Search

The increasing use of electronic medical records during the clinical encounter brings not only benefits but also barriers that may affect the doctor-patient relationship and increase the work burden of the physician. We evaluated whether the use of an electronic medical record scribe in an academic urology program would ameliorate these problems.We randomly assigned electronic medical record scribes to the office hours of 5 academic urologists, and using surveys we evaluated patient and physician acceptance and satisfaction.Patients were accepting of an electronic medical record scribe and satisfaction rates were high (93% vs 87% in the absence of a scribe, p = 0.36). Patients were comfortable disclosing urological information in the presence of the scribe. Physicians were dramatically more satisfied with office hours when a scribe was present (69% vs 19%, p0.001). We were unable to determine whether the presence of a scribe improves productivity.Electronic medical record scribes in a urology practice may be a practical solution to provide documentation while maintaining or improving the doctor-patient relationship because they increase physician satisfaction and do not detract from patient satisfaction.

TGF-β signaling disorder has emerged as a cause for aortic aneurysm formation. However, mechanistic details of this disorder remain poorly defined. This study sought to understand the TGF-β signaling propagation and its impact on aortic structural homeostasis under conditions of receptor deficiency. An inducible gene deletion system driven by Myh11-CreER was utilized for selective removal of receptors Alk5, Tgfbr2, or both in SMCs, termed Alk5iko, Tgfbr2iko, and Alk5iko Tgfbr2iko, respectively. Alk5-floxed (Alk5f/f) mice served as controls. Animals (male, 9-11 weeks of age) were followed up to six months following gene deletion. Alk5iko caused progressive aortic enlargement (ultrasound scan). In four weeks, 23% of animals (n=42) died from aortic rupture, with the survivals all showing severe aneurysmal degeneration at locations of ascending (100%), descending (43%) and/or suprarenal (50%) aortas. Surprisingly, Tgfbr2iko in age-matched males (n=26) was well tolerated. Neither rupture nor aortic dilation was noted in four weeks. Evidence of aortic pathology was limited to scattered elastic fiber breaks. To evaluate the role of TGF-β in aortic aneurysm formation in Alk5iko animals, we deleted Tgfbr2 simultaneously with Alk5. The additional Tgfbr2iko completely recused aortic rupture, attenuated aortic dilation from 68% to 25%, and significantly improved aortic histology. Compared to the Alk5f/f controls, Alk5iko, Tgfbr2iko, and Alk5iko Tgfbr2iko aortas all displayed a similar but reduced level of Smad2 phosphorylation at various time points, indicating that loss of the canonical TGF-β signal is not the primary driver for the aortic phenotype of Alk5iko aortas. Meanwhile, the Alk5iko aortas produced 3-fold more pERK than Alk5f/f controls, and this elevation was completely abolished by the additional Tgfbr2 deletion. Pharmaceutical treatment of the Alk5iko mice with ERK inhibitor RDEA-119 significantly inhibited aortic dilation and prevented aortic wall from degeneration while those treated with vehicle control exhibited aortic dilation and intimal/medial tears. In conclusion, loss of Alk5 in SMCs triggers a non-Alk5 but Tgfbr2 dependent signal that promotes aortic aneurysm formation through exacerbating ERK activity.

It has been proposed that various groups of cells, such as medial SMCs (mSMCs), bone marrow progenitors, and mature ECs (mECs) hold the potential to become neointimal SMCs via phenotypic switching, differentiation, or endothelial-mesenchymal-transition (EMT). However, no definitive evidence has been provided to support these claims, which renders the in vivo significance of these events in question. Using an inducible Cre-loxP system, where the production of a reporter (e.g. β-gal) is driven by a highly definitive marker gene for mSMCs (e.g. SMC myosin heavy chain, SMMHC) or mECs (e.g. stem cell leukemia, SCL), we traced the fate of these cells during neointimal hyperplasia (NIH) in ligated common carotid and wire-injured femoral arteries. Tamoxifen induction resulted in a homogeneous labeling of mSMCs of the unmanipulated arteries of R26R;SMMHC-CreERtm mice. Following arterial injury, SMCs that were initially located in the medial layer presented in neointimal lesions; however, the fraction of these cells varied widely among vessels with either type of injury. This heterogeneity was not secondary to the random loss of the genetic label as evidenced by the stable β-gal activity in SMC culture. Addition of a second (4wks after surgery) induction did not change the pattern and fraction of the labeled SMCs in the neointima, indicating that few recruited progenitors transform into mature SMCs. This observation is further supported through examination of mice chimeric for R26R;SMMHC-CreERtm bone marrow, where β-gal activity was not detected in injured arteries though strongly induced in culture following PDGF treatment. Neointima formed in R26R;SCL-CreERtm arteries demonstrated a co-localization of β-gal activity to the repopulated ECs, with none being detected in cells underneath the EC monolayer, suggesting a role for mECs in re-endothelialization and indicating EMT as a rare event in NIH development. We have provided direct evidence for the contribution of mSMCs to NIH. The recruited vascular progenitors, particularly bone marrow cells, do not differentiate into fully mature SMCs in NIH lesion. EMT does not serve as a mechanism for populating neointimal cells following vascular injury while occurring under other vascular disease conditions.