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The ionospheric radiance and electron density observed by the tiny ionospheric photometer (TIP) and GPS occultation experiment (GOX) payloads on FORMOSAT-3/COSMIC satellites are applied to determine the boundaries of the auroral oval and its width in the winter nighttime ionosphere for both hemispheres. The TIP collects ionospheric emission at 135.6 nm due to electron impact excitation, while the GOX offers ionospheric electron density profiles with radio occultation (RO) technique. Comparison between them shows similar patterns of the plasma structure in the polar caps. The mean width of the auroral bands ranges between about 2 and 11° latitude in the winter nighttime and it varies with longitudes. The comparison by month suggests that the mean radius of the auroral ovals varies with the intensity of the auroral radiance.

A new era of studying the ionospheric space weather effects has come after launch of the innovative satellite constellation, named as Formosa Satellite 3 or Constellation Observing System for Meteorology, Ionosphere, and Climate (abbreviated as FORMOSAT-3/COSMIC or F3/C in short), performing a radio occultation experiment capable of observing the global ionosphere three-dimensionally. This is the first time that a satellite constellation provides instantaneously both the lower and upper parts of the ionospheric electron density up to the satellite altitude. With more than 2500 soundings of the ionospheric vertical electron density profiles every day, ionospheric plasma structures over many continents and most of oceans, where ground-based observation is limited, are now observed continuously. Important ionospheric research topics, such as space weather effects to the ionosphere, variations of ionospheric plasma structure and dynamics produced by solar outputs, and atmosphere-ionosphere coupling processes, can be widely studied and modeled based on the three-dimensional ionospheric images constructed by the F3/C observations. After one year in orbit, a great amount of radio occultation soundings allow us to construct global ionospheric maps to study the ionospheric seasonal effects and atmosphere-ionosphere interactions. Taking advantage of the uniqueness of dense global coverage, the major physical mechanisms of the two studies are given. For study of the seasonal variation during solstice, electron density images of the mid- and low-latitude ionosphere show a clear north-to-south asymmetry which may be affected by the summer-to-winter neutral wind. Meanwhile a significant longitudinal variation at midnight is also seen in the solstitial season. Another interesting result is the four stronger equatorial ionization anomaly (EIA) regions located at different longitudes. This four-peaked EIA structure may result from upward propagating nonmigrating tides originated from troposphere. F3/C's observation of the daytime four-peaked structure provides an important evidence to support the proposed forming mechanism.

The tiny ionospheric photometer (TIP) and GPS occultation experiment (GOX) onboard FORMOSAT-3/COSMIC (F3/C) are employed to measure the OI 135.6 nm intensities in the nadir direction and the total electron content (TEC) between the F3/C and GPS satellite in the ionosphere, respectively. Due to its very high sensitivity ~600 counts/Rayleigh and rather narrow nadir pointing 3.8° ncircular field-of-view, the TIP provides accurate characterization of ionospheric electron density gradients in the horizontal direction. Meanwhile, a technique of the low earth orbit (LEO) tomography is applied to analyze the GOX data obtaining the 3D distribution of ionosphere electron density. Here, we combine the two observations to carry out the LEO-TIP tomographic inversions, and demonstrate that the peak electron density (NmF2) retrieved from the TIP combined together with the peak altitude (hmF2) information from the LEO tomography profiles provides more realistic electron density.

Interleukin (IL)-25 is a cytokine released by airway epithelial cells responding to pathogens. Excessive production of reactive oxygen species (ROS) leads to airway inflammation and remodeling in asthma. Mitochondria are the major source of ROS. After stress, defective mitochondria often undergo selective degradation, known as mitophagy. In this study, we examined the effects of IL-25 on ROS production and mitophagy and investigated the underlying mechanisms. The human monocyte cell line was pretreated with IL-25 at different time points. ROS production was measured by flow cytometry. The involvement of mitochondrial activity in the effects of IL-25 on ROS production and subsequent mitophagy was evaluated by enzyme-linked immunosorbent assay, Western blotting, and confocal microscopy. IL-25 stimulation alone induced ROS production and was suppressed by N-acetylcysteine, vitamin C, antimycin A, and MitoTEMPO. The activity of mitochondrial complex I and complex II/III and the levels of p-AMPK and the mitophagy-related proteins were increased by IL-25 stimulation. The CCL-22 secretion was increased by IL-25 stimulation and suppressed by mitophagy inhibitor treatment and PINK1 knockdown. The Th2-like cytokine IL-25 can induce ROS production, increase mitochondrial respiratory chain complex activity, subsequently activate AMPK, and induce mitophagy to stimulate M2 macrophage polarization in monocytes.

Diabetic patients normally have enlarged or normal-sized kidneys throughout their lifetime, but some diabetic uremic patients have small kidneys. It is uncertain if kidney size could have any negative impact on outcome in hemodialysis patients. This longitudinal, observational cohort study recruited 301 diabetic hemodialysis patients in 2015, and followed until 2019. Patients were stratified into two subgroups according to their kidney sizes before dialysis, as small (n = 32) or enlarged or normal (n = 269). Baseline demographic, hematological, biochemical, nutritional, inflammatory and dialysis related data were collected for analysis. Patients with small kidney size were not only older (P<0.001) and had lower body mass index (P = 0.016), but had also higher blood uric acid concentration (P<0.001) compared with patients with enlarged or normal kidney size. All patients received adequate doses of hemodialysis since the Kt/V and urea reduction ratio was 1.7±0.3 and 0.7±0.1, respectively. Patients with small size kidneys received higher erythropoietin dose than patients with enlarged or normal kidney size (P = 0.031). At the end of analysis, 92 (30.6%) patients expired. Kaplan-Meier analysis revealed no survival difference between both groups (P = 0.753). In a multivariate logistic regression model, it was demonstrated that age (P<0.001), dialysis duration (P<0.001), as well as blood albumin (P = 0.012) and low-density lipoprotein (P = 0.009) concentrations were significantly correlated with mortality. Small kidney size on starting hemodialysis was not related with an augmented risk for death in diabetic patients receiving hemodialysis. Further studies are necessary.

Post-traumatic stress disorder (PTSD) occurs when an individual experiences a traumatic event that exceeds the limits of psychological endurance. Many veterans experience PTSD. PTSD can negatively impact veterans’ quality of life, functioning, life satisfaction, and overall well-being. It is important to analyze the concept of PTSD in the veteran population. This concept analysis aimed to investigate the defining attributes, a model case, antecedents, consequences, and empirical referents related to the concept of PTSD among veterans. Walker and Avant’s method was used to guide this concept analysis of PTSD. The results showed that three attributes were determined from the analysis: intrusive memories of traumatic events, feelings of isolation and estrangement, and negative cognitions. PTSD is conceptualized as a collection of symptoms that arise from highly traumatic experiences. The military environment predisposes veterans to traumatic events that should be identified or acknowledged. A better understanding of the concept of PTSD can facilitate the development of effective interventions for the veteran population and enhance their mental health.

The association of anosmia/ageusia with a positive severe respiratory syndrome coronavirus 2 (SARS-CoV-2) test is well-established, suggesting these symptoms are reliable indicators of coronavirus disease 2019 (COVID-19) infection. This study investigates the clinical characteristics and systemic inflammatory markers in hospitalized COVID-19 patients in Taiwan, focusing on those with anosmia/ageusia. We conducted a retrospective observational study on 231 hospitalized COVID-19 patients (alpha variant) from April to July 2021. Clinical symptoms, dyspnea grading, and laboratory investigations, including neutrophil-lymphocyte ratios (NLRs), platelet-lymphocyte ratios (PLRs), and ANDC scores (an early warning score), were analyzed. Cough (64.1%), fever (58.9%), and dyspnea (56.3%) were the most common symptoms, while anosmia/ageusia affected 9% of patients. Those with anosmia/ageusia were younger, had lower BMI, lower systemic inflammatory markers, and better ANDC scores than those without these symptoms. Female patients exhibited lower NLR values and ANDC scores compared to male patients (all p  < 0.05). Multivariable regression analysis demonstrated significant associations between NLR and CRP and ferritin levels (all p  < 0.01), and between PLR and ESR and ferritin levels ( p  < 0.01). Categorized ANDC scores significantly correlated with the total hospital length of stay (all p  < 0.05). Despite ethnic differences in the prevalence of anosmia/ageusia, our study highlights similar clinical presentations and inflammatory profiles to those observed in Western countries. The ANDC score effectively predicted hospital stay duration. These findings suggest that anosmia/ageusia may be associated with less severe disease and a lower inflammatory response, particularly in younger and female patients. The ANDC score can serve as a valuable prognostic tool in assessing the severity and expected hospital stay of COVID-19 patients.

Few studies assess cord blood biomarkers to predict prenatal exposure to di(2-ethylhexyl) phthalate (DEHP) on the development of allergic diseases later in childhood. IL-33 has been indicated to play an important role in allergic diseases. We evaluated the association of prenatal DEHP exposure and IL-33 in cord blood on the development of allergic diseases. We also investigated the mechanism of DEHP in human lung epithelial cells and asthma animal models. 66 pregnant women were recruited, and their children followed when they were aged 3 years. Maternal urinary DEHP metabolites were determined using liquid chromatography-electrospray-ionization-tandem mass spectrometry. The effect of DEHP on IL-33 production was investigated in human lung epithelial cells and club cell-specific aryl hydrocarbon receptor (AhR) deficiency mice. ELISA and RT-PCR, respectively, measured the IL-33 cytokine concentration and mRNA expression. The concentrations of maternal urinary DEHP metabolites and serum IL-33 in cord blood with childhood allergy were significantly higher than those in the non-childhood allergy group. DEHP and MEHP could induce IL-33 production and reverse by AhR antagonist and flavonoids . Enhanced ovalbumin-induced IL-4 and IL-33 production in bronchoalveolar lavage fluid (BALF) by DEHP exposure and suppressed in club cell-specific AhR null mice. Kaempferol has significantly reversed the DEHP effect in the asthma animal model. Cord blood IL-33 level was correlated to childhood allergy and associated with maternal DEHP exposure. IL-33 might be a potential target to assess the development of DEHP-related childhood allergic disease. Flavonoids might be the natural antidotes for DEHP.

Arsenic is an environmental factor associated with epithelial–mesenchymal transition (EMT). Since macrophages play a crucial role in regulating EMT, we studied the effects of arsenic on macrophage polarization. We first determined the arsenic concentrations to be used by cell viability assays in conjunction with previous studies. In our results, arsenic treatment increased the alternatively activated (M2) macrophage markers, including arginase 1 (ARG-1) gene expression, chemokine (C-C motif) ligand 16 (CCL16), transforming growth factor-β1 (TGF-β1), and the cluster of differentiation 206 (CD206) surface marker. Arsenic-treated macrophages promoted A549 lung epithelial cell invasion and migration in a cell co-culture model and a 3D gel cell co-culture model, confirming that arsenic treatment promoted EMT in lung epithelial cells. We confirmed that arsenic induced autophagy/mitophagy by microtubule-associated protein 1 light-chain 3-II (LC3 II) and phosphor-Parkin (p-Parkin) protein markers. The autophagy inhibitor chloroquine (CQ) recovered the expression of the inducible nitric oxide synthase (iNOS) gene in arsenic-treated M1 macrophages, which represents a confirmation that arsenic indeed induced the repolarization of classically activated (M1) macrophage to M2 macrophages through the autophagy/mitophagy pathway. Next, we verified that arsenic increased M2 cell markers in mouse blood and lungs. This study suggests that mitophagy is involved in the arsenic-induced M1 macrophage switch to an M2-like phenotype.