• Title/Summary/Keyword: disease-model animal

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Review of Experimental Researches on Gastrointestinal Activity of Agastache rugosa (Fisch. & C. A. Mey.) Kuntze and Pogostemon cablin (Blanco) Benth. (곽향(藿香) 및 광곽향(廣藿香)의 위장관 효능에 대한 실험연구 고찰)

  • Jerng, Ui Min;Oh, Yong Taek;Kim, Jung Hoon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.31 no.2
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    • pp.138-144
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    • 2017
  • The pharmacological rationale of Agastache rugosa (AR) or Pogostemon cablin (PC), which have been used in traditional Korean medicine to treat dampness pattern or syndrome in gastrointestinal tract, was investigated on the gastrointestinal disorders. In-vivo model studies that examined the effect on the gastrointestinal disorders of AR or PC were collected. They were classified into disease-induced in-vivo models or non-disease in vivo models. The target disease, animal species, induction method, administration, and outcomes (changes in morphological and histological parameter, or blood and fluid) of each study were analyzed. The therapeutic mechanism of AR or PC extract was evaluated by the induced diseases and the changes in outcomes. There were contradictory reports on gastrointestinal motility of AR or PC in disease non-disease in-vivo model. AR or PC inhibited gastrointestinal motility in disease model of increased gastrointestinal motility, while promoted motility in disease model of decreased gastrointestinal motility. AR or PC also inhibited inflammatory changes in gastrointestinal inflammation model. These results suggest that the bidirectional regulation of gastrointestinal motility and the improvement of gastrointestinal inflammatory disorders might underpin traditional therapeutic effect of AR or PC, that is effect to resolve dampness of gastrointestinal tract.

Generation of Transgenic Mice with Overexpression of Mouse Resistin

  • Lee, H. T.;J. R. Chun.;K. S. Chung
    • Korean Journal of Animal Reproduction
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    • v.26 no.4
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    • pp.321-328
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    • 2002
  • The hormone resistin is associated with type II diabetes mellitus in rodent model. Resistin impairs glucose tolerance and insulin action. A new class of anti-diabetic drugs were called thiazolidinediones (TZDs) downreguates a resistin. Resistin gene expression is induced during adipocyte differentiation and resistin polypeptide is secreted by adipocytes. But, the correlation between increased adiposity and resistin remains unknown. The objectives of this study was to clone a mouse resistin CDNA and to generate transgenic mice overexpressing mouse resistin gene. The pCMV-mus/resistin gene was prepared from previous recombinant pTargeT$^{TM}$-mus/resistin by digestion of Bgl II, and has used for microin- jection into pronuclei of one cell embryos. Mouse resistin expression was detected in transgenic F$_1$mice by RT-PCR. The transgenic mouse with resistin gene expression has heavier body weight which was measured higher level of plasma glucose than that of normal mouse. And in diet-induced experiments, in fasting group, resistin expression was higher than that of re-feeding group. This result demonstrates that the resistin gene overexpressing mice may be became to obesity and be useful as an animal disease model to be diabetes caused by insulin resistance of resistin.n.

Production and Characterization of a Transgenic Mouse Model of Human Liver Cancer (형질 전환 기법을 이용한 인체 간암의 마우스 모델 제작 및 특성 규명)

  • Li, Zhong-Shu;Lee, Jung-Woong;Hyun, Byung-Hwa;Lee, Chul-Ho;Jeong, Kyu-Shick;Fang, Nan-Zhu;Yeom, Young-Il
    • Reproductive and Developmental Biology
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    • v.31 no.3
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    • pp.145-152
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    • 2007
  • Transgenic mice were generated by microinjecting a plasmid DNA containing the SV40 (simian virus 40) large T antigen (Tag) gene fused with mouse albumin promoter/enhancer sequences into fertilized one-cell mouse embryos. Among eleven founder transgenic animals, four developed hepatocellular carcinoma, two showed kidney cancer and one developed skin and brain tumors. Three stable transgenic lines, #1-2, #1-6 and #1-11 were established. Members of the lines #1-6 and #1-11 reproducibly developed liver tumors by 8 to 10 weeks of age but did not exhibit any phenotypic changes in other tissues. Histological changes loading to liver tumor formation occurred with predictable kinetics and could be classified into three distinct stages; (a) newborn to 3 weeks of age, characterized by hyperplastic hepatocytes with reduced amounts of cytoplasm without any nuclear alterations, (b) between 4 to 8 weeks of age, characterized by diffuse liver cell dysplasia without observable tumor nodules, and (c) 9 weeks of age and thereafter, characterized by hepatocellular carcinomas in the background of extensive liver dysplasia. Metastasis to the lung from a liver carcinoma was observed in #1-11 founder animal. This transgenic mouse system displays similarities with human liver cancers in a number of aspects and provides a useful model for the study of molecular events involved in hepatocarcinogenesis.

A Study on the Introduction of Livestock U-healthcare (가축 U-Healthcare 도입방안 연구)

  • Koo, Jee-Hee;Jung, Tae-Woong;Ahn, Ji-Yeon;Lee, Sang-Rak
    • Journal of Animal Environmental Science
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    • v.18 no.2
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    • pp.85-90
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    • 2012
  • In Korea, livestock has grown into the most value-added business in the agricultural and forest industry. But due to the recent outbreak of deadly infectious diseases such as foot-and-mount disease and avian influenza (AI), the demand for IT-enabled cutting-edge management system is getting stronger. As for humans, pilot projects and researches concerning U-healthcare have been carried out since early 2000. So this study explored the current progress of U-healthcare introduction, and suggested the strategies to develop technologies of collecting, processing, and utilizing information; to apply elements for a service model development and prioritization; to provide policy and institutional support. Therefore it is expected to vitalize the livestock U-healthcare in the future through continuous study based on these results.

A Study on Brain Disease Research Trends and Need to Conduct Mechanism Studies on Temporomandibular Joint Disorder Related Cerebrovascular Diseases (뇌질환 연구 동향 조사 및 턱관절 장애 관련 뇌질환 기전 연구의 필요성)

  • Lee, Se-Eun;Lee, Min Ji;Lee, Byoungho;Lim, Sehyun;Cho, Suin
    • Journal of TMJ Balancing Medicine
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    • v.8 no.1
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    • pp.11-15
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    • 2018
  • Recently, clinical efficacies of the intraoral balancing appliance therapy have been reported by several researchers, and it has been found that there are various kinds of diseases that can be effectively applied. However, studies on cerebrovascular disease, one of the main diseases with a high mortality rate, are still poorly reported, and studies of temporomandibular joint disorder (TMD)-induced changes in brain function suggest that cerebrovascular disease is more appropriate as an adaptive disorder of the temporomandibular joint (TMJ) balancing device. In the developed countries, the importance of research on the structure and function of the brain has been recognized and spurred on the related research. In Korea, the research on brain function and cognitive disorders should have promoted more massively. In order to regain its former reputation in the Korean medicine in the field of cerebrovascular disease, it should be spurred on basic research and clinical case studies. In addition, extensive and in-depth studies including animal studies are needed to establish the basis of underlying mechanisms of the TMJ balancing therapies.

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Improvement of Motor Behavior of Parkinson′s Disease Animal Model by Nurr1-Transfected Human Embryonic Stem Cells.

  • Lee, Chang-Hyun;Cho, Hwang-Yoon;Kil, Kwang-Soo;Lee, Gun-Soup;Yoon, Ji-Yeon;Lee, Young-Jae;Kim, Eun-Young;Park, Se-Pill;Lim, Jin-Ho
    • Proceedings of the Korean Society of Developmental Biology Conference
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    • 2003.10a
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    • pp.103-103
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    • 2003
  • The purpose of this study is to evaluate an efficacy of in vitro differentiated human embryonic stem (hES, MB03) cells expressing Nurr1 in relief of symptomatic motor behavior of Parkinson's disease (PD) animal models MB03 was genetically modified to express Nurr1 protein and was induced to differentiate according to 2-/4+ protocol using retinoic acid and ascorbic acid. The differentiation-induced cells were selected for 10 to 20 days thereafter in N2 medium. Upon selection, cells expressing GFAP, TH, or NF200 were 38.8%, 11%, and 20.5%, respectively. in order to examine therapeutic effects of the differentiated cells in PD animal model, rats were unilaterally lesioned by administration of 6-kydroxydopamine HCI (6-OHDA) into medial forebrain region (MFB, AP -4.4 mm, ML 1.2 mm, DV 78 mm with incision bar set at -2.4 mm), as a reference to bregma and the surface of the skull. Confirmation of successful lesion by apomorphine-induced rotational behavior, differentiated cells were transplanted into the striatum (AP 1.0, ML 3.5, DV -5.0; AP 0.6, ML 2.5, DV -4.5). Improvements of asymmetric motor behavior by the transplantation were examined every two weeks after the surgery. In two weeks, numbers of rotation by the experimental rats were $-14.8 \pm 33.9%$ (P<0.05) of the number before transplantation, however, the ratio increased slightly to $13.6 \pm 56.3%$ in six weeks. In contrast, the ratio of sham-grafted animals ranged from 112.3+8.5% to 139.2+28.9% during the examination. Immunohistochemical studies further confirmed the presence, survival, migration, and expression of TH of the transplanted human cells.

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Induced neural stem cells from human patient-derived fibroblasts attenuate neurodegeneration in Niemann-Pick type C mice

  • Hong, Saetbyul;Lee, Seung-Eun;Kang, Insung;Yang, Jehoon;Kim, Hunnyun;Kim, Jeyun;Kang, Kyung-Sun
    • Journal of Veterinary Science
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    • v.22 no.1
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    • pp.7.1-7.13
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    • 2021
  • Background: Niemann-Pick disease type C (NPC) is caused by the mutation of NPC genes, which leads to the abnormal accumulation of unesterified cholesterol and glycolipids in lysosomes. This autosomal recessive disease is characterized by liver dysfunction, hepatosplenomegaly, and progressive neurodegeneration. Recently, the application of induced neural stem cells (iNSCs), converted from fibroblasts using specific transcription factors, to repair degenerated lesions has been considered a novel therapy. Objectives: The therapeutic effects on NPC by human iNSCs generated by our research group have not yet been studied in vivo; in this study, we investigate those effects. Methods: We used an NPC mouse model to efficiently evaluate the therapeutic effect of iNSCs, because neurodegeneration progress is rapid in NPC. In addition, application of human iNSCs from NPC patient-derived fibroblasts in an NPC model in vivo can give insight into the clinical usefulness of iNSC treatment. The iNSCs, generated from NPC patientderived fibroblasts using the SOX2 and HMGA2 reprogramming factors, were transplanted by intracerebral injection into NPC mice. Results: Transplantation of iNSCs showed positive results in survival and body weight change in vivo. Additionally, iNSC-treated mice showed improved learning and memory in behavior test results. Furthermore, through magnetic resonance imaging and histopathological assessments, we observed delayed neurodegeneration in NPC mouse brains. Conclusions: iNSCs converted from patient-derived fibroblasts can become another choice of treatment for neurodegenerative diseases such as NPC.

Effect of Polylysine on Scrapie Prion Protein Propagation in Spleen during Asymptomatic Stage of Experimental Prion Disease in Mice

  • Titlow, William B.;Waqas, Muhammad;Lee, Jihyun;Cho, Jae Youl;Lee, Sang Yeol;Kim, Dae-Hwan;Ryou, Chongsuk
    • Journal of Microbiology and Biotechnology
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    • v.26 no.9
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    • pp.1657-1660
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    • 2016
  • Prion diseases are incurable neurodegenerative disorders. Our previous study demonstrated that polylysine was effective in prolonging the incubation period in a rodent model and in alleviating the scrapie prion protein (PrPSc) burden in the brain at the terminal stage of the disease. Here, we report that intraperitoneal administration of polylysine suppresses the accumulation of prions in the spleen during the early stages of the disease. This study supports the congruence of PrPSc inhibition by polylysine in both the spleen and brain.