Journal of Education Health and Sport,
Год журнала:
2023,
Номер
46(1), С. 11 - 21
Опубликована: Авг. 25, 2023
Introduction:
Iqos
and
other
heat-not-burn
products
according
to
tobacco
companies
are
a
safer
alternative
cigarettes.
The
aim
of
this
article
is
objectively
review
the
potential
impact
iQOS®
on
human
health
by
searching
for
integrating
published
research
findings.
This
provides
comprehensive
analysis
scientific
conducted
effects
use
health,
distinguishing
between
specific
medical
fields.
Materials
methods:
study
based
articles
collected
from
PubMed
database
spanning
years
2016-2023.
was
through
keywords
such
as
"Iqos",
"Heat
not
burn",
"Iqos
impact".
Results:
Tobacco
heaters
seen
potentially
less
harmful.
However,
emerging
their
harmfulness
clearly
shows
that
despite
reduced
concentrations
compounds
hazardous
aerosol
produced
still
contains
same
harmful
substances.
Further
studies
show
toxic
at
similar
level
smoke
traditional
cigarettes.
Antioxidants,
Год журнала:
2024,
Номер
13(11), С. 1395 - 1395
Опубликована: Ноя. 15, 2024
Electronic
cigarettes
and
heated
tobacco
products
have
seen
significant
growth
in
sales
usage
recent
years.
Initially
promoted
as
potentially
less
harmful
alternatives
to
traditional
tobacco,
scientific
evidence
has
raised
serious
concerns
about
the
risks
they
pose,
particularly
relation
atherosclerosis.
While
atherosclerosis
long
been
associated
with
conventional
smoking,
emerging
research
suggests
that
electronic
may
also
contribute
development
of
this
condition
related
cardiovascular
complications.
In
a
narrative
review,
we
examined
potential
effects
on
oxidative
stress
Several
studies
shown
e-cigarettes
increase
through
activation
enzymes
such
NADPH
oxidase.
One
primary
these
is
their
pro-thrombotic
pro-atherosclerotic
impact
endothelial
cells
platelets,
which
promotes
inflammatory
processes
within
arteries.
Furthermore,
chemicals
found
cigarette
liquids
exacerbate
inflammation
cause
dysfunction.
systematic
analyzed
chronic
exposure
function,
assessed
by
brachial
flow-mediated
dilation
(FMD).
Although
are
often
perceived
safer
could
still
present
health.
It
essential
raise
public
awareness
dangers
implement
protective
measures,
for
young
people.
Respiratory Research,
Год журнала:
2024,
Номер
25(1)
Опубликована: Май 16, 2024
Mitogen-activated
protein
kinase
(MAPK)signaling-mediated
smoking-associated
pulmonary
vascular
remodeling
(PVR)
plays
an
important
role
in
the
pathogenesis
of
group
3
hypertension
(PH).
And
G
pathway
suppressor
2
(GPS2)
could
suppress
G-protein
signaling
such
as
Ras
and
MAPK,
but
its
cigarette
smoking
-induced
PVR
(CS-PVR)
is
unclear.
An
vivo
model
smoke-exposed
rats
was
constructed
to
assess
GPS2
smoking-induced
PH
PVR.
In
vitro,
effects
overexpression
silencing
on
function
human
arterial
smooth
cells
(HPASMCs)
underlying
mechanisms
were
explored.
expression
downregulated
rat
arteries
(PAs)
HPASMCs
after
CS
exposure.
More
importantly,
CS-exposed
with
had
lower
right
ventricular
systolic
pressure
(RVSP),
hypertrophy
index
(RVHI),
wall
thickness
(WT%)
than
those
without.
enhanced
proliferation
migration
induced
by
extract
(CSE)
can
be
evidently
inhibited
overexpressed
GPS2.
Besides,
GPS2siRNA
significantly
proliferation,
well
activated
Raf/ERK
signaling,
while
these
zoledronic
acid
(ZOL).
addition,
promoter
methylation
level
PAs
increased
exposure,
5-aza-2-deoxycytidine
(5-aza)
CSE-induced
hypermethylation
downregulation
vitro.
improve
CS-PVR,
suggesting
that
might
serve
a
novel
therapeutic
target
for
PH-COPD
future.
International Journal of General Medicine,
Год журнала:
2024,
Номер
Volume 17, С. 2955 - 2965
Опубликована: Июль 1, 2024
Purpose:
Early
identification
of
new
residual
risk
factors
for
coronary
heart
disease
(CHD)
is
warranted.
In
this
study,
we
aim
to
investigate
the
association
between
serine
concentration,
an
important
amino
acid
in
one-carbon
metabolism,
and
CHD
Chinese
hospitalized
patients.
Patients
Methods:
This
case–control
study
included
428
pairs
comprising
patients
with
a
maximum
artery
stenosis
degree
>
70%
controls
<
30%.
The
individuals
were
matched
by
age,
sex,
date
angiography
at
Peking
University
First
Hospital
from
January
1,
2016,
December
31,
2019.
Conditional
logistic
regression
was
used
associations
concentration
CHD.
Results:
aged
63.48
±
10.38
years,
43.73%
male.
Compared
controls,
had
slightly
lower
(13.35
4.20
vs
13.77
4.08
μg/mL),
but
difference
not
significant.
multivariable
conditional
analysis,
every
1
μg/mL
increase
odds
decreased
6%
(95%
confidence
interval
[CI]
0.90–
0.99;
P
=
0.010).
≥
13.41
than
those
(odds
ratio
[OR]
0.57,
95%
CI
0.39–
0.84;
0.004).
Subgroup
analyses
showed
that
sex
interacted
relationship
(
interaction
0.039),
which
more
significant
males
(OR
0.93,
0.87–
0.98;
0.013)
females.
Conclusion:
observed
inverse
prevalence
patients,
revealed
might
play
protective
role
Keywords:
serine,
disease,
case–control,
metabolism
Technology and Health Care,
Год журнала:
2023,
Номер
32(3), С. 1781 - 1794
Опубликована: Дек. 6, 2023
BACKGROUND:
Endothelial
dysfunction,
the
earliest
stage
of
atherosclerosis,
can
be
caused
by
smoking,
but
its
molecular
mechanism
requires
further
investigation.
OBJECTIVE:
This
study
aimed
to
use
bioinformatics
analysis
identify
potential
mechanisms
involved
in
smoking-related
atherosclerotic
endothelial
dysfunction.
METHODS:
The
transcriptome
data
used
for
this
were
obtained
from
Gene
Expression
Omnibus
(GEO)
database.
GSE137578
and
GSE141136
datasets
common
differentially
expressed
genes
(co-DEGs)
cells
treated
with
oxidized
low-density
lipoprotein
(ox-LDL)
tobacco.
co-DEGs
annotated
using
Ontology
(GO)
Kyoto
Encyclopedia
Genes
Genomics
(KEGG)
databases.
Additionally,
a
protein-protein
interaction
(PPI)
network
was
constructed
visualize
their
interactions
screen
hub
genes.
GSE120521
dataset
verify
expression
unstable
plaques.
miRNA
profile
GSE137580
online
databases
(starBase
2.0,
TargetScan
8.0
DGIdb
v4.2.0)
predict
related
non-coding
RNAs
drugs.
RESULTS:
A
total
232
identified,
including
113
up-regulated
119
down-regulated
These
DEGs
primarily
enriched
detrimental
autophagy,
cell
death,
transcription
factors,
cytokines,
implicated
ferroptosis,
abnormal
lipid
metabolism,
inflammation,
oxidative
stress
pathways.
Ten
screened
PPI
network,
such
as
FOS,
HMOX1,
SQSTM1,
PTGS2,
ATF3,
DDIT3,
MCM4,
KIF15,
UHRF1,
CCL2.
Importantly,
HMOX1
plaques
(p=
0.034).
Finally,
regulatory
involving
lncRNA/circRNA-miRNA-hub
drug-hub
established.
CONCLUSION:
Atherosclerotic
dysfunction
is
associated
smoking-induced
injury.
Through
analysis,
we
identified
provided
therapeutic
targets.
Journal of Oral Biology and Craniofacial Research,
Год журнала:
2024,
Номер
14(2), С. 152 - 157
Опубликована: Фев. 5, 2024
Smoking
is
a
significant
health
hazard
and
contributes
to
cardiovascular
pulmonary
diseases.
It
can
increase
postoperative
complications
during
oral
maxillofacial
surgery
due
its
topical
effect
on
the
mucosa.
New
alternatives
traditional
tobacco
products
are
gaining
popularity,
in
particular,
electronic
cigarettes.
This
pilot
study
investigated
acute
effects
of
nicotine-containing
nicotine-free
cigarettes
palatal
blood
flow
(PBF),
compared
their
14
medically
healthy
volunteers
(8
males,
6
females,
age:
34.7
±
7.0)
were
recruited
for
study.
All
patients
(N
=
14)
requested
smoke
(ECN)
(EC0)
mouthpiece
(end
cigarette)
as
control
sham
smoking
blind
test
(BT).
EC
users
did
not
cigarette
(TC),
resulting
10
people
TC
group.
Palatal
was
measured
by
Laser
Speckle
Contrast
Imager
before,
immediately
after,
15
min
after
exposures.
Exhaled
carbon
monoxide
(eCO)
carboxyhemoglobin
(COHb)
before
with
piCO+
Smokerlyzer
machine.
In
all
groups,
no
differences
observed
changes
between
time
points.
significantly
higher
(TC)
group
both
exposure
(p
<
0.05).
Acute
use
either
or
may
have
minimal
impact
flow,
but
additional
studies
required
clarify
Cardiovascular Research,
Год журнала:
2023,
Номер
119(9), С. 1781 - 1783
Опубликована: Июнь 30, 2023
Journal
Article
Smoke
on
the
blood
stream:
novel
insights
in
cigarette
smoke-induced
atherosclerosis
and
plaque
erosion
Get
access
Henning
Morawietz
Division
of
Vascular
Endothelium
Microcirculation,
Department
Medicine
III,
Faculty
University
Hospital
Carl
Gustav
Carus,
TUD
Dresden
Technology,
Fetscherstr.
74,
D-01307
Dresden,
Germany
Corresponding
author.
Tel:
+49
351
458
6625;
fax:
6354,
E-mail:
[email protected]
https://orcid.org/0000-0001-9360-9736
Search
for
other
works
by
this
author
on:
Oxford
Academic
PubMed
Google
Scholar
Cardiovascular
Research,
Volume
119,
Issue
9,
July
2023,
Pages
1781–1783,
https://doi.org/10.1093/cvr/cvad097
Published:
01
2023
history
Corrected
typeset:
04