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1 d applied to rhesus monkeys with and without Helicobacter pylori infection.
2 by nonsteroidal anti-inflammatory drugs and Helicobacter pylori infection.
3 en validated, with subsequent eradication of Helicobacter pylori infection.
4 ctiveness of standard therapies to eradicate Helicobacter pylori infection.
5 oid tissue type is closely linked to chronic Helicobacter pylori infection.
6 incided with a decrease in the prevalence of Helicobacter pylori infection.
7 in the inflammatory response associated with Helicobacter pylori infection.
8 genetic and environmental factors, including Helicobacter pylori infection.
9 phoid tissue (MALT) lymphoma is dependent on Helicobacter pylori infection.
10 attention as a cause of tissue damage due to Helicobacter pylori infection.
11 a consequence of chronic gastritis caused by Helicobacter pylori infection.
12 nicopathologic entity, often associated with Helicobacter pylori infection.
13 ial serologic assays accurately detect adult Helicobacter pylori infection.
14 in urease vaccine-induced protection against Helicobacter pylori infection.
15 Chronic gastritis was induced in B6 mice by Helicobacter pylori infection.
16 ptic ulcer disease pathogenesis secondary to Helicobacter pylori infection.
17 the expression of which is increased during Helicobacter pylori infection.
18 roposed as first-line empiric treatments for Helicobacter pylori infection.
19 ens, drugs, colonizing bacteria and possibly Helicobacter Pylori infection.
20 cell signals produced by immune responses to Helicobacter pylori infection.
21 nd/or parietal cell loss, and during chronic Helicobacter pylori infection.
22 tients receiving aspirin are associated with Helicobacter pylori infection.
23 ortance with declining prevalence of chronic Helicobacter pylori infection.
24 rror-prone DNA repair pathway in response to Helicobacter pylori infection.
25 tric submucosal vessels in a murine model of Helicobacter pylori infection.
26 ct the gastric epithelium, especially during Helicobacter pylori infection.
27 's population and are largely due to chronic Helicobacter pylori infection.
28 ecimens show evidence of gastric atrophy and Helicobacter pylori infection.
29 2), a gene associated with susceptibility to Helicobacter pylori infection.
30 mation and gastritis but leads to persistent Helicobacter pylori infection.
31 f non-steroidal anti-inflammatory drugs, and Helicobacter pylori infection.
32 sia (GIN) with 80% prevalence 6 months after Helicobacter pylori infection.
33 istories reflect the overriding influence of Helicobacter pylori infection.
34 ies, and new approaches to the management of Helicobacter pylori infection.
35 ve recently been shown to be associated with Helicobacter pylori infections.
37 y, small intestinal bacterial overgrowth and Helicobacter pylori infection affect motor fluctuations
38 role of serologic testing to confirm cure of Helicobacter pylori infection after antimicrobial therap
40 ially housed rhesus monkeys rapidly acquired Helicobacter pylori infection, although the organism was
41 Current guidelines recommend testing for Helicobacter pylori infection among users of low-dose as
45 a new immunoblot assay (Helicoblot 2.1) for Helicobacter pylori infection and CagA and VacA status b
51 e made significant progress in understanding Helicobacter pylori infection and gastric motility in th
52 are needed to clarify the natural history of Helicobacter pylori infection and identify predictors of
53 lass I- and class II-restricted functions in Helicobacter pylori infection and immunity upon oral imm
54 icting data regarding an association between Helicobacter pylori infection and iron deficiency anemia
56 ding the nature of cell-mediated immunity in Helicobacter pylori infection and its role in pathogenes
57 lial cells (GECs) are the primary target for Helicobacter pylori infection and may act as APCs regula
58 ociated lymphoid tissue (MALT) is related to Helicobacter pylori infection and may depend on this inf
59 l and infant plasma vitamin A, reduce infant Helicobacter pylori infection and nasopharyngeal pneumoc
60 risk factors for bleeding peptic ulcers are Helicobacter pylori infection and non-steroidal anti-inf
61 tatistically significant association between Helicobacter pylori infection and Primary Open-Angle Gla
62 ize the evidence for the association between Helicobacter pylori infection and Primary Open-Angle Gla
64 ested a link between a high-salt diet during Helicobacter pylori infection and the development of hyp
69 eal adenocarcinoma (EAC) in individuals with Helicobacter pylori infection, and a network meta-analys
71 of gastric epithelial cells is a hallmark of Helicobacter pylori infection, and altered epithelial ce
72 eradication, NOD1 contributes to controlling Helicobacter pylori infection, and NOD2 is involved in m
74 ce of peptic ulcers, strategies to eradicate Helicobacter pylori infection, and prophylaxis against u
75 gastric mucosa as a result of long standing Helicobacter pylori infection, and this acquired MALT ma
76 de antibiotic widely used for eradication of Helicobacter pylori infection, and thus resistance to th
77 Although consensus supports eradication of Helicobacter pylori infections, antimicrobial resistance
78 ive protein (aOR: 0.82; 95% CI: 0.73, 0.92), Helicobacter pylori infection (aOR: 0.11; 95% CI: 0.05,
82 valence rates in developed nations, most new Helicobacter pylori infections are primarily acquired du
85 egulation of iNOS has been observed in human Helicobacter pylori infection, but the cellular sources
96 cing identified more IM patients with active Helicobacter pylori infection compared with histopatholo
99 ence from developed countries indicates that Helicobacter pylori infection correlates with a reduced
101 Key risk factors for gastric cancer include Helicobacter pylori infection, diet, obesity, smoking, a
104 dard proton-pump inhibitor-based therapy for Helicobacter pylori infection fails in up to one quarter
105 ity and reflux for cardia gastric cancer and Helicobacter pylori infection for non-cardia gastric can
109 stigated for centuries, the association with Helicobacter pylori infection has been recognized for on
112 of the humoral immune responses of people to Helicobacter pylori infection has facilitated the invest
113 une response of gastric T cells during acute Helicobacter pylori infection has not been previously ch
114 tment failure of three standard regimens for Helicobacter pylori infections has increased and represe
115 l therapies for the effective eradication of Helicobacter pylori infection have been identified and a
117 ication rates of standard triple therapy for Helicobacter pylori infections have decreased in recent
118 c adenocarcinoma is strongly associated with Helicobacter pylori infection; however, most infected pe
120 amed stomachs (from TxA23 mice and mice with Helicobacter pylori infection) identified more metaplast
123 en made in understanding the epidemiology of Helicobacter pylori infection in developing countries an
124 acute antibody and T-cell immune response to Helicobacter pylori infection in humans has not been stu
125 lymphoid tissue (MALT) lymphoma linked with Helicobacter pylori infection in humans was observed in
128 5 Ser-536 phosphorylation also occurs during Helicobacter pylori infection in macrophages and gastric
132 level I evidence supporting the treatment of Helicobacter pylori infection in patients with duodenal
133 between water sources and the prevalence of Helicobacter pylori infection in Peruvian children was s
134 ter pylori infection, screening and treating Helicobacter pylori infection in selected transplant pat
136 duced immune mechanisms that protect against Helicobacter pylori infection in the mouse model have no
169 ey (1999-2000), the authors assessed whether Helicobacter pylori infection is associated with iron de
200 gastric inflammatory and immune response in Helicobacter pylori infection may be due to the effect o
215 easured a strong transcriptional response to Helicobacter pylori infection only in this cell type.
217 ric cancer (OR = 0.80, 95% CI 0.72-0.89) and Helicobacter Pylori infection (OR = 0.72, 95% CI 0.60-0.
219 mHSP65 antibody titers were correlated with Helicobacter pylori infection (P=0.004), which maintaine
221 10 responses and increased susceptibility to Helicobacter pylori infection, phenotypes observed in NO
222 plastic cell lineages in response to chronic Helicobacter pylori infection predisposes to gastric neo
227 ously established roles in susceptibility to Helicobacter pylori infection, response to counteract in
230 immunosuppressed transplant recipients with Helicobacter pylori infection, screening and treating He
232 histologic subtype and anatomic subsite, by Helicobacter pylori infection status, by geographic loca
234 nificantly less effective for eradication of Helicobacter pylori infection than are 5-day concomitant
235 umor tissues were more likely to have active Helicobacter pylori infection than those with stable tum
236 andomised controlled trial of eradication of Helicobacter pylori infection, the association between b
237 ns of household and environmental factors to Helicobacter pylori infection, the authors examined H. p
239 ncer databases, which do not include data on Helicobacter pylori infection, the most well-known risk
240 mal inductive sites for immunization against Helicobacter pylori infection, the protective efficacy o
241 y focus on atrophic gastritis due to chronic Helicobacter pylori infection-the most common etiology-o
242 with Helicobacter felis to create a model of Helicobacter pylori infection--the most common human chr
243 ancer and peptic ulcer disease attributed to Helicobacter pylori infections, there is still only a li
248 e presence of chronic atrophic gastritis and Helicobacter pylori infection was determined by measurem
253 principal causes of peptic ulcer disease are Helicobacter pylori infection, which affects approximate
254 (49%) of the 100 patients had biopsy-proved Helicobacter pylori infection with chronic active gastri
255 iological evidence links high-salt diets and Helicobacter pylori infection with increased risk of dev
256 nally, 57.1% of patients tested positive for Helicobacter pylori infection, with its prevalence reach
257 We examined the longitudinal changes of Helicobacter pylori infection within 46 families with ch