6 research outputs found
Perioperative passport: empowering people with diabetes along their surgical journey
© 2017 Diabetes UK Aim: To determine whether a handheld ‘perioperative passport’ could improve the experience of perioperative care for people with diabetes and overcome some of the communication issues commonly identified in inpatient extracts. Methods: Individuals with diabetes undergoing elective surgery requiring at least an overnight stay were identified via a customized information technology system. Those allocated to the passport group were given the perioperative passport before their hospital admission. A 26-item questionnaire was completed after surgery by 50 participants in the passport group (mean age 69 years) and by 35 participants with diabetes who followed the usual surgical pathway (mean age 70 years). In addition, the former group had a structured interview about their experience of the passport. Results: The prevalence of those who reported having received prior information about their expected diabetes care was 35% in the control group vs 92% in the passport group (
Regulation of myofibroblast transdifferentiation by DNA methylation and MeCP2: implications for wound healing and fibrogenesis
Regulation of myofibroblast transdifferentiation by DNA methylation and MeCP2: implications for wound healing and fibrogenesis
Myofibroblasts are critical cellular elements of wound healing generated at sites of injury by transdifferentiation of resident cells. A paradigm for this process is conversion of hepatic stellate cells (HSC) into hepatic myofibroblasts. Treatment of HSC with DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-azadC) blocked transdifferentiation. 5-azadC also prevented loss of IB and PPAR expression that occurs during transdifferentiation to allow acquisition of proinflammatory and profibrogenic characteristics. ChIP analysis revealed IB promoter is associated with transcriptionally repressed chromatin that converts to an active state with 5-azadC treatment. The methyl-CpG-binding protein MeCP2 which promotes repressed chromatin structure is selectively detected in myofibroblasts of diseased liver. siRNA knockdown of MeCP2 elevated IB promoter activity, mRNA and protein expression in myofibroblasts. MeCP2 interacts with IB promoter via a methyl-CpG-dependent mechanism and recruitment into a CBF1 corepression complex. We conclude that MeCP2 and DNA methylation exert epigenetic control over hepatic wound healing and fibrogenesis.Abbreviations: ECM, the extracellular matrix; MTD, myofibroblast transdifferentiation; HSC, hepatic stellate cells; HM, hepatic myofibroblast; ?-SMA, smooth muscle-alpha actin; HDACs, histone deacetylase