S
Susanta Mondal
Researcher at Rush University Medical Center
Publications - 29
Citations - 5247
Susanta Mondal is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: Encephalomyelitis & T cell. The author has an hindex of 14, co-authored 25 publications receiving 4675 citations. Previous affiliations of Susanta Mondal include Harvard University & Veterans Health Administration.
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Journal ArticleDOI
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
Sharon Maynard,Jiang Yong Min,Jaime R. Merchan,Kee-Hak Lim,Jianyi Li,Susanta Mondal,Towia A. Libermann,James P. Morgan,Frank W. Sellke,Isaac E. Stillman,Franklin H. Epstein,Vikas P. Sukhatme,S. Ananth Karumanchi +12 more
TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
Journal ArticleDOI
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) could contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
Sharon Maynard,Jiang-Yong Min,Jaime R. Merchan,Kee-Hak Lim,Jianyi Li,Susanta Mondal,Towia A. Libermann,James P. Morgon,Frank W. Sellke,Isaac E. Stillman,Franklin H. Epstein,Vikas P. Sukhatme,S. Ananth Karumanchi +12 more
TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
Journal ArticleDOI
Selective disruption of TLR2-MyD88 interaction inhibits inflammation and attenuates Alzheimer’s pathology
Suresh B. Rangasamy,Malabendu Jana,Avik Roy,Grant T. Corbett,Madhuchhanda Kundu,Sujyoti Chandra,Susanta Mondal,Sridevi Dasarathi,Elliott J. Mufson,Rama K. Mishra,Chi Hao Luan,David A. Bennett,Kalipada Pahan,Kalipada Pahan +13 more
TL;DR: WT TIDM peptide suppressed the disease process in mice with experimental allergic encephalomyelitis and collagen-induced arthritis and inhibited microglial activation induced by fibrillar A&bgr;1-42 and lipoteichoic acid, but not 1-methyl-4-phenylpyridinium, dsRNA, bacterial lipopolysaccharide, flagellin, or CpG DNA.
Journal ArticleDOI
Protection of Tregs, suppression of Th1 and Th17 cells, and amelioration of experimental allergic encephalomyelitis by a physically-modified saline.
TL;DR: RNS60 treatment exhibited immunomodulation and ameliorated adoptive transfer of experimental allergic encephalomyelitis, an animal model of MS, via Tregs and is suggested for therapeutic intervention in MS and other autoimmune disorders.
Journal ArticleDOI
Role of elongin-binding domain of von hippel lindau gene product on HuR-mediated VPF/VEGF mRNA stability in renal cell carcinoma
Kaustubh Datta,Susanta Mondal,Sutapa Sinha,Jinping Li,Enfeng Wang,Bertrand Knebelmann,S. Ananth Karumanchi,Debabrata Mukhopadhyay +7 more
TL;DR: The experiments presented here suggest that the association of the elongin-bindingdomain of VHL with a specific RNA-binding domain of HuR (RRM1) is important for the destabilizing function of V HL on VPF/VEGF mRNA.