49 research outputs found

    Aquaporins: A promising target for drug development

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    10.1517/14728222.10.6.889Expert Opinion on Therapeutic Targets106889-909EOTT

    Optimisation of storage driven denitrification by using on-line specific oxygen uptake rate monitoring during SND in a SBR

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    This study builds on previous experience of maximising the formation of COD as poly-hydroxybutyrate (PHB) and now describes a feedback technique of preserving the use of PHB for denitrification resulting in enhanced nitrogen removal rather than allowing its wasteful oxidation by oxygen. The feedback technique uses on-line SOUR monitoring for detecting the end-point of nitrification and controlling the aerobic phase length accordingly. The laboratory SBR was operated such that all organic substrate (acetate) was rapidly converted to PHB, which then served as the electron donor for nitrogen removal via simultaneous nitrification and denitrification (SND) during the aerobic phase (up to 70% SND). During SBR cycling with a fixed aeration length (240 minutes), PHB was unnecessarily oxidised after ammonium depletion, resulting in little denitrification and poor total nitrogen removal (69%). However, when the aerobic phase length was controlled via the SOUR, up to 1.8 CmM PHB (58 mg L -1 COD) could be preserved, enabling improved total nitrogen removal (86%). The drop in the SOUR after ammonium depletion was a reproducible event that could be detected even when using raw wastewater and fresh activated sludge. The SOUR-control technique holds promise to build up PHB over a number of SBR cycles. While advanced oxygen-control is used for improved N-removal in several existing WWTPs, this study investigates the importance of oxygen control with relevance to PHB driven SND in sequencing batch reactors

    MicroRNAs Involved in Regulating Spontaneous Recovery in Embolic Stroke Model

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    10.1371/journal.pone.0066393PLoS ONE86e6639

    MiR-335 regulates Hif-1 alpha to reduce cell death in both mouse cell line and rat ischemic models

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    Hypoxia inducible factor-1α facilitates cellular adaptation to hypoxic conditions. Hence its tight regulation is crucial in hypoxia related diseases such as cerebral ischemia. Changes in hypoxia inducible factor-1α expression upon cerebral ischemia influence the expression of its downstream genes which eventually determines the extent of cellular damage. MicroRNAs are endogenous regulators of gene expression that have rapidly emerged as promising therapeutic targets in several diseases. In this study, we have identified miR-335 as a direct regulator of hypoxia inducible factor-1α and as a potential therapeutic target in cerebral ischemia. MiR-335 and hypoxia inducible factor-1α mRNA showed an inverse expression profile, both in vivo and in vitro ischemic conditions. Given the biphasic nature of hypoxia inducible factor-1α expression during cerebral ischemia, miR-335 mimic was found to reduce infarct volume in the early time (immediately after middle cerebral artery occlusion) of embolic stroke animal models while the miR-335 inhibitor appears to be beneficial at the late time of stroke (24 hrs after middle cerebral artery occlusion). Modulation of hypoxia inducible factor-1α expression by miR-335 also influenced the expression of crucial genes implicated in neurovascular permeability, cell death and maintenance of the blood brain barrier. These concerted effects, resulting in a reduction in infarct volume bring about a beneficial outcome in ischemic stroke
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