• 대한본초학회지
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• 제22권2호
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• pp.175-180
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• 2007

Objective : The application of Sam So Eum (蔘蘇飮, SSE) as a herbal medicine to treat asthma in mice has been studied and the mechanism of cytokine production in asthmatic mice was discussed. Recently, SSE was known to have anti-allergic activity. However, its therapeutic mechanisms are unclear. Methods : So, we investigated the effects of SSE on levels of several cytokines in bronchoalveolar lavage fluid (BALF) using flow cytometric analysis in allergen-induced asthma. Results : In this experiment, SSE decreased levels of IL-la, IL-17 and GM-CSF respectively. Contrary, SSE restored level of IFN-g toward naive level in BALF. Conclusion : In conclusion, we demonstrate that SSE is useful to treat asthma and it's therapeutic mechanisms are involved in Thl skewing reaction.

• BMB Reports
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• 제29권3호
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• pp.200-204
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• 1996

Nerve growth factor (NGF) is literally known to promote neural differentiation and survival in several peripheral and central neurons. Thus, it is Widely believed that NGF may serve as a therapeutic agent for many types of neuronal diseases. One of the mechanisms suggested to explain the protective role of NGF is that the trophic factor can prevent the increase of intracellular calcium ions which might be responsible for neural death. To examine whether or not the calcium hypothesis works even under pathological conditions, we applied NGF to cultures deprived of glucose. Surprisingly, what was observed here is that NGF rather promoted cell death under a glucose-deprived condition. What we call the NGF paradox phenomenon occurred in a calcium concentration-dependent manner, indirectly suggesting that NGF might increase intracellular calcium ions in cells deprived of glucose. This suggestion is further supported by the fact that nifedipine, a well-known L-type calcium channel blocker, could block the cell death potentiated by NGF. Here it is still premature to propose the complete mechanism underlying the NGF paradox phenomenon. However, this study certainly indicates that NGF as a therapeutic agent for neuronal diseases should be carefully considered before use.

• 대한물리의학회지
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• 제3권1호
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• pp.21-25
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• 2008

Purpose : The objective of this study was conducted to find out the facilitation therapy. Therapeutic exercise concepts are changed from classical therapeutic exercise and neurophysiolosical approach to facilitation therapy. Methods : This is literature study with books and PNF international course books. Results : Facilitation concepts are changed. Complex movements are the result of spinal reflex-mechanism. It was changed the to reflex-reponses are variable and organization of complex movements are determined by the necessity to move. Therefore therapy goals and concepts of spasticity have to change. Conclusion : Facilitation therapy approach by use input systems, which are needed to interact with environmental and task demands. The systems are visual, tactile, propriocepsis, vestibular, acoustical and olfactory. Facilitation therapy need these system all together with shaping.

• Journal of Microbiology and Biotechnology
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• 제30권2호
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• pp.306-312
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• 2020

Despite the importance of brown adipocytes as a therapeutic target for the prevention and treatment of obesity, the molecular mechanism underlying brown adipocyte differentiation is not fully understood. In particular, the role of post-translational modifications in brown adipocyte differentiation has not been extensively studied. Histidine phosphorylation is increasingly recognized an important process for protein post-translational modifications. In this study, we show that histidine phosphorylation patterns change during brown adipocyte differentiation. In addition, the expression level of protein histidine phosphatase 1 (PHPT1), a major mammalian phosphohistidine phosphatase, is reduced rapidly at the early phase of differentiation and recovers at the later phase. During white adipocyte differentiation of 3T3-L1 preadipocytes, however, the expression level of PHPT1 do not significantly change. Knockdown of PHPT1 promotes brown adipocyte differentiation, whereas ectopic expression of PHPT1 suppresses brown adipocyte differentiation. These results collectively suggest that histidine phosphorylation is closely linked to brown adipocyte differentiation and could be a therapeutic target for obesity and related metabolic diseases.

• 한국한의학연구원논문집
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• 제6권1호
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• pp.99-105
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• 2000

Lithium, a simple monovalent cation, is the mainstay in the treatment of manic-depressive illness, but despite extensive research, its mechanism of action remains to be elucidated. Because lithium requires chronic administration for therapeutic efficacy and because its beneficial effects last well beyond its discontinuation, it has been postulated that lithium may exert major effects at the genomic level. We have previously shown that Yungmijihwangwon (YM) increase TH protein expression through antioxidant activity and unknown effects in vivo. In the pressent study, we have sought to determine if lithium in herbal medicine also increases the expression of endogenous gene known to be regulated by AP-1 and have therefore investigated the effects of herbal medicine on tyrosine hydroxylase (TH) levels. Male mice were treated with LiCl and herbal medicine for 30 days, and TH levels and dopamine level were measured in striatum using immunoblotting and ECD-HPLC. Herbal medicine treatment resulted in statistically nonsignificant increase in TH levels in mouse striatum. The precise therapeutic relevance of these effects is presently unknown.

• 혜화의학회지
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• 제14권2호
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• pp.55-70
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• 2005

In oriental medicine, Gamibangpungtongsungsan (KBTS) has been used as a therapeutic agent for the treatments of acute stage of cerebrovascular diseases and hypertension. In the present study, underlying mechanism on KBTS effects was investigated using spontaneously hypertensive rats (SHR) by determining related parameters such as blood pressure, heart-beat rates, and hormones and plasma constituents. The major finding are summarized as follows. 1. KBTS treatment at concentrations lower than $125\;{\mu}g/m{\ell}$ did not show any cytotoxicity on cultured human fibroblast cells. 2. KBTS treatment in SHR significantly decreased blood pressure and heart-beat rate compared with untreated control. 3. KBTS treatment in SHR decreased aldosterone levels in the blood compared with untreated control, but the difference was not statistically significant. 4. KBTS treatment in SHR significantly decreased dopamine, norepinephrine and epinephrine levels in the blood compared with untreated control. 5. KBTS treatment in SHR decreased plasma ion concentrations such as Na+, K+, Ca2+, Cl- compared with untreated control; decreases in Na+ and Cl- were statistically significant. 6. KBTS treatment in SHR significantly decreased TNF-$\alpha$, IL-6, and IL-10 levels in the blood compared with untreated control. Thus, the present data show evidence on anti-hypertension activity of KBTS in an experimental animal system, which can provide further insights into the development of anti-hypertension therapeutic agents.

• BMB Reports
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• 제49권8호
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• pp.405-413
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• 2016

Tau proteins, which stabilize the structure and regulate the dynamics of microtubules, also play important roles in axonal transport and signal transduction. Tau proteins are missorted, aggregated, and found as tau inclusions under many pathological conditions associated with neurodegenerative disorders, which are collectively known as tauopathies. In the adult human brain, tau protein can be expressed in six isoforms due to alternative splicing. The aberrant splicing of tau pre-mRNA has been consistently identified in a variety of tauopathies but is not restricted to these types of disorders as it is also present in patients with non-tau proteinopathies and RNAopathies. Tau mis-splicing results in isoform-specific impairments in normal physiological function and enhanced recruitment of excessive tau isoforms into the pathological process. A variety of factors are involved in the complex set of mechanisms underlying tau mis-splicing, but variation in the cis-element, methylation of the MAPT gene, genetic polymorphisms, the quantity and activity of spliceosomal proteins, and the patency of other RNA-binding proteins, are related to aberrant splicing. Currently, there is a lack of appropriate therapeutic strategies aimed at correcting the tau mis-splicing process in patients with neurodegenerative disorders. Thus, a more comprehensive understanding of the relationship between tau mis-splicing and neurodegenerative disorders will aid in the development of efficient therapeutic strategies for patients with a tauopathy or other, related neurodegenerative disorders.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1999년도 제38차 춘계학술대회
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• pp.228-241
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• 1999

Percutaneous coronary angioplasty is well established therapeutic modality in the management of coronary artery disease. However, the high restenosis rate of 30 to 50% limits its usefulness. The principal mechanism of restenosis, intimal hyperplasia, is the proliferative response of vessel wall to injury, which consists largely of smooth muscle cells. A large body of animal investigations and a limited number of clinical studies have established the ability of ionizing radiation to reduce neointimal proliferation and restenosis rate significantly. Human studies have been reported that intravascular radiation after first restenosis inhibits a second restenosis. Encouraged by these reports, we are also conducting a double blind, placebo-controlled, randomized trial to evaluate this new therapeutic modality in patients with coronary artery stenosis. The objective of our trial is to determine the safety and efficacy of catheter-based solutional beta emitting radioisotope system in preventing restenosis after angioplasty. This review describes the vascular brachytherapy systems and isotopes that have been utilized in the initial clinical trials performed in this area of post PTCA coronary restenosis. The results of many worldwide ongoing clinical trials will determine whether this new technology will change the future practice of vascular intervention.

• Molecules and Cells
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• 제25권4호
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• pp.457-461
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• 2008

DNA damage checkpoint is an important self-defense mechanism for the maintenance of genome stability. Defects in DNA damage signaling and repair lead to various disorders and increase tumor incidence in humans. In the past 10 years, we have identified many components involved in the DNA damage-signaling pathway, including the product of breast cancer susceptibility gene 1 (BRCA1). Mutations in BRCA1 are associated with increased risk of breast and ovarian cancers, highlighting the importance of this DNA damage-signaling pathway in tumor suppression. While it becomes clear that BRCA1 plays a crucial role in the DNA damage responsive pathway, exactly how BRCA1 receives DNA damage signals and exerts its checkpoint function has not been fully addressed. A series of recent studies reported the discovery of many novel components involved in DNA damage-signaling pathway. These newly identified checkpoint proteins, including RNF8, RAP80 and CCDC98, work in concern in recruiting BRCA1 to DNA damage sites and thus regulate BRCA1 function in G2/M checkpoint control. This review will summarize these recent findings and provide an updated view of the regulation of BRCA1 in response to DNA damage.

• BMB Reports
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• 제50권7호
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• pp.345-354
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• 2017

Autophagy, a catabolic process necessary for the maintenance of intracellular homeostasis, has recently been the focus of numerous human diseases and conditions, such as aging, cancer, development, immunity, longevity, and neurodegeneration. However, the continued presence of autophagy is essential for cell survival and dysfunctional autophagy is thought to speed up the progression of neurodegeneration. The actual molecular mechanism behind the progression of dysfunctional autophagy is not yet fully understood. Emerging evidence suggests that basal autophagy is necessary for the removal of misfolded, aggregated proteins and damaged cellular organelles through lysosomal mediated degradation. Physiologically, neurodegenerative disorders are related to the accumulation of amyloid ${\beta}$ peptide and ${\alpha}-synuclein$ protein aggregation, as seen in patients with Alzheimer's disease and Parkinson's disease, respectively. Even though autophagy could impact several facets of human biology and disease, it generally functions as a clearance for toxic proteins in the brain, which contributes novel insight into the pathophysiological understanding of neurodegenerative disorders. In particular, several studies demonstrate that natural compounds or small molecule autophagy enhancer stimuli are essential in the clearance of amyloid ${\beta}$ and ${\alpha}-synuclein$ deposits. Therefore, this review briefly deliberates on the recent implications of autophagy in neurodegenerative disorder control, and emphasizes the opportunities and potential therapeutic application of applied autophagy.