Research Square (Research Square),
Год журнала:
2023,
Номер
unknown
Опубликована: Июль 14, 2023
Abstract
Purpose
This
study
aimed
to
evaluate
the
factors
associated
with
constipation
and
efficacy
of
distal
resection
length
(DRL)
not
less
than
3cm
in
males
anorectal
malformation
(ARM).
Methods
Demographic,
anomalies,
clinical
features,
bowel
function
ARM
rectourethral/rectovesical
fistula
(RUF/RVF)
were
evaluated.
The
Krickenbeck
scores
used
assess
function.
Univariate
multivariate
analysis
identify
constipation.
was
evaluated
between
groups
categorized
by
DRL
after
1:1
propensity
score
matching
(PSM).
Result
A
total
153
a
median
follow-up
period
6
years,
54(35.2%)
suffered
from
Multivariate
revealed
that
(OR
=
0.68,
P
0.007)
is
only
independent
protective
factor
potty
training.
After
PSM,
35
patients
included
each
DRL≥3.0cm
DRL<3cm,
well-balanced.
No
significant
differences
noted
postoperative
complications
(11.4%
vs.
25.7%
0.218)
constant
soiling
(17.1%
31.4%,
0.718).
However,
incidence
group
significantly
lower
DRL<3cm
group(37.1%
71.4%,
0.028).
Conclusion
longer
for
constipation,
suggesting
excessive
preservation
rectal
pouch
cause
And
rate
≥3cm
without
increment
which
may
be
fibrosis
last
pouch.
Thus,
recommended
resect
ARM.
World Journal of Gastroenterology,
Год журнала:
2024,
Номер
30(31), С. 3689 - 3704
Опубликована: Авг. 13, 2024
Inflammatory
bowel
disease,
particularly
Crohn's
disease
(CD),
has
been
associated
with
alterations
in
mesenteric
adipose
tissue
(MAT)
and
the
phenomenon
termed
"creeping
fat".
Histopathological
evaluations
showed
that
MAT
intestinal
tissues
were
significantly
altered
patients
CD,
these
characterized
by
inflammation
fibrosis.
Frontiers in Medicine,
Год журнала:
2024,
Номер
11
Опубликована: Июнь 14, 2024
Intestinal
fibrosis
is
a
common
complication
of
chronic
intestinal
diseases
with
the
characteristics
fibroblast
proliferation
and
extracellular
matrix
deposition
after
inflammation,
leading
to
lumen
narrowing,
structural
functional
damage
intestines,
life
inconvenience
for
patients.
However,
anti-inflammatory
drugs
are
currently
generally
not
effective
in
overcoming
making
surgery
main
treatment
method.
The
development
slow
process
its
onset
may
be
result
combined
action
inflammatory
cells,
local
cytokines,
stromal
cells.
aim
this
study
elucidate
pathogenesis
[e.g.,
(ECM),
cytokines
chemokines,
epithelial-mesenchymal
transition
(EMT),
differentiation
myofibroblast
microbiota]
underlying
explore
therapeutic
advances
(such
as
regulating
ECM,
EMT,
targeting
TGF-
β
)
based
on
order
gain
new
insights
into
prevention
fibrosis.
Frontiers in Cell and Developmental Biology,
Год журнала:
2023,
Номер
11
Опубликована: Сен. 26, 2023
In
inflammatory
bowel
disease
(IBD),
chronic
inflammation
in
the
gastrointestinal
tract
can
lead
to
tissue
damage
and
remodelling,
which
ultimately
result
fibrosis.
Prolonged
injury
trigger
activation
of
fibroblasts
extracellular
matrix
(ECM)
components.
As
fibrosis
progresses,
becomes
increasingly
stiff
less
functional,
complications
such
as
intestinal
strictures,
obstructive
symptoms,
eventually,
organ
dysfunction.
Epithelial
cells
play
a
key
role
fibrosis,
they
secrete
cytokines
growth
factors
that
promote
fibroblast
ECM
deposition.
Additionally,
epithelial
undergo
process
called
epithelial-mesenchymal
transition,
acquire
more
mesenchymal-like
phenotype
contribute
directly
Overall,
interactions
between
cells,
immune
critical
development
progression
IBD.
Understanding
these
complex
may
provide
new
targets
for
therapeutic
interventions
prevent
or
treat
this
review,
we
have
collected
discussed
recent
literature
highlighting
contribution
pathogenesis
fibrotic
IBD,
including
evidence
EMT,
epigenetic
control
potential
influence
microbiome
possible
strategies
target
EMT.
Finally
discuss
pro-fibrotic
epithelial-immune
epithelial-fibroblasts
cells.
World Journal of Gastroenterology,
Год журнала:
2024,
Номер
30(13), С. 1801 - 1809
Опубликована: Апрель 2, 2024
Advancements
in
murine
modeling
systems
for
ulcerative
colitis
have
diversified
our
understanding
of
the
pathophysiological
factors
involved
disease
onset
and
progression.
This
has
fueled
identification
molecular
targets,
resulting
a
rapidly
expanding
therapeutic
armamentarium.
Subsequently,
management
strategies
evolved
from
symptomatic
resolution
to
well-defined
objective
endpoints,
including
clinical
remission,
endoscopic
remission
mucosal
healing.
While
incorporation
these
assessment
modalities
permitted
targeted
intervention
context
natural
history
prevention
complications,
studies
consistently
depicted
discrepancies
associated
with
ascertaining
status
through
measures.
Current
recommendations
lack
consideration
histological
The
simultaneous
achievement
clinical,
endoscopic,
histologic
not
been
fully
investigated.
laid
groundwork
novel
outcome
termed
clearance
(DC).
article
summarizes
concept
DC
its
current
evidence.
Foods,
Год журнала:
2023,
Номер
12(6), С. 1192 - 1192
Опубликована: Март 11, 2023
Polyacetylene
phytochemicals
are
emerging
as
potentially
responsible
for
the
chemoprotective
effects
of
consuming
apiaceous
vegetables.
There
is
some
evidence
suggesting
that
polyacetylenes
(PAs)
impact
carcinogenesis
by
influencing
a
wide
variety
signalling
pathways,
which
important
in
regulating
inflammation,
apoptosis,
cell
cycle
regulation,
etc.
Studies
have
shown
correlation
between
human
dietary
intake
PA-rich
vegetables
with
reduced
risk
inflammation
and
cancer.
PA
supplementation
can
influence
growth,
gene
expression
immunological
responses,
has
been
to
reduce
tumour
number
rat
mouse
models.
Cancer
chemoprevention
PAs
involves
several
mechanisms,
including
on
inflammatory
cytokines,
NF-κB
pathway,
antioxidant
response
elements,
unfolded
protein
(UPR)
growth
factor
signalling,
progression
apoptosis.
This
review
summarises
published
research
falcarinol-type
compounds
their
mechanisms
action
regarding
cancer
also
identifies
gaps
our
current
understanding
health
benefits
these
PAs.
Fibrosis
represents
a
process
characterized
by
excessive
deposition
of
extracellular
matrix
(ECM)
proteins.
It
often
the
evolution
pathological
conditions,
causes
organ
failure,
and
can,
in
extreme
cases,
compromises
functionality
organs
to
point
causing
death.
In
recent
years,
considerable
efforts
have
been
made
understand
molecular
mechanisms
underlying
fibrotic
identify
possible
therapeutic
strategies.
Great
interest
has
aroused
discovery
association
between
epithelial
mesenchymal
plasticity
(EMP),
particular
transition
(EMT),
fibrogenesis,
which
led
identification
complex
closely
interconnected
with
each
other,
could
explain
EMT-dependent
fibrosis.
However,
result
remains
unsatisfactory
from
view.
advances
epigenetics,
is
based
on
chromatin
remodeling
through
various
histone
modifications
or
intervention
non-coding
RNAs
(ncRNAs),
provided
more
information
process,
this
represent
promising
path
forward
for
innovative
strategies
review,
we
summarize
current
research
epigenetic
involved
fibrosis,
focus
regulation
EMP/EMT-dependent
Inflammation Research,
Год журнала:
2024,
Номер
73(8), С. 1359 - 1370
Опубликована: Июнь 6, 2024
Abstract
Background
and
aims
Intestinal
fibrosis
is
a
common
complication
of
Inflammatory
Bowel
Disease
(IBD),
namely
Crohn's
disease
(CD)
ulcerative
colitis
(UC),
but
the
precise
mechanism
by
which
it
occurs
incompletely
understood
hampering
development
effective
therapeutic
strategies.
Here,
we
aimed
at
inducing
characterizing
an
inflammation-mediated
in
patient-derived
organoids
(PDOs)
issued
from
crypts
isolated
colonic
mucosal
biopsies
IBD
pediatric
patients
age
matched-control
subjects
(CTRLs).
Methods
Inflammatory-driven
was
induced
exposing
CTRL-,
CD-
UC-PDOs
to
pro-inflammatory
cytokine
TNF-α
for
one
day,
followed
co-treatment
with
TGF-β1
three
days.
Fibrotic
response
proven
analyzing
inflammatory
fibrotic
markers
RT-qPCR
immunofluorescence.
Transcriptomic
changes
were
assessed
RNA-sequencing.
Results
Co-treatment
caused
CTRL-
IBD-PDOs
morphological
towards
mesenchymal-like
phenotype
up-regulation
inflammatory,
mesenchymal,
markers.
profiling
highlighted
that
all
intestinal
PDOs,
regardless
disease,
co-exposure
regulated
EMT
genes
specifically
increased
involved
positive
regulation
cell
migration.
Finally,
demonstrated
CD-PDOs
display
specific
compared
both
UC-PDOs,
mainly
characterized
upregulation
nuclear
factors
controlling
transcription.
Conclusions
This
study
demonstrates
PDOs
may
develop
inflammatory-derived
thus
representing
promising
tool
fibrogenesis
IBD.
show
expression
genes.
In
particular,
gene
signature
UC
CTRL-PDOs.
Journal of Inflammation Research,
Год журнала:
2025,
Номер
Volume 18, С. 1413 - 1423
Опубликована: Фев. 1, 2025
Purpose:
Intestinal
fibrous
stenosis
due
to
Crohn's
disease
(CD)
is
highly
prevalent.
Although
several
clinical
risk
factors
for
have
been
identified,
such
as
perianal
fistulizing
disease,
small
bowel
location,
and
deep
mucosal
ulceration,
predicting
remains
challenging.
The
intestinal
microbiota
plays
a
crucial
role
in
the
development
progression
of
CD.
However,
its
poorly
understood.
Leveraging
single-center
cross-sectional
study,
we
aimed
investigate
fecal
CD-associated
stenosis.
Methods:
Using
metagenomic
analysis,
examined
differences
between
CD
patients
with
those
without
We
identified
specific
assessed
their
predictive
accuracy
Additionally,
explored
functional
two
groups.
Results:
:
Our
investigation
samples
revealed
no
significant
gut
structure
taxonomically,
found
70
taxa
significantly
different
abundance
(p
<
0.05)
Furthermore,
LEfSe
analysis
indicated
that
g_Bacteroides
g_Enterocloster
could
predict
while
p_Actinobacteria,
c_Actinomycetia,
c_Bacilli,
o_Lactobacillales,
f_Streptococcaceae
g_Streptococcus
Functional
differential
enrichment
five
metabolic
pathways
at
KEGG
pathway
level
stenosis,
including
sphingolipid
metabolism,
lipoic
acid
biosynthesis
neomycin,
kanamycin
gentamicin.
In
eggNOG
database,
observed
four
categories
groups,
encompassing
cellular
process,
signaling,
metabolism.
Conclusion:
Fecal
impacted
there
were
alpha
beta
diversities,
was
associated
changes
composition
function,
suggesting
potential
Keywords:
microbiota,
Chronische
Leberschäden,
wie
die
mit
metabolischer
Dysfunktion
assoziierte
steatotische
Lebererkrankung
(MASLD),
virale
Hepatitis
B
oder
C,
cholestatische
Hepatitiden
(PBC,
PSC),
toxische
Schädigungen
(Alkohol)
genetische
Alterationen
(Hämochromatose,
Morbus
Wilson
usw.)
verursachen
in
der
Regel
eine
chronische
Entzündungsreaktion
Leberzellen
Gallengangepithelien.
Diese
kann
über
längere
Zeit
zu
einer
Vernarbung
Leber,
sog.
Fibrose
führen.
Die
Leberfibrose
ist
dabei
größtenteils
unabhängig
vom
schädigenden
Agens,
obwohl
das
Muster
anfänglichen
(periportal,
perizentral
sinusoidal)
durchaus
variieren
kann.
unbehandelte
und
fortschreitende
Darm
anderen
parenchymatösen
Organen
teils
vollständiger
architektonischer
Dekonstruktion
Ablagerung
von
Bindegewebe,
sukzessivem
Funktionsverlust
Im
Endstadium
Leberzirrhose
können
portale
Hypertension,
Enzephalopathie,
Blutungen
Karzinome
(hepatozelluläres
Karzinom
[HCC],
intrahepatische
cholangiozelluläre
[iCCCa])
auftreten.
intestinale
schwerwiegendsten
Komplikationen
bei
Crohn.
Durch
neuartige
konsequente
therapeutische
Interventionen
fibrotische
Prozesse
gestoppt
reversibel
gemacht
werden.
Neue
Forschungstechnologien
haben
unser
Wissen
Leberfibrogenese
Darmfibrose
erheblich
verbessert.
Der
Schwerpunkt
dieser
Übersichtsarbeit
liegt
auf
MASLD
dem
Crohn,
chronischen
entzündlichen
Erkrankungen
Leber
steigender
Prävalenz
großen
Auswirkungen
Allgemeinbevölkerung.
aktuellen
Grundlagen
potenziellen
Möglichkeiten
präventiver
therapeutischer
antifibrotischer
werden
illustriert.