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Esophageal Helicobacter pylori colonization aggravates esophageal injury caused by reflux.
[esophageal adenocarcinoma]
To
investigate
esophageal
Helicobacter
pylori
(
H
.
pylori
)
colonization
on
esophageal
injury
caused
by
reflux
and
the
related
mechanisms
.
An
esophagitis
model
,
with
acid
and
bile
reflux
,
was
surgically
produced
in
male
rats
.
The
rats
were
randomly
divided
into
either
:
(
1
)
an
esophagogastroduodenal
anastomosis
(
EGDA
)
group
;
(
2
)
an
EGDA
with
H
.
pylori
infection
group
;
(
3
)
a
pseudo-operation
with
H
.
pylori
infection
group
;
or
(
4
)
a
pseudo-operation
group
.
All
rats
were
kept
for
36
wk
.
Based
on
the
location
of
H
.
pylori
colonization
,
the
EGDA
rats
with
H
.
pylori
infection
were
subdivided
into
those
with
concomitant
esophageal
H
.
pylori
colonization
or
those
with
only
gastric
H
.
pylori
colonization
.
The
esophageal
injuries
were
evaluated
grossly
and
microscopically
.
The
expressions
of
CDX
2
and
MUC
2
were
determined
by
real-time
polymerase
chain
reaction
(
RT-PCR
)
and
immunohistochemistry
.
Ki-
67
antigen
expression
was
determined
by
immunohistochemistry
.
The
mRNA
levels
of
cyclin
D
1
,
c-
Myc
,
Bax
and
Bcl-
2
were
determined
by
RT-PCR
.
Cell
apoptosis
was
evaluated
using
the
TdT-mediated
dUTP
nick
-end
labeling
method
.
Esophagitis
,
Barrett
's
esophagus
(
BE
)
,
and
esophageal
adenocarcinoma
(
EAC
)
developed
in
rats
that
underwent
EGDA
.
When
comparing
rats
with
EGDA
and
concomitant
esophageal
H
.
pylori
colonization
to
EGDA-only
rats
,
the
severity
of
injury
(
87
.
9
±
5
.
2
vs
77
.
2
±
8
.
6
,
macroscopically
,
92
.
5
±
8
.
0
vs
83
.
8
±
5
.
5
,
microscopically
,
both
P
<
0
.
05
)
and
the
incidences
of
BE
(
80
.
0
%
vs
33
.
3
%
,
P
=
0
.
055
)
and
EAC
(
60
.
0
%
vs
11
.
1
%
,
P
<
0
.
05
)
were
increased
.
These
increases
were
associated
with
upregulation
of
CDX
2
and
MUC
2
mRNA
(
10
.
1
±
5
.
4
vs
3
.
0
±
2
.
9
,
8
.
4
±
4
.
6
vs
2
.
0
±
3
.
2
,
respectively
,
Ps
<
0
.
01
)
and
protein
(
8
.
1
±
2
.
3
vs
3
.
3
±
3
.
1
,
7
.
3
±
4
.
0
vs
1
.
8
±
2
.
7
,
respectively
,
all
P
<
0
.
05
)
.
The
expression
of
Ki-
67
(
8
.
9
±
0
.
7
vs
6
.
0
±
1
.
7
,
P
<
0
.
01
)
and
the
presence
of
apoptotic
cells
(
8
.
3
±
1
.
1
vs
5
.
3
±
1
.
7
,
P
<
0
.
01
)
were
also
increased
significantly
in
rats
with
EGDA
and
concomitant
esophageal
H
.
pylori
colonization
compared
with
rats
with
EGDA
only
.
The
mRNA
levels
of
cyclin
D
1
(
5
.
8
±
1
.
9
vs
3
.
4
±
1
.
3
,
P
<
0
.
01
)
,
c-
Myc
(
6
.
4
±
1
.
7
vs
3
.
7
±
1
.
2
,
P
<
0
.
01
)
,
and
Bax
(
8
.
6
±
1
.
6
vs
5
.
1
±
1
.
3
,
P
<
0
.
01
)
were
significantly
increased
,
whereas
the
mRNA
level
of
Bcl-
2
(
0
.
6
±
0
.
3
vs
0
.
8
±
0
.
3
,
P
<
0
.
01
)
was
significantly
reduced
in
rats
with
EGDA
and
concomitant
esophageal
H
.
pylori
colonization
compared
with
rats
with
EGDA
only
.
Esophageal
H
.
pylori
colonization
increases
esophagitis
severity
,
and
facilitates
the
development
of
BE
and
EAC
with
the
augmentation
of
cell
proliferation
and
apoptosis
in
esophageal
mucosa
.
Diseases
Validation
Diseases presenting
"esophageal injuries"
symptom
esophageal adenocarcinoma
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