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Jong-Seon Byun,Yoon Hee Han,Sung-Jun Hong,Sung-Mi Hwang,Yong-Soo Kwon,Hee Jae Lee,Sung-Soo Kim,Myong-Jo Kim,Wanjoo Chun 대한생리학회-대한약리학회 2010 The Korean Journal of Physiology & Pharmacology Vol.14 No.5
Urushinol, a plant allergen, has significantly restricted the medical application of Rhus verniciflua, although it has been reported to possess a wide variety of biological activities such as anti-inflammatory, antioxidant, and anti-cancer actions. To reduce the urushinol content while maintaining the beneficial biological activities, mushroom-mediated fermentation of Rhus verniciflua was carried out and this method resulted in significantly attenuated allergenicity [1]. In the present study, to examine the neuroprotective properties of mushroom-fermented stem bark of Rhus verniciflua, two constituents were isolated from mushroom-fermented bark and their neuroprotective properties were examined in a mouse model of kainic acid (KA)-induced excitotoxicity. KA resulted in significant apoptotic neuronal cell death in the CA3 region of mouse hippocampus. However, seven daily administrations of RVH-1 or RVH-2 prior to KA injection significantly attenuated KA-induced pyramidal neuronal cell death in the CA3 region. Furthermore, pretreatment with RVH-1 and RVH-2 also suppressed KA-induced microglial activation in the mouse hippocampus. The present study demonstrates that RVH-1 and RVH-2 isolated from Rhus verniciflua and detoxified using mushroom species possess neuroprotective properties against KA-induced excitotoxicity. This leads to the possibility that detoxified Rhus verniciflua can be a valuable asset in herbal medicine.
Jong-Seon Byun,Sang-Hyun Lee,Seong-Ho Jeon,Yong-Soo Kwon,Hee Jae Lee,Sung-Soo Kim,Young-Myeong Kim,Myong-Jo Kim,Wanjoo Chun 대한생리학회-대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.4
Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS<sup>−/−</sup>) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.
Short Segment Hiatal Hernia: Is It a Clinically Significant Entity?
( Jong Jin Hyun ),( Ji Hoon Kim ),( Jong Eun Yeon ),( Jong Jae Park ),( Jae Seon Kim ),( Kwan Soo Byun ),( Young Tae Bak ) 대한소화기기능성질환·운동학회 2010 Journal of Neurogastroenterology and Motility (JNM Vol.16 No.1
Introduction: Hiatal hernia (HH) is a well-known contributory factor of gastroesophageal reflux disease (GERD). However, studies on the clinical significance of simple small HH are Lacking. We conducted a study to clarify the clinical significance of short segment HH (SSHH) in relation to GERD. Methods: 4,592 consecutive cases (male/female: 2,076/2,516, median age: 49 years) examined with diagnostic esophagogastroduodenoscopy for the first time were enrolled. During the insertion of endoscope, presence of HH was determined and the Length was measured, if present. The relationships between gender, age, presence of erosive esophagitis, and columnar-lined esophagus (CLE) and the Lengths of HH were analyzed. Results: Among 4,592 cases, HH was present in 428 cases (9.3%); SSHH was found in 255 cases (5.6%) and Long segment HH (LSHH) in 173 cases (3.8%). HH was more frequent among males and patients with LSHH tended to be older. Erosive esophagitis was observed in 4.8%, 22.0%, and 37.0% of no HH, SSHH, and LSHH group, respectively (p 0.05). CLE was observed in 14.4%, 36.5%, and 24.3% of no HH, SSHH, and LSHH group, respectively (p 0.05). Conclusions: SSHH is not a clinically silent and innocent entity, but rather a condition with a significant pathologic significance similar to LSHH in regard to GERD.(J Neurogastroenterol Motil 2010;16:35-39)
Byun, Jong-Seon,Lee, Sang-Hyun,Jeon, Seong-Ho,Kwon, Yong-Soo,Lee, Hee-Jae,Kim, Sung-Soo,Kim, Young-Myeong,Kim, Myong-Jo,Chun, Wan-Joo The Korean Society of Pharmacology 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.4
Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice ($iNOS^{-1-}$) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.
Byun, Jong-Seon,Han, Yoon-Hee,Hong, Sung-Jun,Hwang, Sung-Mi,Kwon, Yong-Soo,Lee, Hee-Jae,Kim, Sung-Soo,Kim, Myong-Jo,Chun, Wan-Joo The Korean Society of Pharmacology 2010 The Korean Journal of Physiology & Pharmacology Vol.14 No.5
Urushinol, a plant allergen, has significantly restricted the medical application of $Rhus$ $verniciflua$, although it has been reported to possess a wide variety of biological activities such as anti-inflammatory, antioxidant, and anti-cancer actions. To reduce the urushinol content while maintaining the beneficial biological activities, mushroom-mediated fermentation of $Rhus$ $verniciflua$ was carried out and this method resulted in significantly attenuated allergenicity [1]. In the present study, to examine the neuroprotective properties of mushroom-fermented stem bark of $Rhus$ $verniciflua$, two constituents were isolated from mushroom-fermented bark and their neuroprotective properties were examined in a mouse model of kainic acid (KA)-induced excitotoxicity. KA resulted in significant apoptotic neuronal cell death in the CA3 region of mouse hippocampus. However, seven daily administrations of RVH-1 or RVH-2 prior to KA injection significantly attenuated KA-induced pyramidal neuronal cell death in the CA3 region. Furthermore, pretreatment with RVH-1 and RVH-2 also suppressed KA-induced microglial activation in the mouse hippocampus. The present study demonstrates that RVH-1 and RVH-2 isolated from $Rhus$ $verniciflua$ and detoxified using mushroom species possess neuroprotective properties against KA-induced excitotoxicity. This leads to the possibility that detoxified $Rhus$ $verniciflua$ can be a valuable asset in herbal medicine.
내시경 검사시 Phenol Red 분무에 의한 Helicobacter pylori 감염 진단의 의의
김종극(Jong Guk Kim),이창홍(Chang Hong Lee),박영태(Young Tae Bak),김진호(Jin Ho Kim),원남희(Nam Hee Won),김재선(Jae Seon Kim),변관수(Kwan Soo byun) 대한소화기학회 1993 대한소화기학회지 Vol.25 No.1
N/A A strong association between Helicobacter pylori (H. pylori) and chronic active inflammation of the gastric antrum and duodenal ulceration has been recognized. Although various rnethods have been proposed to detect this microorganism, no unanimity exists among investigators concerning which method represents a gold standard. H. pylori producee urease that converts urea to ammonia which then raises the pH, therefore we have utilized an endoscopic spray technique using phenol red (pH indicator) in vivo to assess H. pylori infection itself and its distribution. 87 patients with dyspepsia were pre-medicated with ranitidine 150 mg p.o. 3 houre before endoscopy to maintain a gastric pH between 3-6. During endoscopy, 20 ml of a mixture containing 0.05% phenol red and 0.5% urea was sprayed over the antral mucosa using a spray catheter. It was defined as positivc if any area of the mucosa turned red within 3 min after spraying. Antral biopsies were taken from all patients. Biopsies were assessed in a blind fashion after H&E, Giemsa and Warthin-Starry silver stain. The phenol red positive patients were 54.0%, and diffuse pattern of positive staining was 85.1% and regional pattern was 14.9%. Diagnostic sensitivity and specificity of the endoscoic spray technique were 87.2%. and 85.0% respectively. In conclusion, the endoscopic phenol red spray technique may be one of the simple and useful screening tests for diagnosis of H. pylori infection and for dilineating its probahle pattern of distributionvn gastric mucosa in vivo, but this method seems not useful for confirmatory diagnosis of H. pylori infection and needs further study.
김종극(Jong Guk Kim),이창홍(Chang Hong Lee),박영태(Young Tae Bak),김진호(Jin Ho Kim),김재선(Jae Seon Kim),변관수(Kwan Soo byun),지종대(Jong Dae Ji),송훤택(Hwun Taig Song) 대한소화기학회 1993 대한소화기학회지 Vol.25 No.4
N/A Adenomatous polyps are known to be precursors for cancer, and identifying of persons with adenomatous polyps is practically important because these individuals should constitute a disproportionate percentage of persons destined to have colorectal cancer. There is enough reason to believe that regclar endoscopic screening of persons with adenomatous polyps and removal of these polyps can reduce the incidence of colorectal cancer. But hyperplastic colonic polyps are generally regarded as being of little or no clinical consequence. Recentlyl, however, controversy has not been settled down on the significance of distal colonic hyperplastic polyp as a marker for proximal colonic adenomatous polyp (s). To establish the prevalence of proximal neoplasms in subjects with or without hyperplastic polyps in distal colon and to determine whether the presence of hypcrplastic polyps in the distal colon could serve as a market for proximal synchronous adenomatous colonic polyps, we prospectively analyzed 895 consecutive subjects who were examined with colcnoscopy between March 1990 and October l992. 191 of 895 subjects (21.4%) had one or more colonic polyps. The prevalence of adenomatous polyps alone was 10.2% hyperplastic polyps 8.4%, and both 1.9%. The proportion of subjects with both proximal adenomatous polyp and distal hyperplastic polyps (6.0%) was not significantly different from the proportion of those without distal hyperplistic polyps(5.1%), But subjects with distal adenomatous polyps (s) were si!nificantly more likely to have proximal adenomatous polyp (s) than those without distal adenomatous polyp (s). The result of this study suggests that hyperplastir. polyps of distal colon do not serve as a marker for neoplastic polyps of proximai colon.
장결핵의 감별진단에 있어서 3 개월 추적 대장내시경 검사의 의의
연종은(Jong Eun Youn),박이병(Ie Byung Park),권소영(So Yung Kwon),김재선(Jae Seon Kim),변관수(Kwan Soo Byun),박영태(Young Tae Bak),김종극(Jong Guk Kim),이창홍(Chang Hong Lee),김진호(Jin Ho Kim) 대한내과학회 1996 대한내과학회지 Vol.50 No.2
N/A Objectives: A therapeutic trial with antituberculous drugs is reasonable if the clinical and colonoscopic features are compatible, in countries with a high prevalence of intestinal tuberculosis. But Crohn's disease, lymphoma and other infectious disease should be differentiated from the disease. There have been no established monitoring modalities to assess the efficacy of the therapeutic trial and to differentiate these diseases yet. Therefore, this study was done to assess the usefulness of follow-up colonoscopy at 3 months of antituberculous treatment as a monitoring modality. Methods: 42 patients with tentative diagnosis of intestinal tuberculosis which was made on the basis of clinical and colonoscopic findings were enrolled, The patients were divided into 2 groups according to the symptomatic improvement after the therapy : (A) 30 patients with improved symptom : (B) 12 patients with persistent symptom. Colonoscopy with biopsy was performed before and at 3 months of therapeutic trial. Standard four-drug antituberculous chemotherapy was done at least for 9 months and patients were followed for more than a year after completion of therapy. Final diagnoses were made on the basis of satisfactory outcome of therapeutic trial, operative findings and another follow-up colonoscopy. Results: 1) colonscopic findings at 3 months of therapy improved in 31 cases. 27 of them were finally diagnosed as tuberculosis, 1 was as ulcerative colitis and 3 were lost. Among 11 endoscopically unimproved cases, 7 were finally diagnosed as Crohn's disease, 2 were as tuberculosis and 2 were lost. 2) 27 of 29 patients with final diagnosis of intestinal tuberculosis improved colonoscopically at 3 months of therapy. 2 unimproved cases had a complicated disease(stenosis) or an atypical mycobacterial infection, respectively. 3) In group A, 1 was diagnosed as ulcerative colitis and in group H, 3 were diagnosed as tuberculosis finally. Conclusion: Follow-up colonoscopy at 3 months of antituberculous therapeutic trial in patients with tentative diagnosis of intestinal tuberculosis seems to be a valuable modality for monitoring the efficacy of therapy and differentiating intestinal tuberculosis from other diseases.