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위장관 ; 혈류가 유지된 채 분리된 흰 쥐 결장에 대한 Urocortin 1의 영향
유일영 ( Il Young You ),이승호 ( Seung Ho Lee ),김기배 ( Ki Bae Kim ),이희승 ( Hee Seung Lee ),장종순 ( Jong Soon Jang ),연명호 ( Myeong Ho Yeon ),한정호 ( Joung Ho Han ),윤순만 ( Soon Man Yoon ),채희복 ( Hee Bok Chae ),박선미 ( S 대한소화기학회 2015 대한소화기학회지 Vol.65 No.5
Background/Aims: Urocortin 1, a corticotropin-releasing factor related peptide, increases colonic motility under stressful conditions. We investigated the effect of urocortin 1 on colonic motility using an experimental model with isolated rat colon in which the blood flow and intestinal nerves were preserved. Furthermore, we assessed whether this effect was mediated by adrenergic or cholinergic nerves. Methods: Colonic motility was measured in the proximal and distal parts of resected rat colon. The colon resected from the peritoneum was stabilized, and then urocortin 1 (13.8, 138, 277, and 1,388 pM) was administered via a blood vessel. Motility index was measured in the last 5 min of the 15 min administration of urocortin 1 and expressed as percentage change from baseline. Subsequently, the change in motility was measured by perfusing urocortin 1 in colons pretreated with phentolamine, propranolol, hexamethonium, atropine, or tetrodotoxin. Results: At concentrations of 13.8, 138, 277, and 1,388 pM, urocortin 1 increased the motility of proximal colon (20.4±7.2%, 48.4±20.9%, 67.0±25.8%, and 64.2±20.9%, respectively) and the motility of distal colon (3.3±3.3%, 7.8±7.8%, 71.1±28.6%, and 87.4±32.5%, respectively). The motility induced by urocortin 1 was significantly decreased by atropine to 2.4 2.4% in proximal colon and 3.4±3.4% in distal colon (p<0.05). However, tetrodotoxin, propranolol, phentolamine, and hexamethonium did not inhibit motility. Conclusions: Urocortin 1 increased colonic motility and it is considered that this effect was directly mediated by local muscarinic cholinergic receptors. (Korean J Gastroenterol 2015;65:283-290)
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간흡충으로 인한 총담관의 양성 협착과 감별이 어려운악성 협착
김현 ( Hyun Kim ),한정호 ( Joung Ho Han ),박선미 ( Seon Mee Park ),김정태 ( Jeong Tae Kim ),장종순 ( Jong Soon Jang ),이희승 ( Hee Seung Lee ),이승호 ( Seung Ho Lee ),연명호 ( Myeong Ho Yeon ) 대한췌장담도학회 2015 대한췌담도학회지 Vol.20 No.1
Accurate and early diagnosis of indeterminate bile duct stricture is difficult. There are numerous cases suggesting similarity between benign tumors and malignancy. Therefore, meticulous evaluation with endoscopic retrograde cholangiopancreatography (ERCP), endoscopic ultrasound and computed tomography (CT) is necessary. A 50 year-old male presented with painless jaundice. Abdominal CT scan showed distal biliary stricture without definite pancreatic mass. Repeated brush cytology and endobiliary biopsy during ERCP did not reveal malignancy except for eggs of Clonorchis sinensis. The patient declined surgical resection without definite evidence of malignancy. Abdominal CT scan one month later showed progressive parenchymal atrophy and pancreatic duct dilatation. The patient underwent pylorus preserving pancreatoduodenectomy. Pathology revealed pancreatic adenocarcinoma in the head portion. Since accurate preoperative diagnosis of malignant biliary obstruction can be evasive, patients with biliary stricture should undergo evaluation with high index of suspicion.
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과용량 반코마이신이 투여된 환자에서 신생검으로 확진한 급성 세뇨관 괴사 1예
심영광 ( Young Kwang Shim ),김정은 ( Jung Eun Kim ),연명호 ( Myeong Ho Yeon ),최재현 ( Jae Hyun Choi ),김미경 ( Mi Kyung Kim ),성문혁 ( Mun Hyuk Sung ),김선문 ( Sun Moon Kim ),권순길 ( Soon Kil Kwon ),김혜영 ( Hye Young Kim ),이 대한신장학회 2011 Kidney Research and Clinical Practice Vol.30 No.3
Vancomycin has been associated with acute kidney injury, particularly in the concomitant treatment with aminoglycoside or in the presence of other risk factor such as preexisting renal disease, sepsis, or hemodynamic instability. Vancomycin-related nephrotoxicity typically manifests as acute tubulointerstitial nephritis. Biopsy-proven acute tubular necrosis associated with vancomycin intoxication in the absence of aminoglycoside has been reported only in very few cases. We report a case of biopsy-proven acute tubular necrosis associated with vancomycin intoxication that was treated by continuous venovenous hemodiafiltration. A 28-year-old male without preexisting renal disease received a massive overdose of vancomycin. The plasma vancomycin level was 440.3 g/mL. μ Renal biopsy revealed acute tubular necrosis that there is marked thinning of the tubular epithelium with dilatation of the tubular lumens and severe foamy epithelial cell changes in tubules. Continuous venovenous hemodiafiltration resulted in efficient reduction of serum vancomycin levels, which was followed clinically by recovered of renal function.
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신장 ; 아밀로라이드 유발 신세뇨관산증 흰쥐 신장에서 암모니아 운반체의 발현
김승중 ( Seung Jung Kim ),김혜영 ( Hye Young Kim ),최재현 ( Jae Hyun Choi ),김정태 ( Jung Tae Kim ),김정은 ( Jeong Eun Kim ),연명호 ( Myeong Ho Yeon ),김선문 ( Sun Moon Kim ),권순길 ( Soon Kil Kwon ),신경섭 ( Kyung Sub Shin ) 대한내과학회 2011 대한내과학회지 Vol.80 No.6
목적: 신세뇨관산증은 요중 산 배설이 감소하는 질환으로, 대부분 요 암모니아 배설의 감소에 의한 것이다. 본 연구는 아밀로라이드로 유발된 신세뇨관산증 흰쥐에서 산 배설의 변화와 암모니아 운반체인 Rh B Glycoprotein (Rhbg)와 Rh C Glycoprotein (Rhcg)의 발현 변화를 확인하여 신세뇨관산증의 병인에 암모니아 운반체의 역할을 규명하고자 하였다. 방법: Sprague-Dawley계 웅성 흰쥐를 사용하였으며, 실험군에는 amiloride (3 mg/kg/day)를 6일간 복강 내 주입하였다. 7일째 대사케이지에 mineral oil을 처리하여 24시간 동안 요를 수집하였다. Rhbg와 Rhcg의 단백 발현을 평가하기 위하여 immunoblot와 면역조직화학염색을 시행하였고, 면역조직화학염색법을 정량화 분석하였다. 결과: 아밀로라이드 투여군에서 혈중 tCO2 농도는 대조군 25.6±1.5 mEq/L에 비하여 23.0±1.5 mEq/L로 감소하였으며 (p<0.05), 혈중 K+농도는 대조군 3.84±0.34 mmol/L에 비하여 4.50±0.46 mmol/L로 약간 높았다(p<0.05). 아밀로라이드 투여군에서 24시간 요 암모니아 배설은 대조군 0.52±0.07 mmol에 비하여 0.30±0.03 mmol으로 요 암모니아 배설이 감소하였으며(p<0.05), Urine pH는 양 군 간에 차이가없어 아밀라이드 투여에 의해 신세뇨관산증이 유발되었음을 확인하였다. 반정량적 immunoblot 검사에서 Rhbg와 Rhcg의 단백 발현은 양 군 간에 유의한 차이가 없었다. 면역조직화학염색과 정량화 분석 결과 아밀로라이드 유발 신세뇨관산증군에서 Rhcg의 면역반응성은 감소하였으나, Rhbg의 면역반응성은 유의한 차이가 없었다. 결론: 아밀로라이드 투여 흰쥐에서 암모니아 배설 감소와 Rhcg의 면역반응성의 감소가 동반되었다. 따라서 아밀로라이드 유발 신세뇨관 산증의 병인에 암모니아 운반체 Rhcg가 중요한 역할을 할 것으로 생각한다. Background/Aims: Renal tubular acidosis (RTA) decreases the net acid excretion, predominantly due to a decrease in urinary ammonia excretion. This study examined whether this decrement is associated with changes in the renal expression of the ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg), in rats with amiloride-induced RTA. Methods: Male Sprague-Dawley rats were treated intraperitoneally with amiloride (3 mg/kg/day) for 6 days. Rhbg and Rhcg expression was evaluated by immunoblotting and immunohistochemistry. Cell height, total cellular expression, expression in the apical 25% of the cell, and apical expression as a percentage of total expression were quantified using immunohistochemistry with quantitative morphometric analysis. Results: After amiloride treatment for 6 days, the serum bicarbonate level was decreased, and serum potassium was increased. The total urinary ammonia excretion and potassium excretion were decreased. The total Rhbg and Rhcg protein expression levels were not changed in the cortex or outer medulla of the kidney. Light microscopy and immunohistochemistry with quantitative morphometric analysis demonstrated that total Rhcg expression was decreased in the cortical collecting duct (CCD) and outer medullary collecting duct (OMCD) in amiloride-induced RTA, whereas Rhbg immunoreactivity was unchanged. Conclusions: Rats with amiloride-induced RTA have decreased urinary ammonia excretion associated with decreased Rhcg expression in the CCD and OMCD, suggesting that the ammonia transporter Rhcg plays an important role in the pathogenesis of amiloride-induced RTA. (Korean J Med 2011;80:687-696)
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