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Syamal Roy

Researcher at Indian Institute of Chemical Biology

Publications -  119
Citations -  4292

Syamal Roy is an academic researcher from Indian Institute of Chemical Biology. The author has contributed to research in topics: Leishmania donovani & Visceral leishmaniasis. The author has an hindex of 34, co-authored 111 publications receiving 3679 citations. Previous affiliations of Syamal Roy include Massachusetts Institute of Technology & Council of Scientific and Industrial Research.

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Use of antimony in the treatment of leishmaniasis: current status and future directions.

TL;DR: It has been shown that some of the peroxovanadium compounds have Sb(V)-resistance modifying ability in experimental infection with Sb (V) resistant Leishmania donovani isolates in murine model, and vanadium compounds may be used in combination with S b(V) in the treatment of Sb.(V) resistance cases of kala-azar.
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Sodium Antimony Gluconate Induces Generation of Reactive Oxygen Species and Nitric Oxide via Phosphoinositide 3-Kinase and Mitogen-Activated Protein Kinase Activation in Leishmania donovani-Infected Macrophages

TL;DR: This study has provided the first evidence that SAG treatment induces activation of some important components of the intracellular signaling pathway, which results in an early wave of ROS- dependent parasite killing and a stronger late wave of NO-dependent parasite killing.
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Leishmania donovani Targets Dicer1 to Downregulate miR-122, Lower Serum Cholesterol, and Facilitate Murine Liver Infection

TL;DR: Restoration of miR-122 or Dicer1 levels in VL mouse liver increased serum cholesterol and reduced liver parasite burden and altered expression of lipid metabolic genes, many of which are direct or indirect targets of the liver-specific microRNA-122.
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Leishmania donovani suppresses activated protein 1 and NF-κB activation in host macrophages via ceramide generation: involvement of extracellular signal-regulated kinase

TL;DR: The induction of ceramide synthesis in host macrophages appears to be instrumental and one of the turning points leading to silencing of the macrophage antileishmanial responses.