• The Korean Journal of Zoology
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• v.11 no.4
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• pp.103-117
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• 1968

Insect hemocytes during metamorphosis were studies by histchemical and autoradiographic methods is Pieris rapae (Lepidoptera). The hemocytes were classified into six types, prohemocytes, plasmatocytes, podocytes, granular hemocytes, spherule cells and oenocytoids on the basis of the transitions in shapes and inclnsions of cytoplasms. Proteins, nucleic acids, polysaccharides and lipids in the hemocytes were detected histochemically from larval to pupal stages to learn the rise and fall of them during growth and metamorphosis. Most of the granules consisted of glycogen, neutral mucopolysaccharides and mucoprotein in addition to some granules of neutral fats and phospholipids were found in the granular hemocytes and spherule cells. Mitotic figures and DNA synthetic activities were observed in every type of hemocytes from 2nd to 5th instars, suggesting the all types of hemocytes originated from the prohemocytes. The cytoplasmic filaments of plasmatocytes and pdocytes extended very long in prepupa and pupa and the vermiform cells were the transformed plasmatocytes due to their further differentiation.

• Childhood Kidney Diseases
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• v.15 no.2
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• pp.138-145
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• 2011

Purpose : To test whether the expression of ${\beta}$-catenin, a component of podocyte as a filtration molecule, would be altered by puromycin aminonucleoside (PAN) in the cultured podocyte in vitro. Methods : We cultured rat glomerular epithelial cells (GEpC) with various concentrations of PAN and examined the distribution of ${\beta}$-catenin by confocal microscope and measured the change of ${\beta}$-catenin expression by Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). Results :We found that ${\beta}$-catenin relocalized from peripheral cytoplasm to inner cytoplasm, therefore, intercellular separations were seen in confluently cultured cells by high concentrations of PAN in immunofluorescence views. In Western blotting of GEpC, PAN ($50{\mu}g/mL$) decreased ${\beta}$-catenin expression by 34.9% at 24 hrs and 34.3% at 48 hrs, compared to those in without PAN condition (P<0.05). In RT-PCR, high concentrations ($50{\mu}g/mL$) of PAN also decreased ${\beta}$-catenin mRNA expression similar to protein suppression by 25.4% at 24 hrs and 51.8% at 48 hrs (P<0.05). Conclusion : Exposure of podocytes to PAN in vitro relocates ${\beta}$-catenin internally and reduces ${\beta}$-catenin mRNA and protein expression, which could explain the development of proteinuria in experimental PAN-induced nephropathy.

• Childhood Kidney Diseases
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• v.21 no.2
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• pp.152-155
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• 2017

Orthostatic or postural proteinuria is the most common cause of asymptomatic proteinuria in children. As orthostatic proteinuria (OP) is a benign disease with relatively good prognosis, it has no specific management, and patients only need to be observed. However, if OP shows a persistently high level of proteinuria, in theory, glomerular changes can occur. An 11-year-old girl was referred to the hospital due to asymptomatic proteinuria and was diagnosed as having OP based on the results of clinical and laboratory examinations, urinalysis, and protein/creatinine (TP/Cr) ratio at both supine and erect positions. During follow-up observation, the 24-hour TP/Cr ratio was persistently higher than 1.5 mg/mg for 2 years. We performed renal biopsy, which showed mesangial proliferative glomerular lesions with focal effacement of the podocyte foot processes, but without immune depositions. OP can be accompanied by glomerular lesions if moderate to severe proteinuria persists.

• Clinical and Experimental Pediatrics
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• v.60 no.3
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• pp.55-63
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• 2017

Advances in podocytology and genetic techniques have expanded our understanding of the pathogenesis of hereditary steroid-resistant nephrotic syndrome (SRNS). In the past 20 years, over 45 genetic mutations have been identified in patients with hereditary SRNS. Genetic mutations on structural and functional molecules in podocytes can lead to serious injury in the podocytes themselves and in adjacent structures, causing sclerotic lesions such as focal segmental glomerulosclerosis or diffuse mesangial sclerosis. This paper provides an update on the current knowledge of podocyte genes involved in the development of hereditary nephrotic syndrome and, thereby, reviews genotype-phenotype correlations to propose an approach for appropriate mutational screening based on clinical aspects.

• Molecules and Cells
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• v.38 no.4
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• pp.285-296
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• 2015

Oxidative stress has been linked to the pathogenesis of diabetic nephropathy, the complication of diabetes in the kidney. NADPH oxidases of the Nox family, and in particular the homologue Nox4, are a major source of reactive oxygen species in the diabetic kidney and are critical mediators of redox signaling in glomerular and tubulointerstitial cells exposed to the diabetic milieu. Here, we present an overview of the current knowledge related to the understanding of the role of Nox enzymes in the processes that control mesangial cell, podocyte and tubulointerstitial cell injury induced by hyperglycemia and other predominant factors enhanced in the diabetic milieu, including the renin-angiotensin system and transforming growth factor-${\beta}$. The nature of the upstream modulators of Nox enzymes as well as the downstream targets of the Nox NADPH oxidases implicated in the propagation of the redox processes that alter renal biology in diabetes will be highlighted.

• Journal of Trauma and Injury
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• v.32 no.2
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• pp.111-114
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• 2019

Minimal change disease (MCD) in children has a favorable long-term prognosis, and development of end-stage renal disease is very uncommon; less than 5%. In the first case of its kind, we report a 21-year-old female with a history of MCD at the age of 6, who had late relapse subsequent to a motorcycle accident resulting in a de-gloving skin injury and intensive care unit admission. MCD was confirmed by normal light microscopy, podocyte effacement on electron microscopy and absence of any deposits on immunofluorescence 3 weeks after the incident due to critical illness. It is postulated that the skin injury is what caused the relapse of MCD.

• Childhood Kidney Diseases
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• v.27 no.1
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• pp.1-10
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• 2023

Pediatric nephrotic syndrome (NS) is a clinical syndrome characterized by massive proteinuria, hypoalbuminemia, and generalized edema. Most childhood NS cases are idiopathic (with an unknown etiology). Traditional therapeutic approaches based on immunosuppressive agents largely support the key role of the immune system in idiopathic NS (INS), especially in the steroid-sensitive form. Although most previous studies have suggested the main role of T cell dysfunction and/or the abnormal secretion of certain glomerular permeability factors, recent studies have emphasized the role of B cells since the therapeutic efficacy of B cell depletion therapy in inducing and/or maintaining prolonged remission in patients with INS was confirmed. Furthermore, several studies have detected circulating autoantibodies that target podocyte proteins in a subset of patients with INS, suggesting an autoimmune-mediated etiology of INS. Accordingly, a new therapeutic modality using B cell-depleting drugs has been attempted, with significant effects in a subset of patients with INS. Currently, INS is considered an immune-mediated disorder caused by a complex interplay between T cells, B cells, soluble factors, and podocytes, which may vary among patients. More in-depth investigations of the pathogenic pathways of INS are required for an effective personalized therapeutic approach and to define precise targets for therapeutic intervention.

• Journal of Acupuncture Research
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• v.15 no.2
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• pp.43-60
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• 1998

This study examined the histomorphomeric and histological changes of the left and right kidney in uninephrectomized rat. The results were as follows: 1. In the control, the right kidney was more prominent than the left in the basement membrane of glomerular capillaries. The podocyte had well developed Golgi apparatus in the left kidney and rough endoplasmic reticulum in the right kidney. 2. At the 30 days after unilateral nephrectomy, the basal lamina of glomerular capillaries was prominently thickened in the right kidney. The cytoplasm of the podocyte of the left kidney was markedly increased and had free ribosomes, developed Golgi apparatus and rough endoplasmic reticulum. 3. At the 30 days, the section of the glomeruli were more enlarged in the left kidney than in the right. 4. At the 20 day, the nuclear section of the podocytes were markedly enlarged in the right kidney, but those of the left kidney were diminished. The mitochondrial section of the podocytes were prominently increased in the right kidney. 5. The nuclear section of the parietal layer lining cells was no significant change in the right kidney. That of the left kidney was increased at the 20 days and decreased at the 40 days. The nuclear section of glomerular endothelium of the left kidney increased earlier than the right. 6. In the morphometry of the control kidney, the section areas, long and short diameters, the nuclear section, the mitochondrial section of the proximal tubule cells, and the changes of those were more large in the right kidney than in the left. 7. The luminal secretory vesicles and peroxisomes of the left kidney were more than the right at the 20 days. The increase of mitochodrial section in the proximal tubule cells of the left kidney was more prominent than the right. The large cytoplasmic vacuoles were more prominent in the left kidney than in the right. 8. The thickness of cytoplasm and brush border was more thick in the control left kidney than in the control right. The change of cytoplasmic thickness of the left kidney was increased earlier than in the right and both kineys were increased in the thickness of brush border at the 30 days.

• Korean Journal of Veterinary Research
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• v.34 no.4
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• pp.653-664
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• 1994

This study was carried out to investigate diabetic renal changes in cyclophosphamide(CY) treated nonobese diabetic(NOD) mice and to develop animal model of diabetic human nephropathy. The 8-week-old NOD and ICR mice were injected with cyclophosphamide intraperitoneally at 200mg/kg body weight and compared the chemical effects on these mice with the non-treated NOD and ICR mice respectively. The renal glomeruli in ICR, cyclophosphamide-treated ICR(ICR+CY), NOD and cyclophosphamide-treated NOD(NOD+CY) mice were observed by the light and electron microscopes. The results obtained were summarized as follows ; 1. Spontaneous incidences of diabetes mellitus in NOD mice were significantly promoted by dosing with cyclophosphamide. 2. Glomerulohypertrophy, proliferation of mesangium, partial thickening of glomerular basement membrane, and partial fusion of pedicels of podocyte were observed in NOD mice and NOD+CY mice. These changes were not observed in both ICR mice and ICR+CY mice. 3. The diabetic nephropathy observed in NOD+CY mice was more severe than that of non-treated NOD mice.

• Childhood Kidney Diseases
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• v.13 no.2
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• pp.99-117
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• 2009

Diabetic nephropathy is a major cause of chronic renal failure in developing countries, and the prevalence rate has markedly increased during the past decade. Diabetic nephropathy shows various specific histological changes not only in the glomeruli but also in the tubulointerstitial region. In the early stage, the effacement of podocyte foot processes and thickened glomerular basement membrane (GBM) is noticed even at the stage of microalbuminuria. Nodular, diffuse, and exudative lesions, so-called diabetic glomerulosclerosis, are well known as glomerular lesions. Interstitial lesions also exhibit fibrosis, edema, and thickened tubular basement membrane. Diabetic nephropathy is considered to be multifactorial in origin with increasing evidence that one of the major pathways involved in the development and progression of diabetic nephropathy as a result of hyperglycemia. Hyperglycemia induces renal damage directly or through hemodynamic alterations, such as, glomerular hyperfiltration, shear stress, and microalbuminuria. Chronic hyperglycemia also induces nonhemodynamic dysregulations, such as, increased production of advanced glycosylation endproducts, oxidative stress, activation of signal pathway, and subsequent various cytokines. Those pathogenic mechanisms resulted in extracellular matrix deposition including mesangial expansion and GBM thickening, glomerular hypertrophy, inflammation, and proteinuria. In this review, recent opinions on the histopathologic changes and pathophysiologic mechanisms leading to initiation and progression of diabetic nephropathy will be introduced.