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Träfflista för sökning "WFRF:(Mohan Pooja) "

Search: WFRF:(Mohan Pooja)

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1.
  • Kumar, A. Naresh, et al. (author)
  • Upgrading the value of anaerobic fermentation via renewable chemicals production : A sustainable integration for circular bioeconomy
  • 2022
  • In: Science of the Total Environment. - : Elsevier. - 0048-9697 .- 1879-1026. ; 806, part 1
  • Research review (peer-reviewed)abstract
    • The single bioprocess approach has certain limitations in terms of process efficiency, product synthesis, and effective resource utilization. Integrated or combined bioprocessing maximizes resource recovery and creates a novel platform to establish sustainable biorefineries. Anaerobic fermentation (AF) is a well-established process for the transformation of organic waste into biogas; conversely, biogas CO2 separation is a challenging and cost-effective process. Biological fixation of CO2 for succinic acid (SA) mitigates CO2 separation issues and produces commercially important renewable chemicals. Additionally, utilizing digestate rich in volatile fatty acid (VFA) to produce medium-chain fatty acids (MCFAs) creates a novel integrated platform by utilizing residual organic metabolites. The present review encapsulates the advantages and limitations of AF along with biogas CO2 fixation for SA and digestate rich in VFA utilization for MCFA in a closed-loop approach. Biomethane and biohydrogen process CO2 utilization for SA production is cohesively deliberated along with the role of biohydrogen as an alternative reducing agent to augment SA yields. Similarly, MCFA production using VFA as a substrate and function of electron donors namely ethanol, lactate, and hydrogen are comprehensively discussed. A road map to establish the fermentative biorefinery approach in the framework of AF integrated sustainable bioprocess development is deliberated along with limitations and factors influencing for techno-economic analysis. The discussed integrated approach significantly contributes to promote the circular bioeconomy by establishing carbon-neutral processes in accord with sustainable development goals.
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2.
  • Maxwell, Christopher A., et al. (author)
  • Interplay between BRCA1 and RHAMM Regulates Epithelial Apicobasal Polarization and May Influence Risk of Breast Cancer
  • 2011
  • In: PLoS Biology. - : Public Library of Science (PLoS). - 1545-7885 .- 1544-9173. ; 9:11
  • Journal article (peer-reviewed)abstract
    • Differentiated mammary epithelium shows apicobasal polarity, and loss of tissue organization is an early hallmark of breast carcinogenesis. In BRCA1 mutation carriers, accumulation of stem and progenitor cells in normal breast tissue and increased risk of developing tumors of basal-like type suggest that BRCA1 regulates stem/progenitor cell proliferation and differentiation. However, the function of BRCA1 in this process and its link to carcinogenesis remain unknown. Here we depict a molecular mechanism involving BRCA1 and RHAMM that regulates apicobasal polarity and, when perturbed, may increase risk of breast cancer. Starting from complementary genetic analyses across families and populations, we identified common genetic variation at the low-penetrance susceptibility HMMR locus (encoding for RHAMM) that modifies breast cancer risk among BRCA1, but probably not BRCA2, mutation carriers: n = 7,584, weighted hazard ratio ((w)HR) = 1.09 (95% CI 1.02-1.16), p(trend) = 0.017; and n = 3,965, (w)HR = 1.04 (95% CI 0.94-1.16), p(trend) = 0.43; respectively. Subsequently, studies of MCF10A apicobasal polarization revealed a central role for BRCA1 and RHAMM, together with AURKA and TPX2, in essential reorganization of microtubules. Mechanistically, reorganization is facilitated by BRCA1 and impaired by AURKA, which is regulated by negative feedback involving RHAMM and TPX2. Taken together, our data provide fundamental insight into apicobasal polarization through BRCA1 function, which may explain the expanded cell subsets and characteristic tumor type accompanying BRCA1 mutation, while also linking this process to sporadic breast cancer through perturbation of HMMR/RHAMM.
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