tbuckley/cabot-search huggingface dataset:
Comparative Access to and Use of Digital Breast Tomosynthesis Screening by Women’s Race/Ethnicity and Socioeconomic Status
Authors: Christoph I. Lee, Weiwei Zhu, Tracy Onega, Louise M. Henderson, Karla Kerlikowske, Brian L. Sprague, Garth H. Rauscher, Ellen S. O’Meara, Anna N. A. Tosteson, Jennifer S. Haas, Roberta diFlorio-Alexander, Celia Kaplan, Diana L. Miglioretti
Journal: JAMA Network Open (2021)

Digital breast tomosynthesis (DBT) has reduced recall and increased cancer detection compared with digital mammography (DM), depending on women's age and breast density. Whether DBT screening access and use are equitable across groups of women based on race/ethnicity and socioeconomic characteristics is uncertain.To determine women's access to and use of DBT screening based on race/ethnicity, educational attainment, and income.This cross-sectional study included 92 geographically diverse imaging facilities across 5 US states, at which a total of 2 313 118 screening examinations were performed among women aged 40 to 89 years from January 1, 2011, to December 31, 2017. Data were analyzed from June 13, 2019, to August 18, 2020.Women's race/ethnicity, educational level, and community-level household income.Access to DBT (on-site access) at time of screening by examination year and actual use of DBT vs DM screening by years since facility-level DBT adoption (≤5 years).Among the 2 313 118 screening examinations included in the analysis, the proportion of women who had DBT access at the time of their screening appointment increased from 11 558 of 354 107 (3.3%) in 2011 to 194 842 of 235 972 (82.6%) in 2017. In 2012, compared with White women, Black (relative risk [RR], 0.05; 95% CI, 0.03-0.11), Asian American (RR, 0.28; 95% CI, 0.11-0.75), and Hispanic (RR, 0.38; 95% CI, 0.18-0.80) women had significantly less DBT access, and women with less than a high school education had lower DBT access compared with college graduates (RR, 0.18; 95% CI, 0.10-0.32). Among women attending facilities with both DM and DBT available at the time of screening, Black women experienced lower DBT use compared with White women attending the same facility (RRs, 0.83 [95% CI, 0.82-0.85] to 0.98 [95% CI, 0.97-0.99]); women with lower educational level experienced lower DBT use (RRs, 0.79 [95% CI, 0.74-0.84] to 0.88 [95% CI, 0.85-0.91] for non-high school graduates and 0.90 [95% CI, 0.89-0.92] to 0.96 [95% CI, 0.93-0.99] for high school graduates vs college graduates); and women within the lowest income quartile experienced lower DBT use vs women in the highest income quartile (RRs, 0.89 [95% CI, 0.87-0.91] to 0.99 [95% CI, 0.98-1.00]) regardless of the number of years after facility-level DBT adoption.In this cross-sectional study, women of minority race/ethnicity and lower socioeconomic status experienced lower DBT access during the early adoption period and persistently lower DBT use when available over time. Future efforts should address racial/ethnic, educational, and financial barriers to DBT screening.
SAT0701-HPR SLE EXACERBATION PREDICTORS IN PATIENTS OF KYRGYZ NATIONALITY
Authors: Gulazyk Koilubaeva, Elmira Karimova, Altynai Moldobaeva, Aijamal Jumakadyrova, A. Moldobaeva
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Taken into account the wave-like multivariate flow of SLE, there are still difficulties in diagnosing conditions such as "remission" and "exacerbation". The questions of SLE "exacerbation" predictors and their influence on the further nature of the course and outcome of the disease remain little studied. <h3>Objectives</h3> Study of SLE exacerbations predictors in patients living in Kyrgyzstan. <h3>Methods</h3> The study included 150 (26.31%) Kyrgyz patients out of 570 with a reliable diagnosis of SLE, female (96%), young age (median - 34 [26; 44]), Kyrgyz nationality (89.33%), high - 61 (40.66%) and very high activity - 40 (26.67%), with the duration of SLE at 1 observation point from 7 months to 10 years, with dynamic observation from 1 year to 3 years. To determine the gradation of the degree of reduction in glomerular filtration rate (GFR) and the severity of proteinuria in patients with lupus nephritis, used the classification of chronic kidney disease (CKD) according to KDIGO (2013). The characteristic and frequency of SLE exacerbations were assessed by the SFI - R index: mild, moderate or severe. <h3>Results</h3> The results of the study showed that 84 (56%) Kyrgyz patients out of 150 had 192 SLE exacerbations by using the SFI index during 3 years of follow-up, with a frequency of 1 to 4 cases (2.82 ± 2.21) per patient. A mild exacerbation was observed predominantly in 103 patients (53.65%), manifested by skin - mucous syndrome - in 81 (78.64%) and febrile fever - in 22 (21.36%). A moderate exacerbation was noted in 48 (25%) patients in the form of polyserositis - in 18 (37.5%), articulations - in 16 (33.33%) and nephritis with minimal urinary syndrome - in 14 (29.17%) of them. Severe exacerbation was recorded in 41 (21.35%) patients, manifested mainly by kidney damage - in 28 (68.29%), lungs - in 4 (9.76%), central nervous system - in 4 (9.76%) and hematological disorders - in 5 (12.19%). Severe exacerbations of the kidneys were characterized by nephritis with CKD C1 A1 in 6, CKD C1 A3 in 6, with CKD C2 A3 in 6, severe nephritis with CKD C3a A3 in 3, CKD C3b A3 in 2 and nephritis with nephrotic syndrome - in 5 patients. SLE exacerbations in most cases resulted from self-withdrawal of glucocorticoid and cytostatic therapy in 44 (52.38%) and activation of the pathological process in 35 (41.67%) patients and in 5 (5.95%) of them were unknown. <h3>Conclusion</h3> On the background of careful dynamic monitoring of patients, predominantly mild SLE exacerbation was observed (53.65%), due to self-withdrawal of glucocorticoid and cytostatic therapy (52.38%). <h3>Acknowledgement</h3> I would like to express my deep gratitude to Professor E. Nosonov and Professor S. Soloviev, my research assistances, for their patient guidance, enthusiastic encouragement and useful critiques of this research work.
Work-exacerbated Asthma
Journal: American Journal of Respiratory and Critical Care Medicine (2018)

Who gets work-exacerbated asthma?Any person with a diagnosis of asthma who works can get WEA.For example, teachers, healthcare workers, cleaning staff, office workers, animal handlers, as well as workers in more industrial "dirty" workplaces, such as construction workers, factory workers, painters, firefighters, carpenters, and welders are exposed to substances or conditions that can cause WEA.(For more information on asthma and on other work related lung diseases, see the ATS Patient Information Series at http://www.thoracic.org/patients/patient-resources/resources/occupational-lung-disease.pdf) How common is work-exacerbated asthma?Work-exacerbated asthma is very common.About 25% to up to 50% of working adults with known asthma have exacerbations with asthma symptoms related to their workplace.These symptoms include wheezing, cough, chest tightness and/or shortness of breath.
Timing of Dialysis Initiation and End-stage Kidney Disease Incidence
Authors: Qi Zhi Clayton Yang
Journal: JAMA Internal Medicine (2021)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
A Fusion Transcription Factor–Driven Cancer Progresses to a Fusion-Independent Relapse via Constitutive Activation of a Downstream Transcriptional Target
Authors: Salah Boudjadi, Puspa Raj Pandey, Bishwanath Chatterjee, Thanh Hung Nguyen, Wenyue Sun, Frederic G. Barr
Journal: Cancer Research (2021)

Abstract Targeted monotherapies usually fail due to development of resistance by a subgroup of cells that evolve into recurrent tumors. Alveolar rhabdomyosarcoma is an aggressive myogenic soft-tissue cancer that is associated with a characteristic PAX3-FOXO1 gene fusion encoding a novel fusion transcription factor. In our myoblast model of PAX3-FOXO1–induced rhabdomyosarcoma, deinduction of PAX3-FOXO1 simulates a targeted therapy that antagonizes the fusion oncoprotein. This simulated therapy results initially in regression of the primary tumors, but PAX3-FOXO1–independent recurrent tumors eventually form after a delay. We report here that upregulation of FGF8, a direct transcriptional target of PAX3-FOXO1, is a mechanism responsible for PAX3-FOXO1–independent tumor recurrence. As a transcriptional target of PAX3-FOXO1, FGF8 promoted oncogenic activity in PAX3-FOXO1–expressing primary tumors that developed in the myoblast system. In the recurrent tumors forming after PAX3-FOXO1 deinduction, FGF8 expression was necessary and sufficient to induce PAX3-FOXO1–independent tumor growth through an autocrine mechanism. FGF8 was also expressed in human PAX3-FOXO1–expressing rhabdomyosarcoma cell lines and contributed to proliferation and transformation. In a human rhabdomyosarcoma cell line with reduced PAX3-FOXO1 expression, FGF8 upregulation rescued oncogenicity and simulated recurrence after PAX3-FOXO1–targeted therapy. We propose that deregulated expression of a PAX3-FOXO1 transcriptional target can generate resistance to therapy directed against this oncogenic transcription factor and postulate that this resistance mechanism may ultimately be countered by therapeutic approaches that antagonize the corresponding downstream pathways. Significance: In a model of cancer initiated by a fusion transcription factor, constitutive activation of a downstream transcriptional target leads to fusion oncoprotein-independent recurrences, thereby highlighting a novel progression mechanism and therapeutic target.
How to Advise Persons Who Are Antibody Positive for SARS-CoV-2 About Future Infection Risk
Authors: Mitchell H. Katz
Journal: JAMA Internal Medicine (2021)

Raymond A. Harvey, MPH; Jeremy A. Rassen, ScD; Carly A. Kabelac, BS; Wendy Turenne, MS; Sandy Leonard, MPH; Reyna Klesh, MS; William A. Meyer III, PhD, D(ABMM), MLS(ASCP)CM; Harvey W. Kaufman, MD, MBA; Steve Anderson, PhD; Oren Cohen, MD; Valentina I. Petkov, MD, MPH; Kathy A. Cronin, PhD; Alison L. Van Dyke, MD, PhD; Douglas R. Lowy, MD; Norman E. Sharpless, MD; Lynne T. Penberthy, MD, MPH
Late-onset hidradenitis suppurativa: A cluster analysis of the National Italian Registry IRHIS
Authors: Simone Cazzaniga, Elena Pezzolo, Simone Garcovich, Luigi Naldi, Vincenzo Bettoli, Damiano Abeni, Angelo V. Marzano, Annalisa Patrizi, Laura Atzori, Gabriella Fabbrocini, Annamaria Offidani, Claudia Lasagni, Valentina Dini, Marzia Caproni, Serafinella Patrizia Cannavò
Journal: Journal of the American Academy of Dermatology (2021)
Preexisting and Post–COVID-19 Immune Responses to SARS-CoV-2 in Patients with Cancer
Authors: Tatjana Bilich, Malte Roerden, Yacine Maringer, Annika Nelde, Jonas S. Heitmann, Marissa L. Dubbelaar, Andreas Peter, Sebastian Hörber, Jens Bauer, Jonas Rieth, Marcel Wacker, Fiamma Berner, Lukas Flatz, Stefanie Held, Peter Brossart, Melanie Märklin, Philipp Wagner, Eva Erne, Reinhild Klein, Hans-Georg Rammensee, Helmut R. Salih, Juliane S. Walz
Journal: Cancer Discovery (2021)

Abstract Patients with cancer, in particular patients with hematologic malignancies, are at increased risk for critical illness upon COVID-19. We here assessed antibody as well as CD4+ and CD8+ T-cell responses in unexposed and SARS-CoV-2–infected patients with cancer to characterize SARS-CoV-2 immunity and to identify immunologic parameters contributing to COVID-19 outcome. Unexposed patients with hematologic malignancies presented with reduced prevalence of preexisting SARS-CoV-2 cross-reactive CD4+ T-cell responses and signs of T-cell exhaustion compared with patients with solid tumors and healthy volunteers. Whereas SARS-CoV-2 antibody responses did not differ between patients with COVID-19 and cancer and healthy volunteers, intensity, expandability, and diversity of SARS-CoV-2 T-cell responses were profoundly reduced in patients with cancer, and the latter associated with a severe course of COVID-19. This identifies impaired SARS-CoV-2 T-cell immunity as a potential determinant for dismal outcome of COVID-19 in patients with cancer. Significance: This first comprehensive analysis of SARS-CoV-2 immune responses in patients with cancer reports on the potential implications of impaired SARS-CoV-2 T-cell responses for understanding pathophysiology and predicting severity of COVID-19, which in turn might allow for the development of therapeutic measures and vaccines for this vulnerable patient population. See related commentary by Salomé and Horowitz, p. 1877. This article is highlighted in the In This Issue feature, p. 1861
Prediction of postpartum hemorrhage in pregnant women with immune thrombocytopenia: Development and validation of the <scp>MONITOR</scp> model in a nationwide multicenter study
Authors: Qiu‐Sha Huang, Xiao‐Lu Zhu, Qing‐Yuan Qu, Xiao Liu, Gao‐Chao Zhang, Yan Su, Qi Chen, Feng‐Qi Liu, Xue‐Yan Sun, Mei‐Ying Liang, Yi Liu, Ming Jiang, Hui Liu, Ru Feng, Hong‐Xia Yao, Lei Zhang, Shen‐Xian Qian, Tong‐Hua Yang, Jing‐Yu Zhang, Xu‐Liang Shen, Lin‐Hua Yang, Jian‐Da Hu, Ren‐Wei Huang, Zhong‐Xing Jiang, Jing‐Wen Wang, Hong‐Yu Zhang, Zhen Xiao, Si‐Yan Zhan, Hui‐Xin Liu, Ying‐Jun Chang, Qian Jiang, Hao Jiang, Jin Lu, Lan‐Ping Xu, Xiao‐Hong Zhang, Cheng‐Hong Yin, Jian‐Liu Wang, Xiao‐Jun Huang, Xiao‐Hui Zhang
Journal: American Journal of Hematology (2021)

Abstract Globally, postpartum hemorrhage (PPH) is the leading cause of maternal death. Women with immune thrombocytopenia (ITP) are at increased risk of developing PPH. Early identification of PPH helps to prevent adverse outcomes, but is underused because clinicians do not have a tool to predict PPH for women with ITP. We therefore conducted a nationwide multicenter retrospective study to develop and validate a prediction model of PPH in patients with ITP. We included 432 pregnant women (677 pregnancies) with primary ITP from 18 academic tertiary centers in China from January 2008 to August 2018. A total of 157 (23.2%) pregnancies experienced PPH. The derivation cohort included 450 pregnancies. For the validation cohort, we included 117 pregnancies in the temporal validation cohort and 110 pregnancies in the geographical validation cohort. We assessed 25 clinical parameters as candidate predictors and used multivariable logistic regression to develop our prediction model. The final model included seven variables and was named MONITOR ( m aternal complication, WH O bleeding score, a n tepartum platelet transfusion, placental abnormal i ties, pla t elet count, previ o us uterine surgery, and p r imiparity). We established an easy‐to‐use risk heatmap and risk score of PPH based on the seven risk factors. We externally validated this model using both a temporal validation cohort and a geographical validation cohort. The MONITOR model had an AUC of 0.868 (95% CI 0.828–0.909) in internal validation, 0.869 (95% CI 0.802–0.937) in the temporal validation, and 0.811 (95% CI 0.713–0.908) in the geographical validation. Calibration plots demonstrated good agreement between MONITOR‐predicted probability and actual observation in both internal validation and external validation. Therefore, we developed and validated a very accurate prediction model for PPH. We hope that the model will contribute to more precise clinical care, decreased adverse outcomes, and better health care resource allocation.
Calling a Code
Authors: Christina Dimopoulos
Journal: Annals of Internal Medicine (2021)

On Being a DoctorFebruary 2021Calling a CodeChristina Dimopoulos, MDChristina Dimopoulos, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M20-4617 Audio Reading - “Calling a Code” Audio. Virginia L. Hood, MD, a physician from the University of Vermont, reads “Calling a Code” by Christina Dimopoulos, MD Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail The repetitive, staccato tone of the code pager sounds, followed by a voice overhead announcing the patient's location. I spin down four flights of stairs and see people in yellow contact gowns forming a line for chest compressions.I feel nauseous.A resident calls out in my general direction that the family needs to be contacted. When no one volunteers, I step outside to the hallway to find a computer. I locate a phone number for the patient's emergency contact—his sister—but hesitate before calling.She is about to learn from a stranger that her brother has died and we are ... Author, Article, and Disclosure InformationAffiliations: Corresponding Author: Christina Dimopoulos, MD, Yale-New Haven Hospital, 20 York Street, New Haven, CT 06510; e-mail, christina.[email protected]edu. PreviousarticleNextarticle Advertisement Audio Reading - “Calling a Code” Audio. Virginia L. Hood, MD, a physician from the University of Vermont, reads “Calling a Code” by Christina Dimopoulos, MD Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics February 2021Volume 174, Issue 2Page: 268-269KeywordsBloodBlood pressureHeartHeart ratePharynxResuscitationShockSternumThoraxTouch ePublished: 16 February 2021 Issue Published: February 2021 Copyright & PermissionsCopyright © 2021 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
The Role of DNA Methylation Reprogramming During Sex Determination and Transition in Zebrafish
Authors: Xinxin Wang, Xin Ma, Gaobo Wei, Weirui Ma, Zhen Zhang, Xuepeng Chen, Lei Gao, Zhenbo Liu, Yue Yuan, Lizhi Yi, Jun Wang, Toshinobu Tokumoto, Junjiu Huang, Dahua Chen, Jian Zhang, Jiang Liu
Journal: Genomics Proteomics & Bioinformatics (2021)

Abstract DNA methylation is a prevalent epigenetic modification in vertebrates, and it has been shown to be involved the regulation of gene expression and embryo development. However, it remains unclear how DNA methylation regulates sexual development, especially in species without sex chromosomes. To determine this, we utilized zebrafish to investigate DNA methylation reprogramming during juvenile germ cell development and adult female-to-male sex transition. We reveal that primordial germ cells (PGCs) undergo significant DNA methylation reprogramming during germ cell development, and the methylome of PGCs is reset to an oocyte/ovary-like pattern at 9 days post fertilization (9 dpf). When DNA methyltransferase (DNMT) activity in juveniles was blocked after 9 dpf, the zebrafish developed into females. We also show that Tet3 is involved in PGC development. Notably, we find that DNA methylome reprogramming during adult zebrafish sex transition is similar to the reprogramming during the sex differentiation from 9 dpf PGCs to sperm. Furthermore, inhibiting DNMT activity can prevent the female-to-male sex transition, suggesting that methylation reprogramming is required for zebrafish sex transition. In summary, DNA methylation plays important roles in zebrafish germ cell development and sexual plasticity.
Audio Interview: Viral Variants and Covid-19
Authors: Eric J. Rubin, Lindsey R. Baden, Jeremy J. Farrar, Stephen Morrissey
Journal: New England Journal of Medicine (2021)

Viral Variants and Covid-19 In this audio interview conducted on February 17, 2021, the editors are joined by British infectious disease expert Jeremy Farrar to discuss emerging SARS-CoV-2 variants...
Abstract PS17-33: Sumo-modified androgen receptors support the metastatic phenotype of endocrine-resistant hormone receptor-positive breast cancer
Authors: Tasneem Bawa-Khalfe, Shaymaa Bahnassy, Hariprasad Thangavel, Maram Quttina, Ashfia Fatima Khan, Dhanya Dhanyalayam, Joan Ritho, Samaneh Karami, Jing Ren
Journal: Cancer Research (2021)

Abstract Background: Conventional endocrine therapy is the first-line treatment for hormone receptor positive (HR+) breast cancer (BCa) subtype. Frequently, intrinsic and acquired ET resistance (ET-R) persists to support a disease with poor prognosis and limited therapy than the ET-sensitive carcinoma. High levels of androgen receptors (AR) in HR+ BCa correlate with insensitivity to ET tamoxifen and greater susceptibility to cancer metastasis. However, targeting AR with antagonist enzalutamide (Enz) in ET-R HR+ BCa present conflicting results. In the current report, we present novel findings of a constitutively active modified AR population that accumulates in the ET-R HR+ BCa cells to drive cell migration and metastatic phenotype. Methods: Cell-free protein modification tests, in-house SUMOylation assays, and PLA imaging were used to determine the AR protein profile in multiple ET-sensitive, intrinsic-, and acquired-ET HR+-BCa lines. Reporter assay and targeted transcriptome studies evaluate the genomic activity of native and modified-AR mimetic. Finally, the inhibitory effect of Enz with or without combination therapy was determined using migration and spheroid growth studies. Results: In acquired and intrinsic ET-R BCa cell lines, a constitutively active, higher molecular weight SUMO-modified AR (SUMO-AR) persists at the chromatin. The SUMO-AR is resilient to ubiquitin-mediated proteasomal degradation. We now report that the canonical AR chaperone protein HSPB1/Hsp27 functions as a novel SUMO-E3 ligase for AR. SUMO-AR interacts with a unique repertoire of biomolecules as compared to unmodified AR in the same cell lines. An increase in the SUMO protein and global SUMO-modified proteome supports this multimeric complex. The ligand-independent SUMO-AR activity promotes a gene-expression profile that favors epithelial-mesenchymal transition. Treatment with Enz alone or in combination with a SUMO inhibitor attenuates migration and metastatic phenotype of ET-R HR+ BCa. Conclusion: SUMO-AR dictates metastatic susceptibility and Enz responsiveness of ET-R HR+ BCa. Consistently, targeting both unmodified and SUMO-modified AR serves as a better therapeutic strategy for advanced HR+ BCa. Citation Format: Tasneem Bawa-Khalfe, Shaymaa Bahnassy, Hariprasad Thangavel, Maram Quttina, Ashfia Fatima Khan, Dhanya Dhanyalayam, Joan Ritho, Samaneh Karami, Jing Ren. Sumo-modified androgen receptors support the metastatic phenotype of endocrine-resistant hormone receptor-positive breast cancer [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS17-33.