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“Atopic dermatitis, also known as atopic eczema, is a chronic pruritic skin condition affecting approximately 17.8 million persons in the United States. It can lead to significant morbidity. GS-9973 supplier A simplified version of the U.K. Working Party’s Diagnostic Criteria can help make the diagnosis. Asking about the presence and frequency of symptoms can allow physicians to grade the severity of the disease and response to treatment. Management consists of relieving symptoms and lengthening time between flare-ups. Regular,

liberal use of emollients is recommended. The primary pharmacologic treatment is topical corticosteroids. Twice-daily or more frequent application has not been shown to be more effective than once-daily application. A maintenance regimen of GNS-1480 topical corticosteroids may reduce relapse rates in patients who have recurrent moderate to severe atopic dermatitis. Pimecrolimus and tacrolimus are calcineurin inhibitors that are recommended as second-line treatment for persons with moderate to severe atopic dermatitis and who are at risk of atrophy from topical corticosteroids. Although the U.S. Food

and Drug Administration has issued a boxed warning about a possible link between these medications and skin malignancies and lymphoma, studies have not demonstrated a clear link. Topical and oral antibiotics may be used to treat secondary bacterial infections, but are not effective in preventing atopic dermatitis flare-ups. The effectiveness of alternative therapies, such as Chinese herbal preparations, homeopathy, hypnotherapy/biofeedback, and massage therapy, has not been established. (Am Fam Physician. 2012;86(1):35-42. Copyright (c) 2012 American Academy of Family Physicians.)”
“In BV-6 order to explore the response of photosynthetic electron transport chain to heat stress, chlorophyll

a fluorescence and modulated 820 nm reflection transients were examined in the leaves of Jerusalem artichoke (Helianthus tuberosus L.). J step was elevated at 43 degrees C, suggesting that electron transport beyond primary quinone electron acceptor of photosystem II (Q(A)) was inhibited. I step was elevated at 45 degrees C due to the lowered plastoquinol re-oxidation rate. Significant decrease in the QA reducing reaction centers per photosystem II (PSII) antenna chlorophyll and marked increase in relative variable fluorescence intensity at 300 mu s also occurred at 45 degrees C, indicating that the electron transport chain from PSII donor side to QA was injured. Overall, the fragment between QA and plastoquinol is the most susceptible to heat in the electron transport chain before photosystem I (PSI). The maximal photochemical capacity of PSI was not affected by heat stress even at 48 degrees C, and the interaction between PSII and PSI become unbalanced, when temperature rose to 45 degrees C.