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Angiopathy

Acute myocardial infarction Angiopathy Aortic aneurysm Aortic balloon assist devices Giant hemangiomas Peripheral vascular disease Postcardiac arrest Prosthetic devices Raynaud s syndrome Infectious Arbovirus Aspergillus Candida albicans Cytomegalovirus Ebola virus... [Pg.996]

The pathogenesis of diabetic foot infection stems from three key factors neuropathy, angiopathy, and immunopathy. Aerobic gram-positive cocci, such as S. aureus and P-hemolytic streptococci, are the predominant pathogens in acutely infected diabetic foot ulcers. However, chronically infected wounds are subject to polymicrobial infection and require treatment with broad-spectrum antibiotics. [Pg.1075]

Angiopathy of large (macroangiopathy) and small (microangiopathy) vessels is also the result of high blood glucose concentrations. Angiopathy results in ischemia and skin breakdown. [Pg.1082]

Wisniewski HM, Frackowiak J, Mazur Kolecka B. In vitro production of beta-amyloid in smooth muscle cells isolated from amylid angiopathy-affected vessels. Neurosci Lett 1995 183 120-123. [Pg.280]

Walker LC. Animal models of cerebral beta-amyloid angiopathy. Brain Res Brain Res Rev 1997 25 70-84. [Pg.281]

Creutzfeldt-Jakob disease (CJD) Alzheimer s disease (AD) Hemodialysis-related amyloidosis Primary systemic amyloidosis Secondary systemic amyloidosis Familial amyloid polyneuropathy I Familial amyloid polyneuropathy III Cerebral amyloid angiopathy Finnish hereditary systemic amyloidosis Type II diabetes Injection-localized amyloidosis Medullary thyroid carcinoma Atrial amyloidosis... [Pg.199]

Olafsson, I., and Grubb, A. (2000). Hereditary cystatin C amyloid angiopathy. Amyloid 7, 70-79. [Pg.279]

APOE genotypes directly influence lipid metabolism and atherosclerosis (see Fig. 10.17). The presence of the APOE-4 allele contributes to the phenotypic manifestation of atherosclerosis, brain amyloid angiopathy, and cerebral white... [Pg.308]

Olichney, J.M., Hansen, L.A., Galasko, D., et al. (1996) The apolipoprotein E epsylon-4 allele is associated with increased neuiific plaques and cerebral amyloid angiopathy in Alzheimer s disease and Lewy body variant. Neurology, 47, 190-196. [Pg.349]

Tian, J., Shi, J., Bailey, K., Lendon, C.L., Pickering-Brown, S.M., Mann, D.M.A. (2004) Association between apolipoprotein E E4 allele and arteriosclerosis, cerebral amyloid angiopathy, and cerebral white matter damage in Alzheimer s disease. J. Neurol. Neurosurg. Psychiatry, 75, 696-699. [Pg.351]

Haller H, Drab M, Luft FC. (1996) The role of hyperglycemia and hyper-insulinemia in the pathogenesis of diabetic angiopathy. Clin Nephrol 46 246-255. [Pg.581]

The massive amyloid deposition in the form of parenchymal plaques and/or in cerebrovascular amyloid (cerebral amyloid angiopathy) is associated with neuronal loss and dysfunction. In particular the cholinergic neurons of the basal forebrain, which are involved in the memory processes, are affected and neuron loss in these nuclei accounts for some of the AD symptoms. [Pg.25]

Diabetes mellitus can have serious secondary effects. A constantly raised blood sugar level can lead in the long term to changes in the blood vessels (diabetic angiopathy), kidney damage (nephropathy) and damage to the nervous system (neuropathy), as well as to cataracts in the eyes. [Pg.160]

The closed-loop type artificial pancreas (specifically 8-cell), which consists of an automatic continuous monitor of blood glucose level (BGL) and an automatic injector of insulin which are coupled with feed-back system, has great potential for prevention of diabetic complication such as micro-angiopathies(l). A large-scale closed-loop type artificial pancreas for bedside use has already been developed and is clinically used at some laboratories and hospitals (2-4). However, this device is limited to only bedside use. On the other hand, the open-loop type artificial pancreas which consists of only a insulin injecting pump without an automatic continuous monitor of BGL, has been developed and is going to be clinically used(5-7). This system, however, can not completely control BGL as well as the bare pancreas in a normal body and often causes lower BGL(8-9). [Pg.373]

In particular, conditions of Aft overproduction or impaired cerebral Aft clearance mechanisms result in elevated Aft levels that promote Aft aggregation, oligomerization, and fibrillogenesis [20]. Deposition of Aft in an insoluble beta-pleated conformation (amyloid) occurs as plaques in the neuropil and as amyloid angiopathy in the cerebral vasculature. The deposition of amyloid initiates a cascade of injurious events, including free radical production, glial activation, and direct neuronal damage. Kinase activation in response to amyloid-induced injury may increase the amount... [Pg.110]

Flyvbjerg A, Orskov H. Diabetic angiopathy new experimental and clinical aspects. Hormone and Metabolic Research 2005, 37, 1-3. [Pg.110]

Barelli, H Lebeau, A., Vizzavona, J., et al. (1997) Characterization of new polyclonal antibodies specific for 40 and 42 amino acid-long amyloid beta peptides their use to examine the cell biology of presenilins and the immunohistochemistry of sporadic Alzheimer s disease and cerebral amyloid angiopathy cases. Mol. Med. 3, 695-707. [Pg.86]

Yu, P.H. 1998. Deamination of methylamine and angiopathy toxicity of formaldehyde, oxidative stress and relevance to protein glycoxidation in diabetes. J Neural Transm Suppl 52 201-216. [Pg.208]

Macro-angiopathy, leading to increased risk of cardiovascular events. [Pg.143]

Fig. 13.5. T2 -weighted gradient echo images in a patient with biopsy proven cerebral amyloid angiopathy (CAA). Extensive low signal abnormality is noted on the brain surfaces and in the parenchyma indicating the previous hemorrhages. Periventricular high intensity lesions, a common finding in CAA is also noted... Fig. 13.5. T2 -weighted gradient echo images in a patient with biopsy proven cerebral amyloid angiopathy (CAA). Extensive low signal abnormality is noted on the brain surfaces and in the parenchyma indicating the previous hemorrhages. Periventricular high intensity lesions, a common finding in CAA is also noted...
Greenberg SM, Briggs ME, Hyman BT et al (1996b) Apoli-poprotein E e4 is associated with the presence and earlier onset of hemorrhage in cerebral amyloid angiopathy. Stroke 27 1333-1337... [Pg.206]

Greenberg SM, O Donnell HC, Schaefer PW, Kraft E (1999) MRI detection of new hemorrhages potential marker of progression in cerebral amyloid angiopathy. Neurology 53 1135-1138... [Pg.206]

Itoh Y, Yamada M, Hayakawa M, Otomo E, Miyatake T (1993) Cerebral amyloid angiopathy a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly. J Neurol Sci 116 135-141... [Pg.206]


See other pages where Angiopathy is mentioned: [Pg.73]    [Pg.185]    [Pg.1082]    [Pg.321]    [Pg.253]    [Pg.223]    [Pg.231]    [Pg.235]    [Pg.237]    [Pg.237]    [Pg.250]    [Pg.260]    [Pg.490]    [Pg.103]    [Pg.19]    [Pg.20]    [Pg.160]    [Pg.168]    [Pg.193]    [Pg.203]    [Pg.203]    [Pg.204]    [Pg.205]   


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Cerebral amyloid angiopathy

Cerebral amyloid angiopathy hemorrhage

Cystatin C amyloid angiopathy

Hereditary cystatin C amyloid angiopathy

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