Publications by authors named "Gloria I Viboud"

Objectives: Despite the growing importance of bioinformatics in molecular diagnostics, not all medical laboratory sciences (MLS) programs provide instruction in this field. We developed and assessed a virtual laboratory learning unit to introduce basic bioinformatics concepts and tools to MLS students.

Methods: The unit included a video tutorial, written instructions for the online laboratory activity, and a postactivity review video.

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Objectives: The implementation of nucleic acid testing in laboratory medicine has revolutionized clinical diagnosis. Unfortunately, incorporation of these technologies in less developed countries remains a challenge. Despite Romania's recent economic growth, the country is in dire need of medical and laboratory staff trained in modern technologies.

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, the causative agent of plague, has a complex infectious cycle that alternates between mammalian hosts (rodents and humans) and insect vectors (fleas). Consequently, it must adapt to a wide range of host environments to achieve successful propagation. PhoP is a response regulator of the PhoP/PhoQ two-component signal transduction system that plays a critical role in the pathogen's adaptation to hostile conditions.

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A common virulence mechanism among bacterial pathogens is the use of specialized secretion systems that deliver virulence proteins through a translocation channel inserted in the host cell membrane. During Yersinia infection, the host recognizes the type III secretion system mounting a pro-inflammatory response. However, soon after they are translocated, the effectors efficiently counteract that response.

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The innate immune system of mammals responds to microbial infection through detection of conserved molecular determinants called 'pathogen-associated molecular patterns' (PAMPs). Pathogens use virulence factors to counteract PAMP-directed responses. The innate immune system can in turn recognize signals generated by virulence factors, allowing for a heightened response to dangerous pathogens.

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Yersinia pseudotuberculosis binds to beta1 integrin receptors, and uses the type III secretion proteins YopB and YopD to introduce pores and to translocate Yop effectors directly into host cells. Y. pseudotuberculosis lacking effectors that inhibit Rho GTPases, YopE and YopT, have high pore forming activity.

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Pathogenic Yersinia species share a type III secretion system that translocates Yop effector proteins into host cells to counteract signalling responses during infection. Two of these effectors, YopE and YopT, downregulate Rho GTPases by different mechanisms. Here, we investigate whether YopT and YopE are functionally redundant by dissecting the contribution of these two effectors to the pathogenesis of Yersinia pseudotuberculosis in a mouse infection and tissue culture model.

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A type III secretion system (TTSS) is encoded on a virulence plasmid that is common to three pathogenic Yersinia species: Y. enterocolitica, Y. pseudotuberculosis, and Y.

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Type III secretion systems are used by several pathogens to translocate effector proteins into host cells. Yersinia pseudotuberculosis delivers several Yop effectors (e.g.

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Human enterotoxigenic Escherichia coli (ETEC) produces a type IV pilus termed longus which is encoded on large plasmids in association with colonization factor antigens (CFAs) and enterotoxins. A plasmid-derived 7 kbp BamHI DNA fragment hybridizing with an oligonucleotide probe designed from the amino-terminal amino acid sequence of the denatured 22 kDa structural longus pilin subunit was subcloned and sequenced. DNA sequencing analysis revealed an open reading frame, designated lngA, whose predicted amino acid sequence matched perfectly the N-terminal sequence of LngA obtained by Edman degradation.

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