Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rapid-onset cataracts were induced in SPF C57 bl/6 mice by intraperitoneal administration of naphthalene following cytochrome P-450 isozyme induction with phenobarbital. Several L-cysteine prodrugs with masked sulfhydryl groups in the form of thiazolidine-4-carboxylic acids, as well as N-acetyl-L-cysteine, N,S-bis-acetyl-L-cysteine and glutathione ethyl ester, were evaluated for their ability to maintain hepatic and lenticular glutathione at near-normal levels and to prevent naphthalene-induced cataract formation. Each prodrug was administered at three specified times to a cumulative total of 1.5 mole equivalents of the single dose of naphthalene. Three L-cysteine prodrugs delayed but did not prevent cataract formation in 40-60% of the mice over a 72-hr period, while eight of the 13 compounds produced cataract yields similar to the naphthalene control animals, i.e. 83% in 72 hr. However, two L-cysteine prodrugs, 2(R,S)-methylthiazolidine-4(R)-carboxylic acid (MTCA) and 2(R,S)-n-propylthiazolidine-4(R)-carboxylic acid (PTCA), prevented cataract formation in 20 of 21 and 12 of 12 mice, respectively, and maintained hepatic reduced glutathione levels at 82% and 51% of untreated controls. In contrast, glutathione was depressed to 3% of the normal value in those animals treated with naphthalene alone. Lenticular glutathione values were depressed, albeit minimally, in all naphthalene-treated mice regardless of administration of either MTCA or PTCA. The mice protected with either MTCA or PTCA showed no visible effects of naphthalene toxicity or lens opacities at any time. It can be concluded that these L-cysteine prodrugs were effective in preventing naphthalene-induced cataract and maintaining near-normal hepatic glutathione levels.
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PMID:Prevention of naphthalene-induced cataract and hepatic glutathione loss by the L-cysteine prodrugs, MTCA and PTCA. 879 61

Dysplastic nevus is an acquired or hereditary nevus that clinically seems atypical and pathohistologically dysplastic. The term of dysplastic nevus has changed through history and even until now the dermatologists and pathologists have not found the same conclusion for name and definition of dysplastic nevus. Epidemiology of dysplastic nevus is different depending on geographic lattitude, being three times higher in Australia than in Great Britain. Genetic factors play a role in etiology of dysplastic nevus but are still not well defined. UV radiation is indisputable main etiological factor in developing dysplastic nevus. Many studies confirm that children who have been using sun protection creams with SPF have less dysplastic nevi than those who did not. Nevus with geographic shape and muddy borders, dominately macular, red to brown colored and has 5 mm or more in diameter is clinically dysplastic nevus. ABCDE rules count for dysplastic nevus as well as for melanoma but prefferable diagnostic criteria for dysplastic nevus would be "ugly duckling sign". Pathohistologic analysis is the key in confirming the diagnosis of dysplastic nevus. Great experience and knowledge in dermatopathology field is essential for pathologists to make a distinction between dysplastic nevus and melanoma in situ. Likewise great experience in dermatooncology field is essential in differentiating dysplastic nevus from other nevi. Surgical excision is the only therapy that should be done for dysplastic nevus. Regular follow up is highly recommended for patients with dysplastic nevus and syndroma naevi dysplastic. Education about sun protection measures and self-examination techniques is essential for all patients with dysplastic nevi and their family.
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PMID:Dysplastic nevus--risk factor or disguise for melanoma. 2222 Apr 61

Athletes practicing and competing outdoors are exposed to considerable UV radiation and at an increased risk for the development of UV-related skin conditions, including skin cancer. Risk factors for skin cancer include genetics, immune status, and particularly UV radiation. Independent factors, such as phototype, family or personal history of melanoma, number of nevi, atypical nevi and solar lentigines, as well as sunburn history are also important risk indicators for skin cancer, especially melanoma (1-3). Additionally, exercise-induced immunosuppression may contribute to the development of skin cancers (4). To the best of our knowledge, only one article has been previously published analyzing the effects of UV exposure in triathlon athletes (5). Our aim was to analyze sun protection habits of athletes competing in the Croatian Olympic and Super Sprint triathlon and screen them for skin cancer and other skin lesions. Participants completed a questionnaire consisting of questions regarding personal and family history, phenotypic characteristics, training habits, and sunlight-related risk factors. Additionally, a total body skin examination was performed by a board-certified dermatologist. Skin type, number of melanocytic nevi, presence of atypical nevi, solar lentigines, as well as suspicious lesions were recorded (Figure 1). The study population consisted of 95 participants, 65 (68%) men and 30 (32%) women. Approximately 30% of participants spent 4 to 6 hours per week outdoors, while 21% spent more than 10 hours outdoors per week. Regarding sun protection habits, more than 90% of participants stated it was important to use sunscreen, however, almost 50% rarely used sunscreen while training, 27% frequently used sunscreen, while only 3% always used sunscreen. A staggering 20% of participants never used sunscreen. Unsurprisingly, almost a third of the athletes (26%) reported previously having severe sunburns with blisters. Almost 10% reported a positive family history of melanoma and one reported positive personal history of melanoma. Skin examinations revealed that nearly half of the participants (46%) had solar lentigines, 25% had atypical nevi, while 2 participants presented with actinically damaged skin and 2 participants with actinic keratoses. The majority of the triathletes (around 57%) had less than 20 nevi on their skin, while only around 10% had between 50 and 100 nevi. No lesions that were suggestive of invasive skin cancer - non-melanoma skin cancer or melanoma - were identified. UV exposure is usually exceeded in most activities performed outdoors with exposed skin, even if they are performed in sunny conditions for only a short amount of time. The limit for UV exposure was exceeded more than 30 times during the Ironman Triathlon World Championship 1999 in Hawaii, as reported by Moehrle. Additionally, despite the application of water-resistant sunscreen (SPF 25+), these triathletes showed sunburn on sun-exposed skin, which was most probably due to water exposure, sweating, and friction (5). Other studies evaluating skin cancer and sun protection habits of outdoor athletes indicate that most do not appear to be aware of the serious potential health risks of extensive sun exposure (6-8). Even though no invasive skin cancer was detected in our athletes, a significant number of participants presented with solar lentigines and a fair amount with atypical nevi, both considered risk factors for skin cancer. Additionally, a large proportion of participants had a history of severe blistering sunburns, which is not surprising given that 20% never use sunscreen. Our results indicate that it is necessary to advise and educate outdoor athletes about sun-smart behavior. Avoiding training and competing in periods with high sun exposure, wearing adequate clothing, and applying water-resistant high-protection sunscreen regularly and sufficiently are practices and habits that should be encouraged. Screening for skin cancer is a valuable measure and should be performed in high-risk individuals such as triathletes.
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PMID:Do Athletes Practicing Outdoors Know and Care Enough About the Importance of Photoprotection? 3265 Aug 51