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Namratta Manhas

Researcher at Central Drug Research Institute

Publications -  5
Citations -  787

Namratta Manhas is an academic researcher from Central Drug Research Institute. The author has contributed to research in topics: Neuroprotection & Brain ischemia. The author has an hindex of 5, co-authored 5 publications receiving 741 citations. Previous affiliations of Namratta Manhas include Sanjay Gandhi Post Graduate Institute of Medical Sciences.

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Molecular targets in cerebral ischemia for developing novel therapeutics.

TL;DR: The current status on the molecular mechanisms of stroke pathophysiology is covered with an endeavour to identify potential molecular targets such as targeting postsynaptic density-95 (PSD-95)/N-methyl-d-aspartate (NMDA) receptor interaction, certain key proteins involved in oxidative stress, CaMKs and MAPKs (ERK, p38 and JNK) signalling, inflammation and cell death pathways.
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Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia.

TL;DR: Application of a cell-permeable STEP-derived peptide that is resistant to degradation and binds to p38 MAPK protects cultured neurons from hypoxia-reoxygenation injury and reduces ischemic brain damage when injected up to 6 h after the insult.
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Hyperthyroidism induces apoptosis in rat liver through activation of death receptor-mediated pathways

TL;DR: Hyperthyroidism-induced apoptosis in rat liver involves the activation of death receptor-mediated pathways, including p75NTR, a member of tumor necrosis factor (TNF) receptor superfamily, in rat Liver.
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Inhibiting the Na+/H+ exchanger reduces reperfusion injury: a small animal MRI study.

TL;DR: High resolution T2 images can be used for consistent and precise calculation of lesion volumes, while changes of DWI are a sensitive early marker of ischemic injury.
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Energy metabolism during cutaneous wound healing in immunocompromised and aged rats.

TL;DR: The results suggest that significant alterations in the activities of energy metabolizing enzymes in the granulation tissues in both immunocompromised as well as in aged rats may overall affect the energy availability for cellular activity needed for repair process.