Proteomic Analysis of Kunitz-Type Trypsin Inhibitor Deleted Soybean

Russian Journal of Plant Physiology - To explore proteomic characters of Kunitz-type trypsin inhibitors (KTIs) deleted soybean (Glycine max (L.) Merr.), seeds without KTIs and its female parent...     

miR-129-5p improves cardiac function in rats with chronic heart failure through targeting HMGB1

Mammalian Genome - Increasing evidence shows that miRNAs play pivotal roles in cardiovascular diseases, including heart failure (HF). The aim of this study was to investigate the role of miR-129-5p...     

慢性乙型肝炎患者肠道菌群与肝脏生化指标的相关性

乙型肝炎病毒感染引起的慢性乙型肝炎(Chronic hepatitis B,CHB)是一种全球性流行疾病,严重时可引起肝功能衰竭,甚至发展成肝硬化和肝癌.也已发现CHB的发生和发展与肠道菌群的组成和结构的变化密切相关.为进一步探究肠道菌群结构与肝脏生化指标之间的联系,文中随机纳入14名CHB患者和11名健康对照者(Co...     

Procyanidin B1 promotes in vitro maturation of pig oocytes by reducing oxidative stress

Oxidative stress negatively affects the in vitro maturation (IVM) of oocytes. Procyanidin B1 (PB1) is a natural polyphenolic compound that has antioxidant properties. In this study, we investigated the effect of PB1 supplementation during IVM of porcine oocytes. Treatment with 100 μM PB1 significantly increased the MII oocytes rate (p <0.05), the parthenogenetic (PA) blastocyst rate (p <0.01) and the total cell number in the PA blastocyst (p < 0.01) which were cultured in regular in vitro culture (IVC) medium. The PA blastocyst rate of regular MII oocytes activated and cultured in IVC medium supplemented with 100 and 150 μM PB1 significantly increased compared with control (p < 0.01 and p < 0.05). We also evaluated the reactive oxygen species (ROS) levels, mitochondrial membrane potential (Δψm) levels, glutathione (GSH) levels, and apoptotic levels in MII oocytes and cumulus cells following 100 μM PB1 treatment. The results showed that the PB1 supplementation decreased ROS production and apoptotic levels. In addition, PB1 was found to increase Δψm levels and GSH levels. In conclusion, PB1 inhibited apoptosis of oocytes and cumulus cells by reducing oxidative stress. Moreover, PB1 improved the quality of oocytes and promoted PA embryo development. Taken together, our results suggest that PB1 is a promising antioxidant additive for IVM of oocytes.     

益生菌调控肠道屏障功能预防家禽球虫病的研究进展

球虫病给养禽业带来巨大经济损失,人们对绿色健康食品的迫切需求使球虫病的防控面临新的挑战.伴随世界"禁抗"进程的不断推进,家禽养殖业亟需一种安全有效的新型抗球虫方法.益生菌可竞争性排斥病原菌定殖以防止球虫病继发感染,可刺激宿主抗菌肽、黏蛋白和紧密连接蛋白的分泌以抵御球虫入侵,还可激活免疫反应以增强机体抗球虫感染的能力.本...     

Melatonin inhibits triple-negative breast cancer progression through the Lnc049808-FUNDC1 pathway

Melatonin has been reported to have tumor-suppressive effects via comprehensive molecular mechanisms, and long non-coding RNAs (lncRNAs) may participate in this process. However, the mechanism by which melatonin affects the function of lncRNAs in triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer, is still unknown. Therefore, we aimed to investigate the differentially expressed mRNAs and lncRNAs in melatonin-treated TNBC cells and the interaction mechanisms. Microarray analyses were performed to identify differentially expressed mRNAs and lncRNAs in TNBC cell lines after melatonin treatment. To explore the functions and underlying mechanisms of the mRNAs and lncRNAs candidates, a series of in vitro experiments were conducted, including CCK-8, Transwell, colony formation, luciferase reporter gene, and RNA immunoprecipitation (RIP) assays, and mouse xenograft models were established. We found that after melatonin treatment, FUNDC1 and lnc049808 downregulated in TNBC cell lines. Knockdown of FUNDC1 and lnc049808 inhibited TNBC cell proliferation, invasion, and metastasis. Moreover, lnc049808 and FUNDC1 acted as competing endogenous RNAs (ceRNAs) for binding to miR-101. These findings indicated that melatonin inhibited TNBC progression through the lnc049808-FUNDC1 pathway and melatonin could be used as a potential therapeutic agent for TNBC.Subject terms: Breast cancer, Non-coding RNAs     

PIK-75 promotes homology-directed DNA repair

Homo!ogy-directed repair(HDR)is one of two major DNA repair pathways to mend the double-strand breaks(DSBs)formed in the genome(Liang et al.,1998;Pardo et al.,2009).Although less efficient compared with another DNA repair pathway,nonhomologous end joining(NHEJ),HDR is a type of precise repair to restore DNA damage and sustain genomic stability(Pardo et al.,2009;Ceccaldi et al.,2016).By contrast,NHEJ usually introduces mutations into the repaired site,thus probably harming the genomic integrity(Lieber et al.,2003).The error-free property enables HDR to be harnessed to correct a faulty mutation for therapeutic purpose in cells or in the body(Wu et al.,2013).In add让ion,HDR possesses great potential in the generation of genome-edited animals with precise genetic modifications,such as point mutation,DNA replacement,and DNA insertion in a specific genomic site(Wang et al.,2013).However,the low repair frequency mediated by HDR significantly limits让s application for efficient gene correction or establishment of various genetically modified animal models.Currently,multiple site-specific endonucleases have emerged as highly efficient tools to create targeted DSBs and markedly promote subsequent DNA repair either via HDR or NHEJ(Gaj et al.,2013).Nonetheless,the HDR-mediated modifications following the cleavage of engineering nucleases are still inefficient,usually with an efficiency less than 20%in cultured mammalian cells and embryos(Mali et al..2013;Wang et al.,2013;Yang et al.,2013).