Biomedicines,
Journal Year:
2021,
Volume and Issue:
9(9), P. 1220 - 1220
Published: Sept. 14, 2021
Background.
Emerging
evidences
suggest
that
in
severe
COVID-19,
multi-organ
failure
is
associated
with
a
hyperinflammatory
state
(the
so-called
“cytokine
storm”)
combination
the
development
of
prothrombotic
state.
The
central
role
endothelial
dysfunction
pathogenesis
disease
to
date
accepted,
but
precise
mechanisms
underlying
coagulopathy
remain
unclear.
Whether
alterations
vascular
homeostasis
directly
depend
upon
SARS-CoV-2
infection
cells
or,
rather,
occur
secondarily
activation
inflammatory
response
still
matter
debate.
Here,
we
address
effect
spike
S1
protein
on
human
lung
microvascular
(HLMVEC).
In
particular,
existence
an
endothelium-macrophage
crosstalk
has
been
explored.
Methods
and
Results.
addressed
(HLMVEC),
either
or
after
incubation
conditioned
medium
(CM)
monocyte-derived
macrophages
(MDM)
previously
activated
by
(CM-MDM).
Both
MDM
HLMVEC
are
protein,
increased
expression
pro-inflammatory
mediators.
However,
when
exposed
CM-MDM,
enhanced
cell
occurs
terms
adhesion
molecules,
pro-coagulant
markers,
chemokines.
Under
this
experimental
condition,
ICAM-1
VCAM-1,
chemokines
CXCL8/IL-8,
CCL2/MCP1,
CXCL10/IP-10
as
well
tissue
factor
(TF)
markedly
induced.
Instead,
decrease
thrombomodulin
(THBD)
observed.
Conclusion.
Our
data
mediators
released
spike-activated
amplify
cells,
likely
contributing
impairment
integrity
pro-coagulative
endothelium.
Gevher Nesibe Journal IESDR,
Journal Year:
2021,
Volume and Issue:
6(12), P. 56 - 72
Published: May 25, 2021
In
early
December
2019,
an
outbreak
of
coronavirus
2019
(COVID-19)
caused
by
a
novel
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
occurred
in
Wuhan,
China's
Hubei
province.
On
30
January
2020,
the
World
Health
Organization
and
International
Public
declared
emergency,
as
23.03.2021,
laboratory-approved
123,097,155
cases
2,716,151
deaths
were
reported
worldwide.
The
perceived
risk
disease
has
led
many
countries
to
adopt
various
control
measures.
Emerging
genetic
clinical
evidence
suggests
pathway
similar
SARS
MERS.
Potential
therapeutic
strategies
that
are
currently
being
evaluated
derive
mainly
from
previous
experience
with
Covid-19
treatment.
Although
several
potential
treatments
for
COVID-19
MERS
have
been
identified
animal
vitro
models,
human
trials
still
lacking,
which
hinders
progress
This
review
requires
overview
three
major
deadly
coronaviruses
assessment
factors
applicable
lessons
stop
their
spread
leveraging
learned
first
two
outbreaks
identifying
areas
improvement
future
preparedness
plans.
persistence
can
help
inform
public
health
officials
medical
practitioners
efforts
combat
its
progress.
Also,
this
review,
pathogenesis,
epidemiology,
diagnosis,
treatment,
vaccine
reviewed.
Brain Sciences,
Journal Year:
2021,
Volume and Issue:
11(2), P. 235 - 235
Published: Feb. 13, 2021
Considering
the
mechanisms
capable
of
causing
brain
alterations
in
COVID-19,
we
aimed
to
study
occurrence
cognitive
abnormalities
months
following
hospital
discharge.
We
recruited
38
(aged
22–74
years;
27
males)
patients
hospitalized
for
complications
SARS-CoV-2
infection
nonintensive
COVID
units.
Participants
underwent
neuropsychological
testing
about
5
after
Of
all
patients,
42.1%
had
processing
speed
deficits,
while
26.3%
showed
delayed
verbal
recall
deficits.
Twenty-one
percent
presented
with
deficits
both
and
memory.
Bivariate
analysis
revealed
a
positive
correlation
between
lowest
arterial
oxygen
partial
pressure
(PaO2)
fractional
inspired
(FiO2)
(P/F)
ratio
during
hospitalization
memory
consolidation
performance
(SRT-LTS
score,
r
=
0.404,
p
0.027),
as
well
SpO2
levels
upon
arrival
(SRT-D
rs
0.373,
0.042).
Acute
respiratory
distress
syndrome
(ARDS)
was
associated
worse
(ARDS
vs.
no
ARDS:
SRT-LTS
mean
score
30.63
±
13.33
44.50
13.16,
0.007;
SRT-D
5.95
2.56
8.10
2.62,
0.029).
Cognitive
can
frequently
be
found
COVID-19
Increased
fatigability,
concentration
memory,
overall
decreased
discharge
interfere
work
daily
activities.
Cardiovascular Research,
Journal Year:
2022,
Volume and Issue:
119(2), P. 336 - 356
Published: July 25, 2022
Abstract
Long
COVID
has
become
a
world-wide,
non-communicable
epidemic,
caused
by
long-lasting
multiorgan
symptoms
that
endure
for
weeks
or
months
after
SARS-CoV-2
infection
already
subsided.
This
scientific
document
aims
to
provide
insight
into
the
possible
causes
and
therapeutic
options
available
cardiovascular
manifestations
of
long
COVID.
In
addition
chronic
fatigue,
which
is
common
symptom
COVID,
patients
may
present
with
chest
pain,
ECG
abnormalities,
postural
orthostatic
tachycardia,
newly
developed
supraventricular
ventricular
arrhythmias.
Imaging
heart
vessels
provided
evidence
chronic,
post-infectious
perimyocarditis
consequent
left
right
failure,
arterial
wall
inflammation,
microthrombosis
in
certain
patient
populations.
Better
understanding
underlying
cellular
molecular
mechanisms
will
aid
development
effective
treatment
strategies
its
manifestations.
A
number
have
been
proposed,
including
those
involving
direct
effects
on
myocardium,
microthrombotic
damage
endothelium,
persistent
inflammation.
Unfortunately,
existing
circulating
biomarkers,
coagulation,
inflammatory
markers,
are
not
highly
predictive
either
presence
outcome
when
measured
3
infection.
Further
studies
needed
understand
mechanisms,
identify
specific
guide
future
preventive
treatments
address
sequelae.
Clinical Infectious Diseases,
Journal Year:
2021,
Volume and Issue:
74(9), P. 1525 - 1533
Published: Aug. 9, 2021
Abstract
Background
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
viral
RNA
(vRNA)
is
detected
in
the
bloodstream
of
some
patients
with
disease
2019
(COVID-19),
but
it
not
clear
whether
this
RNAemia
reflects
viremia
(ie,
virus
particles)
and
how
relates
to
host
immune
responses
outcomes.
Methods
SARS-CoV-2
vRNA
was
quantified
plasma
samples
from
observational
cohorts
51
COVID-19
including
9
outpatients,
19
hospitalized
(non–intensive
care
unit
[ICU]),
23
ICU
patients.
levels
were
compared
cross-sectional
indices
severity
prospective
clinical
We
used
multiple
imaging
methods
visualize
virions
plasma.
Results
100%,
52.6%,
11.1%
ICU,
non-ICU,
respectively.
Virions
pellets
using
electron
tomography
immunostaining.
Plasma
significantly
higher
>
non-ICU
outpatients
(P
<
.0001);
for
inpatients,
strongly
associated
World
Health
Organization
(WHO)
score
at
admission
=
.01),
maximum
WHO
.002),
discharge
disposition
.004).
A
level
>6000
copies/mL
mortality
(hazard
ratio,
10.7).
Levels
several
inflammatory
biomarkers
.01)
neutralizing
antibody
titers
.8).
Conclusions
Visualization
particles
indicates
that
due,
least
part,
viremia.
The
correlate
severity,
patient
outcome,
specific
titers.
Thrombotic
and
microvascular
complications
are
frequently
seen
in
deceased
COVID-19
patients.
However,
whether
this
is
caused
by
direct
viral
infection
of
the
endothelium
or
inflammation-induced
endothelial
activation
remains
highly
contentious.Here,
we
use
patient
autopsy
samples,
primary
human
cells
an
vitro
model
pulmonary
epithelial-endothelial
cell
barrier.We
show
that
express
very
low
levels
SARS-CoV-2
receptor
ACE2
protease
TMPRSS2,
which
blocks
their
capacity
for
productive
infection,
limits
to
produce
infectious
virus.
Accordingly,
can
only
be
infected
when
they
overexpress
ACE2,
exposed
high
concentrations
SARS-CoV-2.
We
also
does
not
infect
3D
vessels
under
flow
conditions.
further
demonstrate
a
co-culture
with
Endothelial
do
however
sense
respond
adjacent
epithelial
cells,
increasing
ICAM-1
expression
releasing
pro-inflammatory
cytokines.Taken
together,
these
data
suggest
vivo,
unlikely
may
occur
if
epithelium
denuded
(basolateral
infection)
load
present
blood
(apical
infection).
In
such
scenario,
whilst
occur,
it
contribute
amplification.
still
play
key
role
pathogenesis
sensing
mounting
response
Andrology,
Journal Year:
2021,
Volume and Issue:
9(4), P. 1053 - 1059
Published: March 20, 2021
Abstract
Background
Erectile
dysfunction
(ED),
as
the
hallmark
of
endothelial
dysfunction,
could
be
a
short‐
or
long‐term
complication
COVID‐19.
Additionally,
being
ED
clinical
marker
and
predictor
non‐communicable
chronic
diseases,
particularly
cardiovascular,
subjects
with
potentially
have
higher
risk
contracting
Objectives
To
investigate
prevalence
among
reported
diagnosis
COVID‐19
to
measure
association
ED.
Materials
methods
We
reviewed
data
from
Sex@COVID
online
survey
(performed
between
April
7
May
4,
2020,
in
Italy)
retrieve
sample
Italian
male
sexually
active
SARS‐CoV‐2
infection.
A
matching
COVID‐19‐negative
was
also
retrieved
using
propensity
score
3:1
ratio.
The
used
different
standardized
psychometric
tools
effects
lockdown
social
distancing
on
intrapsychic,
relational,
sexual
health
subjects.
Results
One
hundred
were
included
analysis
(25
COVID‐positive;
75
COVID‐negative).
ED,
measured
Sexual
Health
Inventory
for
Men,
significantly
COVID+
group
(28%
vs.
9.33%;
p
=
0.027).
Logistic
regression
models
confirmed
significant
effect
development
independently
other
variables
affecting
erectile
function,
such
psychological
status,
age,
BMI
[OR
5.66,
95%
CI:
1.50–24.01].
Likewise,
more
likely
COVID‐19,
once
corrected
age
5.27,
1.49–20.09].
Discussion
conclusion
On
top
well‐described
pathophysiological
mechanisms,
there
is
preliminary
evidence
real‐life
population
factor
developing
possibly
occurring
consequence
Universal
vaccination
against
personal
protective
equipment
added
benefit
preventing
dysfunctions.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: March 7, 2022
Microvascular
thrombosis
is
associated
with
multiorgan
failure
and
mortality
in
coronavirus
disease
2019
(COVID-19).
Although
thrombotic
complications
may
be
ascribed
to
the
ability
of
SARS-CoV-2
infect
replicate
endothelial
cells,
it
has
been
poorly
investigated
whether,
complexity
viral
infection
human
host,
specific
elements
alone
can
induce
damage.
Detection
circulating
spike
protein
sera
severe
COVID-19
patients
was
evaluated
by
ELISA.