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1 tic therapy for children with non-dysenteric Shigella infection.
2 n to be altered during the course of natural Shigella infection.
3 dentified that surface loops of OmpA mediate Shigella infection.
4 lgi-associated ARF/ARL family GTPases during Shigella infection.
5 for the reduction of immune responses during Shigella infection.
6 e intestine by 24 hours post-intraperitoneal Shigella infection.
7 e; however, adult mice are resistant to oral Shigella infection.
8  protective efficacy against intraperitoneal Shigella infection.
9 p90 host-cell vinculin fragment generated by Shigella infection.
10 is essential to resistance following primary Shigella infection.
11 e interleukin-1beta is cleaved shortly after Shigella infection.
12 y help identify patients most likely to have Shigella infection.
13 tional cell death pathways during oral mouse Shigella infection.
14 n factor CREB3 under Golgi stress induced by Shigella infection.
15  SMAC release in the immune response against Shigella infection.
16 rating the importance of SIRT2 to counteract Shigella infection.
17 nd -8 renders mice hyper-susceptible to oral Shigella infection.
18 vel therapeutics and preventatives to combat Shigella infection.
19 Ciprofloxacin is a recommended treatment for Shigella infections.
20 ProD was associated with Cryptosporidium and Shigella infections.
21 equencing for the laboratory surveillance of Shigella infections.
22 ella infection, 28.3 {CI, 7.2-112.2}; OR for Shigella infection, 14.5 {CI 1.5-141.0} or any recreatio
23     Among 24 patients with culture-confirmed Shigella infection, 4 were treated with azithromycin; al
24 Abl and Arg are catalytically activated upon Shigella infection, accumulate at the site of bacterial
25          The mechanism of protection against Shigella infection and disease in endemic areas is uncer
26 l the spatiotemporal variation in paediatric Shigella infection and map its predicted prevalence acro
27 eficient mice are highly susceptible to oral Shigella infection and recapitulate the clinical feature
28                LGF is a secondary outcome of Shigella infection and reduction in LGF is not often qua
29 d. vaccination with IpaB and IpaD to prevent Shigella infection and support further studies in humans
30  or programmed cell death, is induced during Shigella infections and has been proposed to be a key ev
31        The associations between asymptomatic Shigella infections and impaired linear growth at age 2
32 value of dysentery for the identification of Shigella infection, and the efficacy of antibiotics for
33                                              Shigella infections are a leading cause of diarrhoeal de
34 he human intestinal xenograft in response to shigella infection but failed to significantly alter tis
35 n, improved sanitation decreased the odds of Shigella infection by 19% (odds ratio [OR]=0.81 [95% CI
36 -5p and miR-6073 exert a selective effect on Shigella infection by impairing bacterial actin-based mo
37                               Probability of Shigella infection exceeded 20% when both precipitation
38            Real-time genomic surveillance of Shigella infections has been implemented in several coun
39 Antimicrobial therapy is often necessary for Shigella infections; however, we are reaching a crisis p
40 on towards understanding the biomechanics of Shigella infection, (ii) the zebrafish infection model,
41 es contribute to protective immunity against Shigella infection in a high-burden setting.
42  enterotoxigenic Escherichia coli (ETEC) and shigella infection in children younger than 5 years from
43 ith human intestine in vivo, we have studied shigella infection in human intestinal xenografts in sev
44  changes in species prevalence, diagnoses of Shigella infections in England are persistently most com
45      Essential events in the pathogenesis of Shigella infections include bacterial invasion of epithe
46 ction of MSD cases that were attributable to Shigella infection increased from 9.6% (n = 129) for cul
47                  Western blots revealed that Shigella infection induces vinculin proteolysis in PtK2
48 el and discuss where the future of modelling Shigella infection lies.
49 sentery for identification and management of Shigella infection might miss an opportunity to reduce S
50 g infection, the susceptibility to pulmonary Shigella infection of each of various mouse strains that
51 h has been previously described for virulent Shigella infection of HMDM and is termed oncosis.
52 animal models to study mechanisms underlying Shigella infection of humans.
53 onfirm a potential pathogenic role of HD5 in Shigella infection of not only epithelial cells but also
54 o and in vivo Whether and how HD5 influences Shigella infection of resident macrophages following its
55                                       During Shigella infections of human macrophages, interleukin-1b
56 served a reduced prevalence of Trichuris and Shigella infection relative to the same age group at bas
57 xhibited a 10-fold-greater susceptibility to Shigella infection than immunocompetent mice.
58  SIRT2 knockout mice are more susceptible to Shigella infection than wildtype mice, demonstrating the
59                   The GI panel detected more Shigella infections than did culture; six of 31 (19.4%)
60 and suggest a novel approach to treatment of Shigella infections through inhibition of host cell sign
61                                              Shigella infection was associated with human intestinal
62                                              Shigella infection was associated with mortality (pooled
63 NAs chosen among the strongest inhibitors of Shigella infection, we discovered that miR-3668, miR-473
64 the need for preventive strategies targeting Shigella infection, which could potentially reduce the d
65  dysentery identified 1.9-85.9% of confirmed Shigella infections, with sensitivity decreasing over ti