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Alteration of Tight Junction Protein Expression in Dahl Salt-Sensitive Rat Kidney
Jo, Chor Ho,Kim, Sua,Oh, Il Hwan,Park, Joon-Sung,Kim, Gheun-Ho Karger Medical and Scientific Publishers 2018 Kidney & blood pressure research Vol. No.
<P>Background/Aims: Altered pressure natriuresis is an important mechanism of hypertension, but it remains elusive at the molecular level. We hypothesized that in the kidney, tight junctions (TJs) may have a role in pressure natriuresis because paracellular NaCl transport affects interstitial hydrostatic pressure. Methods: To assess the association of salt-sensitive hypertension with altered renal TJ protein expression, Dahl salt-sensitive (SS) and salt-resistant (SR) rats were put on an 8% NaCl-containing rodent diet for 4 weeks. Systolic blood pressure (SBP) and urine NaCl excretion were measured weekly, and kidneys were harvested for immunoblotting and quantitative PCR analysis at the end of the animal experiments. Results: SBP was significantly higher in SS rats than in SR rats during the first to fourth weeks of the animal experiments. During the first and second week, urinary NaCl excretion was significantly lower in SS rats as compared with SR rats. However, the difference between the two groups vanished at the third and fourth weeks. In the kidney, claudin-4 protein and mRNA were significantly increased in SS rats as compared with SR rats. On the other hand, occludin protein and mRNA were significantly decreased in SS rats as compared with SR rats. The expression of claudin-2, claudin-7, and claudin-8 did not vary significantly between the two groups. Conclusions: In SS rats, SS hypertension was associated with differential changes in renal TJ protein expression. Both upregulation of claudin-4 and downregulation of occludin might increase paracellular NaCl transport in the kidney, resulting in impaired pressure natriuresis in SS rats. (c) 2017 The Author(s) Published by S. Karger AG, Basel</P>
Association of Proteinuria with Urinary Concentration Defect in Puromycin Aminonucleoside Nephrosis
( Chor Ho Jo ),( Sua Kim ),( Gheun-ho Kim ) 대한전해질학회 2020 Electrolytes & Blood Pressure Vol.18 No.2
Background: Puromycin aminonucleoside (PA) can induce nephrotic syndrome in rats, and proteinuria is an important mediator of tubulointerstitial injury in glomerulopathy. We assumed that glomerular proteinuria may affect tubular function, such as urinary concentration, and investigated whether a urinary concentration defect is associated with proteinuria in puromycin aminonucleoside nephrosis (PAN). We also investigated the defect response to enalapril. Methods: Glomerular proteinuria was induced by a single intraperitoneal injection of PA (150mg/kg BW) in male Sprague-Dawley rats. In a half of these rats, enalapril (35mg/kg BW) was administered daily in a food mixture for two weeks. After the animal experiment, kidneys were harvested for immunoblot analysis and histopathologic examination. Results: Compared with the control group, PA-treated rats had severe proteinuria, polyuria, and a lower urine osmolality. PA treatment induced remarkable tubulointerstitial injury and significant reductions in protein abundances of aquaporin-1 and Na-K-2Cl co-transporter type 2 (NKCC2). Proteinuria significantly correlated with osteopontin expression in the kidney and inversely correlated with renal expression of aquaporin-1, aquaporin-2, and NKCC2. The degree of tubulointerstitial injury significantly correlated with proteinuria, urine output, and osteopontin expression and inversely correlated with urine osmolality and renal expression of aquaporin-1, aquaporin-2, and NKCC2. No significant differences in parameters were found between PA-treated rats with and without enalapril. Conclusion: In PAN, glomerular proteinuria was associated with tubulointerstitial injury and water diuresis. Downregulation of aquaporin-1 and NKCC2 can impair countercurrent multiplication and cause a urinary concentration defect in PAN.
Effects of Dietary Salt Restriction on Puromycin Aminonu cleoside Nephrosis: Preliminary Data
( Chor Ho Jo ),( Sua Kim ),( Joon Sung Park ),( Gheun Ho Kim ) 대한전해질학회 2011 Electrolytes & Blood Pressure Vol.9 No.2
Proteinuria is a major promoter that induces tubulointerstitial injury in glomerulopathy. Dietary salt restriction may reduce proteinuria, although the mechanism is not clear. We investigated the effects of dietary salt restriction on rat kidneys in an animal model of glomerular proteinuria. Male SpragueDawley rats were used and divided into 3 groups: vehicletreated normalsalt controls, puromycin aminonucleoside (PA)treated normalsalt rats, and PAtreated lowsalt rats. PA was given at a dose of 150 mg/kg BW at time 0, followed by 50 mg/kg BW on days 28, 35, and 42. Sodiumdeficient rodent diet with and without additional NaCl (0.5%) were provided for normalsalt rats and lowsalt rats, respectively. On day 63, kidneys were harvested for histopathologic examination and immunohistochemistry. PA treatment produced overt proteinuria and renal damage. Dietary salt restriction insignificantly reduced proteinuria in PAtreated rats, and PAtreated lowsalt rats had lower urine output and lower creatinine clearance than vehicletreated normalsalt controls. When tubulointerstitial injury was semiquantitatively evaluated, it had a positive correlation with proteinuria. The tubulointerstitial injury score was significantly increased by PA treatment and relieved by lowsalt diet. ED1positive infiltrating cells and immunostaining for interstitial collagen III were significantly increased by PA treatment. These changes appeared to be less common in PAtreated lowsalt rats, although the differences in PAtreated normalsalt versus lowsalt rats did not reach statistical significance. Our results suggest that renal histopathology in PA nephrosis may potentially be improved by dietary salt restriction. Nonhemodynamic mechanisms induced by lowsodium diet might contribute to renoprotection.
구치부 지지의 상실과 마모로 인해 교합이 붕괴된 환자에서 수직고경 회복을 동반한 구강회복 증례
조유진,정수아,양홍서,박상원,임현필,윤귀덕,박찬,Jo, Yu Jin,Jung, Sua,Yang, Hong-So,Park, Sang-Won,Lim, Hyun-Pil,Yun, Kwi-Dug,Park, Chan 대한치과보철학회 2018 대한치과보철학회지 Vol.56 No.4
다수의 치아 상실과 치아 마모로 인해 교합이 붕괴된 경우 교합 고경의 변경이 필요할 수 있다. 그리고 이러한 경우 심미적이면서도 근신경계와 조화를 이룰 수 있는 고경을 결정하는 것이 중요하다. 본 증례는 치아상실 및 마모로 인해 교합 수직 고경의 감소가 관찰된 환자에서 진단 모형과 방사선 사진 및 다양한 임상적 검사 등의 교합관계분석을 통해 교합 수직 고경을 회복을 동반한 보철 수복을 진행한 경우로, 기능적인 면과 심미적인 면에서 양호한 결과를 얻었기에 이를 보고하는 바이다. Multiple tooth loss and excessive occlusal wear can result in damage to occlusal disharmony, functional disorders and esthetic problems, requiring comprehensive prosthetic treatments. Changing vertical dimension harmonized with surrounding muscle tissue is important. In this case, the patient with loss of vertical dimension caused by severe tooth loss and tooth wear was treated with the analysis of vertical dimension, such as diagnostic model, radiography and various clinical exams. the patient was satisfied with favorable functions and esthetics for 1 years of follow-up.