Temporal transcriptomics reveal the molecular mechanism of dormancy and germination regulated by temperature in Paris polyphylla seed

The mature seed of Paris polyphylla var.chinensis(PPC)is morphophysiologically dormant and develops differently under warm and cold temperatures.To elucidate the molecular mechanisms underlying temperature-dependent regulation of PPC seed dormancy and germination,we investigated the dynamic changes in PPC seed transcript levels under warm and cold temperature stratifications(WS and CS,respectively)by time-resolved RNA sequencing,focusing on genes related to hormone metabolism and signaling and cell wall remodeling(CWRM)and encoding transcription factors/regulators(TFs/TRs).A total of 48765 and 47836 differentially expressed genes(DEGs)were associated with WS and CS,respectively.Of these,17581 and 16652 DEGs,respectively,unique to WS and CS,and 5386 were common to both temperature stratifications across nine analyzed growth stages.The expression of hormone metabolism and signaling,TF/TR,and CWRM genes were closely associated with temperature.More genes related to gibberellin(GA),cytokinin,auxin,and brassinosteroid biosynthetic were upregulated in WS as compared to CS seeds,while genes related to dormancy release and germination were downregulated in WS seeds.However,only GA and abscisic acid levels were altered in PPC seeds breaking morphophysiological dormancy(MPD).Overall,37 TF and five TR families were upregulated whereas 24 TF and 16 TR families were downregulated in WS as compared to CS seeds.Most CWRM families were highly expressed under WS as compared to CS,suggesting that they promote endosperm weakening and embryo growth of WS seeds and facilitate MPD release and germination.A coexpression analysis revealed positive correlations between TFs/TRs and DEGs involved in hormone metabolism and signaling and CWRM.These results provided a basis for investigating the interaction between the endosperm and underdeveloped embryo in the regulation of PPC seed germination and seedling emergence.

Computational study of bubble coalescence/break-up behaviors and bubble size distribution in a 3-D pressurized bubbling gas-solid fluidized bed of Geldart A particles

A computational study was carried out on bubble dynamic behaviors and bubble size distributions in a pressurized lab-scale gas-solid fluidized bed of Geldart A particles.High-resolution 3-D numerical simulations were performed using the two-fluid model based on the kinetic theory of granular flow.A finegrid,which is in the range of 3–4 particle diameters,was utilized in order to capture bubble structures explicitly without breaking down the continuum assumption for the solid phase.A novel bubble tracking scheme was developed in combination with a 3-D detection and tracking algorithm(MS3 DATA)and applied to detect the bubble statistics,such as bubble size,location in each time frame and relative position between two adjacent time frames,from numerical simulations.The spatial coordinates and corresponding void fraction data were sampled at 100 Hz for data analyzing.The bubble coalescence/break-up frequencies and the daughter bubble size distribution were evaluated by using the new bubble tracking algorithm.The results showed that the bubble size distributed non-uniformly over cross-sections in the bed.The equilibrium bubble diameter due to bubble break-up and coalescence dynamics can be obtained,and the bubble rise velocity follows Davidson’s correlation closely.Good agreements were obtained between the computed results and that predicted by using the bubble break-up model proposed in our previous work.The computational bubble tracking method showed the potential of analyzing bubble motions and the coalescence and break-up characteristics based on time series data sets of void fraction maps obtained numerically and experimentally.

钠离子电池O3型层状氧化物正极的现状与展望:稳定性、可逆性及其反应机理

近年来,钠离子二次电池(SIBs)正逐渐成为研究的焦点.正极材料是决定SIBs性能的关键因素之一,对于高性能SIBs商业化至关重要. O3相层状过渡金属氧化物在能量密度、工作电压和合成成本方面具有独特优势,是目前最受关注的商业化钠离子正极材料.然而O3相材料在实际应用过程中依然存在着较大的缺陷,包括充放电循环中结构相变不可逆, Na^(+)扩散势垒高和空气稳定性差等问题.本文从材料组成结构、相变演化、反应机制和改性策略及其所面临的挑战等方面对典型的O3相钠离子层状材料研究现状进行全面总结及评述,并对其未来的发展趋势进行展望.

Correlation between Expression of DcR3 on Tumor Cells and Sensitivity to FasL

To investigate the correlation between sensitivity to Fas ligand （FasL） and expression level of decoy receptor 3 （DcR3） on tumor cell surface, Fas/DcR3 mRNA expression was detected by RT-PCR. Anti-DcR3 mAb was used to detect expression level of DcR3 on surface of tumor cells by flow cytometry. Caspase-8, caspase-9, caspase-3, Bcl-2 expressions were analyzed by Western blot, respectively. Sensitivity to apoptosis induced by FasL was determined by Annexin V apoptosis kit. The expressions of DcR3 on the surface of tumor cells from high to low were approximately 35.3% in BGC823 cells, and 21.6% in MCF-7 cells, respectively. The apoptotic rates induced by FasL from low to high were 15.6% in BGC823 cells, and 58.2% in MCF-7 cells, respectively. There was a significant correlation between the expression levels of DcR3 with FasL-inducing apoptosis. Cellular ＆ Molecular Immunology.

Combination of Human Fas （CD95/Apo-1） Ligand with Adriamycin Significantly Enhances the Efficacy of Antitumor Response

The prognosis of hepatocellular carcinoma （HCC） is poor, even with the combined treatment of curative resection and adjuvant chemoradiotherapy. To solve this problem, many biologic therapies have been investigated. Fas ligand （FasL, CD95L） is mainly expressed in activated T lymphocytes and natural killer （NK） cells, and plays a central role in both cell-mediated immunity and immune downregulation. Several studies have shown that FasL is expressed in HCC. In the present report, we prepared recombinant human pET-22b（＋）/FasL protein and investigated the effect of FasL on HCC cells in vitro and on tumor growth in a murine HCC tumor model. The well-known cytotoxic chemotherapeutic reagent adriamycin （ADM） served as a control. We found that FasL effectively suppressed the viability of H22 tumor cells and significantly induced the apoptosis of H22 cells. The apoptotic levels of cells treated with FasL-ADM were significantly higher than those treated with FasL or ADM alone, and the FasL-ADM combination resulted in a more than additive effect on tumor growth delay in this model. The results suggested that combined treatment of FasL and other chemotherapeutic agents may be a new approach to improve the efficacy of chemotherapy for HCC.

Induction of Tumor Cell Apoptosis via Fas/DR5

The apoptosis inducing effects on tumor cell lines MGC803, BEL7402 and HL60 by Fas ligand and anti-human DR5 monoclonal antibodies （anti-DR5 mAb） and the underlying mechanism was studied. Fas/DR5 mRNA was detected by RT-PCR. Cytotoxicity exerted by FasL/anti-DR5 mAb on tumor cell lines was measured by MTT assay and the induced apoptosis was determined by agarose gel electrophoresis. Flow cytometry was employed to analyze the mode of cell death. The mRNA expression of DR5 in MGC803 and BEL7402 cells after giving anti-DR5 mAb was up-regulated compared with control group, while it was down-regulated in HL60 cells in the same condition. The mRNA expression of Fas in HL60 was higher after giving FasL compared with control group, while it was lower in MGC803 and BEL7402. MGC803 and BEL7402 were sensitive to anti-DR5 mAb but partially to FasL, and HL60 was sensitive to FasL but less sensitive to anti-DR5 mAb. Apoptosis induced by Fas ligand and anti-DR5 mAb vary among tumor cell lines. The underlying mechanism may be relevant to Fas/DR5 mRNA expression, which was presented as the release of caspase-8 and Bcl-2.

RGD-FasL Induces Apoptosis in Hepatocellular Carcinoma

Despite impressive results obtained in animal models, the clinical use of Fas ligand （FasL） as an anticancer drug is limited by severe toxicity. Systemic toxicity of death ligands may be prevented by using genes encoding membrane-bound death ligands and by targeted transgene expression through either targeted transduction or targeted transcription. Selective induction of tumor cell death is a promising anticancer strategy. A fusion protein is created by fusing the extracellular domain of Fas ligand （FasL） to the peptide arginine-glycine-aspartic acid （RGD） that selectively targets avβ-integrins on tumor endothelial cells. The purpose of this study is to evaluate the effects of RGD-FasL on tumor growth and survival in a murine hepatocellular carcinoma （HCC） tumor model. Treatment with RGD-FasL displaying an obvious suppressive effect on the HCC tumor model as compared to that with FasL （p 〈 0.05） and resulted in a more additive effect on tumor growth delay in this model. RGD-FasL treatment significantly enhanced mouse survival and caused no toxic effect, such as weight loss, organ failure, or other treatment-related toxicities. Apoptosis was detected by flow cytometric analysis and TUNEL assays; those results also showed that RGD-FasL is a more potent inducer of cell apoptosis for H22 and H9101 cell lines than FasL （p 〈 0.05）. In conclusion, RGD-FasL appears to be a low-toxicity selective inducer of tumor cell death, which merits further investigation in preclinical and clinical studies. Furthermore, this approach offers a versatile technology for complexing target ligands with therapeutic recombinant proteins. To distinguish the anti-tumor effects of FasL in vivo, tumor and liver tissues were harvested to examine for evidence of necrotic cells, tumor cells, or apoptotic cells by Hematoxylin and eosin （H＆E） staining.

Expression of rabbit defensin NP-1 gene in transgenic tobacco plants and its activity against bacterial wilt

A cDNAderived 200 bp fragment encoding a rabbit defensin NP1 mature peptide was ligated into the GUSless pBI121 to yield pBIC35NP1. Tobacco leaf discs were genetically transformed with an Agrobacterium tumefaciens strain harbouring pBIC35NP1. Northern blot analysis showed that the defensin NP1 expression cassette was normally transcribed in transgenic plants. Resistance tests demonstrated that expression of native defensin NP1 can confer partial resistance to the bacterial wilt pathogen, Ralstonia solanacearum.