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951.
In Vietnam's coastal wetlands, fluoroquinolones, a widely used class of antibiotics in shrimp farming, are frequently detected in sediments of former shrimp farms. This phenomenon could lead to negative impacts on the aquatic ecosystem, since the antibiotic residues could induce changes in the microorganism communities of the water body. The potential of native wetland plants (Acrostichum aureum L. and Rhizophora apiculata Blume Fl. Javae) for phytoremediation of fluoroquinolones (ciprofloxacin and norfloxacin) was investigated. The half-life for each antibiotic was estimated at approximately 10 days in the planted sediment. With respect to the accumulation of ciprofloxacin and norfloxacin in plants, these antibiotics were found mainly in roots. Antibiotic translocation from root to stem and leaves occurred at a low rate. The results showed that A. aureum and R. apiculata can be valuable for the phytoremediation of antibiotic-contaminated sediments. Additionally, the initial findings of the presence of resistant bacteria indicated that bacteria could play a role in facilitating the phytodegradation.  相似文献   
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Endothelial progenitor cells (EPCs) play an important role in angiogenesis. However, they exist in limited numbers in the human body. This study was aimed to produce EPCs, for autologous transplantation, using direct reprogramming of skin fibroblasts under GMP-compliant conditions. Fibroblasts were collected and cultured from the skin in DMEM/F12 medium supplemented with 5% activated platelet-rich plasma and 1% antibiotic-antimycotic solution. They were then transfected with mRNA ETV2 and incubated in culture medium under hypoxia (5% oxygen) for 14 d. Phenotype analysis of transfected cells confirmed that single-factor ETV2 transfection successfully reprogrammed dermal fibroblasts into functional EPCs. Our results showed that ETV2 mRNA combined with hypoxia can give rise to functional EPCs. The cells exhibited functional phenotypes similar to endothelial cells derived from umbilical cord vein; they expressed CD31 and VEGFR2, and formed capillary-like structures in vitro. Moreover, these EPCs could significantly improve hindlimb ischemia in mouse models. Although the direct conversion efficacy was low (3.12 ± 0.98%), altogether our study demonstrates that functional EPCs can be produced from fibroblasts and can be used in clinical applications.  相似文献   
953.
Recently, we mapped genomic regions associated with resistance to wheat diseases and insensitivity to Pyrenophora tritici-repentis (Ptr) toxins using 81 historical and modern Canadian western spring wheat cultivars genotyped with genome-wide single nucleotide polymorphic (SNP) markers. Here, we investigate the frequency and effects of allelic variants of 50 markers associated with 16 candidate genes that regulate resistance to leaf rust (Puccinia triticina), yellow or stripe rust (P. striiformis f. sp. tritici), tan spot (P. tritici-repentis), and Ptr ToxA reaction in a subset of 70 of the 81 spring wheat cultivars. We evaluated the 70 cultivars in the field for all diseases except Ptr ToxA, which was evaluated in a greenhouse. Using Spearman rank correlation, stepwise discriminant analysis, and partial least squares regression, we identified between 4 and 11 markers as best predictors of each phenotypic trait. Overall, 23 of the 50 markers were associated with one or more of the phenotypic traits of which analysis of variance showed significant differences between allelic variants of 19 markers. In most analyses, markers for Lr34/Yr18 and Tsn1 loci were identified consistently as the best predictor of disease resistance and Ptr ToxA sensitivity, respectively. The same alleles from two Lr34/Yr18 diagnostic SNP markers (wMAS000003 and wMAS000004) not only decreased stripe rust scores up to 1.6 (on a 1 to 9 scale), but also increased grain yield up to 196 kg ha?1 without affecting maturity. Results from this study could aid spring wheat breeders in selecting the best parental combinations and/or marker-assisted selection to integrate disease resistance with early maturity and short stature.  相似文献   
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多基因植物表达载体的构建   总被引:9,自引:0,他引:9  
将功能互补的抗真菌病基因或抗虫基因共同转化水稻植株,可望获得既抗病又抗虫的转基因水稻植株,马铃薯蛋白酶抑制剂Ⅱ基因PinⅡ,苏云金杆菌毒蛋白CryⅠ(b)基因B.t.,以及PPT乙酰转移酶基因bar构建在一个载体上,水稻碱性几丁质酶基因RC24与大麦核糖体失活蛋白基因B-RIP构建在另一个载体上,两载体共同转化水稻植株的工作正在进行之中。Ⅱ  相似文献   
956.
朱道立 《动物学研究》2001,22(6):437-441
以细胞培养技术与自然凝胶电泳系统方法证明,在周围神经再生过程中,损伤的坐骨神经远侧端,即起衍生的靶器官诱导神经突起的定向生长。分析探讨与神经诱向性再生相关的活性因子,其结果提示在远侧端神经组织中出现的90kDa蛋白组分具有很强的诱向性作用,诱导神经突起在神经再生过程中能够准确地到达靶器官。由此说明雪旺细胞在神经再生过程中扮演着重要角色。  相似文献   
957.
Apatinib, a highly selective inhibitor of vascular endothelial growth factor receptor‐2 (VEGFR‐2), inhibits the angiogenesis of tumours. The function and mechanism of apatinib in oesophageal squamous cell carcinoma (ESCC) remain unknown. In present study, we found that the development of ESCC in patients was controlled by treatment of combination of apatinib and a chemotherapeutic drug. Moreover, apatinib efficiently promotes cell apoptosis, inhibits cell proliferation, invasion, epithelial‐mesenchymal transition (EMT) and activity of the Akt/mTOR pathway in ESCC cells. Western blot analysis showed that apatinib significantly increased vimentin protein levels, decreased Bcl2, matrix metalloproteinase 9 (MMP9), E‐cadherin, p‐Akt and p‐mTOR protein levels in ESCC cells. Furthermore, apatinib enhanced chemosensitivity of cytotoxic drugs paclitaxel (TAX), 5‐fluorouracil (5‐FU) and cisplatin (DDP) by upregulating expression of vimentin protein, and downregulating expression of Bcl2, MMP9 and E‐cadherin protein in vitro. Compared with single‐agent groups, the combination of apatinib with each chemotherapeutic drug significantly repressed tumour growth and angiogenesis through blocking the expression of Ki67 and VEGFR‐2 in vivo. Taken together, apatinib efficiently inhibits cell growth through blocking Bcl2 and Akt/mTOR pathway, and suppresses metastasis via inhibiting MMP9 and EMT in ESCC cells. Apatinib promoted antitumour effect of chemotherapeutic agents through promoting cell apoptosis and inhibiting EMT and angiogenesis in ESCC.  相似文献   
958.
We report the synthesis, binding affinities to the recombinant human somatostatin receptors, and structure‐activity relationship studies of compounds related to the cyclic hexapeptide, c‐[Pro6‐Phe7‐D‐Trp8‐Lys9‐Thr10‐Phe11], L‐363,301 (the numbering in the sequence refers to the position of the residues in native somatostatin). The Pro residue in this compound is replaced with the arylalkyl peptoid residues Nphe (N‐benzylglycine), (S)βMeNphe [(S)‐N‐[(α‐methyl)benzyl]glycine] or (R)βMeNphe [(R)‐N‐[(α‐methyl)benzyl]glycine] and l ‐1‐naphthylalanine is incorporated into either position 7 or 11 of the parent compound. The synthesis and binding data of the Nnal6 ([N‐naphthylmethyl]glycine) analog of L‐363,301 is also reported. The incorporation of the Nnal residue into position 6 of L‐363,301 resulted in an analog with weaker binding affinities to all hsst receptors but enhanced selectivity towards the hsst2 receptor compared with the parent compound. The other compounds bind effectively to the hsst2 receptor but show some variations in the binding to the hsst3 and hsst5 receptors resulting in different ratios of binding affinities to the hsst5 and hsst2 or hsst3 and hsst2, respectively. The incorporation of the Nphe residue into position 6 and the Nal residue into position 7 of L‐363,301 led to a compound which binds potently to the hsst2 and has increased selectivity towards this receptor (weaker binding to hsst3 and hsst5 receptors) compared with the parent compound. The analogs with β‐methyl chiral substitutions in the aromatic peptoid side chain and Nal in position 7 or 11 bind effectively to the hsst2 and hsst5 receptors. They exhibit similar ratios of binding affinities to the hsst5 and hsst2 receptors as observed for L‐363,301. There are however minor differences in binding to the hsst3 receptor among these analogs. These studies allow us to investigate the influence of additional hydrophobic groups on the binding activity to the isolated human somatostatin receptors and the results are important for the design of other somatostatin analogs. Copyright © 1999 European Peptide Society and John Wiley & Sons, Ltd.  相似文献   
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