http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Helicobacter pylori의 Kato III 세포내 발견
백승철,이정희,고경혁,조명제,조중현,김유경,윤희상,이우곤,이광호,강수민 대한소화기학회 1998 대한소화기학회지 Vol.31 No.6
Background/Aims; Some investigaters reported that the invasion of H. pylori into the gastric epithelial cells or lamina propria had been detected by light microscopie examination using various staining methods (i,e. the Warthin-Starry stain, immunohistologic stain) or by electron microscopic examination. However, the results are hardly convinced because they may be nonspecifically stained, or the intracytoplasmic organelles of the gastric epithelial cells may be mistaken for bacteria. Thus, we combined an immunohistologic method with an electron microscopy to deterrnine whether H. pylori is invasive into the gastric epithelial cells. Metbods: To enhance bacterial invasion, we adapted an in vitro system using Kato III cells, a gastric carcinoma eell line. The cells were infected with H. pylori. The infection was confirmed by staining with polyelonal antibody against H. pylori. and an electron microscopy. Resnlts: H. pylori was found within the cytoplasm of several Kato III cells. The intracellular bacteria could be differentiated from intracellular organelles or other bacteria-looking materials by gold particles attached to the bacteria, Conclusions: We could not elucidate the invasiveness of H. pylori, but we found the presence of H. pylori in the cytoplasm of the Kato III cells. These results indicate that the invasiveness of H. pylori will remain as one of the factors participating in the pathogenesis oF H. pylori-induced chronic gastritis and peptic ulcer. Further studies will be needed to demonstrate the invasiveness of H. pylori.
당뇨병성 족부 합병증에 따른 하지 절단술의 위험 인자에 대한 분석
정홍근,김유진,심상호,김희진,Jung, Hong-Geun,Kim, You-Jin,Shim, Shang-Ho,Kim, Hee-Jin 대한족부족관절학회 2007 대한족부족관절학회지 Vol.11 No.2
Purpose: To evaluate the possible risk factors of lower extremity amputations in diabetic foot patients. Materials and Methods: The study is based on 37 patients who received lower extremity amputations from April, 1997 to February 2005 due to diabetic foot complications with at least 1 year follow up. As for the control group, 49 diabetes patients who had been treated at the endocrinology department for at least 1 year without any diabetic foot complication were evaluated. As for the possible risk factors, age, gender, duration of diabetes mellitus, body mass index, Hb A1c, blood glucose level, total cholesterol, s-creatinine, C-peptide, smoking, alcohol, hypertension, cardiovascular disease, CVA, retinopathy and neuropathy were investigated. Results: Among the possible risk factors evaluated, age, Hb A1c, smoking, neuropathy and blood glucose level factors showed statistically significant difference between the diabetic amputation and the control group. Conclusion: In reducing the risk of the lower extremity amputations in the diabetic patients due to diabetic foot complications, strict control of blood glucose level and cessation of smoking were found to be utmost important.
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,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>