Sanchita Ghosh

ORCID: 0000-0002-0261-460X
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About
Contact & Profiles
Research Areas
  • Effects of Radiation Exposure
  • Radiation Therapy and Dosimetry
  • Wireless Communication Networks Research
  • Hematopoietic Stem Cell Transplantation
  • Advanced Wireless Network Optimization
  • EEG and Brain-Computer Interfaces
  • Radiopharmaceutical Chemistry and Applications
  • Vitamin C and Antioxidants Research
  • Antioxidant Activity and Oxidative Stress
  • Advanced MIMO Systems Optimization
  • Free Radicals and Antioxidants
  • Advanced Memory and Neural Computing
  • Smart Grid Security and Resilience
  • PARP inhibition in cancer therapy
  • Cell death mechanisms and regulation
  • MicroRNA in disease regulation
  • Nanofluid Flow and Heat Transfer
  • Renal Diseases and Glomerulopathies
  • Fluid Dynamics and Turbulent Flows
  • Cloud Computing and Resource Management
  • Neuroscience and Neural Engineering
  • Mitochondrial Function and Pathology
  • Glutathione Transferases and Polymorphisms
  • Radioactive element chemistry and processing
  • Metal-Catalyzed Oxygenation Mechanisms

Homi Bhabha National Institute
2023-2025

Bhabha Atomic Research Centre
2023-2025

Uniformed Services University of the Health Sciences
2015-2024

Albert Einstein College of Medicine
2021-2024

Texas Tech University
2023-2024

University of Engineering & Management
2018-2024

Pacific Northwest National Laboratory
2024

National Institute of Allergy and Infectious Diseases
2024

Birla Institute of Technology, Mesra
2008-2023

Sharda University
2021-2023

Abstract Endoplasmic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological relevance and the mechanisms that compromise adaptive ER signalling in podocytes remain unknown. Here we show nuclear translocation of transcription factor spliced X-box binding protein-1 (sXBP1) selectively impaired DN, inducing activating factor-6 (ATF6) C/EBP homology protein (CHOP). Podocyte-specific genetic ablation XBP1 or inducible expression ATF6 mice aggravates DN....

10.1038/ncomms7496 article EN cc-by Nature Communications 2015-03-10

Materials and methods: To optimise its dose time regimen, gamma-tocotrienol (GT3) was injected subcutaneously (SC) at different doses into male CD2F1 mice [LD50/30 (lethal radiation that results in the mortality of 50% 30 days) 8.6 Gy with vehicle]. The were given 10.5, 11 11.5 cobalt-60 radiation, 30-day survival-protection determined. Time optimisation done by SC administration GT3 intervals before irradiation. Dose reduction factor (DRF) determined probit analysis using as end point six...

10.1080/09553000902985128 article EN International Journal of Radiation Biology 2009-01-01

Glomerular apoptosis may contribute to diabetic nephropathy (dNP), but the pathophysiologic relevance of this process remains obscure. Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) CIX caspase-3, -8, -10). Notably, despite reduction glomerular cell death caspase-3 activity by both inhibitors, only ameliorated dNP. Nephroprotection was associated with reduced renal caspase-1 inflammasome...

10.1681/asn.2015060676 article EN Journal of the American Society of Nephrology 2016-02-01

The search for treatments to counter potentially lethal radiation-induced injury over the past several decades has led development of multiple classes radiation countermeasures. However, date only granulocyte colony-stimulating factor (G-CSF; filgrastim, Neupogen)and pegylated G-CSF (pegfilgrastim, Neulasta) have been approved by United States Food and Drug Administration (FDA) treatment hematopoietic acute syndrome (ARS). Gamma-tocotrienol (GT3) demonstrated strong radioprotective efficacy...

10.1667/rr14127.1 article EN Radiation Research 2016-03-01

Established therapies for diabetic nephropathy (dNP) delay but do not prevent its progression. The shortage of established may reflect the inability to target tubular compartment. chemical chaperone tauroursodeoxycholic acid (TUDCA) ameliorates maladaptive endoplasmic reticulum (ER) stress signaling and experimental dNP. Additionally, TUDCA activates farnesoid X receptor (FXR), which is highly expressed in cells. We hypothesized that ER via FXR agonism specifically Indeed, induced expression...

10.1681/asn.2016101123 article EN Journal of the American Society of Nephrology 2017-07-10

We analyzed the radioprotective effects of gamma-tocotrienol (GT3) on hematopoietic stem cells (HSCs) and progenitor (HPCs) in sublethally irradiated mice. Flow cytometry analysis indicated that radiation depleted HPCs (c-Kit(+), Lin(-)) to 40% at days 2 4 after total-body irradiation (TBI) all treatment groups. The HPC numbers GT3-treated mice recovered almost completely (90%) day 7 but remained vehicle-treated (30%) even 13 TBI. An vitro colony-forming assay sorted HSCs (Lin(-), Sca1(+),...

10.1667/rr1824.1 article EN Radiation Research 2010-06-01

Ghosh, S. P., Perkins, M. W., Hieber, K., Kulkarni, S., Kao, T-C., Reddy, E. V. R., Maniar, M., Seed, T. and Kumar, K. Radiation Protection by a New Chemical Entity, Ex-RadTM : Efficacy Mechanisms. Radiat. Res. 171, 173–179 (2009).Ex-Rad™ is among series of small molecule kinase inhibitors developed for modifying cell cycle distribution patterns in cancer cells subjected to radiation therapy, it has been identified as potential candidate protection studies. We have investigated its...

10.1667/rr1367.1 article EN Radiation Research 2009-01-21

The aim of the present study was to assess recovery from hematopoietic and gastrointestinal damage by Ex-RAD®, also known as ON01210.Na (4-carboxystyryl-4-chlorobenzylsulfone, sodium salt), after total body radiation. In our previous study, we reported that Ex-RAD, a small-molecule radioprotectant, enhances survival mice exposed gamma radiation, prevents radiation-induced apoptosis measured inhibition protein 53 (p53) expression in cultured cells. We have expanded this determine best...

10.1093/jrr/rrs001 article EN cc-by-nc Journal of Radiation Research 2012-06-06

The goal of this study was to establish a model partial-body irradiation (PBI) sparing 2.5% the bone marrow (BM2.5-PBI) that accurately recapitulates radiological/nuclear exposure scenarios. Here we have reported which produces gastrointestinal (GI) damage utilizing clinical linear accelerator (LINAC) with precise dosimetry, can be used develop medical countermeasures (MCM) for GI acute radiation syndrome (ARS) under FDA animal rule. PBI (1 hind leg spared) developed in male and female...

10.1667/rade-23-00068.1 article EN Radiation Research 2023-11-28

Abstract Background Acute radiation syndrome (ARS) manifests after exposure to high doses of in the instances radiologic accidents or incidents. Facilitating regeneration bone marrow (BM), namely hematopoietic stem and progenitor cells (HSPCs), is key mitigating ARS multi-organ failure. JNJ-26366821, a PEGylated thrombopoietin mimetic (TPOm) peptide, has been shown as an effective medical countermeasure (MCM) treat hematopoietic-ARS (H-ARS) mice. However, activity TPOm on regulating BM...

10.1186/s13287-024-03734-z article EN cc-by Stem Cell Research & Therapy 2024-04-29

Enhancing therapeutic effectiveness is crucial for translating anticancer nanomedicines from laboratory to clinical settings. In this study, we have developed radioactive rhenium oxide nanoparticles encapsulated in human serum albumin ([188Re]ReOx-HSA NPs) concurrent radiotherapy (RT) and photothermal therapy (PTT), aiming optimize treatment outcomes. [188Re]ReOx-HSA NPs were synthesized by a controlled reduction of 188ReO4− HSA medium extensively characterized. The effect was demonstrated...

10.1007/s00259-025-07074-9 article EN cc-by-nc-nd European Journal of Nuclear Medicine and Molecular Imaging 2025-01-25

The threat of a nuclear attack has increased in recent years highlighting the benefit developing additional therapies for treatment victims suffering from Acute Radiation Syndrome (ARS). In this work, we evaluated impact PEGylated thrombopoietin mimetic peptide, JNJ-26366821, on mortality and hematopoietic effects associated with ARS mice exposed to lethal doses total body irradiation (TBI). JNJ-26366821 was efficacious as mitigator thrombocytopenia both CD2F1 C57BL/6 TBI cobalt-60 gamma-ray...

10.1038/s41598-022-07426-7 article EN cc-by Scientific Reports 2022-03-03

δ-Tocotrienol (DT3), a vitamin E isoform, is associated with strong antioxidant and immunomodulatory properties. We confirmed the potent activity in membrane systems showed that DT3 an effective radiation protector mitigator. (4 μM, P < 0.001) inhibited lipid peroxidation mouse liver microsomes nitric oxide (NO) formation (20 μM DT3, 0.01) RAW264.7 cells, murine alveolar macrophage line. In CD2F1 mice exposed to lethal total-body from 60Co γ-radiation source, single subcutaneous (s.c.)...

10.1667/rr2460.1 article EN Radiation Research 2011-03-24

We reported that microRNA-30c (miR-30c) plays a key role in radiation-induced human cell damage through an apoptotic pathway. Herein we further evaluated miR-30 expression and mechanisms of delta-tocotrienol (DT3), radiation countermeasure candidate, for regulating mouse model hematopoietic CD34+ cells. CD2F1 mice were exposed to 0 (control) or 7–12.5 Gy total-body gamma-radiation, cells irradiated with 0, 2 4 radiation. Single doses DT3 (75 mg/kg, subcutaneous injection μM culture)...

10.1371/journal.pone.0122258 article EN public-domain PLoS ONE 2015-03-27

We recently demonstrated that natural delta-tocotrienol (DT3) significantly enhanced survival in total-body irradiated (TBI) mice, and protected mouse bone marrow cells from radiation-induced damage through Erk activation-associated mTOR pathways. Here, we further evaluated the effects mechanisms of DT3 on acute gastrointestinal syndrome. (75-100 mg/kg) or vehicle was administered as a single subcutaneous injection to CD2F1 mice 24 h before 10-12 Gy (60)Co irradiation at dose rate 0.6 Gy/min...

10.1667/rr13398.1 article EN Radiation Research 2013-12-01
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