10 research outputs found

    Participatory on-farm evaluation of wheat genotypes

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    In wheat development programs, the evaluation and identification of superior genotypes  is the first and leading step in a crop improvement program. Coordinated Farmer’s Field Trial (CFFT) was conducted during the three successive wheat growing season of 2010/11, 2011/12 and 2012/13. In CFFT six different wheat genotypes were planted in different outreach sites of research stations of Nepal Agricultural Research Council (NARC) at varying geographical regions. CFFT was conducted according to standard recommended practices of wheat at farmers’ field with different sets of genotypes for Terai and hill. In CFFT for Terai Tar and Lower valley (TTL) under timely sown irrigated (TSI) condition wheat genotype NL 1073 produced the grain yield of 3695 kg/ha and under the timely sown rainfed (TSR) that was 2738 kg/ha in 2010/11. In 2011/12, wheat genotype NL 1073 had the highest recorded grain yield of 3691 kg/ha in mid western region which was followed by check variety Vijay in CFFT-TTL in 2011/12 in the same region. Similarly in 2012/13, check variety Vijay showed the highest grain yield of 3818 kg/ha and 3044 kg/ha followed by NL 1094 (2938 kg/ha and 3468 kg/ha) in TSR and TSI environments, respectively. In CFFT for Mid and High Hill (MHH) WK 1204 had the highest grain yield of 3967 kg/ha in TSI which was followed by NL 1008 with the yield of 3890 in 2010/11. In 2011/12 the highest mean grain yield was observed in WK 1204 (4242 kg/ha) followed by BL 3872 (3922 kg/ha). Similarly, in 2012/13 NL 1008 was the best genotypes on the basis of grain yield (3297 kg/ha) followed by NL 1055 (3131 kg/ha) under CFFT-MHH

    Topical Application of an Irreversible Small Molecule Inhibitor of Lysyl Oxidases Ameliorates Skin Scarring and Fibrosis

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    Scarring is a lifelong consequence of skin injury, with scar stiffness and poor appearance presenting physical and psychological barriers to a return to normal life. Lysyl oxidases are a family of enzymes that play a critical role in scar formation and maintenance. Lysyl oxidases stabilize the main component of scar tissue, collagen, and drive scar stiffness and appearance. Here we describe the development and characterisation of an irreversible lysyl oxidase inhibitor, PXS-6302. PXS-6302 is ideally suited for skin treatment, readily penetrating the skin when applied as a cream and abolishing lysyl oxidase activity. In murine models of injury and fibrosis, topical application reduces collagen deposition and cross-linking. Topical application of PXS-6302 after injury also significantly improves scar appearance without reducing tissue strength in porcine injury models. PXS-6302 therefore represents a promising therapeutic to ameliorate scar formation, with potentially broader applications in other fibrotic diseases

    Secreted factors from keloid keratinocytes modulate collagen deposition by fibroblasts from normal and fibrotic tissue: A pilot study

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    Interactions between keratinocytes and fibroblasts in the skin layers are crucial in normal tissue development, wound healing, and scarring. This study has investigated the role of keloid keratinocytes in regulating collagen production by primary fibroblasts in vitro. Keloid cells were obtained from removed patients’ tissue whereas normal skin cells were discarded tissue obtained from elective surgery procedures. Fibroblasts and keratinocytes were isolated, cultured, and a transwell co-culture system were used to investigate the effect of keratinocytes on collagen production using a ‘scar-in-a-jar’ model. Keloid fibroblasts produced significantly more collagen than normal skin fibroblasts in monoculture at the RNA, secreted protein, and stable fibrillar protein level. When keloid keratinocytes were added to normal skin fibroblasts, expression of collagen was significantly upregulated in most samples, but when added to keloid fibroblasts, collagen I production was significantly reduced. Interestingly, keloid keratinocytes appear to decrease collagen production by keloid fibroblasts. This suggests that signaling in both keratinocytes and fibroblasts is disrupted in keloid pathology
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