Abstract Background Both air pollution and weather impact hospitalization for respiratory diseases. However, few studies have investigated the contribution of weather to hospitalization related to ...the adverse effects of air pollution. This study analyzed the effects of particulate matter (PM) on daily respiratory-related hospital admissions, taking into account meteorological factors. Methods Daily hospital admissions for respiratory diseases (acute bronchitis, allergic rhinitis, and asthma) between 2007 and 2010 were extracted from the National Health Insurance Corporation, Korea. Patients were divided into three age-based groups (0–15, 16–64, and ≥65 years). PM levels were obtained from 19 monitoring stations in Busan. Results The mean number of patients admitted for acute bronchitis, allergic rhinitis, and asthma was 5.8 ± 11.9, 4.4 ± 6.1, and 3.3 ± 3.3, respectively. During that time, the daily mean PM10 and PM2.5 concentrations were 49.6 ± 20.5 and 24.2 ± 10.9 μg/m3 , respectively. The mean temperature anomaly was 7.0 ± 2.3 °C; the relative humidity was 62.0 ± 18.0%. Hospital admission rates for respiratory diseases increased with increasing PM and temperature, and with decreasing relative humidity. A multivariate analysis including PM, temperature anomaly, relative humidity, and age showed a significant increase in respiratory-related admissions with increasing PM levels and a decreasing relative humidity. Higher PM2.5 levels had a greater effect on respiratory-related hospital admission than did PM10 levels. Children and the elderly were the most susceptible to hospital admission for respiratory disease. Conclusions PM levels and meteorological factors impacted hospitalization for respiratory diseases, especially in children and the elderly. The effect of PM on respiratory diseases increased as the relative humidity decreased.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Stress-induced glucocorticoids disturb mitochondrial bioenergetics and dynamics; however, instead of being removed via mitophagy, the damaged mitochondria accumulate. Therefore, we investigate the ...role of glucocorticoids in mitophagy inhibition and subsequent synaptic defects in hippocampal neurons, SH-SY5Y cells, and ICR mice. First, we observe that glucocorticoids decrease both synaptic density and vesicle recycling due to suppressed mitophagy. Screening data reveal that glucocorticoids downregulate BNIP3-like (BNIP3L)/NIX, resulting in the reduced mitochondrial respiration function and synaptic density. Notably, we find that glucocorticoids direct the glucocorticoid receptor to bind directly to the PGC1α promoter, downregulating its expression and nuclear translocation. PGC1α downregulation selectively decreases NIX-dependent mitophagy. Consistent with these results, NIX enhancer pre-treatment of a corticosterone-exposed mouse elevates mitophagy and synaptic density in hippocampus, improving the outcome of a spatial memory task. In conclusion, glucocorticoids inhibit mitophagy via downregulating NIX and that NIX activation represents a potential target for restoring synapse function.
Objective
To examine the relationship between metabolically healthy and unhealthy obesity phenotypes and risk of vasomotor symptoms (VMS) in premenopausal women.
Design
Prospective cohort study.
...Setting
Middle‐aged women in a cohort based on regular health screening examinations.
Population
Premenopausal Korean women aged 42–52 years were recruited and were followed up for a median of 4.2 years. The cross‐sectional and cohort studies comprised 4672 women and 2590 women without VMS at baseline, respectively.
Methods
Adiposity measures included body mass index (BMI), waist circumference and percentage body fat. Being metabolically healthy was defined as not having any metabolic syndrome components or a homeostasis model assessment of insulin resistance of 2.5 or more.
Main outcomes measures
VMS (hot flushes and night sweats) assessed using the questionnaire.
Results
All adiposity measures were positively associated with an increased risk of VMS in both cross‐sectional and longitudinal studies. The multivariable‐adjusted prevalence ratio (95% confidence interval CI) for VMS comparing percentage body fat of 35% or more with the reference was 1.47 (95% CI 1.14–1.90) in metabolically healthy women, and the corresponding prevalence ratio was 2.32 (95% CI 1.42–3.78) in metabolically unhealthy women (Pinteraction = 0.334). The multivariable‐adjusted hazard ratio for incident VMS comparing percentage body fat of 35% or more with the reference was 1.34 (95% CI 1.00–1.79) in metabolically healthy women, whereas the corresponding hazard ratio was 3.61 (95% CI 1.81–7.20) in metabolically unhealthy women (Pinteraction = 0.036). The association between BMI, waist circumference and VMS did not significantly differ by metabolic health status.
Conclusions
Maintaining normal weight and being metabolically healthy may help to prevent VMS in premenopausal women.
Tweetable
Avoiding obesity and a metabolically unhealthy status may help reduce vasomotor symptoms in premenopausal women.
Tweetable
Avoiding obesity and a metabolically unhealthy status may help reduce vasomotor symptoms in premenopausal women.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
To forecast haze pollution episodes caused by high concentrations of long-range transported pollutants emitted in the areas upstream of South Korea, it is crucial to study and identify their ...behaviour. We analysed the three-dimensional air quality structure in Seoul using ground observation data and aerosol lidar measurements to identify vertical aerosol intrusion into the Korean Peninsula during the spring of 2016. The intrusions were particularly affected by the development of the atmospheric boundary layer (ABL) in the leeward regions. The nocturnal pollutant intrusion into the Korean peninsula via the Yellow Sea was examined using measured data. The pollutants first reached the area above the nocturnal boundary layer (548 ± 180 m) and approached ground level on the following day due to convective mixing depending on the convective ABL growth (1182 ± 540 m) in daytime. These intrusion mechanisms were mostly attributed to extremely high concentrations (i.e. >100 μg m
) of fine particulate matter in the leeward regions, accounting for four of the total of six cases for which the warnings and alerts were issued in Seoul Metropolitan Area over a year-long period (2016). The horizontal and vertical pathways of the long-range transported pollutants and the atmospheric vertical structure were identified as key factors affecting the surface air quality concentration in the leeward regions.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Mesoporous NiO/NiFe2O4 multi-composite hollow nanocages via monodisperse Ni3Fe(CN)62 prussian blue analogue nanocube precursors were successfully synthesized. The three-dimensional (3D) mesoporous ...and hollow structures provided an efficient electrolyte diffusion path and a high surface area, resulting in the enhancement of electrocatalytic activities for the oxygen evolution reaction. The overpotential and Tafel slope of mesoporous NiO/NiFe2O4 multi-composite hollow nanocages were as low as 303 mV at a current density of 10 mA cm-2 and 58.5 mV dec-1, respectively. In addition, the composite showed excellent durability at approximately 60 mA cm-2 for 12 h.
Prime editing can induce a desired base substitution, insertion, or deletion in a target gene using reverse transcriptase after nick formation by CRISPR nickase. In this study, we develop a ...technology that can be used to insert or replace external bases in the target DNA sequence by linking reverse transcriptase to the Francisella novicida Cas9, which is a CRISPR-Cas9 ortholog. Using FnCas9(H969A) nickase, the targeting limitation of existing Streptococcus pyogenes Cas9 nickase SpCas9(H840A)-based prime editing is dramatically extended, and accurate prime editing is induced specifically for the target genes in human cell lines.
Peroxidasin (PXDN) has been reported to crosslink the C‐terminal non‐collagenous domains of collagen IV (Col IV) by forming covalent sulfilimine bond. Here, we explored the physiological role of PXDN ...and its mechanism of action in endothelial cell survival and growth. Silencing of PXDN using siRNAs decreased cell proliferation without increase of the number of detached cells and decreased cell viability under serum‐starved condition with increased fragmented nuclei and caspase 3/7 activity. Conditioned medium (CM) containing wild‐type PXDN restored the proliferation of PXDN‐depleted cells, but CM containing mutant PXDN with deletion of either N‐terminal extracellular matrix (ECM) motifs or peroxidase domain failed to restore PXDN function. Accordingly, anti‐PXDN antibody raised against IgC2 (3‐4) subdomain within ECM motifs and peroxidase inhibitor phloroglucinol prevented the rescue of the PXDN‐depleted cells by PXDN‐containing CM. PXDN depletion resulted in loss of sulfilimine crosslinks, and decreased dense fibrillar network assembly of not only Col IV, but also fibronectin and laminin like in Col IV knockdown. Exogenous PXDN‐containing CM restored ECM assembly as well as proliferation of PXDN‐depleted cells. Accordingly, purified recombinant PXDN protein restored the proliferation and ECM assembly, and prevented cell death of the PXDN‐depleted cells. PXDN depletion also showed reduced growth factors‐induced phosphorylation of FAK and ERK1/2. In addition, siPXDN‐transfected cell‐derived matrix failed to provide full ECM‐mediated activation of FAK and ERK1/2. These results indicate that both the ECM motifs and peroxidase activity are essential for the cellular function of PXDN and that PXDN is crucial for ECM assembly for survival and growth signaling.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Nicotinamide adenine dinucleotide (NAD
) acts as a cofactor for multiple biological processes. While previous research has revealed that the NAD
declines associated with aging contributes to an ...impairment of immune cells, its role in mast cell function, especially in response to an anaphylactic condition, has remained unexplored. We tested whether the restoration of cellular NAD
concentration by the supplementation of NAD
boosting molecules prevented mast cell degranulation and anaphylactic responses.
Bone marrow derived mast cells (BMMCs) and human cord blood derived mast cells were treated with NAD
precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR), and FcεRI downstream signaling was assessed. Animal models of passive systemic anaphylaxis (PSA) and passive cutaneous anaphylaxis (PCA) were used to investigate the effects of NAD
precursors in the anaphylactic responses of mice.
Treatment of murine BMMCs and human cord blood derived mast cells with NAD
precursors repressed intracellular signaling downstream of FcεRI, as well as the release of inflammatory cytokines and lipid mediators. The intraperitoneal administration of NMN or NR also markedly attenuated IgE-mediated anaphylactic responses in mouse models of PSA and PCA. These beneficial effects of NAD
precursors, however, were attenuated in mast cell-specific
knockout mice, indicating a Sirt6 dependency for their action.
NAD
precursors may serve as an effective therapeutic strategy that limits mast cell-mediated anaphylactic responses.
Hyperglycemia in diabetes mellitus (DM) patients is a causative factor for amyloidogenesis and induces neuropathological changes, such as impaired neuronal integrity, neurodegeneration, and cognitive ...impairment. Regulation of mitochondrial calcium influx from the endoplasmic reticulum (ER) is considered a promising strategy for the prevention of mitochondrial ROS (mtROS) accumulation that occurs in the Alzheimer's disease (AD)-associated pathogenesis in DM patients. Among the metabolites of ellagitannins that are produced in the gut microbiome, urolithin A has received an increasing amount of attention as a novel candidate with anti-oxidative and neuroprotective effects in AD. Here, we investigated the effect of urolithin A on high glucose-induced amyloidogenesis caused by mitochondrial calcium dysregulation and mtROS accumulation resulting in neuronal degeneration. We also identified the mechanism related to mitochondria-associated ER membrane (MAM) formation. We found that urolithin A-lowered mitochondrial calcium influx significantly alleviated high glucose-induced mtROS accumulation and expression of amyloid beta (Aβ)-producing enzymes, such as amyloid precursor protein (APP) and β-secretase-1 (BACE1), as well as Aβ production. Urolithin A injections in a streptozotocin (STZ)-induced diabetic mouse model alleviated APP and BACE1 expressions, Tau phosphorylation, Aβ deposition, and cognitive impairment. In addition, high glucose stimulated MAM formation and transglutaminase type 2 (TGM2) expression. We first discovered that urolithin A significantly reduced high glucose-induced TGM2 expression. In addition, disruption of the AIP-AhR complex was involved in urolithin A-mediated suppression of high glucose-induced TGM2 expression. Markedly, TGM2 silencing inhibited inositol 1, 4, 5-trisphosphate receptor type 1 (IP3R1)-voltage-dependent anion-selective channel protein 1 (VDAC1) interactions and prevented high glucose-induced mitochondrial calcium influx and mtROS accumulation. We also found that urolithin A or TGM2 silencing prevented Aβ-induced mitochondrial calcium influx, mtROS accumulation, Tau phosphorylation, and cell death in neuronal cells. In conclusion, we suggest that urolithin A is a promising candidate for the development of therapies to prevent DM-associated AD pathogenesis by reducing TGM2-dependent MAM formation and maintaining mitochondrial calcium and ROS homeostasis.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Atrial fibrillation (AF) is a major risk factor for ischemic stroke and associated with a 5-fold higher risk of stroke. In this retrospective cohort study, the incidence of and risk factors for ...ischemic stroke in patients with AF were identified. All patients (≥30 years old) without previous stroke who were diagnosed with AF in 2007-2013 were selected from the National Health Insurance Service-National Sample Cohort. To identify factors that influenced ischemic stroke risk, Cox proportional hazard regression analysis was conducted. During a mean follow-up duration of 3.2 years, 1022 (9.6%) patients were diagnosed with ischemic stroke. The overall incidence rate of ischemic stroke was 30.8/1000 person-years. Of all the ischemic stroke that occurred during the follow-up period, 61.0% occurred within 1-year after AF diagnosis. Of the patients with CHA2DS2-VASc score of ≥2, only 13.6% were receiving warfarin therapy within 30 days after AF diagnosis. Relative to no antithrombotic therapy, warfarin treatment for >90 days before the index event (ischemic stroke in stroke patients and death/study end in non-stroke patients) associated with decreased ischemic stroke risk (Hazard Ratio = 0.41, 95%confidence intervals = 0.32-0.53). Heart failure, hypertension, and diabetes mellitus associated with greater ischemic stroke risk. AF patients in Korea had a higher ischemic stroke incidence rate than patients in other countries and ischemic stroke commonly occurred at early phase after AF diagnosis. Long-term (>90 days) continuous warfarin treatment may be beneficial for AF patients. However, warfarin treatment rates were very low. To prevent stroke, programs that actively detect AF and provide anticoagulation therapy are needed.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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