Similar Datasets
Project description:Interventions: No Group:No intervention
Primary outcome(s): CRE screening results
Study Design: Sequential
| 2699279 | ecrin-mdr-crc
Project description:Design: double blind controlled randomized trial with a parallel design and 3 treatment groups Description of subjects: Patients admitted in study centers for colorectal surgery under laporoscopy and/or laparotomy.
Product:
Product 1: BB536 and LA1 (10E9) Product 2: BB536 and LA1 (10E7) Placebo: Maltodextrin Number of patients: enrolled subjects: n=33, ITT data set: n=31, PP data set: n=30
Primary objective:
Colonization (biopsy+stools) of each bacteria for one of the dose at D0 (surgical procedure)
Secondary objectives:
* Influence of the probiotic bacteria on the gut microflora
* Modulation of the immune and inflammatory response
Additional objectives:
* Investigate dose effect on La1 colonization
* Investigate the effect of La1 colonization, treatment without La1 colonization, and absence of treatment and La1 colonization on other bacteria and on immunological parameters
| 2074940 | ecrin-mdr-crc
Project description:We here performed a proteomics study on the colon tissues of ckmt1 KOIEC or. WT (flox+/+) mice after DSS treatment for 8 days (n=3). KOIEC mice (Ckmt1flox/flox, Vil-Cre) means mice with intestinal epithelial conditional knockout (C57BL/6J). Cre-negative Ckmt1 flox/flox littermates were used as controls. Group 1: DSSCKO (Ckmt1flox/flox, Vil-Cre) Group 2: DSSflox (Cre-negative Ckmt1 flox/flox littermates)
2025-05-07 | PXD057053 | Pride
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâs genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâs major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify HNS binding sites across the genome to determine the direct regulon of HNS
2016-03-23 | E-GEOD-72471 | biostudies-arrayexpress
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâs genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâs major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify ToxR binding sites across the genome to determine the direct regulon of ToxR
2016-03-23 | E-GEOD-72473 | biostudies-arrayexpress
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâ??s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâ??s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify TcpP binding sites across the genome to determine the direct regulon of TcpP
2016-03-23 | E-GEOD-72472 | biostudies-arrayexpress
Project description:We performed proteomic analyses on the kidneys of Tmod1 flox/flox/Ksp-Cre- (TF) and Tmod1 flox/flox/Ksp-Cre+ (TFK) mice.
2019-06-10 | MSV000083953 | MassIVE
Project description:Dhps<fl/fl> mice and Dhps<fl/fl>;Vil1<cre/+> mice were infected or not with Citrobacter rodentium (10^9 bacteria/mouse) for 14 days, and cell lysates were prepared for analysis. A total of 4 mice per group were used for the following groups: (1) Vil1<+> no C. Rod; (2) Vil1<cre> no C. Rod; (3) Vil1<+> with C. Rod; (4) Vil1<cre> with C. Rod
2025-05-06 | PXD051536 | Pride