Samir Kumar‐Singh

ORCID: 0000-0001-9466-6732
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Amyotrophic Lateral Sclerosis Research
  • SARS-CoV-2 and COVID-19 Research
  • Parkinson's Disease Mechanisms and Treatments
  • COVID-19 Clinical Research Studies
  • Antibiotic Resistance in Bacteria
  • Neurological diseases and metabolism
  • Occupational and environmental lung diseases
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • Prion Diseases and Protein Misfolding
  • Neurogenetic and Muscular Disorders Research
  • Parasite Biology and Host Interactions
  • Parasitic Diseases Research and Treatment
  • Dementia and Cognitive Impairment Research
  • Bacterial biofilms and quorum sensing
  • Long-Term Effects of COVID-19
  • Antimicrobial Resistance in Staphylococcus
  • Nosocomial Infections in ICU
  • Gut microbiota and health
  • Cholinesterase and Neurodegenerative Diseases
  • Medical Imaging and Pathology Studies
  • COVID-19 and healthcare impacts
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Ubiquitin and proteasome pathways
  • Computational Drug Discovery Methods

University of Antwerp
2016-2025

University of Medicine and Pharmacy of Craiova
2020

Central Pollution Control Board
2014

VIB-UAntwerp Center for Molecular Neurology
2006-2013

Virginia Commonwealth University
2012

Vlaams Instituut voor Biotechnologie
2000-2009

Mayo Clinic in Florida
2007

Hertie Institute for Clinical Brain Research
2007

German Center for Neurodegenerative Diseases
2006

University of Manchester
2006

We identified a novel plasmid-mediated colistin-resistance gene in porcine and bovine colistin-resistant Escherichia coli that did not contain mcr-1. The gene, termed mcr-2, 1,617 bp phosphoethanolamine transferase harboured on an IncX4 plasmid, has 76.7% nucleotide identity to Prevalence of mcr-2 E. (11/53) Belgium was higher than mcr-1 (7/53). These data call for immediate introduction screening ongoing molecular epidemiological surveillance Gram-negative pathogens.

10.2807/1560-7917.es.2016.21.27.30280 article EN cc-by Eurosurveillance 2016-07-07
Vivianna M. Van Deerlin Patrick Sleiman María Martínez-Lage Alice Chen‐Plotkin Li-San Wang and 95 more Neill R. Graff‐Radford Dennis W. Dickson Rosa Rademakers Bradley F. Boeve Murray Grossman Steven E. Arnold David Mann Stuart Pickering‐Brown Harro Seelaar Peter Heutink John C. van Swieten Jill R. Murrell Bernardino Ghetti Salvatore Spina Jordan Grafman John R. Hodges Maria Grazia Spillantini Sid Gilman Andrew P. Lieberman Jeffrey Kaye Randall L. Woltjer Eileen H. Bigio Marsel Mesulam Safa Al‐Sarraj Claire Troakes Roger N. Rosenberg Charles L. White Isidró Ferrer Albert Lladó Manuela Neumann Hans A. Kretzschmar Christine M. Hulette Kathleen A. Welsh‐Bohmer Bruce L. Miller Ainhoa Alzualde Adolfo López de Munain Ann C. McKee Marla Gearing Allan I. Levey James J. Lah John Hardy Jonathan D. Rohrer Tammaryn Lashley Ian R. Mackenzie Howard Feldman Ronald L. Hamilton Steven T. DeKosky Julie van der Zee Samir Kumar‐Singh Christine Van Broeckhoven Richard Mayeux Jean Paul Vonsattel Juan C. Troncoso Jillian J. Kril John B. Kwok Glenda M. Halliday Thomas D. Bird Paul G. Ince Pamela J. Shaw Nigel J. Cairns John C. Morris Catriona McLean Charles DeCarli William G. Ellis Stefanie H. Freeman Matthew P. Frosch John H. Growdon Daniel P. Perl Mary Sano David A. Bennett Julie A. Schneider Thomas G. Beach Eric M. Reiman Bryan K. Woodruff Jeffrey L. Cummings Harry V. Vinters Carol A. Miller Helena C. Chui Irina Alafuzoff Päivi Hartikainen Danielle Seilhean Douglas Galasko Eliezer Masliah Carl W. Cotman MJ Tuñón Mònica Martínez David G. Muñoz Steven L. Carroll Daniel Marson Peter Riederer Nenad Bogdanović Daniela Berg Hákon Hákonarson John Q. Trojanowski Virginia M.‐Y. Lee

10.1038/ng.536 article EN Nature Genetics 2010-02-14

Neuronal cytoplasmic and intranuclear aggregates of RNA-binding protein TDP-43 are a hallmark feature neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) frontotemporal lobar degeneration (FTLD). ALS FTLD show considerable clinical pathological overlap occur both familial sporadic forms. Though missense mutations in cause rare forms ALS, it is not yet known whether this due to loss function or gain aberrant function. Moreover, the role wild-type (WT) TDP-43, associated...

10.1073/pnas.0912417107 article EN Proceedings of the National Academy of Sciences 2010-02-04
Elisa Gentilotti Anna Górska Adriana Tami Roy Gusinow Massimo Mirandola and 95 more Jesús Rodríguez‐Baño Zaira R. Palacios‐Baena Elisa Rossi Jan Hasenauer Iris Lopes-Rafegas Elda Righi Natascia Caroccia Salvatore Cataudella Zeno Pasquini Thomas Osmo Lidia Del Piccolo Alessia Savoldi Samir Kumar‐Singh Fulvia Mazzaferri Maria Giulia Caponcello Gerolf de Boer Gabriel Levy Hara Pasquale De Nardo Surbhi Malhotra Lorenzo Maria Canziani Jade Ghosn Aline-Marie Florence Nadhem Lafhej Bernardina T.F. van der Gun Maddalena Giannella Cédric Laouénan Evelina Tacconelli Mariana Guedes Gaia Maccarrone Maria Diletta Pezzani Marcella Sibani Ruth Joanna Davies Stefania Vitali Giorgia Franchina Giorgia Tomassini Concetta Sciammarella Riccardo Cecchetto Davide Gibellini Chiara Konishi De Toffoli Giulia Rosini Chiara Perlini Marco Meroi Filippo Cioli Puviani Daniele Fasan Claudio Micheletto Stefania Montemezzi Nicolò Cardobi Gianluca Vantini Gloria Mazzali Giovanni Stabile Maddalena Marcanti Marco Pattaro Zonta D Calì Anna Mason Cinzia Perlini Paolo Gisondi Maria Mongardi Simona Sorbello Karin I. Wold María F. Vincenti‐González A.C.M. Veloo Valerie P. R. Harmsma Daniele Pantano Margriet van der Meer Lilli Gard Erley Lizarazo Marjolein Knoester Alex W. Friedrich Hubert G.M. Niesters Pierluigi Viale Domenico Marzolla Federica Cosentino Michela Di Chiara Giacomo Fornaro Cecilia Bonazzetti Beatrice Tazza Alice Toschi Oana Vetamanu Maria Eugenia Giacomini Filippo Trapani Lorenzo Marconi Luciano Attard Sara Tedeschi Liliana Gabrielli Tiziana Lazzarotto Paula Olivares Javier Castilla J. Velez Virginia Almadana Pacheco Lucía Martín-Barrera Ana Belén Martín-Gutiérrez David Gutiérrez-Campos Marta Fernández-Regaña Ana Silva-Campos Patricia Fernández‐Riejos

Lack of specific definitions clinical characteristics, disease severity, and risk preventive factors post-COVID-19 syndrome (PCS) severely impacts research discovery new therapeutics drugs.This prospective multicenter cohort study was conducted from February 2020 to June 2022 in 5 countries, enrolling SARS-CoV-2 out- in-patients followed at 3-, 6-, 12-month diagnosis, with assessment biochemical features, antibody (Ab) response, Variant Concern (VoC), physical mental quality life (QoL)....

10.1016/j.eclinm.2023.102107 article EN cc-by EClinicalMedicine 2023-07-21

The varied ways in which mutations presenilins (PSEN1 and PSEN2) affect amyloid b precursor protein (APP) processing causing early-onset familial Alzheimer disease (FAD) are complex not yet properly understood. Nonetheless, one useful diagnostic marker is an increased ratio of Ab42 to Ab40 (Ab42/Ab40) patients' brain biological fluids as well transgenic mice cells. We studied Ab APP for a set nine clinical PSEN on novel highly reproducible enzyme-linked immunosorbent assay (ELISA)-based...

10.1002/humu.20336 article EN Human Mutation 2006-06-02

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, present here the first comprehensive analysis of these cases in terms neuropathology, genetics, demographics clinical data. 92% (34/37) had fused sarcoma (FUS) pathology, indicating that FTLD-FUS is important FTLD subtype. This collection specifically focussed on aFTLD-U one three recently defined subtypes FTLD-FUS. The subtype...

10.1007/s00401-010-0698-6 article EN cc-by-nc Acta Neuropathologica 2010-05-19

Abstract Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding microtubule‐associated protein tau (MAPT). However, rare familial without MAPT have been reported, suggesting other tauopathy‐related genetic defects. Interestingly, two presenilin 1 (PS1) (Leu113Pro and insArg352) recently associated FTD albeit neuropathological confirmation. We report here a novel PS1 mutation patient Pick‐type absence extracellular β‐amyloid...

10.1002/ana.20083 article EN Annals of Neurology 2004-04-26

<h3>Background</h3> Progranulin gene (<i>PGRN</i>) haploinsufficiency was recently associated with ubiquitin-positive frontotemporal lobar degeneration linked to chromosome 17q21 (FTLDU-17). <h3>Objective</h3> To assess whether<i>PGRN</i>genetic variability contributed other common neurodegenerative brain diseases, such as Alzheimer disease (AD) or Parkinson (PD). <h3>Design</h3> Mutation analysis of<i>PGRN</i> <h3>Setting</h3> Memory Clinic of the Middelheim General Hospital....

10.1001/archneur.64.10.1436 article EN Archives of Neurology 2007-10-01

Double or multiple antigen labeling in IHC classically relies on the existence of primary antibodies raised different species IgG isotypes to ensure specific with secondary detection systems. However, suitable pairs are not always available best choice (e.g., as diagnostic tools). During last few years, several methods have been proposed overcome this, but none them offers flexibility needed for reliable double enzymatic fluorescent IHC. We present here a procedure that elutes after first...

10.1369/jhc.2009.953240 article EN Journal of Histochemistry & Cytochemistry 2009-02-16

Abstract Loss‐of‐function mutations in progranulin ( GRN ) are associated with frontotemporal lobar degeneration intraneuronal ubiquitinated protein accumulations composed primarily of hyperphosphorylated TDP‐43 (FTLD‐TDP). The mechanism by which deficiency causes pathology or neurodegeneration remains elusive. To explore the role vivo , we established Grn knockout mice using a targeted genomic recombination approach and Cre‐LoxP technology. Constitutive homozygous (Grn −/− were born an...

10.1002/path.4043 article EN The Journal of Pathology 2012-06-25

The initial report of the mcr-1 (mobile colistin resistance) gene has led to many reports variants and other mcr genes from different bacterial species originating human, animal environmental samples in geographical locations. Resistance nomenclature is complex unfortunately problems such as names being used for same gene/protein or name genes/proteins are not uncommon. Registries exist some families, bla (β-lactamase) genes, but there yet no agreed scheme genes. National Center...

10.1093/jac/dky262 article EN public-domain Journal of Antimicrobial Chemotherapy 2018-06-22

Abstract It is well established that antibiotic treatment selects for resistance, but the dynamics of this process during infections are poorly understood. Here we map responses Pseudomonas aeruginosa to in high definition a lung infection single ICU patient. Host immunity and therapy with meropenem suppressed P. , second wave emerged due growth oprD wbpM resistant mutants evolved situ. Selection then led loss resistance by decreasing prevalence low fitness mutants, increasing frequency...

10.1038/s41467-021-22814-9 article EN cc-by Nature Communications 2021-04-28

Abstract Bacteria have the potential to translocate between sites in human body, but dynamics and consequences of within-host bacterial migration remain poorly understood. Here we investigate link gut lung Pseudomonas aeruginosa populations an intensively sampled ICU patient using a combination genomics, isolate phenotyping, host immunity profiling, clinical data. Crucially, show that colonization was driven by translocation P. from gut. Meropenem treatment for suspected urinary tract...

10.1038/s41467-022-34101-2 article EN cc-by Nature Communications 2022-11-22

Abstract Objectives To determine the susceptibility profiles and resistome of Pseudomonas aeruginosa isolates from European ICUs during a prospective cohort study (ASPIRE-ICU). Methods 723 respiratory samples or perianal swabs 402 patients 29 sites in 11 countries were studied. MICs 12 antibiotics determined by broth microdilution. Horizontally acquired β-lactamases analysed through phenotypic genetic assays. The first 105 providing such WGS, including analysis previously defined genotypic...

10.1093/jac/dkac122 article EN Journal of Antimicrobial Chemotherapy 2022-04-14

BackgroundThe role of host immunity in emergence evasive SARS-CoV-2 Spike mutations under therapeutic monoclonal antibody (mAb) pressure remains to be explored.MethodsIn a prospective, observational, monocentric ORCHESTRA cohort study, conducted between March 2021 and November 2022, mild-to-moderately ill COVID-19 patients (n = 204) receiving bamlanivimab, bamlanivimab/etesevimab, casirivimab/imdevimab, or sotrovimab were longitudinally studied over 28 days for viral loads, de novo...

10.1172/jci166032 article EN cc-by Journal of Clinical Investigation 2023-02-02

Vascular endothelial growth factor (VEGF), acidic and basic fibroblast factors (FGF-1 -2), transforming β (TGFβ) are potent angiogenic cytokines. Malignant mesothelioma of the pleura presents with a high intra-tumoural microvascular density (IMD) which also has prognostic relevance. This study was designed to verify immunohistochemical expression cytokines in as well non-neoplastic human mesothelial cells individual combined these relation both IMD prognosis. In addition, four cell lines...

10.1002/(sici)1096-9896(199909)189:1<72::aid-path401>3.0.co;2-0 article EN The Journal of Pathology 1999-09-01

Amyloidogenic processing of the amyloid precursor protein (APP) with deposition in brain 42 amino acid long beta-peptide (A beta(42)) is considered central to Alzheimer's disease (AD) pathology. However, it generally believed that nonfibrillar pre-amyloid A beta(42) deposits have mature presence beta(40) into fibrillar plaques cause neurodegeneration. Here, we describe an aggressive form AD caused by a novel missense mutation APP (T714I) directly involving gamma-secretase cleavages APP. The...

10.1093/hmg/9.18.2589 article EN Human Molecular Genetics 2000-11-01
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