BPB Reports,
Год журнала:
2023,
Номер
6(6), С. 209 - 216
Опубликована: Янв. 1, 2023
Ethanol,
a
widely
used
toxic
chemical
in
human
cultures,
exerts
its
toxicity
throughout
the
body,
with
nervous
system
being
particularly
vulnerable,
leading
to
various
neurological
disorders.
Despite
prevalence
of
peripheral
neuropathies
associated
alcohol
abuse,
causal
mechanism
ethanol-induced
remains
largely
unknown.
This
study
investigated
impact
repeated
ethanol
intake
on
histological
features
trigeminal
ganglia
mice.
Histological
analysis
revealed
that
blood
vessels
exhibited
distinct
morphological
and
molecular
characteristics
based
their
location,
specifically
regions
where
neuronal
cell
bodies
or
axonal
fibers
predominate.
Administration
binge
level
for
four
consecutive
days
induced
significant
vessel
remodeling
both
regions.
Unexpectedly,
morphology
neurons
axons
remained
unaffected
by
ethanol.
Given
observed
suppression
IBA1/AIF1-positive
microglia-like
cells
ethanol,
we
explored
whether
manipulative
activity
minocycline
could
recapitulate
effects.
Remarkably,
administration
minocycline,
instead
resulted
similar
remodeling,
suggesting
causes
through
ganglia.
These
findings
provide
valuable
insights
into
complex
interplay
between
exposure,
activity,
vascular
changes
Psychological Medicine,
Год журнала:
2024,
Номер
54(10), С. 2482 - 2491
Опубликована: Март 12, 2024
Abstract
Background
Cerebral
microvascular
dysfunction
may
contribute
to
depression
via
disruption
of
brain
structures
involved
in
mood
regulation,
but
evidence
is
limited.
We
investigated
the
association
retinal
function,
a
proxy
for
function
brain,
with
incidence
and
trajectories
clinically
relevant
depressive
symptoms.
Methods
Longitudinal
data
are
from
The
Maastricht
Study
5952
participants
(59.9
±
8.5
years/49.7%
women)
without
symptoms
at
baseline
(2010–2017).
Central
arteriolar
equivalent
central
venular
(CRAE
CRVE)
composite
score
flicker
light-induced
dilation
were
assessed
baseline.
(9-item
Patient
Health
Questionnaire
⩾10).
Trajectories
included
continuously
low
prevalence
(low,
n
=
5225
[87.8%]);
early
increasing,
then
chronic
high
(early-chronic,
157
[2.6%]);
low,
increasing
(late-increasing,
247
[4.2%]);
remitting
(remitting,
323
[5.4%]).
Results
After
median
follow-up
7.0
years
(range
1.0–11.0),
806
(13.5%)
individuals
had
incident
full
adjustment,
larger
CRAE
CRVE
each
associated
lower
risk
(hazard
ratios
[HRs]
per
standard
deviation
[
s.d.
]:
0.89
[95%
confidence
interval
(CI)
0.83–0.96]
0.93
[0.86–0.99],
respectively),
while
was
higher
(HR
:
1.10
[1.01–1.20]).
Compared
trajectory,
odds
belonging
early-chronic
trajectory
(OR:
0.83
[0.69–0.99])
1.23
[1.07–1.43]).
Conclusions
These
findings
support
hypothesis
that
cerebral
contributes
development
The Clinician,
Год журнала:
2024,
Номер
18(1), С. 31 - 36
Опубликована: Июнь 23, 2024
Alcoholic
cardiomyopathy
is
the
most
common
form
of
myocardial
damage
caused
by
ethanol.
Ethanol
and
its
main
active
metabolite
acetaldehyde
have
a
direct
toxic
effect
on
myocardium.
The
mechanisms
cardiotoxic
ethanol
are
diverse
include
membranotropic
action,
to
cellular
organelles,
activation
lipid
peroxidation,
number
others.
Dissolving
in
lipids
biological
membranes,
changes
their
physico-chemical
properties,
disrupts
activity
membrane
receptors,
eventually
disconnecting
connection
excitation
with
contraction
cardiomyocytes.
Particular
importance
pathogenesis
alcoholic
attached
ability
cause
structural
functional
mitochondria,
which
directly
related
violation
oxidative
processes
energy
supply
myocardium
as
whole.
Under
influence
alcohol,
free-radical
oxidation
products
content
increases
antioxidants
decreases,
indicates
stress
development.
deterioration
contractility
due
chronic
alcohol
intoxication
triggers
cascade
compensatory
cardiomyocyte
hypertrophy
progressive
fibrosis,
while
adaptive
reactions
become
factor
further
pathological
changes.
causes
dose-dependent
manner.
probability
occurrence
derivative
total
accumulated
dose
individual
predisposition.
considered
variant
secondary
dilated
all
clinical
manifestations
consequences:
dilation
heart
chambers,
low
left
ventricular
ejection
fraction,
circulatory
insufficiency,
cardiac
arrhythmias.
A
relatively
favorable
prognosis
provided
partial
reversibility
under
condition
abstinence
from
consumption.
Specific
drugs
for
treatment
not
been
developed.
New
strategies
use
growth
regulation
factors
synthesized
cardiomyocytes,
well
stimulation
muscle
regeneration
repair
processes.
IntroductionWe
first
examined
the
role
of
age
at
cardiovascular
disease
(CVD)
onset
for
incident
dementia,
and
then
whether
lifestyle
factors
guideline-recommended
levels
in
those
with
CVD
mitigate
dementia
risk.
MethodsWe
used
population-based
data
(Whitehall
II;
n=10,308;
baseline
1985-1988;
examinations
every
4
to
5
years).Lifestyle
(nonsmoking,
body
mass
index,
physical
activity
diet)
were
extracted
from
clinical
examination
after
diagnosis.
ResultsOver
a
median
31.6
years,
3,275
(32.1%)
developed
CVD.At
70,
risk
was
higher
before
(hazard
ratio
(HR)
participants
60,
using
without
70
as
reference
1.56
(95%
CI
1.18;
2.08))
but
not
60
years.In
CVD,
greater
number
recommended
diagnosis
associated
lower
(per
factor
level
HR
0.73
0.59;
0.92)).
DiscussionOur
results
suggest
that
early
is
older
ages.In
if
following
diagnosis.Chapter
2
34
Table
2.1
Characteristics
total
study
population,
according
status.Total
population
(n=10,216)
Dementia
status
end
follow-up
,
March
2019
No
(n=9,566,
93.6%)
(n=650,
6.4%)
Age
follow-up,
years
74.7
(7.2)
74.6
76.7
(6.0)
Female
sex,
n
(%)
3,361
(32.9)
3,089
(32.3)
272
(41.9)Married/cohabiting,
7,568
(74.1)
7,108
(74.3)
190
(29.2)
Education
≤Partial
secondary
school,
4,848
(47.5)
4,462
(46.6)
386
(59.4)
High
school
diploma,
2,714
(26.6)
2,578
(27.0)
136
(20.9)
≥University
degree,
2,654
(26.0)
2,526
(26.4)
128
(19.7)Race/ethnicity
White,
9,181
(89.9)
8,626
(90.2)
555
(85.4)
non-White,
1,035
(10.1)
940
(9.8)
95
(14.6)Cardiovascular
disease,
(32.1)
2,917
(30.5)
358
(55.1)Coronary
heart
2,290
(22.4)
2,075
(21.7)
215
(33.1)Stroke,
511
(5.0)
403
(4.2)
108
(16.6)Atrial
fibrillation,
1,343
(13.2)
1.149
(12.0)
194
(29.9)Heart
failure,
635
(6.2)
531
(5.6)
104
(16.0)Type
diabetes
1,663
(16.3)
1,497
(15.7)
166
(25.6)Hypertension
6,730
(65.9)
6,201
(64.8)
529
(81.4)
Lifestyle
b
n=7,940
n=7,444
n=496
Body
kg/m
26.3
(4.3)
<30
6,647
(83.7)
6,235
(83.8)
412
(83.1)Nonsmokers,
6,974
(87.8)
6,551
(88.0)
423
(85.3)Moderate-to-vigorous
activity,
min/week
165
(56;
315)
167
122
(36;
300)
Moderate-to-vigorous
≥150
min/week,
4,223
(53.2)
3,978
(53.4)
245
(49.4)
Dietary
habits
optimal
c
1,977
(24.9)
1.892
(25.4)
85
(17.1)Number
3
(2;
3)
Data
are
means
(SD)
or
(interquartile
range),
unless
otherwise
indicated.a
Median
range)
overall
follow
up
(31.1;
32.6)
it
31.8
32.7)
27.5
(24.6;
30.2)
follow-up.b
on
shown
2,276
participants,
6
excluded
due
341
died
1,929
had
missing
factors.c
defined
consumption
fruit
vegetable
twice
day
more
high
fibre
bread.
Association
dementiaThe
association
prevalent
55,
65
2.2.Results
show
(i.e.ages
65)
dementia.At
compared
(HR
1.52
1.09;
2.13)).This
also
case
1.59
1.23;
2.05))
BPB Reports,
Год журнала:
2023,
Номер
6(6), С. 209 - 216
Опубликована: Янв. 1, 2023
Ethanol,
a
widely
used
toxic
chemical
in
human
cultures,
exerts
its
toxicity
throughout
the
body,
with
nervous
system
being
particularly
vulnerable,
leading
to
various
neurological
disorders.
Despite
prevalence
of
peripheral
neuropathies
associated
alcohol
abuse,
causal
mechanism
ethanol-induced
remains
largely
unknown.
This
study
investigated
impact
repeated
ethanol
intake
on
histological
features
trigeminal
ganglia
mice.
Histological
analysis
revealed
that
blood
vessels
exhibited
distinct
morphological
and
molecular
characteristics
based
their
location,
specifically
regions
where
neuronal
cell
bodies
or
axonal
fibers
predominate.
Administration
binge
level
for
four
consecutive
days
induced
significant
vessel
remodeling
both
regions.
Unexpectedly,
morphology
neurons
axons
remained
unaffected
by
ethanol.
Given
observed
suppression
IBA1/AIF1-positive
microglia-like
cells
ethanol,
we
explored
whether
manipulative
activity
minocycline
could
recapitulate
effects.
Remarkably,
administration
minocycline,
instead
resulted
similar
remodeling,
suggesting
causes
through
ganglia.
These
findings
provide
valuable
insights
into
complex
interplay
between
exposure,
activity,
vascular
changes
