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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Retinoids have effects on the metabolism of keratinization and on the metabolism of connective tissue. Recent results have indicated that they may be helpful for treating dermatological diseases which involve marked connective tissue changes such as scleroderma, keloids and actinic skin damage. In addition, retinoids have been shown to reduce the clinical and histological alterations occurring in vulvar lichen sclerosus. For these reasons, etretinate was tried in a patient with extensive lichen sclerosus et atrophicus (LSA). Clinical improvement was seen after three months' treatment, i.e. a decrease in pruritus and softening of the skin. The degenerated zone in the lesional skin was shown by histological analyses to have reduced markedly. The immunohistochemistry, with unaltered staining for type III procollagen and fibronectin, disclosed no signs of enhanced collagen synthesis. Thus the reparation mechanism remained obscure.
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PMID:Etretinate reduces connective tissue degeneration in lichen sclerosus et atrophicus. 257 15

Albino hairless mice (Skh: HR-1) exposed chronically to sub-erythemal doses of UV radiation display physical, visible and histological alterations. Using narrow bandwidth radiation covering the UV radiation spectrum from 280-380 nm, the wavelength dependence of these alterations was determined. The wavelength dependence spectra indicate that for all but one parameter measured (skin sagging), UV-B radiation is considerably more efficient than UV-A radiation in producing changes in the skin. However, in natural sunlight there is considerably more UV-A than UV-B radiation, providing the potential for UV-A to have a larger contribution to skin damage than UV-B. This argues in favor of using broad spectrum photoprotective agents to shield the skin adequately from UV-induced aging. The spectra were also used to develop potential associations among events by determining which events occur at similar wavelengths. There seems to be a correspondence between mouse visible skin wrinking (UV-B event) and two histological events: increase in glycosaminoglycans and alteration in collagen. There was no obvious correspondence among UV-A-induced events.
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PMID:Wavelength dependence of histological, physical, and visible changes in chronically UV-irradiated hairless mouse skin. 262 90

Light and electron microscopy of mouse skin damage caused by intradermal infection with a virulent strain of Vibrio vulnificus and by a single intradermal injection of the cytolytic toxin produced by the bacterium revealed similar structural alterations. The epidermis was intact; however, the infection and toxin produced acute cellulitis characterized by extensive extracellular edema; disorganization of collagen bundles; large accumulations of cell debris and plasma proteins; damaged or necrotic fat cells, capillary endothelial cells, and muscle cells; and mild inflammatory cell infiltration. The virulent strain of V. vulnificus produced a capsule and was resistant to phagocytosis in vivo, whereas a weakly virulent strain of the bacterium did not produce a capsule and was readily phagocytized and digested. Factors that may be important in the pathogenesis of V. vulnificus wound infections include a capsule that inhibits phagocytosis and an extracellular cytolytic toxin that is responsible, at least in part, for the severe tissue damage characteristic of such wound infections.
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PMID:Mouse skin damage caused by cytolysin from Vibrio vulnificus and by V. vulnificus infection. 380 62

Ulcerated and nonulcerated skin from 5 patients with chronic radiation skin damage was examined using electron microscopy. Noticeable fibroblast disorganization was seen, with swollen and degenerating mitochondria, multiple vacuoles, and dilated irregular rough endoplasmic reticulum. Unusual crystalline inclusions were seen in some fibroblasts. In the ulcerated skin, contractile fibroblasts (myofibroblasts) were seen in 2 of 4 specimens. Stroma showed dense collagen and prominent elastosis. The microvasculature in the radiation-damaged tissue showed occasional lumen occlusion and vacuolization of endothelial cells, without consistent abnormality. These data suggest that permanent damage to fibroblasts or fibroblast stem cells may play an important role in chronic radiation skin ulceration.
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PMID:The ultrastructure and etiology of chronic radiotherapy damage in human skin. 714 58

The cytotoxicity of monoterpenes, percutaneous absorption enhancers, to cultured human skin cells was investigated in order to quantitatively estimate their skin damage. A neutral red bioassay with epidermal keratinocytes and a contraction test of collagen gel in which dermal fibroblasts were cultured were employed for evaluating the cytotoxicity of terpenes. In the neutral red bioassay, keratinocyte proliferation was inhibited on the addition of terpenes, and cell survival remarkably decreased with an increase in the concentration of terpenes fed into the culture well. When the fibroblasts were cultured in a collagen gel matrix, the lattice of collagen contracted as the cells grew. Therefore, the application of cytotoxic agents brings about an inhibition of collagen gel contraction induced by the fibroblasts. Strong inhibition was observed in the cases of hydrocarbons in terpenes, and the inhibition was dependent on the concentration of these compounds added in the culture medium. The cytotoxicity of terpenes was compared with the skin damage evoked by the application of terpenes in rats in vivo. As a result, it was considered that the skin irritation caused by terpenes was predictable to a certain extent by means of the cytotoxic study of cultured human skin cells.
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PMID:Evaluation of skin damage of cyclic monoterpenes, percutaneous absorption enhancers, by using culture human skin cells. 826 59

In this ultrastructural study, albino hairless mice were irradiated with long-wavelength ultraviolet (UVA) (340-400 nm) thrice weekly for 32 weeks for a cumulative dose of 8000 J/cm2. Biopsies were taken from these mice, from age-matched unirradiated controls, and from mice irradiated with UVB for 20-30 weeks with a cumulative dose of approximately 6-9 J/cm2. The most striking UVA-induced changes were 1) elastic fiber hyperplasia without evidence of fiber disintegration, 2) a large increase in randomly deposited microfibrils; 3) massive duplication of vascular basement membrane; 4) extensive endothelial cell damage; and 5) collagen fibers with smaller diameters but without apparent damage. By contrast, after UVB, the hyperplastic elastic fibers frequently appeared to be degraded. Microfibrils were only moderately increased and remained in an organized array. Also, unlike with UVA, the epidermal basement membrane was duplicated whereas that of the vessels was mainly spared. Collagen fibers showed evidence of dissolution. Thus, ultrastructural features provide further evidence that skin damage induced by UVA can be dissimilar to that induced by UVB.
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PMID:UVA-induced ultrastructural changes in hairless mouse skin: a comparison to UVB-induced damage. 842 42

Several recent investigations collectively suggest that the role of ultraviolet A (UVA) in chronic actinic skin damage may be greater than originally thought. In the present work, the output of a xenon-arc solar-simulator passed through a Bausch & Lomb monochromator in conjunction with a 2-mm Schott WG-320 filter produced narrow-band UVA centered at 338 nm, half-band width 24 nm, I0 = 3.4 +/- 0.3 mW/cm2. We chronically irradiated 10 Sk-1 albino hairless mice 5 times per week for 18 weeks, starting with 1.25 J/cm2, for 33 irradiation days, sequentially followed by 1.50 J/cm2 (34 days), 1.8 J/cm2 (10 days), 2.0 J/cm2 (22 days) to afford a total UVA dose of 154.3 J/cm2 over 99 irradiation days. Erythema was noted clinically by day 6, which persisted throughout the irradiation. During the irradiation period, some scaling, consistent with mild epidermal hyperplasia was noted during irradiation days 37-56. This response later regressed despite continued chronic irradiation. Hematoxylin and eosin examination immediately after the final irradiation revealed a mild inflammatory response, with some dermal restructuring. At the end of the experiment, no significant signs of epidermal hyperplasia or (pre)malignant lesions were seen, although some stratum corneum thickening was noted. Marked dermal collagen damage and moderate elastosis was also evident. We believe that the observed differences in results reported in previous studies are in large part due to differences in light sources and irradiation protocols.
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PMID:Chronic exposure of Sk-1 hairless mice to narrow-band ultraviolet A (320-355 nm) 911 83

Vibrio vulnificus wound infection is characterized by an intense acute cellulitis which spreads along the subcutaneous tissue with severe tissue destruction. Toxins produced by the bacteria appear to be involved in the pathogenesis of skin necrosis and to facilitate microbial dissemination in vivo. We report microscopic studies of mouse skin damage caused by a single intradermal injection of V. vulnificus or of an extracellular metalloprotease isolated from this organism. The gene encoding this metalloprotease has been cloned and expressed in Escherichia coli. The crude metalloprotease extract obtained from the periplasmic fraction by osmotic shock was used in this study. Intradermal injection of this preparation resulted in marked edematous changes of the skin, which extended throughout the dermis and subcutaneous tissues and into adjacent muscles. The collagen and elastic fibers degenerated and some muscle cells even appeared necrotic. Blood vessels became congested, with moderate perivascular neutrophil and mononuclear cell infiltration. There was no evidence of necrotic changes in the blood vessel itself. These results show that the damage to the connective tissues caused by V. vulnificus is at least partly attributable to its protease. Therefore, the protease seems to be an important virulence factor of this microbe.
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PMID:Mouse skin damage caused by a recombinant extracellular metalloprotease from Vibrio vulnificus and by V. vulnificus infection. 930 19

For preventing or minimizing acute and chronic skin damage caused by UV radiation, the use of sunscreens is probably the most important measure. To screen the protective efficacy of new sunscreen molecules or formulations against UV rays, we evaluated as in vitro testing methods the use of two three-dimensional models, a dermal equivalent (DE) and a skin equivalent (SE). The DE is composed of a porous collagen-glycosaminoglycans-chitosan matrix populated by normal human fibroblasts. The SE is comprised of a fully differentiated epidermis realized by seeding keratinocytes onto the DE. In this study, we demonstrated that the DE and SE models react to the deleterious effects of UVA and UVB. Then, we extended our research to the evaluation of their usefulness for photoprotection trials. Sunscreen agents (Eusolex 8020 and 6300) and commercially available sunscreens (chemical and physical filter formulations) that protect the skin against either UVA or UBV were evaluated. The tested products were applied (n = 6) topically (10 microL) and incubated for 30 min prior to irradiation over a range of UVA (0-50 J/cm2) or UVB (0-5 J/cm2). The photoprotection provided by the tested sunscreen molecules and formulations was evaluated by measurement of residual cellular viability 24 h postirradiation using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test and assessment of the inflammation response by interleukin-1 alpha release assay. When sunscreens were applied prior to UV exposure, a higher residual cellular viability versus control was obtained, demonstrating the photoprotective effects of the tested products. These in vitro models could be used for screening tests to evaluate the protective effects of sunscreen molecules and formulations, especially for UVA trials because there is a lack of consensus for an in vivo method.
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PMID:Measurements of the protective effect of topically applied sunscreens using in vitro three-dimensional dermal and skin equivalents. 942 71

Blister formation and skin damage can be induced by BaP1, a haemorrhagic metalloproteinase from the venom of the snake Bothrops asper. Pathological changes in the skin were investigated after intramuscular injections of Bothrops asper haemorrhagic metalloproteinase BaP1. Blisters developed within the first hour, with separation of epidermis from the dermal-epidermal junction, whereas acantholysis of epithelial cells was not observed. After the third hour there was ulceration with formation of a proteinaceous scab and inflammatory infiltrate. By 7 to 14 days there was evidence of a regenerative process in dermis and epidermis. Haemorrhage occurred in both dermis and hypodermis as a consequence of BaP1 injection, together with damage of sebaceous glands and an inflammatory reaction in which enlarged macrophages were the predominant cell type. Zymography assays showed the presence of several endogenous metalloproteinases in the exudate, skin homogenates and plasma. In addition, BaP1 was detected in exudates and plasma by immunoblotting. This technique also demonstrated the presence of components immunologically related to laminin and collagen type IV in exudates. It is suggested that BaP1, and probably endogenous matrix metalloproteinases, degrade some protein components at the dermal-epidermal junction, inducing the formation of blisters.
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PMID:Blister formation and skin damage induced by BaP1, a haemorrhagic metalloproteinase from the venom of the snake Bothrops asper. 979 20


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