• International Journal of Advanced Culture Technology
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• 제4권4호
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• pp.45-50
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• 2016

This is a humanistic study to trace phenomena logically the comprehensive therapeutic mechanism of the human body which is coded by the smart emotion of the rated signal conveyed by the Rated Sijo. The Gestalt, which is structured in the form of therapeutic metastasis conveyed by sentences, is intended to embody the principle of human response. So, this researcher explored the metastatic structure toward Gestalt of original human being through the passage of foreground and background by ergonomic and chemical structure. In the meantime, this researcher focused on revealing the structure of the field of existence by the symbol system in which the therapeutic mechanism of the human body is embodied. As a result, the basic framework of Gestalt literary therapy, which contributes to the improvement of the Quality of Life metaphorized as a mechanism of the symbol system by the metastasis of literary therapy or the electrical operation of the human body. As a result, the human body as a conductor through literature has turned out to be an original Gestalt structure pursued by literature. In addition, it was analyzed that the human body would accept signals such as emotions and Rated Emotions planted in the sentence, and synapse them into the human physiological psycho analytical symbol system. Therefore, it has been confirmed possibility that human existent environment and trauma are separated from the whole universe can push fully implement therapeutic techniques toward totalization by a combination of literary devices, especially appropriate electric signal combination of the Rated Sijo.

• 한국전문물리치료학회지
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• 제2권2호
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• pp.98-107
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• 1995

Physical therapists use assumptions about motor control in every aspect of their work in treating stroke patients. An understanding of the recovery process after stroke, some neural mechanism of recovery and therapeutic model is critical factor for physical therapist to evaluate and obtain a higher final stage of recovery. The purpose of this article was to review the recovery process after stroke, some neural mechanism of recovery, the role of rehabilitation in the process of recovery, therapeutic model and its limitation. This article will help understanding of recovery process. evaluation, and treatment of the stroke patients. Each therapeutic method consists of a different set of assumptions and they are not completely independent of one another. Therefore specializing in any techniques of physical therapy will not be enough to treat stroke, so we are in need of integrated approach and objective measurement instrument to adequately evaluate and treat stroke patients.

• International Journal of Oral Biology
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• 제46권2호
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• pp.74-80
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• 2021

Autophagy is an evolutionarily well-conserved cellular homeostasis program that responds to various cellular stresses and degrades unnecessary or harmful intracellular materials in lysosomes. Accumulating evidence has shown that autophagy dysfunction often results in various human pathophysiological conditions, including metabolic disorders, cancers, and neurodegenerative diseases. The discovery of an autophagy machinery protein network has revealed underlying molecular mechanisms of autophagy, and advances in the understanding of its regulatory mechanism have provided novel therapeutic targets for treating human diseases. Recently, reports have emerged on the involvement of autophagy in oral squamous cell carcinoma (OSCC). Although the role of autophagy in cancer therapy is controversial, the beneficial use of the induction of autophagic cell death in OSCC has drawn significant attention. In this review, the types of autophagy, mechanism of autophagosome biogenesis, and modulating molecules and therapeutic candidates affecting the induction of autophagic cell death in OSCC are briefly described.

• 한국발생생물학회지:발생과생식
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• 제27권1호
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• pp.1-7
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• 2023

Small-cell lung cancer (SCLC) continues to be the deadliest of all lung cancer types. Its high mortality is largely attributed to the unchangeable development of resistance to standard chemo/radiotherapies, which have remained invariable for the past 30 years, underlining the need for new therapeutic approaches. Recent studies of SCLC genome revealed a large number of somatic alterations and identified remarkable heterogeneity of the frequent mutations except for the loss of both RB and P53 tumor suppressor genes (TSGs). Identifying the somatic alterations scattered throughout the SCLC genome will help to define the underlying mechanism of the disease and pave the way for the discovery of therapeutic vulnerabilities associated with genomic alterations. The new technique made it possible to determine the underlying mechanism for the discovery of therapeutic targets. To these ends, the techniques have been focused on understanding the molecular determinants of SCLC.

• IMMUNE NETWORK
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• 제2권2호
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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.

• BMB Reports
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• 제53권6호
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• pp.291-298
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• 2020

Tumor angiogenesis is an essential process for growth and metastasis of cancer cells as it supplies tumors with oxygen and nutrients. During tumor angiogenesis, many pro-angiogenic factors are secreted by tumor cells to induce their own vascularization via activation of pre-existing host endothelium. However, accumulating evidence suggests that vasculogenic mimicry (VM) is a key alternative mechanism for tumor vascularization when tumors are faced with insufficient supply of oxygen and nutrients. VM is a tumor vascularization mechanism in which tumors create a blood supply system, in contrast to tumor angiogenesis mechanisms that depend on pre-existing host endothelium. VM is closely associated with tumor progression and poor prognosis in many cancers. Therefore, inhibition of VM may be a promising therapeutic strategy and may overcome the limitations of anti-angiogenesis therapy for cancer patients. In this review, we provide an overview of the current anti-angiogenic therapies for ovarian cancer and the current state of knowledge regarding the links between microRNAs and the VM process, with a focus on the mechanism that regulates associated signaling pathways in ovarian cancer. Moreover, we discuss the potential for VM as a therapeutic strategy against ovarian cancer.

• Biomolecules & Therapeutics
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• 제19권4호
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• pp.398-410
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• 2011

Over the past few decades, our understanding of the epidemiology and immunopathogenesis of Hodgkin lymphoma (HL) has made enormous advances. Consequently, the treatment of HL has changed significantly, rendering this disease of the most curable human cancers. To date, about 80% of patients achieve long-term disease-free survival. However, therapeutic challenges still remain, particularly regarding the salvage strategies for relapsed and refractory disease, which need further identification of better prognostic markers and novel therapeutic schemes. Although the precise molecular mechanism by which Epstein-Barr virus (EBV) contributes to the generation of malignant cells present in HL still remains unknown, current increasing data on the role of EBV in the pathobiology of HL have encouraged people to start developing novel and specific therapeutic strategies for EBV-associated HL. This review will provide an overview of therapeutic approaches for acute EBV infection and the classical form of HL (cHL), especially focusing on EBV-associated HL cases.

• 대한한의학회지
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• 제34권2호
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• pp.29-40
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• 2013

Objectives: To investigate therapeutic mechanisms of Gyejibokryeong-hwan (GJBRH) against gynaecological diseases, articles on biological assay were gathered and analyzed. Methods: The articles were classified as being from domestic or international journals, and by their year of publication. The mechanisms of the biological effects against gynaecological diseases were noted. Results: Of the 14 articles analyzed, 13 were published in China and 1 was from Japan. GJBRH showed therapeutic effect against uterine and mammary gland diseases. Uterine-related diseases such as endometriosis, hysteromyoma, adenomyosis, cancer, and inflammation can be improved by the administration of GJBRH through anti-angiogenesis, anti-inflammation, the modulation of immune cell and immunoglobulin, and the regulation of hormone secretion. GJBRH also reduced mammary hyperplasia by regulating hormone and cytokine release. Conclusions: We speculate that the inhibitory effect against uterine and mammary gland diseases could be related to the therapeutic efficacy of GJBRH in improving gynaecological diseases.

• Molecules and Cells
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• 제38권5호
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• pp.381-389
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• 2015

Autophagy is a lysosome-dependent intracellular degradation process that allows recycling of cytoplasmic constituents into bioenergetic and biosynthetic materials for maintenance of homeostasis. Since the function of autophagy is particularly important in various stress conditions, perturbation of autophagy can lead to cellular dysfunction and diseases. Accumulation of abnormal protein aggregates, a common cause of neurodegenerative diseases, can be reduced through autophagic degradation. Recent studies have revealed defects in autophagy in most cases of neurodegenerative disorders. Moreover, deregulated excessive autophagy can also cause neurodegeneration. Thus, healthy activation of autophagy is essential for therapeutic approaches in neurodegenerative diseases and many autophagy-regulating compounds are under development for therapeutic purposes. This review describes the overall role of autophagy in neurodegeneration, focusing on various therapeutic strategies for modulating specific stages of autophagy and on the current status of drug development.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.59-59
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• 2001

The purpose of this study was to investigate the molecular mechanism by which environmental pH alters the radiation-induced expression of p53, the key regulator of cellular responses to radiation. We have already reported that an acidic environment markedly prolongs the radiation-induced expression of p53 and also prolongs the radiation-induced G2/M arrest.(omitted)