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1. |
The pathogenesis and biochemistry of amyloidosis |
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The Journal of Pathology,
Volume 151,
Issue 1,
1987,
Page 1-10
Alan S. Cohen,
Lawreen Heller Connors,
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摘要:
AbstractThe transformation of serum proteins into Congo red‐sensitive fibrillar material is requisite for the onset and progression of amyloid disease. All the mechanisms which lead to the disease itself have not been elucidated, but our knowledge has increased significantly. It is apparent that in all types of amyloid fibrils, three common features are displayed by the major protein constituents. These are that the fibril protein has (1) a serum precursor, (2) a high degree of anti‐parallel beta‐sheet conformation and (3) a distinctive ultrastructure on electron microscopy. In the AL and AA forms of amyloidosis, the putative precursors appear to undergo limited degradation to form the protein component of amyloid fibrils. It has been suggested that there may be certain primary structural characteristics inherent in precursor molecules which make them amyloidogenic, thus predisposing them to amyloid fibril formation.33This would include certain subtypes of immunoglobulin light chains, possibly kappa I and lambda VI, in the AL type of amyloidosis and one of the polymorphic SAA species, SAA2, which has been identified as the predominating isotype found in AA amyloid fibrils.32,33,110In AH amyloidosis, the mechanism of amyloid fibril formation appears to be simply a concentration phenomenon where elevated concentrations of B2‐M are not handled normally and amyloid deposition is the result. Amyloidogenesis in the hereditary form of systemic amyloidosis may involve other factors in addition to the presence of a variant precursor prealbumin as indicated by the delayed onset of the disease. It is evident that the elucidation of the mechanism(s) which governs the onset and progression of the amyloidoses will allow future regulation and treatment of these all too often complex di
ISSN:0022-3417
DOI:10.1002/path.1711510102
出版商:John Wiley&Sons, Ltd.
年代:1987
数据来源: WILEY
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2. |
Lesions of the renal papilla induced by paracetamol |
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The Journal of Pathology,
Volume 151,
Issue 1,
1987,
Page 11-19
M. A. Henry,
J. D. Tange,
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摘要:
AbstractThe acute nephrotoxic effects of paracetamol in the uninephrectomized homozygous Gunn rat are different from those of aspirin. Both compounds induce renal papillary necrosis but paracetamol produces accumulation of non‐cellular material in the interstitial space, less damage to interstitial cells, more damage to tubular epithelium, and more severe necrosis of proximal convoluted tubules. In both cortex and papilla only a small fraction of the cells at risk are affected. It is concluded that the findings are consistent with a synergistic nephrotoxic effect between the two compounds, but that the lesions are not sufficiently severe for the natural history of analgesic nephropathy to be wholly explicable by such synergis
ISSN:0022-3417
DOI:10.1002/path.1711510103
出版商:John Wiley&Sons, Ltd.
年代:1987
数据来源: WILEY
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3. |
Announcement |
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The Journal of Pathology,
Volume 151,
Issue 1,
1987,
Page 21-21
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ISSN:0022-3417
DOI:10.1002/path.1711510104
出版商:John Wiley&Sons, Ltd.
年代:1987
数据来源: WILEY
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4. |
Synopsis of papers presented at the 15th Meeting of the Pathological Society of Great Britain and Ireland |
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The Journal of Pathology,
Volume 151,
Issue 1,
1987,
Page 23-102
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ISSN:0022-3417
DOI:10.1002/path.1711510105
出版商:John Wiley&Sons, Ltd.
年代:1987
数据来源: WILEY
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5. |
Masthead |
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The Journal of Pathology,
Volume 151,
Issue 1,
1987,
Page -
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PDF (92KB)
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ISSN:0022-3417
DOI:10.1002/path.1711510101
出版商:John Wiley&Sons, Ltd.
年代:1987
数据来源: WILEY
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