α‐ketoglutarate delays age‐related fertility decline in mammals

The fecundity reduction with aging is referred as the reproductive aging which comes earlier than that of chronological aging. Since humans have postponed their childbearing age, to prolong the reproductive age becomes urgent agenda for reproductive biologists. In the current study, we examined the potential associations of α‐ketoglutarate (α‐KG) and reproductive aging in mammals including mice, swine, and humans. There is a clear tendency of reduced α‐KG level with aging in the follicle fluids of human. To explore the mechanisms, mice were selected as the convenient animal model. It is observed that a long term of α‐KG administration preserves the ovarian function, the quality and quantity of oocytes as well as the telomere maintaining system in mice. α‐KG suppresses ATP synthase and alterations of the energy metabolism trigger the nutritional sensors to down‐regulate mTOR pathway. These events not only benefit the general aging process but also maintain ovarian function and delay the reproductive decline. Considering the safety of the α‐KG as a naturally occurring molecule in energy metabolism, its utility in reproduction of large mammals including humans deserves further investigation.     

A Human Active Lower Limb Model for Chinese Pedestrian Safety Evaluation

A subsystem impactor test for pedestrian lower limb injury evaluation has been brought in China New Car Assessment Protocol(CNCAP).Concerning large anthropometr...     

TEB/POLQ plays dual roles in protecting Arabidopsis from NO-induced DNA damage

Nitric oxide (NO) is a key player in numerous physiological processes. Excessive NO induces DNA damage, but how plants respond to this damage remains unclear. We screened and identified an Arabidopsis NO hypersensitive mutant and found it to be allelic to TEBICHI/POLQ, encoding DNA polymerase θ. The teb mutant plants were preferentially sensitive to NO- and its derivative peroxynitrite-induced DNA damage and subsequent double-strand breaks (DSBs). Inactivation of TEB caused the accumulation of spontaneous DSBs largely attributed to endogenous NO and was synergistic to DSB repair pathway mutations with respect to growth. These effects were manifested in the presence of NO-inducing agents and relieved by NO scavengers. NO induced G2/M cell cycle arrest in the teb mutant, indicative of stalled replication forks. Genetic analyses indicate that Polθ is required for translesion DNA synthesis across NO-induced lesions, but not oxidation-induced lesions. Whole-genome sequencing revealed that Polθ bypasses NO-induced base adducts in an error-free manner and generates mutations characteristic of Polθ-mediated end joining. Our experimental data collectively suggests that Polθ plays dual roles in protecting plants from NO-induced DNA damage. Since Polθ is conserved in higher eukaryotes, mammalian Polθ may also be required for balancing NO physiological signaling and genotoxicity.     

Osteoimmunology: The correlation between osteoclasts and the Th17/Treg balance in osteoporosis

Osteoporosis is a bone disease that is caused by disorder of the skeletal microenvironment, and it characterized by a high disability rate and the occurrence of low energy fractures. Studies on osteoporosis and related treatment options have always been hot spots in the field of bone biology. In the past, the understanding of osteoporosis has been rather limited; research has only shown that osteoporosis involves the imbalance of bone resorption and bone formation, and recent studies have not provided cutting‐edge theories of the basic understanding of osteoporosis. Recent studies have shown crosstalk between bone and immune responses. RANKL, an essential factor for osteoclasts (OCs), is associated with the immune system. T helper (Th17)/regulatory T (Treg) cells are two different kinds of T cells that can self‐interact and regulate the differentiation and formation of OCs. Therefore, understanding the correlation between the skeletal and immune systems and further revealing the roles and the cooperation between RANKL and the Th17/Treg balance will help to provide new insights for the treatment of osteoporosis.     

喀斯特生态脆弱区贫困化时空动态特征与影响因素——以贵州省为例

贵州省属于西南喀斯特生态脆弱与集中连片特困的复合区域,研究其贫困化的时空动态与影响因素,对该地区精准脱贫具有重要意义。以贫困发生率为指标,采用ESTDA框架对2003—2015年贵州省贫困化时空动态特征进行分析,并结合地理探测器分析其影响因素。结果表明:(1)贵州省贫困化具有显著的空间正相关性,出现了贫困化相似县域相邻分布的空间集聚效应,局部趋势上两级分化趋势明显,空间结构呈典型的"核心边缘"模式。(2)贫困化局部空间结构和空间依赖方向上都具有较强的稳定性;出现协同增长型的县域有53个,表明贫困化空间格局具有明显的空间整合性。(3)贫困化具有较强的局部空间关联模式和空间转移惰性,表现为一定的路径依赖或空间锁定特征。(4)各因素对贫困化的影响力存在一定差异,农民可支配收入是影响贫困化主要因素,海拔、坡度和植被覆盖度等自然因素影响较小;任意两个因素交互探测后对贫困化的影响均强于单个因素的影响,且解释力表现为非线性增强和双线性增强两种类型。     

Caveolin-1 identified as a key mediator of acute lung injury using bioinformatics and functional research

Acute lung injury (ALI) is a potentially life-threatening, devastating disease with an extremely high rate of mortality. The underlying mechanism of ALI is currently unclear. In this study, we aimed to confirm the hub genes associated with ALI and explore their functions and molecular mechanisms using bioinformatics methods. Five microarray datasets available in GEO were used to perform Robust Rank Aggregation (RRA) to identify differentially expressed genes (DEGs) and the key genes were identified via the protein-protein interaction (PPI) network. Lipopolysaccharide intraperitoneal injection was administered to establish an ALI model. Overall, 40 robust DEGs, which are mainly involved in the inflammatory response, protein catabolic process, and NF-κB signaling pathway were identified. Among these DEGs, we identified two genes associated with ALI, of which the CAV-1/NF-κB axis was significantly upregulated in ALI, and was identified as one of the most effective targets for ALI prevention. Subsequently, the expression of CAV-1 was knocked down using AAV-shCAV-1 or CAV-1-siRNA to study its effect on the pathogenesis of ALI in vivo and in vitro. The results of this study indicated that CAV-1/NF-κB axis levels were elevated in vivo and in vitro, accompanied by an increase in lung inflammation and autophagy. The knockdown of CAV-1 may improve ALI. Mechanistically, inflammation was reduced mainly by decreasing the expression levels of CD3 and F4/80, and activating autophagy by inhibiting AKT/mTOR and promoting the AMPK signaling pathway. Taken together, this study provides crucial evidence that CAV-1 knockdown inhibits the occurrence of ALI, suggesting that the CAV-1/NF-κB axis may be a promising therapeutic target for ALI treatment.Subject terms: Cell signalling, Respiratory tract diseases     

短期增温对中亚热带杉木人工幼林土壤氮磷耦合作用的影响

全球变暖引起陆地生态系统和整个生物圈一系列生态问题,未来全球平均气温的持续增加将使这些问题进一步加剧。目前增温、氮沉降和森林更新方式对中亚热带土壤氮磷等养分的影响已有部分研究,但增温对亚热带森林的氮磷耦合作用的影响仍然未知。以中亚热带杉木(Cunninghamia lanceolate)幼苗为研究对象,设置埋设电缆以加热土壤增温实验(增温幅度(5±0.5)℃),研究短期增温对土壤含水量、微生物生物量氮(MBN)、微生物生物量磷(MBP)、土壤氮磷养分,以及氮(N)、磷(P)耦合作用的影响。结果表明:短期增温对全氮、全磷无显著影响;增温第1年显著提高了有效氮、铵态氮(NH_4~+)和有效磷的含量,显著降低了MBN含量。增温第2年,土壤中有效磷、NH_4~+和MBP含量显著下降;短期增温虽然对土壤全N/P,有效N/P的影响不显著,但是增温使铵态氮/硝态亚硝态氮(NH_4~+/(NO_3~-+NO_2~-))显著降低;此外,增温显著降低了MBN/MBP,缓解了微生物对磷的限制。相关性分析表明,耦合作用不仅受N和P之间相互作用的影响,也受土壤温度、水分含量等其他因素的影响。研究表明,短期增温并未对中亚热带杉木人工幼林土壤氮磷耦合作用产生显著影响,但增温后降低了有效氮、有效磷的含量。因此,在未来全球变暖背景下,研究结果为中亚热带森林生态系统的的健康发展和科学管理提供重要的理论依据。