GLORIA

GEOMAR Library Ocean Research Information Access

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Glucocorticoid-induced apoptosis of rat mesangial cells in culture (1998)
    Springer
    Clinical and experimental nephrology 2 (1998), S. 12-17 
    Details
    ISSN: 1437-7799
    Keywords: mesangial cell ; apoptosis ; glucocorticoid ; cell culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background Apoptosis of glomerular mesangial cells is shown in experimental and human glumerulonephritis. But it is unclear whether or not glucocorticoids can induce apoptosis in mesangial cells. Methods Rat mesangial cells in culture were incubated with dexamethazone and methylprednisolone. Apoptosis was evaluated by DNA-specific staining with fluorescent dye (H33258), in situ nick end labeling, gel electrophoresis of extracted DNA, and electron microscopy. Results The proportion of lysed cells and cells positive for nick end labeling increased at a concentration of 0.2 to 5 mmol/L of dexamethazone and methylprednisolone. Chromatin condensation and DNA ladders in those cells were also seen. Actinomycin D, a transcriptional inhibitor, or cycloheximide, a translational inhibitor, partially blocked glucocorticoid-induced apoptosis of rat mesangial cells. Conclusions Glucocorticoids induced typical apoptosis in rat mesangial cells. These data provide new information on the pharmacologic action of glucocorticoids on mesangial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02480618
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Immunoelectron microscopic localization of membrane attack complex and hepatitis B e antigen in membranous nephropathy (1989)
    Springer
    Virchows Archiv 414 (1989), S. 325-330 
    Details
    ISSN: 1432-2307
    Keywords: Membranous nephropathy ; Membrane attack complex ; Hepatitis B virus ; Hepatitis B e antigen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Immunoelectron microscopy was used to localize membrane attack complex (MAC) and hepatitis B e (HBe) antigen in renal tissue specimens from a total of 9 patients with membranous nephropathy (MN); 6 with MN associated with a hepatitis B virus (HBV) infection, 2 with idiopathic MN, and 1 with lupus nephritis. All the patients were proteinuric, and 2 patients were classified as stage I-II, 6 as stage II, and 1 as stage IV. MAC, along with IgG and C3, was distributed within the subepithelial electron dense deposits in all the stages. MAC was also stained in the striated membranous structures within the glomerular basement membrane and mesangial matrix of some patients. In HBV-associated MN, HBe antigen was localized in the subepithelial electron dense deposits of 5 patients, while it was absent from the subepithelial deposits in a patient that was sero-positive for hepatitis B s antigen but negative for HBe antigen. This patient also lacked MAC deposition in these loci. These results suggest that MAC is associated with the formation of subepithelial deposits and proteinuria in MN. In HBV-associated MN, HBe antigen-antibody immune complex makes up the subepithelial deposits and is likely to activate the terminal components of complementin situ.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00734087
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Immunohistochemical study of the membrane attack complex of complement in IgA nephropathy (1988)
    Springer
    Virchows Archiv 413 (1988), S. 77-86 
    Details
    ISSN: 1432-2307
    Keywords: IgA nephropathy ; Membrane attack complex ; Complement ; Striated membrane structures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The localization of the membrane attack complex of complement (MAC) was examined in the normal human kidneys and in biopsy specimens from patients with primary IgA nephropathy by immunofluorescent and immunoelectron microscopies. Immunofluorescent staining for MAC was significantly more intense than in the normal kidneys, and was observed in the mesangium and occasionally along the glomerular capillary walls of 22 of 30 patients with IgA nephropathy. By dualstaining, the MAC deposits were generally concordant with the deposits of IgA, C3, C5 and C9, or of IgG, when present. C1q or C4 was infrequently observed in the glomeruli. Immunoelectron microscopy revealed various staining patterns of glomerular MAC deposition; homogeneous fine-granular staining beneath the glomerular basement membrane (GBM) in the paramesangial zone, patchy staining within the mesangial electron dense deposits (EDD), and ring-shaped or ribbon-like staining, associated with the striated membrane structures (SMS), in the matrix of the mesangium, GBM and tubular basement membrane (TBM). This study suggests that the terminal complement system is activated, mainly by an alternative complement pathway mechanism, in the mesangium of IgA nephropathy, and is associated with the paramesangial lesion and EDD. MAC deposition in glomerular SMS may also result from in situ activation rather than trapping from the circulation. There was little correlation between glomerular MAC deposition and proteinuria or renal histology of patients with IgA nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00844284
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Urinary transforming growth factor-β in patients with glomerular diseases (1997)
    Springer
    Pediatric nephrology 11 (1997), S. 334-336 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Transforming growth factor-β  ;   Glomerulonephritis   ;   Urine   ;   Mesangial matrix
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We measured the urinary levels of active transforming growth factor-β (TGF-β) by enzyme-linked immunosorbent assay in 12 healthy controls and 42 patients with various glomerular diseases, including mesangial proliferative (IgA nephritis, Henoch-Schönlein purpura nephritis, and IgA-negative mesangial proliferative glomerulonephritis) and non-proliferative (minimal change nephrotic syndrome and focal glomerulosclerosis) types. Urinary TGF-β, expressed as a ratio to urinary creatinine (ng/mg creatinine), was elevated in patients with IgA nephritis and focal glomerulosclerosis, and was significantly higher than in patients with other types of glomerular diseases and healthy controls. There was a significant correlation between urinary TGF-β levels and the grade of interstitial fibrosis. Among patients with proliferative-type disease, urinary TGF-β was significantly correlated with the grade of mesangial matrix increase and the magnitude of proteinuria. The relationship between urinary TGF-β levels and the immunostaining intensity of TGF-β in the glomeruli was not significant. These results indicated that urinary TGF-β reflects the grade of interstitial fibrosis in glomerular diseases and also the mesangial matrix increase in proliferative-type glomerulonephritis. Measuring TGF-β levels in the urine might be helpful in monitoring patients with some types of glomerular disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050289
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Acute interstitial nephritis and uveitis syndrome: activated immune cell infiltration in the kidney (1991)
    Springer
    Pediatric nephrology 5 (1991), S. 232-234 
    Details
    ISSN: 1432-198X
    Keywords: Acute interstitial nephritis ; Uveitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Infiltrating cells were analysed in renal biopsy tissue obtained from a 15-year-old girl with acute interstitial nephritis and uveitis using monoclonal antibodies specific for mononuclear cell surface markers. The interstitial infiltrates consisted mainly of T cells and monocytes/macrophages. A considerable proportion of the infiltrating cells were identified by a monoclonal antibody against the interleukin-2 receptor, indicating that a majority of those immune cells are activated. This observation documents the participation of cell-mediated immune injury in interstitial nephritis associated with uveitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01095961
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Immunotactoid glomerulopathy in a child with Down syndrome (1993)
    Springer
    Pediatric nephrology 7 (1993), S. 86-88 
    Details
    ISSN: 1432-198X
    Keywords: Immunotactoid glomerulopathy ; Fibrillary glomerulonephritis ; Down syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 9-year-old girl with Down (21-trisomy) syndrome was found to have proteinuria and microscopic haematuria at age 6 years. Proteinuria gradually increased during the next 3 years, although blood pressure and renal function remained normal. The patient exhibited no underlying systemic diseases, monoclonal gammopathy, cryoglobulinaemia or histological evidence of plasmacytoma. A percutaneous renal biopsy revealed immunotactoid glomerulopathy (fibrillary glomerulonephritis) characterized by thickening of the glomerular basement membrane, diffuse mesangial expansion and various-sized acid-Schiff-positive nodules that were intensely positive for IgG, light chains (κ and λ) and complement components (C3, C4, C1q) along the glomerular capillaries in the mesangium. Congo red dye and amyloid thioflavine T staining were negative. Fibrils (15–17 nm in diameter — larger than amyloid fibrils) were present in the mesangial area and within the glomerular basement membrane. We are not aware of a previous report of immunotactoid glomerulopathy and a patient with chromosomal abnormalities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00861584
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Absence of α6(IV) collagen in kidney and skin of X-linked Alport syndrome patients (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 742-744 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Alport syndrome   ;   Type IV collagen   ;   Basement membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Ab stract. To identify the abnormalities of the type IV collagen α6 chain, α6(IV), in Alport syndrome, we examined renal and skin tissue using rat monoclonal antibodies against non-consensus amino acid sequences of α6(IV). Immunofluorescence of normal human kidney and skin tissue revealed linear α6(IV) staining in the basement membrane (BM) of Bowman’s capsule, in some tubules, and also in the epidermal BM. Renal specimens from five male patients of four families with X-linked Alport syndrome showed no reactivity for α6(IV) in Bowman’s capsules and tubules. In these patients, α1(IV) and α2(IV) were normal, whereas α3(IV), α4(IV), and α5(IV) were absent from the BMs of the kidney. In skin tissue of male patients, neither α5(IV) nor α6(IV) were detected. The epidermal BM of female heterozygotes with X-linked Alport syndrome showed a mosaic staining for α5(IV) and α6(IV). These findings indicate that, in addition to a disturbed α3(IV)-α4(IV)-α5(IV) network, patients with X-linked Alport syndrome have abnormalities in α6(IV) of the renal and epidermal BMs at the protein level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050206
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...