Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-two patients with malignant melanoma were treated with boron neutron capture therapy (BNCT) using 10B-p-boronophenylalanine (BPA). The estimation of absorbed dose and optimization of treatment dose based on the pharmacokinetics of BPA in melanoma patients is described. The doses of gamma-rays were measured using small TLDs of Mg2SiO4 (Tb) and thermal neutron fluence was measured using gold foil and wire. The total absorbed dose to the tissue from BNCT was obtained by summing the primary and capture gamma-ray doses and the high LET radiation doses from 10B(n, alpha)7Li and 14N(n,p)14C reactions. The key point of the dose optimization is that the skin surrounding the tumour is always irradiated to 18 Gy-Eq, which is the maximum tolerable dose to the skin, regardless of the 10B-concentration in the tumor. The neutron fluence was optimized as follows. (1) The 10B concentration in the blood was measured 15-40 min after the start of neutron irradiation. (2) The 10B-concentration in the skin was estimated by multiplying the blood 10B value by a factor of 1.3. (3) The neutron fluence was calculated. Absorbed doses to the skin ranged from 15.7 to 37.1 Gy-Eq. Among the patients, 16 out of 22 patients exhibited tolerable skin damage. Although six patients showed skin damage that exceeded the tolerance level, three of them could be cured within a few months after BNCT and the remaining three developed severe skin damage requiring skin grafts. The absorbed doses to the tumor ranged from 15.7 to 68.5 Gy-Eq and the percentage of complete response was 73% (16/22). When BNCT is used in the treatment of malignant melanoma, based on the pharmacokinetics of BPA and radiobiological considerations, promising clinical results have been obtained, although many problems and issues remain to be solved.
Australas Phys Eng Sci Med 2003 Sep
PMID:Boron neutron capture therapy (BNCT) for malignant melanoma with special reference to absorbed doses to the normal skin and tumor. 1462 47

Local skin trauma induces inflammatory responses resulting in local tissue and distant organ injury. EGF, a polypeptide hormone, mainly produced in saliva, is one of the major accelerators in wound healing. Wistar albino rats of both sexes received either bovine serum albumin or EGF (10 microg/kg) subcutaneously before a circular (18 mm diameter) partial thickness burn was induced. Afterwards, some rats were placed in separate cages to prevent licking, while the others were caged together to allow wound-licking. Treatments were continued for 5 more days and on the 5th day animals were decapitated. Histopathological analysis of skin damage and dermal myeloperoxidase (MPO) activity, as an index for neutrophil activity, were evaluated. Oxidant injury to the liver and intestines was determined by measuring glutathione (GSH) and malondialdehyde (MDA) levels, as well as MPO activity. The results demonstrate that healing of the burn wound on the skin is accelerated by both wound-licking and EGF administration, which also attenuated tissue neutrophil accumulation, suggesting the role of neutrophils as the source of mediators involved in delayed epithelial regeneration. Moreover, local dermal burn results in oxidant injury to the liver, concomitant with significant elevations in hepatic and intestinal GSH levels. Exogenous administration of EGF at physiological doses had no effect on inflammatory responses of the distant organs, while allowing the rats to lick the wound reduced the oxidant injury to the liver. Since saliva or EGF enhances skin wound healing, topical use of EGF-rich artificial saliva merits consideration for its use in burn patients.
Burns 2004 Sep
PMID:The healing-promoting effect of saliva on skin burn is mediated by epidermal growth factor (EGF): role of the neutrophils. 1530 17

Ultraviolet (UV) irradiation from the sun reduces production of type I procollagen (COLI), the major structural protein in human skin. This reduction is a key feature of the pathophysiology of premature skin aging (photoaging). Photoaging is the most common form of skin damage and is associated with skin carcinoma. TGF-beta/Smad pathway is the major regulator of type I procollagen synthesis in human skin. We have previously reported that UV irradiation impairs transforming growth factor-beta (TGF-beta)/Smad signaling in mink lung epithelial cells. We have investigated the mechanism of UV irradiation impairment of the TGF-beta/Smad pathway and the impact of this impairment on type I procollagen production in human skin fibroblasts, the major collagen-producing cells in skin. We report here that UV irradiation impairs TGF-beta/Smad pathway in human skin by down-regulation of TGF-beta type II receptor (TbetaRII). This loss of TbetaRII occurs within 8 hours after UV irradiation and precedes down-regulation of type I procollagen expression in human skin in vivo. In human skin fibroblasts, UV-induced TbetaRII down-regulation is mediated by transcriptional repression and results in 90% reduction of specific, cell-surface binding of TGF-beta. This loss of TbetaRII prevents downstream activation of Smad2/3 by TGF-beta, thereby reducing expression of type I procollagen. Preventing loss of TbetaRII by overexpression protects against UV inhibition of type I procollagen gene expression in human skin fibroblasts. UV-induced down-regulation of TbetaRII, with attendant reduction of type I procollagen production, is a critical molecular mechanism in the pathophysiology of photoaging.
Am J Pathol 2004 Sep
PMID:Solar ultraviolet irradiation reduces collagen in photoaged human skin by blocking transforming growth factor-beta type II receptor/Smad signaling. 1533 99

Polysaccharides from aloe are always considered an effective radioprotector on irradiation-induced skin damage. The aim of this study was to determine if aloe polysaccharides (AP) have radioprotective effects on normal human cells in vitro and mouse survival in vivo and to explore the mechanism. Pretreatment with 50 microg/ml AP could improve the surviving fraction at 2 Gy (SF2) of three normal cell lines 293, ECV304, and C. liver from 41.5%, 46.5%, and 40.9% to 49.4%, 72.1%, and 89.1%, respectively. AP could also reduce the apoptotic rate of C. liver cells from 9.5% and 43.0% to 2.2% and 10.9% 48 h and 72 h after 2 Gy irradiation, respectively. Western blot analysis showed that pretreatment with AP could block the upregulation of pro-apoptotic p53, Bax, and Bad and the downregulation of Bcl-2 by irradiation. AP could lower thymocyte apoptosis of mice in vivo after 6 Gy irradiation and abrogate the cell cycle perturbation. Fifty mg/kg of AP treatment for 30 min before 7.5 Gy irradiation provided the best radioprotective effect and improved the 30-day survival rate of mice to 86.0%, from 10.0%. AP exerted radioprotective effects in vitro and in vivo through an inhibition of apoptosis.
J Radiat Res 2004 Sep
PMID:Aloe polysaccharides mediated radioprotective effect through the inhibition of apoptosis. 1561 91

Sauna-related burns are rare, even in Finland where sauna bathing is a popular leisure pastime. Burns induced by hot air are even more rare and constitute a very small subgroup of all sauna burns. Hot air burns are characterised by a combination of full thickness skin damage with deep tissue destruction. We report here on six consecutive patients suffering from hot air sauna burns with rhabdomyolysis. All six patients were middle-aged, the majority of them men. Acute excessive consumption of alcohol exacerbated by a hot environment resulted in dehydration and loss of consciousness. Immobility and prolonged exposure to hot, dry air resulted in third degree regional burns with 5-32% TBSA. Rhabdomyolysis was evident on admission. The laboratory values of plasma creatine kinase (P-CK), plasma myoglobin (PM), blood pH, and serum potassium (S-K) during the first five days were evaluated. Aggressive fluid management and correction of acidosis and myoglobinuria were started on admission. Surgical management consisted of early, aggressive excision at fascial level, in some patients involving sacrifice of the upper layers of muscle. Even so, mortality in this small series was 50%. The best indicator of poor prognosis was a highly elevated CK value on the second post-injury day.
Burns 2005 Sep
PMID:Rhabdomyolysis caused by hot air sauna burn. 1604 74

Whereas in Australia the high incidence of UV-induced skin cancer and chronic UV-damage is epidemiologically well proved, comparable figures in Europe and particularly in Germany are missing. Presumably, the prevalence and incidence of actinic keratoses, basal cell carcinoma and squamous cell carcinoma are significantly underestimated. The importance of chronic skin damage is discussed in accordance with new epidemiologic studies recently published in international journals. Since the percentage of older people is increasing in Germany the therapeutic importance of UV-damage and its relevance for preventive medicine will be of increasing importance in the next years.
J Dtsch Dermatol Ges 2005 Sep
PMID:[Epidemiology of chronic UV-damage]. 1611 42

Protection against ultraviolet (UV) irradiation prevents from the development of acute skin damage such as erythema formation and chronic skin changes such as premature skin ageing. Especially those sunscreens with higher sun protection factors do not only protect against solar dermatitis but also inhibit UV-induced immunosuppression by blocking the release of immunosuppressive mediators from UV-exposed epidermis. In particular, the protection against UV-induced immunosuppression by sunscreens is supposed to reduce the development of UV-induced skin cancer. Besides immunosuppression UV-irradiation is also able to induce "UV signature" mutations within UV-exposed DNA. Topical application of DNA repair enzymes induces nucleotide excision repair and corrections of DNA damages. Thereby, the risk to develop UV-induced skin malignancies is markedly reduced. Accordingly, future perspectives in the development of sunscreens include DNA repair enzymes or factors, which can induce the endogenous cellular DNA repair system. Until these developments come to practice reasonable sun protection according to the skin complexion is of primary importance.
J Dtsch Dermatol Ges 2005 Sep
PMID:[Sunprotection: possibilities and limitations]. 1611 44

Although the combination of pale skin and intense sun exposure results in an important health risk for the individual, it is less clear if at the population level this risk has possessed an evolutionary meaning. In this sense, a number of adaptive hypotheses have been put forward to explain the evolution of human skin pigmentation, such as photoprotection against sun-induced cancer, sexual selection, vitamin D synthesis or photoprotection of photolabile compounds, among others. It is expected that if skin pigmentation is adaptive, we might be able to see the signature of positive selection on some of the genes involved. In order to detect this signature, we analyze a battery of 81 candidate loci by means of phylogenetic and population genetic tests. Our results indicate that both light and dark skin may possess adaptive value. Of the main loci presenting this signature, TP53BP1 shows clear evidence of adaptive selection in Africans, whereas TYRP1 and SLC24A5 show evidence of adaptive selection in Caucasians. Although we cannot offer a mechanism that based on these genes explains the advantage of light skin, if TP53BP1, and perhaps RAD50, have truly conferred an adaptive value to the African population analyzed, photoprotection against sun-induced skin damage/cancer might be proposed as a mechanism that has driven the evolution of human skin pigmentation.
Mol Biol Evol 2006 Sep
PMID:A scan for signatures of positive selection in candidate loci for skin pigmentation in humans. 1675 56

Ultraviolet radiation is the major environmental cause of skin damage. Although only 0.5% of ultraviolet B (UVB) radiation reaches the earth, it is the main cause of sunburn and inflammation and the most carcinogenic constituent of sunlight. We investigated whether the topical application of a novel, water-soluble gamma-tocopherol (gamma-Toc) derivative, gamma-tocopherol-N,N-dimethylglycinate hydrochloride (gamma-TDMG), could protect against UV-induced skin damage. Topical pre- or postapplication of gamma-TDMG solution significantly prevented sunburn cell formation, lipid peroxidation, and edema/inflammation that were induced by exposure to a single dose of UV irradiation. Cyclooxygenase-2 (COX-2)-catalyzed synthesis of prostaglandin E(2) (PGE(2)) levels seen after UV exposure were significantly suppressed by pre- or posttreatment with gamma-TDMG. The increase in COX-2 activity was significantly inhibited by gamma-TDMG, suggesting that the reduction in PGE(2) concentration was due to the direct inhibition of COX-2 activity by gamma-TDMG. The derivative strongly inhibited inducible nitric oxide synthase mRNA expression and nitric oxide production. With the application of gamma-TDMG, the pigmentation in melanocytes was lightened and the increase melanin concentration was suppressed. Gamma-TDMG is converted to gamma-Toc in the skin and has higher bioavailability than gamma-Toc itself. These results suggest that gamma-TDMG-derived gamma-Toc acts as an antioxidant, antiinflammatory and antipigmentation agent. Our data further suggest that the topical application of gamma-TDMG may be efficacious in preventing and reducing UV-induced skin damage in humans.
Yakugaku Zasshi 2006 Sep
PMID:[UVB-induced skin damage and the protection/treatment--effects of a novel, hydrophilic gamma-tocopherol derivative]. 1694 83

Over the last decades, the incidence of ultraviolet B (UVB)-related skin problems has been increasing. Damages induced by UVB radiation are related to mutations that occur as a result of direct DNA damage and/or the production of reactive oxygen species. We investigated the anti-oxidant effects of a Polygonum multiflorum thumb extract against skin damage induced by UVB irradiation. Female SKH-1 hairless mice were divided into three groups: control (N = 7), distilled water- (N = 10), and P. multiflorum extract-treated (PM, N = 10) groups. The PM (10 g) was extracted with 100 mL distilled water, cryo-dried and 9.8 g was obtained. The animals received a topical application of 500 microL distilled water or PM extract (1, 2, 4, 8, and 16%, w/v, dissolved in distilled water) for 30 min after UVB irradiation (wavelength 280-320 nm, 300 mJ/cm(2); 3 min) of the dorsal kin for 14 days, and skin immunohistochemistry and Cu,Zn-superoxide dismutase (SOD1) activity were determined. SOD1 immunoreactivity, its protein levels and activities in the skin were significantly reduced by 70% in the distilled water-treated group after UVB irradiation compared to control. However, in the PM extract-treated groups, SOD1 immunoreactivity and its protein and activity levels increased in a dose-dependent manner (1-16%, w/v, PM extract) compared to the distilled water-treated group. SOD1 protein levels and activities in the groups treated with 8 and 16%, w/v, PM extract recovered to 80-90% of the control group levels after UVB. These results suggest that PM extract strongly inhibits the destruction of SOD1 by UV radiation and probably contains anti-skin photoaging agents.
Braz J Med Biol Res 2006 Sep
PMID:An extract of Polygonum multiflorum protects against free radical damage induced by ultraviolet B irradiation of the skin. 1697 4


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