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1.


Evidence is emerging that certain technologies such as computerized provider order entry may reduce the likelihood of patient harm. However, many technologies that should reduce medical errors have been abandoned because of problems with their design, their impact on workflow, and general dissatisfaction with them by end users. Patient safety researchers have therefore looked to human factors engineering for guidance on how to design technologies to be usable (easy to use) and useful (improving job performance, efficiency, and/or quality). While this is a necessary step towards improving the likelihood of end user satisfaction, it is still not sufficient. Human factors engineering research has shown that the manner in which technologies are implemented also needs to be designed carefully if benefits are to be realized. This paper reviews the theoretical knowledge on what leads to successful technology implementation and how this can be translated into specifically designed processes for successful technology change. The literature on diffusion of innovations, technology acceptance, organisational justice, participative decision making, and organisational change is reviewed and strategies for promoting successful implementation are provided. Given the rapid and ever increasing pace of technology implementation in health care, it is critical for the science of technology implementation to be understood and incorporated into efforts to improve patient safety.  相似文献   
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Objective. Rheumatoid arthritis (RA) is characterized by decreased expression of CD7 in the peripheral blood and in the synovium. The present study was designed to identify the basis for and functional consequences of this decreased expression. Methods. Peripheral blood lymphocytes from normal controls and from patients with RA or systemic lupus erythematosus (SLE), and T cell lines derived from rheumatoid synovium, were evaluated using 3-color fluorescence-activated cell sorter analysis. Results. Normal subjects and most SLE patients expressed homogeneous, bright CD7 on CD4+, CD45RA+ cells, whereas RA patients demonstrated a significantly increased proportion of CD7– cells. T cell lines derived from rheumatoid synovium demonstrated a striking deficiency of CD7 on CD4+, CD45RA– cells. CD4+, CD45RA+ cells from RA patients changed phenotype after in vitro activation to CD45RA negativity, with up-regulation of CD7. CD7–, CD4+, CD45RA– cells were assessed for their ability to induce pokeweed mitogen-driven IgM and IgM-rheumatoid factor synthesis, and they were found to be potent helper/inducer cells. An increased population of CD7-, CD4+ cells in peripheral blood was found to predict a low response to recall antigens. Conclusion. The low expression of CD7 in RA may explain some of the immune abnormalities which may contribute to the pathogenesis of this disease.  相似文献   
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Apalutamide, an androgen receptor signaling inhibitor, in combination with androgen-deprivation therapy (ADT), is approved for treatment of patients with nonmetastatic castration-resistant prostate cancer and metastatic castration-sensitive prostate cancer, based on the data from the phase 3 SPARTAN and TITAN studies respectively. Apalutamide is an inducer of cytochrome P450 enzymes and P-glycoprotein, which are involved in the metabolism of oral anticoagulants (OACs) and may thus have potential drug-drug interactions when co-administered with OACs. Concomitant use of certain OACs such as apixaban, rivaroxaban, edoxaban, dabigatran, and warfarin was allowed in the SPARTAN and TITAN studies. A post-hoc analysis was conducted to evaluate the incidence of treatment-emergent thrombotic and embolic adverse events (AEs) in patients receiving concomitant OACs with apalutamide + ADT or placebo + ADT in both the studies. Anticoagulants were identified by WHO Drug Anatomical Therapeutic Chemical level 4 classifications. Thrombotic and embolic AEs were coded using the Medical Dictionary for Regulatory Activities Version 22.1. Data were analyzed from patients receiving concurrent OACs among all treated patients in SPARTAN (apalutamide + ADT: 95/803 [11.8%]; placebo + ADT: 48/398 [12.1%]) and TITAN (apalutamide + ADT: 31/524 [5.9%]; placebo + ADT: 28/527 [5.3%]). No consequential differences were observed in the occurrence of thrombotic and embolic events between apalutamide + ADT and placebo + ADT groups receiving concomitant OACs in SPARTAN (11.6% vs 12.5%) or TITAN (19.4% vs 21.4%). Grade 3/4 thrombotic and embolic AEs observed in patients receiving concomitant OACs with apalutamide + ADT or placebo + ADT were 6 (6.3%) vs 5 (10.4%) in SPARTAN and 3 (9.7%) vs 1 (3.6%) in TITAN. This analysis suggests that when necessary, concomitant OACs can be used with apalutamide with appropriate monitoring.  相似文献   
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The principal causes of death of 68 patients with lupus glomerulonephritis were reviewed. Renal failure (40%), vascular events (25%), and infections (16%) were the predominant causes. Diffuse proliferative glomerulonephritis was associated with an increased frequency of renal failure. A bimodal pattern of early deaths due to active lupus and sepsis and late deaths from vascular events was found superimposed on a constant rate of death from renal failure.  相似文献   
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A nucleation and crystallization schedule was adapted to produce 40% crystalline Bioglass ceramic particulates. These particles were placed in a dynamic environment in a simulated physiologic solution (SBF-9) for time periods ranging from 10 min to 7 days. Fourier transform Raman spectroscopy (FT-Raman) and infrared spectroscopy (FTIR) were used to analyze the apatite layer formation on the particulates. FTIR determined that amorphous apatite formation took place within 2 h, with the appearance of crystalline apatite in 14 h. The vibrational frequencies obtained through FT-Raman were equivalent to those obtained using FTIR. These analyses showed that a fully crystallized apatite layer was present on the particulate after 3 days of exposure in SBF solution. These findings are consistent with those associated with amorphous Bioglass particles.  相似文献   
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Alpha-1-antitrypsin phenotypes were determined in 37 patients with rheumatoid arthritis and 40 patients with systemic lupus erythematosus. No significant increase in non-MM phenotypes was found. It appears that alpha-1-antitrypsin phenotypes neither predispose to the development nor enhance the severity of the two rheumatic diseases.  相似文献   
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