• 생물정신의학
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• 제15권4호
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• pp.275-287
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• 2008

본 논문에서는 우울증과 관상동맥 질환의 연관성에 대해 병태생리학적 기전을 중심으로 고찰하였다. 현재까지 선행 연구들을 통해 제시된 주요 병태생리학적 기전으로는 우울증에서의 증가된 혈액 응고 경향, HPA 축 기능 및 ANS 조절 이상, 상승된 염증 반응 상태 등과 더불어 관상동맥 질환과 우울증이 공통된 유전적 위험 인자를 공유하고 있을 가능성 등이 있다. 혈액 응고와 관련되어서는 혈소판의 활성 및 반응성 증가, 혈관 내피 기능 이상, 혈액 응고 인자의 증가 등이 구체적인 병리 기전으로 제시 되었으며, HPA 축 및 ANS 기능 이상과 관련되어서는 혈장내 카테콜라민의 증가와 이와 연관된 심박수 증가 및 심박 변이성의 감소, 기타 혈역학적 스트레스의 증가 등으로 인한 부정맥 및 죽상경화증의 촉진이 주요한 기전으로 제시되었다. 또한 CRP 등과 같은 염증 표지자 연구를 통해 우울증에서의 증가된 염증 반응이 죽상경화증이나 혈전 형성과 관계 되어있을 가능성 역시 제시되었다. 하지만 역으로 관상동맥 질환과 우울증의 동반 이환율이 높다는 사실은 잘 알려져 있음에도 불구하고 관상동맥 질환에서의 어떤 병태생리적 변화가 우울증의 발병 및 경과와 관련되어 있는지에 대해서는 체계적인 연구가 매우 적은 것이 사실이다. 이 이외에도 우울증과 관상동맥 질환 외의 제3의 요인 즉, 유전적 위험 인자가 두 질환에 선행함을 제시하여 우울증과 관상동맥 질환이 공통된 유전적 취약성을 공유하고 있을 가능성을 제기한 연구들도 있다. 그 밖에도 우울증과 대사 증후군과의 연관성에 기반한 연구나 ${\Omega}$-3 지방산, homocystein 수준에 주목한 일부 연구들이 존재하며, 관상동맥 질환을 가진 환자는 뇌혈관에도 죽상경화증이 있을 가능성이 높고 이로 인해 뇌의 특정 부위에 혈류장애가 있을 가능성이 높아서 이것이 혈관성 우울증을 야기할 가능성이 있다는 보고를 한 연구들도 있다. 우울증이 관상동맥 질환의 발생 및 경과에 부정적인 영향을 끼친다는 많은 연구 결과들은 우울증과 관상동맥 질환의 원인적 연관성에 대한 연구를 지속적으로 촉진시키고 있다. 하지만 우울증이라는 대상 질환 자체의 이질성과 관상동맥 질환을 가지고 있는 환자들은 대부분 항응고제 등의 약물을 투여하고 있다는 사실 등이 병태생리 규명 연구에 어려움을 주고 있는 것이 사실이다. 우울증과 관상동맥 질환의 병태생리적 연관성에 대한 지속적이고 다각적인 연구는 향후 관상동맥 질환 환자에서의 우울증의 중요성을 치료자에게 인식시키는 계기가 될 수 있으며 더 나아가 관상동맥 질환의 치료 예후의 개선으로 이어질 수 있는 통로를 제공할 것이다.

• Clinical and Experimental Pediatrics
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• 제50권4호
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• pp.328-334
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• 2007

Sinusitis is a common medical problem in children. The prevalence of penicillin-resistant S. pneumoniae infection has been increased during the last decade. The medical management is based on the choice of antimicrobial agents. This article reviews current literatures on the management of acute bacterial sinusitis and chronic sinusitis, with an emphasis on penicillin-resistant S. pneumoniae infection. This article also explores the potential pathophysiologic mechanisms of chronic sinusitis.

• Journal of Genetic Medicine
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• 제18권1호
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• pp.8-15
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• 2021

Recent genetic advances allow for identification of the genetic etiologies of epilepsy within individual patients earlier and more frequently than ever. Specific targeted treatments have emerged from improvements in understanding of the underlying epileptogenic pathophysiology. These targeted treatment strategies include modifications of ion channels or other cellular receptors and their function, mechanistic target of rapamycin signaling pathways, and substitutive therapies in hereditary metabolic epilepsies. In this review, we explore targeted treatments based on underlying pathophysiologic mechanisms in specific genetic epilepsies.

• BMB Reports
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• 제49권5호
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• pp.263-269
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• 2016

The intestine represents the largest and most elaborate immune system organ, in which dynamic and reciprocal interplay among numerous immune and epithelial cells, commensal microbiota, and external antigens contributes to establishing both homeostatic and pathologic conditions. The mechanisms that sustain gut homeostasis are pivotal in maintaining gut health in the harsh environment of the gut lumen. Intestinal epithelial cells are critical players in creating the mucosal platform for interplay between host immune cells and luminal stress inducers. Thus, knowledge of the epithelial interface between immune cells and the luminal environment is a prerequisite for a better understanding of gut homeostasis and pathophysiologies such as inflammation. In this review, we explore the importance of the epithelium in limiting or promoting gut inflammation (e.g., inflammatory bowel disease). We also introduce recent findings on how small RNAs such as microRNAs orchestrate pathophysiologic gene regulation.

• Annals of Clinical Neurophysiology
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• 제11권1호
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• pp.1-8
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• 2009

Orthostatic intolerance is defined as the development of various symptoms during standing that are relieved by recumbency. Postural tachycardia syndrome (POTS) is another nomenclature of orthostatic intolerance. POTS characterized by a heart rate increase ${\geq}30$ bpm from supine to standing or >120 bpm at standing without orthostatic hypotension. POTS is a heterogenous in presentation with various pathophysiologic mechanisms. Important mechanisms are hypovolemia, denervation, hyperadrenergic and deconditioning state. There are presented as lightheadness or dizziness, palpitations, presyncope, sense of weakness, tremulousness, shortness of breath. POTS are classified under 3 groups that are neuropathic, hyperadrenergic, and deconditioning POTS. Most patients can be improved from a pathophysiologically based regimen of management.

• Clinical and Experimental Pediatrics
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• 제50권4호
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• pp.335-339
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• 2007

The link between upper airway disease (allergic rhinitis and sinusitis) and lower airway disease (asthma) has long been of interest to physicians. Many epidemiological and pharmacological studies have provided a better understanding of pathophysiologic interrelationship between allergic rhinitis and asthma. The vast majority of patients with asthma have allergic rhinitis, and rhinitis is a major independent risk factor for asthma in cross-sectional and longitudinal studies. The association between sinusitis and asthma has long been appreciated. Through the recent evidences, allergic rhinitis, sinusitis, and asthma may not be considered as different diseases but rather as the expression in different parts of the respiratory tract of same pathological process in nature. Various mechanisms have been proposed to explain the relationship between asthma and upper airway diseases, but the underlying mechanisms are not completely discovered. The implications for the one-airway hypothesis are important not only academically but also clinically for diagnostic and therapeutic purposes.

• 대한기관식도과학회지
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• 제5권2호
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• pp.113-118
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• 1999

Background & Objectives : Nasal resistance which is halfly responsible for airway resistance is known to be influenced by hypoxia, hypercapnia, exercise, pregnancy, alcohol, ammonia and smoking. Smoking is a common part of our sociocultural environment and we have many a times been introduced to its various adverse effects, which have usually been more focused on lung problems. The purpose of this study is to determine any relationship between smoking and nasal resistance and to evaluate it's effective sites. Materials and Methods : Acoustic rhinometry was performed in 25 smokers and 25 nonsmokers who had no nasal symptoms nor abnormal rhinoscopic findings, and used an acoustic rhinometry to measure the distance from nose-piece to the C-notch, cross sectional area at the C-notch, and volume of the nasal cavity from nose-piece to 7cm. The authors compared the data between the two groups. Results : The cross sectional area at the C-notch was significantly decreased(p<0.05) in smoking group. The distance to the C-notch and the volume of nasal cavity were decreased likely in smoking group but there were no significant difference(p>0.05). Conclusion : Smoking reduced the cross sectional area at the C-notch, so increased the nasal resistance. The underlying mechanisms seems to be decreased nasal mucosal reactivity and congestion of the nasal mucosa. The authors believe there should follow more studies on pathophysiologic mechanisms and the histopathologic changes which involve the effect of smoking on nasal structures.

• 수면정신생리
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• 제6권1호
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• pp.19-25
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• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.

• 생물정신의학
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• 제18권2호
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• pp.72-79
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• 2011

Recent advances in brain imaging research are remarkable. Among them, many results from a variety of neuroimaging modalities in Alzheimer's dementia accompanied by the development and growing of imaging techniques have been presented in the research field. In this review we are focused on the imaging biomarkers for the Alzheimer's dementia to investigate the pathophysiologic mechanism. Future research on biomarkers for Alzheimer's dementia will provide more diverse and complex mechanisms or hypotheses than have been proposed in the current hypothesis about the pathogenesis of Alzheimer's dementia.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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• pp.69-69
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• 2003

There are now increasing evidences that free radicals and reactive oxygen species are involved in a variety of pathological events. Reactive Oxygen Species (ROS) are produced during normal cellular function. ROS lead to lipid peroxidation, massive protein oxdiation and degradation. Under normal conditions, antioxidant are substnaces that either directly or indirectly protect cell against adverse effect of ROS. several biologically important compound include ${\beta}$-carotene, taruine and flavonoids reported have antioxidant function. The various antioxidant either scavange superoxide and free radicals or stimulate the detoxification mechanisms within cells resulting in increased detoxification of free radicals formation and thus in prevention of many pathophysiologic processes. This study carried out to investigate the antioxidant activity of flavonoids, myricetin with other antioxidants, ${\beta}$-carotene and taurine on B16Fl0. In order to investigate the efficacy of antioxidant activity, we measured cell viability, antioxidant enzyme activity (SOD, GPX, CAT) and intracellular reactive oxygen intermediate (ROI). In this results, we show that these flavonoids with other antioxidant substrates are increased antioxidant activity level.