in human skin, we developed a model of human skin wounds in sterile culture. Health of human skin preserved as fragments Operationsr��ckst Walls were cut into 1   � 0 Groups mm and  <a href=”http://www.selleckbio.com/a-674563-S2670.html”>A-674563</a> in a medium of keratinocytes incubated under sterile conditions. On days 0, 1, 2, 3 and 4 samples for immunohistochemistry, RNA isolation or extraction of the proteins were Processed. We examined the expression of three human  Defensins in the skin, hBD 1, 2 and hBD hBD third Northern blot, big amounts of e hBD 3 mRNA detected in the wounded skin at day 4 and was replaced by IHC, hBD-3 peptide also present in keratinocytes of 4 days. The intensive R Staining hBD 3 was the R Santander of wound of skin slices.<br> Used in order  <a href=”http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=131480678″>PF-04217903</a> to lay on the induction of hBD peptide 3 in extracts from the skin of 0 and 4 days after injury by urea-PAGE, by S ure blot nonstandard abbreviations that followed analyzed were: AMP, antimicrobial peptide, the AU side, side urea, S acid hBD, human  Defensin, HB EGF, heparin-binding EGF, IHC, immunohistochemistry, MBD 14,  mouse Defensin 14, NGAL, neutrophil gelatinase-associated lipocalin, qRT-PCR, quantitative RT-PCR, SLPI, secretory leukocyte an inhibitor of the protease, TAPI-1, tumor necrosis factor  �� � �p rotease inhibitor-1, TBS, an L solution Tris-buffered salt solutions solution, the TSB, CASO-Bouillon. Conflict of interest: The authors have explained rt that no conflict of interest. Citation for this article: J. blinking. Investment. 116:1878, 1885. doi: 10.1172/JCI28422.<br> The research article Journal of Clinical Investigation, Volume 116 Number 7th JCI July 2006 in 1879 with the fight against HBD-3 Antique Body. Only small amounts of hBD 3 were found in normal skin at day 0, but the level increased hte Significantly by 4 days. However, we found no expression of HBD 1 and HBD 2 in human skin induced by Northern blots or IHC wounded. To investigate whether a simple injury sufficient of the epithelium of the skin, was to induce the expression of hBD 3, we have organotypic cultures of epidermal keratinocytes by a cut with a sterile scalpel injured. After 4 days of intensive R Compared staining hBD 3-peptide to the R Change of the incision to nonwounded cultures. We also found that two other antimicrobial proteins in human skin, neutrophil gelatinase associated lipocalin and secretory leukocyte protease inhibitor, which were in our model induced with hBD third In line with previous findings, the basal expression of SLPI in the skin was low.<br> SLPI was previously to be induced as in the skin after wounding, through unknown mechanisms. Figure 1: Expression of hBD 3, NGAL and SLPI in human skin wounds. The human skin was cut into a   � 0 mm plates and incubated for 4 days in culture 0th Every day, the samples were processed for IHC or extract RNA or proteins. Northern blots of total RNA from whole skin. The blots were hybridized with probes for hBD 3, NGAL and SLPI G3PD. The graphs show the expression of hBD 3, NGAL and SLPI normalized to G3PD mRNA expression. hBD 3, NGAL and SLPI mRNA levels in the skin on day 4, the value 1 was assigned. Slices of the skin on days 0 and 4 with and without treatment with AG 1478 were for hBD 3, NGAL and SLPI found Rbt. Red color was developed with chromogen fast, and Harris H matoxylin Was used for color-cons. The proteins Extracted from the skin of both injured and the medium by AU PAGE and SDS-PAGE using synthetic hBD 3 were analyzed as a standard, then a gel Deleted