Implementing technology in healthcare : insights from physicians

Technology has significantly changed the way health organizations operate. However, the role it plays in healthcare systems remains unclear. This aim of this study was to evaluate the opinion of physicians regarding e-health and determine what factors influence their opinion and describe the advantages, inconveniences and threats they may perceive by its use. A cross-sectional questionnaire-based study. A questionnaire which had been previously designed and validated by the authors was used to interview physicians from the Barcelona Medical Association. 930 physicians were contacted by phone to participate in the study. Seven hundred sixty physicians responded to the questionnaire (response rate: 82%). The usefulness of telemedicine scored 7.4 (SD 1.8) on a scale from 1-10 (from the lowest to the highest) and the importance of the Internet in the workplace was 8.2 points (SD 1.8). Therapeutic compliance (7.0 -SD 1.8-) and patient health (7.0 -SD 1.7-) showed the best scores, and there were differences between professionals who had and had not previously participated in a telemedicine project (p < 0.05). The multivariate regression model explained the 41% of the variance for 7 factors: participation in telemedicine project (p < 0.001), quality of clinical practice (p < 0.001), patient health (p < 0.001), professional workload (p = 0.005), ease-of-use of electronic device (p = 0.007), presence of incentives for telemedicine (p = 0.011) and patient preference for in-person visits (p = 0.05). Physicians believe in the usefulness of e-health. Professionals with previous experience with it are more open to its implementation and consider that the benefits of technology outweigh its possible difficulties and shortcomings. Physicians demanded projects with appropriate funding and technology, as well as specific training to improve their technological abilities. The relationship of users with technology differs according to their personal or professional life. Although a 2.0 philosophy has been incorporated into many aspects of our lives, healthcare systems still have a long way to go in order to adapt to this new understanding of the relationship between patients and their health. The online version of this article (doi:10.1186/s12911-017-0489-2) contains supplementary material, which is available to authorized users

Insulin protects acinar cells during pancreatitis by preserving glycolytic ATP supply to calcium pumps.

From Europe PMC via Jisc Publications RouterHistory: ppub 2021-07-01, epub 2021-07-19Publication status: PublishedFunder: Medical Research Council; Grant(s): MR/P00251X/1Funder: NIDDK NIH HHS; Grant(s): P30 DK089503, R01 DK059578, P30 DK020572, P60 DK020572, U2C DK110768Funder: Wellcome TrustAcute pancreatitis (AP) is serious inflammatory disease of the pancreas. Accumulating evidence links diabetes with severity of AP, suggesting that endogenous insulin may be protective. We investigated this putative protective effect of insulin during cellular and in vivo models of AP in diabetic mice (Ins2Akita) and Pancreatic Acinar cell-specific Conditional Insulin Receptor Knock Out mice (PACIRKO). Caerulein and palmitoleic acid (POA)/ethanol-induced pancreatitis was more severe in both Ins2Akita and PACIRKO vs control mice, suggesting that endogenous insulin directly protects acinar cells in vivo. In isolated pancreatic acinar cells, insulin induced Akt-mediated phosphorylation of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2) which upregulated glycolysis thereby preventing POA-induced ATP depletion, inhibition of the ATP-dependent plasma membrane Ca2+ ATPase (PMCA) and cytotoxic Ca2+ overload. These data provide the first mechanistic link between diabetes and severity of AP and suggest that phosphorylation of PFKFB2 may represent a potential therapeutic strategy for treatment of AP

Identification and characterization of a fatty acyl reductase from a Spodoptera littoralis female gland involved in pheromone biosynthesis

© 2014 Royal Entomological Society. Fatty acyl-CoA reductases (FARs), the enzymes that catalyse reduction of a fatty acyl-CoA to the corresponding alcohol in insect pheromone biosynthesis, are postulated to play an important role in determining the proportion of each component in the pheromone blend. For the first time, we have isolated and characterized from the Egyptian cotton leaf worm Spodoptera littoralis (Lepidoptera: Noctuidae) a FAR cDNA (Slit-FAR1), which appeared to be expressed only in the pheromone gland and was undetectable in other female tissues, such as fat body, ovaries, wings, legs or thorax. The encoded protein has been successfully expressed in a recombinant system, and the recombinant enzyme is able to produce the intermediate fatty acid alcohols of the pheromone biosynthesis of S. littoralis from the corresponding acyl-CoA precursors. The kinetic variables Km and Vmax, which have been calculated for each acyl-CoA pheromone precursor, suggest that in S. littoralis pheromone biosynthesis other biosynthetic enzymes (e.g. desaturases, acetyl transferase) should also contribute to the final ratio of components of the pheromone blend. In a phylogenetic analysis, Slit-FAR1 appeared grouped in a cluster of other FARs involved in the pheromone biosynthesis of other insects, with little or non-specificity for the natural pheromone precursors.This research was supported by the European Commission through the Biosynthetic Infochemical Communication (‘iCHEM’) project, contract no. 032275.Peer Reviewe

Regulation of transforming growth factor β-induced responses by protein kinase A in pancreatic acinar cells

TGF-β is an important regulator of growth and differentiation in the pancreas and has been implicated in pancreatic tumorigenesis. We have recently demonstrated that TGF-β can activate protein kinase A (PKA) in mink lung epithelial cells (Zhang L, Duan C, Binkley C, Li G, Uhler M, Logsdon C, Simeone D. Mol Cell Biol 24: 2169–2180, 2004). In this study, we sought to determine whether TGF-β activates PKA in pancreatic acinar cells, the mechanism by which PKA is activated, and PKA's role in TGF-β-mediated growth regulatory responses. TGF-β rapidly activated PKA in pancreatic acini while having no effect on intracellular cAMP levels. Coimmunoprecipitation experiments demonstrated a physical interaction between a Smad3/Smad4 complex and the regulatory subunits of PKA. TGF-β also induced activation of the PKA-dependent transcription factor CREB. Both the specific PKA inhibitor H89 and PKI peptide significantly blocked TGF-β's ability to activate PKA and CREB. TGF-β-mediated growth inhibition and TGF-β-induced p21 and SnoN expression in pancreatic acinar cells were blocked by H89 and PKI peptide. This study demonstrates that this novel cross talk between TGF-β and PKA signaling pathways may play an important role in regulating TGF-β signaling in the pancreas