Literature DB >> 1869651

A study of elastic tissue and actinic radiation in "aging," temporal arteritis, polymyalgia rheumatica, and atherosclerosis. The actinic storm in the modern world.

J P O'Brien1, W Regan.   

Abstract

Solar radiation provokes a lifelong series of destructive changes in the supporting elastic tissues of "exposed" skin. Called actinic elastosis/lysis (or actinic "aging"), the sequence begins in early life as simple elastic hyperplasia, converts in middle life to progressive actinic elastotic degeneration, and, in late life, typically ends with a stage of resorption (elastolysis) and atrophy ("aged" skin). Superficial "exposed" arteries such as the temporal artery participate in the same sequence of degenerative elastotic changes, which, as in the skin, may provoke granulomatous responses in a few of the many subjects affected. In the case of the temporal artery, a contingent outcome may be giant cell (temporal) arteritis and its recognized systemic vascular expression, polymyalgia rheumatica. Actinic commotion at the surface of the body is often massive in degree and extent and may be expected to exert a deleterious autoimmune impact on the essential elastic tissues of the arterial system. For this reason, solar radiation should be recognized as a risk factor for other elastic-related vascular diseases, including atherosclerosis and aneurysms. Man-made radiations may be exacerbating the effects of predominant solar radiation. Of the many radiant bands that make up the actinic (electromagnetic) spectrum, little is known for certain about the identity of those that cause these prevalent disorders of elastic tissue. Until this void is filled, more care should be taken with solar and the other "safe" radiations.

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Year:  1991        PMID: 1869651     DOI: 10.1016/0190-9622(91)70118-l

Source DB:  PubMed          Journal:  J Am Acad Dermatol        ISSN: 0190-9622            Impact factor:   11.527


  6 in total

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2.  Giant cell arteritis.

Authors:  J P O'Brien; W Regan; E G Cleary
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3.  Post-cardiac transplant arteriopathy in piglets is associated with fragmentation of elastin and increased activity of a serine elastase.

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4.  Fingerprinting desmosine-containing elastin peptides.

Authors:  Christoph U Schräder; Andrea Heinz; Petra Majovsky; Christian E H Schmelzer
Journal:  J Am Soc Mass Spectrom       Date:  2015-01-21       Impact factor: 3.109

5.  Elafin, a serine elastase inhibitor, attenuates post-cardiac transplant coronary arteriopathy and reduces myocardial necrosis in rabbits afer heterotopic cardiac transplantation.

Authors:  B Cowan; O Baron; J Crack; C Coulber; G J Wilson; M Rabinovitch
Journal:  J Clin Invest       Date:  1996-06-01       Impact factor: 14.808

6.  The endogenous vascular elastase that governs development and progression of monocrotaline-induced pulmonary hypertension in rats is a novel enzyme related to the serine proteinase adipsin.

Authors:  L Zhu; D Wigle; A Hinek; J Kobayashi; C Ye; M Zuker; H Dodo; F W Keeley; M Rabinovitch
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  6 in total

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