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Inhibitory Effect of Elastase on the Glomerular Capillary Basement Membrane Thickening of the Experimental Congenital Diabetic Mice (N.S.Y. Mice)YASUDA, BUNJI, SASAKI, MAKOTO, KUNO, TSUNEJI, KOBAYASHI, KAIZO, KISHI, TSUNEKI, KAWANISHI, ATSUKO, SHIBATA, MASAO 03 1900 (has links)
No description available.
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Carbohydrate of rat glomerular basement membraneLui, Sylvia Wai-Lan. January 1972 (has links)
No description available.
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Carbohydrate of rat glomerular basement membraneLui, Sylvia Wai-Lan. January 1972 (has links)
No description available.
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Identification of a mutation in COL4A5 causative for X-linked Alport syndrome in the domestic dog and analysis of gene expression in the kidneys of affected and nonaffected siblingsCox, Melissa Luanne 30 September 2004 (has links)
The domestic dog, Canis lupus familiaris, plays many roles in the lives of humans. Additionally, the dog is recognized for its potential as a model for many human hereditary diseases. Thus, the genetics and genomics of the dog are being studied extensively in order to facilitate its use as a model, as well as to help the dog for its own sake. As part of this research effort, our laboratory has added type I markers (i.e., the acidic and basic keratins, c-kit, type I and IV collagens, and the gene encoding uromodulin) to the emerging map of the canine genome. The mapping of genes, particularly those in large gene families such as the collagens, is valuable because it rapidly increases the density of gene loci on the map and provides insight regarding conservation of synteny between the dog and other mammals. The major focus of work reported here is the genetics of X-linked Alport syndrome (XLAS), a terminal renal disease that affects the human and the dog. The disease results from mutations in COL4A5, a type IV collagen gene. Reported here are the 1) sequencing and mapping of the canine cDNA encoding uromodulin, 2) mapping of the type I and type IV collagen genes, 3) sequencing of the full-length cDNA of canine COL4A5, 4) identification of a 10 bp deletion in COL4A5, causative for XLAS in our colony of mixed breed dogs, 5) development of a genetic test for identification of affected and carrier dogs in the colony and 6) assessment of gene expression in the kidneys of normal and XLAS-dogs. This assessment was performed using a canine-specific oligonucleotide microarray. XLAS dogs demonstrated up-regulation of many genes involved in extracellular matrix reorganization, cell structure, and immune response, as expected in a glomerulopathy with tubulointerstitial nephritis. Trends were verified by quantitative RT-PCR. A review of the current status of canine genetics research, and current understanding of hereditary diseases in the dog, concludes this dissertation.
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Glomerular Basement Membrane Thickening in Renal AllograftsWAKABAYASHI, TOMO 03 1900 (has links)
No description available.
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Identification of a mutation in COL4A5 causative for X-linked Alport syndrome in the domestic dog and analysis of gene expression in the kidneys of affected and nonaffected siblingsCox, Melissa Luanne 30 September 2004 (has links)
The domestic dog, Canis lupus familiaris, plays many roles in the lives of humans. Additionally, the dog is recognized for its potential as a model for many human hereditary diseases. Thus, the genetics and genomics of the dog are being studied extensively in order to facilitate its use as a model, as well as to help the dog for its own sake. As part of this research effort, our laboratory has added type I markers (i.e., the acidic and basic keratins, c-kit, type I and IV collagens, and the gene encoding uromodulin) to the emerging map of the canine genome. The mapping of genes, particularly those in large gene families such as the collagens, is valuable because it rapidly increases the density of gene loci on the map and provides insight regarding conservation of synteny between the dog and other mammals. The major focus of work reported here is the genetics of X-linked Alport syndrome (XLAS), a terminal renal disease that affects the human and the dog. The disease results from mutations in COL4A5, a type IV collagen gene. Reported here are the 1) sequencing and mapping of the canine cDNA encoding uromodulin, 2) mapping of the type I and type IV collagen genes, 3) sequencing of the full-length cDNA of canine COL4A5, 4) identification of a 10 bp deletion in COL4A5, causative for XLAS in our colony of mixed breed dogs, 5) development of a genetic test for identification of affected and carrier dogs in the colony and 6) assessment of gene expression in the kidneys of normal and XLAS-dogs. This assessment was performed using a canine-specific oligonucleotide microarray. XLAS dogs demonstrated up-regulation of many genes involved in extracellular matrix reorganization, cell structure, and immune response, as expected in a glomerulopathy with tubulointerstitial nephritis. Trends were verified by quantitative RT-PCR. A review of the current status of canine genetics research, and current understanding of hereditary diseases in the dog, concludes this dissertation.
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Nidogen-2 in der Pathogenese Kollagen IV-assoziierter Nephropathien bei zusätzlicher Podocin-Mutation / Nidogen-2 in the pathogenesis of collagen IV-related nephropathies with additional podocin mutationPrinz, Carolin Susanne 16 November 2016 (has links)
Kollagen IV assoziierte Nephropathien sind hereditäre Erkrankungen, die die glomeruläre Basalmembran betreffen. Homozygote Aberrationen des COL4A3- oder des COL4A4-Gens zeigen wie X-chromosomal dominant vererbte Mutationen des COL4A5-Gens das klinische Bild des Alport-Syndroms mit frühzeitigem terminalem Nierenversagen. Heterozygote COL4A3-Mutationen sind ursächlich für die benigne familiäre Hämaturie. Ein zusätzlicher Polymorphismus in Nphs2, welches das Schlitzmembranprotein Podocin kodiert, könnte hierbei zu einem aggravierten Krankheitsverlauf führen. Um diese These zu überprüfen, ist eine Analyse des glomerulären Filters, bestehend aus glomerulärer Basalmembran, der zwischen den Podozytenfüßen liegenden Schlitzmembran und Kapillarendothel notwendig. Nidogen-2 ist als Verbindungsprotein essenzieller Bestandteil der glomerulären Basalmembran. Die Ergebnisse der Untersuchungen des Proteins in der Basalmembran COL4A3 heterozygoter Mäuse mit zusätzlichem Podocin-Polymorphismus wichen stark von denen bei einfach COL4A3 heterozygoten Tieren ab. Es ergeben sich daher anhand von Nidogen-2 Hinweise, dass eine Mutation in Nphs2 den Krankheitsverlauf Kollagen IV assoziierter Erkrankungen modifizieren könnte.
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Die Interaktion zwischen der glomerulären Basalmembran und der Schlitzmembran im col43+/-/nphs2+/R140Q-Tiermodell / The interaction between the glomerular basement membrane and the slit diaphragm in the col4a3+/-/nphs2+/R140Q-animal modelGrönemeyer, Lisa-Lena 04 October 2011 (has links)
No description available.
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Die Bedeutung der glomerulären Basalmembrankomponente Nidogen-1 bei podozytären Erkrankungen der Niere / The significance of the glomerular basement membrane component nidogen-1 in podocytic kidney diseasesSpieker, Christine 12 June 2017 (has links)
No description available.
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Die Bedeutung des Kollagenrezeptors α2β1- Integrin bei der Pathogenese und Prävention der Nierenfibrose in hereditären Typ IV- Kollagen- Erkrankungen / The importance of the collagen- receptor integrin α2β1 in the pathogenesis and prevention of renal fibrosis in hereditary type IV collagen diseasesMartin, Maria 09 May 2011 (has links)
No description available.
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