Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.

/pdf/nadph-oxidase-in-brain-injury-and-neurodegenerative-1jgawyhr3r.pdf

NADPH oxidase in brain injury and neurodegenerative disorders.

Oxidative stress has been linked to various disease states as well as physiological aging. The lungs are uniquely exposed to a highly oxidizing environment and have evolved several mechanisms to attenuate oxidative stress. Idiopathic pulmonary fibrosis (IPF) is a progressive age-related disorder that leads to architectural remodeling, impaired gas exchange, respiratory failure, and death. In this article, we discuss cellular sources of oxidant production, and antioxidant defenses, both enzymatic and nonenzymatic. We outline the current understanding of the pathogenesis of IPF and how oxidative stress contributes to fibrosis. Further, we link oxidative stress to the biology of aging that involves DNA damage responses, loss of proteostasis, and mitochondrial dysfunction. We discuss the recent findings on the role of reactive oxygen species (ROS) in specific fibrotic processes such as macrophage polarization and immunosenescence, alveolar epithelial cell apoptosis and senescence, myofibroblast differentiation and senescence, and alterations in the acellular extracellular matrix. Finally, we provide an overview of the current preclinical studies and clinical trials targeting oxidative stress in fibrosis and potential new strategies for future therapeutic interventions. © 2020 American Physiological Society. Compr Physiol 10:509-547, 2020.

Oxidative Stress in Pulmonary Fibrosis.

The NLRP3 inflammasome is activated by a variety of external or host-derived stimuli and its activation initiates an inflammatory response through caspase-1 activation, resulting in inflammatory cytokine IL-1β maturation and secretion. The NLRP3 inflammasome activation is a kind of innate immune response, most likely mediated by myeloid cells acting as a host defense mechanism. However, if this activation is not properly regulated, excessive inflammation induced by overactivated NLRP3 inflammasome can be detrimental to the host, causing tissue damage and organ dysfunction, eventually causing several diseases. Previous studies have suggested that mitochondrial damage may be a cause of NLRP3 inflammasome activation and autophagy, which is a conserved self-degradation process that negatively regulates NLRP3 inflammasome activation. Recently, mitochondria-selective autophagy, termed mitophagy, has emerged as a central player for maintaining mitochondrial homeostasis through the elimination of damaged mitochondria, leading to the prevention of hyperinflammation triggered by NLRP3 inflammasome activation. In this review, we will first focus on the molecular mechanisms of NLRP3 inflammasome activation and NLRP3 inflammasome-related diseases. We will then discuss autophagy, especially mitophagy, as a negative regulator of NLPP3 inflammasome activation by examining recent advances in research. [BMB Reports 2016; 49(10): 529-535].

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/153051/1/T201606049.pdf

Mitophagy: a balance regulator of NLRP3 inflammasome activation

Acute and chronic lung injuries are among the leading causes of mortality worldwide. Lung injury can affect several components of the respiratory system, including the airways, parenchyma, and pulmonary vasculature. Although acute and chronic lung injuries represent an enormous economic and clinical burden, currently available therapies primarily focus on alleviating disease symptoms rather than reversing and/or preventing lung pathology. Moreover, some supportive interventions, such as oxygen and mechanical ventilation, can lead to (further) deterioration of lung function and even the development of permanent injuries. Lastly, sepsis, which can originate extrapulmonary or in the respiratory system itself, contributes to many cases of lung-associated deaths. Considering these challenges, we aim to summarize molecular and cellular mechanisms, with a particular focus on airway inflammation and oxidative stress that lead to the characteristic pathophysiology of acute and chronic lung injuries. In addition, we will highlight the limitations of current therapeutic strategies and explore new antioxidant-based drug options that could potentially be effective in managing acute and chronic lung injuries.

/pdf/oxidative-stress-and-inflammation-in-acute-and-chronic-lung-3i8vt6vm.pdf

Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries

Molecular mechanisms underlying hyperoxia acute lung injury.

A fully autonomous vehicle must ensure not only fully autonomous driving but also the safety and comfort of its passengers. However, the self-driving technology that is currently completed focuses only on perfect driving and does not guarantee the safety and comfort of passengers. This paper proposes a braking-pressure and driving-direction determination system (BDDS), which computes the brake pressure and steering angle optimized for passenger safety by utilizing more diverse information than existing autonomous vehicles. The BDDS proposed in this paper consists of two modules. The road roughness classification module (RRCM) classifies the roughness of the road by using the pressure data applied to the suspension and the K-NN algorithm and computes the optimal brake pressure. The passenger recognition and sharing module (PRSM) identifies the current occupant status of the vehicle by using a body pressure sensor and CNN, shares the information with surrounding vehicles, and computes the optimal steering angle using passenger information and road information. As a result of the simulations described in this paper, the parameters of AI models were optimized. In addition, the RRCS was about 7% more accurate than the K-means clustering algorithm, and PRS was about 9% more accurate than the existing seat recognition system.

/pdf/the-braking-pressure-and-driving-direction-determination-26d9tc1l.pdf

The Braking-Pressure and Driving-Direction Determination System (BDDS) Using Road Roughness and Passenger Conditions of Surrounding Vehicles

본 연구는 유아교사의 직무 스트레스와 학부모와의 관계, 사회적 지지가 그들의 소진에 미치는 영향을 알아보기 위한 목적으로 이루어졌다. 이를 위하여 대구, 경북 지역 유아교사 205명을 대상으로 약 3주간 비대면 설문을 실시하고, 설문 자료를 토대로, 기술통계 분석, 상관관계 분석, 중다회귀분석을 실시하였다. 분석을 통해 도출된 결과를 제시하면 다음과 같다. 첫째, 유아교사의 직무 스트레스, 학부모와의 관계, 사회적 지지, 소진 사이의 상관관계를 분석한 결과 유아교사의 직무 스트레스는 그들의 학부모와의 관계, 사회적 지지와 유의미한 부적 상관을 가지고, 소진과는 유의미한 정적 상관을 가지고 있었다. 둘째, 유아교사의 직무 스트레스, 학부모와의 관계, 사회적 지지가 소진에 미치는 영향을 탐색하기 위해 중다회귀분석을 실시한 결과, 직무 스트레스, 학부모와의 관계, 사회적 지지 모두 그들의 소진에 유의한 영향을 미치는 것으로 나타났다. 본 논문은 유아교사의 소진을 예방하기 위해 그들의 직무 스트레스를 최소화하고, 학부모와의 관계에서 발생하는 부정적 감정 소모를 감소시키기 위한 정책적 지원과 더불어 주변 및 조직의 지지 형성을 위한 사회적인 지원도 필요함을 시사한다. 

The Effect of Job Stress, Human Relation with Parent, Social Support on Burnout of Early Childhood Teacher

Aims: Acute lung injury (ALI) induced by excessive hyperoxia has been employed as a model of oxidative stress imitating acute respiratory distress syndrome. Under hyperoxic conditions, overloading quantities of reactive oxygen species (ROS) are generated in both lung epithelial and endothelial cells, leading to ALI. Some NADPH oxidase (NOX) family enzymes are responsible for hyperoxia-induced ROS generation in lung epithelial and endothelial cells. However, the molecular mechanisms of ROS production in type II alveolar epithelial cells (AECs) and ALI induced by hyperoxia are poorly understood. Results: In this study, we show that dual oxidase 2 (DUOX2) is a key NOX enzyme that affects hyperoxia-induced ROS production, particularly in type II AECs, leading to lung injury. In DUOX2 mutant mice (DUOX2thyd/thyd) or mice in which DUOX2 expression is knocked down in the lungs, hyperoxia-induced ALI was significantly lower than in wild-type (WT) mice. DUOX2 was mainly expressed in type II AECs, but not ...

/pdf/dual-oxidase-2-in-lung-epithelia-is-essential-for-hyperoxia-2q5ppkr15w.pdf

Dual Oxidase 2 in Lung Epithelia Is Essential for Hyperoxia-Induced Acute Lung Injury in Mice

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The Braking-Pressure and Driving-Direction Determination System (BDDS) Using Road Roughness and Passenger Conditions of Surrounding Vehicles

The Effect of Job Stress, Human Relation with Parent, Social Support on Burnout of Early Childhood Teacher

Dual Oxidase 2 in Lung Epithelia Is Essential for Hyperoxia-Induced Acute Lung Injury in Mice