SIMULATED MEDICAL ENCOUNTERS TO ANALYZE PATIENT-PHYSICIAN COMMUNICATION DURING ELECTRONIC MEDICAL RECORDS\u27 USE IN PRIMARY CARE

The implications of the patient-physician relationship and communication on healthcare quality have been widely discussed in previous research. Communication has been characterized as one of the most powerful, encompassing, and versatile instruments available to the physician and it has been suggested that good patient-physician communication can improve healthcare outcomes. The incorporation of Electronic Medical Records (EMRs) in primary care provides an opportunity for improving healthcare services and quality of care. EMRs have, without a doubt, transformed the dynamics of the medical encounter. Implications of EMRs on the patient-physician communication, and thus on healthcare quality, have not yet reached a full understanding. Existing physician communication skills assessment tools do not take into account the physician\u27s need to divert his/her attention from the patient to the computer, and vise versa. One such tool is the SEGUE. This research-in-progress paper aims to describe the preliminary steps taken to assess the adequacy of the existing SEGUE tool in evaluating physicians\u27 communication skills in a computerized environment based on simulated medical encounters. Assuming that the existing SEGUE tool does not capture the new dynamics of the medical encounter; we suggest that it should be enhanced to include best-practices for physicians\u27 EMR use while maintaining effective communication with patients. We intend to develop a set of items which reflect recommendations for EMR use aimed at maintaining effective communication with the patient. These new items will be formulated based on an extant literature review and experts panel, and will eventually be incorporated into the existing SEGUE tool to provide a comprehensive tool for analyzing physicians\u27 communication skills in the computerized clinic

Hemodynamic support with TandemHeart™ in tako-tsubo cardiomyopathy – a case report

Tako-tsubo cardiomyopathy is characterized by chest pain, electrocardiographic abnormalities mimicking acute myocardial infarction, akinesis or dyskinesis of apical or mid left ventricular segments, and the absence of obstructive coronary artery disease. Tako-tsubo cardiomyopathy is usually a potentially reversible form of cardiac dysfunction. A careful literature search revealed no previous report of a patient requiring mechanical circulatory support in tako-tsubo cardiomyopathy. We report a patient with tako-tsubo cardiomyopathy, ventricular fibrillation, and hemodynamic instability requiring a left ventricular assist device (TandemHeart™) followed by improvement of left ventricular ejection fraction to 45%

Distribution of shortest cycle lengths in random networks

We present analytical results for the distribution of shortest cycle lengths (DSCL) in random networks. The approach is based on the relation between the DSCL and the distribution of shortest path lengths (DSPL). We apply this approach to configuration model networks, for which analytical results for the DSPL were obtained before. We first calculate the fraction of nodes in the network which reside on at least one cycle. Conditioning on being on a cycle, we provide the DSCL over ensembles of configuration model networks with degree distributions which follow a Poisson distribution (Erdos-R\'enyi network), degenerate distribution (random regular graph) and a power-law distribution (scale-free network). The mean and variance of the DSCL are calculated. The analytical results are found to be in very good agreement with the results of computer simulations.Comment: 44 pages, 11 figure

Individual and collective stock dynamics: intra-day seasonalities

We establish several new stylised facts concerning the intra-day seasonalities of stock dynamics. Beyond the well known U-shaped pattern of the volatility, we find that the average correlation between stocks increases throughout the day, leading to a smaller relative dispersion between stocks. Somewhat paradoxically, the kurtosis (a measure of volatility surprises) reaches a minimum at the open of the market, when the volatility is at its peak. We confirm that the dispersion kurtosis is a markedly decreasing function of the index return. This means that during large market swings, the idiosyncratic component of the stock dynamics becomes sub-dominant. In a nutshell, early hours of trading are dominated by idiosyncratic or sector specific effects with little surprises, whereas the influence of the market factor increases throughout the day, and surprises become more frequent.Comment: 9 pages, 7 figure

Temporal pattern of C1q deposition after transient focal cerebral ischemia

Recent studies have focused on elucidating the contribution of individual complement proteins to post-ischemic cellular injury. As the timing of complement activation and deposition after cerebral ischemia is not well understood, our study investigates the temporal pattern of C1q accumulation after experimental murine stroke. Brains were harvested from mice subjected to transient focal cerebral ischemia at 3, 6, 12, and 24 hr post reperfusion. Western blotting and light microscopy were employed to determine the temporal course of C1q protein accumulation and correlate this sequence with infarct evolution observed with TTC staining. Confocal microscopy was utilized to further characterize the cellular localization and characteristics of C1q deposition. Western Blot analysis showed that C1q protein begins to accumulate in the ischemic hemisphere between 3 and 6 hr post-ischemia. Light microscopy confirmed these findings, showing concurrent C1q protein staining of neurons. Confocal microscopy demonstrated co-localization of C1q protein with neuronal cell bodies as well as necrotic cellular debris. These experiments demonstrate the accumulation of C1q protein on neurons during the period of greatest infarct evolution. This data provides information regarding the optimal time window during which a potentially neuroprotective anti-C1q strategy is most likely to achieve therapeutic success. © 2006 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50651/1/20775_ftp.pd

Overground walking speed changes when subjected to body weight support conditions for nonimpaired and post stroke individuals

<p>Abstract</p> <p>Background</p> <p>Previous research has shown that body weight support (BWS) has the potential to improve gait speed for individuals post-stroke. However, body weight support also reduces the optimal walking speed at which energy use is minimized over the gait cycle indicating that BWS should reduce walking speed capability.</p> <p>Methods</p> <p>Nonimpaired subjects and subjects post-stroke walked at a self-selected speed over a 15 m walkway. Body weight support (BWS) was provided to subjects at 0%, 10%, 20%, 30%, and 40% of the subject's weight while they walked overground using a robotic body weight support system. Gait speed, cadence, and average step length were calculated for each subject using recorded data on their time to walk 10 m and the number of steps taken.</p> <p>Results</p> <p>When subjected to greater levels of BWS, self-selected walking speed decreased for the nonimpaired subjects. However, subjects post-stroke showed an average increase of 17% in self-selected walking speed when subjected to some level of BWS compared to the 0% BWS condition. Most subjects showed this increase at the 10% BWS level. Gait speed increases corresponded to an increase in step length, but not cadence.</p> <p>Conclusions</p> <p>The BWS training environment results in decreased self-selected walking speed in nonimpaired individuals, however self-selected overground walking speed is facilitated when provided with a small percentage of body weight support for people post-stroke.</p

Fat1 deletion promotes hybrid EMT state, tumour stemness and metastasis

FAT1, which encodes a protocadherin, is one of the most frequently mutated genes in human cancers1–5. However, the role and the molecular mechanisms by which FAT1 mutations control tumour initiation and progression are poorly understood. Here, using mouse models of skin squamous cell carcinoma and lung tumours, we found that deletion of Fat1 accelerates tumour initiation and malignant progression and promotes a hybrid epithelial-to-mesenchymal transition (EMT) phenotype. We also found this hybrid EMT state in FAT1-mutated human squamous cell carcinomas. Skin squamous cell carcinomas in which Fat1 was deleted presented increased tumour stemness and spontaneous metastasis. We performed transcriptional and chromatin profiling combined with proteomic analyses and mechanistic studies, which revealed that loss of function of FAT1 activates a CAMK2–CD44–SRC axis that promotes YAP1 nuclear translocation and ZEB1 expression that stimulates the mesenchymal state. This loss of function also inactivates EZH2, promoting SOX2 expression, which sustains the epithelial state. Our comprehensive analysis identified drug resistance and vulnerabilities in FAT1-deficient tumours, which have important implications for cancer therapy. Our studies reveal that, in mouse and human squamous cell carcinoma, loss of function of FAT1 promotes tumour initiation, progression, invasiveness, stemness and metastasis through the induction of a hybrid EMT state

Postnatal PPARδ Activation and Myostatin Inhibition Exert Distinct yet Complimentary Effects on the Metabolic Profile of Obese Insulin-Resistant Mice

BACKGROUND: Interventions for T2DM have in part aimed to mimic exercise. Here, we have compared the independent and combined effects of a PPARdelta agonist and endurance training mimetic (GW501516) and a myostatin antibody and resistance training mimetic (PF-879) on metabolic and performance outcomes in obese insulin resistant mice. METHODOLOGY/PRINCIPAL FINDINGS: Male ob/ob mice were treated for 6 weeks with vehicle, GW501516, PF-879, or GW501516 in combination with PF-879. The effects of the interventions on body composition, glucose homeostasis, glucose tolerance, energy expenditure, exercise capacity and metabolic gene expression were compared at the end of study. GW501516 attenuated body weight and fat mass accumulation and increased the expression of genes of oxidative metabolism. In contrast, PF-879 increased body weight by driving muscle growth and altered the expression of genes involved in insulin signaling and glucose metabolism. Despite their differences, both interventions alone improved glucose homeostasis. Moreover, GW501516 more effectively improved serum lipids, and PF-879 uniquely increased energy expenditure, exercise capacity and adiponectin levels. When combined the robust effects of GW501516 and/or PF-879 on body weight, adiposity, muscle mass, glycemia, serum lipids, energy expenditure and exercise capacity were highly conserved. CONCLUSIONS/SIGNIFICANCE: The data, for the first time, demonstrate postnatal inhibition of myostatin not only promotes gains in muscle mass similar to resistance training,but improves metabolic homeostasis. In several instances, these effects were either distinct from or complimentary to those of GW501516. The data further suggest that strategies to increase muscle mass, and not necessarily oxidative capacity, may effectively counter insulin resistance and T2DM