• Title/Summary/Keyword: Kidney glomerulus

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Morphological and Physiological Effects of Lead (Pb) Exposure on Tissues of Carassius auratus (납 노출에 따른 붕어(Carassius auratus) 조직의 미세구조 및 생리적 변화)

  • Kim, Jeong-Sook;Shin, Myung-Ja;Lee, Jong-Eun;Seo, Eul-Won
    • Korean Journal of Ecology and Environment
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    • v.43 no.3
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    • pp.409-417
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    • 2010
  • Present study aimed to investigate morphological and physiological change in the tissues of Carassius auratus after exposure against Pb (lead) with various rearing condition. We measured the level of accumulated heavy metal and analyzed ultrastructure with transmission electron microscopy. The heavy metal, Pb, was accumulated in the gill, bone and integument increased drastically for exposure periods, the 40 days. The accumulation of Pb in the gill showed relatively higher than that in other tissues. And accumulated Pb amounts also were increased with exposure time dependent manner in the gill, bone and integument tissues. Also, specific activities of antioxidation enzymes in all tissue after exposure to Pb were increased in the course of exposure. And the activities of SOD from tissues exposed to Pb were increased 2 folds than those from the unexposed but GPX activities were maintained constant. The increased numbers of mucous cells in gill tissues exposed to Pb were determined and morphological changes, such as clubbing and fusion, were shown secondary lamella. Also, exposure of Pb for 40 days on gills tissues cause membrane damage in mitochondria and nucleus. In kidney tissues, the atrophied glomerulus was observed, and the empty space in Bowman's capsule was expanded. Based on the all results, it is suggested that the exposure to the high level of Pb for long period affect on the morphology of tissues, and change the enzymatic balance in C. auratus.

High Glucose and Advanced Glycosylation Endproducts(AGE) Modulate the P-cadherin Expression in Glomerular Epithelial Cells(GEpC) (배양한 사구체 상피세포에서 고농도 당과 후기 당화합물에 의한 P-cadherin의 변화)

  • Ha Tae-Sun;Koo Hyun-Hoe;Lee Hae-Soo;Yoon Ok-Ja
    • Childhood Kidney Diseases
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    • v.9 no.2
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    • pp.119-127
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    • 2005
  • Purpose : Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the integrity of slit diaphragm(SD) proteins including nephrin, p-cadherin, and others. Diabetic proteinuric condition demonstrates defects in SD molecules as well as ultrastructural changes in podocytes. We examined the molecular basis for this alteration of SD molecules especially on P-cadherin as a candidate regulating the modulation of pathogenic changes in the barrier to protein filtration. Methods : To investigate whether high glucose and AGE induce changes in SD, we cultured rat GEpC under normal(5 mM) or high glucose(30 mM) and AGE- or BSA-added conditions and measured the change of P-cadherin expression by Western blotting and RT-PCR. Results : We found that administration of high glucose decreased the P-cadherin production significantly in the presence or absence of AGE by Western blotting. In RT-PCR high glucose with or without AGE also significantly decreased the expression of P-cadherin mRNA compared to those of controls. Such changes were not seen in the osmotic control. Conclusion : We suggest that high glucose with or without AGE suppresses the Production of P-cadherin at the transcriptional level and that these changes nay explain the functional changes of SD in diabetic conditions. (J Korean Soc Pediatr Nephrol 2005;9:119-127)

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Diagnosis and Treatment of Hematuria (혈뇨의 진단과 치료)

  • Jong Hwan Jung
    • The Korean Journal of Medicine
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    • v.99 no.5
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    • pp.243-252
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    • 2024
  • Hematuria is a common manifestation caused by various factors such as infection, inflammation, trauma, urinary stone and malignancy. Hematuria reflects pathological state of urinary system. Isolated microscopic hematuria without any abnormalities besides of hematuria on urine microscopic examination usually presents a good clinical course or outcome. However, significant proteinuria or hypertension, which accelerates renal dysfunction, can often develop during follow-up period in patients with isolated microscopic hematuria. Compared with non-glomerular hematuria, glomerular hematuria shows several characteristic findings such as dysmorphic red blood cell (RBC) or RBC casts or significant proteinuria on urinalysis. If glomerular hematuria is strongly suspected, a kidney biopsy may be required to differentiate the cause of glomerulonephritis. In this review, we tried to review the differential diagnosis and diagnostic approach and treatment of hematuria.

Pharmacokinetic Study of Pyrazinamide Related to the Mechanism of the Renal Excretion (Pyrazinamide의 신배설기전에 관한 약동학적 연구)

  • Choi, Eung-Sang;Shin, Sang-Goo;Lee, Sun-Hee;Choi, Cheol-Hee;Kim, Yong-Sik;Lim, Jung-Kyoo;Park, Chan-Woong
    • The Korean Journal of Pharmacology
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    • v.23 no.1
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    • pp.1-7
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    • 1987
  • The renal handling and tissue distribution of pyrazinamide were studied after administration of single dose intravenous injection for 15 min or constant infusion in New Zealand White rabbits. Peak pyrazinamide serum concentration ranged from 57.3 to $105.0{\mu}g/ml$ ($mean{\pm}SD;83.0{\pm}17.8$). The mean half-life of the a phase was $0.143{\pm}0.047$ hr while the ${\beta}$ phase ranged from 1.66 to 3.25 hr($mean{\pm}SD;2.38{\pm}0.57$). The mean steady-state volume of distribution in non-compartmental model was $0.935{\pm}0.362\;L/kg$ Excretion ratio of pyrazinamide was dramatically reduced from 1.02 to 0.30 when unbound serum pyrazinamide concentration was increased from 6.04 to $60.9\;{\mu}g/ml$. The urine flow dependency of renal clearance of pyrazinamide was demonstrated in steady-state serum concentration. The tissue/serum concentration ratio of pyrazinamide was highest in kidney and lowest in skeletal muscle among the tissues examined. The results suggested that a large fraction of pyrazinamide filtered by glomerulus and secreted by renal tubule was reabsorbed and this tubular reabsorption of pyrazinamide might be greatly influenced by urine flow.

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Effect of Antler Velvet Ethanol Extract on Common Serum Chemistry Panels and Histopathological Change in Rats Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (녹용 에탄올 추출물이 2,3,7,8 Tetrachlorodibenzo-p-dioxin에 노출된 랫드의 일반 혈액 화학 지수 및 조직 병변에 미치는 효과)

  • Choi, Kyung-Yun;Hwang, Seock-Yeon;Lee, Su-Chan;Kim, Si-Kwan
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.35 no.9
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    • pp.1178-1184
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    • 2006
  • This study was carried out to investigate the effect of ethanol extract of antler velvet (EAV) on common serum chemistry panels and histopathological change in rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Administration of TCDD ($50{\mu}g/kg$ body weight) induced significant decrease in platelet count (p<0.01), creatine phosphokinase (CPK, p<0.01), lactatate dehydrogenase (LDH, p<0.05) and glucose (p<0.05) levels and increase in hemoglobin (p<0.05), aspartate aminotransferase (AST, p<0.01), alanine amino transferase (ALT, p<0.05) and lipase activities (p<0.05), and blood urea nitrogen (BUN, p<0.05), triglyceride (p<0.01) and low density lipoptotein cholesterol (LDL-C, p<0.05) levels. However, pretreatment of EAV at daily dose of 20 mg/kg b.w. from 1 wk before TCDD exposure for 5 wks attenuated the abnormality of the overall serum chemistry panels but statistical difference between TE and TA groups was observed only in testicular weight (p<0.01), LDH activity (p<0.05), glucose (p<0.05) and lipase activity (p<0.01). In addition, TCDD induced significant histopathological changes including swelling, fatty metamorphosis, and vacuolar degeneration in liver; edema in proximal and distal convoluted tubules, and glomerulus in kidney; severe atrophy of red purple and appearance of significant number of macrophage in spleen; prominent atrophy and decrease in immune cells in thymus. On the other hand, administration of EAV attenuated histopathological damage induced by TCDD. These results further suggest that administration of EAV attenuates TCDD induced testicular, liver, pancreatic, hematopoietic and nephrotic toxicities in rats.