• Title/Summary/Keyword: pathogenesis mechanism

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A Study on Implications for Korean Medicine Education by Comparing International Competence Frameworks in Medical Education (국제적인 의학교육 역량체계 비교를 통한 한의학교육에의 시사점 연구)

  • Shin, Sang Woo;Park, Jongbae Jay
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.31 no.1
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    • pp.36-45
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    • 2017
  • In order to gain implications for establishing competency-based education system in Korean medicine education, we examined several competence frameworks of medical education developed at international or national level, and compared the basic constitution and common elements. The competence frameworks of medical education consist of seven categories of communication, professionalism, critical thinking, medical knowledge, patient care, management, and public health. Medical knowledge consists of five sub-groups: normal structure and function; pathogenesis and mechanism of disease; principles of drug and treatment; psychological, behavioral and sociological principles; and public health and lifelong learning. In principle, competencies are further divided into sub-categories or combined with learning outcomes, and the field and the level of achievement is presented per item. This article aims at summarizing the competencies of a few globally leading medical institutions with the educational standard of Korean Medicine in mind.

Degradation of Insect Humoral Immune Proteins by the Proteases Secreted from Enterococcus faecalis

  • Park, Shin-Yong;Kim, Koung-Mi;Kim, Ik-Soo;Lee, Sang-Dae;Lee, In-Hee
    • International Journal of Industrial Entomology and Biomaterials
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    • v.13 no.1
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    • pp.37-43
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    • 2006
  • Enterococcus faecalis was isolated from the body fluid of dead Galleria mellonella larvae. Upon injection of E. faecalis into the hemocoel of G. mellonella, the bacteria destroyed parts of humoral defense systems in the hemolymph. In a test for the proteolytic activity of E. faecalis CS, it was confirmed that the enzyme degraded three well-known a-helical antimicrobial peptides, cecropin A, melittin and halocidin, and abolished their activities. We also determined putative cleavage sites on the primary sequences of three peptides through purification and mass analysis of peptide fragments digested by E. faecalis CS. Furthermore it was found that apolipophorin-III, recently known as a critical recognition protein for invading microbes in the hemolymph of G. mellonella, was also degraded by E. faecalis CS. Taken together, the present work shows that the protease in secretions from E. faecalis destroyed two critical humoral immune factors in the hemolymph of G. mellonella larvae. In addition, this paper demonstrates that the relationship between the host insect and the pathogenic bacteria might provide a valuable model system to study the enterococcal virulence mechanism, which may be relevant to mammalian pathogenesis.

Effects of Sunghyangchungisan(SHCS) on Oxidant-induced Cell Death in Human Neuroglioma Cells

  • Kim Na-Ri;Kwon Jung-Nam;Kim Young-Kyun
    • The Journal of Korean Medicine
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    • v.26 no.2 s.62
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    • pp.63-76
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    • 2005
  • Objectives: Reactive oxygen species (ROS) have been implicated in the pathogenesis of a wide range of acute and longterm neurodegenerative diseases. This study was undertaken to examine whether Sunghyangchungisan(SHCS), a well-known prescription in Korean traditional medicine, might have beneficial effects on ROS-induced brain cell injury. Methods: Human neuroglioma cell line A172 and H2O2 were employed as an experimental model cell and oxidant. Results: SHCS effectively protected the cells against both the necrotic and apoptotic cell death induced by H2O2. The effect of SHCS was dose-dependent at concentrations ranging from 0.2 to 5mg/ml. SHCS significantly prevented depletion of cellular ATP and activation of poly (ADP-ribose) polymerase induced by H2O2. It also helped mitochondria to preserve its functional integrity estimated by MTT reduction ability. Furthermore, SHCS significantly prevented H202-induced release of cytochrome c into cytosol. Determination of intracellular ROS showed that SHCS might exert its role as a powerful scavenger of intracellular ROS. Conclusions: The present study provides clear evidence for the beneficial effect of SHCS on ROS-induced neuroglial cell injury. The action of SHCS as an ROS-scavenger might underlie the mechanism.

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β-Adrenergic Receptor and Insulin Resistance in the Heart

  • Mangmool, Supachoke;Denkaew, Tananat;Parichatikanond, Warisara;Kurose, Hitoshi
    • Biomolecules & Therapeutics
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    • v.25 no.1
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    • pp.44-56
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    • 2017
  • Insulin resistance is characterized by the reduced ability of insulin to stimulate tissue uptake and disposal of glucose including cardiac muscle. These conditions accelerate the progression of heart failure and increase cardiovascular morbidity and mortality in patients with cardiovascular diseases. It is noteworthy that some conditions of insulin resistance are characterized by up-regulation of the sympathetic nervous system, resulting in enhanced stimulation of ${\beta}$-adrenergic receptor (${\beta}$AR). Overstimulation of ${\beta}$ARs leads to the development of heart failure and is associated with the pathogenesis of insulin resistance in the heart. However, pathological consequences of the cross-talk between the ${\beta}$AR and the insulin sensitivity and the mechanism by which ${\beta}$AR overstimulation promotes insulin resistance remain unclear. This review article examines the hypothesis that ${\beta}$ARs overstimulation leads to induction of insulin resistance in the heart.

Induction of Resistance by TMV Infection in Capsicum annuum Against Phytophthora Blight (TMV 감염에 의한 고추의 역병 저항성 유도)

  • 이성희;이주연;차재순
    • Korean Journal Plant Pathology
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    • v.14 no.4
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    • pp.319-324
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    • 1998
  • Induction of systemic acquired resistance (SAR) against phytophthora blight and pathogenesis-related (PR) protein accumulation by TMV infection in pepper plant (Capsicum annuum cv. Nockwang) were examined to understand the mechanism of the systemic acquired resistance in pepper plant. The zoospore suspension of Phytophthora capsici was inoculated on stem of pepper plant in which TMV-pepper strain had been inoculated on fully expanded upper leaves, and thephytopha blight incidence was examined. Both disease severity and lesion length of phytophthora blight were much smaller in TMV pre-inoculated pepper plant than in uninoculated control plants. The phytophthora blight incidence was decreased about 50% in the TMV pre-inoculated pepper, compared to the uninoculated control plant at 10 days after P. capsici inoculation. Accumulation of PR1 and PR5 proteins in intercellular fluid of TMV-inoculated and uninoculated upper leaves were monitored by immuno-blot with tobacco P1b and PR5a, antibody during induction of SAR. PR1 and PR5 were detected from 24 hours after TMV inoculation in both TMV-inoculated and uninouclated upper leaves, and increased rapidly in TMV-inoculation in uninoculated upper leaves were defoliated. PR5 could be detected upto 20 days after TMV inoculation in uninoculated upper leaves. These results suggest that TMV infection induces SAR against phytophthora blight in pepper plant, and that PR proteins are accumulated very rapidly during induction of SAR and maintained for quite long time in pepper plant.

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Estrogen Effect on the Na,K-ATPase Activity Repressed by IgE-Dependent Histamine-Releasing factor in HeLa Cells (HeLa 세포에서 Estrogen이 Na,K-ATPase활성에 미치는 영향)

  • Lee Si-Nae;Kim Hwa-Jung;Lee Kyunglim
    • Microbiology and Biotechnology Letters
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    • v.33 no.4
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    • pp.322-326
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    • 2005
  • IgE-dependent histamine-releasing factor (HRF) is found extracellularly to regulate the degranulation process of histamine in mast cells and basophils and known to play a predominant role in the pathogenesis of chronic allergic disease. HRF has been also identified in the intracellular region of the cell. Previously, we reported that HRF interacts with the 3rd cytoplasmic domain of the alpha subunit of Na,K-ATPase and inhibits Na,K-ATPase activity. Since it is known that estroaen activates the sarcolemmal Na,K-ATPase, we tested whether estrogen recovers the Na,K-ATPase activity repressed by HRF. In this study, we showed that estrogen activates Na,K-ATPase repressed by HRF. RT-PCR and western blot analysis showed that estrogen doesn't reduce the expression level of HRF in HeLa cell, suggesting that this recovery effects of estrogen probably occur via indirect mechanism on HRF and Na,K-ATPase.

Effects of Seman Armenicae and Radix Trichosanthis on the iNOS expression and superoxide formation in the RAW264.7 cells (행인 과루인 추출물이 마우스 대식세포주인 RAW264.7 세포주의 iNOS 발현 및 Superoxide 형성에 미치는 영향)

  • Park, Joug-Un;Moon, Seok-Jae;Moon, Goo;Won, Jin-Hee
    • THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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    • v.5 no.1
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    • pp.137-150
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    • 1999
  • Macrophage play a major role in host defence against infection and tumor development and this activity is regulated through the production of several mediators. In particular, the production of NO by macrophages mediates killing or growth inhibition of tumor cells, bacteria, fungi and parasites. However, over-expression of iNOS by various stimuli, resulting in over-production of NO, contributes to the pathogenesis of septic shock and some inflammator and auto-immune disease. Therefore, it would be valuable to develop potent and selective inhibitors of for potential therapeutic use. Thus the agent that supprees the expression of iNOS mRNA or enzyme protein will be usefull for the prevention of various diseases. We are intersted in identifying selective inhibitiors of iNOS which might be useful intreating inflammatory human diseases. In summary, we have demenstrated that scopoletin, isolated from Seman Armenicae and Radix Trichosanthis the production of NO induced by $IFN-\gammer$ plus LPS in RAW 264.7 macrophages, The mechanism for the inhibition of NO production was due to suppression of the expression of iNOS mRNA or enzyme protein.

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Dialysis Disequilibrium Syndrome in Neurosurgical Patient - Case Report - (신경외과 환자 치료 중 발생한 Dialysis Disequilibrium Syndrome - 증례보고 -)

  • Woo, Hee-Kyung;Yoo, Do-Sung;Kim, Dal-Soo;Huh, Pil-Woo;Cho, Kyoung-Suok;Kang, Joon-Ki
    • Journal of Korean Neurosurgical Society
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    • v.30 no.3
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    • pp.381-383
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    • 2001
  • Neurological symptoms may develope when the blood urea nitrogen is lowered too rapidly by hemodialysis. It is known that these symptoms, known as dialysis disequilibrium are associated with cerebral edema. However, the pathogenesis of brain swelling and neurological deterioration after rapid hemodialysis is controversial. The reverse urea hypothesis suggests that hemodialysis removes urea more slowly from the brain than from the plasma, creating an osmotic gradient that results in cerebral edema. The idiogenic osmole hypothesis proposes that an osmotic gradient between brain and plasma develops during rapid dialysis because of newly formed brain osmoles. Authors report a such case and discuss the possible mechanism and preventive methods.

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Role of Nucleotide-binding and Oligomerization Domain 2 Protein(NOD2) in the Development of Atherosclerosis

  • Kim, Ha-Jeong
    • 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.

Recent Progress in HER2 Associated Breast Cancer

  • Wang, Wei-Jia;Lei, Yuan-Yuan;Mei, Jin-Hong;Wang, Chun-Liang
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.7
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    • pp.2591-2600
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    • 2015
  • Breast cancer is the most common cancer worldwide among women and the second most common cancer. Approximately 15-23% of breast cancers over-express human epidermal growth factor receptor2 (HER2), a 185-kDa transmembrane tyrosine kinase, which is mainly found at the cell surface of tumor cells. HER2-positive breast cancer, featuring amplification of HER2/neu and negative expression of ER and PR, has the three following characteristics: rapid tumor growth, lower survival rate, and better response to adjuvant therapies. Clinically, it is notable for its role in a pathogenesis that is associated with increased disease recurrence and acts as a worse prognosis. At the same time, it represents a good target for anti-cancer immunotherapy despite the prevalence of drug resistance. New treatments are a major topic of research, and a brighter future can be expected. This review discusses the role of HER2 in breast cancer, therapeutic modalities available and prognostic factors.