• 한국항행학회논문지
• /
• 제27권4호
• /
• pp.356-364
• /
• 2023

항행 정밀도 증가는 항공교통 수용량을 개선함으로써 효율적인 공역 환경을 조성하였으나, 항공안전 측면에서는 항공기 간 충돌확률을 증가시키는 요인으로 작용하였다. 항공기가 고도 분리에 실패하더라도 좌우 위치 오차를 갖는 경우 충돌로 이어지지 않지만, 좌우 위치 정밀도가 증가하면 위치 랜덤성이 줄어들어 항공기 충돌확률이 증가하게 된다. 이에 따라 국제민간항공기구는 항공기를 항공로 중심선으로부터 의도적으로 이탈시키는 SLOP (Strategic Lateral Offset Procedures) 절차를 도입하였으며, 우리나라 또한 이와 유사한 Offset 절차를 운영하고 있다. Y579 항공로는 22년 말 복선화되기 전까지 offset 절차로 운영되었으며, Y579 offset 항적 분석결과 SLOP 절차와 달리 단방향 복선 항공로와 유사함을 확인하였다. 본 논문은 단방향 복선 항공로 및 offset 절차에 적용 가능한 안전평가 방법론을 개발하고 이를 활용하여 Y579 Offset 절차에 대한 안전평가를 수행하였다.

• 한국항공운항학회지
• /
• 제28권1호
• /
• pp.7-13
• /
• 2020

A significant growth in local air traffic volume is leading to airway congestion and flight delays especially for Incheon-China and Incheon-Europe sectors. A key method to increase the airway capacity is to place a supplemental airway parallel to the existing one and in cooperation between the aviation authorities between China and Korea, a dual airway track was implemented on December 6, 2018. Here, we use airline A's flight data to analyze the congestion change effect of the new airway. Results show total delay time to Europe is reduced 51% (13.4 to 6.6 minutes) as the delay distribution for 16-30 minutes, 31 minutes and greater decreased from 23.2% to 8.2% and 8.7% to 1.0% respectively. The delay to China also decreased but the drop is not as significant as flights to Europe. This is caused by the difference in flight distance, traffic volume, and characteristics of flights landing and transiting China. Flights to Europe show a broad distribution in altitude allocation and reduction in aircraft separation demonstrating the effectiveness of a dual airway track.

• Biomolecules & Therapeutics
• /
• 제32권4호
• /
• pp.460-466
• /
• 2024

Asthma is characterized by chronic inflammation and respiratory tract remodeling. Peroxisome proliferator-activated receptors (PPARs) play important roles in the pathogenesis and regulation of chronic inflammatory processes in asthma. The role of PPARγ has been studied using synthetic PPARγ agonists in patients with asthma. However, involvement of PPARα/δ has not been studied in asthma. In the present study, we investigated if elafibranor, a PPARα/δ dual agonist, can modulate ovalbumin (OVA)-induced allergic asthma, which is a potential drug candidate for non-alcoholic fatty liver in obese patients. Elafibranor suppresses antigen-induced degranulation in RBL-2H3 mast cells without inducing cytotoxicity in vitro. In mice with OVA-induced allergic asthma, the administration of elafibranor suppressed OVA-induced airway hyper-responsiveness at a dose of 10 mg/kg. Elafibranor also suppressed the OVA-induced increase in immune cells and pro-inflammatory cytokine production in the bronchoalveolar lavage fluid (BALF). Histological studies suggested that elafibranor suppressed OVA-induced lung inflammation and mucin hyper-production in the bronchial airways. In addition, elafibranor suppressed OVA-induced increases in serum immunoglobulin E and IL-13 levels in BALF. Conversely, the present study suggests that elafibranor has the potential for use in patients with allergic asthma.

• BMB Reports
• /
• 제36권1호
• /
• pp.95-109
• /
• 2003

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.

• Tuberculosis and Respiratory Diseases
• /
• 제42권5호
• /
• pp.744-751
• /
• 1995

연구배경: 여러 종류의 자극으로 감각신경(C-fiber)의 말단부에서 분비되는 신경단백질인 substance P와 neurokinin A는 기관지 평활근의 수축, 점막의 혈장 유출 및 점액의 과분비를 일으켜 기관지 천식 발병 기전에 중요한 역활을 한다. 이러한 기도 신경단백질은 $NK_1$, $NK_2$, $NK_3$ 등의 3종류의 수용체를 통하여 작용하며, $NK_1$ 수용체에 주로 작용하는 substance P는 기도의 혈관확장과 혈장 유출에 관여하며 $NK_2$ 수용체에 작용하는 neurokinin A는 기도의 수축에 주로 작용하며 기도혈장 유출에도 관여하는 것으로 알려져 있다. 목적: 저지들은 백서의 미주신경인 비교감 및 비부교감 신경을 전기적 자극으로 유발된 기도 혈장 유출에서 $NK_1$과 $NK_2$ 수용체 차단제인 FK224를 이용하여 기도내 신경성 염증에서 혈장유출에 대한 효과를 기도 부위별로 확인하였다. 대상 및 방법: 백서 21마리를 7마리씩 3군으로 나누어 미주신경에 전기적 자극을 하지 않은 대조군(control group), 2분간 자극한 군(NANC2군)과 신경 단백 수용체 차단제인 FK224를 미주신경 자극 전에 사용한 군(FK224군)에서 Evans blue dye를 이용하여 기도 부위별 혈장 유출의 정도를 각 군간에 비교하여 다음과 같은 결과를 얻었다. 결과: 1) 2분간 신경 자극한 군(NANC2군)은 대조군에 비하여 기관에서 49.7(${\pm}2.5$)ng/mg으로 353%, 주기관지에서 38.7(${\pm}2.8$)ng/mg으로 221%의 증가와 말초기관지 19.1(${\pm}1.6$)ng/mg으로 151%로 혈장 유출이 모두 유의하게 높았으며(p<0.05), 주로 상부 기도에서 혈장 유출 정도가 심하였으나, 폐실질은 13.0(${\pm}1.8$)ng/mg, 76%로 대조군과 차이는 없었다(p>0.05). 2) 신경 단백질 수용체 차단제를 사용한 FK224군은 2분간 신경 자극한 군에 비하여 기관에서 24.3(${\pm}2.2$)ng/mg으로 49%, 주기관지에서 22.3(${\pm}1.6$)ng/mg 으로 58%의 억제와 말초기관지 13.3(${\pm}0.8$) ng/mg으로 70%로 혈장 유출이 모두 유의하게 감소되었다(p<0.05). 결론: 이상의 결과에 의하면 백서에서 미주신경(NANC)의 전기적 자극으로 유발된 혈장유출은 기도에서만 발생되고 주로 상부기도에서 혈장유출이 심하며, $NK_1$과 $NK_2$ 수용체 차단제인 FK224를 전처치하여 substance P와 neurokinin A의 수용체 차단으로 기도 혈장 유출이 억제됨을 알 수 있었다.

• 대한통합의학회지
• /
• 제12권1호
• /
• pp.27-39
• /
• 2024

Purpose : Smoking is a major factor in chronic obstructive pulmonary disease (COPD), but the effect of electrical cigarette smoking on COPD development is still uncertain. This study aimed to compare the functions of airways and lungs exposed to combustible cigarettes and electrical cigarettes based on the pulmonary function test (PFT) results from the Korean National Health and Nutrition Examination Survey (NHANES). Methods : This study used data from 8,942 participants with PFT results out of 47,309 total subjects from the 6th to 8th Korean NHANES (2014-2015, 2016-2018, and 2019, respectively). Individuals with diseases such as cancer, ex-smokers, and dual tobacco users were excluded. The PFT results were analyzed according to the COPD diagnostic criteria. After adjusting for confounding variables, a complex sample generalized linear model ANOVA test was performed to investigate the association between PFT results and combustible smoker or electrical cigarette user groups. Results : In an analysis based on the obstructive ventilatory disorders (forced expiratory volume in 1 second[FEV₁]/forced vital capacity[FVC]<.7), combustible cigarette smokers showed a 3.46 times higher risk of COPD compared to non-smokers, while electrical cigarette smokers exhibited no significant difference in terms of COPD-related risks compared to non-smokers. FEV₁ showed a negative relation with combustible cigarette smokers as reported elsewhere (B=-.07, p<.001). FEV₁/FVC was negatively related to both combustible cigarette smokers (B=-.03, p<.001) and electrical cigarette smokers (B=-.02, p<.001). Conclusion : FEV₁/FVC decreases were observed in the long-term exposure to both combustible and electrical cigarettes. The lower FEV₁ in the combustible cigarette group implies the worsening of the severity of COPD, suggesting more damage to the airways and lungs in the short term. Therefore, the temporary electrical cigarettes use for the transition period in order to smoking cessation potentially aids to reduce the harmful effect of combustible cigarettes in COPD development.