• Journal of Sasang Constitutional Medicine
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• v.14 no.1
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• pp.26-33
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• 2002

1. Purpose The purpose of this article was to find the change of Dong-mu's conceptions about constitutional disease through comparing with ${\ulcorner}$Sasang-Yihak-chobonguen${\lrcorner}$, ${\ulcorner}$Dongyi Soose Bowon${\lrcorner}$ written in 1894(Old edition) and ${\ulcorner}$Dongyi Soose Bowon${\lrcorner}$ published in 1901(In Edition) 2. Methods Comparing with ${\ulcorner}$Sasang-Yihak-chobonguen${\lrcorner}$, ${\ulcorner}$Dongyi Soose Bowon${\lrcorner}$ written in 1894(Old edition) and ${\ulcorner}$Dongyi Soose Bowon${\lrcorner}$ published in 1901(In Edition) we found the change of Dong-mu's conceptio ns about constitutional disease 3. Result 1) In ${\ulcorner}$Sasang-Yihak-chobonguen${\lrcorner}$, diseases were classified 'Oi-Gam(外感)‘, ’Nae-sang(內傷)‘, ’Ok-roi(牢獄)‘. ’Wi-gyoung(危傾)‘. In ${\ulcorner}$Sasang-Yihak-chobonguen${\lrcorner}$ ordinary symptoms was more impotant than disease, and good life style was emplasized for health 2) In ${\ulcorner}$Dongyi Soose Bowon${\lrcorner}$ written in 1894(Old edition), diseases were classified 'Oi-Gam(外感)‘, ’Nae-sang(內傷)‘. siseases from exterior causes was classified into 'Oi-gam-noi-chu-byoung(外傷腦?頁病)’, and diseases from interior causes was classified into 'Nae-sang-wi-wan-byoung(內觸胃脘病).‘ Herbal medication yet was't used by Disease 3) In ${\ulcorner}$Dongyi Soose Bowon${\lrcorner}$ published in 1901(In Edition), diseases was classified not by causes of disease but by mechanism and symptom of disease, so into Exterior-cold disease' and 'Interior-hot disease'. Herbal medication was used by pattern of Disease. 4) Conception of constitutional diseases was gradualy complished through edition.

• IMMUNE NETWORK
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• v.2 no.2
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• pp.65-71
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• 2002

The immunological mechanism of the responses to ultraviolet (UV) B radiation in mouse models were investigated by the suppression of contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH), and susceptibility to infection. However, there are some differences in immune suppression according to the different models as well as the irradiation protocols. Therefore, this review focused on the differences in the suppressive effects on CHS and DTH, and susceptibility to infection in relation to the different in vivo models. Recent advances in cytokine knockout mice experiments have the reexamination of the role of the critical cytokines in UVB-induced immune suppression, which was investigated previously by blocking antibodies. The characteristics of the suppressor cells responsible for UVB-induced tolerance were determined. The subcellular mechanism of UVB-induced immune suppression was also explained by the induction of apoptotic cells through the Fas and Fas-ligand interaction. The phagocytosis of the apoptotic cells is believed to induce the production of the immune suppressive cytokine like interleukin-10 by macrophages. Therefore, the therapeutic UVB response to a skin disease, such as psoriasis, by the depletion of infiltrating T cells could be considered in the extension line of apoptosis and immune suppression.

• Journal of Korean Neurosurgical Society
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• v.57 no.6
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• pp.436-439
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• 2015

The majority of clinical studies on moyamoya disease (MMD) have focused on anterior circulation. The disease involvement of posterior circulation in MMD, mainly in the posterior cerebral artery (PCA), has been mentioned since the early 1980s, and it has been repeatedly emphasized as one of the most important factors related to poor prognosis in MMD. However, its clinical features and outcome have only been elucidated during the last few years. In this review, the angiographic definition of PCA stenosis is summarized. The clinical features are elucidated as being either early-onset or delayed-onset, according to the time of PCA stenosis diagnosis in reference to the anterior circulation revascularization surgeries. The surgical strategy and hypothesis on the mechanism of PCA stenosis is also briefly mentioned. It appears that some MMD patients may show PCA stenosis during the early or late course of the disease and that the presenting symptoms may vary. Because the hemodynamic compromise caused by PCA stenosis may respond well to surgical treatment, clinicians should be aware of the condition, especially during follow-up of MMD patients.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.4953-4960
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• 2013

Primary liver cancer is one of the most common cancers at the global level, accounting for half of all cancers in some undeveloped countries. This disease tends to occur in livers damaged through alcohol abuse, or chronic infection with hepatitis B and C, on a background of cirrhosis. Various cancer-causing substances are associated with primary liver cancer, including certain pesticides and such chemicals as vinyl chloride and arsenic. The strong association between HBV infection and liver cancer is well documented in epidemiological studies. It is generally acknowledged that the virus is involved through long term chronic infection, frequently associated with cirrhosis, suggesting a nonspecific mechanism triggered by the immune response. Chronic inflammation of liver, continuous cell death, abnormal cell growth, would increase the occurrence rate of genetic alterations and risk of disease. However, the statistics indicated that only about one fifth of HBV carries would develop HCC in lifetime, suggesting that individual variation in genome would also influence the susceptibility of HCC. The goal of this review is to highlight present level of knowledge on the role of viral infection and genetic variation in the development of liver cancer.

• Molecules and Cells
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• v.42 no.10
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• pp.729-738
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• 2019

Autophagy is an important process for protein recycling. Oligomerization of p62/SQSTM1 is an essential step in this process and is achieved in two steps. Phox and Bem1p (PB1) domains can oligomerize through both basic and acidic surfaces in each molecule. The ZZ-type zinc finger (ZZ) domain binds to target proteins and promotes higher-oligomerization of p62. This mechanism is an important step in routing target proteins to the autophagosome. Here, we determined the crystal structure of the PB1 homo-dimer and modeled the p62 PB1 oligomers. These oligomer models were represented by a cylindrical helix and were compared with the previously determined electron microscopic map of a PB1 oligomer. To accurately compare, we mathematically calculated the lead length and radius of the helical oligomers. Our PB1 oligomer model fits the electron microscopy map and is both bendable and stretchable as a flexible helical filament.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.34-63
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• 2003

Idiopathic Parkinson's disease (IPD) represents a common neurodegenerative disorder. While epidemiological studies have suggested a number of risk factors including age, gender, race, and inherited disorder, the cumulative evidence supports the view that environmental or occupational exposure to certain chemicals may contribute to the initiation and progress of Parkinsonism.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.6
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• pp.479-484
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• 2015

NOD2 (nucleotide-binding and oligomerization domain 2) was initially reported as a susceptibility gene for Crohn's disease, with several studies focused on elucidating its molecular mechanism in the progression of Crohn's disease. We now know that NOD2 is an intracellular bacterial sensing receptor, and that MDP-mediated NOD2 activation drives inflammatory signaling. Various mutations in NOD2 have been reported, with NOD2 loss of function being associated with the development of Crohn's disease and other autoimmune diseases. These results suggest that NOD2 not only has an immune stimulatory function, but also an immune regulatory function. Atherosclerosis is a chronic inflammatory disease of the arterial wall; its pathologic progression is highly dependent on the immune balance. This immune balance is regulated by infiltrating monocytes and macrophages, both of which express NOD2. These findings indicate a potential role of NOD2 in atherosclerosis. The purpose of this review is to outline the known roles of NOD2 signaling in the pathogenesis of atherosclerosis.

• Journal of Oral Medicine and Pain
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• v.43 no.3
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• pp.61-69
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• 2018

Obstructive sleep apnea (OSA) is a relatively common, but greatly underdiagnosed sleep-related breathing disorder, characterized by recurrent collapse of the upper airway during sleep. OSA has been associated with a variety of cardiometabolic disease, such as hypertension, coronary artery disease, cardiac arrhythmia, cerebrovascular disease and metabolic dysfunction. Neurocognitive impairment, including excessive daytime sleepiness, increased risk of motor vehicle accidents, is also related to OSA. Sleep fragmentation and related arousals during sleep lead to intermittent hypoxia, sympathetic activation, oxidative stress, systemic inflammation and metabolic dysregulation which provide biological plausibility to this pathologic mechanism. Extensive studies demonstrated that OSA is a modifiable risk factor for the above mentioned diseases and oral appliances (OAs), although continuous positive air pressure (CPAP) is a first-line therapy of OSA, are not inferior to CPAP at least in mild OSA, and may be an alternative to CPAP in CPAP-intolerant subjects with OSA. The goal of this article is to provide a current knowledge of pathologic link between OSA and cardiovascular disease, focusing on intermittent hypoxia, sympathetic activation, oxidative stress and metabolic dysregulation. Then, previous epidemiologic studies will be reviewed to understand the causal relationship between OSA and cardiovascular disease. Finally, the effects of OAs will be updated via recent metaanalyses compared to CPAP.

• BMB Reports
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• v.53 no.1
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• pp.47-55
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• 2020

Alzheimer's disease (AD) is a multifactorial neurodegenerative disease and has become a major socioeconomic issue in many developed countries. Currently available therapeutic agents for AD provide only symptomatic treatments, mainly because the complete mechanism of the AD pathogenesis is still unclear. Although several different hypotheses have been proposed, mitochondrial dysfunction has gathered interest because of its profound effect on brain bioenergetics and neuronal survival in the pathophysiology of AD. Various therapeutic agents targeting the mitochondrial pathways associated with AD have been developed over the past decade. Although most of these agents are still early in the clinical development process, they are used to restore mitochondrial function, which provides an alternative therapeutic strategy that is likely to slow the progression of the disease. In this mini review, we will survey the AD-related mitochondrial pathways and their small-molecule modulators that have therapeutic potential. We will focus on recently reported examples, and also overview the current challenges and future perspectives of ongoing research.

• BMB Reports
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• v.53 no.7
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• pp.373-378
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• 2020

Phosphorylation of the signaling component by protein kinase often leads to a kinase cascade or feedback loop. 3-Phosphoinositide-dependent kinase 1 (PDK1) signaling pathway diverges into various kinases including Akt and p70 S6 kinase (p70S6k). However, the PDK1 feedback mechanism remains elusive. Here, we demonstrated that UNC-51-like kinase (ULK1), an autophagy initiator kinase downstream of mechanistic target of rapamycin (mTOR), directly phosphorylated PDK1 on serine 389 at the linker region. Furthermore, our data showed that this phosphorylation affected the kinase activity of PDK1 toward downstream substrates. These results suggest a possible negative feedback loop between PDK1 and ULK1.