Operationalizing Programmatic Assessment: The CBME Programmatic Assessment Practice Guidelines.

PROBLEM: Assessing the development and achievement of competence requires multiple formative and summative assessment strategies and the coordinated efforts of trainees and faculty (who often serve in multiple roles, such as academic advisors, program directors, and competency committee members). Operationalizing programmatic assessment (PA) in competency-based medical education (CBME) requires comprehensive practice guidelines, written in accessible language with descriptions of stakeholder activities, to move assessment theory into practice and to help guide the trainees and faculty who enact PA. APPROACH: Informed by the Appraisal of Guidelines for Research and Evaluation II (AGREE II) framework, the authors used a multiphase, multimethod approach to develop the CBME Programmatic Assessment Practice Guidelines (PA Guidelines). The 9 guidelines are organized by phases of assessment and include descriptions of stakeholder activities. A user guide provides a glossary of key terms and summarizes how the guidelines can be used by different stakeholder groups across postgraduate medical education (PGME) contexts. The 4 phases of guideline development, including internal stakeholder consultations and external expert review, occurred between August 2016 and March 2020. OUTCOMES: Local stakeholders and external experts agreed that the PA Guidelines hold potential for guiding initial operationalization and ongoing refinement of PA in CBME by individual stakeholders, residency programs, and PGME institutions. Since July 2020, the PA Guidelines have been used at Queen's University to inform faculty and resident development initiatives, including online CBME modules for faculty, workshops for academic advisors/competence committee members, and a guide that supports incoming residents' transition to CBME. NEXT STEPS: Research exploring the use of the PA Guidelines and user guide in multiple programs and institutions will gather further evidence of their acceptability and utility for guiding operationalization of PA in different contexts.

Competency-based education calls for programmatic assessment: But what does this look like in practice?

RATIONALE, AIMS, AND OBJECTIVES: Programmatic assessment has been identified as a system-oriented approach to achieving the multiple purposes for assessment within Competency-Based Medical Education (CBME, i.e., formative, summative, and program improvement). While there are well-established principles for designing and evaluating programs of assessment, few studies illustrate and critically interpret, what a system of programmatic assessment looks like in practice. This study aims to use systems thinking and the 'two communities' metaphor to interpret a model of programmatic assessment and to identify challenges and opportunities with operationalization. METHOD: An interpretive case study was used to investigate how programmatic assessment is being operationalized within one competency-based residency program at a Canadian university. Qualitative data were collected from residents, faculty, and program leadership via semi-structured group and individual interviews conducted at nine months post-CBME implementation. Data were analyzed using a combination of data-based inductive analysis and theory-derived deductive analysis. RESULTS: In this model, Academic Advisors had a central role in brokering assessment data between communities responsible for producing and using residents' performance information for decision making (i.e., formative, summative/evaluative, and program improvement). As system intermediaries, Academic Advisors were in a privileged position to see how the parts of the assessment system contributed to the functioning of the whole and could identify which system components were not functioning as intended. Challenges were identified with the documentation of residents' performance information (i.e., system inputs); use of low-stakes formative assessments to inform high-stakes evaluative judgments about the achievement of competence standards; and gaps in feedback mechanisms for closing learning loops. CONCLUSIONS: The findings of this research suggest that program stakeholders can benefit from a systems perspective regarding how their assessment practices contribute to the efficacy of the system as a whole. Academic Advisors are well positioned to support educational development efforts focused on overcoming challenges with operationalizing programmatic assessment.

Quick action a credit to NHS.

Good on the health professionals who rushed out to help those involved in the Westminster attack last week (news online, 23 March).

No PJs in the day room.

In response to your story about Nottingham University Hospitals NHS Trust's campaign to get inpatients out of pyjamas to help speed up recovery (news, 8 February), I trained as a nurse in the late 1980s and getting people dressed was a fundamental part of our training.

Moho topography, ranges and folds of Tibet by analysis of global gravity models and GOCE data.

The determination of the crustal structure is essential in geophysics, as it gives insight into the geohistory, tectonic environment, geohazard mitigation, etc. Here we present the latest advance on three-dimensional modeling representing the Tibetan Mohorovicic discontinuity (topography and ranges) and its deformation (fold), revealed by analyzing gravity data from GOCE mission. Our study shows noticeable advances in estimated Tibetan Moho model which is superior to the results using the earlier gravity models prior to GOCE. The higher quality gravity field of GOCE is reflected in the Moho solution: we find that the Moho is deeper than 65 km, which is twice the normal continental crust beneath most of the Qinghai-Tibetan plateau, while the deepest Moho, up to 82 km, is located in western Tibet. The amplitude of the Moho fold is estimated to be ranging from -9 km to 9 km with a standard deviation of ~2 km. The improved GOCE gravity derived Moho signals reveal a clear directionality of the Moho ranges and Moho fold structure, orthogonal to deformation rates observed by GPS. This geophysical feature, clearly more evident than the ones estimated using earlier gravity models, reveals that it is the result of the large compressional tectonic process.

Disruption of microtubules sensitizes the DNA damage-induced apoptosis through inhibiting nuclear factor κB (NF-κB) DNA-binding activity.

The massive reorganization of microtubule network involves in transcriptional regulation of several genes by controlling transcriptional factor, nuclear factor-kappa B (NF-κB) activity. The exact molecular mechanism by which microtubule rearrangement leads to NF-κB activation largely remains to be identified. However microtubule disrupting agents may possibly act in synergy or antagonism against apoptotic cell death in response to conventional chemotherapy targeting DNA damage such as adriamycin or comptothecin in cancer cells. Interestingly pretreatment of microtubule disrupting agents (colchicine, vinblastine and nocodazole) was observed to lead to paradoxical suppression of DNA damage-induced NF-κB binding activity, even though these could enhance NF-κB signaling in the absence of other stimuli. Moreover this suppressed NF-κB binding activity subsequently resulted in synergic apoptotic response, as evident by the combination with Adr and low doses of microtubule disrupting agents was able to potentiate the cytotoxic action through caspase-dependent pathway. Taken together, these results suggested that inhibition of microtubule network chemosensitizes the cancer cells to die by apoptosis through suppressing NF-κB DNA binding activity. Therefore, our study provided a possible anti-cancer mechanism of microtubule disrupting agent to overcome resistance against to chemotherapy such as DNA damaging agent.

Disruption of Microtubules Sensitizes the DNA Damage-induced Apoptosis Through Inhibiting Nuclear Factor kappaB (NF-kappaB) DNA-binding Activity

The massive reorganization of microtubule network involves in transcriptional regulation of several genes by controlling transcriptional factor, nuclear factor-kappa B (NF-kappaB) activity. The exact molecular mechanism by which microtubule rearrangement leads to NF-kappaB activation largely remains to be identified. However microtubule disrupting agents may possibly act in synergy or antagonism against apoptotic cell death in response to conventional chemotherapy targeting DNA damage such as adriamycin or comptothecin in cancer cells. Interestingly pretreatment of microtubule disrupting agents (colchicine, vinblastine and nocodazole) was observed to lead to paradoxical suppression of DNA damage-induced NF-kappaB binding activity, even though these could enhance NF-kappaB signaling in the absence of other stimuli. Moreover this suppressed NF-kappaB binding activity subsequently resulted in synergic apoptotic response, as evident by the combination with Adr and low doses of microtubule disrupting agents was able to potentiate the cytotoxic action through caspase-dependent pathway. Taken together, these results suggested that inhibition of microtubule network chemosensitizes the cancer cells to die by apoptosis through suppressing NF-kappaB DNA binding activity. Therefore, our study provided a possible anti-cancer mechanism of microtubule disrupting agent to overcome resistance against to chemotherapy such as DNA damaging agent.

The prevalence of pressure ulcers in a tertiary care pediatric and adult hospital.

OBJECTIVE: To describe the pressure ulcer prevalence, stage and body location, and demographic characteristics of patients with pressure ulcers at a tertiary care adult hospital and a tertiary care pediatric hospital. DESIGN: Prevalence survey. SETTING AND SUBJECTS: A total of 513 inpatients, including 416 adults admitted to a tertiary care hospital and 97 children admitted to a tertiary care pediatric hospital. Only inpatients with mental health-related diagnoses were excluded. INSTRUMENTS: The Kinetics Concepts International's Prevalence and Incidence Study Collection Form was used to assess variables, including demographic information; presence, location, and stage of pressure ulcers; and presence of special support surfaces. METHODS: All patients had head-to-toe skin assessments performed during an 8-hour period by teams of 3 multidisciplinary staff members. Kinetics Concepts International's Prevalence and Incidence Program software and Microsoft Excel were used for data entry and analysis. RESULTS: Combined pressure ulcer prevalence was 26.3%, with 29.2% in adult patients and 13.1% in pediatric patients. The most common body locations for pressure ulcers were the sacrum (22.1%), heels (14.8%), ears (12.9%), elbows (10.6%), and the buttocks (6.8%). Forty-eight percent of the ulcers were stage I, 36% Stage II, 6% Stage III-IV, and 10% unable to stage. CONCLUSIONS: Overall combined pressure ulcer prevalence and common body locations were consistent with findings from comparable hospitals. Patients at the extreme ends of the age spectrum had an increased risk of pressure ulcers. Stage I and II ulcers occurred most frequently. Potential prevention and early management strategies may be effective in decreasing the prevalence of these ulcers.

The effect of auricular acupuncture on psychophysiological measures of cocaine craving.

This study used a randomized pretest/posttest control group design to test the effectiveness of auricular acupuncture interventions in diminishing psychological and physiological changes associated with cocaine craving in 30 treatment-seeking cocaine-dependent patients. The experimental group received the real auricular acupuncture intervention, insertion of needles into ear point locations specifically targeted for drug withdrawal. The control group received sham or placebo auricular acupuncture, insertion of needles into ear point locations not targeted for any specific therapeutic benefit. Psychological (Cocaine Craving Questionnaire - Now) and physiological (skin conductance activity) changes associated with cocaine craving were measured. Results showed no differences between the control and the experimental group in diminishing psychological and physiological measures associated with craving. There were differences from pre- to posttest on measures of psychological but not physiological craving for the combined experimental and control groups.

Ethanol extract of propolis inhibits nitric oxide synthase gene expression and enzyme activity.

Propolis obtained from honeybee hives has been used in Oriental folk medicine as an anti-inflammatory, anti-carcinogenic, or immunomodulatory agent. However, the molecular basis for anti-inflammatory properties of propolis has not yet been established. Since nitric oxide (NO) synthesized by inducible nitric oxide synthase (iNOS) has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of NO synthesis or action represents a new approach to the treatment of inflammatory and autoimmune diseases. The present study, therefore, examined effects of ethanol extract of propolis (EEP) on iNOS expression and activity of iNOS enzyme itself. Treatment of RAW 264.7 cells with EEP significantly inhibited NO production and iNOS protein expression induced by lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma). EEP also inhibited iNOS mRNA expression and nuclear factor-kappa B (NF-kappaB) binding activity in a concentration-dependent manner. Furthermore, transfection of RAW 264.7 cells with iNOS promoter linked to a chloramphenicol acetyltransferase (CAT) reporter gene, revealed that EEP inhibited the iNOS promoter activity induced by LPS plus IFN-gamma through the NF-kappaB sites of the iNOS promoter. In addition, EEP directly interfered with the catalytic activity of murine recombinant iNOS enzyme. These results suggest that EEP may exert its anti-inflammatory effect by inhibiting the iNOS gene expression via action on the NF-kappaB sites in the iNOS promoter and by directly inhibiting the catalytic activity of iNOS.

Caffeic acid phenethyl ester inhibits nitric oxide synthase gene expression and enzyme activity.

Since nitric oxide (NO) synthesized by inducible nitric oxide synthase (iNOS) has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of NO synthesis or action represents a new approach to the treatment of inflammatory and autoimmune diseases. Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been identified to show anti-inflammatory, anti-viral and anti-cancer activities. The present study, therefore, examined effects of CAPE on iNOS expression and activity of iNOS enzyme itself. Treatment of RAW 264.7 cells with CAPE significantly inhibited NO production and iNOS protein expression induced by lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma). CAPE also inhibited iNOS mRNA expression and nuclear factor-kappa B (NF-kappaB) binding activity in a concentration-dependent manner. Furthermore, transfection of RAW 264.7 cells with iNOS promoter linked to a chloramphenicol acetyltransferase reporter gene, revealed that CAPE inhibited the iNOS promoter activity induced by LPS plus IFN-gamma through the NF-kappaB sites of the iNOS promoter. In addition, CAPE directly interfered with the catalytic activity of murine recombinant iNOS enzyme. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting the iNOS gene expression at the transcriptional level through the suppression of NF-kappaB activation, and by directly inhibiting the catalytic activity of iNOS.

Diclofenac inhibits IFN-gamma plus lipopolysaccharide-induced iNOS gene expression via suppression of NF-kappaB activation in RAW 264.7 macrophages

Diclofenac, a phenylacetic acid derivative, is a widely used non-steroidal anti-inflammatory drug (NSAID) to provide effective relief of inflammation and pain. Nitric oxide (NO) synthesized by inducible nitric oxide synthase (iNOS) has been implicated as a mediator of inflammation. We examined the inhibitory effects of diclofenac on the induction of iNOS in RAW 264.7 macrophages which were activated with lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma). Treatment of RAW 264.7 cells with diclofenac and other NSAIDs (aspirin and indomethacin) significantly inhibited NO production and iNOS protein expression induced by LPS plus IFN-gamma. Also, diclofenac but not aspirin and indomethacin, inhibited iNOS mRNA expression and nuclear factor-kappa B (NF-kappaB) binding activity concentration-dependently. Furthermore, transfection of RAW 264.7 cells with iNOS promoter linked to a CAT reporter gene revealed that only diclofenac inhibited the iNOS promoter activity induced by LPS plus IFN-gamma through the NF-kappaB sites of iNOS promoter. Taken together, these suggest that diclofenac may exert its anti-inflammatory effect by inhibiting iNOS gene expression at the transcriptional level through suppression of NF-kappaB activation.

Role of NF- kappaB binding sites in the regulation of inducible nitric oxide synthase by tyrosine kinase

In macrophages, lipopolysaccharide (LPS) alone or in combination with interferon- gamma (IFN- gamma) has been shown to release a nitric oxide (NO) through the increase of the transcription of the inducible nitric oxide synthase (iNOS) gene. To investigate the exact intracellular signaling pathway of the regulation of iNOS gene transcription by LPS plus IFN- gamma, the effects of protein tyrosine kinase (PTK) inhibitor and protein kinase C (PKC) inhibitors on NO production, iNOS mRNA expression, nuclear factor- kappaB (NF- kappaB) binding activity and the promoter activity of iNOS gene containing two NF- kappaB sites have been examined in a mouse macrophage RAW 264.7 cells. LPS or IFN- gamma, stimulated NO production, and their effect was enhanced synergistically by mixture of LPS and IFN- gamma. The PTK inhibitor such as tyrphostin reduced LPS plus IFN- gamma-induced NO production, iNOS mRNA expression and NF- kappaB binding activity. In contrast, PKC inhibitors such as H-7, Ro-318220 and staurosporine did not show any effect on them. In addition, transfection of RAW 264.7 cells with iNOS promoter linked to a CAT reporter gene revealed that tyrphostin inhibited the iNOS promoter activity through the NF- kappaB binding site, whereas PKC inhibitors did not. Taken together, these suggest that PTK, but not PKC pathway, is involved in the regulation of the iNOS gene transcription through the NF- kappaB sites of iNOS promoter in RAW 264.7 macrophages by LPS plus IFN- gamma.