• Journal of fish pathology
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• v.22 no.3
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• pp.263-273
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• 2009

There is an increasing number of reports describing Streptococcus parauberis as an important pathogen of cultured olive flounder Paralichthys olivaceus and starry flounder Platichthys stellatus in Korea. We tried to determine the effects of water temperature (14${^{\circ}C}$ and 21${^{\circ}C}$) on the pathogenicity in Streptococcal disease caused by S. parauberis. We have challenged 180 olive flounder by i.p injection to $2.0{\times}10^{7}$ live cells/fish. Mortality was monitored for 21 days post challenge. And histopathological characterizations as infection degree, tissue degeneration and/or bacterial distribution were investigated with H&E stain and in situ hybridization technique. Fifty percent and 16.7% of mortality occurred within 21 days at 21${^{\circ}C}$ and 14${^{\circ}C}$ water temperature, respectively. In most cases, the typical symptoms of olive flounder infected with S. parauberis were darkness of the skin, lethargy, mild abdominal distension cause by ascites, splenomegaly, congested liver and internal organs paleness. The pericardial sac contained large amounts of cloudy fluid. Numerous whitish nodules, which were variable in size and often confluent, were randomly scattered throughout the myocardium. Especially, pericarditis and/or myocarditis was observed in all tested fishes after death. Positive in reaction with S. parauberis were found in all tissues in situ hybridization analysis. The relative numbers of S. parauberis in heart were much more than in liver, spleen, kidney and stomach. We evaluated that S. parauberis strain causes serious damage in the pericardium, shortness of breath and the blood disorder. Therefore, pericarditis and myocarditis caused by S. parauberis were closely related to mortality of olive flounder.

• The Korean Journal of Nuclear Medicine
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• v.28 no.1
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• pp.75-84
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• 1994

The need for assessment of ureteric function in the patient with an obviousely dilated ureter has increased particularly with the added spectrum of asymptomatic patients presenting with hydrone-phrosis and hydroureter on antenatal and perinatal ultrasound. To assess the influence of ureteral status on kidney washout during $^{99m}Tc$-DTPA diuretic renography, ureteral images were reviewed in 80 children referred for hydronephrosis. A scintigraphically abnormal ureter was defined as an intense and continuous image of > 10 min during diuretic renography. Out of them, a total of 16 nephroureteral systems in 12 children with scintigraphically abnormal ureter were analyzed. A diuretic washout index using response half time (t1/2) by linear fitting after lasix injection, was determined on renal (Kt1/2) and ureteral (Ut1/2) curves (diuretic renogram vs. diuretic ureterogram). Diuretic ureterogram curve patterns corresponding to normal (type I), obstructive (II) and non-obstructive (III) cases were described. Compared with X-ray data, diuretic renography was highly sensitive (88%) and specific (99%) for detecting any ureteral abnormality. Despite an obstructive Kt1/2 (>20 min), no patient with an abnormal ureter underwent therapy at the ureteropelvic junction because the hydronephrosis regressed after surgery at the lower level. Our data indicate that the abnormal ureter findings during diuretic renography have to be recognized before therapy for children with hydeonephrosis.

• The Korean Journal of Nuclear Medicine
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• v.37 no.6
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• pp.382-392
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• 2003

Purpose: Uptakes of Tc-99m MIBI (MIBI) and Tc-99m tetrofosmin (tetrofosmin) in human non-small cell lung cancer A549, multidrug-resistance associated protein (MRP) expressing cell, were investigated in vitro and in vivo. Materials and Methods: Western blot analysis and immunohistochemistry were used for detection of MRP in A549 cells with anti-MRPr1 antibody. Cellular uptakes of two tracers were evaluated at $100{\mu}M$ of verapamil (Vrp), $50{\mu}M$ of cyclosporin A (CsA) and $25{\mu}M$ of butoxysulfoximide (BSO) after incubation with MIBI and tetrofosmin for 30 and 50 min at $37^{\circ}C$, using single cell suspensions at $1{\times}10^6cells/ml$. Radioactivities in supernatants and pellets were measured with gamma well counter. A549 cells were inoculated in each flanks of 24 nude mice. Group 1 (Gr1) and Gr3 mice were treated with only MIBI or tetrofosmin, and Gr2 and Gr4 mice were treated with 70mg/kg of CsA i.p. for 1 hour before injection of 370KBq of MIBI or tetrofosmin. Mice were sacrificed at 10, 60 and 240 min. Radioactivities of organs and tumors were expressed as percentage injected dose per gram of tissue (%ID/gm). Results: Western blot analysis of the A549 cells detected expression of MRPr1 (190 kDa) and immunohistochemical staining of tumor tissue for MRPr1 revealed brownish staining in cell membrane but not P-gp. Upon incubating A549 cells for 60 min with MIBI and tetrofosmin, cellular uptake of MIBI was higher than that of tetrofosmin. Coincubation with modulators resulted in an increase in cellular uptakes of MIBI and tetrofosmin. Percentage increase of MIBI was higher than that of tetrofosmin with Vrp by 623% and 427%, CsA by 753% and 629% and BSO by 219% and 140%, respectively. There was no significant difference in tumoral uptakes of MIBI and tetrofosmin between Gr1 and Gr3. Percentage increases in MIBI (114% at 10 min, 257% at 60 min, 396% at 240 min) and tetrofosmin uptake (110% at 10 min, 205% at 60 min, 410% at 240 min) were progressively higher by the time up to 240 min with CsA. Conclusion: These results indicate that MIBI and tetrofosmin are suitable tracers for imaging MRP-mediated drug resistance in A549 tumors. MIBI may be a better tracer than tetrofosmin for evaluating MRP reversal effect of modulators.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.115-128
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• 1992

The training of male wistar rats for active conditioned response (ACR) was performed by one daily training session of 30 consecutive trials for 10 successive days using a two-way shuttle box, and the rats that showed 10 or more ACRs on the last day were treated for further 10 days with electroconvulsive shock (ECS : 50 mA, 0.5 msec; 100 Hz; 1.5 sec) and the following compounds. On the 20th day, all the rats were tested for the ACR rention. The ECS regimens were one ECS per day for 10 days with one day interval $(5{\times}ECS)$, one ECS at 3 hrs (ECS-3h), and one ECS at 24 hrs (ECS-24h), respectively, before the ACR retention test. And CDP-choline (cc: 250 mg/kg), spermine (SM: 10 mg/kg), ${\alpha}-difluoromethylornithine$ (DO: 250 mg/kg), or aminoguanidine (AG: 100 mg/kg) was administered by one daily i.p. injection for 10 days. The ACR number $(13.7{\pm}1.0)$ obtained on the last training day was increased by 37.23% on the 20th day in the control rats. And the ACR increase was significantly suppressed by 5-ECS, ECS-3h, CC, or SM but was little affected by ECS-24h, DO, or AG. However, the 5-ECS induced impairment of ACR retention was significantly suppressed by AG, SM, and CC in the order of potency but was little affected by DFMO. And the ECS-3h induced impairment was moderately worsened by SM or AG. The acetylcholine (ACh) of the rat hypothalamus (HT), hippocampus (HC), and entorhinal cortex (EC) was markedly increased by CC and moderately increased by SM, but little affected by ECS-3h, ECS-24h, DO, or AG. But $5{\times}ECS$ slightly increased the ACh content. The brain putrescine (Pt) content was significantly increased by AG and little affected by CC, SM, or DO. But the $5{\times}ECS$ markedy decreased the brain Pt content, and the decrease was significantly suppressed by CC, SM, or AG. CC induced the marked increases of the spermidine (Sd) and spermine (Sm) contents of all the areas. SM increased the Sd contents of all the areas and the EC-Sm content. DO decreased the brain Sd and Sm contents. And AG increased the HT-Sd content and the Sm contents of all the brain areas. The $5{\times}ECS$ induced decrease of the HC-Sm content was suppressed by CC, SM and AG. These results suggest that the improving effect of aminoguanidine on the $5{\times}ECS$ induced impairment of ACR retention may be ascribed in part to its activity as a diamine oxidase inhibitor.