Asian American and Pacific Islander patients with melanoma have increased odds of treatment delays: A cross-sectional study.

BACKGROUND: Asian American and Pacific Islander (AAPI) melanoma patients have higher mortality than non-Hispanic White (NHW) patients. Treatment delays may contribute, but whether AAPI patients have longer time from diagnosis to definitive surgery (TTDS) is unknown. OBJECTIVES: Investigate TTDS differences between AAPI and NHW melanoma patients. METHODS: Retrospective review of AAPI and NHW melanoma patients in the National Cancer Database (NCD) (2004-2020). The association of race with TTDS was evaluated by multivariable logistic regression, controlling for sociodemographic characteristics. RESULTS: Of 354,943 AAPI and NHW melanoma patients identified, 1155 (0.33%) were AAPI. AAPI patients had longer TTDS for stage I, II, and III melanoma (P < .05 for all). Adjusting for sociodemographic factors, AAPI patients had 1.5 times the odds of a TTDS between 61 and 90 days and twice the odds of a TTDS >90 days. Racial differences in TTDS persisted in Medicare and private insurance types. Uninsured AAPI patients had the longest TTDS (mean, 53.26 days), while those with private insurance had the shortest TTDS (mean, 34.92 days; P < .001 for both). LIMITATION: AAPI patients comprised 0.33% of the sample. CONCLUSIONS: AAPI melanoma patients have increased odds of treatment delays. Associated socioeconomic differences should inform efforts to reduce disparities in treatment and survival.

Abnormal thrombosis and neutrophil activation increase hospital-acquired sacral pressure injuries and morbidity in COVID-19 patients.

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, multi-hospital, 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 COVID-19 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.

Factors associated with matching into research-focused dermatology residency programs.

Although dermatology is one of the most competitive specialties to match into, there is limited transparency in the residency match process. In this retrospective cohort study of 2234 allopathic medical graduates, we identify applicant characteristics associated with matching into research oriented dermatology programs. Many of the statistically significant variables in our study, including PhD/MD status, graduating from a Top-25 NIH funded medical school, increasing total number of pre-residency publications (PRPs), and increasing number of high-impact PRPs, correlate with future academic employment. Although literature shows an association between an increasing number of first author PRPs and future academic employment, we did not find number of first or last author PRPs to be predictive of matching into a research oriented residency program. A more comprehensive evaluation of an applicant's research output, considering both the final products of an applicant's research endeavors and an applicant's role in various projects, may better approximate an applicant's commitment to academics.

Trends of Research Output of Allopathic Medical Students Matching Into Dermatology, 2007-2018.

IMPORTANCE: According to the National Residency Matching Program's biennial Charting Outcomes in the Match (NRMP ChOM) reports, the mean number of research items of matched allopathic dermatology applicants has nearly tripled since 2007, rising from 5.7 to 14.7. Research items are self-reported by applicants and serve as an approximation of research output. Because the NRMP research items field is unverified and reported as an aggregate of several different research pursuits, it may not be an accurate representation of applicant research output. OBJECTIVE: To determine if the rise in NRMP-reported data is associated with a rise in verifiable, indexed publications from matched allopathic dermatology applicants from 2007 to 2018. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional study including a bibliometric analysis on accepted applicant research output among 2234 matched allopathic dermatology applicants, with a total of 6229 publications, in dermatology residency programs for the years 2007, 2009, 2011, 2014, 2016, and 2018. MAIN OUTCOME AND MEASURES: The primary outcomes were the mean number of peer-reviewed indexed publications and mean number of NRMP ChOM research items. Secondary outcomes assessed the quality of indexed publications by analyzing article type and journal of publication. RESULTS: From 2007 to 2018, the mean number of indexed publications per matched dermatology applicant increased from 1.6 to 4.7 (203% increase). Indexed publications consistently compose a minority of NRMP ChOM research items (28.8% across the 6 years of the study). Nonindexed research items increased at more than double the rate of indexed publications. Bibliometric analysis showed that all other types of publications are increasing at a rate of 6 to 9 times that of basic science publications, dermatology-related publications increased at 5 times the rate of non-dermatology publications, and publications in lower-impact factor dermatology journals increased at 4 times the rate of publications in higher-impact factor dermatology journals. CONCLUSIONS AND RELEVANCE: This cross-sectional study provides data on the research output of matched dermatology applicants. Indexed publications compose a minority of NRMP research items. Medical student self-reports of research output may emphasize research quantity over quality.

Identifying Key Genetic Regions for Cell Sheet Morphogenesis on Chromosome 2L Using a Drosophila Deficiency Screen in Dorsal Closure.

Cell sheet morphogenesis is essential for metazoan development and homeostasis of animal form - it contributes to developmental milestones including gastrulation, neural tube closure, heart and palate formation and to tissue maintenance during wound healing. Dorsal closure, a well-characterized stage in Drosophila embryogenesis and a model for cell sheet morphogenesis, is a remarkably robust process during which coordination of conserved gene expression patterns and signaling cascades regulate the cellular shape changes and movements. New 'dorsal closure genes' continue to be discovered due to advances in imaging and genetics. Here, we extend our previous study of the right arm of the 2nd chromosome to the left arm of the 2nd chromosome using the Bloomington deficiency kit's set of large deletions, which collectively remove 98.9% of the genes on the left arm of chromosome two (2L) to identify 'dorsal closure deficiencies'. We successfully screened 87.2% of the genes and identified diverse dorsal closure defects in embryos homozygous for 49 deficiencies, 27 of which delete no known dorsal closure gene. These homozygous deficiencies cause defects in cell shape, canthus formation and tissue dynamics. Within these deficiencies, we have identified pimples, odd-skipped, paired, and sloppy-paired 1 as dorsal closure genes on 2L that affect lateral epidermal cells. We will continue to identify novel 'dorsal closure genes' with further analysis. These forward genetic screens are expected to identify new processes and pathways that contribute to closure and links between pathways and structures already known to coordinate various aspects of closure.

Identifying Genetic Players in Cell Sheet Morphogenesis Using a Drosophila Deficiency Screen for Genes on Chromosome 2R Involved in Dorsal Closure.

Cell sheet morphogenesis characterizes key developmental transitions and homeostasis, in vertebrates and throughout phylogeny, including gastrulation, neural tube formation and wound healing. Dorsal closure, a process during Drosophila embryogenesis, has emerged as a model for cell sheet morphogenesis. ∼140 genes are currently known to affect dorsal closure and new genes are identified each year. Many of these genes were identified in screens that resulted in arrested development. Dorsal closure is remarkably robust and many questions regarding the molecular mechanisms involved in this complex biological process remain. Thus, it is important to identify all genes that contribute to the kinematics and dynamics of closure. Here, we used a set of large deletions (deficiencies), which collectively remove 98.5% of the genes on the right arm of Drosophila melanogaster's 2nd chromosome to identify "dorsal closure deficiencies". Through two crosses, we unambiguously identified embryos homozygous for each deficiency and time-lapse imaged them for the duration of closure. Images were analyzed for defects in cell shapes and tissue movements. Embryos homozygous for 47 deficiencies have notable, diverse defects in closure, demonstrating that a number of discrete processes comprise closure and are susceptible to mutational disruption. Further analysis of these deficiencies will lead to the identification of at least 30 novel "dorsal closure genes". We expect that many of these novel genes will identify links to pathways and structures already known to coordinate various aspects of closure. We also expect to identify new processes and pathways that contribute to closure.