Refining the results of a whole-genome screen based on 4666 microsatellite markers for defining predisposition factors for multiple sclerosis

2004 ◽  
Vol 25 (14) ◽  
pp. 2212-2218 ◽  
Author(s):  
René Gödde ◽  
Viktoria Nigmatova ◽  
Peter Jagiello ◽  
Eckhart Sindern ◽  
Michael Haupts ◽  
...  
2003 ◽  
Vol 143 (1-2) ◽  
pp. 107-111 ◽  
Author(s):  
Bartosz Bielecki ◽  
Marcin P. Mycko ◽  
Ewa Tronczyńska ◽  
Marek Bieniek ◽  
Stephen Sawcer ◽  
...  

2003 ◽  
Vol 143 (1-2) ◽  
pp. 17-24 ◽  
Author(s):  
M. Eraksoy ◽  
M. Kurtuncu ◽  
G. Akman-Demir ◽  
M. Kılınc ◽  
M. Gedizlioglu ◽  
...  

2003 ◽  
Vol 143 (1-2) ◽  
pp. 112-115 ◽  
Author(s):  
M. Santos ◽  
J. Pinto-Basto ◽  
M.E. Rio ◽  
M.J. Sá ◽  
A. Valença ◽  
...  

Brain ◽  
2002 ◽  
Vol 125 (6) ◽  
pp. 1337-1347 ◽  
Author(s):  
Stephen Sawcer ◽  
Mel Maranian ◽  
Efrosini Setakis ◽  
Val Curwen ◽  
Eva Akesson ◽  
...  

2002 ◽  
Vol 111 (3) ◽  
pp. 270-277 ◽  
Author(s):  
Rene Goedde ◽  
Stephen Sawcer ◽  
Stefan Boehringer ◽  
Bianca Miterski ◽  
Eckhart Sindern ◽  
...  

2003 ◽  
Vol 143 (1-2) ◽  
pp. 97-100 ◽  
Author(s):  
Maria Liguori ◽  
Stephen Sawcer ◽  
Efrosini Setakis ◽  
Alastair Compston ◽  
Mara Giordano ◽  
...  

2020 ◽  
Vol 75 (9) ◽  
pp. 2516-2525
Author(s):  
A Keith Turner ◽  
Sabine E Eckert ◽  
Daniel J Turner ◽  
Muhammud Yasir ◽  
Mark A Webber ◽  
...  

Abstract Objectives A whole-genome screen at sub-gene resolution was performed to identify candidate loci that contribute to enhanced or diminished ciprofloxacin susceptibility in Salmonella enterica serovar Typhi. Methods A pool of over 1 million transposon insertion mutants of an S. Typhi Ty2 derivative were grown in a sub-MIC concentration of ciprofloxacin, or without ciprofloxacin. Transposon-directed insertion site sequencing (TraDIS) identified relative differences between the mutants that grew following the ciprofloxacin treatment compared with the untreated mutant pool, thereby indicating which mutations contribute to gain or loss of ciprofloxacin susceptibility. Results Approximately 88% of the S. Typhi strain’s 4895 annotated genes were assayed, and at least 116 were identified as contributing to gain or loss of ciprofloxacin susceptibility. Many of the identified genes are known to influence susceptibility to ciprofloxacin, thereby providing method validation. Genes were identified that were not known previously to be involved in susceptibility, and some of these had no previously known phenotype. Susceptibility to ciprofloxacin was enhanced by insertion mutations in genes coding for efflux, other surface-associated functions, DNA repair and expression regulation, including phoP, barA and marA. Insertion mutations that diminished susceptibility were predominantly in genes coding for surface polysaccharide biosynthesis and regulatory genes, including slyA, emrR, envZ and cpxR. Conclusions A genomics approach has identified novel contributors to gain or loss of ciprofloxacin susceptibility in S. Typhi, expanding our understanding of the impact of fluoroquinolones on bacteria and of mechanisms that may contribute to resistance. The data also demonstrate the power of the TraDIS technology for antibacterial research.


2010 ◽  
Vol 28 (4) ◽  
pp. 585-596 ◽  
Author(s):  
Haitao Li ◽  
Xun Chen ◽  
Yuan Yang ◽  
Jinsong Xu ◽  
Jianxun Gu ◽  
...  

2018 ◽  
Vol 6 (6) ◽  
pp. 642-650
Author(s):  
Vasu Arora ◽  
Neera Kapoor ◽  
Samar Fatma ◽  
Sarika Jaiswal ◽  
Mir Asif Iquebal ◽  
...  

2008 ◽  
Vol 25 (3) ◽  
pp. 175-180 ◽  
Author(s):  
Kei Kitahara ◽  
Shigeyuki Kawa ◽  
Yoshihiko Katsuyama ◽  
Takeji Umemura ◽  
Yayoi Ozaki ◽  
...  

Alcohol abuse is one of the most common risk factor for chronic pancreatitis, but the underlying pathophysiological mechanisms remain unclear. The aim of this study was to identify genes that contribute to susceptibility or resistance for alcoholic chronic pancreatitis by screening the whole genome. Sixty-five patients with alcoholic chronic pancreatitis (63 men and 2 women, mean age 55.2 years) and 99 healthy Japanese controls were enrolled in this study. This was an association study using 400 polymorphic microsatellite markers with an average spacing of 10.8 cM distributed throughout the whole genome. This search revealed 10 candidate susceptibility regions and 5 candidate resistant regions throughout the genome. No specific microsatellite markers were detected in association with previously reported susceptibility genes for chronic pancreatitis, such asPRSS1, PRSS2, CTRC, SPINK1, CFTR, ALDH2, and CYP2E1. Among the statistically significant markers,D15S1007on chromosome 15q14 showed strong evidence for disease susceptibility (70.8% vs. 35.1%,Pc= 0.0001). Within 500 kb of D15S1007, several genes were candidate genes for susceptibility, includingFMN1, DKFZP686C2281, LOC440268, RYR3, and AVEN, This study identified 10 candidate susceptibility and 5 candidate resistant regions that may contain genes involved in ACP pathogenesis.


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