tbuckley/cabot-search huggingface dataset:
Autoimmune Pulmonary Alveolar Proteinosis
Authors: Cormac McCarthy, Brenna C. Carey, Bruce C. Trapnell
Journal: American Journal of Respiratory and Critical Care Medicine (2022)

Autoimmune pulmonary alveolar proteinosis (PAP) is a rare disease characterized by myeloid cell dysfunction, abnormal pulmonary surfactant accumulation, and innate immune deficiency. It has a prevalence of 7-10 per million; occurs in individuals of all races, geographic regions, sex, and socioeconomic status; and accounts for 90% of all patients with PAP syndrome. The most common presentation is dyspnea of insidious onset with or without cough, production of scant white and frothy sputum, and diffuse radiographic infiltrates in a previously healthy adult, but it can also occur in children as young as 3 years. Digital clubbing, fever, and hemoptysis are not typical, and the latter two indicate that intercurrent infection may be present. Low prevalence and nonspecific clinical, radiological, and laboratory findings commonly lead to misdiagnosis as pneumonia and substantially delay an accurate diagnosis. The clinical course, although variable, usually includes progressive hypoxemic respiratory insufficiency and, in some patients, secondary infections, pulmonary fibrosis, respiratory failure, and death. Two decades of research have raised autoimmune PAP from obscurity to a paradigm of molecular pathogenesis-based diagnostic and therapeutic development. Pathogenesis is driven by GM-CSF (granulocyte/macrophage colony-stimulating factor) autoantibodies, which are present at high concentrations in blood and tissues and form the basis of an accurate, commercially available diagnostic blood test with sensitivity and specificity of 100%. Although whole-lung lavage remains the first-line therapy, inhaled GM-CSF is a promising pharmacotherapeutic approach demonstrated in well-controlled trials to be safe, well tolerated, and efficacious. Research has established GM-CSF as a pulmonary regulatory molecule critical to surfactant homeostasis, alveolar stability, lung function, and host defense.
Antibody-Peptide Epitope Conjugates for Personalized Cancer Therapy
Authors: Songfa Zhang, Chuan Yan, David G. Millar, Qiqi Yang, James M. Heather, Adam Langenbucher, Laura T. Morton, Sean Sepulveda, Eric Alpert, Lauren R. Whelton, Dominique T. Zarrella, Mei Guo, Eleanor Minogue, Michael S. Lawrence, Bo R. Rueda, David R. Spriggs, Weiguo Lu, David M. Langenau, Mark Cobbold
Journal: Cancer Research (2021)

Abstract Antibody–peptide epitope conjugates (APEC) are a new class of modified antibody–drug conjugates that redirect T-cell viral immunity against tumor cells. APECs contain a tumor-specific protease cleavage site linked to a patient-specific viral epitope, resulting in presentation of viral epitopes on cancer cells and subsequent recruitment and killing by CD8+ T cells. Here we developed an experimental pipeline to create patient-specific APECs and identified new preclinical therapies for ovarian carcinoma. Using functional assessment of viral peptide antigen responses to common viruses like cytomegalovirus (CMV) in patients with ovarian cancer, a library of 192 APECs with distinct protease cleavage sequences was created using the anti-epithelial cell adhesion molecule (EpCAM) antibody. Each APEC was tested for in vitro cancer cell killing, and top candidates were screened for killing xenograft tumors grown in zebrafish and mice. These preclinical modeling studies identified EpCAM-MMP7-CMV APEC (EpCAM-MC) as a potential new immunotherapy for ovarian carcinoma. Importantly, EpCAM-MC also demonstrated robust T-cell responses in primary ovarian carcinoma patient ascites samples. This work highlights a robust, customizable platform to rapidly develop patient-specific APECs. Significance: This study develops a high-throughput preclinical platform to identify patient-specific antibody–peptide epitope conjugates that target cancer cells and demonstrates the potential of this immunotherapy approach for treating ovarian carcinoma.
Noncanonical Function of AGO2 Augments T-cell Receptor Signaling in T-cell Prolymphocytic Leukemia
Authors: Till Braun, Johanna Stachelscheid, Nadine Bley, Sebastian Oberbeck, Moritz Otte, Tony Andreas Müller, Linus Wahnschaffe, Markus Glaß, Katharina Ommer, Marek Franitza, Birgit Gathof, Janine Altmüller, Michael Hallek, Daniel Auguin, Stefan Hüttelmaier, Alexandra Schrader, Marco Herling
Journal: Cancer Research (2022)

Abstract T-cell prolymphocytic leukemia (T-PLL) is a chemotherapy-refractory T-cell malignancy with limited therapeutic options and a poor prognosis. Current disease concepts implicate TCL1A oncogene-mediated enhanced T-cell receptor (TCR) signaling and aberrant DNA repair as central perturbed pathways. We discovered that recurrent gains on chromosome 8q more frequently involve the argonaute RISC catalytic component 2 (AGO2) gene than the adjacent MYC locus as the affected minimally amplified genomic region. AGO2 has been understood as a protumorigenic key regulator of miRNA (miR) processing. Here, in primary tumor material and cell line models, AGO2 overrepresentation associated (i) with higher disease burden, (ii) with enhanced in vitro viability and growth of leukemic T cells, and (iii) with miR-omes and transcriptomes that highlight altered survival signaling, abrogated cell-cycle control, and defective DNA damage responses. However, AGO2 elicited also immediate, rather non–RNA-mediated, effects in leukemic T cells. Systems of genetically modulated AGO2 revealed that it enhances TCR signaling, particularly at the level of ZAP70, PLCγ1, and LAT kinase phosphoactivation. In global mass spectrometric analyses, AGO2 interacted with a unique set of partners in a TCR-stimulated context, including the TCR kinases LCK and ZAP70, forming membranous protein complexes. Models of their three-dimensional structure also suggested that AGO2 undergoes posttranscriptional modifications by ZAP70. This novel TCR-associated noncanonical function of AGO2 represents, in addition to TCL1A-mediated TCR signal augmentation, another enhancer mechanism of this important deregulated growth pathway in T-PLL. These findings further emphasize TCR signaling intermediates as candidates for therapeutic targeting. Significance: The identification of AGO2-mediated activation of oncogenic T cells through signal amplifying protein–protein interactions advances the understanding of leukemogenic AGO2 functions and underlines the role of aberrant TCR signaling in T-PLL.
2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines
Authors: Paul A. Heidenreich, Biykem Bozkurt, David Aguilar, Larry A. Allen, Joni J. Byun, Monica M. Colvin, Anita Deswal, Mark H. Drazner, Shannon M. Dunlay, Linda R. Evers, James C. Fang, Savitri E. Fedson, Gregg C. Fonarow, Salim S. Hayek, Adrian F. Hernandez, Prateeti Khazanie, Michelle M. Kittleson, Christopher S. Lee, Mark S. Link, Carmelo A. Milano, Lorraine C. Nnacheta, Alexander T. Sandhu, Lynne Warner Stevenson, Orly Vardeny, Amanda R. Vest, Clyde W. Yancy
Journal: Circulation (2022)

The "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure" replaces the "2013 ACCF/AHA Guideline for the Management of Heart Failure" and the "2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure." The 2022 guideline is intended to provide patient-centric recommendations for clinicians to prevent, diagnose, and manage patients with heart failure.
Haemophagocytic lymphohistiocytosis associated with bartonella peliosis hepatis following kidney transplantation in a patient with HIV
Authors: Danielle Steed, Jeffrey Collins, Alton B Farris, Jeannette Guarner, Dilek Yarar, Rachel Friedman-Moraco, Tristan Doane, Stephanie Pouch, G Marshall Lyon, Michael H Woodworth
Journal: The Lancet Infectious Diseases (2022)

Bacillary peliosis hepatis is a well recognised manifestation of disseminated Bartonella henselae infection that can occur in immunocompromised individuals. Haemophagocytic lymphohistiocytosis is an immune-mediated condition with features that can overlap with a severe primary infection such as disseminated Bartonella spp infection. We report a case of bacillary peliosis hepatis and secondary haemophagocytic lymphohistiocytosis due to disseminated Bartonella spp infection in a kidney-transplant recipient with well controlled HIV. The patient reported 2 weeks of fever and abdominal pain and was found to have hepatomegaly. He recalled exposure to a sick dog but reported no cat exposures. Laboratory evaluation was notable for pancytopenia and cholestatic injury. The patient met more than five of eight clinical criteria for haemophagocytic lymphohistiocytosis. Pathology review of a bone marrow core biopsy identified haemophagocytosis. A transjugular liver biopsy was done, and histopathology review identified peliosis hepatis. Warthin-Starry staining of the bone marrow showed pleiomorphic coccobacillary organisms. The B henselae IgG titre was 1:512, and Bartonella-specific DNA targets were detected by peripheral blood PCR. Treatment with doxycycline, increased prednisone, and pausing the mycophenolate component of his transplant immunosuppression regimen resulted in an excellent clinical response. Secondary haemophagocytic lymphohistiocytosis can be difficult to distinguish from severe systemic infection. A high index of suspicion can support the diagnosis of systemic Bartonella spp infection in those who present with haemophagocytic lymphohistiocytosis, especially in patients with hepatomegaly, immunosuppression, and germane animal exposures.
Are TEMs Canceled? Questioning the Functional Relevance of Tie2-Expressing Macrophages
Authors: Yuqing Zhang, Rolf A. Brekken
Journal: Cancer Research (2022)

Abstract Inflammatory cells are a vital component of the tumor stroma and, of these, tumor-associated macrophages (TAM) are the major cell type. TAMs are recruited early in tumorigenesis and generally promote metastasis, stimulate tumor angiogenesis, and drive immunosuppression. TAMs have been shown to express the endothelial cell markers that enable chemotaxis and proangiogenic capacity. In this issue of Cancer Research, Jakab and colleagues challenge the functional significance of Tie2-expressing monocytes/macrophages (TEM) in the context of tumor growth and progression. By employing myeloid-specific deletion of the angiopoietin receptor Tie2 and comprehensive analysis of myeloid cell single-cell RNA sequencing datasets, they provide compelling data that Tie2-positive macrophages do not contribute to tumor angiogenesis or relapse after chemotherapy, two major biologic processes previously attributed to tumor-associated TEMs. The study highlights that the concept of macrophage-expressed Tie2 as a therapeutic target or prognostic indicator needs reconsideration. See related article by Jakab et al., p. 1353
Gut-derived lipopolysaccharide promotes alcoholic hepatosteatosis and subsequent hepatocellular carcinoma by stimulating neutrophil extracellular traps through toll-like receptor 4
Authors: Yang Liu, Xin Zhang, Shuo Chen, Jiazhong Wang, Shuo Yu, Yiming Li, Meng Xu, Harouna Aboubacar, Junhui Li, Tao Shan, Jixin Wang, Gang Cao
Journal: Clinical and Molecular Hepatology (2022)

Binge drinking leads to many disorders, including alcoholic hepatosteatosis, which is characterized by intrahepatic neutrophil infiltration and increases the risk of hepatocellular carcinoma (HCC). Molecular mechanisms may involve the migration of bacterial metabolites from the gut to the liver and the activation of neutrophil extracellular traps (NETs).Serum samples from both binge drinking and alcohol-avoiding patients were analyzed. Mouse models of chronic plus binge alcohol-induced hepatosteatosis and HCC models were used.A marker of NETs formation, lipopolysaccharide (LPS), was significantly higher in alcoholic hepatosteatosis and HCC patients and mice than in controls. Intrahepatic inflammation markers and HCC-related cytokines were decreased in mice with reduced NET formation due to neutrophil elastase (NE) deletion, and liver-related symptoms of alcohol were also alleviated in NE knockout mice. Removal of intestinal bacteria with antibiotics led to decreases in markers of NETs formation and inflammatory cytokines upon chronic alcohol consumption, and development of alcoholic hepatosteatosis and HCC was also attenuated. These functions were restored upon supplementation with the bacterial product LPS. When mice lacking toll-like receptor 4 (TLR4) received chronic alcohol feeding, intrahepatic markers of NETs formation decreased, and hepatosteatosis and HCC were alleviated.Formation of NETs following LPS stimulation of TLR4 upon chronic alcohol use leads to increased alcoholic steatosis and subsequent HCC.
Bitter taste signaling in tracheal epithelial brush cells elicits innate immune responses to bacterial infection
Authors: Monika I. Hollenhorst, Rajender Nandigama, Saskia B. Evers, Igor Gamayun, Noran Abdel Wadood, Alaa Salah, Mario Pieper, Amanda Wyatt, Alexey Stukalov, Anna Gebhardt, Wiebke Nadolni, Wera Burow, Christian Herr, Christoph Beisswenger, Soumya Kusumakshi, Fabien Ectors, Tatjana I. Kichko, Lisa Hübner, Peter Reeh, Antje Munder, Sandra-Maria Wienhold, Martin Witzenrath, Robert Bals, Veit Flockerzi, Thomas Gudermann, Markus Bischoff, Peter Lipp, Susanna Zierler, Vladimir Chubanov, Andreas Pichlmair, Peter König, Ulrich Boehm, Gabriela Krasteva-Christ
Journal: Journal of Clinical Investigation (2022)

Constant exposure of the airways to inhaled pathogens requires efficient early immune responses protecting against infections. How bacteria on the epithelial surface are detected and first-line protective mechanisms are initiated are not well understood. We have recently shown that tracheal brush cells (BCs) express functional taste receptors. Here we report that bitter taste signaling in murine BCs induces neurogenic inflammation. We demonstrate that BC signaling stimulates adjacent sensory nerve endings in the trachea to release the neuropeptides CGRP and substance P that mediate plasma extravasation, neutrophil recruitment, and diapedesis. Moreover, we show that bitter tasting quorum-sensing molecules from Pseudomonas aeruginosa activate tracheal BCs. BC signaling depends on the key taste transduction gene Trpm5, triggers secretion of immune mediators, among them the most abundant member of the complement system, and is needed to combat P. aeruginosa infections. Our data provide functional insight into first-line defense mechanisms against bacterial infections of the lung.
Updated Overall Survival of Ribociclib plus Endocrine Therapy versus Endocrine Therapy Alone in Pre- and Perimenopausal Patients with HR+/HER2− Advanced Breast Cancer in MONALEESA-7: A Phase III Randomized Clinical Trial
Authors: Yen-Shen Lu, Seock-Ah Im, Marco Colleoni, Fabio Franke, Aditya Bardia, Fatima Cardoso, Nadia Harbeck, Sara Hurvitz, Louis Chow, Joohyuk Sohn, Keun Seok Lee, Saul Campos-Gomez, Rafael Villanueva Vazquez, Kyung Hae Jung, K. Govind Babu, Paul Wheatley-Price, Michelino De Laurentiis, Young-Hyuck Im, Sherko Kuemmel, Nagi El-Saghir, Ruth O'Regan, Claudia Gasch, Nadia Solovieff, Craig Wang, Yongyu Wang, Arunava Chakravartty, Yan Ji, Debu Tripathy
Journal: Clinical Cancer Research (2021)

Abstract Purpose: Ribociclib plus endocrine therapy (ET) demonstrated a statistically significant progression-free survival and overall survival (OS) benefit in the phase III MONALEESA-7 trial of pre-/perimenopausal patients with hormone receptor (HR)-positive (HR+), HER2-negative (HER2−) advanced breast cancer (ABC). The median OS was not reached in the ribociclib arm in the protocol-specified final analysis; we hence performed an exploratory OS and additional outcomes analysis with an extended follow-up (median, 53.5 months). Patients and Methods: Patients were randomized to receive ET [goserelin plus nonsteroidal aromatase inhibitor (NSAI) or tamoxifen] with ribociclib or placebo. OS was evaluated with a stratified Cox proportional hazard model and summarized with Kaplan–Meier methods. Results: The intent-to-treat population included 672 patients. Median OS was 58.7 months with ribociclib versus 48.0 months with placebo [hazard ratio = 0.76; 95% confidence interval (CI), 0.61–0.96]. Kaplan–Meier estimated OS at 48 months was 60% and 50% with ribociclib and placebo, respectively. Subgroup analyses were generally consistent with the OS benefit, including patients who received NSAI and patients aged less than 40 years. Subsequent antineoplastic therapies following discontinuation were balanced between the ribociclib (77%) and placebo (78%) groups. Use of cyclin-dependent kinase 4/6 inhibitors after discontinuation was higher with placebo (26%) versus ribociclib (13%). Time to first chemotherapy was significantly delayed with ribociclib versus placebo. No drug–drug interactions were observed between ribociclib and either NSAI. Conclusions: Ribociclib plus ET continued to show significantly longer OS than ET alone in pre-/perimenopausal patients, including patients aged less than 40 years, with HR+/HER2− ABC with 53.5 months of median follow-up (ClinicalTrials.gov, NCT02278120).
Editor's Note: Peptide Aptamers Targeting Mutant p53 Induce Apoptosis in Tumor Cells
Authors: Elisa Guida, Andrea Bisso, Cristina Fenollar-Ferrer, Marco Napoli, Claudio Anselmi, Javier E. Girardini, Paolo Carloni, Giannino Del Sal
Journal: Cancer Research (2022)

The editors are publishing this note to alert readers to a concern about this article. The authors made the editors aware they had mistakenly duplicated Western blot bands in Fig. 4B. The same image was used for both the p53 R175H and p53 R273H cell lines.
The Effect of Corticosteroids on Prostate Cancer Outcome Following Treatment with Enzalutamide: A Multivariate Analysis of the Phase III AFFIRM Trial
Authors: Jimmy L. Zhao, Karim Fizazi, Fred Saad, Kim N. Chi, Mary-Ellen Taplin, Cora N. Sternberg, Andrew J. Armstrong, Johann S. de Bono, William T. Duggan, Howard I. Scher
Journal: Clinical Cancer Research (2021)

Abstract Purpose: The clinical impact of concurrent corticosteroid use (CCU) on enzalutamide-treated patients with metastatic castration-resistant prostate cancer (mCRPC) is unknown. We investigated the association of CCU with overall survival (OS), radiographic progression-free survival (rPFS), and time to prostate-specific antigen progression (TTPP) in post-chemotherapy, enzalutamide-treated patients with mCRPC. Patients and Methods: Post hoc analysis of AFFIRM (NCT00974311) with patients (n = 1,199) randomized 2:1 to enzalutamide 160 mg/day or placebo. Treatment group, CCU, and known prognostic factors were evaluated for impact on OS, rPFS, and TTPP using a multivariate Cox proportional hazards model. CCU was defined as “baseline” (use started at baseline) or “on-study” (baseline plus use that was started during the trial). Results: Enzalutamide significantly improved OS, rPFS, and TTPP independent of baseline CCU but was associated with inferior clinical outcomes when compared with no baseline CCU, including a shorter OS [10.8 months vs. not reached (NR); HR for use vs. no use, 2.13; 95% confidence interval (CI), 1.79–2.54], rPFS (5.2 months vs. 8.0 months; HR, 1.49; 95% CI, 1.29–1.72], and TTPP (4.6 months vs. 5.7 months; HR, 1.50; 95% CI, 1.25–1.81). These findings held in a multivariate analysis adjusting for baseline prognostic factors wherein baseline CCU was independently associated with decreased OS (HR, 1.71; 95% CI, 1.43–2.04; P &amp;lt; 0.0001) and rPFS (HR, 1.28; 95% CI, 1.11–1.48; P = 0.0007). Conclusions: Patients with mCRPC benefited from enzalutamide treatment independent of CCU, but CCU was associated with worse baseline prognostic factors and outcomes.
Improving Transitional Care and Reducing Hospitalization for Nursing Facility Residents
Authors: Peter A. Boling
Journal: JAMA Network Open (2022)

Kelly Birtwell, PhD; Claire Planner, PhD; Alexander Hodkinson, PhD; Alex Hall, PhD; Sally Giles, PhD; Stephen Campbell, PhD; Natasha Tyler, PhD; Maria Panagioti, PhD; Gavin Daker-White, PhD
英格兰和威尔士的大疱性表皮松解症
Journal: British Journal of Dermatology (2022)

British Journal of DermatologyVolume 186, Issue 5 p. e213-e213 Plain Language Summary 英格兰和威尔士的大疱性表皮松解症 First published: 02 May 2022 https://doi.org/10.1111/bjd.21266AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract Linked Article: Petrof et al. Br J Dermatol 2022; 186:843–848. 大疱性表皮松解症(EB)是一组罕见遗传性疾病，在此类疾病中，皮肤非常脆弱。二十年前，英国国家医疗服务体系(NHS)为EB患者设立了专项服务，向英格兰和威尔士的所有患者提供专家建议、治疗和基因检测。EB有不同类型，严重类型的患者和大多数较轻类型的EB患者都已在该专项服务中登记，从而有可能精确计算出这类疾病的罕见程度。 作者研究了来自英格兰和威尔士EB患者数据库的匿名患者信息。2021年3月时有2361位EB患者，即每百万人口中有35位患者。作者还研究了患有不同类型EB的人数。例如，每百万人口中有17位患者属单纯型EB，11位患者属营养不良型EB，1位患者属交界型EB。2002年1月至2021年4月期间，有1200名新生儿患有EB。 在所研究的19年期间，严重类型EB的出生率有所下降，可能因为接受遗传咨询的情况有所改善。此外，患有致命亚型交界型EB的婴儿的预期寿命略有提高，可能是因为有了更好的新生儿护理。较轻类型EB患者的数据不太可靠，因为他们中有些人不需要专项服务。本研究发现，英国的患者人数高于很多其他国家，因为每位患者都在NHS中有登记。 Volume186, Issue5May 2022Pages e213-e213 RelatedInformation
Complicated Carotid Artery Plaques and Risk of Recurrent Ischemic Stroke or TIA
Authors: Anna Kopczak, Andreas Schindler, Dominik Sepp, Anna Bayer-Karpinska, Rainer Malik, Mia L. Koch, Julia Zeller, Christoph Strecker, Daniel Janowitz, Frank A. Wollenweber, Johann-Martin Hempel, Tobias Boeckh-Behrens, Clemens C. Cyran, Andreas Helck, Andreas Harloff, Ulf Ziemann, Sven Poli, Holger Poppert, Tobias Saam, Martin Dichgans
Journal: Journal of the American College of Cardiology (2022)

Complicated nonstenosing carotid artery plaques (CAPs) are an under-recognized cause of stroke.The purpose of this study was to determine whether complicated CAP ipsilateral to acute ischemic anterior circulation stroke (icCAP) are associated with recurrent ischemic stroke or transient ischemic attack (TIA).The CAPIAS (Carotid Plaque Imaging in Acute Stroke) multicenter study prospectively recruited patients with ischemic stroke restricted to the territory of a single carotid artery. Complicated (AHA-lesion type VI) CAP were defined by multisequence, contrast-enhanced carotid magnetic resonance imaging obtained within 10 days from stroke onset. Recurrent events were assessed after 3, 12, 24, and 36 months. The primary outcome was recurrent ischemic stroke or TIA.Among 196 patients enrolled, 104 patients had cryptogenic stroke and nonstenosing CAP. During a mean follow-up of 30 months, recurrent ischemic stroke or TIA occurred in 21 patients. Recurrent events were significantly more frequent in patients with icCAP than in patients without icCAP, both in the overall cohort (incidence rate [3-year interval]: 9.50 vs 3.61 per 100 patient-years; P = 0.025, log-rank test) and in patients with cryptogenic stroke (10.92 vs 1.82 per 100 patient-years; P = 0.003). The results were driven by ipsilateral events. A ruptured fibrous cap (HR: 4.91; 95% CI: 1.31-18.45; P = 0.018) and intraplaque hemorrhage (HR: 4.37; 95% CI: 1.20-15.97; P = 0.026) were associated with a significantly increased risk of recurrent events in patients with cryptogenic stroke.Complicated CAP ipsilateral to acute ischemic anterior circulation stroke are associated with an increased risk of recurrent ischemic stroke or TIA. Carotid plaque imaging identifies high-risk patients who might be suited for inclusion into future secondary prevention trials. (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT01284933).
Reply by Elmaleh-Sachs <i>et al</i>. to Townsend and Cowl, and to Miller <i>et al.</i>
Authors: Arielle Elmaleh-Sachs, Pallavi Balte, Elizabeth C. Oelsner, Norrina B. Allen, Aaron Baugh, Alain G. Bertoni, John L. Hankinson, James S. Pankow, Wendy S. Post, Joseph E. Schwartz, Benjamin M. Smith, Karol Watson, R. Graham Barr
Journal: American Journal of Respiratory and Critical Care Medicine (2022)