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Wiep Klaas Smits

Researcher at Leiden University Medical Center

Publications -  87
Citations -  4709

Wiep Klaas Smits is an academic researcher from Leiden University Medical Center. The author has contributed to research in topics: Clostridium difficile & Biology. The author has an hindex of 29, co-authored 72 publications receiving 4082 citations. Previous affiliations of Wiep Klaas Smits include Massachusetts Institute of Technology & University of Groningen.

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Bistability, epigenetics, and bet-hedging in bacteria.

TL;DR: Heterogeneous populations can demonstrate increased fitness compared with homogeneous populations and the possible roles of interlinked bistable networks, epigenetic inheritance, and bet-hedging in bacteria are discussed.
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Clostridium difficile infection.

TL;DR: Infection of the colon with the Gram-positive bacterium Clostridium difficile is potentially life threatening, especially in elderly people and in patients who have dysbiosis of the gut microbiota following antimicrobial drug exposure.
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Phenotypic variation in bacteria: the role of feedback regulation

TL;DR: The ubiquity of these processes throughout nature, as well as the presumed molecular mechanisms responsible for the heterogeneity observed in a selection of bacterial species are discussed.
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Characterization of the virulence of a non-RT027, non-RT078 and binary toxin-positive Clostridium difficile strain associated with severe diarrhea

TL;DR: The data indicate that LC693 may be more virulent than strain 1379, an epidemic strain from the same hospital, and provide the first phenotypic characterization of a non- RT027 and non-RT078 binary toxin-positive ST201 isolate.
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Stripping Bacillus: ComK auto-stimulation is responsible for the bistable response in competence development

TL;DR: It is argued that transcriptional regulation determines the threshold of ComK to initiate the auto‐stimulatory response, and that the fraction of cells that reach this threshold, and thus develop competence, in a wild‐type strain governed by MecA‐mediated proteolytic control.