• Title/Summary/Keyword: Disease models

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Strategies to reduce risk factors of non-communicable diseases in South Korea (만성질환 위험요인 감소를 위한 전략과 방향)

  • Khang, Young-Ho
    • Korean Journal of Health Education and Promotion
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    • v.33 no.4
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    • pp.1-9
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    • 2016
  • Objectives: This review is to suggest strategies to reduce risk factors of non-communicable diseases (NCD) in South Korea. Methods: Prior research findings on the burden of NCD and associated risk factors and the effectiveness of intervention programs were reviewed. Strategies regarding the control of NCD risk factors were conceived. Results: The author presented research findings from the Global Burden of Disease study on the burden of non-communicable disease (NCD) and associated risk factors in South Korea. Strengths and limitations of population and high-risk strategies for preventing NCDs were introduced. The author also reviewed the evidence on the effectiveness of multiple cardiovascular risk factor interventions and community-based intervention programs on cardiovascular diseases conducted in industrialized countries. Finally, strategies to reduce NCD risk factors in South Korea were suggested. Conclusions: The evidence-based interventions and the importance of population strategies in NCD prevention were highlighted. The author indicated that strategies employed by unhealthy commodity industries to undermine effective public health policies and programs should be actively monitored. It has been suggested that effective high-risk strategies with ecological models to address social risks rather than medical risks among disadvantaged population should be further developed in South Korea.

Drosophila as a model for unfolded protein response research

  • Ryoo, Hyung Don
    • BMB Reports
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    • v.48 no.8
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    • pp.445-453
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    • 2015
  • Endoplasmic Reticulum (ER) is an organelle where most secretory and membrane proteins are synthesized, folded, and undergo further maturation. As numerous conditions can perturb such ER function, eukaryotic cells are equipped with responsive signaling pathways, widely referred to as the Unfolded Protein Response (UPR). Chronic conditions of ER stress that cannot be fully resolved by UPR, or conditions that impair UPR signaling itself, are associated with many metabolic and degenerative diseases. In recent years, Drosophila has been actively employed to study such connections between UPR and disease. Notably, the UPR pathways are largely conserved between Drosophila and humans, and the mediating genes are essential for development in both organisms, indicating their requirement to resolve inherent stress. By now, many Drosophila mutations are known to impose stress in the ER, and a number of these appear similar to those that underlie human diseases. In addition, studies have employed the strategy of overexpressing human mutations in Drosophila tissues to perform genetic modifier screens. The fact that the basic UPR pathways are conserved, together with the availability of many human disease models in this organism, makes Drosophila a powerful tool for studying human disease mechanisms. [BMB Reports 2015; 48(8): 445-453]

Analysis of studies on Maekmundong-tang (맥문동탕(麥門冬湯)에 대한 연구 논문 분석)

  • Kim, Hyoung-Won;Yang, Su-Young;Kim, Min-Hee;NamGung, Uk;Park, Yang-Chun
    • Journal of Haehwa Medicine
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    • v.19 no.2
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    • pp.165-171
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    • 2011
  • Objectives: This study analyzed the contents of the research papers of Maekmundong-tang (MMDT). This study was conducted to help development of new clinical application and clinical studies for treating COPD with Oriental medicine. Materials and Methods: We inspected 26 theses and scrutinized their classification, objective diseases, study design, participants, methodological quality of clinical trial. Results: The following results were obtained in this study. 1. The studies of MMDT started in 1989 and have continuously increased, but it decreased recently. 2. The studies were mainly focused on experimental models rather than clinical studies. The topics of studies were mainly relaxation of airway contraction and anti-asthmatic effect. 3. MMDT was showed to have effects on chronic cough and asthma in these papers. Conclusion: MMDT is being used in respiratory disease. However, mechanism study should be conducted at experimental study and more clinical studies on the efficacy of MMDT for chronic respiratory disease are needed.

Temporal Changes in the Hepatic Fatty Liver in Mice Receiving Standard Lieber-DeCarli Diet

  • Yin, Hu-Quan;Lee, Byung-Hoon
    • Toxicological Research
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    • v.24 no.2
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    • pp.113-117
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    • 2008
  • Chronic exposure to ethanol induces cumulative damage to the liver starting from fatty infiltration to cirrhosis depending on the dose and duration of exposure. The whole process leading to the development of alcoholic liver disease is very complex and the mechanisms involved are not fully understood. Among many experimental animal models, Lieber-DeCarli liquid diet provides moderate to severe pathophysiological outcome depending on the compositional changes. In the present study, we investigated the temporal changes in the early phase hepatic disease in rats fed with standard Lieber-DeCarli diet. Male Wistar rats were fed with Lieber-Decarli ethanol diet for 6 weeks and the liver samples were obtained after 2, 4 and 6 weeks. Mild fatty infiltration was observed in 2 weeks of feeding and it became evident in 4 and 6 week samples. The level of hepatic triglyceride showed a good agreement with the data obtained in the pathological analysis. Feeding mice with ethanol diet resulted in the maturation and translocation of SREBP-1 to nucleus in the liver. Western blot analysis of the pooled liver sample of control and ethanol fed animals showed a clear-cut time-dependent increase in the expression of nSREBP-1. These data provide important information for selecting proper time point in experimental intervention study in the field of drug development for alcoholic liver disease.

Perspectives for Ginsenosides in Models of Parkinson's Disease

  • Wei-Ming, Lin;Gille, Gabriele;Radad, Khaled;Rausch, Wolf-Dieter
    • Journal of Ginseng Research
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    • v.31 no.3
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    • pp.127-136
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    • 2007
  • Ginseng, the root of Panax species, is a well-known herbal medicine. It has been used as traditional medicine in Korea, China and Japan for thousands of years and now is a popular and worldwide natural medicine. The active principles of ginseng are ginsenosides which are also called ginseng saponins. Traditionally ginseng has been used primarily as a tonic to invigorate weak body functions and help the restoration of homeostasis. Current in vivo and in vitro studies demonstrate its beneficial effects in a wide range of pathological conditions such as cardiovascular diseases, cancer, immune deficiency and hepatotoxicity. Moreover, recent research indicates that some of ginseng's active ingredients exert beneficial actions on aging and neurodegenerative disorders such as Parkinson´s disease. Essentially, antioxidant, antiinflammatory, anti-apoptotic and immunostimulant activities are mostly underlying the postulated ginseng-mediated protective mechanisms. Next to animal studies, data from neural cell cultures contribute to the understanding of these mechanisms which involve decreasing nitric oxide, scavenging of free radicals and counteracting excitotoxicity. This paper focuses on own and other neuroprotective data on ginseng for dopaminergic neurons and intends to show aspects where neuroprotection e.g. by ginsenosides, additionally or preceding standard Parkinson therapy, could come about as a valuable contribution to slow neurodegenerative processes.

Cardiovascular Diseases and Panax ginseng: A Review on Molecular Mechanisms and Medical Applications

  • Kim, Jong-Hoon
    • Journal of Ginseng Research
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    • v.36 no.1
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    • pp.16-26
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    • 2012
  • Ginseng is one of the most widely used herbal medicines and is reported to have a wide range of therapeutic and pharmacological applications. Ginseng may also be potentially valuable in treating cardiovascular diseases. Research concerning cardiovascular disease is focusing on purified individual ginsenoside constituents of ginseng to reveal specific mechanisms instead of using whole ginseng extracts. The most commonly studied ginsenosides are $Rb_1$, $Rg_1$, $Rg_3$, $Rh_1$, Re, and Rd. The molecular mechanisms and medical applications of ginsenosides in the treatment of cardiovascular disease have attracted much attention and been the subject of numerous publications. Here, we review the current literature on the myriad pharmacological functions and the potential benefits of ginseng in this area. In vitro investigations using cell cultures and in vivo animal models have indicated ginseng's potential cardiovascular benefits through diverse mechanisms that include antioxidation, modifying vasomotor function, reducing platelet adhesion, influencing ion channels, altering autonomic neurotransmitters release, and improving lipid profiles. Some 40 ginsenosides have been identified. Each may have different effects in pharmacology and mechanisms due to their different chemical structures. This review also summarizes results of relevant clinical trials regarding the cardiovascular effects of ginseng, particularly in the management of hypertension and improving cardiovascular function.

Mitochondrial Complex I Inhibition Accelerates Amyloid Toxicity

  • Joh, Yechan;Choi, Won-Seok
    • Development and Reproduction
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    • v.21 no.4
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    • pp.417-424
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    • 2017
  • Alzheimer's disease (AD) is neurodegenerative disease, characterized by the progressive decline of memory, cognitive functions, and changes in personality. The major pathological features in postmortem brains are neurofibrillary tangles and amyloid beta ($A{\beta}$) deposits. The majority of AD cases are sporadic and age-related. Although AD pathogenesis has not been established, aging and declining mitochondrial function has been associated. Mitochondrial dysfunction has been observed in AD patients' brains and AD mice models, and the mice with a genetic defect in mitochondrial complex I showed enhanced $A{\beta}$ level in vivo. To elucidate the role of mitochondrial complex I in AD, we used SH-SY5Y cells transfected with DNA constructs expressing human amyloid precursor protein (APP) or human Swedish APP mutant (APP-swe). The expression of APP-swe increased the level of $A{\beta}$ protein in comparison with control. When complex I was inhibited by rotenone, the increase of ROS level was remarkably higher in the cells overexpressing APP-swe compared to control. The number of dead cell was significantly increased in APP-swe-expressing cells by complex I inhibition. We suggest that complex I dysfunction accelerate amyloid toxicity and mitochondrial complex I dysfunction in aging may contribute to the pathogenesis of sporadic AD.

Adenosine monophosphate-activated protein kinase in diabetic nephropathy

  • Kim, Yaeni;Park, Cheol Whee
    • Kidney Research and Clinical Practice
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    • v.35 no.2
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    • pp.69-77
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    • 2016
  • Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and its pathogenesis is complex and has not yet been fully elucidated. Abnormal glucose and lipid metabolism is key to understanding the pathogenesis of DN, which can develop in both type 1 and type 2 diabetes. A hallmark of this disease is the accumulation of glucose and lipids in renal cells, resulting in oxidative and endoplasmic reticulum stress, intracellular hypoxia, and inflammation, eventually leading to glomerulosclerosis and interstitial fibrosis. There is a growing body of evidence demonstrating that dysregulation of 50 adenosine monophosphate-activated protein kinase (AMPK), an enzyme that plays a principal role in cell growth and cellular energy homeostasis, in relevant tissues is a key component of the development of metabolic syndrome and type 2 diabetes mellitus; thus, targeting this enzyme may ameliorate some pathologic features of this disease. AMPK regulates the coordination of anabolic processes, with its activation proven to improve glucose and lipid homeostasis in insulin-resistant animal models, as well as demonstrating mitochondrial biogenesis and antitumor activity. In this review, we discuss new findings regarding the role of AMPK in the pathogenesis of DN and offer suggestions for feasible clinical use and future studies of the role of AMPK activators in this disorder.

Implementation of Cough Detection System Using IoT Sensor in Respirator

  • Shin, Woochang
    • International journal of advanced smart convergence
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    • v.9 no.4
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    • pp.132-138
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    • 2020
  • Worldwide, the number of corona virus disease 2019 (COVID-19) confirmed cases is rapidly increasing. Although vaccines and treatments for COVID-19 are being developed, the disease is unlikely to disappear completely. By attaching a smart sensor to the respirator worn by medical staff, Internet of Things (IoT) technology and artificial intelligence (AI) technology can be used to automatically detect the medical staff's infection symptoms. In the case of medical staff showing symptoms of the disease, appropriate medical treatment can be provided to protect the staff from the greater risk. In this study, we design and develop a system that detects cough, a typical symptom of respiratory infectious diseases, by applying IoT technology and artificial technology to respiratory protection. Because the cough sound is distorted within the respirator, it is difficult to guarantee accuracy in the AI model learned from the general cough sound. Therefore, coughing and non-coughing sounds were recorded using a sensor attached to a respirator, and AI models were trained and performance evaluated with this data. Mel-spectrogram conversion method was used to efficiently classify sound data, and the developed cough recognition system had a sensitivity of 95.12% and a specificity of 100%, and an overall accuracy of 97.94%.

Botulinum Toxin A Ameliorates Neuroinflammation in the MPTP and 6-OHDA-Induced Parkinson's Disease Models

  • Ham, Hyeon Joo;Yeo, In Jun;Jeon, Seong Hee;Lim, Jun Hyung;Yoo, Sung Sik;Son, Dong Ju;Jang, Sung-Su;Lee, Haksup;Shin, Seung-Jin;Han, Sang Bae;Yun, Jae Suk;Hong, Jin Tae
    • Biomolecules & Therapeutics
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    • v.30 no.1
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    • pp.90-97
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    • 2022
  • Recently, increasing evidence suggests that neuroinflammation may be a critical factor in the development of Parkinson's disease (PD) in addition to the ratio of acetylcholine/dopamine because dopaminergic neurons are particularly vulnerable to inflammatory attack. In this study, we investigated whether botulinum neurotoxin A (BoNT-A) was effective for the treatment of PD through its anti-neuroinflammatory effects and the modulation of acetylcholine and dopamine release. We found that BoNT-A ameliorated MPTP and 6-OHDA-induced PD progression, reduced acetylcholine release, levels of IL-1β, IL-6 and TNF-α as well as GFAP expression, but enhanced dopamine release and tyrosine hydroxylase expression. These results indicated that BoNT-A had beneficial effects on MPTP or 6-OHDA-induced PD-like behavior impairments via its anti-neuroinflammation properties, recovering dopamine, and reducing acetylcholine release.