Impact of COVID-19 on Out-of-Hospital Cardiac Arrest in Korea

Background@#Coronavirus disease 2019 (COVID-19) is a global public health crisis that has had a significant impact on emergency medical services (EMS). Several studies have reported an increase in the incidence of out-of-hospital cardiac arrest (OHCA) and a decreased survival due to COVID-19, which has been limited to a short period or has been reported in some regions. This study aimed to investigate the effect of COVID-19 on OHCA patients using a nationwide database. @*Methods@#We included adult OHCA patients treated by EMS providers from January 19, 2019 to January 20, 2021. The years before and after the first confirmed case in Korea were set as the non-COVID-19 and COVID-19 periods, respectively. The main exposure of interest was the COVID-19 period, and the primary outcome was prehospital return of spontaneous circulation (ROSC). Other OHCA variables were compared before and after the COVID-19 pandemic and analyzed. We performed a multivariable logistic regression analysis to understand the independent effect of the COVID-19 period on prehospital ROSC. @*Results@#The final analysis included 51,921 eligible patients, including 25,355 (48.8%) during the non-COVID-19 period and 26,566 (51.2%) during the COVID-19 period. Prehospital ROSC deteriorated during the COVID-19 period (10.2% vs. 11.1%, P = 0.001). In the main analysis, the adjusted odds ratios (AORs) for prehospital ROSC showed no significant differences between the COVID-19 and non-COVID-19 periods (AOR [95% confidence interval], 1.02 [0.96–1.09]). @*Conclusion@#This study found that the proportion of prehospital ROSC was lower during the COVID-19 period than during the non-COVID-19 period; however, there was no statistical significance when adjusting for potential confounders. Continuous efforts are needed to restore the broken chain of survival in the prehospital phase and increase the survival rate of OHCA patients.

The Impact of the COVID-19 Outbreak on Emergency Medical Service:An Analysis of Patient Transportations and Time Intervals

Background@#This study aimed to investigate the impact of the coronavirus disease 2019 (COVID-19) outbreak on the Emergency Medical Service (EMS) system in South Korea. The study focused on the differences in EMS time intervals following the COVID-19 outbreak, particularly for patients with fever. @*Methods@#A retrospective analysis of EMS patient transportation data from 2017 to 2022 was conducted using the national EMS database. @*Results@#Starting from the year 2020, coinciding with the COVID-19 outbreak, all EMS time intervals experienced an increase. For the years 2017 to 2022, the mean response time interval values were 8.6, 8.6, 8.6, 10.2, 12.8, and 11.4 minutes, and the mean scene time interval values were 7.1, 7.2, 7.4, 9.0, 9.8, and 10.9 minutes. The mean transport time interval (TTI) values were 12.1, 12.3, 12.4, 14.2, 16.9, and 16.2 minutes, and the mean turnaround time interval values were 27.6, 27.9, 28.7, 35.2, 42.0, and 43.1 minutes. Fever (≥ 37.5°C) patients experienced more pronounced prolongations in EMS time intervals compared to non-fever patients and had a higher probability of being non-transported. The mean differences in TTI between fever and non-fever patients were 0.8, 0.8, 0.8, 4.3, 4.8, and 3.2 minutes, respectively, from 2017 to 2022. Furthermore, the odds ratios for fever patients being transported to the emergency department were 2.7, 2.9, 2.8, 1.1, 0.8, and 0.7, respectively, from 2017 to 2022. @*Conclusion@#The study findings highlight the significant impact of the COVID-19 outbreak on the EMS system and emphasize the importance of ongoing monitoring to evaluate the burden on the EMS system.

Circulating Anti-Elastin Antibody Levels and Arterial Disease Characteristics: Associations with Arterial Stiffness and Atherosclerosis

PURPOSE: Elastin is a major arterial structural protein, and elastin-derived peptides are related to arterial change. We previously reported on a novel assay developed using aortic elastin peptides; however, its clinical implications remain unclear. In this study, we assessed whether anti-elastin antibody titers reflect the risk of coronary artery disease (CAD) or its characteristics. MATERIALS AND METHODS: We included 174 CAD patients and 171 age- and sex-matched controls. Anti-elastin antibody titers were quantified by enzyme-linked immunosorbent assay. Parameters of arterial stiffness, including the augmentation index (AI) and heart-to-femoral pulse wave velocity (hfPWV), were measured non-invasively. The clinical and angiographic characteristics of CAD patients were also evaluated. Associations between anti-elastin levels and vascular characteristics were examined by linear regression analysis. RESULTS: The median blood level of anti-elastin was significantly lower in the CAD group than in the controls [197 arbitrary unit (a.u.) vs. 63 a.u., p<0.001]. Levels of anti-elastin were significantly lower in men and in subjects with hypertension, diabetes mellitus, hyperlipidemia, or high hfPWV. Nevertheless, anti-elastin levels were not dependent on atherothrombotic events or the angiographic severity of CAD. In a multivariate analysis, male sex (beta=-0.38, p<0.001), diabetes mellitus (beta=-0.62, p<0.001), hyperlipidemia (beta=-0.29, p<0.001), and AI (beta=-0.006, p=0.02) were ultimately identified as determinants of anti-elastin levels. CONCLUSION: Lower levels of anti-elastin are related to CAD. The association between antibody titers and CAD is linked to arterial stiffness rather than the advancement of atherosclerosis.

Interplay between Inflammatory Responses and Lymphatic Vessels

Lymphatic vessels are routes for leukocyte migration and fluid drainage. In addition to their passive roles in migration of leukocytes, increasing evidence indicates their active roles in immune regulation. Tissue inflammation rapidly induces lymphatic endothelial cell proliferation and chemokine production, thereby resulting in lymphangiogenesis. Furthermore, lymphatic endothelial cells induce T cell tolerance through various mechanisms. In this review, we focus on the current knowledge on how inflammatory cytokines affect lymphangiogenesis and the roles of lymphatic vessels in modulating immune responses.

Mechanism of Allergic Asthma Pathogenesis by Protease Allergen / 한양의대학술지

Asthma is a complex immune mediated chronic inflammatory lung disease characterized by chronic inflammation of the airways, airway hyper-responsiveness and airway obstruction, and the prevalence of this disease has increased in recent years. It is well known that many features of allergic asthma are consequences of Th2 cell dominated immune responses against allergens, thus allergen specific Th2 cells play a critical role in the pathogenesis. In this review, we will discuss the properties of common indoor and outdoor allergens including house dust mite, fungus, pollen and cockroach, the activation and differentiation of naive CD4 T cells by protease allergens, how specific allergens modify host's immune system to mediate immune evasion, and regulation of homing receptor expression and trafficking of allergen specific Th2 cells. Lastly, we will also overview the general course of pathogenesis of allergic asthma and discuss prospects of development of novel immuno-therapies to asthma.

Role of Citrullinated Fibrinogen Peptides in the Activation of CD4 T Cells from Patients with Rheumatoid Arthritis

This study was conducted to determine whether CD4 T cell responses to citrullinated fibrinogen occur in patients with rheumatoid arthritis (RA), especially in HLA-DR4-positive subjects. Whole peripheral blood mononuclear cells (PBMCs) of RA patients and control subjects were stimulated with citrullinated fibrinogen peptides, and T-cell production of proliferation and proinflammatory cytokines, such as interferon-gamma(IFN-gamma) and interleukin-17A (IL-17A), were measured. In addition, CD4 T cells from RA patients were stimulated with the citrullinated fibrinogen peptide, Fib-alpha R84Cit, identified as a DRB1*0401-restricted T cell epitope in HLA-DR4 transgenic mice, and the degree of T cell activation was examined similarly. No proliferative responses to the citrullinated fibrinogen peptides were observed in whole PBMCs or CD4 T cells from RA patients. Furthermore, no increased production of IFN-gamma or IL-17A was found in whole PBMCs or CD4 T cells stimulated with the citrullinated fibrinogen peptides, although these cells responded to recall antigen, a mixture of tetanus toxoid, purified protein derivative (PPD) from Mycobacterium tuberculosis, and Candida albicans. The results of this study indicate that anti-citrulline immunity in RA patients may be mediated by fibrinogen because there is no evidence of CD4 T cell-mediated immune responses to citrullinated fibrinogen peptides.

Serum Elastin-Derived Peptides and Anti-Elastin Antibody in Patients with Systemic Sclerosis

The elastin metabolism in systemic sclerosis (SSc) has been known to be abnormal. The authors investigated relationship between the clinical manifestations of systemic sclerosis (SSc) and serum levels of soluble elastin-derived peptide (S-EDP) and anti-elastin antibodies. Serum samples were obtained from 79 patients with SSc and 79 age- and sex-matched healthy controls. Concentrations of serum S-EDP and anti-elastin antibodies were measured by ELISA. The serum concentrations of S-EDP in SSc patients were significantly higher than in healthy controls (median, 144.44 ng/mL vs 79.59 ng/mL, P < 0.001). Serum EDP concentrations were found to be correlated with disease duration in SSc (P = 0.002) and particularly in diffuse cutaneous SSc (P = 0.005). Levels of anti-elastin antibodies were found to be more elevated in SSc patients than in healthy controls (median, 0.222 U vs 0.191 U, P = 0.049), more increased in diffuse cutaneous SSc than limited cutaneous SSc (median, 0.368 U vs 0.204 U, P = 0.031). In addition, levels of anti-elastin antibodies were also found to be negatively associated with presence of anti-centromere antibody (P = 0.023). The S-EDP levels were not found to be correlated with levels of anti-elastin antibodies. The increased S-EDP and anti-elastin antibody levels and association with clinical and laboratory characteristics may reflect the abnormal metabolism in SSc.

Role of Th17 Cell and Autoimmunity in Chronic Obstructive Pulmonary Disease

The molecular mechanisms involved in the pathogenesis of chronic obstructive pulmonary disease (COPD) are poorly defined. Accumulating evidences indicate that chronic inflammatory responses and adaptive immunity play important roles in the development and progression of the disease. Recently, it has been shown that IL-17 producing CD4 T cells, named Th17 cells, which have been implicated in the pathogenesis of several inflammatory and autoimmune diseases, are involved in airway inflammation and COPD. In addition, we and others suggest that autoimmunity may play a critical role in the pathogenesis of COPD. Here, we will review the current understanding of roles of Th17 cells and autoimmune responses in COPD.

A Novel Cell Line for Screening of Immunosuppressor Specific to T Lymphocytes / 대한면역학회지

The systematic study of products from bacteria and fungi has led to the development of two immunosuppressive drugs, cyclosporin A and FK 506 (tacrolimus) which are useful to suppress adaptive immune responses to the grafted tissue. However, they affect all immune responses indiscriminately and are both toxic to kidneys and other organs. To facilitate the development of immunosuppressor to block the T cell receptor (TcR)-mediated signaling cascade specifically, a novel Jurkat T cell transfectants, JK NFAT-SEAP were generated in which the expression of the secreted alkaline phosphatase (SEAP) is driven by the multiple NFAT binding sites plus minimal IL-2 promoter. Upon stimulation with ionomycin or anti-TcR mAb OKT3 in the presence of PMA, these transfectants secreted high level of SEAP into the medium, which was conveniently analyzed by SEAP analysis. The secretion of SEAP was effectively inhibited by cyclosporin A or FK 506 at the concentration of [10 ' ug/ml], [10 ug/ml] respectively. JK NFAT-SEAP transfectants will provide two major advantages for the development of a novel immunosuppressor. First, analysis of SEAP secreted into the culture medium by SEAP analysis enables us to test a large number of samples within a short period of time. Second, Usage of IL-2 promoter for the expression of SEAP makes us identify bioproducts to target specifically on TcR-mediated signaling pathway.