Kawasaki disease was associated with higher IL-17A and IL-6, a cytokine profile similar to other autoimmune diseases. IVIG therapy resulted in increased expression of Treg-related FoxP3. IVIG resistance was associated with higher levels of IL-10 and IL-17A. Our findings provide further evidence that Kawasaki disease is an autoimmune-like disease.
Background Pneumonia, the leading reason underlying childhood deaths, may be triggered or exacerbated by air pollution. To date, only a few studies have examined the association of air pollution with emergency department (ED) visits for pediatric pneumonia, with inconsistent results. Therefore, we aimed to elucidate the impact of short-term exposure to particulate matter (PM) and other air pollutants on the incidence of ED visits for pediatric pneumonia. Methods PM 2.5 , PM 10 , and other air pollutant levels were measured at 11 air quality-monitoring stations in Kaohsiung City, Taiwan, between 2008 and 2014. Further, we extracted the medical records of non-trauma patients aged ≤17 years and who had visited an ED with the principal diagnosis of pneumonia. A time-stratified case–crossover study design was employed to determine the hazard effect of air pollution in a total of 4024 patients. Results The single-pollutant model suggested that per interquartile range increment in PM 2.5 , PM 10 , nitrogen dioxide (NO 2 ), and sulfur dioxide (SO 2 ) on 3 days before the event increased the odds of pediatric pneumonia by 14.0% [95% confidence interval (CI), 5.1–23.8%], 10.9% (95% CI, 2.4–20.0%), 14.1% (95% CI, 5.0–24.1%), and 4.5% (95% CI, 0.8–8.4%), respectively. In two-pollutant models, PM 2.5 and NO 2 were significant after adjusting for PM 10 and SO 2 . Subgroup analyses showed that older children (aged ≥4 years) were more susceptible to PM 2.5 (interaction p = 0.024) and children were more susceptible to NO 2 during warm days (≥26.5 °C, interaction p = 0.011). Conclusions Short-term exposure to PM 2.5 and NO 2 possibly plays an important role in pediatric pneumonia in Kaohsiung, Taiwan. Older children are more susceptible to PM 2.5 , and all children are more susceptible to NO 2 during warm days.
Background: Air pollution exposure is associated with greater risk for cardiovascular events. This study aims to examine the effects of increased exposure to short-term air pollutants on ST-segment elevation myocardial infarction (STEMI) and determine the susceptible groups. Methods: Data on particulate matter PM2.5 and PM10 and other air pollutants, measured at each of the 11 air-quality monitoring stations in Kaohsiung City, were collected between 2011 and 2016. The medical records of non-trauma adult (>17 years) patients who had visited the emergency department (ED) with a typical electrocardiogram change of STEMI were extracted. A time-stratified and case-crossover study design was used to examine the relationship between air pollutants and daily ED visits for STEMI. Results: An interquartile range increment in PM2.5 on lag 0 was associated with an increment of 25.5% (95% confidence interval, 2.6%–53.4%) in the risk of STEMI ED visits. Men and persons with ≥3 risk factors (male sex, age, hypertension, diabetes, current smoker, dyslipidemia, history of myocardial infarction, and high body mass index) for myocardial infarction (MI) were more sensitive to the hazardous effects of PM2.5 (interaction: p = 0.039 and p = 0.018, respectively). The associations between PM10, NO2, and O3 and STEMI did not achieve statistical significance. Conclusion: PM2.5 may play an important role in STEMI events on the day of exposure in Kaohsiung. Men and persons with ≥3 risk factors of MI are more susceptible to the adverse effects of PM2.5 on STEMI.
Background: The use of focused assessment with sonography in trauma (FAST) enables clinicians to rapidly screen for injury at the bedsides of patients. Pre-hospital FAST improves diagnostic accuracy and streamlines patient care, leading to dispositions to appropriate treatment centers. In this study, we determine the accuracy of artificial intelligence model-assisted free-fluid detection in FAST examinations, and subsequently establish an automated feedback system, which can help inexperienced sonographers improve their interpretation ability and image acquisition skills.Methods: This is a single-center study of patients admitted to the emergency room from January 2020 to March 2021. We collected 324 patient records for the training model, 36 patient records for validation, and another 36 patient records for testing. We balanced positive and negative Morison's pouch free-fluid detection groups in a 1:1 ratio. The deep learning (DL) model Residual Networks 50-Version 2 (ResNet50-V2) was used for training and validation.Results: The accuracy, sensitivity, and specificity of the model performance for ascites prediction were 0.961, 0.976, and 0.947, respectively, in the validation set and 0.967, 0.985, and 0.913, respectively, in the test set. Regarding feedback prediction, the model correctly classified qualified and non-qualified images with an accuracy of 0.941 in both the validation and test sets.Conclusions: The DL algorithm in ResNet50-V2 is able to detect free fluid in Morison's pouch with high accuracy. The automated feedback and instruction system could help inexperienced sonographers improve their interpretation ability and image acquisition skills.
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Focal cortical dysplasia (FCD) is a congenital malformation of cortical development where the cortical neurons located in the brain area fail to migrate in the proper formation. Epilepsy, particularly medically refractory epilepsy, is the most common clinical presentation for all types of FCD. This study aimed to explore the expression change of circulating miRNAs in patients with FCD from serum exosomes. A total of nine patients with FCD and four healthy volunteers were enrolled in this study. The serum exosomes were isolated from the peripheral blood of the subjects. Transmission electron microscopy (TEM) was used to identify the exosomes. Both exosomal markers and neuronal markers were detected by Western blotting analysis to prove that we could obtain central nervous system-derived exosomes from the circulation. The expression profiles of circulating exosomal miRNAs were assessed using next-generation sequencing analysis (NGS). We obtained a total of 107 miRNAs with dominant fold change (>2-fold) from both the annotated 5p-arm and 3p-arm of 2780 mature miRNAs. Based on the integrated platform of HMDD v3.2, miRway DB and DIANA-miRPath v3.0 online tools, and confirmed by MiRBase analysis, four potentially predicted miRNAs from serum exosomes in patients with FCD were identified, including miR194-2-5p, miR15a-5p, miR-132-3p, and miR-145-5p. All four miRNAs presented upregulated expression in patients with FCD compared with controls. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and pathway category of four target miRNAs, we found eight possible signaling pathways that may be related to FCD. Among them, we suggest that the mTOR signaling pathway, PI3K-Akt signaling pathway, p53 signaling pathway, and cell cycle regulation and TGF-beta signaling pathway are high-risk pathways that play a crucial role in the pathogenesis of FCD and refractory epilepsy. Our results suggest that the circulating miRNAs from exosomes may provide a potential biomarker for diagnostic, prognostic, and therapeutic adjuncts in patients with FCD and refractory epilepsy.
Purpose: Cervical traumas are frequent in emergency department and X-ray, CT, and MRI are the essential imaging modalities in the diagnosis. However, especially for pregnant and morbid obese patients and children, these techniques can be challenging. We tested the success of point-of-care ultrasound in the evaluation of cervical traumas. Methods: This is a case series of cervical vertebra imaging with ultrasound in emergency department. We used linear probe and placed it anterolaterally to the neck, parallel to cervical spine. Images were obtained by an ultrasound-certified emergency physician. The height of the anterior wall of vertebral body, irregularity in vertebral body, and intervertebral space were assessed. Results: We presented a case series of six patients. Ultrasound images of cervical vertebral bodies and intervertebral spaces were able to obtain for all the patients. Any pathology was not observed in ultrasound imaging. This finding was compatible with cervical X-ray and CT scans and all the patients were discharged. Conclusions: However, this is a case series report of minor cervical trauma, and we were able to obtain ultrasound images of cervical vertebra bodies with point-of-care ultrasound examination by an emergency physician. This technique can be important for the patients contraindicated to CT or MRI. Also, it can give additional information to X-ray and CT scans especially for soft tissues. A2 A new technique in verifying the placement of a nasogastric tube: obtaining the longitudinal view of nasogastric tube in addition to transverse view with ultrasound
Status epilepticus may cause molecular and cellular events, leading to hippocampal neuronal cell death. Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) is an important regulator of vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), also known as fetal liver kinase receptor 1 (Flk-1). Resveratrol is an activator of PGC-1α. It has been suggested to provide neuroprotective effects in epilepsy, stroke, and neurodegenerative diseases. In the present study, we used microinjection of kainic acid into the left hippocampal CA3 region in Sprague Dawley rats to induce bilateral prolonged seizure activity. Upregulating the PGC-1α pathway will increase VEGF/VEGFR2 (Flk-1) signaling and further activate some survival signaling that includes the mitogen activated protein kinase kinase (MEK)/mitogen activated protein kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways and offer neuroprotection as a consequence of apoptosis in the hippocampal neurons following status epilepticus. Otherwise, downregulation of PGC-1α by siRNA against pgc-1α will inhibit VEGF/VEGFR2 (Flk-1) signaling and suppress pro-survival PI3K/AKT and MEK/ERK pathways that are also accompanied by hippocampal CA3 neuronal cell apoptosis. These results may indicate that the PGC-1α induced VEGF/VEGFR2 pathway may trigger the neuronal survival signaling, and the PI3K/AKT and MEK/ERK signaling pathways. Thus, the axis of PGC-1α/VEGF/VEGFR2 (Flk-1) and the triggering of downstream PI3K/AKT and MEK/ERK signaling could be considered an endogenous neuroprotective effect against apoptosis in the hippocampus following status epilepticus.
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