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Nandi Simpson

Researcher at University College London

Publications -  15
Citations -  1403

Nandi Simpson is an academic researcher from University College London. The author has contributed to research in topics: Effector & Type three secretion system. The author has an hindex of 10, co-authored 15 publications receiving 1085 citations. Previous affiliations of Nandi Simpson include Imperial College London & University of Paris.

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Stunted microbiota and opportunistic pathogen colonization in caesarean-section birth

TL;DR: The disrupted transmission of maternal Bacteroides strains, and high-level colonization by opportunistic pathogens associated with the hospital environment (including Enterococcus, Enterobacter and Klebsiella species), in babies delivered by caesarean section are reported.
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Rac Regulates Endothelial Morphogenesis and Capillary Assembly

TL;DR: It is found that the small GTPase Rac is essential for the matrix-induced changes in endothelial cell morphology, whereas p21-activated kinase, an effector of Rac, is required for cell motility.
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Identification of a novel Citrobacter rodentium type III secreted protein, EspI, and roles of this and other secreted proteins in infection.

TL;DR: It is found that EspF, EspG, and EspH are not required for efficient colonization of the mouse colon or for the production of hyperplasia, and a novel secreted protein, EspI encoded outside the LEE, whose secretion is also dependent on a functional type III secretion system.
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Pathogenic Neisseria meningitidis utilizes CD147 for vascular colonization

TL;DR: It is reported that the immunoglobulin superfamily member CD147 (also called extracellular matrix metalloproteinase inducer (EMMPRIN) is a critical host receptor for the meningococcal pilus components PilE and PilV, and interfering with this interaction potently inhibited the primary attachment ofMeningococci to human endothelial cells in vitro and prevented colonization of vessels in human brain tissue explants ex vivo.
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Subversion of actin dynamics by EPEC and EHEC.

TL;DR: During the course of infection, enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC and EHEC) subvert the host cell signalling machinery and hijack the actin cytoskeleton to tighten their interaction with the gut epithelium, while avoiding phagocytosis by professional phagocytes.