bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 14, 2024
Advancements
in
long-read
transcriptome
sequencing
(long-RNA-seq)
technology
have
revolutionized
the
study
of
isoform
diversity.
These
full-length
transcripts
enhance
detection
various
structural
variations,
including
novel
isoforms,
alternative
splicing
events,
and
fusion
transcripts.
By
shifting
open
reading
frame
or
altering
gene
expressions,
studies
proved
that
these
transcript
alterations
can
serve
as
crucial
biomarkers
for
disease
diagnosis
therapeutic
targets.
In
this
project,
we
proposed
IFDlong,
a
bioinformatics
biostatistics
tool
to
detect
using
bulk
single-cell
long-RNA-seq
data.
Specifically,
software
performed
annotation
each
long-read,
defined
quantified
expression
by
expectation-maximization
algorithm,
profiled
For
evaluation,
IFDlong
pipeline
achieved
overall
best
performance
when
compared
with
several
existing
tools
large-scale
simulation
studies.
both
quantification,
is
able
reach
more
than
0.8
Spearman's
correlation
truth,
0.9
cosine
similarity
distinguishing
multiple
events.
simulation,
successfully
balance
sensitivity
(higher
90%)
specificity
90%).
Furthermore,
has
its
accuracy
robustness
diverse
in-house
public
datasets
on
healthy
tissues,
cell
lines
types
diseases.
Besides
long-RNA-seq,
compatibility
This
new
may
hold
promise
significant
impact
analysis.
The
available
at
https://github.com/wenjiaking/IFDlong.
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(12), P. 3229 - 3229
Published: Dec. 6, 2023
Inflammatory
bowel
disease
(IBD)
is
a
lifelong
inflammatory
immune
mediated
disorder,
encompassing
Crohn's
(CD)
and
ulcerative
colitis
(UC);
however,
the
cause
specific
pathogenesis
of
IBD
yet
incompletely
understood.
Multiple
cytokines
produced
by
different
cell
types
results
in
complex
functional
networks
that
constitute
highly
regulated
messaging
network
signaling
pathways.
Applying
biological
mechanisms
underlying
at
single
omic
level,
technologies
genetic
engineering
enable
quantification
pattern
released
new
insights
into
cytokine
landscape
IBD.
We
focus
on
existing
literature
dealing
with
biology
pro-
or
anti-inflammatory
interactions
facilitate
cell-based
modulation
system
for
inflammation.
summarize
main
roles
substantial
related
to
homeostatic
tissue
functions
remodeling
IBD,
which
may
be
specifically
valuable
successful
cytokine-targeted
therapies
via
marketed
products.
Cytokines
their
receptors
are
validated
targets
multiple
therapeutic
areas,
we
review
current
strategies
intervention
developing
therapies.
New
biologics
have
shown
efficacy
last
few
decades
management
IBD;
unfortunately,
many
patients
nonresponsive
develop
therapy
resistance
over
time,
creating
need
novel
therapeutics.
Thus,
treatment
options
beyond
immune-modifying
anti-TNF
agents
combination
expanding
rapidly.
Further
studies
needed
fully
understand
response,
cytokines,
direct
pathogenetic
relevance
regarding
individually
tailored,
safe
efficient
targeted-biotherapeutics.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: April 24, 2024
Epigenetic
modifications,
characterized
by
changes
in
gene
expression
without
altering
the
DNA
sequence,
play
a
crucial
role
development
and
progression
of
cancer
significantly
influencing
activity
cellular
function.
This
insight
has
led
to
novel
class
therapeutic
agents,
known
as
epigenetic
drugs.
These
drugs,
including
histone
deacetylase
inhibitors,
acetyltransferase
methyltransferase
aim
modulate
curb
growth
uniquely
landscape
cells.
Ongoing
research
clinical
trials
are
rigorously
evaluating
efficacy
these
particularly
their
ability
improve
outcomes
when
used
combination
with
other
treatments.
Such
therapies
may
more
effectively
target
potentially
overcome
challenge
drug
resistance,
significant
hurdle
therapy.
Additionally,
importance
nutrition,
inflammation
control,
circadian
rhythm
regulation
modulating
responses
been
increasingly
recognized,
highlighting
critical
modifiers
thereby
effectiveness
pharmacological
interventions
patient
outcomes.
drugs
represent
paradigm
shift
treatment,
offering
targeted
that
promise
precise
approach
treating
wide
spectrum
tumors,
fewer
side
effects
compared
traditional
chemotherapy.
progress
marks
step
towards
personalized
interventions,
leveraging
unique
profiles
individual
tumors
optimize
treatment
strategies.
British Journal of Anaesthesia,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 1, 2025
Chronic
neuropathic
pain
generally
has
a
poor
response
to
treatment
with
conventional
drugs.
Sympathectomy
can
alleviate
in
some
patients,
suggesting
that
abnormal
sympathetic-somatosensory
signaling
interactions
might
underlie
forms
of
pain.
The
molecular
mechanisms
underlying
remain
obscure.
Lumbar
sympathectomy
was
performed
spared
nerve
injury
(SNI)
mice
or
rats,
and
the
up-down
method
used
measure
mechanical
paw
withdrawal
threshold.
Dorsal
root
ganglia
(DRG)
injection
perfusion
were
deliver
virus
Methylated
RNA
immunoprecipitation
sequencing,
RNA-sequencing,
immunoelectron
microscopy
identify
neurotransmitters.
We
found
sprouting
tyrosine
hydroxylase-positive
sympathetic
fibres
DRG
mediated
maintenance
allodynia
after
SNI
(day
28,
P<0.001).
further
significantly
increased
N6-methyladenosine
level
CXCL16
messenger
P<0.001),
which
attributable
reduced
demethylase
fat
mass
obesity-associated
protein
(P=0.002)
interaction
YTHDF1
(P=0.013)
ganglion.
Enhanced
expression
lead
increases
release
into
act
synergistically
norepinephrine
from
terminals
enhance
neuronal
excitability.
Norepinephrine
co-released
contribute
rodent
model.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 22, 2025
To
identify
cell
specific
molecular
changes
associated
with
sarcoidosis
risk
and
progression,
we
aimed
to
characterize
the
cellular
composition,
gene
expression
patterns,
cell-cell
interactions
in
BAL
cells
from
patients
(both
progressive
non-progressive)
healthy
controls.
Single
RNA-seq
data
were
collected
on
12
4
control
participants.
We
combined
scRNA-seq
these
participants
our
previously
10
for
a
final
sample
size
of
16
cases
(8
8
14
Following
initial
preprocessing
CellRanger,
quality
controlled,
combined,
clustered
Seurat.
tested
differences
proportions
by
disease
group
using
F-tests
pseudobulk
analysis.
Cell
communication
pathway
analysis
performed
CellChat.
identified
five
macrophage
populations:
resident,
high
metallothionein
(MT)
recruited,
profibrotic
proliferating
macrophages.
Each
subpopulation
displayed
unique
profiles,
notable
differential
genes
pathways
linked
resident
macrophages,
recruited
also
observed
progression
In
non-macrophages
cells,
significant
reduction
number
B
compared
Among
T
populations,
transcriptional
alterations
at
level.
Additionally,
distinct
cell-to-cell
macrophages
between
These
findings
underscore
complexity
immune
involvement
highlight
potential
targets
further
investigation.
HIV Infection and Immunosuppressive Disorders,
Journal Year:
2025,
Volume and Issue:
16(4), P. 28 - 44
Published: Feb. 13, 2025
The
aim
of
the
study
was
to
search
for
candidate
genes
interacting
with
HIV
attachment
receptors
(CCR5,
CXCR4,
CCR2,
CD4)
and
potentially
involved
in
disease
pathogenesis,
based
on
complex
silico
network
algorithms.
Materials
methods.
A
number
web
applications
were
used
analyse
genetic
protein-protein
networks,
algorithms
databases
which
are
complementary.
CD4
receptor
chemokine
co-receptor
CCR5,
CXCR4
CCR2
as
background/baseline
all
cases,
their
protein
products
play
a
key
role
process
virus
cell.
data
analysed,
including
two-stage
ranking
identified
according
interaction
background
presence
results
analysis
different
resources.
Results
discussion.
According
results,
using
three
resources:
HumanNet
—
451
genes,
GeneMania
86,
STRING
61.
Based
crossing
resources,
total
associated
511.
rank
above
4
points
68.
Of
these,
31
(45.6%)
encoding
C-C/C-X-C
family
ligands,
12
(17.6%)
C-C/C-XC
receptors,
8
(11.8%)
other
types,
17
(25%)
proteins
types.
following
that
not
members
C-C/C/C-X-C
families
indicated
groups
have
been
identified:
ARRB2,
TLR2,
ADRA1A,
ARRB1,
FPR1,
FPR3,
GNAI1,
PF4,
PIK3CG,
PPIA,
S1PR3,
GNA11,
GNAI2,
GNG2,
PTPRC,
ADRA1B,
ADRB1,
AFP,
CD164,
DBN1,
GNB1,
ITCH,
RNF113A,
SLC1A1,
USP14.
Conclusion.
Most
pathogenesis
those
progression
infection
is
known
or
under
active
investigation.
At
same
time,
whose
never
considered
possible
participants
identified,
but
suggest
they
may
regulation
entry
and/or
modulation
immune
response
organism.
Further
bioinformatic
experimental
studies
functions
polymorphic
variants
these
will
help
improve
understanding
basis
identify
new
directions
therapeutic
approaches.