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1.  Expectations of iPad Use in an Internal Medicine Residency Program: Is It Worth the “Hype”? 
Background
While early reports highlight the benefits of tablet computing in hospitals, introducing any new technology can result in inflated expectations.
Objective
The aim of the study is to compare anticipated expectations of Apple iPad use and perceptions after deployment among residents.
Methods
115 internal medicine residents received Apple iPads in October 2010. Residents completed matched surveys on anticipated usage and perceptions after distribution 1 month prior and 4 months after deployment.
Results
In total, 99% (114/115) of residents responded. Prior to deployment, most residents believed that the iPad would improve patient care and efficiency on the wards; however, fewer residents “strongly agreed” after deployment (34% vs 15% for patient care, P<.001; 41% vs 24% for efficiency, P=.005). Residents with higher expectations were more likely to report using the iPad for placing orders post call and during admission (71% vs 44% post call, P=.01, and 16% vs 0% admission, P=.04). Previous Apple iOS product owners were also more likely to use the iPad in key areas. Overall, 84% of residents thought the iPad was a good investment for the residency program, and over half of residents (58%) reported that patients commented on the iPad in a positive way.
Conclusions
While the use of tablets such as the iPad by residents is generally well received, high initial expectations highlight the danger of implementing new technologies. Education on the realistic expectations of iPad benefits may be warranted.
doi:10.2196/jmir.2524
PMCID: PMC3650925  PMID: 23656727
iPad; mobile tablet computing; technology; expectation dynamics; hype
2.  Genetic Dissection of a Blood Pressure Quantitative Trait Locus on Rat Chromosome 1 and Gene Expression Analysis Identifies SPON1 as a Novel Candidate Hypertension Gene 
Circulation research  2007;100(7):992-999.
A region with a major effect on blood pressure is located on rat chromosome 1. We have previously isolated this region in reciprocal congenic strains (WKY.SHR-Sa and SHR.WKY-Sa) derived from a cross of the spontaneously hypertensive rat (SHR) with the Wistar-Kyoto rat (WKY) and shown that there are two distinct BP quantitative trait loci (QTLs), BP1 and BP2, in this region. Sisa1, a congenic sub-strain from the SHR.WKY-Sa animals carrying an introgressed segment of 4.3Mb, contains BP1. Here, we report further dissection of BP1 by the creation of two new mutually exclusive congenic sub-strains (Sisa1a and Sisa1b) and interrogation of candidate genes by expression profiling and targeted transcript sequencing. Only one of the sub-strains (Sisa1a) continued to demonstrate a BP difference but with a reduced introgressed segment of 3Mb. Exonic sequencing of the twenty genes located in the Sisa1a region did not identify any major differences between SHR and WKY. However, microarray expression profiling of whole kidney samples and subsequent quantitative RT-PCR identified a single gene, Spon1 that exhibited significant differential expression between the WKY and SHR genotypes at both 6 and 24 weeks of age. Western blot analysis confirmed an increased level of the Spon1 gene product in SHR kidneys. Spon1 belongs to a family of genes with anti-angiogenic properties. These findings justify further investigation of this novel positional candidate gene in BP control in hypertensive rat models and humans.
doi:10.1161/01.RES.0000261961.41889.9c
PMCID: PMC3533402  PMID: 17332427
hypertension; genetics; rats; gene expression; quantitative trait locus
3.  Knockdown of embryonic myosin heavy chain reveals an essential role in the morphology and function of the developing heart 
Development (Cambridge, England)  2011;138(18):3955-3966.
The expression and function of embryonic myosin heavy chain (eMYH) has not been investigated within the early developing heart. This is despite the knowledge that other structural proteins, such as alpha and beta myosin heavy chains and cardiac alpha actin, play crucial roles in atrial septal development and cardiac function. Most cases of atrial septal defects and cardiomyopathy are not associated with a known causative gene, suggesting that further analysis into candidate genes is required. Expression studies localised eMYH in the developing chick heart. eMYH knockdown was achieved using morpholinos in a temporal manner and functional studies were carried out using electrical and calcium signalling methodologies. Knockdown in the early embryo led to abnormal atrial septal development and heart enlargement. Intriguingly, action potentials of the eMYH knockdown hearts were abnormal in comparison with the alpha and beta myosin heavy chain knockdowns and controls. Although myofibrillogenesis appeared normal, in knockdown hearts the tissue integrity was affected owing to apparent focal points of myocyte loss and an increase in cell death. An expression profile of human skeletal myosin heavy chain genes suggests that human myosin heavy chain 3 is the functional homologue of the chick eMYH gene. These data provide compelling evidence that eMYH plays a crucial role in important processes in the early developing heart and, hence, is a candidate causative gene for atrial septal defects and cardiomyopathy.
doi:10.1242/dev.059063
PMCID: PMC3160091  PMID: 21862559
Atrial septal development; Cardiomyopathy; Myosin; Chick
4.  Anomaly and Signature Filtering Improve Classifier Performance For Detection Of Suspicious Access To EHRs 
Our objective is to facilitate semi-automated detection of suspicious access to EHRs. Previously we have shown that a machine learning method can play a role in identifying potentially inappropriate access to EHRs. However, the problem of sampling informative instances to build a classifier still remained. We developed an integrated filtering method leveraging both anomaly detection based on symbolic clustering and signature detection, a rule-based technique. We applied the integrated filtering to 25.5 million access records in an intervention arm, and compared this with 8.6 million access records in a control arm where no filtering was applied. On the training set with cross-validation, the AUC was 0.960 in the control arm and 0.998 in the intervention arm. The difference in false negative rates on the independent test set was significant, P=1.6×10−6. Our study suggests that utilization of integrated filtering strategies to facilitate the construction of classifiers can be helpful.
PMCID: PMC3243249  PMID: 22195129
5.  Structural basis of AMPK regulation by small molecule activators 
Nature Communications  2013;4:3017.
AMP-activated protein kinase (AMPK) plays a major role in regulating cellular energy balance by sensing and responding to increases in AMP/ADP concentration relative to ATP. Binding of AMP causes allosteric activation of the enzyme and binding of either AMP or ADP promotes and maintains the phosphorylation of threonine 172 within the activation loop of the kinase. AMPK has attracted widespread interest as a potential therapeutic target for metabolic diseases including type 2 diabetes and, more recently, cancer. A number of direct AMPK activators have been reported as having beneficial effects in treating metabolic diseases, but there has been no structural basis for activator binding to AMPK. Here we present the crystal structure of human AMPK in complex with a small molecule activator that binds at a site between the kinase domain and the carbohydrate-binding module, stabilising the interaction between these two components. The nature of the activator-binding pocket suggests the involvement of an additional, as yet unidentified, metabolite in the physiological regulation of AMPK. Importantly, the structure offers new opportunities for the design of small molecule activators of AMPK for treatment of metabolic disorders.
Small molecule activators of the energy sensing kinase AMPK are promising candidates as therapies for metabolic disease. Xiao et al. present the crystal structure of AMPK in complex with a small molecule activator, and show that the drug stabilizes interaction between the catalytic and carbohydrate-binding domains.
doi:10.1038/ncomms4017
PMCID: PMC3905731  PMID: 24352254

Results 1-5 (5)