50 research outputs found

    PGPR in Managing Root Rot Disease and Enhancing Growth in Mandarin (Citrus reticulata Blanco.) Seedlings

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    Decline in general plant-health and fruit production in mandarin influenced by abiotic and biotic factors is a major threat to cultivars grown in Darjeeling and Sikkim hills. Fusarium root rot, caused by F. oxysporum, is one of the most serious diseases afflicted during early plant growth stage in Citrus. To address this, seven PGPR isolates - Pseudomonas poae (RMK03), Bacillus stratosphericus (RHS/CL-01), Ochrobactrum anthropi, Paenibacillus lentimorbus, Bacillus pumilus, Bacillus megaterium and Bacillus amyloliquefaciens were isolated from the rhizosphere of Citrus reticulata, C. limonia and Camellia sinensis, and used for evaluating their effect on growth of mandarin seedlings. Pseudomonas poae showed in vitro antagonism to Fusarium oxysporum. Better growth enhancement was noticed with P. poae, B. stratosphericus, O. anthropi and B. pumilus. Enhanced activity of chlorophyll, total protein, phenol, four major defense enzymeschitinase, β-1, 3-glucanase, peroxidase and phenyalanine ammonia lyase was observed upon application of PGPR. P. poae also suppressed root rot caused by Fusarium oxysporum. Use of PGPR, which promote growth besides reducing disease severity to some extent, may lead to use of eco-friendly approaches for controlling plant diseases

    Kernel quantile-based estimation of expected shortfall

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    Since its proposal as an alternative risk measure to value-at-risk (VaR), expected shortfall (ES) has attracted a great deal of attention in financial risk management, primarily owing to its coherent properties. Recently, there has been an upsurge of research on the estimation of ES from a nonparametric perspective. The focus of this paper is on a few kernel-based ES estimators, including jackknife-based bias-correction estimators that have theoretically been documented to reduce bias. Bias reduction is particularly effective in reducing the tail estimation bias as well as the consequential bias that arises in kernel smoothing and finite-sample fitting and, thus, serves as a natural approach to the estimation of extreme quantiles of asset price distributions. By taking advantage of ES as an integral of the quantile function, a new type of ES estimator is proposed. To compare the performance of the estimators, a series of comparative simulation studies are presented and the methods are applied to real data. An estimator that has an analytical form turned out to perform the best

    Balancing repair and tolerance of DNA damage caused by alkylating agents

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    Alkylating agents constitute a major class of frontline chemotherapeutic drugs that inflict cytotoxic DNA damage as their main mode of action, in addition to collateral mutagenic damage. Numerous cellular pathways, including direct DNA damage reversal, base excision repair (BER) and mismatch repair (MMR), respond to alkylation damage to defend against alkylation-induced cell death or mutation. However, maintaining a proper balance of activity both within and between these pathways is crucial for a favourable response of an organism to alkylating agents. Furthermore, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylating agent toxicity

    Transgenic Mice with Pancellular Enhanced Green Fluorescent Protein Expression in Primitive Hematopoietic Cells and All Blood Cell Progeny

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    Transgenic mice homogeneously expressing enhanced green fluorescence protein (EGFP) in primitive hematopoietic cells and all blood cell progeny, including erythrocytes and platelets, have not been reported. Given previous data indicating H2Kb promoter activity in murine hematopoietic stem cells (HSCs), bone marrow (BM), and lymphocytes, an H2Kb enhancer/promoter EGFP construct was used to generate transgenic mice. These mice demonstrated pancellular EGFP expression in both primitive BM Sca-1+Lin-Kit+ cells and side population (SP) cells. Additionally, all peripheral blood leukocytes subsets, erythrocytes, and platelets uniformly expressed EGFP strongly. Competitive BM transplantation assays established that transgenic H2Kb-EGFP HSCs had activity equivalent to wildtype HSCs in their ability to reconstitute hematopoiesis in lethally irradiated mice. In addition, immunohistochemistry revealed EGFP transgene expression in all tissues examined. This transgenic strain should be a useful reagent for both murine hematopoiesis studies and functional studies of specific cell types from particular tissues

    LacZ and interleukin-3 expression in vivo after retroviral transduction of marrow-derived human osteogenic mesenchymal progenitors.

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    Human marrow-derived mesenchymal progenitor cells (hMPCs), which have the capacity for osteogenic and marrow stromal differentiation, were transduced with the myeloproliferative sarcoma virus (MPSV)-based retrovirus, vM5LacZ, that contains the LacZ and neo genes. Stable transduction and gene expression occurred in 18% of cells. After culture expansion and selection in G418, approximately 70% of neo(r) hMPCs co-expressed LacZ. G418-selected hMPC retain their osteogenic potential and form bone in vivo when seeded into porous calcium phosphate ceramic cubes implanted subcutaneously into SCID mice. LacZ expression was evident within osteoblasts and osteocytes in bone developing within the ceramics 6 and 9 weeks after implantation. Likewise, hMPCs transduced with human interleukin-3 (hIL-3) cDNA, adhered to ceramic cubes and implanted into SCID mice, formed bone and secreted detectable levels of hIL-3 into the systemic circulation for at least 12 weeks. These data indicate that genetically transduced, culture-expanded bone marrow-derived hMPCs retain a precursor phenotype and maintain similar levels of transgene expression during osteogenic lineage commitment and differentiation in vivo. Because MPCs have been shown to differentiate into bone, cartilage, and tendon, these cells may be a useful target for gene therapy
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