damage
[용어속성] Term
Repositioning of pentoxifylline as an immunomodulator and regulator of the renin-angiotensin system in the treatment of COVID-19
COVID-19 치료에서 레닌-안지오텐신 시스템의 면역 조절제 및 조절제로서의 펜톡시필린의 재배치
Article
[키워드] activate
adenosine
adenosine monophosphate
alveolar epithelial cells
angiotensin
Anti-inflammatory
approach
AT1R
balance
cells
circulation
Concentration
COVID-19
cyclic adenosine monophosphate
Cytokines
damage
deleterious effect
deleterious effects
Endothelium
epithelial cells
Evidence
expression
helping
highlight
immune response
immune system
immunomodulator
IMPROVE
in vitro
increase
Inflammatory cytokine
Inflammatory cytokines
inhibiting
inhibitor
Microvascular thrombosis
monophosphate
mRNA
offer
patients with COVID-19
Pentoxifylline
Prevent
Proinflammatory cytokine
proinflammatory cytokines
Protein
protein kinase
RAS
receptor
reduce
reduction in
Renin
renin-angiotensin system
repositioning
safety profile
synthesis
Therapeutic treatment
thrombosis
TNF-α
Treatment
treatment of COVID-19
turn
ventilatory parameters
Viral
viral clearance
[DOI] 10.1016/j.mehy.2020.109988 PMC 바로가기 [Article Type] Article
[DOI] 10.1016/j.mehy.2020.109988 PMC 바로가기 [Article Type] Article
COVID-19 and Systemic Lupus Erythematosus: Focus on Immune Response and Therapeutics
COVID-19 및 전신성 홍반성 루푸스: 면역 반응 및 치료에 초점
Review
[키워드] aberrant immune response
affected
Anti-viral
Antiviral
autoantibodies
Autoimmune disease
Better
cause
caused
characterized
circulating
Clinical outcome
clinical outcomes
Comorbidities
Coronavirus infection
Coronaviruses
COVID-19
COVID-19 pandemic
cytokine
Cytokine storm
Cytokines
damage
death
Defense
Disease progression
Ethnicity
focus
immune response
Immune-mediated
in viral
individual
Infection
Infectious disease
lead
lung
Lungs
Lupus
lupus erythematosus
lymphopenia
management
mechanisms
morbidity and mortality
Novel coronavirus
other organs
Patient
patients
Population
populations
progression
Proinflammatory cytokine
proinflammatory cytokines
PROTECT
Regulatory
response
SARS-CoV-2
severity
susceptible
systemic
systemic lupus erythematosus
T cells
the disease
Therapeutic strategies
therapeutic strategy
Therapeutics
tissues
treated
underlying condition
underlying conditions
vice
Viral
viral infections
while
[DOI] 10.3389/fimmu.2020.589474 PMC 바로가기 [Article Type] Review
[DOI] 10.3389/fimmu.2020.589474 PMC 바로가기 [Article Type] Review
Inborn errors of type I IFN immunity in patients with life-threatening COVID-19
생명을 위협하는 COVID-19 환자에서 I형 IFN 면역의 선천적 오류
Research Article
[키워드] a minor
acute respiratory syndrome
acute respiratory syndrome coronavirus
acute respiratory syndrome coronavirus 2
administration
Affect
affecting
age
amplification
amplification pathway
Asymptomatic
autoantibodies
autoantibody
autoantibody system
autosomal-dominant
autosomal-recessive
Beck
biochemically
BOLD
candidate gene approach
caused
cellular
clinical
Clinical course
Clinical outcome
clinical variability
complete penetrance
complex
component
components
core gene
core genes
coronavirus
coronavirus disease
Coronavirus disease 2019
Course
COVID
COVID Human Genetic Effort
COVID-19
COVID-19 patient
COVID-19 pneumonia
Critical
Critical disease
cytokine
Cytokines
damage
dampen
deficiencies
deficiency
defined
Deleterious
dendritic cell
dendritic cells
determine
Diseases
double-stranded RNA
eight
enrichment
epidemiological studies
Exome
fibroblast
fibroblasts
Genes
genes encoding
genetic defect
genetic defects
genetics
Genome
genomics study
had milder phenotype
healthy individuals
highest
Hospitalized
Human
human fibroblasts with mutations
Hypothesis
identify
IFN
IFN response
IFN-α2
IFNAR1
IFNAR1 deficiency
IFNAR2
IFNs
IKBKG
immune system
Immunity
immunological
in healthy individuals
in some
in vitro
Inborn error
Inborn errors
incomplete penetrance
individual
induction pathway
Infection
infection with SARS-CoV-2
Infectious diseases
Influenza
influenza pneumonia
Influenza virus
inheritance
interferon
interferon regulatory factor
interferon regulatory factor 7
interferons
interferons (IFNs)
involved
IRF3
IRF7
IRF9
lack
life-threatening
likelihood
loci
LOF
loss-of-function
male
mechanism
Medical conditions
minor
minor allele frequency
molecular
molecule
molecules
monogenic inborn error
monogenic inborn errors
mutated
Mutation
NEMO
NEMO/IKBKG
Neutralizing
nonsynonymous variant
other variants
outcome
pathogen
pathogen-induced inflammation
pathway
Patient
patients
Perspective
plasmacytoid dendritic cells
pLOF
Pneumonia
predicted
Prevent
produced
rare variant
Rare variants
Regulation
respiratory
reveal
risk
risk factor
SARS-CoV-2
SARS-COV-2 infection
SARS-CoV-2 infection in vitro
Science
selected
sequenced
severe acute respiratory syndrome Coronavirus
severe acute respiratory syndrome coronavirus 2
severe coronavirus disease
severe COVID-19
Severe COVID-19 pneumonia
severe disease
Severe infection
silent infection
Stat1
STAT2
subject
susceptible
TBK1
tested
Therapeutic benefit
this system
TICAM1
TICAM1/TRIF
tissue
TLR3
Toll-like receptor
Toll-like receptor 3
TRAF3
TRIF
Type
type I
Type I IFN
type I IFNs
type I interferon
UNC93B1
underlie
variant
variants
Viral
Viral illness
viral illnesses
[DOI] 10.1126/science.abd4570 PMC 바로가기 [Article Type] Research Article
[DOI] 10.1126/science.abd4570 PMC 바로가기 [Article Type] Research Article
Autoantibodies against type I IFNs in patients with life-threatening COVID-19
생명을 위협하는 COVID-19 환자에서 I형 IFN에 대한 자가항체
Research Article
[키워드] Activation
acute disease
acute respiratory syndrome
acute respiratory syndrome coronavirus
acute respiratory syndrome coronavirus 2
adaptive
Affect
affected
age
antiviral immunity
Asymptomatic
auto-Ab
auto-Abs
autoantibodies
autoantibody
autoantibody system
Autoimmune
Autoimmunity
B cell
Beck
binding
can not
candidate gene approach
cause
causes
Clinical course
clinical phenotype
clinical phenotypes
clinical variability
collected
complex
component
components
Concentration
conditions
coronavirus
coronavirus disease
Coronavirus disease 2019
correlated
Course
COVID-19
COVID-19 pandemic
COVID-19 patients
COVID-19 pneumonia
Critical
Critical disease
cytokine
Cytokines
damage
dampen
death
determine
disease
Diseases
downstream
enrichment
enrolment
epidemiological
excess
explain
Genes
genetics
genomics study
had milder phenotype
healthy control
healthy individual
healthy individuals
highest
Human
Hypothesis
identify
IFN
IFN response
IFN-stimulated genes
IFN-α
IFN-α/β
IFN-α2
IFN-β
IFN-γ
IFNAR
IFNs
IgG
IL-17A
IL-6
immune system
Immunity
Immunoglobulin
Immunoglobulin G
immunological
impair
impairing
in healthy individuals
in vitro
Inborn errors
increase in
individual
infected with SARS-CoV-2
Infection
Infectious diseases
interferon
interferon regulatory factor
interferon-γ
interferons
interferons (IFNs)
interleukin
interleukin-6
intrinsic
involved
IRF
ISGs
lack
life-threatening
life-threatening coronavirus disease
likelihood
male
mechanism
men
mild SARS-CoV-2 infection
morbidity
morbidity and mortality
mucocutaneous candidiasis
Mutation
mycobacterial disease
neutralize
Neutralizing
outcomes
pandemic
pathogen
pathogen-induced inflammation
pathway
Patient
patients
patients hospitalized
Perspective
phosphorylated
Plasmapheresis
Pneumonia
Prevent
pSTAT
receptor
receptors
Regulation
respiratory
rising
risk
risk factor
SARS-CoV-2
SARS-COV-2 infection
Science
searched
serum IFN-α level
severe acute respiratory syndrome Coronavirus
severe coronavirus disease
severe COVID-19
Severe COVID-19 pneumonia
shown
silent infection
staphylococcal
susceptible
tested
the patient
this system
TLR
Toll-like receptor
Transcription
Treatment
trials
type 1 interferon
type 1 interferons
type I
Type I IFN
type I IFNs
underlie
undetectable
Vaccine
Viral
viral infections
viral respiratory diseases
while
women
[DOI] 10.1126/science.abd4585 PMC 바로가기 [Article Type] Research Article
[DOI] 10.1126/science.abd4585 PMC 바로가기 [Article Type] Research Article
Products of Oxidative Guanine Damage Form Base Pairs with Guanine
Review
[키워드] 2019 novel coronavirus
addition
antiviral agent
base
base incorporation
base pair
base pairs
bases
caused
damage
experiments
form
G-C transversions
guanine
implication
involved
knowledge
oxidative
oxidative guanine damage
pair
product
RdRP
RNA virus
RNA-dependent RNA polymerase
SARS-CoV-2
urea
[DOI] 10.3390/ijms21207645 PMC 바로가기 [Article Type] Review
[DOI] 10.3390/ijms21207645 PMC 바로가기 [Article Type] Review
COVID-19-Induced Thrombosis in Patients without Gastrointestinal Symptoms and Elevated Fecal Calprotectin: Hypothesis Regarding Mechanism of Intestinal Damage Associated with COVID-19
Brief Report
[키워드] abnormality
Admission
Asymptomatic
bowel
bowel perforation
calprotectin
Concentration
coronavirus
COVID-19
D-dimer
damage
disease pathogenesis
enrolled
fecal
fecal calprotectin
Gastrointestinal
Gastrointestinal symptom
gastrointestinal symptoms
hypoxic
individuals with COVID-19
Infectious disease
Inflammatory bowel disease
Inpatient
intestinal
Ischemia
median value
Patient
pilot study
Pneumonia
positive correlation
SARS-CoV-2
thrombosis
Two patient
with COVID-19
[DOI] 10.3390/tropicalmed5030147 PMC 바로가기 [Article Type] Brief Report
[DOI] 10.3390/tropicalmed5030147 PMC 바로가기 [Article Type] Brief Report
Neurological Damage by Coronaviruses: A Catastrophe in the Queue!
Immunology
[키워드] animal model
anomalies
Anxiety
Brain
bystander
catastrophe
caused
cellular
CNS
cognitive
Coronaviruses
Cytokine storm
damage
develop
disease
disorder
dysfunction
Encephalitis
explain
Infection
Inflammation
Influenza
manifestation
massive
measles virus
MERS-CoV
microglial priming
Neuroinflammation
neurological
neurological manifestation
pathogenic
pathology
Patient
peripheral
Primary infection
reported
SARS-CoV-1
SARS-CoV-2
susceptibility
syndrome
viral infection
virus
[DOI] 10.3389/fimmu.2020.565521 PMC 바로가기 [Article Type] Immunology
[DOI] 10.3389/fimmu.2020.565521 PMC 바로가기 [Article Type] Immunology
Cardiovascular Damage in COVID-19: Therapeutic Approaches Targeting the Renin-Angiotensin-Aldosterone System
Review
[키워드] ACE2
ACE2/Ang-(1–7)/MasR
Activation
acute respiratory syndrome
age
agonist
alterations
angiotensin-converting enzyme inhibitor
anomalies
Antiviral
apoptotic
ARB
association
blocker
cardiovascular
cardiovascular damage
Cell
clinical trial
components
Coronavirus disease 2019
Coronavirus-2
COVID-19
COVID-19 patients
damage
decrease
disease
endothelial cells
Genetic
help
homeostasis
hypercoagulable
hyperinflammation
Hyperinflammatory
hypertension
hypertensive
immunomodulator
IMPROVE
individual
infect
Infection
liver
lung
Mortality
multiple tissue
outcome
Pathologies
pathology
pathway
peptides
plasma
polymorphism
RAAS
receptor
reduce
regulate
responses
SARS-CoV-2
SARS-COV-2 infection
severity
sex hormone
soluble ACE2
Stage
susceptibility
System
targeting
Therapies
therapy
thrombotic
Treatment
Vaccine
vessel
viral particle
viral propagation
[DOI] 10.3390/ijms21186471 PMC 바로가기 [Article Type] Review
[DOI] 10.3390/ijms21186471 PMC 바로가기 [Article Type] Review
Quantitative CT Extent of Lung Damage in COVID-19 Pneumonia Is an Independent Risk Factor for Inpatient Mortality in a Population of Cancer Patients: A Prospective Study
Oncology
[키워드] 95% CI
Analysis
association
C-index
Cancer
cancer patient
Cancer patients
cancer stage
Chest CT
correlated
COVID-19
COVID-19 pneumonia
damage
death
demographic
died
distribution
evaluate
Evidence
Factor
Follow-up
groups
histology
independent
Inpatient
IQR
Laboratory
lung
lung damage
lung lesion
management
median
Mortality
non-survivor
oncology
outcome
Oxygen therapy
Patient
patients with COVID-19
performance status
Pneumonia
Population
potential risk
prognostic
Prognostic factor
prognostic performance
Prospective
Quantitative
quantitative assessment
quantitative chest CT extent
released
risk factor for mortality
severity
survival
survivor
Treatment
was used
were recorded
[DOI] 10.3389/fonc.2020.01560 PMC 바로가기 [Article Type] Oncology
[DOI] 10.3389/fonc.2020.01560 PMC 바로가기 [Article Type] Oncology