Experiential Learning: Critical Analysis of Standardized Patient and Disability Simulation

Current revisions to the accreditation standards for occupational therapy (OT) education include proposed changes to experiential learning. The AOTA Fieldwork/Experiential Learning Ad Hoc Committee recommends that fieldwork Level I experiences be replaced with a new model of experiential education that includes the use of standardized patients and simulation (AOTA, 2017). The purpose of this article is to present critical perspectives about standardized patient simulation and disability simulation to support informed decision-making about the integration of experiential learning in OT professional education. In standardized patient simulation, actors play the roles of clients and important others in therapeutic scenarios; in disability simulation, students act out impairments in a variety of settings. While these forms of simulation are commonly used within OT education, they are critiqued for failing to present participants with authentic lived experiences of disability. This paper presents alternative approaches that would more fully align the OT curriculum with perspectives and priorities of intersectional disability communities. Recommendations to be considered by educators and educational programs include becoming familiar with relevant literature across fields and communities; developing long-term partnerships with disability organizations and community members; involving people with disabilities in the development, implementation, and evaluation of experiential learning opportunities; and providing experiential learning opportunities that take place outside educational and clinical settings and that attend to multiple intersecting dimensions of people with disabilities’ lived experiences. Together, these recommendations can help ensure that students have access to evidence-based educational approaches and best practices that accurately reflect the self-identified needs, concerns, and priorities of intersectional disability communities

Redesigning Systems to Improve Teamwork and Quality for Hospitalized Patients (RESET): Study Protocol Evaluating the Effect of Mentored Implementation to Redesign Clinical Microsystems

Background: A number of challenges impede our ability to consistently provide high quality care to patients hospitalized with medical conditions. Teams are large, team membership continually evolves, and physicians are often spread across multiple units and floors. Moreover, patients and family members are generally poorly informed and lack opportunities to partner in decision making. Prior studies have tested interventions to redesign aspects of the care delivery system for hospitalized medical patients, but the majority have evaluated the effect of a single intervention. We believe these interventions represent complementary and mutually reinforcing components of a redesigned clinical microsystem. Our specific objective for this study is to implement a set of evidence-based complementary interventions across a range of clinical microsystems, identify factors and strategies associated with successful implementation, and evaluate the impact on quality. Methods: The RESET project uses the Advanced and Integrated MicroSystems (AIMS) interventions. The AIMS interventions consist of 1) Unit-based Physician Teams, 2) Unit Nurse-Physician Co-leadership, 3) Enhanced Interprofessional Rounds, 4) Unit-level Performance Reports, and 5) Patient Engagement Activities. Four hospital sites were chosen to receive guidance and resources as they implement the AIMS interventions. Each study site has assembled a local leadership team, consisting of a physician and nurse, and receives mentorship from a physician and nurse with experience in leading similar interventions. Primary outcomes include teamwork climate, assessed using the Safety Attitudes Questionnaire, and adverse events using the Medicare Patient Safety Monitoring System (MPSMS). RESET uses a parallel group study design and two group pretest-posttest analyses for primary outcomes. We use a multi-method approach to collect and triangulate qualitative data collected during 3 visits to study sites. We will use cross-case comparisons to consider how site-specific contextual factors interact with the variation in the intensity and fidelity of implementation to affect teamwork and patient outcomes. Discussion: The RESET study provides mentorship and resources to assist hospitals as they implement complementary and mutually reinforcing components to redesign the clinical microsystems caring for medical patients. Our findings will be of interest and directly applicable to all hospitals providing care to patients with medical conditions. Trial Registration: NCT03745677. Retrospectively registered on November 19, 2018

An Open System for Social Computation

Part of the power of social computation comes from using the collective intelligence of humans to tame the aggregate uncertainty of (otherwise) low veracity data obtained from human and automated sources. We have witnessed a surge in development of social computing systems but, ironically, there have been few attempts to generalise across this activity so that creation of the underlying mechanisms themselves can be made more social. We describe a method for achieving this by standardising patterns of social computation via lightweight formal specifications (we call these social artifacts) that can be connected to existing internet architectures via a single model of computation. Upon this framework we build a mechanism for extracting provenance meta-data across social computations

Coinfection With Influenza A Virus and Klebsiella oxytoca: An Underrecognized Impact on Host Resistance and Tolerance to Pulmonary Infections

Pneumonia is a world health problem and a leading cause of death, particularly affecting children and the elderly (1, 2). Bacterial pneumonia following infection with influenza A virus (IAV) is associated with increased morbidity and mortality but the mechanisms behind this phenomenon are not yet well-defined (3). Host resistance and tolerance are two processes essential for host survival during infection. Resistance is the host's ability to clear a pathogen while tolerance is the host's ability to overcome the impact of the pathogen as well as the host response to infection (4–8). Some studies have shown that IAV infection suppresses the immune response, leading to overwhelming bacterial loads (9–13). Other studies have shown that some IAV/bacterial coinfections cause alterations in tolerance mechanisms such as tissue resilience (14–16). In a recent analysis of nasopharyngeal swabs from patients hospitalized during the 2013–2014 influenza season, we have found that a significant proportion of IAV-infected patients were also colonized with Klebsiella oxytoca, a gram-negative bacteria known to be an opportunistic pathogen in a variety of diseases (17). Mice that were infected with K. oxytoca following IAV infection demonstrated decreased survival and significant weight loss when compared to mice infected with either single pathogen. Using this model, we found that IAV/K. oxytoca coinfection of the lung is characterized by an exaggerated inflammatory immune response. We observed early inflammatory cytokine and chemokine production, which in turn resulted in massive infiltration of neutrophils and inflammatory monocytes. Despite this swift response, the pulmonary pathogen burden in coinfected mice was similar to singly-infected animals, albeit with a slight delay in bacterial clearance. In addition, during coinfection we observed a shift in pulmonary macrophages toward an inflammatory and away from a tissue reparative phenotype. Interestingly, there was only a small increase in tissue damage in coinfected lungs as compared to either single infection. Our results indicate that during pulmonary coinfection a combination of seemingly modest defects in both host resistance and tolerance may act synergistically to cause worsened outcomes for the host. Given the prevalence of K. oxytoca detected in human IAV patients, these dysfunctional tolerance and resistance mechanisms may play an important role in the response of patients to IAV

Terahertz induced transparency in single-layer graphene

We show that the transmission of a terahertz (THz) pulse through single-layer graphene is strongly nonlinear. As the peak electric field of the THz pulse exceeds 50 kV/cm, the graphene becomes increasingly transparent to the THz radiation. When field strength reaches 800 kV/cm, the increased transparency corresponds to a two-fold decrease in the time-average sheet conductivity of the graphene (time averaged over the duration of the pulse). Time-resolved measurements reveal that the leading portion of the pulse creates transparency for the trailing portion, with a 10-fold suppression in sheet conductivity at the tail of the strongest THz pulse. Comparing the THz-induced transparency phenomena in different sample geometries shows that substrate-free graphene is the best geometry for maximizing the nonlinear transparency effect.Keywords: Transistors, Spectroscop

A review of duodenal metastases from squamous cell carcinoma of the cervix presenting as an upper gastrointestinal bleed

Upper gastrointestinal bleeding due to duodenal metastases is extremely uncommon. Extra-pelvic spread of squamous cell carcinoma (SCC) of the cervix to the small bowel is rare with only 6 reported cases in the English literature since 1981(PubMed, Medline)

Regulation of Hepatic Triacylglycerol Metabolism by CGI-58 Does Not Require ATGL Co-activation

SummaryAdipose triglyceride lipase (ATGL) and comparative gene identification 58 (CGI-58) are critical regulators of triacylglycerol (TAG) turnover. CGI-58 is thought to regulate TAG mobilization by stimulating the enzymatic activity of ATGL. However, it is not known whether this coactivation function of CGI-58 occurs in vivo. Moreover, the phenotype of human CGI-58 mutations suggests ATGL-independent functions. Through direct comparison of mice with single or double deficiency of CGI-58 and ATGL, we show here that CGI-58 knockdown causes hepatic steatosis in both the presence and absence of ATGL. CGI-58 also regulates hepatic diacylglycerol (DAG) and inflammation in an ATGL-independent manner. Interestingly, ATGL deficiency, but not CGI-58 deficiency, results in suppression of the hepatic and adipose de novo lipogenic program. Collectively, these findings show that CGI-58 regulates hepatic neutral lipid storage and inflammation in the genetic absence of ATGL, demonstrating that mechanisms driving TAG lipolysis in hepatocytes differ significantly from those in adipocytes

Inhibition of dual-specificity tyrosine phosphorylation-regulated kinase 2 perturbs 26S proteasome-addicted neoplastic progression

Dependence on the 26S proteasome is an Achilles' heel for triple-negative breast cancer (TNBC) and multiple myeloma (MM). The therapeutic proteasome inhibitor, bortezomib, successfully targets MM but often leads to drug-resistant disease relapse and fails in breast cancer. Here we show that a 26S proteasome-regulating kinase, DYRK2, is a therapeutic target for both MM and TNBC. Genome editing or small-molecule mediated inhibition of DYRK2 significantly reduces 26S proteasome activity, bypasses bortezomib resistance, and dramatically delays in vivo tumor growth in MM and TNBC thereby promoting survival. We further characterized the ability of LDN192960, a potent and selective DYRK2-inhibitor, to alleviate tumor burden in vivo. The drug docks into the active site of DYRK2 and partially inhibits all 3 core peptidase activities of the proteasome. Our results suggest that targeting 26S proteasome regulators will pave the way for therapeutic strategies in MM and TNBC

Pol II phosphorylation regulates a switch between transcriptional and splicing condensates

The synthesis of pre-mRNA by RNA polymerase II (Pol II) involves the formation of a transcription initiation complex, and a transition to an elongation complex. The large subunit of Pol II contains an intrinsically disordered C-terminal domain that is phosphorylated by cyclin-dependent kinases during the transition from initiation to elongation, thus influencing the interaction of the C-terminal domain with different components of the initiation or the RNA-splicing apparatus. Recent observations suggest that this model provides only a partial picture of the effects of phosphorylation of the C-terminal domain. Both the transcription-initiation machinery and the splicing machinery can form phase-separated condensates that contain large numbers of component molecules: hundreds of molecules of Pol II and mediator are concentrated in condensates at super-enhancers, and large numbers of splicing factors are concentrated in nuclear speckles, some of which occur at highly active transcription sites. Here we investigate whether the phosphorylation of the Pol II C-terminal domain regulates the incorporation of Pol II into phase-separated condensates that are associated with transcription initiation and splicing. We find that the hypophosphorylated C-terminal domain of Pol II is incorporated into mediator condensates and that phosphorylation by regulatory cyclin-dependent kinases reduces this incorporation. We also find that the hyperphosphorylated C-terminal domain is preferentially incorporated into condensates that are formed by splicing factors. These results suggest that phosphorylation of the Pol II C-terminal domain drives an exchange from condensates that are involved in transcription initiation to those that are involved in RNA processing, and implicates phosphorylation as a mechanism that regulates condensate preference