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( Won Il Park ),( Dae Hyeon Cho ),( Ji Eun Oh ),( Hyun Chin Cho ),( Kwang Min Kim ),( Kil Jong Yu ),( Hyoun Soo Lee ),( Man Je Park ),( Sang Goon Shim ),( Chang Uk Jeong ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Esophageal duplication cysts account for a very small percentage of benign esophageal tumor that is usually diagnosed in childhood, but very rare cases remain asymptomatic until adolescence. They may be asymptomatic or present with complications like infection, bleeding, or mass effect. A 19-years-women visited our hospital presenting chest pain and dysphagia. Contrast enhanced computed tomography of the chest showed a heterogeneous density of mass in left lateral wall of distal thoracic esophagus. On endoscopic ultrasound, a heterogeneously echotextured lesion with anechoic components present and no vascular component in Doppler sonogram at intramural location in the lower esophagus was noted. In view of symptoms of dysphagia and possibility of esophageal submucosal tumor, surgical excision through posterolateral thoracotomy was performed. In gross fi nding, a mass measurred 4. 0 x 4. 0 x 2. 0 cm and formed cyst with hematoma formation in it. Histopathologically the cyst was lined by pseudostratifi ed ciliated columnar epithelium surrounded by inner circular and outer longitudinal smooth muscle layers without cartilage. So it was diagnosed as a complicated esophageal duplication cyst with hematoma formation. Esophageal duplication cyst represent rare benign tumor of congenital foregut anomalies. Up to 80% of these cysts are diagnosed in childhood, less than 7% remain asymptomatic until adolescence. Pain and dysphagia are the most common symptoms in adults. Complications may be infections, rupture or bleeding. Diagnosis is usually made by computed tomography and endoscopic ultrasound. The only defi nite treatment is surgical excision. Pathologically, the cyst is covered with nonkeratinizing squamous or ciliated columnar epithelium, and the cyst wall contains two layers of smooth muscle. These fi ndings, accompanied by a lack of cartilage in the cyst wall, can differentiate an esophageal duplication cyst from a bronchogenic cyst.
Chin Hee Mun,Won Taek Lee,Kyung Ah Park,Jong Eun Lee 대한해부학회 2010 Anatomy & Cell Biology Vol.43 No.3
Nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS) plays a protective role in cerebral ischemia by maintaining vascular permeability, whereas NO derived from neuronal and inducible NOS is neurotoxic and can participate in neuronal damage occurring in ischemia. Matrix metalloproteinases (MMPs) are up-regulated by ischemic injury and degrade the basement membrane if brain vessels to promote cell death and tissue injury. We previously reported that agmatine, synthesized from L-arginine by arginine decarboxylase (ADC) which is expressed in endothelial cells, has shown a direct increased eNOS expression and decreased MMPs expression in bEnd3 cells. But, there are few reports about the regulation of eNOS by agmatine in ischemic animal model. In the present study, we examined the expression of eNOS and MMPs by agmatine treatment after transient global ischemia in vivo. Global ischemia was induced with four vessel occlusion (4-VO) and agmatine (100 mg/kg) was administered intraperitoneally at the onset of reperfusion. The animals were euthanized at 6 and 24 hours after global ischemia and prepared for other analysis. Global ischemia led severe neuronal damage in the rat hippocampus and cerebral cortex, but agmatine treatment protected neurons from ischemic injury. Moreover, the level and expression of eNOS was increased by agmatine treatment, whereas inducible NOS (iNOS) and MMP-9 protein expressions were decreased in the brain. These results suggest that agmatine protects microvessels in the brain by activation eNOS as well as reduces extracellular matrix degradation during the early phase of ischemic insult.
Upregulation of Galectin-3 by <i>Corynebacterium kutscheri</i> Infection in the Rat Lung
WON, Young-Suk,JEONG, Eui-Suk,PARK, Hyun-Ji,LEE, Chul-Ho,NAM, Ki-Hoan,KIM, Hyoung-Chin,PARK, Jong-Im,CHOI, Yang-Kyu KINOKUNIYA CO LTD 2007 EXPERIMENTAL ANIMALS Vol.56 No.2
<P><I>Corynebacterium</I> (C) <I>kutscheri</I> and <I>Staphylococcus</I> aureus were isolated from two Sprague-Dawley (SD) rats with a hemisected spinal cord. Grossly, gray-white bulging foci and abscesses were distributed throughout the parenchyma of the lung. Pathologically, severe necrotizing lobar pneumonia with abscesses and fibrinous pleuritis were observed. Immunohistochemical analysis found accumulation of galectin-3 in alveolar macrophages and the alveolar interstitial region. No other viral or bacterial pathogens were detected in these animals. In addition, similar pathogenic changes and accumulation of galectin-3 were observed in the lungs of SD rats experimentally infected with <I>C. kutscheri</I>. Using northern blot analysis, the relative galectin-3 and GAPDH mRNA levels were 4.6 to 9.3 times higher in <I>C. kutscheri</I>-infected lung than in uninfected controls. These results demonstrate that a single <I>C. kutscheri</I> infection can induce the upregulation of galectin-3 in the lung and that this molecule may have an important pathogenic role in <I>C. kutscheri</I> infections in rats.</P>
Free fatty acid as a determinant of ischemic lesion volume in nonarterial-origin embolic stroke
Chung, Jong-Won,Seo, Woo-Keun,Kim, Gyeong-Moon,Chung, Chin-Sang,Lee, Kwang Ho,Bang, Oh. Young Elsevier 2017 Journal of the neurological sciences Vol.382 No.-
<P><B>Abstract</B></P> <P><B>Goals</B></P> <P>This study aimed to determine whether the plasma levels of free fatty acid (FFA) are associated with ischemic lesion characteristics in nonarterial-origin embolic stroke.</P> <P><B>Materials and methods</B></P> <P>We prospectively recruited 254 patients with acute cerebral infarction caused by cardioembolic stroke (CES, <I>n</I> =121) or with embolic stroke of undetermined source (ESUS, <I>n</I> =133). Plasma levels of FFA were measured during the acute stage (median of 2days after stroke onset). Acute ischemic lesions on diffusion-weighted imaging were measured in terms of size, composition, and pattern. Transthoracic echocardiography parameters were evaluated in all patients.</P> <P><B>Findings</B></P> <P>Plasma levels of FAA were not different in CES and ESUS patients (mEq/L, 0.78±0.52 vs. 0.67±0.61, <I>P</I> =0.120). Echocardiography parameters, including left atrium volume index and E/e', were higher, and the ischemic lesion volume was larger in patients with CES than in those with ESUS. The ischemic lesion volume and the proportion of patients with mixed (small and large) and large cortical lesions increased with FFA quartile in both CES and ESUS groups. In a multivariable analysis, FFA level (coefficient, 5.249; standard error, 3.447; <I>P</I> =0.001), atrial fibrillation (coefficient, 7.673; standard error, 1.855; <I>P</I> <0.001), and fasting glucose (coefficient, 0.104; standard error, 0.023; <I>P</I> <0.001) were associated with ischemic lesion volume in nonarterial-origin embolic stroke.</P> <P><B>Conclusion</B></P> <P>Elevated plasma FFA levels are associated with larger ischemic lesion volumes and a higher prevalence of large cortical infarcts in patients with nonarterial-origin embolic stroke regardless of the presence of a high-risk cardioembolic source.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Plasma FFA levels were not different in CES and ESUS patients. </LI> <LI> Topographic infarct patterns were determined by FFA levels in nonarterial-origin embolic stroke. </LI> <LI> Increased FFA level is associated with larger infarct volume in nonarterial-origin embolic stroke. </LI> </UL> </P>