Background: This study aimed to determine the relationship between dyslipidemia and dry eye disease (DED) in a Korean population. Methods: This population-based study enrolled 5,627 adults (aged >19 years) who were participating in the first year of the fifth annual Korea National Health and Nutrition Examination Survey from 2010 to 2011. Clinically diagnosed DED and its symptoms were surveyed, and biochemical blood analysis data were collected. Dyslipidemia was defined as any of the following: hypercholesterolemia (total cholesterol > 200 mg/dL), hypertriglyceridemia (triglyceride > 150 mg/dL), low levels of high-density lipoprotein (100 mg/dL). Results: After adjusting for demographics (age and body mass index), lifestyle (smoking, drinking, exercise, and residential district), and medical factors (diabetes, hypertension, previous ophthalmic surgery, menopause, and rheumatologic disease), elevated serum cholesterol level was found to be associated with increased likelihood of DED (odds ratio, 1.77; 95% confidence interval, 1.127–2.78) in women. Conclusions: DED in a Korean population was found to be associated with high serum cholesterol levelsThe results of this study highlight the significance of eye examinations and independent lipid profile monitoring in patients with dyslipidemia because of its possible correlation with DED progression.

Metabolic syndrome and dyslipidemia contribute to the development of a pro-inflammatory state in asthma. However, studies investigating the association between asthma and dyslipidemia have reported conflicting results. This study aimed to uncover the relationship between asthma and lipid profiles in adolescents using a national health and nutrition survey. This cross-sectional study analyzed the 2010–2012 Korea National Health and Nutrition Examination Survey data and included 2841 subjects aged 11–18 years with fasting blood sample data. Serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels were analyzed. We compared asthma prevalence between high-risk and low-risk lipid groups. There were 123 adolescents with asthma and 2718 without asthma (controls). The TC/HDL-C ratio, LDL-C/HDL-C ratio, and non-HDL-C levels were significantly higher in the asthma group than in the non-asthma group (P < 0.05). The high-risk groups displayed significantly higher asthma prevalence with higher TC, TG, LDL-C, and non-HDL-C levels and TG/HDL-C ratio than the low-risk groups (P < 0.05). After adjusting for potential confounding factors, the high-risk groups were associated with asthma according to their higher TC levels (adjusted odds ratio, 1.69; 95% confidence interval, 1.012–2.822) and TG/HDL-C ratios (adjusted odds ratio, 1.665; 95% confidence interval, 1.006–2.756). Asthma prevalence was greater in adolescents with a high TC level and TG/HDL-C ratio. In addition to the standard lipid profile, elevated TG/HDL-C ratio can be used as a useful additional lipid measure to evaluate interactions between dyslipidemia and asthma.

BACKGROUND: Computational modeling indicated that pathological high shear stress (HSS; 100 dyn/cm ² ) is generated in pulmonary arteries (PAs; 100–500 µm) in congenital heart defects causing PA hypertension (PAH) and in idiopathic PAH with occlusive vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is a feature of PAH. We hypothesize that HSS induces EndMT, contributing to the initiation and progression of PAH. METHODS: We used the Ibidi perfusion system to determine whether HSS applied to human PA endothelial cells (ECs) induces EndMT when compared with physiological laminar shear stress (15 dyn/cm ² ). The mechanism was investigated and targeted to prevent PAH in a mouse with HSS induced by an aortocaval shunt. RESULTS: EndMT, a feature of PAH not previously attributed to HSS, was observed. HSS did not alter the induction of transcription factors KLF (Krüppel-like factor) 2/4, but an ERG (ETS-family transcription factor) was reduced, as were histone H3 lysine 27 acetylation enhancer-promoter peaks containing ERG motifs. Consequently, there was reduced interaction between ERG and KLF2/4, a feature important in tethering KLF and the chromatin remodeling complex to DNA. In PA ECs under laminar shear stress, reducing ERG by siRNA caused EndMT associated with decreased BMPR2 (bone morphogenetic protein receptor 2), CDH5 (cadherin 5), and PECAM1 (platelet and EC adhesion molecule 1) and increased SNAI1/2 (Snail/Slug) and ACTA2 (smooth muscle α2 actin). In PA ECs under HSS, transfection of ERG prevented EndMT. HSS was then induced in mice by an aortocaval shunt, causing progressive PAH over 8 weeks. An adeno-associated viral vector (AAV2-ESGHGYF) was used to replenish ERG selectively in PA ECs. Elevated PA pressure, EndMT, and vascular remodeling (muscularization of peripheral arteries) in the aortocaval shunt mice were markedly reduced by ERG delivery. CONCLUSIONS: Pathological HSS reduced lung EC ERG, resulting in EndMT and PAH. Agents that upregulate ERG could reverse HSS-mediated PAH and occlusive vascular remodeling resulting from high flow or narrowed PAs.

OBJECTIVES: Aspiration of foreign bodies into the tracheobronchial tree is a common accident in children. This study aimed to evaluate the safety and outcome of foreign body removal by flexible bronchoscopy using a retrieval basket in children. METHODS: This was a retrospective study of children treated for foreign bodies in the airway via flexible bronchoscopy using a retrieval basket at a tertiary hospital in Korea between February 2014 and October 2017. The medical records of the patients were retrospectively reviewed and analyzed. RESULTS: A total of 20 children underwent foreign body removal from the airway via flexible bronchoscopy using a retrieval basket. The median age of the patients was 16 (range, 10–21.5) months, and 12 (60%) were male. Foreign bodies removed included 16 (80%) organic items including peanuts, almond, and beans, and 4 (20%) inorganic items including a plastic bag, metal screw, spring, and Lego brick. The locations of the foreign bodies included the central airway (n = 5; trachea, n = 4; subglottic area, n = 1), right bronchial tree (n = 9), and left bronchial tree (n = 6). Successful removal was observed in 18 (90%) cases. The only complication that occurred was mild laryngeal edema (n = 2) after the procedure; both improved with corticosteroid administration. CONCLUSION: Flexible bronchoscopic extraction of a foreign body in the airway using a retrieval basket in children can be performed successfully with minimal complications.

Activation of cell surface CD30 by immobilized anti-CD30 monoclonal antibodies (mAb) induces strong apoptosis in human eosinophils. This anti-CD30 mAb-induced eosinophil apoptosis is inhibited by the addition of inhibitors of p38, ERK1/2 mitogen-activated protein kinases, and phosphatidylinositol 3-kinase. However, there is little data investigating the role of Bcl-2 and caspases in eosinophil apoptosis induced by anti-CD30 mAb. We sought to determine whether anti-CD30 mAb induces human eosinophil apoptosis via Bcl-2 and caspase pathways. Peripheral blood was drawn from 37 healthy volunteers. The CD30 expression on eosinophils was measured at various time points. Eosinophils were then cultured in plates precoated with anti-CD30 mAb (clone Ber-H8), isotype control immunoglobulin G1, interleukin (IL)-5, or dexamethasone. Western blot analysis was performed to determine the expression of Bcl-2, procaspase-8, -9, and -3, and caspase-8, -9, and -3 after cross-linking of CD30. Human eosinophils were also cultured in plates precoated with anti-CD30 mAb (clone Ber-H8) in the presence or absence of caspase-9 or -3 inhibitors. Eosinophil apoptosis was assessed using flow cytometry. The addition of anti-CD30 mAb significantly increased eosinophil apoptosis compared with controls. In western blot analysis, the addition of anti-CD30 mAb significantly decreased the expression of Bcl-2 and procaspase-9 and -3 and increased the expression of caspase-9 and -3. The addition of caspase-9 or -3 inhibitors decreased anti-CD30 mAb-induced human eosinophil apoptosis. Procaspase-8 or caspase-8 expression was not changed in response to various stimuli. Anti-CD30 mAb-induced human eosinophil apoptosis is likely to be mediated through Bcl-2 and caspase-9 and -3.