Clinical usefulness of NT-proBNP as a prognostic factor for septic shock patients presenting to the emergency department.

Plasma N-terminal prohormone of brain natriuretic peptide (NT-proBNP) level is primarily used as a biomarker for left ventricular (LV) dysfunction. It is influenced by various conditions, such as myocardial strain and situations affecting the clearance of NT-proBNP, including sepsis and shock. In this study, we investigated the appropriateness of NT-proBNP as a prognostic factor for septic shock. Patients with septic shock who visited the emergency department of the Ewha Womans' University Mokdong Hospital between January 1, 2018, and December 31, 2020, were classified into the survival group (those who survived in the hospital and were discharged) and the death group (those who died in the hospital). The effectiveness of NT-proBNP, lactate, and blood urea nitrogen as predictive factors of in-hospital mortality was evaluated using the area under the receiver operating characteristic (AUROC) curve. The AUROC curve was 0.678 and 0.648 for lactate and NT-proBNP, respectively, with lactate showing the highest value. However, there was no significant difference between lactate and NT-proBNP levels in the comparison of their AUROC curve (p = 0.6278). NT-proBNP could be a useful predictor of in-hospital mortality in patients with septic shock who present to the emergency department.

Predictors for emergency readmission in patients with ureteral calculi: a focus on pain management and stone location.

BACKGROUND: The management of patients with ureteral calculi in the emergency department (ED) remains challenging due to high revisit rates. PURPOSE: To identify predictors of revisits among patients with ureteral calculi in the ED. DESIGN, SETTING, AND PARTICIPANTS: Data from patients who presented at a tertiary academic hospital in Seoul, Republic of Korea, between February 2018 and December 2019, were analyzed retrospectively. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Variables, including the respiratory rate (RR), estimated glomerular filtration rate (eGFR), duration of pain, number of analgesic doses, location of ureteral calculi, and ED length of stay (LOS) were examined using logistic regression. We also examined some additional variables included in the STONE and CHOKAI scoring systems to examine their association with revisit. RESULTS: Significant predictors of revisits included the number of analgesic doses and the location of ureteral calculi. Patients who required multiple analgesic doses or those with proximal or mid-ureteral calculi were more likely to revisit the ED. Although the STONE and CHOKAI scores could predict uncomplicated ureteral calculi, we found that the CHOKAI score is a valuable tool for predicting the likelihood of patient revisits (p = 0.021). CONCLUSIONS: Effective pain management and consideration of calculi location are important for predicting patient revisits. More research is required to validate findings, develop precise predictive models, and empower tailored care for high-risk patients. In patients with ureteral calculi in the ED, the number of analgesics given and stone location predict return visits. Proximal ureteral calculi on CT may require early urologic intervention to prevent pain-related revisits.

Epidemiology and clinical characteristics of trauma in older patients transferred from long-term care hospitals to emergency departments: A nationwide retrospective study in South Korea.

BACKGROUND: South Korea's aging population had leg to an increased number of long-term care hospitals (LTCHs), and increased transfer of older patients to emergency departments (EDs). This study investigated the epidemiological and injury profiles of LTCH patients aged ≥65 who were transferred from LTCHs to EDs due to trauma. METHOD: This retrospective study conducted between January 2014 and December 2019 in South Korea utilized data from the National Emergency Department Information System. The requirement for informed consent was waived by the IRB due to the retrospective nature of the study. Patient information was anonymized prior to analysis. RESULTS: Of the 1,472,006 trauma cases aged ≥65, 14,469 came from LTCHs. Outcomes varied: 44.1% were discharged, 40.6% were admitted to general wards (GW), 5.9% to intensive care units (ICU), 2.4% to other hospitals, and 6.5% returned to LTCHs. ED length of stay (LOS) was longest in the death (410.28 ± 559.73 min) and GW admission (390.12 ± 621.71 min) groups. Falls were the main cause of injury (50.1%), and the most common fracture was femoral (71.6%). Femoral and shoulder/upper extremity fractures increased hospitalization risk only, whereas self-harm increased both hospitalization and mortality risk. CONCLUSION: Visits to the ED by older patients from LTCH for trauma were avoidable in 50.6% of cases. Additionally, these patients had longer ED LOS and higher hospitalization rates than non-LTCH patients. Falls were the predominant mode of presentation, femoral fracture was the most common fracture among patients from LTCH.

Comparison of antibiotic resistance rates and outcomes among older adult patients with urinary tract infections living in long- term care hospitals and the community.

OBJECTIVE: In this study, we compared the proportion of antibiotic resistance between patients who visited the emergency department (ED) with urinary tract infection (UTI) from long-term care hospitals (LTCH), which is a type of long-term care facilities (LTCF) and the community. We assessed the resulting difference in prognosis. METHOD: Older adults who visited the ED between January and December 2019 and were diagnosed with UTI were divided into community residents and LTCH residents. We investigated the antibiotics sensitivity rates, end of therapy (EOT), and the patient's outcomes were evaluated. RESULTS: The antibiotic resistance rate was higher in LTCH residents. LTCH residents had a higher in hospital mortality rate compared to community residents. EOT was found to be longer, and admission rate and in-hospital mortality rate were also higher in LTCH residents. CONCLUSION: LTCF residents had a higher rate of antibiotic resistance and a poor prognosis.

The Pattern of Injuries in the Emergency Room during the COVID-19 Pandemic.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has obviously caused a remarkable change in patients' emergency department (ED) visits; however, data from multicenter studies are lacking. We aimed to present a comprehensive analysis of injury-related ED visits in Republic of Korea before and during the COVID-19 pandemic. MATERIALS AND METHODS: Data from 23 tertiary hospitals based on Emergency Department-based Injury In-depth Surveillance were used for this retrospective cross-sectional study. A total of 541,515 ED visits (age ≥ 20 years) between 1 January 2018 and 31 December 2020 were included, and the trend of injuries related to motor vehicular accidents, falls, self-harm and suicide, assault, and poisoning were compared between the pre-COVID-19 time period and during the COVID-19 pandemic. RESULTS: In the first year of the COVID-19 period, a decline in the number of ED visits was observed (41,275, 21%) compared to the previous year. Injuries caused by motor vehicles (36,332 in 2019 vs. 27,144 in 2020), falls and slips (61,286 in 2019 vs. 49,156 in 2020), assaults (10,528 in 2019 vs. 8067 in 2020), and poisonings (7859 in 2019 vs. 7167 in 2020) decreased, whereas self-harm and suicide (8917 in 2019 vs. 8911 in 2020) remained unchanged. The hospitalization (16.6% in 2019 vs. 18.8% in 2020) and ED mortality rate (0.6% in 2019 vs. 0.8% in 2020) also increased. CONCLUSION: The COVID-19 pandemic led to a decline in the overall number of trauma patients seeking medical care; however, the proportion of patients requiring hospitalization or intensive care unit admission increased, indicating more severe injuries among those who did seek care. Suicide attempt rates remained unchanged, highlighting the need for targeted care and support for vulnerable patients. During the pandemic, EDs had to continue to provide care to patients with medical emergencies unrelated to COVID-19, which requires a delicate and adaptable approach to ED operations. To manage the increased stress and workload caused by the pandemic, increased resources and support for healthcare workers were needed.

Evidence that gamma-secretase-mediated Notch signaling induces neuronal cell death via the nuclear factor-kappaB-Bcl-2-interacting mediator of cell death pathway in ischemic stroke.

Notch-1 (Notch) is a cell surface receptor that regulates cell-fate decisions in the developing nervous system, and it may also have roles in synaptic plasticity in the adult brain. Binding of its ligands results in the proteolytic cleavage of Notch by the γ-secretase enzyme complex, thereby causing the release of a Notch intracellular domain (NICD) that translocates to the nucleus, in which it regulates transcription. Here we show that activation of Notch modulates ischemic neuronal cell death in vitro and in vivo. Specifically, our findings from the use of Notch-1 siRNA or the overexpression of NICD indicate that Notch activation contributes to cell death. Using modified NICD, we demonstrate an apoptosis-inducing function of NICD in both the nucleus and the cytosol. NICD transfection-induced cell death was reduced by blockade of calcium signaling, caspase activation, and Janus kinase signaling. Inhibition of the Notch-activating enzyme, γ-secretase, protected against ischemic neuronal cell death by targeting an apoptotic protease, cleaved caspase-3, nuclear factor-κB (NF-κB), and the pro-death BH3-only protein, Bcl-2-interacting mediator of cell death (Bim). Treatment of mice with a γ-secretase inhibitor, compound E, reduced infarct size and improved functional outcome in a model of focal ischemic stroke. Furthermore, γ-secretase inhibition reduced NICD, p-p65, and Bim levels in vivo. These findings suggest that Notch signaling endangers neurons after ischemic stroke by modulating the NF-κB, pro-death protein Bim, and caspase pathways.

Evidence that gamma-secretase mediates oxidative stress-induced beta-secretase expression in Alzheimer's disease.

Beta-secretase (BACE1), an enzyme responsible for the production of amyloid beta-peptide (Abeta), is increased by oxidative stress and is elevated in the brains of patients with sporadic Alzheimer's disease (AD). Here, we show that oxidative stress fails to induce BACE1 expression in presenilin-1 (gamma-secretase)-deficient cells and in normal cells treated with gamma-secretase inhibitors. Oxidative stress-induced beta-secretase activity and sAPPbeta levels were suppressed by gamma-secretase inhibitors. Levels of gamma- and beta-secretase activities were greater in brain tissue samples from AD patients compared to non-demented control subjects, and the elevated BACE1 level in the brains of 3xTgAD mice was reduced by treatment with a gamma-secretase inhibitor. Our findings suggest that gamma-secretase mediates oxidative stress-induced expression of BACE1 resulting in excessive Abeta production in AD.

Contribution of gamma-secretase to calcium-mediated cell death.

Presenilins are the catalytic subunit of the large gamma-secretase complex, that promotes intramembranous proteolysis of the beta-amyloid precursor protein (APP), resulting in the production of beta-amyloid (A beta). Mutant presenilin causes early-onset familial Alzheimer's disease (FAD), is related to abnormal Ca(2+) signaling, and render cells vulnerable to cell death. In the present study, we demonstrated that Ca(2+)-mediated cell death is functionally associated with gamma-secretase activity. We found that gamma-secretase activity was elevated during Ca(2+)-mediated cell death. Using selective gamma-secretase inhibitors, we examined the role of gamma-secretase in cell death triggered by increased intracellular Ca(2+). Indeed, treatment with the selective gamma-secretase inhibitors, compound E, DAPT, or L-685.458 significantly decreased Ca(2+)-triggered cell death with that of the controls, but did not affect staurosporin or tunicamycin-mediated cell death. These results implicate the role of gamma-secretase activity in Ca(2+)-mediated cell death.

Characterization of subcellular localization and Ca2+ modulation of calsenilin/DREAM/KChIP3.

Earlier reports found that calsenilin is a transcriptional repressor or a subunit of plasma membrane channel, and indicated that calsenilin was present in the nucleus or plasma membrane. Immunohistochemical and subcellular fractionation analysis, however, revealed that calsenilin/DREAM/KChIP3 was distributed throughout the cytoplasm of SK-N-BE2(C), Jurkat, and HeLa cells. In addition, the expression of calsenilin suppressed the ATP-induced increase in intracellular Ca2+ concentrations. By increase in intracellular calcium concentration, calsenilin was translocated into the nucleus.