Shah, Pranali Nitin

[["dc.bibliographiccitation.firstpage","1179"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Insect Physiology"],["dc.bibliographiccitation.lastpage","1184"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Ganter, G. K."],["dc.contributor.author","Panaitiu, A. E."],["dc.contributor.author","Desilets, J. B."],["dc.contributor.author","Davis-Heim, J. A."],["dc.contributor.author","Fisher, E. A."],["dc.contributor.author","Tan, L. C. H."],["dc.contributor.author","Heinrich, Ralf"],["dc.contributor.author","Buchanan, E. B."],["dc.contributor.author","Brooks, K. M."],["dc.contributor.author","Kenney, M. T."],["dc.contributor.author","Verde, M. G."],["dc.contributor.author","Downey, J."],["dc.contributor.author","Adams, A. M."],["dc.contributor.author","Grenier, Julien"],["dc.contributor.author","Maddula, S."],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Kincaid, K. M."],["dc.contributor.author","O'Brien, J. R. M."],["dc.date.accessioned","2018-11-07T08:52:07Z"],["dc.date.available","2018-11-07T08:52:07Z"],["dc.date.issued","2011"],["dc.description.abstract","Temperature-dependent induction of ecdysteroid deficiency in the ecdysoneless mutant ecd(1) adult Drosophila melanogaster results in altered courtship behavior in males. Ecdysteroid deficiency brings about significantly elevated male-male courtship behavior including song production resembling that directed toward females. Supplementation with dietary 20-hydroxyecdysone reduces male-male attraction, but does not change motor activity, courtship patterns or attraction to females. These observations support the hypothesis that reduced levels of ecdysteroids increase the probability that male fruit flies will display courtship behaviors to male stimuli. (C) 2011 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.jinsphys.2011.05.007"],["dc.identifier.isi","000295441700001"],["dc.identifier.pmid","21704633"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22094"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0022-1910"],["dc.title","Drosophila male courtship behavior is modulated by ecdysteroids"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.journal","Experimental Hematology"],["dc.bibliographiccitation.lastpage","45"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Boieri, Margherita"],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Jalapothu, Dasaradha"],["dc.contributor.author","Zaitseva, Olena"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Rolstad, Bent"],["dc.contributor.author","Naper, Christian"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Inngjerdingen, Marit"],["dc.date.accessioned","2018-11-07T10:23:07Z"],["dc.date.available","2018-11-07T10:23:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Acute graft-versus-host disease (aGvHD) remains a significant hurdle to successful treatment of many hematological disorders. The disease is caused by infiltration of alloactivated donor T cells primarily into the gastrointestinal tract and skin. Although cytotoxic T cells mediate direct cellular damage, T helper (Th) cells differentially secrete inununoregulatory cytokines. aGvHD is thought to be initiated primarily by Thl cells but a consensus is still lacking regarding the role of Th2 and Th17 cells. The aim of this study was to determine the contribution of distinct T-cell subsets to aGvHD in the rat. aGvHD was induced by transplanting irradiated rats with T-cell depleted major histocompatibility complex-mismatched bone marrow, followed 2 weeks later by donor lymphocyte infusion. Near complete donor T-cell chimerism was achieved in the blood and lymphatic tissues, in contrast to mixed chimerism in the skin and gut. Skin and gut donor T cells were predominantly CD4(+), in contrast to T cells in the blood and lymphatic tissues. Genes associated with Th1 cells were upregulated in gut, liver, lung, and skin tissues affected by aGvHD. Increased serum levels of CXCL10 and IL-18 preceded symptoms of aGvHD, accompanied by increased responsiveness to CXCL10 by blood CD4(+) T cells. No changes in the expression of Th2- or Th17-associated genes were observed, indicating that aGvHD in this rat model is mainly Thl driven. The rat model of aGvHD could be instrumental for further investigations of donor T-cell subsets in the skin and gut and for exploring therapeutic options to ameliorate symptoms of aGvHD. Copyright (C) 2017 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc."],["dc.description.sponsorship","European Union [FP7-PEOPLE-2012-ITN-315963]"],["dc.identifier.doi","10.1016/j.exphem.2017.02.002"],["dc.identifier.isi","000403302300005"],["dc.identifier.pmid","28238806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42397"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1873-2399"],["dc.relation.issn","0301-472X"],["dc.title","Rat acute GvHD is Th1 driven and characterized by predominant donor CD4(+) T-cell infiltration of skin and gut"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1028850"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Matos, Carina"],["dc.contributor.author","Mamilos, Andreas"],["dc.contributor.author","Shah, Pranali N."],["dc.contributor.author","Meedt, Elisabeth"],["dc.contributor.author","Weber, Daniela"],["dc.contributor.author","Ghimire, Saroj"],["dc.contributor.author","Hiergeist, Andreas"],["dc.contributor.author","Gessner, André"],["dc.contributor.author","Dickinson, Anne"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Ghimire, Sakhila"],["dc.date.accessioned","2022-12-01T08:31:31Z"],["dc.date.available","2022-12-01T08:31:31Z"],["dc.date.issued","2022"],["dc.description.abstract","The vitamin D receptor (VDR) is critical in regulating intestinal homeostasis and emerging evidence demonstrates that VDR deficiency is a critical factor in inflammatory bowel disease pathology. However, no clinical data exist regarding the intestinal expression of VDR in patients after allogeneic haematopoietic stem cell transplantation (HSCT). Analyzing intestinal biopsies from 90 patients undergoing HSCT with mortality follow-up, we demonstrated that patients with severe acute gastrointestinal graft versus host disease (GI-GvHD) showed significant downregulation of VDR gene expression compared to mild or no acute GI-GvHD patients (p = 0.007). Reduced VDR expression was already detectable at acute GI-GvHD onset compared to GvHD-free patients (p = 0.01). These results were confirmed by immunohistochemistry (IHC) where patients with severe acute GI-GvHD showed fewer VDR+ cells (p = 0.03) and a reduced VDR staining score (p = 0.02) as compared to mild or no acute GI-GvHD patients. Accordingly, low VDR gene expression was associated with a higher cumulative incidence of treatment-related mortality (TRM) (p = 1.6x10-6) but not with relapse-related mortality (RRM). A multivariate Cox regression analysis identified low VDR as an independent risk factor for TRM (p = 0.001, hazard ratio 4.14, 95% CI 1.78-9.63). Furthermore, VDR gene expression significantly correlated with anti-microbial peptides (AMPs) gene expression (DEFA5: r = 0.637, p = 7x10-5, DEFA6: r 0 0.546, p = 0.001). In conclusion, our findings suggest an essential role of the VDR in the pathogenesis of gut GvHD and the prognosis of patients undergoing HSCT."],["dc.identifier.doi","10.3389/fimmu.2022.1028850"],["dc.identifier.pmid","36341397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118189"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Downregulation of the vitamin D receptor expression during acute gastrointestinal graft versus host disease is associated with poor outcome after allogeneic stem cell transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","195"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics Part A"],["dc.bibliographiccitation.lastpage","199"],["dc.bibliographiccitation.volume","140A"],["dc.contributor.author","Mueller, A."],["dc.contributor.author","Schackert, Hans K."],["dc.contributor.author","Lange, B."],["dc.contributor.author","Ruschoff, J."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Willert, J."],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Becker, H."],["dc.contributor.author","Epplen, J. T."],["dc.contributor.author","Stemmler, S."],["dc.date.accessioned","2018-11-07T10:19:50Z"],["dc.date.available","2018-11-07T10:19:50Z"],["dc.date.issued","2006"],["dc.description.abstract","Hereditary non-polyposis colorectal cancer (HNPCC) syndrome is caused by heterozygous germline mutations in DNA mismatch repair genes (MMR), (MSH2, MLH1, MSH6. and PMS2) and it is inherited in an autosomal dominant pattern with high penetrance. Several patients have been reported carrying bi-allelic MMR gene mutations and whose phenotype resembled a syndrome with childhood malignancies including hematological malignancies, brain, and colorectal tumors. This phenotype is similar to the tumor spectrum of MMR knockout mice. Herein we describe two brothers of healthy consanguineous parents from Pakistan, who had developed two and three colorectal cancers at the ages of 11 and 12 years, respectively, and less than 30 polyps. Tumor specimens were microsatellite instable (MSI-H), and expression of MSH2 and MSH6 was lost. Mutation analyses of DNA samples from both patients revealed a novel homozygous c.2006-5T > A mutation in intron 12 of the MSH2 gene. This phenotype of the brothers is unusual as they neither develop hematological malignancies nor brain tumors at an older age of presentation than other patients with homozygous MSH2 mutations. The milder phenotype may be due to the expression of low amounts of MSH2 protein with reduced activity. (c) 2005 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/ajmg.a.31070"],["dc.identifier.isi","000235264400001"],["dc.identifier.pmid","16372347"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41747"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1552-4825"],["dc.title","A novel MSH2 germline mutation in homozygous state in two brothers with colorectal cancers diagnosed at the age of 11 and 12 years"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]