Neurological Research and Practice,
Год журнала:
2024,
Номер
6(1)
Опубликована: Апрель 11, 2024
Abstract
Background
Stroke
is
a
severe
complication
of
infective
endocarditis
(IE),
associated
with
high
rates
mortality.
Data
on
how
IE
patients
and
without
stroke
differ
may
help
to
improve
understanding
contributing
mechanisms.
Methods
All
treated
for
between
2019
2021
were
identified
from
the
medical
records
three
academic
tertiary
care
hospitals
in
Germany,
all
part
Charité
–
Universitätsmedizin
Berlin,
Germany.
Multivariable
logistic
regression
analyses
performed
identify
variables
occurrence
stroke.
Results
The
study
population
consisted
353
diagnosed
IE.
Concomitant
occurred
96/353
(27.2%)
patients.
Acute
was
independently
co-occurring
extracerebral
arterial
embolism
[adjusted
Odds
ratio
(aOR
=
2.52;
95%
confidence
interval
(CI)
1.35–4.71)],
acute
liver
failure
2.62;
CI
1.06–6.50),
dental
focus
infection
3.14;
1.21–8.12)
left-sided
28.26;
3.59-222.19).
found
less
often
congenital
heart
disease
0.20;
0.04–0.99)
atypical
pathogens
isolated
blood
culture
0.31;
0.14–0.72).
Conclusions
more
likely
occur
individuals
systemic
complications
affecting
other
organs,
too.
Special
attention
should
be
addressed
status.
low
incidence
reflect
awareness
prophylactic
measures.
Frontiers in Immunology,
Год журнала:
2023,
Номер
13
Опубликована: Фев. 2, 2023
Ischemic
stroke
(IS)
is
one
of
the
most
fatal
diseases.
Neuroimmunity,
inflammation,
and
oxidative
stress
play
important
roles
in
various
complex
mechanisms
IS.
In
particular,
early
proinflammatory
response
resulting
from
overactivation
resident
microglia
infiltration
circulating
monocytes
macrophages
brain
after
cerebral
ischemia
leads
to
secondary
injury.
Microglia
are
innate
immune
cells
that
constantly
monitor
microenvironment
under
normal
conditions.
Once
occurs,
activated
produce
dual
effects
neurotoxicity
neuroprotection,
balance
two
determines
fate
damaged
neurons.
The
activation
defined
as
classical
(M1
type)
or
alternative
(M2
type).
M1
type
secrete
pro-inflammatory
cytokines
neurotoxic
mediators
exacerbate
neuronal
damage,
while
M2
promote
a
repairing
anti-inflammatory
response.
Fine
regulation
M1/M2
microglial
minimize
damage
maximize
protection
has
therapeutic
value.
This
review
focuses
on
interaction
between
other
involved
IS
phenotypic
characteristics,
mechanism
natural
plant
components
regulating
IS,
providing
novel
candidate
drugs
for
drug
development.
Glia,
Год журнала:
2024,
Номер
72(6), С. 1016 - 1053
Опубликована: Янв. 4, 2024
Abstract
Microglia
play
key
roles
in
the
post‐ischemic
inflammatory
response
and
damaged
tissue
removal
reacting
rapidly
to
disturbances
caused
by
ischemia
working
restore
lost
homeostasis.
However,
modified
environment,
encompassing
ionic
imbalances,
disruption
of
crucial
neuron–microglia
interactions,
spreading
depolarization,
generation
danger
signals
from
necrotic
neurons,
induce
morphological
phenotypic
shifts
microglia.
This
leads
them
adopt
a
proinflammatory
profile
heighten
their
phagocytic
activity.
From
day
three
post‐ischemia,
macrophages
infiltrate
core
while
microglia
amass
at
periphery.
Further,
inflammation
prompts
metabolic
shift
favoring
glycolysis,
pentose‐phosphate
shunt,
lipid
synthesis.
These
shifts,
combined
with
intake,
drive
droplet
biogenesis,
fuel
anabolism,
enable
proliferation.
Proliferating
release
trophic
factors
contributing
protection
repair.
some
accumulate
lipids
persistently
transform
into
dysfunctional
potentially
harmful
foam
cells.
Studies
also
showed
that
either
display
impaired
apoptotic
cell
clearance,
or
eliminate
synapses,
viable
endothelial
Yet,
it
will
be
essential
elucidate
viability
engulfed
cells,
features
local
extent
damage,
temporal
sequence.
Ischemia
provides
rich
variety
region‐
injury‐dependent
stimuli
for
microglia,
evolving
time
generating
distinct
phenotypes
including
those
exhibiting
traits
others
showing
pro‐repair
features.
Accurate
profiling
phenotypes,
alongside
more
precise
understanding
associated
conditions,
is
necessary
step
serve
as
potential
foundation
focused
interventions
human
stroke.
Cell Death Discovery,
Год журнала:
2024,
Номер
10(1)
Опубликована: Янв. 13, 2024
Abstract
Copper
is
an
essential
micronutrient
that
plays
a
pivotal
role
in
numerous
physiological
processes
virtually
all
cell
types.
Nevertheless,
the
dysregulation
of
copper
homeostasis,
whether
towards
excess
or
deficiency,
can
lead
to
pathological
alterations,
such
as
atherosclerosis.
With
advent
concept
copper-induced
death,
termed
cuproptosis,
researchers
have
increasingly
focused
on
potential
dyshomeostasis
In
this
review,
we
provide
broad
overview
cellular
and
systemic
metabolism.
We
then
summarize
evidence
linking
atherosclerosis
elucidate
mechanisms
underlying
development
terms
both
deficiency.
Furthermore,
discuss
for
its
interactions
with
other
modes
highlight
cuproptosis-related
mitochondrial
dysfunction
Finally,
explore
therapeutic
strategy
targeting
novel
form
aiming
some
insights
management
Neural Regeneration Research,
Год журнала:
2023,
Номер
19(3), С. 519 - 528
Опубликована: Июль 20, 2023
Abstract
Local
ischemia
often
causes
a
series
of
inflammatory
reactions
when
both
brain
immune
cells
and
the
peripheral
response
are
activated.
In
human
body,
gut
lung
regarded
as
key
reactional
targets
that
initiated
by
ischemic
attacks.
Mucosal
microorganisms
play
an
important
role
in
regulation
metabolism
affect
blood-brain
barrier
permeability.
addition
to
relationship
between
organs
central
areas
intestine
also
interact
among
each
other.
Here,
we
review
molecular
cellular
mechanisms
involved
pathways
inflammation
across
gut-brain
axis
lung-brain
axis.
We
found
abnormal
intestinal
flora,
microenvironment,
infection,
chronic
diseases,
mechanical
ventilation
can
worsen
outcome
stroke.
This
introduces
influence
on
lungs
after
stroke,
highlighting
bidirectional
feedback
effect
gut,
lungs,
brain.
CNS Neuroscience & Therapeutics,
Год журнала:
2024,
Номер
30(2)
Опубликована: Фев. 1, 2024
Ischemic
stroke,
accounting
for
the
majority
of
stroke
events,
significantly
contributes
to
global
morbidity
and
mortality.
Vascular
recanalization
therapies,
namely
intravenous
thrombolysis
mechanical
thrombectomy,
have
emerged
as
critical
interventions,
yet
their
success
hinges
on
timely
application
patient-specific
factors.
This
review
focuses
early
phase
pathophysiological
mechanisms
ischemic
nuances
recanalization.
It
highlights
dual
role
neutrophils
in
tissue
damage
repair,
involvement
blood-brain
barrier
(BBB)
outcomes.
Special
emphasis
is
placed
ischemia-reperfusion
injury,
characterized
by
oxidative
stress,
inflammation,
endothelial
dysfunction,
which
paradoxically
exacerbates
cerebral
post-revascularization.
The
also
explores
potential
targeting
molecular
pathways
involved
BBB
integrity
inflammation
enhance
efficacy
therapies.
By
synthesizing
current
research,
this
paper
aims
provide
insights
into
optimizing
treatment
protocols
developing
adjuvant
neuroprotective
strategies,
thereby
advancing
therapy
improving
patient
Journal of Nanobiotechnology,
Год журнала:
2024,
Номер
22(1)
Опубликована: Июль 18, 2024
Abstract
Ischemic
stroke
is
a
complex,
high-mortality
disease
with
multifactorial
etiology
and
pathogenesis.
Currently,
drug
therapy
mainly
used
treat
ischemic
in
clinic,
but
there
are
still
some
limitations,
such
as
limited
blood-brain
barrier
(BBB)
penetration
efficiency,
narrow
treatment
time
window
side
effects.
Recent
studies
have
pointed
out
that
delivery
systems
based
on
polymeric
nanocarriers
can
effectively
improve
the
insufficient
for
stroke.
They
provide
neuronal
protection
by
extending
plasma
half-life
of
drugs,
enhancing
drug’s
permeability
to
penetrate
BBB,
targeting
specific
structures
cells.
In
this
review,
we
classified
delivering
drugs
introduced
their
preparation
methods.
We
also
evaluated
feasibility
effectiveness
discussed
existing
limitations
prospects
treatment.
hoped
review
could
theoretical
basis
future
development
nanomedicine
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