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Waxy gene mutations cause the stickiness of maize grains. China is rich in waxy maize landraces and is considered to be the origin of waxy maize. At present, the Waxy alleles found in Chinese waxy maize include wx-D7, wx-D10, wx-Cin4, and wx-124, of which wx-Cin4 and wx-124 are characterized as transposon insertion mutations. The Yunnan area has the most abundant Chinese waxy maize; however, there are still a large number of waxy maize landraces with unknown Waxy alleles. In this study, 20 waxy maize landraces from Yunnan Province of China were used as research materials for waxy gene analysis, and a new Waxy allele was detected. Molecularly, this allele is characterized by an ~ 5.4-Kb retrotransposon Reina inserted in the tenth intron of the Waxy gene, and we named this allele wx-Reina. Reina is a member of the long terminal repeat (LTR) retrotransposon family. This Reina transposon has the same LTR sequence at both ends, so this mutation is a newly formed mutation. Through reverse transcription PCR (RT-PCR) analysis, we found that Reina insertion results in the deletion of exons 10 and 11 in the transcript of wx-Reina, so its original gene function is lost. The discovery of wx-Reina further enriches the knowledge of types of waxy alleles in Chinese waxy maize. Combined with our previous studies, we believe that transposon activity is one of the main driving forces for the formation of Waxy gene alleles in Chinese waxy maize.

Background: LncRNA TSIX has been observed to be abnormally expressed in many human cancers. However, its roles in nasopharyngeal carcinoma (NPC) remains unclear, and this study aims to explore the functions of TSIX in NPC.Methods: The expression of TSIX and miR-342-3p in NPC tissues and corresponding cell lines was detected by qRT-PCR. Bioinformatics analysis and luciferase activity assay and RIP assay were applied to determine the interaction between TSIX, miR-342-3p, and AGR2. The roles of TSIX, miR-342-3p and AGR2 in the proliferation, apoptosis, migration and invasion of NPC cells were explored both in vitro and in vivo. In addition, the rescue experiments were used to confirm the functions of TSIX, miR-342-3p, and AGR2 in NPC progression.Results: Our study firstly found that TSIX was significantly upregulated in NPC tissues and corresponding cell lines. Moreover, upregulation of TSIX obviously exacerbated the NPC progression including the proliferation, apoptosis, migration and invasion, while downregulation of TSIX efficiently attenuated the development of NPC. Further, our results demonstrated that TSIX could increase the expression of AGR2, which was directly targeted by miR-342-3p, and then lead to the facilitated development of NPC cells.Conclusion: In summary, our study revealed that lncRNA TSIX promoted the progression of NPC through targeting miR-342-3p/AGR2 axis, suggested that it might be a potential therapeutic target for NPC.

Acute myocardial infarction (MI) is a common cardiovascular disease with high mortality. In this study, an injectable thermosensitive hydrogel of chitosan (CS)/dextran (DEX)/β-glycerophosphate (β-GP) loaded with umbilical cord mesenchymal stem cells (UCMSCs) was prepared for MI treatment. The good biocompatibility of hydrogels was confirmed by 3T3 cells and HUVECs culture study in vitro. HUVECs encapsulated in the hydrogels showed a cell delivery ability. Furthermore, the results indicated that hydrogel could encapsulate most of UCMSCs and the cells exhibited good viability in CS/ 1.0DEX/β-GP hydrogels. The expression of cardiac markers of cTnI and Cx43 and signaling pathways of p-Akt and p-ERK1/2 were studied, and it showed that UCMSCs differentiate towards myocardium and has a great potential for therapeutic use of cardiac repair. In conclusion, the thermosensitive hydrogel of CS/1.0 DEX/β-GP loaded UCMSCs was a promising candidate as cell delivery vehicle for cardiac repair to reconstitute damaged myocardium.

Cobalt selenide/tin selenide (CoSe/SnSe) hybrid is successfully synthesized via a facile solvothermal method and used as an efficient Pt-free counter electrode (CE) for dye-sensitized solar cells (DSSCs). Field emission scanning electron microscopy observes that CoSe/SnSe hybrid is made up of nanosheets and nanoparticles; the nanosheets are CoSe, while the nanoparticles are SnSe. Cyclic voltammogram measurement indicates that CoSe/SnSe hybrid electrodes have larger current density than CoSe electrode and Pt electrode. Electrochemical impedance spectroscopy shows that the 3CoSe/SnSe hybrid has low charge-transfer resistance of 1.03 Ω cm2. Under simulated solar light irradiation with intensity of 100 mW cm−2 (AM 1.5), the DSSC based on the Co3SnSe4 hybrid CE achieves a power conversion efficiency of 7.71 %, which is higher than that the DSSC based on conventional Pt CE (6.89 %). The DSSCs with all as-prepared CoSe/SnSe hybrid CEs exhibit better photovoltaic performance than the DSSC with conventional Pt CE.

Cobalt selenide (CoSe 2 ) nanorods are prepared by hydrothermal method and used as an efficient Pt-free counter electrode (CE) for dye-sensitized solar cells (DSSCs). Field emission scanning electron microscopy observes that CoSe 2 mostly exhibits a nanorod morphology, which facilitates change carrier transfer from their surface to redox electrolyte. Cyclic voltammogram measurement indicates that CoSe 2 electrode has larger current density than Pt electrode. Electrochemical impedance spectroscopy shows that the CoSe 2 electrode with optimal condition has low series resistance of 8.034 Ω × cm 2 and has low charge-transfer resistance of 0.097 Ω·cm 2 . Under simulated solar light irradiation with intensity of 100 mW·cm −2 (AM 1.5), the DSSC based on the CoSe 2 CE achieves a power conversion efficiency of 8.38 %, which is higher than the solar cell based on Pt CE (7.83%).

Myocardial fibrosis is a characteristic feature of cardiomyopathies. However, no effective strategies to attenuate cardiac fibrosis are currently available. Late-stage endothelial progenitor cells (EPCs) are precursors of endothelial cells (ECs) that repair the heart through a paracrine mechanism. In the present study, we tested whether EPC-derived exosomes regulate the differentiation of fibroblasts into ECs. We isolated late-stage EPCs from human peripheral blood (PB) and used immunofluorescence and flow cytometry to confirm their identity. Next, we isolated exosomes from the EPCs and characterized their morphology using electron microscopy and confirmed the expression of exosome-specific marker proteins using Western blots. We then investigated the in vitro effects of exosomes on the proliferation and angiogenesis of cardiac fibroblasts (CFs) and on the expression of the mesenchymal-endothelial transition (MEndT)-related genes and the myocardial fibrosis-regulated protein, high mobility group box 1 protein B1 (HMGB1). We found that human PB-EPC-derived exosomes enhanced the proliferation and angiogenesis of CFs in vitro. Furthermore, CFs stimulated with these exosomes showed increased expression of the EC-specific markers, like cluster of differentiation 31 and vascular endothelial growth factor receptor 2, and decreased expression of proteins involved in fibrosis, like alpha-smooth muscle actin, vimentin, collagen I, transforming growth factor-beta, and tumor necrosis factor-alpha. In addition, CFs stimulated with human PB-EPC-derived exosomes, inhibited the expression of HMGB1. Taken together, our study demonstrated that EPC-derived exosomes promote the proliferation and angiogenesis of CFs by inhibiting MEndT and decreasing the expression of HMGB1.

Introduction Previous studies have shown that endothelial cell senescence is involved in cardiovascular diseases such as cardiac fibrosis, atherosclerosis and heart failure. Accumulating evidence indicates that apelin exerts protective effects on ageing-related endothelial dysfunction. In this study, we aim to investigate the role of the apelin/APJ axis in angiotensin II (AngII)-induced endothelium senescence and its associated mechanisms. Material and methods Senescence-related β-gal activity assay and western blot were used to evaluate human umbilical vein endothelial cell (HUVEC) senescence. In addition, DCFH-DA staining was carried out to detect the generation of reactive oxygen species (ROS). A validated, high-sensitivity real-time quantitative telomeric repeat amplification protocol (RQ-TRAP) was applied to determine telomerase activity in HUVECs, and a CCK-8 assay was employed to measure cellular viability. Results AngII induced an increase in SA-β-Gal-positive cells and upregulation on expression of P21 and PAI-1 compared to the control group (p < 0.05), while apelin against this process (p < 0.05). The protective effects were attenuated when APJ, AMPK and SIRT1 expression was knocked down (p < 0.05). Furthermore, apelin reduced AngII-induced ROS generation and enhanced telomerase activity in HUVECs (p < 0.05), which contributed to increased HUVEC viability as assessed by the CCK-8 assay (p < 0.05). Conclusions The apelin/APJ axis improved AngII-induced HUVEC senescence via the AMPK/SIRT1 signaling pathway, and the underlying mechanisms might be associated with reduced ROS production and enhanced telomerase activity.

Hyperglycemia, as well as diabetes mellitus, has been shown to impair ATP-sensitive K+ (KATP) channels in human vascular smooth muscle cells. Hydrogen sulfide (H2S) is also known to be an opener of KATP channels. We previously demonstrated the cardioprotective effects exerted by H2S against high-glucose (HG, 35 mM glucose)-induced injury in H9c2 cardiac cells. As such, we hypothesized that KATP channels play a role in the cardioprotective effects of H2S against HG-induced injury. In this study, to examine this hypothesis, H9c2 cardiac cells were treated with HG for 24 h to establish a model of HG-induced insults. Our findings revealed that treatment of the cells with HG markedly decreased the expression level of KATP channels. However, the decreased expression of KATP channels was reversed by the treatment of the cells with 400 µM sodium hydrogen sulfide (NaHS, a donor of H2S) for 30 min prior to exposure to HG. Additionally, the HG-induced cardiomyocyte injuries, including cytotoxicity, apoptosis, oxidative stress and mitochondrial damage, were ameliorated by treatment with NaHS or 100 µM diazoxide (a mitochondrial KATP channel opener) or 50 µM pinacidil (a non-selective KATP channel opener) for 30 min prior to exposure to HG, as indicated by an increase in cell viability, as well as a decrease in the number of apoptotic cells, the expression of cleaved caspase-3, the generation of reactive oxygen species (ROS) and the dissipation of mitochondrial membrane potential (MMP). Notably, treatment of the H9c2 cardiac cells with 100 µM 5-hydroxydecanoic acid (5-HD, a mitochondrial KATP channel blocker) or 1 mM glibenclamide (Gli, a non-selective KATP channel blocker) for 30 min prior to treatment with NaHS and exposure to HG significantly attenuated the above-mentioned cardioprotective effects exerted by NaHS. Notably, treatment of the cells with 500 µM N-acetyl‑L‑cysteine (NAC, a scavenger of ROS) for 60 min prior to exposure to HG markedly reduced the HG-induced inhibitory effect on the expression of KATP channels. Taken together, our results suggest that KATP channels play an important role in the cardioprotective effects of exogenous H2S against HG-induced injury. This study also provides novel data demonstraring that there is an antagonistic interaction between ROS and KATP channels in HG-exposed H9c2 cardiac cells.

With data sets of germination percent and storage time of seed lot of wheat and sorghum stored at three different storage temperature(t, °C) with three different water content (m, %) of seeds, together with data set of buckwheat and lettuce reported in literatures, the possibility that seed survival curve were transformed into line by survival proportion and the relationship that logarithm of average viability period (logp50) and standard deviation of seed death distribution in time (δ)with t, m and interaction between t and m were analysed. Result indicated that survival proportion transformed seed survival curve to line were much easier than the probability adopted by Ellis and Roberts, and the most important factor affecting logp50 and δ of seed lot was interaction between t and m. Thus, Ellis and Roberts viability model were suggested to be improved as Ki=Vi-p/10K-CWT (t×m) to predict longevity of seed lot with initial germination percent unknown, a new model of Gi/G0=A-P/10K-CWT(t×m) was constructed to predict longevity of seed lot with initial germination percent already known.

Congestion control has become a research hotspot, because of the rapid growth of Internet. Random Early Detection (RED) algorithm is the most effective active queue management (AQM) techniques. This paper describes RED algorithm and its derivatives then presents a new algorithm. The packet-marking probability linearly with the average queue length is improper for the arrival packet at the gateway. So we present an improved algorithm named SW-RED, which can adjust weight dynamically and make the packet-marking more reasonable. Simulations by NS2 show that SW-RED has better performance and stability comparing with RED.