Background:Promoters of active genes in eukaryotes are typically depleted of histone proteins. Results: Histone eviction from the induced CHA1 promoter is compromised by mutations in transcription factors, and higher histone occupancy is also seen at constitutively active promoters in such mutants. Conclusion: Preinitiation complex formation promotes reduced histone occupancy at active gene promoters. Significance: Preinitiation complex components participate in chromatin remodeling.

Background Van der Woude syndrome (VWS) is the most common form of syndromic orofacial cleft caused predominantly by mutations in Interferon Regulatory Factor 6 (IRF6). We previously reported that individuals with VWS have increased risk of wound healing complications following cleft repair compared with individuals with nonsyndromic orofacial clefts (nonsyndromic cleft lip and palate—NSCLP). In vitro, absence of IRF6 leads to impaired keratinocyte migration and embryonic wound healing. However, there is currently no data on tissue repair in adult animals and cells with reduced levels of IRF6 like in VWS. Results Excisional wounds of Irf6+/− and wild‐type animals were analyzed 4 and 7 days post‐wounding. Although all wounds were reepithelialized after 7 days, the epidermal and wound volume of repaired wounds was larger in Irf6+/−. These data were supported by increased keratinocyte proliferation in the neoformed epidermis and a less mature granulation tissue with increased cytokine levels. This effect was not cell autonomous, as Irf6+/− neonatal keratinocytes in vitro did not exhibit defects in scratch wound closure or proliferation. Keratinocytes from individuals with VWS also migrated similarly to keratinocytes from NSCLP individuals. Conclusions These data support a role for IRF6 in wound healing by regulating keratinocyte proliferation, granulation tissue maturation, and cytokine levels.

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Compression garments (CGs) such as bandages and stockings are critical in the management of a wide range of lower extremity conditions, particularly venous leg ulcers (VLUs). In order for CGs to deliver therapeutic benefit, the interface pressure between the fabric and the skin much typically reach at least 30 mmHg. However, this threshold value is highly sensitive to the type of CG material used, correct placement by a trained healthcare provider, body position, and leg volume changes. Currently, PicoPressÒ (Microlabitalia, Padua, Italy) is the gold-standard tool to measure interface pressure. Unfortunately, the system is expensive, and requires an air-bladder wired to a large base unit, limiting the system to only point measurements. Using advanced materials science techniques, we report the development of a soft, wearable, flexible and wireless pressure sensor that consists of a gold thin wire (50 nm) integrated on a 3D polyimide structure and elastomer (Ecoflex-30, 2.4 mm in diameter, 1 mm in thickness). Once packaged, this low cost sensor is 15 mm x 45 mm can be comfortably placed between CGs and the skin without the risk of skin injury. Data is transmitted wirelessly to any standard smartphone. Testing in healthy normal subjects, the 3D sensor measured an interface pressure within 10% agreement with the PicoPressÒ across the full range of pressures (0 to 120 mmHg) by detecting the deformation of the elastomer (R 2 >0.98). A wearable interface pressure sensor will enable more effective compression therapy with CGs at the point of application and in the home setting. Future directions include evaluating the performance and tolerability of the device on patients with an active history of VLUs.