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The enclosed material was prepared by Northeast Health Care Quality Foundation NHCQF ; , the Medicare Quality Improvement Organization QIO ; for Maine, New Hampshire and Vermont, under contract with the Centers for Medicare & Medicaid Services CMS ; , an agency of the U.S. Department of Health and Human Services. The contents presented do not necessarily reflect CMS policy.
Activation of corticosteroid regulatory pathway during wound healing O Stojadinovic, B Lee, C Vouthounis and M Tomic Dermatology, NYU School of Medicine, New York, NY Corticosteroids are known as inhibitors of wound healing but the exact mechanism of this inhibition is largely unknown. Therefore, we used two different approaches, immunocytochemistry and global transcriptional analysis to identify the mechanism through which corticosteroids inhibit wound healing. Using immunocytochemistry, we discovered nuclear translocation of the glucocorticoid receptor GR ; at the wound edge that is completely absent from unwounded skin. This suggests that GR is released from its cytoplasmic inhibitor and translocated to the nucleus, directly indicating receptor activation during the process of wound healing. Using Affymetrix HU95A gene chips we compared the expression profiles of human skin 4, 48 and 96 hours upon wounding with human skin unwounded, but treated topically with corticosteroids. These analyses revealed that the expression pattern of corticosteroid treated skin does not have a significant overlap with the pattern of the 4 and 48 hours post-wounded skin. Importantly, we found a strikingly significant overlap with the 96 hours post-wounded skin: 33.2% genes identified as significantly regulated in corticosteroid-treated skin were also significantly regulated in skin 96 hours post wounding. Furthermore, we found 54% of those to be identically regulated, which means that 166 genes were identically regulated in both corticosteroid-treated skin and the skin 96 hours post-wounding. Specifically, we found a similar transcriptional pattern of genes that participate in adhesion, proliferation, migration, Wnt pathway and steroidogenic enzymes, to mention a few. Overall, we found that wound healing activates corticosteroid pathway whereas it dominantly inhibits EGF TNFalpha pathway, resulting in inhibition of migration, increase of proliferation and change of adhesion of keratinocytes. We conclude that corticosteroid serve as natural inhibitors of normal wound healing, i.e. a switch that resets keratinocytes from their activated phenotype back to deifferentiating phenotype and tenormin.
Table III. Necessary, common, occasional and uncommon histologic lesions of NASH see ref. 64 ; Necessary Steatosis, macro-micro Common, but not necessary Perisinusoidal fibrosis in Zone 3; sometimes a component of fibrosis in central-portal bridging Glycogenated nuclei in Zone 1 May be present, but not necessary Mallory's hyaline in Zone 3; typically poorly constituted; may require antibodies with immunohistochemistry cytokeratins 7, 18, 19 ; . Iron detectable in scant amounts in Zone 1 hepatocytes using Prussian blue staining. Megamitochondria in hepatocytes. Uncommon: consider other causes of liver disease Pure or predominantly microvesicular steatosis.

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Where the pharmacist is to substitute a less expensive generically equivalent drug for a brand name drug at the pharmacy, notification to the person presenting the prescription shall be made by the pharmacist, either directly or through a pharmacy intern or other person under the supervision of the pharmacist authorized to assist the pharmacist by the State Board of Pharmacy. Such notification shall be limited to advising the person presenting the prescription that substitution is possible, to advising the person of the amount of the retail price difference between the brand name and the generically equivalent drug product substituted for it, and to informing the person that he may refuse the substitution. Questions by the person presenting the prescription for drug product information shall be answered only by the pharmacist or pharmacy intern. The notification described in this subsection of a possible substitution and retail price difference may be oral or may be in a written statement similar to the following: ``Your , may be physician has indicated that this prescription, identified as filled with one of the generic drug products listed in the Pennsylvania Department of Health Formulary. This lower cost generically equivalent product has been selected by our pharmacy in order to save you, the purchaser, a total of . Please indicate whether you do or do not wish to have the $ lower priced drug. Signed .'' and testosterone. To the Editor: I in agreement with the conclusion by Sirven et al1 that prophylaxis with antiepileptic drugs does not reduce seizure rates in patients who have brain tumors but have never experienced a seizure. However, the authors did not address the serious legal side of this issue. Physicians are also concerned about the family's interpretation of events, and we are "sensitive" to any untoward result, such as a seizure, that may instigate unnecessary frivolous legal action. For this reason, we administer antiseizure medications even though we agree with the results reported by Sirven et al. As a board-certified neurologist, I have consulted on numerous cases in which a patient has had a seizure and the family has reacted in an angry and emotional manner toward the other physicians. It is unfortunate that our society has unrealistic expectations of absolute and guaranteed outcomes in these complicated situations. I do not challenge other physicians or neurosurgeons when they administer prophylactic therapy to patients under these difficult, but understandable, circumstances. Ezra S. Elkayam, MD, PA Safety Harbor, Fla. Diopathic inflammatory bowel disease is divided into 2 major disease processes, Crohn disease CD ; and chronic ulcerative colitis CUC ; . Often, both diseases are characterized by intermittent exacerbation of symptoms and periods of remission that may occur spontaneously or in response to treatment. The etiology of these diseases is unknown but most likely represents an interaction between the environment and host genetic susceptibility. Both medical and surgical treatment are used in the treatment of CD and CUC. However, given the different distribution of disease activity along the intestinal tract and the nature of the inflammatory process, the role and scope of medical and surgical management for each specific disease are different. Crohn disease may arise anywhere along the length of the intestine. It is characterized by transmural inflammation of the bowel wall. Such inflammation leads to a unique set of complications, including abscess and fistula formation and intestinal stenosis. 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