAIR and decreased miR-22 expression. The expression of pyroptosis-associated protein (NLRP3, Caspase-1, GSDMD-N, GSDMD-FL) was increased. The release of LDH, IL-1β and IL-18 in cell supernatants and the sera of model mice was also increased. The proliferation of HUVECs stimulated by HUA was significantly inhibited, and the number of TUNEL-positive cells in hyperuricaemia mouse kidney was increased. Bioinformatics analysis and luciferase reporter and RIP assays confirmed that HOTAIR promoted NLRP3 inflammasome activation by competitively binding miR-22. In gain- or loss-of-function experiments, we found that HOTAIR and NLRP3 overexpression or miR-22 knock down activated the NLRP3 inflammasome and promoted pyroptosis in HUA-treated HUVECs, while NLRP3 and HOTAIR knockdown or a miR-22 mimic exerted the opposite effects. Furthermore, in vivo experiments validated that HOTAIR knockdown alleviated renal inflammation in hyperuricaemia mice. In conclusion, we demonstrated that in hyperuricaemia, lncRNA-HOTAIR promotes endothelial cell pyroptosis by competitively binding miR-22 to regulate NLRP3 expression.     

Numerical Study of an Ultra-Broadband and Wide-Angle Insensitive Perfect Metamaterial Absorber in the UV–NIR Region

Plasmonics - Developing a simple structure using low-cost material that enables both large-scale fabrication and broadband absorption response is highly desirable but very challenging for achieving...