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강혁주,김성욱,최석진,이중현,장재식,서영범,윤병구,박건욱,김성자,김용섭,강승완,이구,양창헌,이창우,김욱년,이광헌,서정일 동국대학교 의학연구소 2000 東國醫學 Vol.7 No.-
과립상 세포종은 Schwann 세포 기원으로 생각되며 인체에 비교적 드물게 발생한다. 과립상 세포종은 전신 어느 곳에서나 발견될 수 있으나 주로 혀, 구강, 피부 혹은 유방 등에서 호발하며 드물게 위장관에서 발견된다. 위장관에서는 식도에서 가장 호발하며 다음으로 위, 대장 순이다. 과립상 세포종은 대부분, 특히 위장관에서는 양성이며 소수의 악성 병변이 보고되었다. 이러한 이유와 함께 수술 전의 진단이 어렵기 때문에 과립상 세포종에 대한 근본적인 치료는 현재까지 외과적 절제술이다. 최근에 시도되는 치료방법들로는 내시경적 레이저 치료, 용종절제술, 내시경적 점막 절제술 등이 있다. 저자들은 상부 소화관 내시경검사를 시행하여 식도 과립상 세포종을 진단하고 내시경적 점막 절제술을 시행하여 합병증 없이 퇴원하여 현재 재발없이 경과 관찰중인 1례를 경험하였기에 보고하는 바이다. Granular cell tumors, which occur infrequently, are probably of Schwann cell origin. They can occur almost anywhere in the body but usually affect the tongue, oral cavity, skin, or breasts and are rarely found in the gastrointestinal tracts. The esophagus is the most frequent gastrointestinal site, followed by the stomach and the colon. Granular cell tumors are generally benign, especially in the gastrointestinal tract, some malignant lesions have been reported. For this reason, and also because preoperative diagnosis is difficult, the standard treatment for granular cell tumor has until now been surgical excision. In recent years, other therapeutic methods is endoscopic laser therapy (ELT), polypectiomy, endoscopic mucosal resection (EMR). We report a case of esophageal granular cell tumor which was diagnosed by an endoscopy and managed using an endoscopic mucosal resection without complication.
Enhanced Bioavailability of Paclitaxel by Bamboo Concentrate Administration
Kang Keon Wook,Choi Jun Shik The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.4
The purpose of this study was to investigate the effect of a cotreatment of bamboo concentrates (Jukcho solution; 0.75, 1.5, and 3.0 mL/kg) with the chemotherapeutic agent paclitaxel on the bioavailability of orally administered paclitaxel (50 mg/kg) in rats. The effect of a pretreatment of bamboo concentrates (1.5 and 3.0 mL/kg for 1.0 h or a consecutive 3 day) was also examined. The paclitaxel plasma concentrations of rats orally administered paclitaxel plus bamboo concentrates (coadministration, 3.0 mL/kg and pretreatment, 1.5 and 3.0 mL/kg) were significantly higher than those of rats treated with paclitaxel alone. Plasma concentrations of paclitaxel in groups pretreated with bamboo concentrates for 3 day were markedly higher than those of a paclitaxel control group at the measured time points. The areas under plasma concentration-time curves (AUCs) of paclitaxel in groups pretreated with bamboo concentrates were elevated and the absolute bioavailability ($AB\%$) and relative bioavailability ($RB\%$) of paclitaxel were also significantly higher than those in the control group. The peak concentration ($C_{max}$), half-life ($t_{1/2}$), and the elimination rate constant ($K_{el}$) of paclitaxel after 3 day of pretreatment with bamboo concentrates were also significantly higher than those in the control, but the time required to reach the maximum plasma concentration ($T_{max}$) of paclitaxel was unaffected by the bamooo concentrates. Western blot analyses demonstrated that the level of CYP3A4 was increased in the livers of rats treated orally with paclitaxel, but this was reversed by pretreating with bamboo concentrates. These results show that bamboo concentrates enhance the bioavailability of orally administered paclitaxel and this effect may be associated with a diminished expression of CYP3A4 in the liver.
Kang, Keon-Wook,Kim, Yoon-Gyoon,Kim, Choon-Won,Kim, Sang-Geon The Pharmaceutical Society of Korea 2002 Archives of Pharmacal Research Vol.25 No.5
Liver fibrosis is a prepathological state wherein damaged liver tissues in chronic liver diseases, such as hepatitis, are not repaired to normal tissues, but converted to fibrous tissue. 5-(2-Pyrazinyl)-4-methyl-1,2-dithiol-3-thione (oltipraz), a cancer chemopreventive agent, is effective against a wide variety of chemical carcinogens. Recently, we reported that oltipraz inhibits liver fibrogenesis (Kang et al., 2002). In the present study, the effects of oltipraz in combination with dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylene dioxybiphenyl-2,2'-dicarboxylate (DDb) on dimethylnitrosamine (DMN)-induced liver fibrogenesis were assessed in rats. Oltipraz (30 mg/kg body weight, po, 3 times per week for 4 weeks) was found to inhibit the increases in plasma ALT, AST and bilirubin by DMN, whereas DDB (30 mg/kg body weight, po, 3 times per week for 4 weeks) attenuated the increases in the plasma ALT and bilirubin. The lowered plasma protein and albumin contents in DMN-treated rats were completely restored by oltipraz, but not by DDB. DDB decreases liver cell injury and inflammation through inhibition of nuclear factor-kB. DMN increased the accumulation of liver collagen, as indicated by the increase in the 4-hydroxyproline content in liver homogenates, which was reduced by treatment with oltipraz, but not by DDB. Given the differential effect between oltipraz and DDB, the potential enhancement of antifibrotic efficacy by the drugs was assessed in the animal model. Despite the minimal effect of DDB on DMN-induced fibrogenesis, DDB (5-25 mg/kg), administered together with oltipraz (25-5 mg/kg), showed an additive protective effect against hepatotoxicity and fibrosis induced by DMN, which was shown by the blood chemistry parameters and histopathological analysis. The adequate composition ratio of oltipraz to DDB was 5:1. These results provide information on the pharmaceutical composition, comprising of oltipraz and DDB as the active components, for the treatment and/or prevention of liver fibrosis and cirrhosis.
Angiotensin II-mediated Nrf2 Down-regulation: A Potential Causing Factor for Renal Fibrosis?
Kang, Keon-Wook 대한약학회 2011 Archives of Pharmacal Research Vol.34 No.5
Epithelial-mesenchymal transition (EMT), a phenotype conversion of epithelial cells to myofibroblasts, is closely related with pathogenesis of renal fibrosis. Although it has been known that angiotensin II (ATII) stimulates EMT process in various cell types, the precise molecular mechanisms had not been clearly demonstrated. In this issue, Kang et al. show that AII suppresses NF-E2-related factor 2 (Nrf2) signaling and enhances transforming growth factor-${\beta}$1's activity to induce EMT in renal epithelial cells (Kang et al., 2011). They suggest that ATII-mediated EMT stimulating effect may result from the increased oxidative stress via defect in Nrf2-antioxidant system. This report proposes a possible mechanism of ATII-mediated renal fibrosis.