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열공형과 비열공형 피질하 혈관성 치매에서 위험인자의 차이에 관한 비교 연구
배희준,정지향,유경호,나덕렬,김상윤,최경규,양동원,손의주,이상도,김재우,박경원,김응규,이재홍,박미영,한일우,함동석,최문성,하충건,최성혜,이애영,이병철,한설희 대한치매학회 2003 Dementia and Neurocognitive Disorders Vol.2 No.2
Backgrounds and Objectives: Vascular dementia is a group of dementing disoders arising from various stroke syndrome. Among these. subcortical ischemic vascular dementia (SIVD) is regarded as a relatively distinct clinical entity. However, MRI patterns of SIVD are not homogenous. In some patients, lacunes are dominant, and in others, subcortical white matter changes are. This study was designed to compare risk factor profiles between SIVD with and without multiple lacunes. Methods: We divided 47 subjects (22 males, mean age. 68 years) recruited from VADAPET (Multicenter Trial For Evaluation Of The Changes In the PET Images Of Subcortical Vascular Dementia Patient) study into two groups one with more than 5 lacunes in deep gray matter (lacune group) and the other with 5 or less(non-lacune group) Clinical characteristics and laboratory findings of two groups were compared. Results: Nineteen of 47 patients (40%) belonged to the lacune group. The lacune and non-lacune groups d d not differ in the following variables: age, hypertension, diabetes mellitus, hyperlipidemia heart disease, history of stroke or TIA, history of trauma or major surgery, family history of hypertension stroke, or dementia, age at diagnosis of dementia, body mass index, white blood cell count, ESR, CRP, fibrinogen, hemoglobin A1C, total cholesterol. LDL cholesterol creatinine, proteinuria, glucosuria, and microhematuria. However, male sex, smoking alcohol. hemoglobin, and HDL cholesterol were possibly associated more with lacune group SIVD than with non-lacune group (p<0 1) Multivariate analyses revealed that smoking, hemoglobin, and HDL cholesterol were independent predictors of SIVD with multiple lacunes Conclusion: Our study suggests that SIVD with multiple lacunes may be significantly different in smoking habits hemoglobin, and HDL cholesterol from SIVD without multiple lacunes.
Park, Yang-Gyu,Jeong, Jae-Kyo,Lee, Ju-Hee,Lee, You-Jin,Seol, Jae-Won,Kim, Shang-Jin,Hur, Tai-Young,Jung, Young-Hun,Kang, Seog-Jin,Park, Sang-Youel D.A. Spandidos 2013 International journal of molecular medicine Vol.31 No.2
<P>Prion disorder-related neurodegenerative diseases are characterized by the accumulation of prion protein (PrP) scrapie isoform (PrPsc) within the central nervous system. PrPsc induces neuronal cell death by increasing intracellular generation of reactive oxygen species (ROS). Lactoferrin (LF) is an 80 kDa protein, which has antioxidant abilities due to the scavenging of ROS. The effects of LF treatment on PrP (106-126)-mediated neurotoxicity and ROS generation were the focus of this study. LF treatment protected against PrP (106-126)-induced neuronal cell death and decreased ROS generation. The reduced ROS generation prevented PrP (106-126)-induced mitochondrial dysfunction. Moreover, PrP (106-126)-induced protein activation including c-Jun N-terminal kinase and caspase-3 were blocked by LF treatment. These results demonstrated that LF protects neuronal cells against PrP (106-126)-mediated neurotoxicity through the scavenging of ROS and provide evidence that LF treatment prevents neuronal cell death caused by PrP (106-126).</P>
Baicalein inhibits tumor progression by inhibiting tumor cell growth and tumor angiogenesis
Park, Yang-Gyu,Choi, Jawun,Jung, Hye-Kang,Kim, Bumseok,Kim, Chan,Park, Sang-Youel,Seol, Jae-Won NATIONAL HELLENIC RESEARCH FOUNDATION 2017 ONCOLOGY REPORTS Vol.38 No.5
<P>Baicalein, a herbal medicine, is a natural flavonoid isolated from the roots of Scutellaria baicalensis Georgi. It is known for its anticancer, anti-inflammatory and neuroprotective properties. Despite these well-known properties, it is not yet clear what effect baicalein has on tumor progression. Therefore, in the present study, we used B16F10 cells, Lewis lung carcinoma (LLC) cells, and human umbilical vein endothelial cells (HUVECs) to investigate the effect of baicalein on cell proliferation and viability, migration and tube formation in vitro. In addition, an experimental animal model was used to observe the growth rate and metastasis of tumors and tumor vessel formation in vivo. Our results showed that baicalein decreased the proliferation and migration and induced tumor cell death via caspase-3 activation in the B16F10 and LLC cells, and strongly inhibited tube formation and cell migration in HUVECs. Furthermore, mouse models showed that baicalein reduced the tumor volume and greatly reduced the tumor growth rate in the early stages of tumor progression, and the baicalein-treated groups had significantly reduced expression of CD31 (endothelial cell marker) and alpha-SMA (mural cell marker) in the tumors, indicating that baicalein inhibits tumor angiogenesis by disrupting tumor vasculature development. Comparison of the lymph node and lung samples collected from the baicalein-treated group, and the untreated group showed that baicalein reduced metastasis of the tumor to these tissues. In summary, baicalein reduced tumor progression and metastasis, directly induced tumor cell death, and inhibited tumor angiogenesis. Our results strongly demonstrate that baicalein is a potential chemotherapeutic agent.</P>
PARK, YANG-GYU,JEONG, JAE-KYO,MOON, MYUNG-HEE,LEE, JU-HEE,LEE, YOU-JIN,SEOL, JAE-WON,KIM, SHANG-JIN,KANG, SEOG-JIN,PARK, SANG-YOUEL Spandidos Publications 2012 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.30 No.5
<P>Insulin-like growth factor-1 (IGF-1) is one of the most important components of bovine colostrum. It exhibits antiapoptotic and antioxidative activities. Prion diseases are neurodegenerative disorders caused by cell death through mitochondrial dysfunction and increasing generation of reactive oxygen species (ROS). This study examined the protective effect of IGF-1 on residues 106-126 of the cellular prion protein [PrP (106-126)]-mediated mitochondrial neurotoxicity and oxidative stress. In SH-SY5Y human neuronal cells, treatment with PrP (106-126) decreased the cell viability and IGF-1 pretreatment markedly blocked the PrP?(106-126)-induced neuronal cell death. IGF-1 inhibited PrP?(106-126)-induced intracellular ROS generation and mitochondrial oxidative stress. In addition, IGF-1 blocked the translocation of the Bax protein to the mitochondria induced by PrP (106-126). These results demonstrate that IGF-1 protects neuronal cells against PrP (106-126)-mediated neurotoxicity through an antioxidative effect and blockage of mitochondrial Bax translocation. The results also suggest that regulation of IGF-1 secretion may have a therapeutic potential in the management of mitochondrial dysfunction and oxidative stress-induced neurodegeneration.</P>
Park, Yang-Gyu,Choi, Jawun,Jung, Hye-Kang,Song, In Kyu,Shin, Yongwhan,Park, Sang-Youel,Seol, Jae-Won UNKNOWN 2017 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.40 No.4
<P>Early pregnancy is characterized by an increase in the blood volume of the uterus for embryonic development, thereby exerting fluid shear stress (FSS) on the vascular walls. The uterus experiences vascular remodeling to accommodate the increased blood flow. The blood flow-induced FSS elevates the expression of vascular endothelial growth factors (VEGFs) and their receptors, and regulates vascular remodeling through the activation of VEGF receptor-3 (VEGFR-3). However, the mechanisms responsible for FSS-induced VEGFR-3 expression in the uterus during pregnancy are unclear. In this study, we demonstrate that vascular remodeling in the uterus during pregnancy is regulated by FSS-induced VEGFR-3 expression. We examined the association between VEGFR-3 and FSS through <I>in vivo</I> and <I>in vitro</I> experiments. <I>In vivo</I> experiments revealed VEGFR-3 expression in the CD31-positive region of the uterus of pregnant mice; VEGF-C (ligand for VEGFR-3) was undetected in the uterus. These results confirmed that VEGFR-3 expression in the endometrium is independent of its ligand. <I>In vitro</I> studies experiments revealed that FSS induced morphological changes and increased VEGFR-3 expression in human uterine microvascular endothelial cells. Thus, VEGFR-3 activation by FSS is associated with vascular remodeling to allow increased blood flow in the uterus during pregnancy.</P>