Epithelial-mesenchymal transition (EMT) describes the global process by which stationary epithelial cells undergo phenotypic changes, including loss of cell-cell adhesion and apical-basal polarity, and acquire mesenchymal characteristics which confer migratory capacity. EMT and its converse, MET (mesenchymal-to-epithelial transition), are integral stages of many physiologic processes, and as such are tightly coordinated by a host of molecular regulators. Converging lines of evidence have identified EMT as a component of cutaneous wound healing, during which otherwise stationary keratinocytes - the resident skin epithelial cells - migrate across the wound bed to restore the epidermal barrier. Moreover, EMT also plays a role in the development of scarring and fibrosis, as the matrix-producing myofibroblast arises from cells of epithelial lineage in response to injury but is pathologically sustained instead of undergoing MET or apoptosis. In this review, we summarize the role of EMT in physiologic repair and pathologic fibrosis of tissues and organs. We conclude that further investigation into the contribution of EMT to the impaired repair of fibrotic wounds may identify components of EMT signaling as common therapeutic targets for impaired healing in many tissues.

Here we describe TRACE (T7 polymerase-driven continuous editing), a method that enables continuous, targeted mutagenesis in human cells using a cytidine deaminase fused to T7 RNA polymerase. TRACE induces high rates of mutagenesis over multiple cell generations in genes Reprints and permissions information is available at www.nature.com/reprints.

Background Medication prescribing discrepancies are used as a quality measure for patients transferred between sites of care. The objective of this study was to quantify the rate of adverse drug events (ADEs) caused by prescribing discrepancies and the discrimination of an index of high-risk transition drug prescribing. Methods We examined medical records of patients transferred between 7 nursing homes and 3 hospitals between 1999–2005 in New York and Connecticut for transfer-associated prescribing discrepancies. ADEs caused by discrepancies were determined by 2 clinician raters. We calculated the fraction of medication discrepancies that caused ADEs in each of 22 drug classes by calculating positive predictive values (PPVs). We calculated the discrimination of a count of high-risk drug discrepancies, selected from published lists of high-risk medications and using observed PPVs. Results 208 patients were hospitalized 304 times. Overall, 65 of 1350 prescribing discrepancies caused ADEs, for a PPV of .048 (95%CI .037–.061). PPVs by drug class ranged from 0 – .28. Drug classes with the highest PPVs were opioid analgesics, metronidazole, and non-opioid analgesics. Patients with 0, 1–2, and ≥ 3 high-risk discrepancies had a 13%, 23%, and 47% chance of experiencing a discrepancy-related ADE, respectively. Conclusions Discrepancies in certain drug classes more often caused ADEs than other types of discrepancies in hospitalized nursing home patients. Information about ADEs caused by medication discrepancies can be used to enhance measurement of care quality, identify high-risk patients, and inform development of decision-support tools at the time of patient transfer.