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1  sensors located 5 and 20 cm above the lower esophageal sphincter).
2 d 3, 6, 9, 12, 15, and 18 cm above the lower esophageal sphincter.
3 incter but an excitatory effect on the upper esophageal sphincter.
4 lion cells in the distal esophagus and lower esophageal sphincter.
5 the evaluation of esophageal peristalsis and esophageal sphincter.
6  outcomes (66%) after treatment of the lower esophageal sphincter.
7 f a new magnetic device to augment the lower esophageal sphincter.
8 uction of the abdominal segment of the lower esophageal sphincter.
9 ion, and electrical stimulation of the lower esophageal sphincter.
10 wed a high prevalence of a hypotensive lower esophageal sphincter (55%) and impaired esophageal peris
11 erized by incomplete relaxation of the lower esophageal sphincter and a loss of normal peristaltic ac
12 of one or more bundles entering at the lower esophageal sphincter and coursing to the forestomach, wh
13                                    The lower esophageal sphincter and crural diaphragm constitute the
14 esophagogastric junction contributors (lower esophageal sphincter and crural diaphragm) during deglut
15 geal reflux (reflux 2 cm distal to the upper esophageal sphincter) and ARS.
16 resolution manometry to determine UES, lower esophageal sphincter, and intraesophageal pressure value
17                                        Lower esophageal sphincter augmentation through injection of m
18  They have an inhibitory effect on the lower esophageal sphincter but an excitatory effect on the upp
19 s was associated with deterioration of lower esophageal sphincter characteristics and increased esoph
20 se were compared between groups (i.e., lower esophageal sphincter characteristics, esophageal acid ex
21  integrated relaxation pressure of the lower esophageal sphincter, did not differ significantly betwe
22 volume into the pharynx 2 cm above the upper esophageal sphincter, directed posteriorly.
23 ker esophagus at 2 and 10 cm above the lower esophageal sphincter during wet swallow.
24     Botulinum toxin injection into the lower esophageal sphincter is an established therapy for the t
25 tulinum toxin (BOTOX) injection of the lower esophageal sphincter largely have replaced cardiomyotomy
26                      Separation of the lower esophageal sphincter (LES) and crural diaphragm was quan
27                  Smooth muscles of the lower esophageal sphincter (LES) and skeletal muscle of the cr
28  those who believed in a morphological lower esophageal sphincter (LES) and those who did not.
29 of the esophagus and relaxation of the lower esophageal sphincter (LES) are mediated by nitric oxide
30                           In contrast, lower esophageal sphincter (LES) circular muscle maintains spo
31 the physiologic signal transduction of lower esophageal sphincter (LES) circular muscle.
32  M(3) and 5-HT(3) receptors as well as lower esophageal sphincter (LES) contraction were determined i
33                                    The lower esophageal sphincter (LES) in patients with gastroesopha
34  was closer to the upper border of the lower esophageal sphincter (LES) in subjects with a large WC (
35               The motor control of the lower esophageal sphincter (LES) is critical for normal swallo
36 ified adrenergic receptor sites in the lower esophageal sphincter (LES) of animals and humans.
37 esophageal acid exposure and increased lower esophageal sphincter (LES) pressure and length based on
38       Responders had higher preoperative low esophageal sphincter (LES) pressure than nonresponders:
39 rgitation after therapy have low or no lower esophageal sphincter (LES) pressure.
40                               Isolated lower esophageal sphincter (LES) relaxation associated with be
41 n the pharynx leads to a long-duration lower esophageal sphincter (LES) relaxation that is an importa
42 proposed that nitrergic nerves mediate lower esophageal sphincter (LES) relaxation with intramuscular
43      On the contrary, during transient lower esophageal sphincter (LES) relaxation, longitudinal musc
44 r discrimination seen during transient lower esophageal sphincter (LES) relaxation-associated reflux
45 s antireflux action is that it reduces lower esophageal sphincter (LES) relaxation.
46 fen reduces the incidence of transient lower esophageal sphincter (LES) relaxations.
47 completeness and propagation velocity, lower esophageal sphincter (LES) resting pressure, LES relaxat
48                     In cat spontaneous lower esophageal sphincter (LES), tone is maintained by the ac
49 veal the anatomical counterpart of the lower esophageal sphincter (LES).
50  and hyoid muscles, esophagus, and the lower esophageal sphincter (LES).
51 ic sphincter augmentation (MSA) on the lower esophageal sphincter (LES).
52 onsisting of 24-hour esophageal pH and lower esophageal sphincter manometry.
53     We have previously used the normal lower esophageal sphincter (N-LES) of human organ donors to ex
54     Botulinum toxin injection into the lower esophageal sphincter of patients with achalasia results
55 ossopalatal junction and the timing of upper esophageal sphincter opening relative to glossopalatal j
56  5 cm above the proximal border of the lower esophageal sphincter (PBLES) as appropriate to the locat
57 nce classically manifests as a reduced lower esophageal sphincter pressure (LESP) and loss of distal
58 esistance, 5 cm H2O/L/sec), adjustable lower esophageal sphincter pressure (LESP) and simulated stoma
59 nometry studies revealed a decrease in lower esophageal sphincter pressure (LESP) from 37 +/- 1 mm Hg
60              No significant changes in lower esophageal sphincter pressure and esophageal peristalsis
61 al acid exposure, esophagitis, resting lower esophageal sphincter pressure and medication use.
62  (pH parameters, endoscopic signs, and lower esophageal sphincter pressure changes).
63  36% decrease in baseline mean resting lower esophageal sphincter pressure in the gastric band group
64 chniques with respect to postoperative lower-esophageal sphincter pressure or postoperative dysphagia
65  extending 5.5 cm proximal to the peak lower esophageal sphincter pressure point was increased by app
66 tion, proton pump inhibitor (PPI) use, lower esophageal sphincter pressure, and patient satisfaction
67 ccording to the size of hiatal hernia, lower esophageal sphincter pressure, Barrett esophagus, and si
68 Life scores, esophageal acid exposure, lower esophageal sphincter pressure, number of beads (size) of
69                                    The lower esophageal sphincter pressure, the motility of the esoph
70 c pressure, and a reduction in resting lower esophageal sphincter pressure.
71                                        Lower esophageal sphincter pressures had also returned to norm
72 ere reduced from 7 to 1 (P < .001) and lower esophageal sphincter pressures were reduced from 28 to 9
73 ignificant improvements in postmyotomy lower esophageal sphincter profiles.
74  vulnerability to reflux and transient lower esophageal sphincter relaxation (tLESR) during gastric d
75 y disorder characterized by incomplete lower esophageal sphincter relaxation and aperistalsis resulti
76 lux disease (e.g. vomiting, disordered lower esophageal sphincter relaxation and gastric accommodatio
77                              Transient lower esophageal sphincter relaxation is central to the pathog
78                              Transient lower esophageal sphincter relaxation is the main mechanism fo
79                          The transient lower esophageal sphincter relaxation nadir also typically occ
80                          The transient lower esophageal sphincter relaxation onset invariably precede
81 r this patient population is transient lower esophageal sphincter relaxation reducers.
82 assessed the relationship of transient lower esophageal sphincter relaxation to gastroesophageal junc
83 ardinal feature of achalasia, impaired lower esophageal sphincter relaxation, can occur in several di
84 ally for the duration of the transient lower esophageal sphincter relaxation.
85 ergic pathways in modulating transient lower esophageal sphincter relaxation.
86 unction (EGJ) opening during transient lower esophageal sphincter relaxations (tLESRs) using high-res
87                              Transient lower esophageal sphincter relaxations and hiatal hernias have
88 sion receptors in triggering transient lower esophageal sphincter relaxations and subsequent reflux.
89  GERD; (2) the mechanism for transient lower esophageal sphincter relaxations and their association w
90 hough there is evidence that transient lower esophageal sphincter relaxations are neurally mediated,
91 dose-dependent inhibition of transient lower esophageal sphincter relaxations in a dog model.
92                      Rather, transient lower esophageal sphincter relaxations must occur before the g
93               Termination of transient lower esophageal sphincter relaxations occurred about the time
94 er school of thought is that transient lower esophageal sphincter relaxations result from gastric dis
95 a refute the hypothesis that transient lower esophageal sphincter relaxations result from passive mec
96                              Transient lower esophageal sphincter relaxations were not increased by t
97 of compounds that can reduce transient lower esophageal sphincter relaxations.
98                                    The lower esophageal sphincter shows normalized pressures and rela
99                Normal responses of the upper esophageal sphincter (UES) and esophageal body to liquid
100 eal junction, laryngeal vestibule, and upper esophageal sphincter (UES) and intraluminal pharyngeal d
101                               Esophago-upper esophageal sphincter (UES) contractile reflex (EUCR) and
102 the effect of laryngeal stimulation on upper esophageal sphincter (UES) pressure and to determine the
103 tudies of the pressure response of the upper esophageal sphincter (UES) to simulated or spontaneous g
104  detailed manometric assessment of the upper esophageal sphincter (UES).
105 rdings were obtained at 2 cm above the lower esophageal sphincter under 2 study conditions in normal
106                         A hypertensive lower esophageal sphincter was diagnosed in three patients, di
107 Nitric oxide-induced relaxation of the lower esophageal sphincter was impaired and achalasia was conf
108 megaesophagus and achalasia, and their lower esophageal sphincter was resistant to nitric oxide-induc
109 t treatments focused on disrupting the lower esophageal sphincter with pneumatic dilation (70%-90% ef

 
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