BMC Microbiology,
Journal Year:
2024,
Volume and Issue:
24(1)
Published: Nov. 29, 2024
Abstract
It
is
critical
to
find
novel
therapeutic
approaches
owing
the
dissemination
of
multidrug
resistance
(MDR)
in
pathogenic
bacteria,
particularly
Staphylococcus
aureus
.
FDA-drug
repurposing
an
important
tactic
fight
MDR
bacteria.
Here,
we
inspected
antibacterial
activity
ambroxol
against
clinical
S.
isolates.
Using
broth
microdilution
method,
revealed
minimum
inhibitory
concentrations
(MICs)
0.75
1.5
mg/mL.
Also,
it
antibiofilm
action
on
42.17%
isolates
by
crystal
violet
assay.
A
scanning
electron
microscope
was
employed
study
ambroxol.
that
association
between
cells
interrupted
ambroxol,
and
biofilm
construction
devastated.
Moreover,
qRT-PCR
utilized
elucidate
consequence
gene
expression
efflux
biofilm.
Remarkably,
has
downregulated
cna
,
fnb
A,
ica
nor
B
genes.
Ambroxol’s
vivo
investigated
using
infected
burn
infection.
Interestingly,
improved
histological
features
skin
tissues,
significantly
diminished
bacterial
burden,
increased
wound
healing
percentage.
a
significant
reduction
immunohistochemical
staining
tumor
necrosis
factor-alpha.
Finally,
silico
investigations
were
performed
potential
five
possible
targets
aureus.
Ambroxol
showed
good
affinities
with
CrtM
being
highest,
proposing
its
probable
role
mechanisms
for
ambroxol’s
Inflammopharmacology,
Journal Year:
2022,
Volume and Issue:
31(1), P. 37 - 56
Published: Dec. 29, 2022
Abstract
Silent
information
regulator
(SIRT)
has
distinctive
enzymatic
activities
and
physiological
functions
to
control
cell-cycle
progression,
gene
expression,
DNA
stability
by
targeting
histone
non-histone
proteins.
SIRT1
enhances
synaptic
formation
activity,
therefore,
can
reduce
the
progression
of
various
degenerative
brain
diseases
including
Parkinson’s
disease
(PD).
activity
is
decreased
aging
with
a
subsequent
increased
risk
for
development
diseases.
Inhibition
promotes
inflammatory
reactions
since
inhibits
transcription
nuclear
factor
kappa
B
(NF-κB)
which
also
activation
via
microRNA
miR-34a
NAD
synthesis.
highly
expressed
in
microglia
as
well
neurons,
antioxidant
anti-inflammatory
effects.
Therefore,
this
review
aimed
find
possible
role
PD
neuropathology.
neuroprotective
effects;
downregulation
during
p53
expression
may
increase
vulnerability
neuronal
cell
deaths.
neuropathology
linked
sequence
changes
release
pro-inflammatory
cytokines
due
signaling
pathways.
In
addition,
oxidative
stress,
disorders,
mitochondrial
dysfunction,
apoptosis
contribute
mutually
Thus,
activators
play
crucial
mitigation
through
amelioration
apoptosis,
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(8), P. 2287 - 2287
Published: Aug. 17, 2023
The
COVID-19
pandemic
caused
much
illness,
many
deaths,
and
profound
disruption
to
society.
production
of
‘safe
effective’
vaccines
was
a
key
public
health
target.
Sadly,
unprecedented
high
rates
adverse
events
have
overshadowed
the
benefits.
This
two-part
narrative
review
presents
evidence
for
widespread
harms
novel
product
mRNA
adenovectorDNA
is
in
attempting
provide
thorough
overview
arising
from
new
technology
that
relied
on
human
cells
producing
foreign
antigen
has
pathogenicity.
first
paper
explores
peer-reviewed
data
counter
attached
these
technologies.
Spike
protein
pathogenicity,
termed
‘spikeopathy’,
whether
SARS-CoV-2
virus
or
produced
by
vaccine
gene
codes,
akin
‘synthetic
virus’,
increasingly
understood
terms
molecular
biology
pathophysiology.
Pharmacokinetic
transfection
through
body
tissues
distant
injection
site
lipid-nanoparticles
viral-vector
carriers
means
‘spikeopathy’
can
affect
organs.
inflammatory
properties
nanoparticles
used
ferry
mRNA;
N1-methylpseudouridine
employed
prolong
synthetic
function;
biodistribution
DNA
codes
translated
spike
proteins,
autoimmunity
via
contribute
harmful
effects.
reviews
autoimmune,
cardiovascular,
neurological,
potential
oncological
effects,
autopsy
spikeopathy.
With
gene-based
therapeutic
technologies
planned,
re-evaluation
necessary
timely.
Frontiers in Neurology,
Journal Year:
2023,
Volume and Issue:
14
Published: July 31, 2023
COVID-19,
caused
by
the
SARS-CoV-2
virus,
is
a
respiratory
infectious
disease.
While
most
patients
recover
after
treatment,
there
growing
evidence
that
COVID-19
may
result
in
cognitive
impairment.
Recent
studies
reveal
some
individuals
experience
deficits,
such
as
diminished
memory
and
attention,
well
sleep
disturbances,
suggesting
could
have
long-term
effects
on
function.
Research
indicates
contribute
to
decline
damaging
crucial
brain
regions,
including
hippocampus
anterior
cingulate
cortex.
Additionally,
identified
active
neuroinflammation,
mitochondrial
dysfunction,
microglial
activation
patients,
implying
these
factors
be
potential
mechanisms
leading
Given
findings,
possibility
of
impairment
following
treatment
warrants
careful
consideration.
Large-scale
follow-up
are
needed
investigate
impact
function
offer
support
clinical
rehabilitation
practices.
In-depth
neuropathological
biological
can
elucidate
precise
provide
theoretical
basis
for
prevention,
intervention
research.
Considering
risks
reinfection,
it
imperative
integrate
basic
research
data
optimize
preservation
patients'
quality
life.
This
integration
will
also
valuable
insights
responding
similar
public
health
events
future.
perspective
article
synthesizes
discussing
outlining
future
directions.
European journal of medical research,
Journal Year:
2024,
Volume and Issue:
29(1)
Published: March 27, 2024
Abstract
Parkinson's
disease
(PD)
is
a
progressive
neurodegenerative
as
result
of
the
degeneration
dopaminergic
neurons
in
substantia
nigra
pars
compacta
(SNpc).
The
fundamental
features
PD
are
motor
and
non-motor
symptoms.
symptoms
develop
due
to
disruption
neurotransmitters
other
such
γ-aminobutyric
acid
(GABA).
potential
role
GABA
neuropathology
concerning
was
not
precisely
discussed.
Therefore,
this
review
intended
illustrate
possible
regarding
pathway
essential
regulating
inhibitory
tone
prevent
excessive
stimulation
cerebral
cortex.
Degeneration
linked
with
reducing
GABAergic
neurotransmission.
Decreasing
activity
promotes
mitochondrial
dysfunction
oxidative
stress,
which
highly
related
neuropathology.
Hence,
restoring
by
agonists
may
attenuate
progression
dysregulation
SNpc
contributes
developing
Besides,
also
pathway,
amelioration
reduce
In
conclusion,
deregulation
might
be
intricate
Improving
novel,
beneficial
approach
control
European journal of medical research,
Journal Year:
2024,
Volume and Issue:
29(1)
Published: Feb. 9, 2024
Abstract
Multiple
sclerosis
(MS)
is
the
most
frequent
inflammatory
and
demyelinating
disease
of
central
nervous
system
(CNS).
The
underlying
pathophysiology
MS
destruction
myelin
sheath
by
immune
cells.
formation
plaques,
inflammation,
injury
neuronal
characterizes
its
neuropathology.
plaques
are
multiple
focal
regions
demyelination
disseminated
in
brain's
white
matter,
spinal
cords,
deep
grey
cerebral
cortex.
Fenofibrate
a
peroxisome
proliferative
activated
receptor
alpha
(PPAR-α)
that
attenuates
reactions
MS.
inhibits
differentiation
Th17
inhibiting
expression
pro-inflammatory
signaling.
According
to
these
findings,
this
review
intended
illuminate
mechanistic
immunoinflammatory
role
fenofibrate
mitigating
In
conclusion,
can
attenuate
neuropathology
modulating
different
pathways,
including
oxidative
stress,
autophagy,
mitochondrial
dysfunction,
inflammatory-signaling
neuroinflammation.
Journal of Translational Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: Nov. 15, 2023
Myalgic
Encephalomyelitis/Chronic
Fatigue
Syndrome
(ME/CFS)
and
post-COVID
condition
can
present
similarities
such
as
fatigue,
brain
fog,
autonomic
neuropathic
symptoms.
