• Korean Journal of Biological Psychiatry
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• v.15 no.4
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• pp.275-287
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• 2008

Depression and coronary artery disease are both highly prevalent diseases. Many previous studies suggest that depression is a common comorbid condition in patients with coronary artery disease and has a significant negative impact on the onset, course, and prognosis of coronary artery disease. However, the exact mechanisms that underlie the association between these two diseases remain unclear. Pathophysiologic mechanisms that may explain the effect of depression on coronary artery disease include hypercoagulability, hypothalamus-pituitary-adrenal axis and autonomic nervous system dysregulation, altered inflammatory response. On the contrary, pathophysiologic mechanisms in coronary artery disease that affect depression are less well known. It is also suggested that both diseases may share a common genetic vulnerability. The authors reviewed the literature on the pathophysiologic relationships of depression and coronary heart disease.

• Clinical and Experimental Pediatrics
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• v.50 no.4
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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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• v.18 no.1
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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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• v.49 no.5
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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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• v.11 no.1
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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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• v.50 no.4
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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.

• Korean Journal of Bronchoesophagology
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• v.5 no.2
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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.

• Sleep Medicine and Psychophysiology
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• v.6 no.1
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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.

• Korean Journal of Biological Psychiatry
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• v.18 no.2
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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.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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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.