Basement membranes fragments

LH3 null mice are embryonic lethal at E9.5-14.5, show fragmentation of basement membrane and possibly some type IV collagen abnormalities... 

A large number of tumor blood vessels increases the opportunity of the tumor cells to enter the circulation. In fact, the newly formed capillaries usually have a fragmented basement membrane, facilitating easier invasion. In the prevascular phase, with little or no angiogenic activity, the tumor is unable to expand beyond a few cubic millimeters, but once angiogenic factors are released in sufficient number, the onset of angiogenic activity stimulates rapid expansion of the tumor. 

Podocyte damage in membranous nephropathy is probably caused by the local activation of complement with the formation of the membranolytic complex C5b-C9. Locally formed chemotactic fragments of complement (e.g., C5a) do not penetrate through the glomerular basement membrane, and that is why in membranous nephropathy glomeruli are not infiltrated with leukocytes. 

Figure 5.1 Schematic illustration of the structure of the wall of different classes of blood capillaries. (1) Continuous capillary (as found in the general circulation). The endothelium is continuous with tight junctions between adjacent endothelial cells. The subendothehal basement membrane is also continuous. (2) Fenestrated capillary (as found in exocrine glands and the pancreas). The endothelium exhibits a series of fenestrae which are sealed by a membranous diaphragm. The subendothehal basement membrane is continuous. (3) Discontinuous (sinusoidal) capillary (as found in the liver, spleen and bone marrow). The overlying endothelium contains numerous gaps of varying size. The subendothehal basement is either absent (hver) or present as a fragmented interrupted structure (spleen, bone marrow)...

Other markers are also available for monitoring the breakdown of the basement membrane components, including collagen breakdown products and laminin fragments. However, at present, few of these markers have found a place in the cHnical laboratory. 

The predominant involvement of the respiratory tract in oxygen toxicity is probably due to the fact that the lungs are the first and only organ to come in contact with the full Pio,. Dyspnea, capillary congestion, alveolar exudation, hemorrhage, atelectasis, swelling of alveolar walls with encroachment on alveolar spaces, fragmentation of basement membranes between alveolar and endothelial cell layers, accumulation of exudate between the basement... 

When tested, the amyloid is of the secondary type, amyloid A protein. Serum amyloid A, an acute phase reactant produced by hepatocy tes, circulates complexes to high density lipoprotein and is cleaved into smaller fragments which subsequently polymerize into the P pleated sheet configuration of amyloid [23, 35]. In heroin related amyloidosis, the amyloid is heavily distributed in the tubular basement membranes, vessel walls, and interstitium as well as the glomeruli. There is greater tubular basement membrane and interstitial amyloid deposition in drug related renal amyloid than in secondary renal amyloid unrelated to heroin abuse... 

Alveolar septa may show some degree of expansion due to capillaritis, edema, and/or interstitial fibrosis (84,85). Capillaritis, characterized by neutrophils within the septa, is usually focal and of mild to moderate intensity. Diffuse or prominent capillaritis, or vasculitis of larger blood vessels is atypical, and if present, suggests another disease process. When interstitial fibrosis is present, it too is usually patchy and mild. Type II pneumocytes may show hyperplasia and reactive atypia in response to alveolar damage. In some cases, hyaline membranes are seen focally (85). Ultrastructural studies have shown fragmentation of alveolar septal basement membranes and wide gaps between endothelial cells (90). 

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