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1 ragastric zinc compared with zinc-sufficient esophagi.
2 ning in ZD esophagi compared with that in ZS esophagi.
3 were detected in the suprabasal layers of ZD esophagi.
4 y resulting in aneurysmal aortas and ectatic esophagi.
5 mens, human esophageal cell lines, and mouse esophagi.
6 enes in the PEITC + NMBA versus NMBA-treated esophagi.
7 -deficient esophagus and in zinc-replenished esophagi after treatment with intragastric zinc compared
8 expressed in the NMBA-treated versus control esophagi and 1,936 genes in the PEITC + NMBA versus NMBA
9  cultured esophageal fibroblasts from normal esophagi and esophagi from patients with severe EoE on a
10 y that many laparoscopic patients with short esophagi are unrecognized and perhaps treated inappropri
11 d levels of DNA damage in reflux-exposed rat esophagi, as observed by reduced levels of phospho-H2A h
12 tly, tumors were consistently observed in ZD esophagi at very early time points.
13 hosphorylated forms of Rb was detected in ZD esophagi by immunoblotting.
14 ng cell nuclear antigen was characterized in esophagi by immunohistochemistry at 0, 24, and 48 h, and
15 6ink4a showed reduced nuclear staining in ZD esophagi compared with that in ZS esophagi.
16 cial and transient infections of tongues and esophagi (detected by histology) at 1 to 2 weeks after o
17 phageal fibroblasts from normal esophagi and esophagi from patients with severe EoE on autologous ver
18 ptosis accelerator, was markedly stronger in esophagi from Zn-/DFMO+ animals that showed increased ap
19       Esophagi were divided into 4 groups (4 esophagi/group): control, Group1 (G1), Group2 (G2), Grou
20 PC) was applied circumferentially in porcine esophagi in vivo.
21                    Here we show that atretic esophagi lack Noggin (NOG) expression, resulting in imma
22 n vitro uniaxial stretching was performed on esophagi (n = 16) obtained from the abattoir within 4-6
23         Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to
24 ell nuclear antigen (PCNA) expression in the esophagi of NMBA treated cyclin D1 mice.
25 y identified 2,261 dysregulated genes in the esophagi of rats that received a 1-week exposure to the
26 n, morphometric changes were observed in the esophagi of rats treated with N-nitrosomethylbenzylamine
27         Lesions developed on the tongues and esophagi of the 4NQO-treated animals and included hyperk
28 udy evaluating the morphological features of esophagi resected for endstage achalasia showed marked d
29 this, we utilized full thickness human donor esophagi to create and validate the ex vivo function of
30 was 88% in ZD rats with highly proliferative esophagi versus 0% in ZS rats.
31                                              Esophagi were assessed by gross morphology, histopatholo
32 h keratinized and nonkeratinized surfaces of esophagi were colonized to a considerably greater extent
33                                              Esophagi were divided into 4 groups (4 esophagi/group):
34 re sacrificed 24 h after the last treatment; esophagi were excised and processed for histologic gradi
35 S) as well as the expression of c-Jun in the esophagi, were evaluated to investigate the mechanism(s)