Hearts,
Journal Year:
2024,
Volume and Issue:
5(4), P. 612 - 627
Published: Dec. 12, 2024
Background:
Cardiovascular
disease
(CVD)
is
the
leading
cause
of
mortality
and
disability
worldwide.
While
sex
differences
in
CVD
have
been
well
documented,
physiological
mechanisms
those
remain
unclear.
As
important
components
cardiovascular
system,
cardiac
vagal
control
baroreflex
serve
as
are
modifiable
factors
for
gender-specific
preventions.
Methods:
Ninety-four
healthy
adults
(18–44
years
age;
Mage
=
21.09
years;
46
female)
were
recruited
to
complete
assessments
heart
rate
variability
(HRV)
at
a
resting
baseline
timing
effect
on
an
R-wave-locked
reaction
time
(RT)
task,
which
used
indicator
novel
behavioral
measure
activity,
respectively.
HRV
metrics
(including
root
mean
square
successive
R-R
interval
differences,
high
frequency
low
variability,
frequency-to-high
ratio),
(the
inhibition
RT
response
phase
systole
compared
diastole),
their
associations
between
female
male
participants.
Results:
Female
participants
showed
higher
levels
vagally
mediated
after
adjusting
basal
rate.
Importantly,
responses
was
positively
correlated
with
among
males
but
not
females.
Conclusions:
Females
exhibited
different
processes
regulate
functions
outcomes.
The
present
findings
will
help
reduce
gender
disparities
preventive
care
improve
health
both
women
men.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 8, 2025
Golgi
Protein
73
(GP73)
is
a
Golgi-resident
protein
that
highly
expressed
in
primary
tumor
tissues.
Initially
identified
as
an
oncoprotein,
GP73
has
been
shown
to
promote
development,
particularly
by
mediating
the
transport
of
proteins
related
epithelial-mesenchymal
transition
(EMT),
thus
facilitating
cell
EMT.
Though
our
previous
review
summarized
functional
roles
intracellular
signal
transduction
and
its
various
mechanisms
promoting
EMT,
recent
studies
have
revealed
plays
crucial
role
regulating
immune
microenvironment.
can
modulate
signaling
pathways
influence
cytokine
chemokine
networks,
resulting
inflammation
caused
viral
bacterial
infection
or
diseases,
leading
microenvironment
deteriorated.
Additionally,
extracellular
also
regulate
target
cells
binding
their
cell-surface
receptors
entering
acceptor
cells,
thereby
development.
In
this
review,
we
aim
summarize
findings,
providing
insights
for
future
investigations
on
potential
therapeutic
ameliorating
chronic
European Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 6, 2024
Abstract
Background
Maintaining
low
concentrations
of
plasma
low‐density
lipoprotein
cholesterol
(LDLc)
over
time
decreases
the
number
LDL
particles
trapped
within
artery
wall,
slows
progression
atherosclerosis
and
delays
age
at
which
mature
atherosclerotic
plaques
develop.
This
substantially
reduces
lifetime
risk
cardiovascular
disease
(ASCVD)
events.
In
this
context,
plaque
development
vulnerability
result
not
only
from
lipid
accumulation
but
also
inflammation.
Results
Changes
in
composition
immune
cells,
including
macrophages,
dendritic
T
B
mast
cells
neutrophils,
along
with
altered
cytokine
chemokine
release,
disrupt
equilibrium
between
inflammation
anti‐inflammatory
mechanisms
sites.
Considering
that
it
is
a
competition
LDLc
inflammation,
instead
they
are
partners
crime,
present
narrative
review
aims
to
give
an
overview
main
inflammatory
molecular
pathways
linked
raised
describe
impact
lipid‐lowering
approaches
on
burden.
Although
remarkable
changes
driven
by
most
recent
lowering
combinations,
relative
reduction
C‐reactive
protein
appears
be
independent
magnitude
lowering.
Conclusion
Identifying
clinical
biomarkers
(e.g.
interleukin‐6)
possible
targets
for
therapy
holds
promise
monitoring
reducing
ASCVD
burden
suitable
patients.
The
central
arterial
pressure
(CAP)
serves
as
a
crucial
parameter
for
assessing
cardiovascular
health
and
evaluating
the
risk
of
related
diseases.
Its
non-invasive,
continuous,
accurate
reconstruction
is
evaluation
prevention
However,
traditional
approaches
often
exhibit
limited
accuracy,
while
certain
deep
learning
models
face
challenges
in
feature
extraction,
which
limits
their
widespread
use
clinical
adoption.
This
study
introduces
novel
waveform
model
(CBL-iTransformer),
built
upon
an
enhanced
iTransformer
architecture.
It
integrates
bidirectional
long
short-term
memory
networks
(BiLSTM)
convolutional
neural
(CNN)
to
augment
extraction
efficiency
precision
during
process.
performance
CBL-iTransformer
reconstructing
CAP
discussed
validated
using
radial
(RAP)
data
obtained
from
62
patients
who
underwent
invasive
measurements
before
after
medication.
metrics,
including
mean
absolute
error
(MAE)
root
square
(RMSE),
are
compared
against
tranditional
method
well
range
models.
research
findings
demonstrate
that
achieves
robust
(
:
0.93
±
0.90
mmHg
,
1.29
mmHg),
also
yielding
reliable
results
aortic
systolic
(CASP)
diastolic
(CADP)
waveforms
1.44
0.84
1.30
0.78
mmHg).
demonstrates
excellent
expected
be
applied
practice
future.
Diagnostics,
Journal Year:
2025,
Volume and Issue:
15(2), P. 187 - 187
Published: Jan. 15, 2025
Background:
The
impact
of
Celiac
Disease
(CD)
is
not
only
limited
to
the
intestinal
system,
but
extraintestinal
manifestations
may
also
be
seen.
In
this
context,
cardiac
have
recently
been
focus
attention.
This
study
aimed
evaluate
myocardial
repolarization
properties
in
CD
patients
by
assessing
frontal
QRS-T
Angle
(fQRS-T)
on
electrocardiography
(ECG).
Methods:
A
total
302
patients,
including
150
and
152
control
group
were
included
study.
ECG
parameters,
fQRS-T,
QRS
interval,
QTc
calculated
for
each
patient
compared
between
groups.
addition,
relationship
these
parameters
with
disease
duration
was
analyzed.
Results:
median
38.5
(16
96)
months
group.
Significantly
wider
interval
(92
(86
vs.
83
(76.3
93),
p
<
0.001)
fQRS-T
(23
(13
37)
18
(6.3
27),
values
observed
Among
those
longer
(>38.5
months)
exhibited
significantly
intervals
(94
(88
98)
88
(84
94),
angles
(29
(14
47)
16
(10
25),
shorter
duration.
positive
correlation
demonstrated
(r
=
0.478,
0.001).
Multivariable
logistic
regression
identified
(OR:
1.060,
95%
CI:
1.032-1.088,
angle
1.028,
1.013-1.043,
as
independent
predictors
CD.
Additionally,
1.066,
1.012-1.124,
0.016)
1.021,
1.003-1.038,
0.021)
significant
linear
analysis
confirmed
that
a
stronger
predictor
widening
(B:
0.389,
0.102-0.677,
age
0.184,
0.123-0.245,
0.008).
Conclusions:
study,
we
chronic
inflammation
secondary
negative
effects
effect
closely
related
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 15, 2025
ABSTRACT
Objective
immune
dysregulation
may
play
a
role
in
cardiovascular
(CV)
risk
excess
rheumatoid
arthritis
(RA).
However,
exact
mediators
are
unknown.
Age-associated
B
cells
(ABCs)
have
emerged
as
multi-faceted
pro-inflammatory
mediators,
also
the
atherosclerosis
microenvironment,
but
their
autoimmunity
is
ill-defined.
Our
aim
was
to
evaluate
ABCs
levels
earliest
stages
of
inflammatory
and
potential
biomarkers
atherosclerosis.
Methods
were
quantified
by
flow
cytometry
58
early
RA
patients,
11
individuals
with
clinical-suspect
arthralgia
(CSA)
33
healthy
controls
(HC).
Atherosclerosis
occurrence
measured
Doppler-ultrasound.
Cytokines
multiplex
immunoassays.
Cardiometabolic-related
proteins
evaluated
using
high-throughput
targeted
proteomics.
Results
Circulating
increased
patients
compared
HC
within
CD19+
PBMCs
pools
(p=0.013
p<0.001,
respectively).
Numerically
higher
found
CSA.
frequency
unrelated
disease
features
traditional
CV
factors
negatively
associated
good
therapeutic
outcomes
upon
csDMARD
at
6
12
months.
positively
correlated
proinflammatory
cytokines
(IFNg,
TNF,
IL-6
IL-21)
proteomic
signatures
related
B-
T-cell
responses
well
cellular
pathways
linked
independently
extent
patients.
Furthermore,
adding
significantly
improved
stratification
over
conventional
instruments.
Conclusions
expansion
an
event
along
course,
outcomes,
milieu
burden.
be
missing
link
between
humoral
autoimmunity.
Journal of Diabetes Research,
Journal Year:
2025,
Volume and Issue:
2025(1)
Published: Jan. 1, 2025
Aims:
This
cross‐sectional
study
is
aimed
at
determining
whether
systemic
inflammation,
diabetic
autoantibodies,
and
islet
β
cell
dysfunction
play
a
role
in
the
progression
of
macrovascular
complications
patients
with
autoimmune
diabetes.
Methods:
202
diabetes
aged
≥
35
years
hospitalized
Peking
Union
Medical
College
Hospital
were
enrolled
this
study.
The
divided
into
three
groups
based
on
severity
peripheral
atherosclerosis.
Biomarkers
function,
other
covariates
validated
to
be
associated
collected.
Correlations
between
atherosclerosis
function
examined
using
an
ordinal
logistic
regression
model.
Results:
Of
patients,
39.1%
male,
median
age
53
(43,
60)
duration
96
(36,
216)
months.
58
had
no
lesions
arteries,
72
carotid
or
lower
extremity
rest
both
arteries.
In
multifactor
test,
positive
cytoplasmic
antibody
(ICA)
long‐term
use
lipid‐lowering
agents
independently
after
adjusting
for
duration.
Conclusions:
correlation
ICA
suggests
inflammation
early
stage
plays
association
need
screening
intervention
dyslipidemia
Radiology,
Journal Year:
2025,
Volume and Issue:
314(2)
Published: Feb. 1, 2025
HomeRadiologyVol.
314,
No.
2
Previous
Reviews
and
CommentaryFree
AccessEditorialCOVID-19
Infection
Coronary
Plaque
Progression:
An
Early
Warning
of
a
Potential
Public
Health
CrisisJonathan
R.
Weir-McCall
,
Jack
S.
BellJonathan
BellAuthor
AffiliationsFrom
the
Department
Cardiovascular
Imaging,
Biomedical
Engineering
Imaging
Sciences,
King's
College
London,
England
(J.R.W.M.);
Radiology,
Royal
Brompton
Hospital,
Guys
St.
Thomas'
NHS
Trust,
Westminster
Bridge
Rd,
4th
Fl,
Lambeth
Wing,
Office
Suite
2,
London
SE1
7EH,
Liverpool
Center
for
Science
at
University
Liverpool,
John
Moores
Heart
Chest
(J.S.B.).Address
correspondence
to
J.R.W.M.
(email:
[email
protected]).Jonathan
BellPublished
Online:Feb
4
2025https://doi.org/10.1148/radiol.243767See
also
article
by
Dai
et
al
in
this
issue.MoreSectionsPDF
ToolsAdd
favoritesCiteTrack
CitationsPermissionsReprints
ShareShare
onFacebookXLinked
In
See
issue.Jonathan
is
senior
lecturer
cardiothoracic
radiologist
Hospital.
His
research
interests
lie
use
cardiovascular
CT
better
understanding
how
these
can
be
used
improve
patient
treatment
outcomes
structural
coronary
artery
disease.
He
sits
on
guideline
committee
SCCT,
Certification
Accreditation
Committee
EACVI
Diagnostics
Advisory
NICE.Download
as
PowerPointJack
Bell
cardiology
registrar
National
Institute
Research
academic
clinical
fellow
Centre
Science.
center
around
integrating
multimodal
data,
including
imaging,
risk
prediction
diseases.Download
PowerPoint
5
years
since
outbreak
COVID-19
pandemic,
there
have
been
over
750
million
documented
cases,
with
100
United
States
alone
(1).
With
advent
mass
vaccinations
growing
population
immunity,
morbidity
mortality
associated
acute
infection
has
improved
substantially.
Resolution
does
not
result
cessation
consequences
COVID-19,
however.
Long-term
sequelae
observed
across
multiple
organ
systems
include
1.6-fold
higher
events
1
year
after
(2).
The
precise
mechanisms
which
influences
remain
uncertain,
although
one
most
compelling
hypotheses
an
interaction
between
atherosclerosis.
Atherosclerosis
chronic
inflammatory
disease,
endothelial
dysfunction
accumulation
low-density
lipoprotein
cholesterol
vessel
intima
leading
complex
cascade
involving
both
innate
adaptive
immune
system.
Both
autoimmune
conditions
(eg,
rheumatoid
arthritis,
bowel
psoriasis)
viral
infections
HIV)
potentiate
relevant
pathways,
accelerated
plaque
formation,
progression,
instability
(3,4).
evidence
less
clear
infections,
studies
calcium
progression
following
pneumonia
reduced
influenza
vaccine
recipients
(5,6).
Preclinical
shown
plausible
could
influence
atherosclerosis,
direct
effects
vascular
endothelium
platelets
via
angiotensin-converting
enzyme
receptor
indirect
through
induction
systemic
inflammation
(7).
However,
atherosclerosis
lacking.
angiography
(CCTA)
ideal
tool
addressing
question.
It
enables
noninvasive
quantitative
assessment
burden
atherosclerotic
within
entire
tree.
This
agree
well
invasive
detect
response,
predict
events.
information
further
complemented
pericoronary
adipose
tissue
(PCAT)
attenuation,
measured
same
time.
elevated
PCAT
attenuation
suggestive
inflammation.
A
recent
study
158
patients
demonstrated
increased
prior
(8).
While
useful
first
glimpse
into
inflammation,
analysis
did
examine
volume,
nor
it
consider
consequence
elevation
attenuation.
issue
(9)
harness
serial
CCTA
scans
alongside
state-of-the-art
image
investigate
associates
outcomes.
retrospective
single-center
analyzed
803
least
two
examinations
performed
median
interval
3
apart.
cohort
was
stratified
according
whether
confirmed
occurred
final
examination.
total
690
2108
plaques
had
113
480
not.
groups
were
matched
baseline
terms
traditional
factors;
medications;
C-reactive
protein
levels;
infection;
vaccination
status;
features,
volumes,
high-risk
key
finding
that
exhibited
greater
annualized
percent
atheroma
volume
(mean,
0.90%
per
±
0.91
[SD]
vs
0.62%
0.68;
P
<
.001)
noncalcified
0.78%
0.79
0.42%
0.45;
compared
without
infection.
Plaques
more
likely
progress
(incidence,
21.0%
15.8%;
=
.03)
exhibit
27.1%
19.8%;
At
causal
mediation
analysis—which
assumes
no
unmeasured
confounders
association
exposure,
mediators,
outcomes—PCAT
accounted
10.3%
between-group
difference
progression.
Clinical
recorded
9
months
examination
defined
lesion
level,
target
failure
end
point
encompassing
cardiac
death,
myocardial
infarction,
revascularization;
major
adverse
all-cause
hospitalization
unstable
angina.
Patients
(10.4%
3.1%;
adjusted
hazard
ratio,
2.90;
(20.1%
3.8%;
4.8;
.002)
those
should
commended
their
comprehensive
large
cohort,
providing
insights
potential
longer-term
COVID-19.
Whereas
findings
certainly
suggest
strong
link
infection,
always
confounding,
inherent
observational
studies.
particular,
behavior
acquiring
such
mask
wearing,
status,
adherence
public
health
regulations,
related
reduction
behaviors,
preventative
lifestyle
measures
medication.
similar
levels
vaccination,
before
period,
medication
use,
provides
some
reassurance
regard,
course
guarantee
adherence.
excluded
who
required
interscan
interval,
thereby
excluding
highest
risk.
Therefore,
possible
severity
consequent
Replication
multicenter
setting,
ideally
range
ethnic
backgrounds,
validate
Asian
rates
are
high.
Overall,
important
hypothesis-generating
clinically
understudied
area.
mild
raises
interesting
questions
about
mechanism.
Although
shared
biologic
pathways
linking
so-called
cytokine
storm
severe
COVID-19—namely
inflammasome
activation
downstream
interleukin
1β,
6,
release—this
Indeed,
high-sensitivity
follow-up
normal
study.
Instead,
incidence
persistent
but
localized
Mechanisms
here
antigen
persistence,
dysregulation,
dysfunction,
oxidative
stress
extending
postacute
phase
Causal
suggested
only
responsible
overall
contribution
underestimated
because
7
months.
If
driving
force
would
expect
maximal
peri-infection
period
then
quiescing.
Consistent
this,
imaged
than
Further
work
aid
temporal
relationship
underlying
association,
determine
specific
question
mechanism
essential
establishing
mitigate
guiding
we
targeting
earliest
during
or
long
term.
From
perspective,
concerning
approach
800
cases
worldwide
replicated
other
populations,
spectrum
severity,
becomes
best
integrate
care
pathway.
Some
calculators,
QRISK3,
already
incorporate
arthritis
lupus
erythematosus
calculations,
reported
ratios
(10).
quantification
may
help
refine
risk,
given
scale
numbers
infected,
integration
cost-effective
manner
challenging.
Given
magnitude
hand,
action
bring
together
trials
necessary
assess
strategies,
anti-inflammatory
medications
statins,
reduce
prevent
future
events.Disclosures
conflicts
interest:
No
relationships.
J.S.B.
supported
fellowship
from
Hospital
Charity.References1.
WHO
dashboard:
cases.
World
Organization.
https://data.who.int/dashboards/covid19/cases.
Accessed
December
3,
2024.
Google
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Al-Aly
Z.
Nat
Med
2022;28(3):583–590.
Medline
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Hemmat
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Badalzadeh
R,
Memar
MY,
Baghi
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J
Clin
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CJ.
Autoimmune
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Scholar5.
Behrouzi
Bhatt
DL,
Cannon
CP,
al.
Association
Influenza
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JAMA
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Scholar6.
Corrales-Medina
VF,
Dwivedi
G,
Taljaard
M,
pneumonia:
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PLoS
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2018;13(2):e0191750.
Scholar7.
Chidambaram
V,
Kumar
Sadaf
MI,
Initiation
Progression
Atherosclerosis:
Pathophysiology
During
Beyond
Acute
Phase.
JACC
Adv
2024;3(8):101107.
Scholar8.
Mátyás
BB,
Benedek
I,
Blîndu
Elevated
FAI
Index
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Vulnerability
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Int
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2023;24(8):7398.
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X,
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SARS-CoV-2
Radiology
2025;314(2):e240876.
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Hippisley-Cox
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Coupland
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Brindle
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Development
validation
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BMJ
2017;357:j2099.
ScholarArticle
HistoryReceived:
Dec
10
2024Revision
requested:
19
received:
2024Accepted:
20
2024Published
online:
Feb
04
2025
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