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1            Those patients who died developed intramucosal acidosis of the sigmoid colon intraoperativ
2 hagectomy for high-grade dysplasia (HGD) and intramucosal adenocarcinoma (IMC) in light of recent adv
3                                              Intramucosal adenocarcinoma and high grade dysplasia hav
4 ing was found in villous adenomas with focal intramucosal adenocarcinoma but was negative in tubular
5                                Survival with intramucosal adenocarcinoma or Barrett's with high-grade
6 ospective review of outcome in patients with intramucosal adenocarcinoma or high grade dysplasia that
7 is the preferred procedure for patients with intramucosal adenocarcinoma or high grade dysplasia.
8 l and en bloc esophagectomy in patients with intramucosal adenocarcinoma or high-grade dysplasia.
9 robability of having high-grade dysplasia or intramucosal adenocarcinoma was 0% (0-4).
10 robability of having high-grade dysplasia or intramucosal adenocarcinoma was 87% (73-95).
11 metastases are rare ( approximately 2%) with intramucosal adenocarcinoma, supporting the use of endos
12 tion with high-grade Barrett's esophagus and intramucosal adenocarcinoma.
13 dysplasia and 22 had high-grade dysplasia or intramucosal adenocarcinoma.
14 m 8 patients who underwent esophagectomy for intramucosal adenocarcinoma.
15                To prove this concept, trans-/intramucosal and lymph-node delivery of PLGA-PEG nanopar
16 define the risk of lymph node metastases for intramucosal and submucosal (T1) esophageal adenocarcino
17                  To validate the presence of intramucosal bacteria ex vivo, CLE was performed in pure
18    In addition, CLE allowed the detection of intramucosal bacteria in vivo.
19 jured intestinal epithelium and clearance of intramucosal bacteria require the presence of intact TLR
20 econd objective was to prove the presence of intramucosal bacteria using CLE.
21 sitivity and specificity for the presence of intramucosal bacteria were 100%.
22                                 In addition, intramucosal bacteria were visualized.
23 d by treatment of patients with dysplasia or intramucosal cancer costs an additional $240 (95% credib
24 tients found to have high-grade dysplasia or intramucosal cancer received endotherapy.
25                     Patients with BE and HGD/intramucosal cancer were studied prospectively from 2002
26 d by treatment of patients with dysplasia or intramucosal cancer would reduce the number of cases of
27 ith BE and neoplasia (72% with HGD, 24% with intramucosal cancer, 4% with low-grade dysplasia [mean a
28 tive endoscopic treatments for dysplasia and intramucosal cancer, coupled with screening programs to
29 ectomy management of high-grade dysplasia or intramucosal cancer, screening by ultrathin nasal endosc
30 tients treated with ablative therapy for HGD/intramucosal cancer.
31  to accelerated (< or = 8 mo) development of intramucosal carcinoma (85%), with submucosal invasion (
32 gressed to high-grade dysplasia and invasive intramucosal carcinoma by 20 months.
33          Lesions consistent with in situ and intramucosal carcinoma were seen in H. pylori-infected m
34 newly diagnosed adenomas, carcinoma in situ, intramucosal carcinoma, and colorectal cancer), they fou
35 cinoma in situ, OR = 2.05, 95% CI 1.01-4.15; intramucosal carcinoma, OR = 1.30, 95% CI 0.61-2.77; and
36 d only WT(Hc) infection caused dysplasia and intramucosal carcinoma.
37 nclude that GCB is associated with selective intramucosal colonization by E. coli.
38 ) had baseline HGD, and 3 (33%) had baseline intramucosal EAC.
39                                              Intramucosal gram-negative coccobacilli were present in
40          Furthermore, an increase in gastric intramucosal hydrogen ion concentration was associated w
41                                        These intramucosal nerve fibers may be a conduit by which intr
42                                              Intramucosal organisms harvested from sinonasal biopsies
43             Continuous monitoring of gastric intramucosal PCO2 and pH is feasible, has potential adva
44 l method for continuously monitoring gastric intramucosal PCO2 and pH was developed and tested.
45           In the animal experiments, gastric intramucosal PCO2 and pH were determined before and afte
46                                              Intramucosal PCO2 by both techniques remained significan
47         By 5 mins after inducing hemorrhage, intramucosal PCO2 by recirculating gas tonometry had inc
48   The technique is able to detect changes in intramucosal PCO2 in response to an induced insult over
49 he conventional method showed an increase in intramucosal PCO2 to 63.0 +/- 20.9 torr (8.4 kPa +/- 2.8
50 , arterial and mixed venous blood gases, and intramucosal PCO2 values were obtained by recirculating
51 gradient between arterial P(CO2) and gastric intramucosal Pco2 was 13+/-3 mm Hg (1.7+/-0.4 kPa) at a
52                         Mean +/- SD baseline intramucosal PCO2 was 47.6 +/- 9.5 torr (6.3 +/- 1.3 kPa
53                                      Gastric intramucosal PCO2 was recorded continuously by capnometr
54             Significant increases in gastric intramucosal PCO2 were detectable by CRGT within 5 min o
55 rfusion by providing on-line measurements of intramucosal PCO2, which can also be used to derive intr
56 % confidence limits, -1.66, 1.72) or gastric intramucosal pH (mean difference, 0.015 pH units; 95% co
57                        Hemodynamics, gastric intramucosal pH (pHi) urine volumes, urinary sodium excr
58  inactivation significantly improved gastric intramucosal pH after aortic occlusion and reperfusion (
59 There were significant correlations between, intramucosal pH and EndoCab antibodies, intramucosal pH
60  feedings for 2 hrs, after which the gastric intramucosal pH and gastric fluid pH measurements were r
61                 The baseline fasting gastric intramucosal pH and gastric fluid pH were determined in
62 een, intramucosal pH and EndoCab antibodies, intramucosal pH and p55 TNF receptor, and p55 TNF recept
63 nsitive than arterial lactate and tonometric intramucosal pH and Pco2.
64 esulted in a significant decrease in gastric intramucosal pH as compared with sham-operated rabbits (
65                      The mean +/- SD gastric intramucosal pH decreased from 7.40 +/- 0.08 to 7.33 +/-
66                 After 30 mins of hemorrhage, intramucosal pH decreased to 6.88 +/- 0.14 (from 7.10 +/
67        Finally, we hypothesized that gastric intramucosal pH is influenced by xanthine oxidase, an ox
68               After induction of anesthesia, intramucosal pH of the sigmoid colon was measured using
69 ating the systemic markers to changes in the intramucosal pH of the sigmoid colon.
70  feeding results in a spuriously low gastric intramucosal pH reading.
71                                  The gastric intramucosal pH returned to the baseline value after 1 h
72                                      Gastric intramucosal pH values improved during reperfusion after
73                                      Gastric intramucosal pH was significantly decreased after hepato
74 1 +/- 1.2 vs. 5.3 +/- 0.7 kPa) and the ileal intramucosal pH was significantly lower (7.07 +/- .28 vs
75 nsumption, SMA blood flow, ileal Pco2, ileal intramucosal pH, and serum lactate levels of mixed venou
76 to arterial Pco2 gap (Pg-Paco2 gap), gastric intramucosal pH, arterial pH, arterial base excess, and
77                                      Gastric intramucosal pH, as determined by recirculating gas tono
78 nsfusion period for Pg-Paco2 gap and gastric intramucosal pH, respectively, was 0.56 kPa (95% confide
79 rtate aminotransferase and decreased gastric intramucosal pH, was significantly (p < 0.0167) attenuat
80 cosal hypercarbia, leading to improvement of intramucosal pH.
81 cosal PCO2, which can also be used to derive intramucosal pH.
82 for at least 1 hr when measuring the gastric intramucosal pH.
83 re was a concomitant significant decrease in intramucosal pH.
84  specimens were examined for the presence of intramucosal S. aureus and characterized to the strain l
85  total gastrectomy which revealed multifocal intramucosal signet ring cell carcinoma.
86 atients (85%) demonstrated 1 or more foci of intramucosal signet ring cell gastric cancer in the exam
87 oid excluding pathogenesis of tumorlets from intramucosal spread from carcinoid tumors.
88 e in interest in endoscopic therapy (ET) for intramucosal (T1a) or submucosal (T1b) esophageal carcin
89                                              Intramucosal terminals were not assessed.
90                                  Increase of intramucosal transforming growth factor alpha (TGFalpha)
91 in the given period, excluding patients with intramucosal tumors (n = 47), palliative resections (n =
92  Lymph node metastases were rare (1.3%) with intramucosal tumors but increased significantly with sub

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