A Comparative Review of Canadian Health Professional Education Accreditation Systems

Canadian governments and various stakeholder groups are advocating greater interprofessional collaboration amongst health care providers as a fundamental strategy for enhancing coordination and quality of care in the health care system. Interprofessional education for collaborative patient-centred practice (IECPCP) is an educational process by which students/learners (or workers) from different health professions learn together to improve collaboration. The educational system is believed to be a main determinant of interprofessional collaborative practice, yet academic institutions are largely influenced by accreditation, certification and licensure bodies. Accreditation processes have been linked to the continuous improvement of curricula in the health professions, and have also been identified as potential avenues for encouraging educational change and innovation. The purpose of this paper is to summarize the characteristics of the national accreditation systems of select Canadian health professional education programs at both the pre- and post-licensure educational levels and to show how these systems support and/or foster IECPCP. A review of the educational accreditation systems of medicine, nursing, pharmacy, social work, occupational therapy and physiotherapy was undertaken through key informant interviews and an analysis of accreditation process documentation. The results of this comparative review suggest that accreditation systems are more prevalent across the health professions at a pre-licensure level. Accreditation at the post- licensure level, particularly at the continuing professional education level, appears to be less well established across the majority of health professions. Overall, the findings of the review also suggest that current accreditation systems do not appear to promote nor foster interprofessional education for collaborative patient-centred practice in a systematic manner through either accreditation processes or standards. Through a critical adult learning perspective we argue that in order for traditional uni-professional structures within the health professional education system to be challenged, the accreditation system needs to place greater value on interprofessional education for collaborative patient-centred practice.Les gouvernements du Canada ainsi que divers groupes d’intervenants appellent à une plus grande collaboration interprofessionnelle entre les fournisseurs de services de santé comme stratégie fondamentale pour rehausser la coordination et la qualité des soins dans le système des soins de santé. L’éducation interprofessionnelle pour la pratique collaborative centrée sur le patient (IECPCP) constitue un processus éducatif qui permet aux étudiants/apprenants (ou travailleurs) de diverses professions de la santé d’apprendre ensemble à mieux collaborer. Le système éducatif est perçu comme le principal déterminant de la pratique collaborative interprofessionnelle; cependant, les institutions éducatives sont fortement infl uencées par les organismes qui octroient les accréditations, certifi cations et autorisations d’exercer. Les processus d’accréditation ont été reliés à l’amélioration continue des programmes d’études dans les professions de santé et ils ont été également identifi és comme avenues potentielles pour encourager le changement et l’innovation en milieu éducatif. L’objectif de cet article est de résumer les caractéristiques des systèmes nationaux d’accréditation de certains programmes de formation des professionnels de la santé au Canada à tous les niveaux (pré- et post-autorisation d’exercer) et de montrer comment ces systèmes soutiennent ou encouragent l’IECPCP. Nous avons passé en revue les systèmes d’accréditation en médecine, soins infirmiers, pharmacie, travail social, ergothérapie et physiothérapie par le biais d’entrevues avec des personnes-clés et par l’analyse de la documentation sur les processus d’accréditation. Les résultats de cette étude comparative suggèrent que les systèmes d’accréditation dans les services de santé sont plus courants avant l’octroi de l’autorisation d’exercer. L’accréditation post-autorisation d’exercer, en particulier dans le domaine de la formation professionnelle continue, semble être moins bien établie dans la majorité des professions de la santé. Globalement, les résultats de l’étude suggèrent aussi que les systèmes actuels d’accréditation ne semblent pas promouvoir ou encourager la formation interprofessionnelle pour la pratique collaborative centrée sur le patient de façon systématique par les processus ou normes d’accréditation. Dans la perspective critique de l’apprentissage des adultes, nous avançons que, pour remettre en question les structures uniprofessionnelles traditionnelles du système éducatif des professions de la santé, le système d’accréditation doit accorder une plus grande place à l’éducation interprofessionnelle sur la pratique collaborative centrée sur le patient.&nbsp

Mutation in Mouse Hei10, an E3 Ubiquitin Ligase, Disrupts Meiotic Crossing Over

Crossing over during meiotic prophase I is required for sexual reproduction in mice and contributes to genome-wide genetic diversity. Here we report on the characterization of an N-ethyl-N-nitrosourea-induced, recessive allele called mei4, which causes sterility in both sexes owing to meiotic defects. In mutant spermatocytes, chromosomes fail to congress properly at the metaphase plate, leading to arrest and apoptosis before the first meiotic division. Mutant oocytes have a similar chromosomal phenotype but in vitro can undergo meiotic divisions and fertilization before arresting. During late meiotic prophase in mei4 mutant males, absence of cyclin dependent kinase 2 and mismatch repair protein association from chromosome cores is correlated with the premature separation of bivalents at diplonema owing to lack of chiasmata. We have identified the causative mutation, a transversion in the 5′ splice donor site of exon 1 in the mouse ortholog of Human Enhancer of Invasion 10 (Hei10; also known as Gm288 in mouse and CCNB1IP1 in human), a putative B-type cyclin E3 ubiquitin ligase. Importantly, orthologs of Hei10 are found exclusively in deuterostomes and not in more ancestral protostomes such as yeast, worms, or flies. The cloning and characterization of the mei4 allele of Hei10 demonstrates a novel link between cell cycle regulation and mismatch repair during prophase I

Assessment of obsessive-compulsive symptom dimensions: development and evaluation

Although several measures of obsessive-compulsive (OC) symptoms exist, most are limited in that they are not consistent with the most recent empirical findings on the nature and dimensional structure of obsessions and compulsions. In the present research, the authors developed and evaluated a measure called the Dimensional Obsessive-Compulsive Scale (DOCS) to address limitations of existing OC symptom measures. The DOCS is a 20-item measure that assesses the four dimensions of OC symptoms most reliably replicated in previous structural research. Factorial validity of the DOCS was supported by exploratory and confirmatory factor analyses of 3 samples, including individuals with OC disorder, those with other anxiety disorders, and nonclinical individuals. Scores on the DOCS displayed good performance on indices of reliability and validity, as well as sensitivity to treatment and diagnostic sensitivity, and hold promise as a measure of OC symptoms in clinical and research settings

Inhibition of p38 MAPK Suppresses Inflammatory Cytokine Induction by Etoposide, 5-Fluorouracil, and Doxorubicin without Affecting Tumoricidal Activity

Cancer patients undergoing treatment with systemic cancer chemotherapy drugs often experience debilitating fatigue similar to sickness behavior, a normal response to infection or tissue damage caused by the production of the inflammatory cytokines IL-1β, TNF-α, and IL-6. The p38 mitogen activated protein kinase (p38 MAPK) plays a central role in the production of these cytokines and consequently the development of sickness behavior. Targeted inhibitors of p38 MAPK can reduce systemic inflammatory cytokine production and the development of sickness behavior. Several systemic cancer chemotherapy drugs have been shown to stimulate inflammatory cytokine production, yet whether this response is related to a common ability to activate p38 MAPK is not known and is the focus of this study. This understanding may present the possibility of using p38 MAPK inhibitors to reduce chemotherapy-induced inflammatory cytokine production and consequently treatment-related fatigue. One caveat of this approach is a potential reduction in chemotherapeutic efficacy as some believe that p38 MAPK activity is required for chemotherapy-induced cytotoxicity of tumor cells. The purpose of this study was to demonstrate proof of principal that p38 MAPK inhibition can block chemotherapy- induced inflammatory cytokine production without inhibiting drug-induced cytotoxicity using murine peritoneal macrophages and Lewis Lung Carcinoma (LLC1) cells as model cell systems. Using these cells we assessed the requirement of etoposide, doxorubicin, 5-flourouracil, and docetaxel for p38 MAPK in inflammatory cytokine production and cytotoxicity. Study findings demonstrate that clinically relevant doses of etoposide, doxorubicin, and 5-FU activated p38 MAPK in both macrophages and LLC1 cells. In contrast, docetaxel failed to activate p38 MAPK in either cell type. Activation of p38 MAPK mediated the drug's effects on inflammatory cytokine production in macrophages but not LLC1 cytotoxicity and this was confirmed with inhibitor studies

A nearby m star with three transiting super-earths discovered by k2

I. J. M. Crossfied, “A Nearby M Star with Three Transiting Super-Earths Discovered by K2”, The Astrophysical Journal, Vol 804(1), April 2015. © 2015. The American Astronomical Society.Small, cool planets represent the typical end-products of planetary formation. Studying the architectures of these systems, measuring planet masses and radii, and observing these planets' atmospheres during transit directly informs theories of planet assembly, migration, and evolution. Here we report the discovery of three small planets orbiting a bright (Ks = 8.6 mag) M0 dwarf using data collected as part of K2, the new ecliptic survey using the re-purposed Kepler spacecraft. Stellar spectroscopy and K2 photometry indicate that the system hosts three transiting planets with radii 1.5-2.1 , straddling the transition region between rocky and increasingly volatile-dominated compositions. With orbital periods of 10-45 days the planets receive just 1.5-10x the flux incident on Earth, making these some of the coolest small planets known orbiting a nearby star; planet d is located near the inner edge of the system's habitable zone. The bright, low-mass star makes this system an excellent laboratory to determine the planets' masses via Doppler spectroscopy and to constrain their atmospheric compositions via transit spectroscopy. This discovery demonstrates the ability of K2 and future space-based transit searches to find many fascinating objects of interest.Peer reviewe

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival