7 research outputs found

    Prioritization and Conservation of Himalayan Medicinal Plants: Angelica glauca Edgew. as a Case Study

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    The present study broadly supports the need for conservation initiatives for Himalayan medicinal plants. An approach is set up for prioritization grading of the importance of medicinal plants that is based upon the knowledge of local communities about the species. The study of Himalayan medicinal plants in general and Angelica glauca Edgew. in particular reveals that the utilization pattern, traditional knowledge base and trade of medicinal plants show trends that are not ideal for sustainability in the Indian Himalaya. The research attempts to integrate the analysis of several aspects of Himalayan trade in medicinal plants to reveal the threat to the plants and to suggest ways to overcome the problem

    Full Length Research Paper Assessment of status and biomass of Swertia angustifolia: a high value Himalayan medicinal plant

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    Studies on population assessment and biomass variation in selected populations of Swertia angustifolia were undertaken in west Himalaya. Low population density across the surveyed populations indicates poor availability of the species in study area. Species showed random distribution and higher frequency of occurrence in most of the population, which is the indicator of better potential of the spe-cies in these sites. Density was positively correlated with biomass. The biomass showed peak value in senescence phase and thus has positive consequences of harvesting for the survival of the species

    Sensitive allele specific oligonucleotide-polymerase chain reaction in detection of preexisting mutations in imatinib-resistant chronic myelogenous leukemia patients: A retrospective analysis

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    Introduction: Pre-existing BCR-ABL kinase domain mutation leads to Imatinib resistance. Methods: Retrospective analysis of 50 patients of Imatinib resistance was done in GCRI, from January 2014 till May 2014. Allelle Specific Oligonucleotide–Polymerase Chain Reaction (ASO-PCR) was performed on Genomic DNA, of peripheral blood mononuclear cells (PBMCs). Results: 47 (94%) were in Chronic phase, 2 (4%) in accelerated phase, 1 (2%) in blastic crisis. Median duration of Imatinib was 48 months. 43/50 had one or more than 1 mutation, T315I mutation in 5 (10%) patients, M351T in 32% (16/50) and F311L in 8. Conclusion: We report low cytogenetic response (25%) and durability of response to 600 mg of Imatinib, even in M351T mutation

    Disabling complement regulatory activities of vaccinia virus complement control protein reduces vaccinia virus pathogenicity

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    Poxviruses encode a repertoire of immunomodulatory proteins to thwart the host immune system. One among this array is a homolog of the host complement regulatory proteins that is conserved in various poxviruses including vaccinia (VACV) and variola. The vaccinia virus complement control protein (VCP), which inhibits complement by decaying the classical pathway C3-convertase (decay-accelerating activity), and by supporting inactivation of C3b and C4b by serine protease factor I (cofactor activity), was shown to play a role in viral pathogenesis. However, the role its individual complement regulatory activities impart in pathogenesis, have not yet been elucidated. Here, we have generated monoclonal antibodies (mAbs) that block the VCP functions and utilized them to evaluate the relative contribution of complement regulatory activities of VCP in viral pathogenesis by employing a rabbit intradermal model for VACV infection. Targeting VCP by mAbs that inhibited the decay-accelerating activity as well as cofactor activity of VCP or primarily the cofactor activity of VCP, by injecting them at the site of infection, significantly reduced VACV lesion size. This reduction however was not pronounced when VCP was targeted by a mAb that inhibited only the decay-accelerating activity. Further, the reduction in lesion size by mAbs was reversed when host complement was depleted by injecting cobra venom factor. Thus, our results suggest that targeting VCP by antibodies reduces VACV pathogenicity and that principally the cofactor activity of VCP appears to contribute to the virulence
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