Development and Validation of the COVID-19 Infection Fear Scale in a Collectivist Cultural Context: A Study From South Korea.

Objective: Understanding the specific fears associated with coronavirus disease-2019 (COVID-19), particularly within different cultural contexts, is crucial for developing effective mental health interventions. This study aims to develop and validate the COVID-19 Infection Fear Scale (CIFS) in a collectivist cultural context such as Korea.

Methods: A total of 1,002 adults aged 19 to 70 participated in an online survey in May 2020.

Exploring Fear of Cancer Recurrence (FCR) in cancer survivors from a medical social work perspective: A qualitative study of medical social workers in South Korea.

Background: Fear of Cancer Recurrence (FCR) in cancer survivors has been insufficiently addressed despite its imperativeness in cancer journey. Although several studies have investigated healthcare professionals' experience with FCR in cancer survivors, a medical social work perspective has rarely been reflected. This study aimed to explore Korean medical social workers' experience with intervening FCR in cancer survivors.

Time-Series Trends of Depressive Levels of Korean Adults During the 2020 COVID-19 Pandemic in South Korea.

Objective: This study aimed to observe the changes in people's depressive levels over 9 months since the coronavirus disease of 2019 (COVID-19) outbreak as well as to identify the predictors of people's depressive levels including COVID-19 infection fear in the context of South Korea in 2020.

Methods: For these purposes, four cross-sectional surveys were periodically implemented from March to December 2020. We randomly recruited 6,142 Korean adults (aged 19 to 70) by using a quota survey.

Factors Related to Anxiety and Depression Among Adolescents During COVID-19: A Web-Based Cross-Sectional Survey.

Background: The coronavirus disease 2019 (COVID-19) outbreak and subsequent disease-containment measures (such as school closures) significantly affected the lives of adolescents. We evaluated the mental-health status and factors associated with anxiety and depression among South Korean adolescents.

Methods: A nationwide online survey was conducted to evaluate the mental-health status of South Korean adolescents during the COVID-19 pandemic.

Platelet-Mediated NET Release Amplifies Coagulopathy and Drives Lung Pathology During Severe Influenza Infection.

The influenza A virus (IAV) causes a respiratory tract infection with approximately 10% of the population infected by the virus each year. Severe IAV infection is characterized by excessive inflammation and tissue pathology in the lungs. Platelet and neutrophil recruitment to the lung are involved in the pathogenesis of IAV, but the specific mechanisms involved have not been clarified.

COVID-19 and Risk Factors of Anxiety and Depression in South Korea.

Objective: The aims of this study were to explore the prevalence of and identify predictors of anxiety and depression related to coronavirus disease of 2019 (COVID-19) in South Korea.

Methods: The analysis is based on a quota survey design and a sampling frame that permitted recruitment of a national sample of 1,014 individuals between March 17-31, 2020. Several standardized measurements were used, including GAD-7, PHQ-9, COVID-19 related fear, restrictions in deaily life, as well as sociodemographic information and physical and psychosocial needs during the pandemic.

Modulation of the liver immune microenvironment by the adeno-associated virus serotype 8 gene therapy vector.

Adeno-associated viruses (AAVs) are emerging as one of the vehicles of choice for gene therapy. However, the potential immunogenicity of these vectors is a major limitation of their use, leading to the necessity of a better understanding of how viral vectors engage the innate immune system. In this study, we demonstrate the immune response mediated by an AAV vector in a mouse model.

Visualizing Oncolytic Virus-Host Interactions in Live Mice Using Intravital Microscopy.

Oncolytic virus (OV) therapy is an emerging cancer treatment that uses replicating viruses to infect and kill tumor cells and incite anticancer immunity. While the approach shows promise, it currently fails most patients, indicating strategies to improve OV activity are needed. Developing these will require greater understanding of OV biology, particularly in the context of OV delivery and clearance, the infection process within a complex tumor microenvironment, and the modulation of anticancer immunity.

Neutrophils in viral infection.

Neutrophils are the first wave of recruited immune cells to sites of injury or infection and are crucial players in controlling bacterial and fungal infections. Although the role of neutrophils during bacterial or fungal infections is well understood, their impact on antiviral immunity is much less studied. Furthermore, neutrophil function in tumor pathogenesis and cancer treatment has recently received much attention, particularly within the context of oncolytic virus infection where neutrophils produce antitumor cytokines and enhance oncolysis.

Platelets as Modulators of Inflammation.

Platelets have classically been considered crucial effector cells in hemostasis, but now are increasingly recognized as players during inflammatory responses in innate and adaptive immunity. Platelets can recognize and kill invading pathogens, and, upon stimulation, also release a wide array of mediators that modify immune and endothelial cell responses. Increased platelet activity can protect the host against infectious insults; however, the excessive activity can lead to inflammation-mediated tissue damage.

Necrostatin-1 Protects Against D-Galactosamine and Lipopolysaccharide-Induced Hepatic Injury by Preventing TLR4 and RAGE Signaling.

Fulminant hepatic failure (FHF) is a life-threatening clinical syndrome results in massive inflammation and hepatocyte death. Necroptosis is a regulated form of necrotic cell death that is emerging as a crucial control point for inflammatory diseases. The kinases receptor interacting protein (RIP) 1 and RIP3 are known as key modulators of necroptosis.

Genipin protects d-galactosamine and lipopolysaccharide-induced hepatic injury through suppression of the necroptosis-mediated inflammasome signaling.

Acute liver failure (ALF) is a life-threatening syndrome resulting from massive inflammation and hepatocyte death. Necroptosis, a programmed cell death controlled by receptor-interacting protein kinase (RIP) 1 and RIP3, has been shown to play an important role in regulating inflammation via crosstalk between other intracellular signaling. The inflammasome is a major intracellular multiprotein that induces inflammatory responses by mediating immune cell infiltration, thus potentiating injury.

Platelets and neutrophil extracellular traps collaborate to promote intravascular coagulation during sepsis in mice.

Neutrophil extracellular traps (NETs; webs of DNA coated in antimicrobial proteins) are released into the vasculature during sepsis where they contribute to host defense, but also cause tissue damage and organ dysfunction. Various components of NETs have also been implicated as activators of coagulation. Using multicolor confocal intravital microscopy in mouse models of sepsis, we observed profound platelet aggregation, thrombin activation, and fibrin clot formation within (and downstream of) NETs in vivo.

Role of platelets in neutrophil extracellular trap (NET) production and tissue injury.

In addition to their well-known role as the cellular mediator of thrombosis, numerous studies have identified key roles for platelets during various disease processes. Importantly, platelets play a critical role in the host immune response, directly interacting with, and eliminating pathogens, from the blood stream. In addition to pathogen clearance, platelets also contribute to leukocyte recruitment at sites of infection and inflammation, and modulate leukocyte activity.

Role of necroptosis in autophagy signaling during hepatic ischemia and reperfusion.

Ischemia and reperfusion (I/R) is a complex phenomenon involving massive inflammation and cell death. Necroptosis refers to a newly described cell death as "programmed necrosis" that is controlled by receptor-interacting protein kinase (RIP) 1 and RIP3, which is involved in the pathogenesis of several inflammatory diseases. Autophagy is an essential cytoprotective system that is rapidly activated in response to various stimuli and involves crosstalk between different modes of cell death and inflammation.

Protective effect of wild ginseng cambial meristematic cells on d-galactosamine-induced hepatotoxicity in rats.

Background: Panax ginseng has a wide range of biological activities including anti-inflammatory, antioxidant, and immunomodulatory functions. Wild ginseng cambial meristematic cells (CMCs) were obtained from P. ginseng cambium.

Activation of NLRP3 and AIM2 inflammasomes in Kupffer cells in hepatic ischemia/reperfusion.

Inflammasome activation by danger signals in ischemia/reperfusion (I/R) injury is responsible for the sterile inflammatory response. Signals triggering formation and activation of the inflammasome involve the generation of oxidative stress. The aim of this study was to examine the molecular mechanisms of inflammasome activation and the involvement of reactive oxygen species in hepatic I/R.

Protective effects of lupeol against D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure in mice.

This study examined the hepatoprotective effects of lupeol (1, a major active triterpenoid isolated from Adenophora triphylla var. japonica) against d-galactosamine (GalN) and lipopolysaccharide (LPS)-induced fulminant hepatic failure. Mice were orally administered 1 (25, 50, and 100 mg/kg; dissolved in olive oil) 1 h before GalN (800 mg/kg)/LPS (40 μg/kg) treatment.

Protective effect of linarin against D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure.

Linarin was isolated from Chrysanthemum indicum L. Fulminant hepatic failure is a serious clinical syndrome that results in massive inflammation and hepatocyte death. Apoptosis is an important cellular pathological process in d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury, and regulation of liver apoptosis might be an effective therapeutic method for fulminant hepatic failure.

Community factors predicting dental care utilization among older adults.

Background: Few investigators have studied the influence of community factors on dental care utilization among older adults. The authors' objective in this study was to investigate the effect of community factors on dental care utilization after adjustment for individual factors.

Methods: Using data from a cross-sectional survey of Ohio residents, the authors assessed dental care utilization in a sample of 2,166 adults 65 years or older.

NLRP3 inflammasome activation in D-galactosamine and lipopolysaccharide-induced acute liver failure: role of heme oxygenase-1.

D-Galactosamine (GalN) and lipopolysaccharide (LPS) are commonly used to study mechanisms of hepatic malfunction that result in hepatic inflammation and subsequent fulminant hepatic failure. Inflammasomes are intracellular multiprotein complexes that in response to cellular danger signals trigger the biological maturation of proinflammatory cytokines. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that induces anti-inflammatory and antioxidant activity against oxidative cellular stress.

Role of heme oxygenase 1 in TNF/TNF receptor-mediated apoptosis after hepatic ischemia/reperfusion in rats.

Hepatocellular apoptosis commonly occurs in ischemia/reperfusion (I/R) injury. The binding of tumor necrosis factor (TNF) to TNF receptor 1 (TNFR1) leads to the formation of a death-inducing signaling complex (DISC), which subsequently initiates a caspase cascade resulting in apoptosis. Heme oxygenase 1 (HO-1) confers cytoprotection against cell death in I/R injury and inhibits stress-induced apoptotic pathways in vitro.

Protective effects of HV-P411 complex against D-galactosamine-induced hepatotoxicity in rats.

This study examined the hepatoprotective effect of the HV-P411 complex, an herbal extract mixture from the seeds of Vitis vinifera, Schisandra chinensis and Taraxacum officinale, against D-galactosamine (D-GalN)-induced hepatitis. Hepatotoxicity was induced by D-GalN (700 mg/kg, i.p.