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A retrospective analysis of patients from a single center in the USA was conducted to explore the association between the development of chilblain lesions during the COVID-19 pandemic and SARS-CoV-2 infection. The study found that chilblain lesions were strongly associated with cold weather, with a significant increase in cases during months when the average temperature was below 50 °F. The majority of patients with chilblains during the pandemic were young, and most had minimal-to-mild COVID-19 symptoms. The study suggests that cold weather may be an important risk factor for developing COVID-19-associated chilblains, but further research is needed to fully understand the association between chilblains and SARS-CoV-2 infection. [Extracted from the article]

Hospitalized patients have an increased risk of developing hospital-acquired sacral pressure injury (HASPI). However, it is unknown whether SARS-CoV-2 infection affects HASPI development. To explore the role of SARS-CoV-2 infection in HASPI development, we conducted a single institution, multihospital, retrospective study of all patients hospitalized for ≥5 days from March 1, 2020 to December 31, 2020. Patient demographics, hospitalization information, ulcer characteristics, and 30-day-related morbidity were collected for all patients with HASPIs, and intact skin was collected from HASPI borders in a patient subset. We determined the incidence, disease course, and short-term morbidity of HASPIs in COVID-19(+) patients, and characterized the skin histopathology and tissue gene signatures associated with HASPIs in COVID19 disease. COVID-19(+) patients had a 63% increased HASPI incidence rate, HASPIs of more severe ulcer stage (OR 2.0, p<0.001), and HASPIs more likely to require debridement (OR 3.1, p=0.04) compared to COVID-19(-) patients. Furthermore, COVID-19(+) patients with HASPIs had 2.2x increased odds of a more severe hospitalization course compared to COVID-19(+) patients without HASPIs. HASPI skin histology from COVID-19(+) patients predominantly showed thrombotic vasculopathy, with the number of thrombosed vessels being significantly greater than HASPIs from COVID-19(-) patients. Transcriptional signatures of a COVID-19(+) sample subset were enriched for innate immune responses, thrombosis, and neutrophil activation genes. Overall, our results suggest that immunologic dysregulation secondary to SARS-CoV-2 infection, including neutrophil dysfunction and abnormal thrombosis, may play a pathogenic role in development of HASPIs in patients with severe COVID-19. [ABSTRACT FROM AUTHOR]

Vascular cutaneous manifestations, especially in men, are associated with a more severe disease course in COVID-19 patients We excluded all patients without evidence of a positive PCR COVID-19 test, patients with photographs of cutaneous abnormalities felt unrelated to COVID-19, and patients whose photographs were uploaded to the EMR >30 days following a positive PCR COVID-19 test (Figure 1). Patients with COVID-19 have been reported to develop various cutaneous eruptions which most commonly are classified into morphologic categories of morbilliform, urticarial, pernio-like, and livedo.[1] Pernio-like lesions are mostly reported in younger patients with mild COVID-19, while livedo manifestations seem to occur in older patients with more severe disease.[2] We performed a retrospective review of documented cutaneous eruptions in COVID-19 patients at a single, tertiary care center and correlated these with clinical data to explore if certain cutaneous lesion morphologies were associated with disease course severity. [Extracted from the article]

We analysed data from a cohort of MD, DO and IMG applicants securing US dermatology residencies during the academic years 2007, 2009, 2011, 2014, 2016 and 2018; the data collection methodology has been previously published2,3 (Supplementary Data S1). In the USA, medical students from allopathic [Doctor of Medicine (MD) degree-granting] and osteopathic [Doctor of Osteopathic Medicine (DO) degree-granting] medical schools may apply to the same specialty training (i.e. residency) programmes for postgraduate training. After controlling for PhD status, matched MD applicants published on average 3.3 more articles than did matched DO applicants, but 4.7 fewer articles than matched IMG applicants (both I P i < 0.001) (Table 2). 1 TableCharacteristics of matched dermatology residency applicants, 2007-2018. [Extracted from the article]

Retiform purpura has been described as a relatively frequent cutaneous finding in patients with coronavirus disease 2019 (COVID‐19). The etiology is hypothesized to be related to thrombotic vasculopathy based on lesional biopsy specimen findings, but the pathogenesis of the vasculopathy is not completely understood. Here, we present a case of a retiform purpuric patch on the sacrum/buttocks in a hospitalized patient prior to subsequent diagnosis of COVID‐19 and an eventual fatal disease course. Two lesional biopsy specimens at different time points in the disease course revealed thrombotic vasculopathy, despite therapeutic anticoagulation. Detailed histopathologic evaluation using immunohistochemical markers suggest the etiology of the vasculopathy involves both persistent complement activation and platelet aggregation, which possibly promote ongoing thrombus formation. This case highlights that sacral/buttock retiform purpuric patches may be a presenting sign of infection with SARS‐CoV‐2 virus and may represent an ominous sign supporting a future severe disease course. In addition, biopsy specimen findings at separate time points demonstrate that cutaneous vasculopathy may persist despite adequate systemic anticoagulation, possibly due to the combination of persistent complement and platelet activation. Finally, occlusive thrombi in sacral/buttock retiform purpuric patches may contribute to future ulceration and significant cutaneous morbidity in patients who survive COVID‐19. [ABSTRACT FROM AUTHOR]

Objectives: Determine whether D-dimer concentration in the absence of imaging can differentiate patients that require anti-coagulation from patients who do not require anti-coagulation.Methods: Data was obtained retrospectively from 366 hemodynamically stable adult ED patients with suspected pulmonary embolism (PE). Patients were categorized by largest occluded artery and aggregated into: 'Require anti-coagulation' (main, lobar, and segmental PE), 'Does not require anti-coagulation' (sub-segmental and No PE), 'High risk of deterioration' (main and lobar PE), and 'Not high risk of deterioration' (segmental, sub-segmental, and No PE) groups. Wilcoxon rank-sum test was used for 2 sample comparisons of median D-dimer concentrations. Receiver operating characteristic (ROC) curve analysis was utilized to determine a D-dimer cut-off that could differentiate 'Require anti-coagulation' from 'Does not require anti-coagulation' and 'High risk of deterioration' from 'Low risk of deterioration' groups.Results: The 'Require anti-coagulation' group had a maximum area under the curve (AUC) of 0.92 at an age-adjusted D-dimer cut-off of 1540 with a specificity of 86% (95% CI, 81-91%), and sensitivity of 84% (79-90%). The 'High risk of deterioration' group had a maximum AUC of 0.93 at an age-adjusted D-dimer cut-off of 2500 with a specificity of 90% (85-93%) and sensitivity of 83% (77-90%).Conclusions: An age-adjusted D-dimer cut-off of 1540 ng/mL differentiates suspected PE patients requiring anti-coagulation from those not requiring anti-coagulation. A cut-off of 2500 differentiates those with high risk of clinical deterioration from those not at high risk of deterioration. When correlated with clinical outcomes, these cut-offs can provide an objective method for clinical decision making when imaging is unavailable. [ABSTRACT FROM AUTHOR]

The article highlights financial conflicts over free open access medical education (FOAMed), collection of educational resources. Topics discussed include focused on quality of educational content; financial conflicts for both general and research payments of all the U.S. based contributors; and highlights majority of financial transactions related to food and beverages.

Study Objective: We aim to characterize the prevalence of financial conflicts of interest among emergency medicine journal editorial board members., Methods: We conducted a cross-sectional study of editorial board members of leading peer-reviewed emergency medicine journals. A list of highly cited emergency medicine journals was curated with Journal Citation Reports and Google Scholar Metrics. Financial conflicts of interest were obtained by curating the Centers for Medicare & Medicaid Services' Open Payments database for the most recently available data (2017). The outcomes of this study were prevalence of financial conflicts of interest and frequency of disclosure on each journal's Web site., Results: Editorial boards of the top 5 journals were analyzed. Of the 198 unique US-based physician-editors, 60 (30.3%) had a financial conflict of interest documented as general or research-based payments. The 52 editors with general payments had a median of 2 payments (interquartile range [IQR] 1 to 8.25), with a median of $202 (IQR $69 to $7,386); the maximum general payment was $115,730 received from industry. For research payments, 26 editors (13.1%) had a median 4 payments (IQR 2 to 9), with a median of $47,095 (IQR $5,328 to $126,025) and maximum of $3,590,000 received from industry. Seven editors in one of the emergency medicine journals included in this study publicly disclosed competing interests; dollar amounts were not reported., Conclusion: Nearly one third of US-based editors at leading emergency medicine journals had financial conflicts of interest, although only one journal publicly disclosed the presence of payments. Public disclosure of editorial board members' financial relationships with industry may allow for more transparency related to the content published in these journals., (Copyright © 2019 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.)

The human chaperonin complex is a ~ 1 MDa nanomachine composed of two octameric rings formed from eight similar but non-identical subunits called CCT. Here, we are elucidating the mechanism of a heritable CCT5 subunit mutation that causes profound neuropathy in humans. In previous work, we introduced an equivalent mutation in an archaeal chaperonin that assembles into two octameric rings like in humans but in which all subunits are identical. We reported that the hexadecamer formed by the mutant subunit is unstable with impaired chaperoning functions. This study quantifies the loss of structural stability in the hexadecamer due to the pathogenic mutation, using differential scanning calorimetry (DSC) and isothermal titration calorimetry (ITC). The disassembly of the wild type complex, which is tightly coupled with subunit denaturation, was decoupled by the mutation without affecting the stability of individual subunits. Our results verify the effectiveness of the homo-hexadecameric archaeal chaperonin as a proxy to assess the impact of subtle defects in heterologous systems with mutations in a single subunit.