Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: July 27, 2024
Methadone
maintenance
treatment
for
opioid
dependent
mothers
is
standard
of
care.
Infants
methadone
maintained
(MMOD)
have
better
outcomes
compared
to
infants
without
treatment.
However,
when
non-exposed
infants,
MMOD
are
associated
with
worse
outcomes.
We
conducted
a
pilot
study
examine
genome
wide
differential
DNA
methylation
using
cord
blood
samples
from
sixteen
term
and
near-term
naïve
mothers,
excluding
chorioamnionitis.
A
total
152
differentially
methylated
loci
were
identified
at
difference
>
+
2,
<
−
2
p-value
0.05.
There
90
hypermethylated
(59
annotated
genes)
62
hypomethylated
(38
observed.
The
changes
involved
multiple
genes,
pathways
networks
that
may
explain
some
the
seen
in
mothers.
Top
genes
areas
cell
growth,
neurodevelopment,
vision
xenobiotic
metabolism
functions.
Our
data
role
key
relevant
neonatal
exposure
pregnancy.
Functional
studies
on
could
lead
improved
understanding
mechanisms
identify
intervention.
Journal of Cardiovascular Development and Disease,
Journal Year:
2024,
Volume and Issue:
11(1), P. 26 - 26
Published: Jan. 16, 2024
In
patent
ductus
arteriosus
(PDA)
in
preterm
infants,
the
relationship
between
treatment
timing
and
long-term
developmental
prognosis
remains
unclear.
The
purpose
of
this
study
was
to
clarify
age
days
when
closure
occurred
development.
Preterm
infants
with
a
birth
weight
less
than
1500
g
who
were
admitted
our
NICU
over
period
9
years
(2011–2019)
diagnosed
PDA
included.
A
new
version
K-type
test
for
corrected
ages
1.5
3
used
as
an
index
duration
evaluated
using
Pearson’s
correlation
coefficient,
multiple
regression
analysis
performed.
Development
quotient
(DQ)
at
showed
date
standard
deviation
(SD)
value
term
weight.
Multiple
positive
DQ
SD
negative
date.
addition,
stronger
found
“posture/motor”
sub-item
years.
On
other
hand,
including
without
that
on
6th
day
or
later
after
had
significantly
lower
3-year-old
exposure
within
5
days.
conclusion,
it
is
suggested
decrease
cerebral
blood
flow
due
has
adverse
effect
neurodevelopment.
Appropriate
interventions,
surgical
delay,
ideally
birth,
may
be
effective
improving
prognosis.
Redox Biology,
Journal Year:
2023,
Volume and Issue:
66, P. 102865 - 102865
Published: Aug. 29, 2023
Oxygen
therapy
is
common
during
the
neonatal
period
to
improve
survival,
but
it
can
increase
risk
of
oxygen
toxicity.
Hyperoxia
damage
multiple
organs
and
systems
in
newborns,
commonly
causing
lung
conditions
such
as
bronchopulmonary
dysplasia
pulmonary
hypertension,
well
other
organs,
including
brain,
gut,
eyes.
These
are
collectively
referred
newborn
radical
disease
indicate
multi-system
caused
by
hyperoxia.
also
lead
changes
metabolic
pathways
production
abnormal
metabolites
through
a
process
called
reprogramming.
Currently,
some
studies
have
analyzed
mechanism
reprogramming
induced
The
focus
has
been
on
mitochondrial
oxidative
stress,
dynamics,
multi-organ
interactions,
lung–gut,
lung–brain,
brain–gut
axes.
In
this
article,
we
provide
an
overview
major
pathway
reported
hyperoxia-associated
diseases
explore
potential
mechanisms
Metabolic
hyperoxia
cause
disorders
glucose,
lipid,
amino
acid
metabolism.
Moreover,
may
predict
occurrence
disease,
suggesting
their
therapeutic
targets.
Although
requires
further
elucidation,
mitochondria
gut–lung–brain
axis
play
key
role
AJP Lung Cellular and Molecular Physiology,
Journal Year:
2024,
Volume and Issue:
326(5), P. L517 - L523
Published: March 12, 2024
Extracellular
vesicle
(EV)
biology
in
neonatal
lung
development
and
disease
is
a
rapidly
growing
area
of
investigation.
Although
EV
research
the
population
lags
behind
adult
diseases,
recent
discoveries
demonstrate
promise
furthering
our
understanding
pathophysiology
bronchopulmonary
dysplasia
potential
use
EVs
clinical
setting,
as
both
biomarkers
therapeutic
agents.
This
review
article
explores
some
advances
this
field
evolving
knowledge
role
dysplasia.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2022,
Volume and Issue:
2022, P. 1 - 12
Published: May 25, 2022
Neonatal
brain
injury
is
often
caused
by
preterm
birth.
Brain
development
vulnerable
to
increased
environmental
stress,
including
oxidative
stress
challenges.
Due
a
premature
change
of
the
fetal
living
environment
from
low
oxygen
in
utero
into
postnatal
high-oxygen
room
air
conditions
ex
utero,
immature
exposed
relative
hyperoxia,
which
can
induce
and
impair
neuronal
cell
development.
To
simulate
drastic
increase
exposure
brain,
5-day-old
C57BL/6
mice
were
hyperoxia
(80%
oxygen)
for
48
hours
or
kept
(normoxia,
21%
analyzed
maturational
alterations
cortical
GABAergic
interneurons.
As
result,
was
indicated
elevated
tyrosine
nitration
proteins.
We
found
perturbation
perineuronal
net
formation
line
with
decreased
density
parvalbumin-expressing
(PVALB)
interneurons
hyperoxic
mice.
Moreover,
deficits
PVALB+
obtained
glutamate
decarboxylase
67
(GAD67)
protein
expression
Western
blot
analysis
lower
gamma-aminobutyric
acid
(GABA)
fluorescence
intensity
immunostaining.
Hyperoxia-induced
affected
synaptogenesis
decreasing
synapsin
1,
2,
synaptophysin
expression.
Developmental
delay
synaptic
marker
demonstrated
together
PI3K-signaling
as
pathway
being
involved
synaptogenesis.
These
results
elucidate
that
neonatal
lead
interneuron
damage
may
serve
an
explanation
high
incidence
psychiatric
behavioral
infants.
Respiratory Research,
Journal Year:
2025,
Volume and Issue:
26(1)
Published: Jan. 24, 2025
Bronchopulmonary
dysplasia
(BPD)
is
a
chronic
lung
condition
of
premature
neonates,
yet
without
an
established
pharmacological
treatment.
The
BPD
rabbit
model
exposed
to
95%
oxygen
has
been
used
in
recent
years
for
drug
testing.
However,
the
toxicity
strong
hyperoxic
hit
precludes
longer-term
follow-up
due
high
mortality
after
first
week
life.
This
study
aimed
extend
preterm
postnatal
day
(PND)
14
mimic
evolving
phase
and
enable
investigation
therapeutic
interventions
at
later
more
relevant
time
points.
Preterm
pups
delivered
on
28th
gestation
were
either
room
air
or
different
degrees
hyperoxia
(50%
70%
O2)
days.
Single
(immediately
birth)
double
(at
birth
PND5)
intratracheal
lipopolysaccharide
(LPS)
administrations
also
tested
combination
with
50%
O2.
Age-matched
rabbits
vaginally
term
as
controls.
Survival,
weight
gain,
function,
pulmonary
artery
micro-ultrasound
Doppler
analysis,
histology
(alveolarization,
injury
score,
design-based
stereology),
longitudinal
micro-CT
imaging
compare
outcomes
PND14.
Premature
itself,
any
other
hit,
was
associated
function
deficits,
delayed
development,
cardiovascular
abnormalities.
BPD-like
phenotype
enhanced
by
O2
but
not
hyperoxia.
Intratracheal
LPS
immediately
significantly
higher
scores
PND14
increased
tissue
damping,
marker
parenchymal
resistance.
Several
strategies
are
feasible
saccular
even
absence
hits,
abnormalities
compared
age-matched
pups.
Enhanced
phenotypes
can
be
further
achieved
continued
exposure
moderate
(70%
administration
LPS.
Frontiers in Pediatrics,
Journal Year:
2025,
Volume and Issue:
13
Published: Feb. 14, 2025
Objective
1st:
To
determine
the
association
of
cerebral
oxygenation
(rcSO
2
)
and
concurrent
neurodevelopmental
outcomes
between
neonates
with
congenital
heart
disease
(CHD)
healthy
controls.
2nd:
examine
fractional
tissue
oxygen
extraction
(FTOE)
in
two
groups.
3rd:
evaluate
how
type
severity
CHD
influenced
associations
our
primary
secondary
objectives.
Study
design
Our
analysis
included
137
(74
63
controls).
We
used
linear
regression
models
to
predictors
(i.e.,
oxygenation,
FTOE,
CHD)
percentage
abnormal
neurobehavioral
scores
(outcome).
The
main
effects
group,
rcSO
,
a
-by-group
interaction
(examined
differences
groups)
covariates
postconceptional
age
at
exam,
sex,
ethnicity,
preductal
peripheral
saturation
on
scores.
also
performed
separate
separately
each
group.
these
for
2nd
3rd
objectives,
replacing
FTOE
as
predictors.
Results
Neonates
had
lower
values
(67%
vs.
79%;
p
<
0.001)
higher
(0.27
0.19;
compared
significantly
differed
groups
(
=
0.004).
In
increased
showed
trend
toward
better
outcomes.
However,
associated
poorer
Additionally,
0.012).
group
towards
Conversely,
Conclusions
different
both
findings
suggest
that
decreased
may
negatively
affect
neonates.
imply
critical
range
values,
where
extreme
either
side
be
harmful.
controls
exhibit
responses
due
differing
metabolic
demands.
Journal of Neuroinflammation,
Journal Year:
2025,
Volume and Issue:
22(1)
Published: Feb. 28, 2025
Abstract
Background
Premature
born
infants
are
at
high
risk
to
develop
white
matter
injury
(WMI).
Hyperoxia
and
perinatal
inflammation
main
factors
for
preterm
birth
associated
brain
injury.
To
date
the
majority
of
experimental
studies
have
focused
on
isolated
insults.
However,
clinically,
WMI
is
a
multifactorial
disorder
caused
by
variety
triggers.
establish
clinically
relevant
rodent
model
WMI,
we
combined
prenatal
with
postnatal
hyperoxia
investigate
individual,
additive
or
synergistic
effects
inflammatory
processes,
myelination
grey
development.
Methods
At
embryonic
day
20,
pregnant
Wistar
rat
dams
received
either
single
intraperitoneal
injection
100
µg/
kg
lipopolysaccharide
(LPS)
sodium
chloride.
Offspring
were
exposed
(80%
O
2
)
normoxia
(21%
from
3
5.
Animals
sacrificed
immediately
after
6
days
later,
corresponding
term-equivalent
age.
White
development
neuroinflammatory
responses
investigated
cellular
molecular
levels
applying
immunohistochemistry,
western
blotting,
real
time
PCR
in
tissues
multiplex
protein
expression
analysis
serum
samples.
Results
Prenatal
resulted
reduced
body
weight
length
offspring,
accompanied
increased
leptin
term
equivalent
The
altered
parameters,
like
weight,
decreased
volume,
thinning
deep
cortical
layers
hypomyelination.
As
potential
underlying
mechanisms,
identified
severe
deficits
an
microglia
activation
elevated
cytokine
tissues,
while
peripheral
reduced.
Interestingly,
size
mainly
mediated
LPS,
independent
hyperoxia,
oligodendrocyte
degeneration
was
induced
inflammation.
pathological
changes,
including
size,
deficits,
expression,
detected.
Conclusion
results
aggravated
compared
insults,
making
it
ideal
improve
our
understanding
complex
pathophysiology
evaluate
urgently
needed
therapies.
Cells,
Journal Year:
2025,
Volume and Issue:
14(6), P. 443 - 443
Published: March 16, 2025
Despite
improved
neonatal
intensive
care,
the
risk
of
premature-born
infants
developing
bronchopulmonary
dysplasia
(BPD)
and
encephalopathy
prematurity
(EoP)
remains
high.
With
hyperoxia
being
a
major
underlying
factor,
both
preterm-birth-related
complications
are
suggested
to
be
closely
interrelated.
However,
experimental
models
lacking
for
assessment
potentially
close
interplay
between
organs.
To
establish
model,
suitable
affected
organs,
Wistar
rats
were
exposed
80%
oxygen
from
postnatal
day
2
(P2)
seven
days.
Brain
lung
tissues
analysed
via
histomorphometry,
immunohistochemistry,
real-time
PCR,
western
blot
at
term
P11.
In
brain,
induced
significant
hypomyelination
accompanied
by
reduction
in
oligodendrocytes
CD68
expression
on
microglia
cells.
These
changes
correlate
with
arrested
alveolarisation
an
increased
number
macrophages
lung.
Interestingly,
contrast
reduced
formation
pulmonary
microvessels,
vascular
density
was
detected
brain.
Seven
days
induces
typical
characteristics
BPD
EoP
rats,
thereby
linking
impaired
disturbed
myelination
brain
providing
model
understanding
pathophysiological
mechanisms
identifying
organ-spanning
novel
therapeutic
interventions
targeting
diseases.