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Objective Clinician distress is a multidimensional condition that includes burnout, decreased meaning in work, severe fatigue, poor work–life integration, reduced quality of life, and suicidal ideation. It has negative impacts on patients, providers, and healthcare systems. In this three-phase qualitative investigation, we identified workplace-related factors that drive clinician distress and co-designed actionable interventions with inter-professional cardiovascular clinicians to decrease their distress and improve well-being within a Canadian quaternary hospital network. Methods Between October 2021 and May 2022, we invited nurses, allied health professionals, and physicians to participate in a three-phase qualitative investigation. Phases 1 and 2 included individual interviews and focus groups to identify workplace-related factors contributing to distress. Phase 3 involved co-design workshops that engaged inter-professional clinicians to develop interventions addressing drivers of distress identified. Qualitative information was analyzed using descriptive thematic analysis. Results Fifty-one clinicians (24 nurses, 10 allied health professionals, and 17 physicians) participated. Insights from Phases 1 and 2 identified five key thematic drivers of distress: inadequate support within inter-professional teams, decreased joy in work, unsustainable workloads, limited opportunities for learning and professional growth, and a lack of transparent leadership communication. Phase 3 co-design workshops yielded four actionable interventions to mitigate clinician distress in the workplace: re-designing daily safety huddles, formalizing a nursing coaching and mentorship program, creating a value-added program e-newsletter, and implementing an employee experience platform. Conclusion This study increases our understanding on workplace-related factors that contribute to clinician distress, as shared by inter-professional clinicians specializing in cardiovascular care. Healthcare organizations can develop effective interventions to mitigate clinician distress by actively engaging healthcare workers in identifying workplace drivers of distress and collaboratively designing tailored, practical interventions that directly address these challenges.

ObjectivesTo assess the prevalence and drivers of distress, a composite of burnout, decreased meaning in work, severe fatigue, poor work–life integration and quality of life, and suicidal ideation, among nurses and physicians during the COVID-19 pandemic.DesignCross-sectional design to evaluate distress levels of nurses and physicians during the COVID-19 pandemic between June and August 2021.SettingCardiovascular and oncology care settings at a Canadian quaternary hospital network.Participants261 nurses and 167 physicians working in cardiovascular or oncology care. Response rate was 29% (428 of 1480).Outcome measuresSurvey tool to measure clinician distress using the Well-Being Index (WBI) and additional questions about workplace-related and COVID-19 pandemic-related factors.ResultsAmong 428 respondents, nurses (82%, 214 of 261) and physicians (62%, 104 of 167) reported high distress on the WBI survey. Higher WBI scores (≥2) in nurses were associated with perceived inadequate staffing (174 (86%) vs 28 (64%), p=0.003), unfair treatment, (105 (52%) vs 11 (25%), p=0.005), and pandemic-related impact at work (162 (80%) vs 22 (50%), p<0.001) and in their personal life (135 (67%) vs 11 (25%), p<0.001), interfering with job performance. Higher WBI scores (≥3) in physicians were associated with perceived inadequate staffing (81 (79%) vs 32 (52%), p=0.001), unfair treatment (44 (43%) vs 13 (21%), p=0.02), professional dissatisfaction (29 (28%) vs 5 (8%), p=0.008), and pandemic-related impact at work (84 (82%) vs 35 (56%), p=0.001) and in their personal life (56 (54%) vs 24 (39%), p=0.014), interfering with job performance.ConclusionHigh distress was common among nurses and physicians working in cardiovascular and oncology care settings during the pandemic and linked to factors within and beyond the workplace. These results underscore the complex and contextual aspects of clinician distress, and the need to develop targeted approaches to effectively address this problem.

Macrophages densely populate the arterial wall, yet their origin and homeostasis are poorly understood. Robbins and colleagues show that arterial macrophages arise from CX3CR1 + embryonic precursors and adult bone marrow–derived monocytes that colonize the tissue immediately after birth. Resident macrophages densely populate the normal arterial wall, yet their origins and the mechanisms that sustain them are poorly understood. Here we use gene-expression profiling to show that arterial macrophages constitute a distinct population among macrophages. Using multiple fate-mapping approaches, we show that arterial macrophages arise embryonically from CX3CR1 + precursors and postnatally from bone marrow–derived monocytes that colonize the tissue immediately after birth. In adulthood, proliferation (rather than monocyte recruitment) sustains arterial macrophages in the steady state and after severe depletion following sepsis. After infection, arterial macrophages return rapidly to functional homeostasis. Finally, survival of resident arterial macrophages depends on a CX3CR1-CX3CL1 axis within the vascular niche.

Pandemic H1N1 influenza A (H1N1pdm) is currently a dominant circulating influenza strain worldwide. Severe cases of H1N1pdm infection are characterized by prolonged activation of the immune response, yet the specific role of inflammatory mediators in disease is poorly understood. The inflammatory cytokine IL-6 has been implicated in both seasonal and severe pandemic H1N1 influenza A (H1N1pdm) infection. Here, we investigated the role of IL-6 in severe H1N1pdm infection. We found IL-6 to be an important feature of the host response in both humans and mice infected with H1N1pdm. Elevated levels of IL-6 were associated with severe disease in patients hospitalized with H1N1pdm infection. Notably, serum IL-6 levels associated strongly with the requirement of critical care admission and were predictive of fatal outcome. In C57BL/6J, BALB/cJ, and B6129SF2/J mice, infection with A/Mexico/4108/2009 (H1N1pdm) consistently triggered severe disease and increased IL-6 levels in both lung and serum. Furthermore, in our lethal C57BL/6J mouse model of H1N1pdm infection, global gene expression analysis indicated a pronounced IL-6 associated inflammatory response. Subsequently, we examined disease and outcome in IL-6 deficient mice infected with H1N1pdm. No significant differences in survival, weight loss, viral load, or pathology were observed between IL-6 deficient and wild-type mice following infection. Taken together, our findings suggest IL-6 may be a potential disease severity biomarker, but may not be a suitable therapeutic target in cases of severe H1N1pdm infection due to our mouse data.

Introduction: Chemokines are small proteins that regulate different cellular functions, such as leukocyte activation, chemoattraction and inflammation. The chemokine CXCL14 (BRAK) is a highly conserved gene among species and through evolution. It has been shown that CXCL14 is locally upregulated during viral infections, also, it has been found that this chemokine possesses direct antibacterial activities. Nonetheless, the exact role that CXCL14 plays during infection remains elusive. Methodology: CXCL14 deficient mice were generated in a C57B6/129 background and followed by phenotypic characterization. Later, the effect of CXCL14 deficiency during influenza infection and E. coli challenge was assessed. Results: Other than a slight weight reduction, CXCL14 deficient mice exhibited no phenotypic alterations. CXCL14 deficiency did not influence the outcome of influenza virus infection or challenge with E. coli, and no statistically significant differences in clinical signs, cellular responses and histopathological findings were observed. Conclusions: CXCL14 does not seem to play a pivotal role during influenza and E. coli infections of the lung; these results are suggestive of functional overlap between CXCL14 and other chemokines that are present during lung infection.

To develop a comprehensive approach for the use of imaging resources, the Ontario Ministry of Health and Long-Term Care formed the Expert Panel on Appropriate Utilization of Diagnostic and Imaging Studies in 2012. The panel includes physicians in academic and community practice, within urban and rural settings.4 It concluded that appropriate use of imaging tests would be optimized if the use of accepted indications for imaging tests, based on guidelines developed by national or international specialty societies, was linked to payment for these tests. To ensure quality, the panel recommended that mandatory independent accreditation of imaging facilities and minimum training requirements for technologists and physicians performing and interpreting the imaging tests be linked to payment for these tests. These general recommendations and recommendations by the Cardiac Care Network of Ontario regarding the use of echocardiography5 have been endorsed by the Government of Ontario and the Ontario Medical Association and await implementation. The panel also recommended that referral and reporting processes for imaging tests be standardized, that regional imaging capacity be planned and coordinated, and that data registries be established to evaluate quality, safety and system effectiveness. In some instances, the physician ordering an imaging study is the owner of the imaging equipment used to conduct the test. A 2012 US Government Accountability Office report to Congress9 noted that financial incentives for self-referring providers, an issue not addressed by the Choosing Wisely or iRefer initiatives, are likely a major factor driving the increase in imaging tests and recommended \"payment reduction for self-referred advanced imaging services.\" Seven Canadian provinces regulate selfreferrals to independent health facilities, and four provinces regulate referrals to health facilities in which immediate family members have investments. The expert panel in Ontario noted that access to imaging studies could be impeded if a financial penalty was applied to imaging tests ordered appropriately by the physician conducting the test, particularly in smaller or more remote communities and in emergency departments. Requiring patients to go back to their primary care physician or other specialist to order an imaging study could delay access to care. Linking mandatory use of guidelines, independent accreditation of imaging facilities and minimum training requirements for health care professionals who perform and interpret imaging tests to payment should promote appropriate use and increase the quality of imaging tests. Reducing the number of imaging tests for inappropriate indications will decrease wait times for tests ordered for appropriate indications and will improve the efficiency of health care systems. Linking the use of guidelines to payment for imaging tests would eliminate the need to impose financial penalties on self-referred services, as recommended by the US Government Accountability Office, and would respect the judgment of the physicians who order the imaging tests.

Resident macrophages densely populate the normal arterial wall, yet their origins and the mechanisms that sustain them are poorly understood. Here we use gene-expression profiling to show that arterial macrophages constitute a distinct population among macrophages. Using multiple fate-mapping approaches, we show that arterial macrophages arise embryonically from [CX3CR1.sup.+] precursors and postnatally from bone marrow-derived monocytes that colonize the tissue immediately after birth. In adulthood, proliferation (rather than monocyte recruitment) sustains arterial macrophages in the steady state and after severe depletion following sepsis. After infection, arterial macrophages return rapidly to functional homeostasis. Finally, survival of resident arterial macrophages depends on a CX3CR1-CX3CL1 axis within the vascular niche.

During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaques in the arterial wall and cause their rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. Here we show that the systemic response to ischaemic injury aggravates chronic atherosclerosis. After myocardial infarction or stroke, Apoe −/− mice developed larger atherosclerotic lesions with a more advanced morphology. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment. Seeking the source of surplus monocytes in plaques, we found that myocardial infarction liberated haematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signalling. The progenitors then seeded the spleen, yielding a sustained boost in monocyte production. These observations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunity to mitigate disease progression. Myocardial infarction accelerates atherosclerosis through activation of the sympathetic nervous system, and the consequent release of haematopoietic stem and progenitor cells. Recurrent heart attack risk Patients who have a myocardial infarction are at high risk of recurrent events. This study shows for the first time that myocardial infarction and stroke accelerate atherosclerosis. The authors were able to demonstrate that myocardial infarction leads to activation of the sympathetic nervous system, which, in turn, leads to the release of haematopoietic stem cells and progenitor cells. These cells seeded in the spleen and augmented the production of monocytes displaying an enhanced atherogenic phenotype. These findings were correlated with patient data showing that prior beta-blocker therapy was associated with a decrease in circulating monocytes after myocardial infarction. These findings suggest that interventions that interrupt the supply of monocytes could attenuate atherosclerosis and may improve long-term patient outcomes.

Resident macrophages densely populate the normal arterial wall, yet their origins and the mechanisms that sustain them are poorly understood. Here we use gene-expression profiling to show that arterial macrophages constitute a distinct population among macrophages. Using multiple fate-mapping approaches, we show that arterial macrophages arise embryonically from CX3CR1 super(+) precursors and postnatally from bone marrow-derived monocytes that colonize the tissue immediately after birth. In adulthood, proliferation (rather than monocyte recruitment) sustains arterial macrophages in the steady state and after severe depletion following sepsis. After infection, arterial macrophages return rapidly to functional homeostasis. Finally, survival of resident arterial macrophages depends on a CX3CR1-CX3CL1 axis within the vascular niche.

We present Clinical Camel, an open large language model (LLM) explicitly tailored for clinical research. Fine-tuned from LLaMA-2 using QLoRA, Clinical Camel achieves state-of-the-art performance across medical benchmarks among openly available medical LLMs. Leveraging efficient single-GPU training, Clinical Camel surpasses GPT-3.5 in five-shot evaluations on all assessed benchmarks, including 64.3% on the USMLE Sample Exam (compared to 58.5% for GPT-3.5), 77.9% on PubMedQA (compared to 60.2%), 60.7% on MedQA (compared to 53.6%), and 54.2% on MedMCQA (compared to 51.0%). In addition to these benchmarks, Clinical Camel demonstrates its broader capabilities, such as synthesizing plausible clinical notes. This work introduces dialogue-based knowledge encoding, a novel method to synthesize conversational data from dense medical texts. While benchmark results are encouraging, extensive and rigorous human evaluation across diverse clinical scenarios is imperative to ascertain safety before implementation. By openly sharing Clinical Camel, we hope to foster transparent and collaborative research, working towards the safe integration of LLMs within the healthcare domain. Significant challenges concerning reliability, bias, and the potential for outdated knowledge persist. Nonetheless, the transparency provided by an open approach reinforces the scientific rigor essential for future clinical applications.