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1. Mastering a Life-Saving Technique: Analysis of Learning from a Cricothyrotomy Workshop

Author

Cole J. Homer, Kristy Carlson, Nolan Marshall, Randi Peavy, Christopher M. Bingcang, John McClain, and Jayme R. Dowdall

Abstract

Cricothyrotomy is an emergency procedure that is utilized in situations that require immediate access to a breathing pathway. This procedure may be performed by professionals in a variety of healthcare fields depending upon the specific emergency scenario, so the development of an interprofessional workshop is imperative for procedural confidence and skill development. Our team developed a training workshop with a specific focus on procedural skills, risks, benefits, and psychological ramifications associated with a cricothyrotomy procedure. Pre-workshop and post-workshop surveys were obtained for comparison of participant confidence. Overall, the organization and delivery of a cricothyrotomy training workshop significantly increased the overall participant confidence surrounding this procedure.

Published
2024

3. TORPEdO: A phase III trial of intensity-modulated proton beam therapy versus intensity-modulated radiotherapy for multi-toxicity reduction in oropharyngeal cancer

Author

David J. Thomson, Clare Cruickshank, Helen Baines, Russell Banner, Matthew Beasley, Guy Betts, Helen Bulbeck, Frances Charlwood, Judith Christian, Matthew Clarke, Olly Donnelly, Bernadette Foran, Callum Gillies, Clare Griffin, Jarrod J. Homer, Johannes A. Langendijk, Lip Wai Lee, James Lester, Matthew Lowe, Andrew McPartlin, Elizabeth Miles, Christopher Nutting, Nachi Palaniappan, Robin Prestwich, James M. Price, Clare Roberts, Justin Roe, Ramkumar Shanmugasundaram, Rita Simões, Anna Thompson, Catharine West, Lorna Wilson, Jane Wolstenholme, and Emma Hall

Subjects
Medical physics. Medical radiology. Nuclear medicine, R895-920, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Published
2023
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4. Culture and characterization of various porcine integumentary-connective tissue-derived mesenchymal stromal cells to facilitate tissue adhesion to percutaneous metal implants

Author

Devaveena Dey, Nicholas G. Fischer, Andrea H. Dragon, Elsa Ronzier, Isha Mutreja, David T. Danielson, Cole J. Homer, Jonathan A. Forsberg, Joan E. Bechtold, Conrado Aparicio, and Thomas A. Davis

Subjects
Transdermal osseointegrated implant, Mesenchymal stromal cells, Integumentary tissues, Cell adhesion, Titanium surfaces, Medicine (General), R5-920, Biochemistry, QD415-436
Abstract

Abstract Background Transdermal osseointegrated prosthesis have relatively high infection rates leading to implant revision or failure. A principle cause for this complication is the absence of a durable impervious biomechanical seal at the interface of the hard structure (implant) and adjacent soft tissues. This study explores the possibility of recapitulating an analogous cellular musculoskeletal-connective tissue interface, which is present at naturally occurring integumentary tissues where a hard structure exits the skin, such as the nail bed, hoof, and tooth. Methods Porcine mesenchymal stromal cells (pMSCs) were derived from nine different porcine integumentary and connective tissues: hoof-associated superficial flexor tendon, molar-associated periodontal ligament, Achilles tendon, adipose tissue and skin dermis from the hind limb and abdominal regions, bone marrow and muscle. For all nine pMSCs, the phenotype, multi-lineage differentiation potential and their adhesiveness to clinical grade titanium was characterized. Transcriptomic analysis of 11 common genes encoding cytoskeletal proteins VIM (Vimentin), cell–cell and cell–matrix adhesion genes (Vinculin, Integrin β1, Integrin β2, CD9, CD151), and for ECM genes (Collagen-1a1, Collagen-4a1, Fibronectin, Laminin-α5, Contactin-3) in early passaged cells was performed using qRT-PCR. Results All tissue-derived pMSCs were characterized as mesenchymal origin by adherence to plastic, expression of cell surface markers including CD29, CD44, CD90, and CD105, and lack of hematopoietic (CD11b) and endothelial (CD31) markers. All pMSCs differentiated into osteoblasts, adipocytes and chondrocytes, albeit at varying degrees, under specific culture conditions. Among the eleven adhesion genes evaluated, the cytoskeletal intermediate filament vimentin was found highly expressed in pMSC isolated from all tissues, followed by genes for the extracellular matrix proteins Fibronectin and Collagen-1a1. Expression of Vimentin was the highest in Achilles tendon, while Fibronectin and Col1agen-1a1 were highest in molar and hoof-associated superficial flexor tendon bone marrow, respectively. Achilles tendon ranked the highest in both multilineage differentiation and adhesion assessments to titanium metal. Conclusions These findings support further preclinical research of these tissue specific-derived MSCs in vivo in a transdermal osseointegration implant model.

Published
2021
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5. Reliability of histopathologic diagnosis of fibrotic interstitial lung disease: an international collaborative standardization project

Author

Robert Camp, Maxwell L. Smith, Brandon T. Larsen, Anja C. Roden, Carol Farver, Andre L. Moreira, Richard Attanoos, Raghavendra Pillappa, Irene Sansano, Alexandre Todorovic Fabro, and Robert J. Homer

Subjects
Interstitial lung disease, Pulmonary fibrosis, Usual interstitial pneumonia, Diseases of the respiratory system, RC705-779
Abstract

Abstract Background Current interstitial lung disease (ILD) diagnostic guidelines assess criteria across clinical, radiologic and pathologic domains. Significant interobserver variation in histopathologic evaluation has previously been shown but the specific source of these discrepancies is poorly documented. We sought to document specific areas of difficulty and develop improved criteria that would reduce overall interobserver variation. Methods Using an internet-based approach, we reviewed selected images of specific diagnostic features of ILD histopathology and whole slide images of fibrotic ILD. After an initial round of review, we confirmed the presence of interobserver variation among our group. We then developed refined criteria and reviewed a second set of cases. Results The initial round reproduced the existing literature on interobserver variation in diagnosis of ILD. Cases which were pre-selected as inconsistent with usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF) were confirmed as such by multi-observer review. Cases which were thought to be in the spectrum of chronic fibrotic ILD for which UIP/IPF were in the differential showed marked variation in nearly all aspects of ILD evaluation including extent of inflammation and extent and pattern of fibrosis. A proposed set of more explicit criteria had only modest effects on this outcome. While we were only modestly successful in reducing interobserver variation, we did identify specific reasons that current histopathologic criteria of fibrotic ILD are not well defined in practice. Conclusions Any additional classification scheme must address interobserver variation in histopathologic diagnosis of fibrotic ILD order to remain clinically relevant. Improvements to tissue-based diagnostics may require substantial resources such as larger datasets or novel technologies to improve reproducibility. Benchmarks should be established for expected outcomes among clinically defined subgroups as a quality metric.

Published
2021
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6. Elevated murine HB-EGF confers sensitivity to diphtheria toxin in EGFR-mutant lung adenocarcinoma

Author

Camila Robles-Oteiza, Deborah Ayeni, Stellar Levy, Robert J. Homer, Susan M. Kaech, and Katerina Politi

Subjects
lung adenocarcinoma, diphtheria toxin, dtr, hbegf, egfr, Medicine, Pathology, RB1-214
Abstract

Conditional ablation of defined cell populations in vivo can be achieved using genetically engineered mice in which the human diphtheria toxin (DT) receptor (DTR) is placed under control of a murine tissue-specific promotor, such that delivery of DT selectively ablates cells expressing this high-affinity human DTR; cells expressing only the endogenous low-affinity mouse DTR are assumed to be unaffected. Surprisingly, we found that systemic administration of DT induced rapid regression of murine lung adenocarcinomas that express human mutant EGFR in the absence of a transgenic allele containing human DTR. DT enzymatic activity was required for tumor regression, and mutant EGFR-expressing tumor cells were the primary target of DT toxicity. In FVB mice, EGFR-mutant tumors upregulated expression of HBEGF, which is the DTR in mice and humans. HBEGF blockade with the enzymatically inactive DT mutant CRM197 partially abrogated tumor regression induced by DT. These results suggest that elevated expression of murine HBEGF, i.e. the low-affinity DTR, confers sensitivity to DT in EGFR-mutant tumors, demonstrating a biological effect of DT in mice lacking transgenic DTR alleles and highlighting a unique vulnerability of EGFR-mutant lung cancers.

Published
2021
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9. Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells

Author

Matteo Forloni, Romi Gupta, Arvindhan Nagarajan, Li-Sha Sun, Yuying Dong, Valentina Pirazzoli, Maria Toki, Anna Wurtz, Mary Ann Melnick, Susumu Kobayashi, Robert J. Homer, David L. Rimm, Scott J. Gettinger, Katerina Politi, Shaillay Kumar Dogra, and Narendra Wajapeyee

Subjects
Biology (General), QH301-705.5
Abstract

Oncogene-induced DNA methylation-mediated transcriptional silencing of tumor suppressors frequently occurs in cancer, but the mechanism and functional role of this silencing in oncogenesis are not fully understood. Here, we show that oncogenic epidermal growth factor receptor (EGFR) induces silencing of multiple unrelated tumor suppressors in lung adenocarcinomas and glioblastomas by inhibiting the DNA demethylase TET oncogene family member 1 (TET1) via the C/EBPα transcription factor. After oncogenic EGFR inhibition, TET1 binds to tumor suppressor promoters and induces their re-expression through active DNA demethylation. Ectopic expression of TET1 potently inhibits lung and glioblastoma tumor growth, and TET1 knockdown confers resistance to EGFR inhibitors in lung cancer cells. Lung cancer samples exhibited reduced TET1 expression or TET1 cytoplasmic localization in the majority of cases. Collectively, these results identify a conserved pathway of oncogenic EGFR-induced DNA methylation-mediated transcriptional silencing of tumor suppressors that may have therapeutic benefits for oncogenic EGFR-mediated lung cancers and glioblastomas.

Published
2016
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10. Update on the Features and Measurements of Experimental Acute Lung Injury in Animals: An Official American Thoracic Society Workshop Report

Author

Hrishikesh S. Kulkarni, Janet S. Lee, Julie A. Bastarache, Wolfgang M. Kuebler, Gregory P. Downey, Guillermo M. Albaiceta, William A. Altemeier, Antonio Artigas, Jason H. T. Bates, Carolyn S. Calfee, Charles S. Dela Cruz, Robert P. Dickson, Joshua A. Englert, Jeffrey I. Everitt, Michael B. Fessler, Andrew E. Gelman, Kymberly M. Gowdy, Steve D. Groshong, Susanne Herold, Robert J. Homer, Jeffrey C. Horowitz, Connie C. W. Hsia, Kiyoyasu Kurahashi, Victor E. Laubach, Mark R. Looney, Rudolf Lucas, Nilam S. Mangalmurti, Anne M. Manicone, Thomas R. Martin, Sadis Matalon, Michael A. Matthay, Daniel F. McAuley, Sharon A. McGrath-Morrow, Joseph P. Mizgerd, Stephanie A. Montgomery, Bethany B. Moore, Alexandra Noël, Carrie E. Perlman, John P. Reilly, Eric P. Schmidt, Shawn J. Skerrett, Tomeka L. Suber, Charlotte Summers, Benjamin T. Suratt, Masao Takata, Rubin Tuder, Stefan Uhlig, Martin Witzenrath, Rachel L. Zemans, and Gutavo Matute-Bello

Subjects
Pulmonary and Respiratory Medicine, Clinical Biochemistry, Cell Biology, Molecular Biology
Published
2022
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12. Supplementary Data from High Expression of Mammalian Target of Rapamycin Is Associated with Better Outcome for Patients with Early Stage Lung Adenocarcinoma

Author

David L. Rimm, Frank Detterbeck, Daniel Boffa, Robert J. Homer, Scott Gettinger, Lynn Tanoue, Konstantinos N. Syrigos, Gerold Bepler, and Valsamo K. Anagnostou

Abstract

Supplementary Data from High Expression of Mammalian Target of Rapamycin Is Associated with Better Outcome for Patients with Early Stage Lung Adenocarcinoma

Published
2023
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13. Data from High Expression of Mammalian Target of Rapamycin Is Associated with Better Outcome for Patients with Early Stage Lung Adenocarcinoma

Author

David L. Rimm, Frank Detterbeck, Daniel Boffa, Robert J. Homer, Scott Gettinger, Lynn Tanoue, Konstantinos N. Syrigos, Gerold Bepler, and Valsamo K. Anagnostou

Abstract

Purpose: Mammalian target of rapamycin (mTOR) is a key kinase downstream of phosphoinositide 3-kinase (PI3K)/AKT predominantly involved in translational control in the presence of nutrients and energy. Despite the well known role of mTOR in carcinogenesis, its prognostic potential in lung cancer has not been investigated. Here, we quantitatively assessed mTOR protein expression in two large data sets to investigate the impact of mTOR expression on patient survival.Experimental Design: Automated quantitative analysis (AQUA), a fluorescent-based method for analysis of in situ protein expression, was used to assess mTOR expression in a training cohort of 167 lung cancer patients. An independent cohort of 235 lung cancer patients (from a second institution) was used for validation.Results: Tumors expressed mTOR in the cytoplasm in 56% and 50% of the cases in training and validation cohorts, respectively; mTOR expression was not associated with standard clinical or pathologic characteristics. Patients with high mTOR expression had a longer median overall survival compared with the low expressers (52.7 versus 38.5 months; log rank P = 0.06), which was more prominent in the adenocarcinoma group (55.7 versus 38.88 months; log rank P = 0.018). Multivariate analysis revealed an independent lower risk of death for adenocarcinoma and adenocarcinoma stage IA patients with mTOR-expressing tumors (hazard ratio, 0.48; 95% confidence interval, 0.24-0.98; P = 0.04, and hazard ratio, 0.12; 95% confidence interval, 0.03-0.72; P = 0.019, respectively).Conclusions: mTOR expression defines a subgroup of patients with a favorable outcome and may be useful for prognostic stratification of lung adenocarcinoma patients as well as incorporation of mTOR into clinical decisions.

Published
2023
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14. Data from A 26-Gene Hypoxia Signature Predicts Benefit from Hypoxia-Modifying Therapy in Laryngeal Cancer but Not Bladder Cancer

Author

Catharine M.L. West, Johannes H.A.M. Kaanders, Adrian L. Harris, Francesca M. Buffa, Peter J. Hoskin, Ana M. Rojas, Jarrod J. Homer, Crispin J. Miller, Helen Denley, Guy N.J. Betts, Janet Taylor, Joely J. Irlam, Paul N. Span, Navin Mani, and Amanda Eustace

Abstract

Purpose: Tumor hypoxia is associated with a poor prognosis, hypoxia modification improves outcome, and hypoxic status predicts benefit from treatment. Yet, there is no universal measure of clinical hypoxia. The aim of this study was to investigate whether a 26-gene hypoxia signature predicted benefit from hypoxia-modifying treatment in both cancer types.Experimental Design: Samples were available from 157 T2–T4 laryngeal cancer and 185 T1–T4a bladder cancer patients enrolled on the accelerated radiotherapy with carbogen and nicotinamide (ARCON) and bladder carbogen nicotinamide (BCON) phase III randomized trials of radiotherapy alone or with carbogen and nicotinamide (CON) respectively. Customized TaqMan low density arrays (TLDA) were used to assess expression of the 26-gene signature using quantitative real-time PCR. The median expression of the 26 genes was used to derive a hypoxia score (HS). Patients were categorized as TLDA-HS low (≤median) or TLDA-HS high (>median). The primary outcome measures were regional control (RC; ARCON) and overall survival (BCON).Results: Laryngeal tumors categorized as TLDA-HS high showed greater benefit from ARCON than TLDA-HS low tumors. Five-year RC was 81% (radiotherapy alone) versus 100% (CON) for TLDA-HS high (P = 0.009). For TLDA-HS low, 5-year RC was 91% (radiotherapy alone) versus 90% (CON; P = 0.90). TLDA-HS did not predict benefit from CON in bladder cancer.Conclusion: The 26-gene hypoxia signature predicts benefit from hypoxia-modifying treatment in laryngeal cancer. These findings will be evaluated in a prospective clinical trial. Clin Cancer Res; 19(17); 4879–88. ©2013 AACR.

Published
2023
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15. Supplementary Tables 1-4, Flowchart 1 from Relation of a Hypoxia Metagene Derived from Head and Neck Cancer to Prognosis of Multiple Cancers

Author

Adrian L. Harris, Catharine M.L. West, Pat Price, Philip Sloan, Nick Slevin, Brian Musgrove, Jarrod J. Homer, Rogan J. Corbridge, Graham J. Cox, Ketan A. Shah, Helen Turley, Helen R. Valentine, Crispin Miller, Priyamal Silva, Francesca M. Buffa, and Stuart C. Winter

Abstract

Supplementary Tables 1-4, Flowchart 1 from Relation of a Hypoxia Metagene Derived from Head and Neck Cancer to Prognosis of Multiple Cancers

Published
2023
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16. Data from Relation of a Hypoxia Metagene Derived from Head and Neck Cancer to Prognosis of Multiple Cancers

Author

Adrian L. Harris, Catharine M.L. West, Pat Price, Philip Sloan, Nick Slevin, Brian Musgrove, Jarrod J. Homer, Rogan J. Corbridge, Graham J. Cox, Ketan A. Shah, Helen Turley, Helen R. Valentine, Crispin Miller, Priyamal Silva, Francesca M. Buffa, and Stuart C. Winter

Abstract

Affymetrix U133plus2 GeneChips were used to profile 59 head and neck squamous cell cancers. A hypoxia metagene was obtained by analysis of genes whose in vivo expression clustered with the expression of 10 well-known hypoxia-regulated genes (e.g., CA9, GLUT1, and VEGF). To minimize random aggregation, strongly correlated up-regulated genes appearing in >50% of clusters defined a signature comprising 99 genes, of which 27% were previously known to be hypoxia associated. The median RNA expression of the 99 genes in the signature was an independent prognostic factor for recurrence-free survival in a publicly available head and neck cancer data set, outdoing the original intrinsic classifier. In a published breast cancer series, the hypoxia signature was a significant prognostic factor for overall survival independent of clinicopathologic risk factors and a trained profile. The work highlights the validity and potential of using data from analysis of in vitro stress pathways for deriving a biological metagene/gene signature in vivo. [Cancer Res 2007;67(7):3441–9]

Published
2023
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18. Interagency approaches to animal models for acute radiation exposure

Author

Lisa S Carnell, Kasandra S Hunter, Mary J. Homer, Corey M Hoffman, Andrea L. DiCarlo, and Shannon G Loelius

Subjects
medicine.medical_specialty, Swine, Disease, Article, Nonclinical, National Institute of Allergy and Infectious Diseases (U.S.), Countermeasure, medicine, Animals, Radiology, Nuclear Medicine and imaging, Radiation Injuries, Intensive care medicine, Acute radiation exposure, Radiation injury, Effective response, Licensure, Radiation, Radiological and Ultrasound Technology, business.industry, Public health, MCM, United States, Clinical trial, Acute Radiation Syndrome, Medical Countermeasures, Radiological weapon, Models, Animal, Swine, Miniature, Rabbits, business, ARS
Abstract

Ionizing radiation can cause devastating injuries including hemorrhage, immune suppression, increased susceptibility to infection, and death. Medical countermeasures (MCMs) that address and mitigate radiation-induced injuries are the most important tools for countering the consequences of radiation exposure. Likewise, in matters of public health security, the development and advancement of radiological MCMs are fundamental for establishing an effective response to radiological and nuclear threats. United States Government agencies such as the Biomedical Advanced Research and Development Authority (BARDA), the National Institute of Allergy and Infectious Diseases (NIAID), and the National Aeronautics and Space Administration (NASA) have dedicated significant efforts to advance the development of MCMs to treat radiation injury and facilitate their introduction into the public sphere. Due to the severe nature of radiation injuries, clinical trials are unethical. Therefore, nonclinical models that accurately replicate clinical manifestations of ionizing radiation injury observed in humans are essential to MCM advancement. The most frequently used nonclinical models of radiation injury are rodents and non-human primates (NHPs). These species reproduce many aspects of human disease caused by ionizing radiation and have been pivotal for the development and licensure of radiological MCMs. Despite these successes, model drawbacks have prompted the exploration and development of additional nonclinical models. Minipigs and rabbits show promise as acceptable models of radiation injury and demonstrate the potential to contribute significantly to MCM advancement. This collection of research showcases the capabilities of minipigs and rabbits in mirroring clinically relevant aspects of radiation-induced disease and documents the potential value these models may hold for radiological and nuclear MCM research. Together, these government-funded studies represent advances in radiological MCM development that can facilitate the emergence of cutting-edge technologies.

Published
2021
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19. Pre-treatment tumour perfusion parameters and initial RECIST response do not predict long-term survival outcomes for patients with head and neck squamous cell carcinoma treated with induction chemotherapy.

Author

Natalie M Lowe, Lucy E Kershaw, Jonathan M Bernstein, Stephanie B Withey, Kathleen Mais, Jarrod J Homer, Nicholas J Slevin, Suzanne C Bonington, Bernadette M Carrington, and Catharine M West

Subjects
Medicine, Science
Abstract

Previously, we showed that pre-treatment tumour plasma perfusion (Fp) predicts RECIST response to induction chemotherapy (ICT) in locoregionally advanced head and neck squamous cell carcinoma (HNSCC). The aim here was to determine whether the pre-treatment tumour Fp estimate, changes in tumour Fp or RECIST response post 2 cycles of ICT were prognostic for long-term survival outcomes.A prospective study enrolled patients with high stage HNSCC treated with docetaxel (T), cisplatin (P) and 5-fluorouracil (F) (ICT) followed by synchronous cisplatin and intensity modulated radiotherapy. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) before and after two cycles of ICT was used to measure Fp and RECIST response.Forty-two patients were recruited and 37 underwent two scans. The median follow-up was 36 (range 23-49) months. Pre-treatment tumour Fp (stratified by median) was not prognostic for overall survival (p = 0.42), disease specific survival (p = 0.20) and locoregional control (p = 0.64). Neither change in tumour Fp nor RECIST response post two cycles of ICT was prognostic for any outcome (p>0.21).DCE-MRI parameters do not predict long-term survival outcomes following ICT and RECIST response to ICT may not be an appropriate endpoint to determine early efficacy of a treatment in HNSCC patients.

Published
2018
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20. "The marriage was no marriage": Crossing Racial Lines in Territorial Arizona.

Author

Thiel, J. Homer

Abstract

This article explores the life of Fannie (Smith) Pogue, an African American woman who lived in Pima County, Arizona Territory, between 1856 and 1912. Fannie was involved in the mining industry and had a relationship with Philip James Garcia, another African American miner. After Philip's death, Fannie became involved with David Pogue, a white man, and they faced legal challenges due to their interracial relationship. Fannie's story highlights the experiences of African Americans in Arizona during this time period and the discrimination they faced. [Extracted from the article]

Published
2024

21. Unadjuvanted intranasal spike vaccine elicits protective mucosal immunity against sarbecoviruses

Author

Tianyang Mao, Benjamin Israelow, Mario A. Peña-Hernández, Alexandra Suberi, Liqun Zhou, Sophia Luyten, Melanie Reschke, Huiping Dong, Robert J. Homer, W. Mark Saltzman, and Akiko Iwasaki

Subjects
Multidisciplinary, COVID-19 Vaccines, SARS-CoV-2, Vaccination, COVID-19, Antibodies, Viral, Immunoglobulin A, Mice, Memory T Cells, Memory B Cells, Spike Glycoprotein, Coronavirus, Animals, Immunity, Mucosal, Immunologic Memory, Administration, Intranasal
Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has highlighted the need for vaccines that not only prevent disease but also prevent transmission. Parenteral vaccines induce robust systemic immunity but poor immunity at the respiratory mucosa. We developed a vaccine strategy that we call “prime and spike,” which leverages existing immunity generated by primary vaccination (prime) to elicit mucosal immune memory within the respiratory tract by using unadjuvanted intranasal spike boosters (spike). We show that prime and spike induces robust resident memory B and T cell responses, induces immunoglobulin A at the respiratory mucosa, boosts systemic immunity, and completely protects mice with partial immunity from lethal SARS-CoV-2 infection. Using divergent spike proteins, prime and spike enables the induction of cross-reactive immunity against sarbecoviruses.

Published
2022

22. Integrated Single-Cell Atlas of Endothelial Cells of the Human Lung

Author

Nicholas E. Banovich, Robert Lafyatis, Laura E. Niklason, Kerstin B. Meyer, Dana Pe'er, Carlos Cosme, Yifan Yuan, Taylor Adams, Austin J. Gutierrez, Maor Sauler, Maurizio Chioccioli, Kadi-Ann Rose, Edward P. Manning, Jonathan A. Kropski, Sergio Poli, Norihito Omote, Xiting Yan, Farida Ahangari, Nir Neumark, Jonas C. Schupp, Arun C. Habermann, Richard W. Pierce, Linh T. Bui, Giuseppe DeIuliis, Micha Sam Brickman Raredon, Martijn C. Nawijn, Robert J. Homer, Naftali Kaminski, Ivan O. Rosas, Sarah A. Teichmann, and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
EXPRESSION, Endothelium, Cell, microcirculation, 030204 cardiovascular system & hematology, Pulmonary Artery, Microcirculation, Human lung, Transcriptome, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), Original Research Articles, Databases, Genetic, Medicine, Humans, Lung, 030304 developmental biology, 0303 health sciences, business.industry, Atlas (topology), Gene Expression Profiling, Computational Biology, High-Throughput Nucleotide Sequencing, respiratory system, endothelial cells, Capillaries, medicine.anatomical_structure, Organ Specificity, Pulmonary Veins, pulmonary circulation, Cancer research, ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, Disease Susceptibility, Single-Cell Analysis, Cardiology and Cardiovascular Medicine, business, transcriptome, Biomarkers
Abstract

Supplemental Digital Content is available in the text., Background: Cellular diversity of the lung endothelium has not been systematically characterized in humans. We provide a reference atlas of human lung endothelial cells (ECs) to facilitate a better understanding of the phenotypic diversity and composition of cells comprising the lung endothelium. Methods: We reprocessed human control single-cell RNA sequencing (scRNAseq) data from 6 datasets. EC populations were characterized through iterative clustering with subsequent differential expression analysis. Marker genes were validated by fluorescent microscopy and in situ hybridization. scRNAseq of primary lung ECs cultured in vitro was performed. The signaling network between different lung cell types was studied. For cross-species analysis or disease relevance, we applied the same methods to scRNAseq data obtained from mouse lungs or from human lungs with pulmonary hypertension. Results: Six lung scRNAseq datasets were reanalyzed and annotated to identify >15 000 vascular EC cells from 73 individuals. Differential expression analysis of EC revealed signatures corresponding to endothelial lineage, including panendothelial, panvascular, and subpopulation-specific marker gene sets. Beyond the broad cellular categories of lymphatic, capillary, arterial, and venous ECs, we found previously indistinguishable subpopulations; among venous EC, we identified 2 previously indistinguishable populations: pulmonary–venous ECs (COL15A1neg) localized to the lung parenchyma and systemic–venous ECs (COL15A1pos) localized to the airways and the visceral pleura; among capillary ECs, we confirmed their subclassification into recently discovered aerocytes characterized by EDNRB, SOSTDC1, and TBX2 and general capillary EC. We confirmed that all 6 endothelial cell types, including the systemic–venous ECs and aerocytes, are present in mice and identified endothelial marker genes conserved in humans and mice. Ligand-receptor connectome analysis revealed important homeostatic crosstalk of EC with other lung resident cell types. scRNAseq of commercially available primary lung ECs demonstrated a loss of their native lung phenotype in culture. scRNAseq revealed that endothelial diversity is maintained in pulmonary hypertension. Our article is accompanied by an online data mining tool (www.LungEndothelialCellAtlas.com). Conclusions: Our integrated analysis provides a comprehensive and well-crafted reference atlas of ECs in the normal lung and confirms and describes in detail previously unrecognized endothelial populations across a large number of humans and mice.

Published
2021

23. Ultrawide Field Imaging of Progressive Retinal Arteriovenous Malformation in a Pediatric Patient with Wyburn-Mason Syndrome

Author

Charlene H, Choo, Irena, Tsui, Ronald J, Homer, and Soh Youn, Suh

Subjects
Arteriovenous Malformations, Retinal Artery, Child, Preschool, Neurocutaneous Syndromes, Arteriovenous Fistula, Humans, Female, Child, Hemangioma
Abstract

Wyburn-Mason syndrome (WMS) is a rare congenital disease that presents with unilateral arteriovenous malformation (AVM) in the visual pathway, midbrain, and/or skin. We report a case of a 5-year-old girl with a history of cerebral and orbital AVM who presented with left exotropia and was found to have group 3 retinal AVM consistent with WMS. Here, we use ultrawide field imaging to show the progression of retinal AVM and peripheral nonperfusion areas for a period of 1 year in a pediatric patient with WMS. [ Ophthalmic Surg Lasers Imaging Retina . 2022;53:46–48.]

Published
2022
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24. Model for Evaluating Antimicrobial Therapy To Prevent Life-Threatening Bacterial Infections following Exposure to a Medically Significant Radiation Dose

Author

Andrew J. Phipps, Julie N. Bergmann, Mark T. Albrecht, Vijay K. Singh, and Mary J. Homer

Subjects
Pharmacology, Ertapenem, Enrofloxacin, Linezolid, Granulocyte-Macrophage Colony-Stimulating Factor, Bacterial Infections, Azithromycin, Radiation Dosage, Anti-Bacterial Agents, Infectious Diseases, Acute Radiation Syndrome, Anti-Infective Agents, Granulocyte Colony-Stimulating Factor, Animals, Pharmacology (medical), Experimental Therapeutics, Gentamicins, Cefepime
Abstract

More evidence is needed to support recommendations for medical management of acute radiation syndrome (ARS) and associated infections resulting from a radiological/nuclear event. While current guidelines recommend the administration of antibiotics to chemotherapy patients with febrile neutropenia, the clinical benefit is unclear for acute radiation injury patients. A well-characterized nonhuman primate (NHP) model of hematopoietic ARS was developed that incorporates supportive care postirradiation. This model evaluated the efficacy of myeloid growth factors within 24 to 48 h after total body irradiation (TBI). However, in this model, NHPs continued to develop life-threatening bacterial infections, even when granulocyte colony-stimulating factor or granulocyte-macrophage colony-stimulating factor was administered in combination with antibiotic monotherapy. In this study, we evaluated the efficacy of combination antibiotic therapies administered to NHPs following 7.4-Gy TBI to understand the occurrence of bacterial infection in NHPs with hematopoietic ARS. We compared enrofloxacin-linezolid, enrofloxacin-cefepime, and enrofloxacin-ertapenem to enrofloxacin monotherapy. The primary endpoint was 60-day postirradiation mortality, with secondary endpoints of overall survival time, incidence of bacterial infection, and bacteriologic culture with antimicrobial susceptibility testing. We observed that enrofloxacin-ertapenem significantly increased survival compared to enrofloxacin monotherapy. Bacteria isolated from nonsurviving macaques with systemic bacterial infections exhibited uniform resistance to enrofloxacin and variable resistance to beta-lactam antibiotics, linezolid, gentamicin, and azithromycin. Multidrug antibiotic resistance was observed in Enterococcus spp. and Escherichia coli. We conclude that antibiotic combination therapies appear to be more effective than monotherapy alone but acknowledge that more work is needed to identify an optimal antimicrobial therapy.

Published
2022

26. Sagittal radiographic parameters in the presence of lumbosacral transitional vertebra (LSTV): relationships between measurements using the upper vs lower transitional vertebra

Author

Jonathan N. Sembrano and Cole J. Homer

Subjects
Orthodontics, 030222 orthopedics, medicine.medical_specialty, business.industry, Radiography, Sagittal plane, Vertebra, 03 medical and health sciences, Femoral head, 0302 clinical medicine, medicine.anatomical_structure, Transitional vertebra, Orthopedic surgery, Spinal deformity, Medicine, Orthopedics and Sports Medicine, business, 030217 neurology & neurosurgery, Lumbosacral joint
Abstract

Optimization of spinopelvic sagittal parameters in spinal deformity surgery have been shown to correlate with surgical outcomes. Commonly used parameters include pelvic incidence (PI), lumbar lordosis (LL) and PI–LL mismatch. Presence of lumbosacral transitional vertebra (LSTV) introduces variability regarding which endplate is considered the sacral endplate. This study aimed to determine the mathematical relationships between measurements using the upper transitional vertebra (UTV) versus the lower transitional vertebra (LTV). The property that internal angles of a triangle sum to 180° was used to create a system of equations to resolve the relationship between the PI–LL mismatch of the UTV and of the LTV. The ultimate relationship was employed on a lateral radiograph of a patient with LSTV for validation. It is possible to compute the PI–LL mismatch using either UTV or LTV and convert to the corresponding PI–LL when using the other vertebra simply by measuring one additional angle (PI–LL)L = (PI–LL)U + X. This angle X is defined by segments connecting the center of the femoral head to the midpoints of the superior endplates of the UTV and LTV. Using the LTV yields a larger PI–LL mismatch value. In patients with LSTV, it is controversial whether the UTV or LTV should be used as the sacral endplate for sagittal measurements. With this mathematical relationship, rather than completing two sets of measurements, the surgeon would only need to measure one set and the additional angle X to determine the resultant PI–LL mismatch for the other transitional vertebra.

Published
2021
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27. Genetic Determinants of EGFR-Driven Lung Cancer Growth and Therapeutic Response In Vivo

Author

Dmitri A. Petrov, Jessica A. Hellyer, Jungmin Choi, Giorgia Foggetti, Laura Andrejka, Chuan Li, Scott N. Gettinger, Deborah Ayeni, Hongchen Cai, Stellar Levy, Wen-Yang Lin, Robert J. Homer, Heather A. Wakelee, Nicholas Rashleigh, Katherine Hastings, Maximilian Diehn, Monte M. Winslow, Katerina Politi, Anna Wurtz, and Dylan Maghini

Subjects
Male, 0301 basic medicine, Lung Neoplasms, Tumor suppressor gene, medicine.drug_class, Adenocarcinoma of Lung, Antineoplastic Agents, Biology, Article, Tyrosine-kinase inhibitor, Mice, 03 medical and health sciences, 0302 clinical medicine, In vivo, medicine, Animals, Humans, Osimertinib, Lung cancer, EGFR inhibitors, Acrylamides, Aniline Compounds, medicine.disease, 3. Good health, ErbB Receptors, Disease Models, Animal, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Cancer research, Adenocarcinoma, Female, Tyrosine kinase
Abstract

In lung adenocarcinoma, oncogenic EGFR mutations co-occur with many tumor suppressor gene alterations; however, the extent to which these contribute to tumor growth and response to therapy in vivo remains largely unknown. By quantifying the effects of inactivating 10 putative tumor suppressor genes in a mouse model of EGFR-driven Trp53-deficient lung adenocarcinoma, we found that Apc, Rb1, or Rbm10 inactivation strongly promoted tumor growth. Unexpectedly, inactivation of Lkb1 or Setd2—the strongest drivers of growth in a KRAS-driven model—reduced EGFR-driven tumor growth. These results are consistent with mutational frequencies in human EGFR- and KRAS-driven lung adenocarcinomas. Furthermore, KEAP1 inactivation reduced the sensitivity of EGFR-driven tumors to the EGFR inhibitor osimertinib, and mutations in genes in the KEAP1 pathway were associated with decreased time on tyrosine kinase inhibitor treatment in patients. Our study highlights how the impact of genetic alterations differs across oncogenic contexts and that the fitness landscape shifts upon treatment. Significance: By modeling complex genotypes in vivo, this study reveals key tumor suppressors that constrain the growth of EGFR-mutant tumors. Furthermore, we uncovered that KEAP1 inactivation reduces the sensitivity of these tumors to tyrosine kinase inhibitors. Thus, our approach identifies genotypes of biological and therapeutic importance in this disease. This article is highlighted in the In This Issue feature, p. 1601

Published
2021
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28. The Native American Adoption of Chilies During the 18th Century in Arizona

Author

Robert B. Ciaccio, Michael W. Diehl, J. Homer Thiel, and Deil Lundin

Subjects
Prehistory, Archeology, History, Geography, Paleoethnobotany, Native american, Anthropology, food and beverages, Domestication, Archaeology, Historical archaeology
Abstract

Despite the analyses of thousands of flotation samples from Arizona and New Mexico, domesticated chili peppers are absent in the prehistoric record, and only one specimen of the chiltipine or “wild...

Published
2021
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31. POU2F3 in SCLC: Clinicopathologic and Genomic Analysis With a Focus on Its Diagnostic Utility in Neuroendocrine-Low SCLC

Author

Marina K. Baine, Christopher A. Febres-Aldana, Jason C. Chang, Achim A. Jungbluth, Shenon Sethi, Cristina R. Antonescu, William D. Travis, Min-Shu Hsieh, Mee Sook Roh, Robert J. Homer, Marc Ladanyi, Jacklynn V. Egger, W. Victoria Lai, Charles M. Rudin, and Natasha Rekhtman

Subjects
Pulmonary and Respiratory Medicine, Repressor Proteins, Lung Neoplasms, Oncology, Biomarkers, Tumor, Carcinoma, Large Cell, Humans, Octamer Transcription Factors, Genomics, Small Cell Lung Carcinoma, Carcinoma, Neuroendocrine
Abstract

POU2F3 is a recent marker of a small cell lung carcinoma (SCLC) subtype related to chemosensory tuft cells (SCLC-P). The characteristics of SCLC-P have not been fully defined, and the data on POU2F3 expression in other lung tumors are scarce.We screened 254 SCLC for POU2F3 expression and comprehensively analyzed histopathologic, genomic, and clinical characteristics of POU2F3-positive tumors. We also explored POU2F3 expression in other major lung cancer types (n = 433) and a targeted set of potential diagnostic mimics of SCLC (n = 123).POU2F3 was expressed in 30 of 254 (12%) SCLC and was strongly associated with low expression of standard neuroendocrine markers (synaptophysin, chromogranin A, CD56, INSM1). Notably, POU2F3 was expressed in 75% of SCLC with entirely negative or minimal neuroendocrine marker expression (15/20) and was helpful in supporting the diagnosis of SCLC in such cases. Broad targeted next-generation sequencing revealed that SCLC-P (n = 12) exhibited enrichment in several alterations, including PTEN inactivation, MYC amplifications, and 20q13 amplifications, but similar rates of RB1 and TP53 alterations as other SCLC (n = 155). Beyond SCLC, POU2F3 expression was exclusively limited to large cell neuroendocrine carcinoma (12%) and basaloid squamous cell carcinoma (22%).This is the largest cohort of SCLC-P clinical samples to date, where we describe the diagnostic utility of POU2F3 in a challenging subset of SCLC with low or absent expression of standard neuroendocrine markers. The distinct genomic alterations in SCLC-P may offer a novel avenue for therapeutic targeting. The role of POU2F3 in a narrow subset of other lung cancer types warrants further study.

Published
2022

32. Luminosity determination in pp collisions at $\sqrt{s} = 7$ TeV using the ATLAS detector at the LHC

Author

The ATLAS Collaboration, G. Aad, B. Abbott, J. Abdallah, A. A. Abdelalim, A. Abdesselam, O. Abdinov, B. Abi, M. Abolins, H. Abramowicz, H. Abreu, E. Acerbi, B. S. Acharya, M. Ackers, D. L. Adams, T. N. Addy, J. Adelman, M. Aderholz, S. Adomeit, P. Adragna, T. Adye, S. Aefsky, J. A. Aguilar-Saavedra, M. Aharrouche, S. P. Ahlen, F. Ahles, A. Ahmad, H. Ahmed, M. Ahsan, G. Aielli, T. Akdogan, T. P. A. Åkesson, G. Akimoto, A. V. Akimov, M. S. Alam, M. A. Alam, S. Albrand, M. Aleksa, I. N. Aleksandrov, M. Aleppo, F. Alessandria, C. Alexa, G. Alexander, G. Alexandre, T. Alexopoulos, M. Alhroob, M. Aliev, G. Alimonti, J. Alison, M. Aliyev, P. P. Allport, S. E. Allwood-Spiers, J. Almond, A. Aloisio, R. Alon, A. Alonso, J. Alonso, M. G. Alviggi, K. Amako, P. Amaral, C. Amelung, V. V. Ammosov, A. Amorim, G. Amorós, N. Amram, C. Anastopoulos, T. Andeen, C. F. Anders, K. J. Anderson, A. Andreazza, V. Andrei, M.-L. Andrieux, X. S. Anduaga, A. Angerami, F. Anghinolfi, N. Anjos, A. Annovi, A. Antonaki, M. Antonelli, S. Antonelli, J. Antos, F. Anulli, S. Aoun, L. Aperio Bella, R. Apolle, G. Arabidze, I. Aracena, Y. Arai, A. T. H. Arce, J. P. Archambault, S. Arfaoui, J.-F. Arguin, E. Arik, M. Arik, A. J. Armbruster, K. E. Arms, S. R. Armstrong, O. Arnaez, C. Arnault, A. Artamonov, G. Artoni, D. Arutinov, S. Asai, R. Asfandiyarov, S. Ask, B. Åsman, L. Asquith, K. Assamagan, A. Astbury, A. Astvatsatourov, G. Atoian, B. Aubert, B. Auerbach, E. Auge, K. Augsten, M. Aurousseau, N. Austin, R. Avramidou, D. Axen, C. Ay, G. Azuelos, Y. Azuma, M. A. Baak, G. Baccaglioni, C. Bacci, A. M. Bach, H. Bachacou, K. Bachas, G. Bachy, M. Backes, E. Badescu, P. Bagnaia, S. Bahinipati, Y. Bai, D. C. Bailey, T. Bain, J. T. Baines, O. K. Baker, S. Baker, F. Baltasar Dos Santos Pedrosa, E. Banas, P. Banerjee, Sw. Banerjee, D. Banfi, A. Bangert, V. Bansal, H. S. Bansil, L. Barak, S. P. Baranov, A. Barashkou, A. Barbaro Galtieri, T. Barber, E. L. Barberio, D. Barberis, M. Barbero, D. Y. Bardin, T. Barillari, M. Barisonzi, T. Barklow, N. Barlow, B. M. Barnett, R. M. Barnett, A. Baroncelli, A. J. Barr, F. Barreiro, J. Barreiro Guimar aes da Costa, P. Barrillon, R. Bartoldus, A. E. Barton, D. Bartsch, R. L. Bates, L. Batkova, J. R. Batley, A. Battaglia, M. Battistin, G. Battistoni, F. Bauer, H. S. Bawa, B. Beare, T. Beau, P. H. Beauchemin, R. Beccherle, P. Bechtle, H. P. Beck, M. Beckingham, K. H. Becks, A. J. Beddall, A. Beddall, V. A. Bednyakov, C. Bee, M. Begel, S. Behar Harpaz, P. K. Behera, M. Beimforde, C. Belanger-Champagne, B. Belhorma, P. J. Bell, W. H. Bell, G. Bella, L. Bellagamba, F. Bellina, G. Bellomo, M. Bellomo, A. Belloni, K. Belotskiy, O. Beltramello, S. Ben Ami, O. Benary, D. Benchekroun, C. Benchouk, M. Bendel, B. H. Benedict, N. Benekos, Y. Benhammou, D. P. Benjamin, M. Benoit, J. R. Bensinger, K. Benslama, S. Bentvelsen, D. Berge, E. Bergeaas Kuutmann, N. Berger, F. Berghaus, E. Berglund, J. Beringer, K. Bernardet, P. Bernat, R. Bernhard, C. Bernius, T. Berry, A. Bertin, F. Bertinelli, F. Bertolucci, M. I. Besana, N. Besson, S. Bethke, W. Bhimji, R. M. Bianchi, M. Bianco, O. Biebel, J. Biesiada, M. Biglietti, H. Bilokon, M. Bindi, A. Bingul, C. Bini, C. Biscarat, R. Bischof, U. Bitenc, K. M. Black, R. E. Blair, J.-B. Blanchard, G. Blanchot, C. Blocker, J. Blocki, A. Blondel, W. Blum, U. Blumenschein, C. Boaretto, G. J. Bobbink, V. B. Bobrovnikov, A. Bocci, R. Bock, C. R. Boddy, M. Boehler, J. Boek, N. Boelaert, S. Böser, J. A. Bogaerts, A. Bogdanchikov, A. Bogouch, C. Bohm, V. Boisvert, T. Bold, V. Boldea, M. Boonekamp, G. Boorman, C. N. Booth, P. Booth, J. R. A. Booth, S. Bordoni, C. Borer, A. Borisov, G. Borissov, I. Borjanovic, S. Borroni, K. Bos, D. Boscherini, M. Bosman, H. Boterenbrood, D. Botterill, J. Bouchami, J. Boudreau, E. V. Bouhova-Thacker, C. Boulahouache, C. Bourdarios, N. Bousson, A. Boveia, J. Boyd, I. R. Boyko, N. I. Bozhko, I. Bozovic-Jelisavcic, S. Braccini, J. Bracinik, A. Braem, E. Brambilla, P. Branchini, G. W. Brandenburg, A. Brandt, G. Brandt, O. Brandt, U. Bratzler, B. Brau, J. E. Brau, H. M. Braun, B. Brelier, J. Bremer, R. Brenner, S. Bressler, D. Breton, N. D. Brett, P. G. Bright-Thomas, D. Britton, F. M. Brochu, I. Brock, R. Brock, T. J. Brodbeck, E. Brodet, F. Broggi, C. Bromberg, G. Brooijmans, W. K. Brooks, G. Brown, E. Brubaker, P. A. Bruckman de Renstrom, D. Bruncko, R. Bruneliere, S. Brunet, A. Bruni, G. Bruni, M. Bruschi, T. Buanes, F. Bucci, J. Buchanan, N. J. Buchanan, P. Buchholz, R. M. Buckingham, A. G. Buckley, S. I. Buda, I. A. Budagov, B. Budick, V. Büscher, L. Bugge, D. Buira-Clark, E. J. Buis, O. Bulekov, M. Bunse, T. Buran, H. Burckhart, S. Burdin, T. Burgess, S. Burke, E. Busato, P. Bussey, C. P. Buszello, F. Butin, B. Butler, J. M. Butler, C. M. Buttar, J. M. Butterworth, W. Buttinger, T. Byatt, S. Cabrera Urbán, M. Caccia, D. Caforio, O. Cakir, P. Calafiura, G. Calderini, P. Calfayan, R. Calkins, L. P. Caloba, R. Caloi, D. Calvet, S. Calvet, A. Camard, P. Camarri, M. Cambiaghi, D. Cameron, J. Cammin, S. Campana, M. Campanelli, V. Canale, F. Canelli, A. Canepa, J. Cantero, L. Capasso, M. D. M. Capeans Garrido, I. Caprini, M. Caprini, M. Caprio, D. Capriotti, M. Capua, R. Caputo, C. Caramarcu, R. Cardarelli, T. Carli, G. Carlino, L. Carminati, B. Caron, S. Caron, C. Carpentieri, G. D. Carrillo Montoya, S. Carron Montero, A. A. Carter, J. R. Carter, J. Carvalho, D. Casadei, M. P. Casado, M. Cascella, C. Caso, A. M. Castaneda Hernandez, E. Castaneda-Miranda, V. Castillo Gimenez, N. F. Castro, G. Cataldi, F. Cataneo, A. Catinaccio, J. R. Catmore, A. Cattai, G. Cattani, S. Caughron, A. Cavallari, P. Cavalleri, D. Cavalli, M. Cavalli-Sforza, V. Cavasinni, A. Cazzato, F. Ceradini, C. Cerna, A. S. Cerqueira, A. Cerri, L. Cerrito, F. Cerutti, M. Cervetto, S. A. Cetin, F. Cevenini, A. Chafaq, D. Chakraborty, K. Chan, B. Chapleau, J. D. Chapman, J. W. Chapman, E. Chareyre, D. G. Charlton, V. Chavda, S. Cheatham, S. Chekanov, S. V. Chekulaev, G. A. Chelkov, H. Chen, L. Chen, S. Chen, T. Chen, X. Chen, S. Cheng, A. Cheplakov, V. F. Chepurnov, R. Cherkaoui El Moursli, V. Chernyatin, E. Cheu, S. L. Cheung, L. Chevalier, F. Chevallier, G. Chiefari, L. Chikovani, J. T. Childers, A. Chilingarov, G. Chiodini, M. V. Chizhov, G. Choudalakis, S. Chouridou, I. A. Christidi, A. Christov, D. Chromek-Burckhart, M. L. Chu, J. Chudoba, G. Ciapetti, A. K. Ciftci, R. Ciftci, D. Cinca, V. Cindro, M. D. Ciobotaru, C. Ciocca, A. Ciocio, M. Cirilli, A. Clark, P. J. Clark, W. Cleland, J. C. Clemens, B. Clement, C. Clement, R. W. Clifft, Y. Coadou, M. Cobal, A. Coccaro, J. Cochran, P. Coe, J. G. Cogan, J. Coggeshall, E. Cogneras, C. D. Cojocaru, J. Colas, A. P. Colijn, C. Collard, N. J. Collins, C. Collins-Tooth, J. Collot, G. Colon, R. Coluccia, G. Comune, P. Conde Mui no, E. Coniavitis, M. C. Conidi, M. Consonni, S. Constantinescu, C. Conta, F. Conventi, J. Cook, M. Cooke, B. D. Cooper, A. M. Cooper-Sarkar, N. J. Cooper-Smith, K. Copic, T. Cornelissen, M. Corradi, S. Correard, F. Corriveau, A. Cortes-Gonzalez, G. Cortiana, G. Costa, M. J. Costa, D. Costanzo, T. Costin, D. Côté, R. Coura Torres, L. Courneyea, G. Cowan, C. Cowden, B. E. Cox, K. Cranmer, M. Cristinziani, G. Crosetti, R. Crupi, S. Crépé-Renaudin, C. Cuenca Almenar, T. Cuhadar Donszelmann, S. Cuneo, M. Curatolo, C. J. Curtis, P. Cwetanski, H. Czirr, Z. Czyczula, S. D’Auria, M. D’Onofrio, A. D’Orazio, A. Da Rocha Gesualdi Mello, P. V. M. Da Silva, C. Da Via, W. Dabrowski, A. Dahlhoff, T. Dai, C. Dallapiccola, S. J. Dallison, M. Dam, M. Dameri, D. S. Damiani, H. O. Danielsson, R. Dankers, D. Dannheim, V. Dao, G. Darbo, G. L. Darlea, C. Daum, J. P. Dauvergne, W. Davey, T. Davidek, N. Davidson, R. Davidson, M. Davies, A. R. Davison, E. Dawe, I. Dawson, J. W. Dawson, R. K. Daya, K. De, R. de Asmundis, S. De Castro, S. De Cecco, J. de Graat, N. De Groot, P. de Jong, E. De La Cruz-Burelo, C. De La Taille, B. De Lotto, L. De Mora, L. De Nooij, M. De Oliveira Branco, D. De Pedis, P. de Saintignon, A. De Salvo, U. De Sanctis, A. De Santo, J. B. De Vivie De Regie, S. Dean, G. Dedes, D. V. Dedovich, J. Degenhardt, M. Dehchar, M. Deile, C. Del Papa, J. Del Peso, T. Del Prete, A. Dell’Acqua, L. Dell’Asta, M. Della Pietra, D. della Volpe, M. Delmastro, P. Delpierre, N. Delruelle, P. A. Delsart, C. Deluca, S. Demers, M. Demichev, B. Demirkoz, J. Deng, S. P. Denisov, C. Dennis, D. Derendarz, J. E. Derkaoui, F. Derue, P. Dervan, K. Desch, E. Devetak, P. O. Deviveiros, A. Dewhurst, B. DeWilde, S. Dhaliwal, R. Dhullipudi, A. Di Ciaccio, L. Di Ciaccio, A. Di Girolamo, B. Di Girolamo, S. Di Luise, A. Di Mattia, R. Di Nardo, A. Di Simone, R. Di Sipio, M. A. Diaz, M. M. Diaz Gomez, F. Diblen, E. B. Diehl, H. Dietl, J. Dietrich, T. A. Dietzsch, S. Diglio, K. Dindar Yagci, J. Dingfelder, C. Dionisi, P. Dita, S. Dita, F. Dittus, F. Djama, R. Djilkibaev, T. Djobava, M. A. B. do Vale, A. Do Valle Wemans, T. K. O. Doan, M. Dobbs, R. Dobinson, D. Dobos, E. Dobson, M. Dobson, J. Dodd, O. B. Dogan, C. Doglioni, T. Doherty, Y. Doi, J. Dolejsi, I. Dolenc, Z. Dolezal, B. A. Dolgoshein, T. Dohmae, M. Donadelli, M. Donega, J. Donini, J. Dopke, A. Doria, A. Dos Anjos, M. Dosil, A. Dotti, M. T. Dova, J. D. Dowell, A. D. Doxiadis, A. T. Doyle, Z. Drasal, J. Drees, N. Dressnandt, H. Drevermann, C. Driouichi, M. Dris, J. G. Drohan, J. Dubbert, T. Dubbs, S. Dube, E. Duchovni, G. Duckeck, A. Dudarev, F. Dudziak, M. Dührssen, I. P. Duerdoth, L. Duflot, M.-A. Dufour, M. Dunford, H. Duran Yildiz, R. Duxfield, M. Dwuznik, F. Dydak, D. Dzahini, M. Düren, J. Ebke, S. Eckert, S. Eckweiler, K. Edmonds, C. A. Edwards, I. Efthymiopoulos, W. Ehrenfeld, T. Ehrich, T. Eifert, G. Eigen, K. Einsweiler, E. Eisenhandler, T. Ekelof, M. El Kacimi, M. Ellert, S. Elles, F. Ellinghaus, K. Ellis, N. Ellis, J. Elmsheuser, M. Elsing, R. Ely, D. Emeliyanov, R. Engelmann, A. Engl, B. Epp, A. Eppig, J. Erdmann, A. Ereditato, D. Eriksson, J. Ernst, M. Ernst, J. Ernwein, D. Errede, S. Errede, E. Ertel, M. Escalier, C. Escobar, X. Espinal Curull, B. Esposito, F. Etienne, A. I. Etienvre, E. Etzion, D. Evangelakou, H. Evans, L. Fabbri, C. Fabre, K. Facius, R. M. Fakhrutdinov, S. Falciano, A. C. Falou, Y. Fang, M. Fanti, A. Farbin, A. Farilla, J. Farley, T. Farooque, S. M. Farrington, P. Farthouat, D. Fasching, P. Fassnacht, D. Fassouliotis, B. Fatholahzadeh, L. Fayard, S. Fazio, R. Febbraro, P. Federic, O. L. Fedin, I. Fedorko, W. Fedorko, M. Fehling-Kaschek, L. Feligioni, D. Fellmann, C. U. Felzmann, C. Feng, E. J. Feng, A. B. Fenyuk, J. Ferencei, D. Ferguson, J. Ferland, B. Fernandes, W. Fernando, S. Ferrag, J. Ferrando, V. Ferrara, A. Ferrari, P. Ferrari, R. Ferrari, A. Ferrer, M. L. Ferrer, D. Ferrere, C. Ferretti, A. Ferretto Parodi, F. Ferro, M. Fiascaris, F. Fiedler, A. Filipčič, A. Filippas, F. Filthaut, M. Fincke-Keeler, M. C. N. Fiolhais, L. Fiorini, A. Firan, G. Fischer, P. Fischer, M. J. Fisher, S. M. Fisher, J. Flammer, M. 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Pilcher, A. D. Pilkington, J. Pina, M. Pinamonti, A. Pinder, J. L. Pinfold, J. Ping, B. Pinto, O. Pirotte, C. Pizio, R. Placakyte, M. Plamondon, W. G. Plano, M.-A. Pleier, A. V. Pleskach, A. Poblaguev, S. Poddar, F. Podlyski, L. Poggioli, T. Poghosyan, M. Pohl, F. Polci, G. Polesello, A. Policicchio, A. Polini, J. Poll, V. Polychronakos, D. M. Pomarede, D. Pomeroy, K. Pommès, L. Pontecorvo, B. G. Pope, G. A. Popeneciu, D. S. Popovic, A. Poppleton, X. Portell Bueso, R. Porter, C. Posch, G. E. Pospelov, S. Pospisil, I. N. Potrap, C. J. Potter, C. T. Potter, G. Poulard, J. Poveda, R. Prabhu, P. Pralavorio, S. Prasad, R. Pravahan, S. Prell, K. Pretzl, L. Pribyl, D. Price, L. E. Price, M. J. Price, P. M. Prichard, D. Prieur, M. Primavera, K. Prokofiev, F. Prokoshin, S. Protopopescu, J. Proudfoot, X. Prudent, H. Przysiezniak, S. Psoroulas, E. Ptacek, J. Purdham, M. Purohit, P. Puzo, Y. Pylypchenko, J. Qian, Z. Qian, Z. Qin, A. Quadt, D. R. Quarrie, W. B. Quayle, F. Quinonez, M. Raas, V. Radescu, B. Radics, T. Rador, F. Ragusa, G. Rahal, A. M. Rahimi, S. Rajagopalan, S. Rajek, M. Rammensee, M. Rammes, M. Ramstedt, K. Randrianarivony, P. N. Ratoff, F. Rauscher, E. Rauter, M. Raymond, A. L. Read, D. M. Rebuzzi, A. Redelbach, G. Redlinger, R. Reece, K. Reeves, A. Reichold, E. Reinherz-Aronis, A. Reinsch, I. Reisinger, D. Reljic, C. Rembser, Z. L. Ren, A. Renaud, P. Renkel, B. Rensch, M. Rescigno, S. Resconi, B. Resende, P. Reznicek, R. Rezvani, A. Richards, R. Richter, E. Richter-Was, M. Ridel, S. Rieke, M. Rijpstra, M. Rijssenbeek, A. Rimoldi, L. Rinaldi, R. R. Rios, I. Riu, G. Rivoltella, F. Rizatdinova, E. Rizvi, S. H. Robertson, A. Robichaud-Veronneau, D. Robinson, J. E. M. Robinson, M. Robinson, A. Robson, J. G. Rocha de Lima, C. Roda, D. Roda Dos Santos, S. Rodier, D. Rodriguez, Y. Rodriguez Garcia, A. Roe, S. Roe, O. Røhne, V. Rojo, S. Rolli, A. Romaniouk, V. M. Romanov, G. Romeo, D. Romero Maltrana, L. Roos, E. Ros, S. Rosati, M. Rose, G. A. Rosenbaum, E. I. Rosenberg, P. L. Rosendahl, L. Rosselet, V. Rossetti, E. Rossi, L. P. Rossi, L. Rossi, M. Rotaru, I. Roth, J. Rothberg, I. Rottländer, D. Rousseau, C. R. Royon, A. Rozanov, Y. Rozen, X. Ruan, I. Rubinskiy, B. Ruckert, N. Ruckstuhl, V. I. Rud, G. Rudolph, F. Rühr, A. Ruiz-Martinez, E. Rulikowska-Zarebska, V. Rumiantsev, L. Rumyantsev, K. Runge, O. Runolfsson, Z. Rurikova, N. A. Rusakovich, D. R. Rust, J. P. Rutherfoord, C. Ruwiedel, P. Ruzicka, Y. F. Ryabov, V. Ryadovikov, P. Ryan, M. Rybar, G. Rybkin, N. C. Ryder, S. Rzaeva, A. F. Saavedra, I. Sadeh, H. F.-W. Sadrozinski, R. Sadykov, F. Safai Tehrani, H. Sakamoto, G. Salamanna, A. Salamon, M. Saleem, D. Salihagic, A. Salnikov, J. Salt, B. M. Salvachua Ferrando, D. Salvatore, F. Salvatore, A. Salzburger, D. Sampsonidis, B. H. Samset, H. Sandaker, H. G. Sander, M. P. Sanders, M. Sandhoff, P. Sandhu, T. Sandoval, R. Sandstroem, S. Sandvoss, D. P. C. Sankey, A. Sansoni, C. Santamarina Rios, C. Santoni, R. Santonico, H. Santos, J. G. Saraiva, T. Sarangi, E. Sarkisyan-Grinbaum, F. Sarri, G. Sartisohn, O. Sasaki, T. Sasaki, N. Sasao, I. Satsounkevitch, G. Sauvage, J. B. Sauvan, P. Savard, V. Savinov, P. Savva, L. Sawyer, D. H. Saxon, L. P. Says, C. Sbarra, A. Sbrizzi, O. Scallon, D. A. Scannicchio, J. Schaarschmidt, P. Schacht, U. Schäfer, S. Schaetzel, A. C. Schaffer, D. Schaile, R. D. Schamberger, A. G. Schamov, V. Scharf, V. A. Schegelsky, D. Scheirich, M. I. Scherzer, C. Schiavi, J. Schieck, M. Schioppa, S. Schlenker, J. L. Schlereth, E. Schmidt, M. P. Schmidt, K. Schmieden, C. Schmitt, M. Schmitz, A. Schöning, M. Schott, D. Schouten, J. Schovancova, M. Schram, A. Schreiner, C. Schroeder, N. Schroer, S. Schuh, G. Schuler, J. Schultes, H.-C. Schultz-Coulon, H. Schulz, J. W. Schumacher, M. Schumacher, B. A. Schumm, Ph. Schune, C. Schwanenberger, A. Schwartzman, D. Schweiger, Ph. Schwemling, R. Schwienhorst, R. Schwierz, J. Schwindling, W. G. Scott, J. Searcy, E. Sedykh, E. Segura, S. C. Seidel, A. Seiden, F. Seifert, J. M. Seixas, G. Sekhniaidze, D. M. Seliverstov, B. Sellden, G. Sellers, M. Seman, N. Semprini-Cesari, C. Serfon, L. Serin, R. Seuster, H. Severini, M. E. Sevior, A. Sfyrla, E. Shabalina, M. Shamim, L. Y. Shan, J. T. Shank, Q. T. Shao, M. Shapiro, P. B. Shatalov, L. Shaver, C. Shaw, K. Shaw, D. Sherman, P. Sherwood, A. Shibata, S. Shimizu, M. Shimojima, T. Shin, A. Shmeleva, M. J. Shochet, D. Short, M. A. Shupe, P. Sicho, A. Sidoti, A. Siebel, F. Siegert, J. Siegrist, Dj. Sijacki, O. Silbert, J. Silva, Y. Silver, D. Silverstein, S. B. Silverstein, V. Simak, Lj. Simic, S. Simion, B. Simmons, M. Simonyan, P. Sinervo, N. B. Sinev, V. Sipica, G. Siragusa, A. N. Sisakyan, S. Yu. Sivoklokov, J. Sjölin, T. B. Sjursen, L. A. Skinnari, K. Skovpen, P. Skubic, N. Skvorodnev, M. Slater, T. Slavicek, K. Sliwa, T. J. Sloan, J. Sloper, V. Smakhtin, S. Yu. Smirnov, L. N. Smirnova, O. Smirnova, B. C. Smith, D. Smith, K. M. Smith, M. Smizanska, K. Smolek, A. A. Snesarev, S. W. Snow, J. Snow, J. Snuverink, S. Snyder, M. Soares, R. Sobie, J. Sodomka, A. Soffer, C. A. Solans, M. Solar, J. Solc, U. Soldevila, E. Solfaroli Camillocci, A. A. Solodkov, O. V. Solovyanov, J. Sondericker, N. Soni, V. Sopko, B. Sopko, M. Sorbi, M. Sosebee, A. Soukharev, S. Spagnolo, F. Spanò, R. Spighi, G. Spigo, F. Spila, E. Spiriti, R. Spiwoks, M. Spousta, T. Spreitzer, B. Spurlock, R. D. St. Denis, T. Stahl, J. Stahlman, R. Stamen, E. Stanecka, R. W. Stanek, C. Stanescu, S. Stapnes, E. A. Starchenko, J. Stark, P. Staroba, P. Starovoitov, A. Staude, P. Stavina, G. Stavropoulos, G. Steele, E. Stefanidis, P. Steinbach, P. Steinberg, I. Stekl, B. Stelzer, H. J. Stelzer, O. Stelzer-Chilton, H. Stenzel, K. Stevenson, G. A. Stewart, T. Stockmanns, M. C. Stockton, M. Stodulski, K. Stoerig, G. Stoicea, S. Stonjek, P. Strachota, A. R. Stradling, A. Straessner, J. Strandberg, S. Strandberg, A. Strandlie, M. Strang, E. Strauss, M. Strauss, P. Strizenec, R. Ströhmer, D. M. Strom, J. A. Strong, R. Stroynowski, J. Strube, B. Stugu, I. Stumer, J. Stupak, P. Sturm, D. A. Soh, D. Su, S. Subramania, Y. Sugaya, T. Sugimoto, C. Suhr, K. Suita, M. Suk, V. V. Sulin, S. Sultansoy, T. Sumida, X. Sun, J. E. Sundermann, K. Suruliz, S. Sushkov, G. Susinno, M. R. Sutton, Y. Suzuki, Yu. M. Sviridov, S. Swedish, I. Sykora, T. Sykora, B. Szeless, J. Sánchez, D. Ta, K. Tackmann, A. Taffard, R. Tafirout, A. Taga, N. Taiblum, Y. Takahashi, H. Takai, R. Takashima, H. Takeda, T. Takeshita, M. Talby, A. Talyshev, M. C. Tamsett, J. Tanaka, R. Tanaka, S. Tanaka, Y. Tanaka, K. Tani, N. Tannoury, G. P. Tappern, S. Tapprogge, D. Tardif, S. Tarem, F. Tarrade, G. F. Tartarelli, P. Tas, M. Tasevsky, E. Tassi, M. Tatarkhanov, C. Taylor, F. E. Taylor, G. Taylor, G. N. Taylor, W. Taylor, M. Teixeira Dias Castanheira, P. Teixeira-Dias, K. K. Temming, H. Ten Kate, P. K. Teng, Y. D. Tennenbaum-Katan, S. Terada, K. Terashi, J. Terron, M. Terwort, M. Testa, R. J. Teuscher, C. M. Tevlin, J. Thadome, J. Therhaag, T. Theveneaux-Pelzer, M. Thioye, S. Thoma, J. P. Thomas, E. N. Thompson, P. D. Thompson, A. S. Thompson, E. Thomson, M. Thomson, R. P. Thun, T. Tic, V. O. Tikhomirov, Y. A. Tikhonov, C. J. W. P. Timmermans, P. Tipton, F. J. Tique Aires Viegas, S. Tisserant, J. Tobias, B. Toczek, T. Todorov, S. Todorova-Nova, B. Toggerson, J. Tojo, S. Tokár, K. Tokunaga, K. Tokushuku, K. Tollefson, M. Tomoto, L. Tompkins, K. Toms, A. Tonazzo, G. Tong, A. Tonoyan, C. Topfel, N. D. Topilin, I. Torchiani, E. Torrence, E. Torró Pastor, J. Toth, F. Touchard, D. R. Tovey, D. Traynor, T. Trefzger, J. Treis, L. Tremblet, A. Tricoli, I. M. Trigger, S. Trincaz-Duvoid, T. N. Trinh, M. F. Tripiana, N. Triplett, W. Trischuk, A. Trivedi, B. Trocmé, C. Troncon, M. Trottier-McDonald, A. Trzupek, C. Tsarouchas, J. C.-L. Tseng, M. Tsiakiris, P. V. Tsiareshka, D. Tsionou, G. Tsipolitis, V. Tsiskaridze, E. G. Tskhadadze, I. I. Tsukerman, V. Tsulaia, J.-W. Tsung, S. Tsuno, D. Tsybychev, A. Tua, J. M. Tuggle, M. Turala, D. Turecek, I. Turk Cakir, E. Turlay, P. M. Tuts, A. Tykhonov, M. Tylmad, M. Tyndel, D. Typaldos, H. Tyrvainen, G. Tzanakos, K. Uchida, I. Ueda, R. Ueno, M. Ugland, M. Uhlenbrock, M. Uhrmacher, F. Ukegawa, G. Unal, D. G. Underwood, A. Undrus, G. Unel, Y. Unno, D. Urbaniec, E. Urkovsky, P. Urquijo, P. Urrejola, G. Usai, M. Uslenghi, L. Vacavant, V. Vacek, B. Vachon, S. Vahsen, C. Valderanis, J. Valenta, P. Valente, S. Valentinetti, S. Valkar, E. Valladolid Gallego, S. Vallecorsa, J. A. Valls Ferrer, H. van der Graaf, E. van der Kraaij, E. van der Poel, D. van der Ster, B. Van Eijk, N. van Eldik, P. van Gemmeren, Z. van Kesteren, I. van Vulpen, W. Vandelli, G. Vandoni, A. Vaniachine, P. Vankov, F. Vannucci, F. VarelaRodriguez, R. Vari, E. W. Varnes, D. Varouchas, A. Vartapetian, K. E. Varvell, V. I. Vassilakopoulos, F. Vazeille, G. Vegni, J. J. Veillet, C. Vellidis, F. Veloso, R. Veness, S. Veneziano, A. Ventura, D. Ventura, S. Ventura, M. Venturi, N. Venturi, V. Vercesi, M. Verducci, W. Verkerke, J. C. Vermeulen, L. Vertogardov, A. Vest, M. C. Vetterli, I. Vichou, T. Vickey, G. H. A. Viehhauser, S. Viel, M. Villa, M. Villaplana Perez, E. Vilucchi, M. G. Vincter, E. Vinek, V. B. Vinogradov, M. Virchaux, S. Viret, J. Virzi, A. Vitale, O. Vitells, I. Vivarelli, F. Vives Vaque, S. Vlachos, M. Vlasak, N. Vlasov, A. Vogel, P. Vokac, M. Volpi, G. Volpini, H. von der Schmitt, J. von Loeben, H. von Radziewski, E. von Toerne, V. Vorobel, A. P. Vorobiev, V. Vorwerk, M. Vos, R. Voss, T. T. Voss, J. H. Vossebeld, A. S. Vovenko, N. Vranjes, M. Vranjes Milosavljevic, V. Vrba, M. Vreeswijk, T. Vu Anh, R. Vuillermet, I. Vukotic, W. Wagner, P. Wagner, H. Wahlen, J. Wakabayashi, J. Walbersloh, S. Walch, J. Walder, R. Walker, W. Walkowiak, R. Wall, P. Waller, C. Wang, H. Wang, J. Wang, J. C. Wang, S. M. Wang, A. Warburton, C. P. Ward, M. Warsinsky, P. M. Watkins, A. T. Watson, M. F. Watson, G. Watts, S. Watts, A. T. Waugh, B. M. Waugh, J. Weber, M. Weber, M. S. Weber, P. Weber, A. R. Weidberg, J. Weingarten, C. Weiser, H. Wellenstein, P. S. Wells, M. Wen, T. Wenaus, S. Wendler, Z. Weng, T. Wengler, S. Wenig, N. Wermes, M. Werner, P. Werner, M. Werth, M. Wessels, K. Whalen, S. J. Wheeler-Ellis, S. P. Whitaker, A. White, M. J. White, S. R. Whitehead, D. Whiteson, D. Whittington, F. Wicek, D. Wicke, F. J. Wickens, W. Wiedenmann, M. Wielers, P. Wienemann, C. Wiglesworth, L. A. M. Wiik, A. Wildauer, M. A. Wildt, I. Wilhelm, H. G. Wilkens, J. Z. Will, E. Williams, H. H. Williams, W. Willis, S. Willocq, J. A. Wilson, M. G. Wilson, A. Wilson, I. Wingerter-Seez, S. Winkelmann, F. Winklmeier, M. Wittgen, M. W. Wolter, H. Wolters, G. Wooden, B. K. Wosiek, J. Wotschack, M. J. Woudstra, K. Wraight, C. Wright, B. Wrona, S. L. Wu, X. Wu, Y. Wu, E. Wulf, R. Wunstorf, B. M. Wynne, L. Xaplanteris, S. Xella, S. Xie, Y. Xie, C. Xu, D. Xu, G. Xu, B. Yabsley, M. Yamada, A. Yamamoto, K. Yamamoto, S. Yamamoto, T. Yamamura, J. Yamaoka, T. Yamazaki, Y. Yamazaki, Z. Yan, H. Yang, S. Yang, U. K. Yang, Y. Yang, Z. Yang, S. Yanush, W.-M. Yao, Y. Yao, Y. Yasu, J. Ye, S. Ye, M. Yilmaz, R. Yoosoofmiya, K. Yorita, R. Yoshida, C. Young, S. Youssef, D. Yu, J. Yu, L. Yuan, A. Yurkewicz, V. G. Zaets, R. Zaidan, A. M. Zaitsev, Z. Zajacova, Yo. K. Zalite, L. Zanello, P. Zarzhitsky, A. Zaytsev, M. Zdrazil, C. Zeitnitz, M. Zeller, P. F. Zema, A. Zemla, C. Zendler, A. V. Zenin, O. Zenin, T. Ženiš, Z. Zenonos, S. Zenz, D. Zerwas, G. Zevi della Porta, Z. Zhan, D. Zhang, H. Zhang, J. Zhang, X. Zhang, Z. Zhang, L. Zhao, T. Zhao, Z. Zhao, A. Zhemchugov, S. Zheng, J. Zhong, B. Zhou, N. Zhou, Y. Zhou, C. G. Zhu, H. Zhu, Y. Zhu, X. Zhuang, V. Zhuravlov, D. Zieminska, B. Zilka, R. Zimmermann, S. Zimmermann, M. Ziolkowski, R. Zitoun, L. Živković, V. V. Zmouchko, G. Zobernig, A. Zoccoli, Y. Zolnierowski, A. Zsenei, M. zur Nedden, V. Zutshi, and L. Zwalinski

Subjects
Astrophysics, QB460-466, Nuclear and particle physics. Atomic energy. Radioactivity, QC770-798
Abstract

Abstract Measurements of luminosity obtained using the ATLAS detector during early running of the Large Hadron Collider (LHC) at $\sqrt{s} = 7$ TeV are presented. The luminosity is independently determined using several detectors and multiple algorithms, each having different acceptances, systematic uncertainties and sensitivity to background. The ratios of the luminosities obtained from these methods are monitored as a function of time and of μ, the average number of inelastic interactions per bunch crossing. Residual time- and μ-dependence between the methods is less than 2% for 0

Published
2011
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33. Inhalable polymer nanoparticles for versatile mRNA delivery and mucosal vaccination

Author

Alexandra Suberi, Molly K. Grun, Tianyang Mao, Benjamin Israelow, Melanie Reschke, Julian Grundler, Laiba Akhtar, Teresa Lee, Kwangsoo Shin, Alexandra S. Piotrowski-Daspit, Robert J. Homer, Akiko Iwasaki, Hee Won Suh, and W. Mark Saltzman

Subjects
respiratory system, Article
Abstract

An inhalable platform for mRNA therapeutics would enable minimally invasive and lung targeted delivery for a host of pulmonary diseases. Development of lung targeted mRNA therapeutics has been limited by poor transfection efficiency and risk of vehicle-induced pathology. Here we report an inhalable polymer-based vehicle for delivery of therapeutic mRNAs to the lung. We optimized biodegradable poly(amine-co-ester) polyplexes for mRNA delivery using end group modifications and polyethylene glycol. Our polyplexes achieved high transfection of mRNA throughout the lung, particularly in epithelial and antigen-presenting cells. We applied this technology to develop a mucosal vaccine for SARS-CoV-2. Intranasal vaccination with spike protein mRNA polyplexes induced potent cellular and humoral adaptive immunity and protected K18-hACE2 mice from lethal viral challenge.One-sentence summaryInhaled polymer nanoparticles (NPs) achieve high mRNA expression in the lung and induce protective immunity against SARS-CoV-2.

Published
2022
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34. Unadjuvanted intranasal spike vaccine booster elicits robust protective mucosal immunity against sarbecoviruses

Author

Tianyang Mao, Benjamin Israelow, Alexandra Suberi, Liqun Zhou, Melanie Reschke, Mario A Peña-Hernández, Huiping Dong, Robert J. Homer, W. Mark Saltzman, and Akiko Iwasaki

Subjects
bacteria, biochemical phenomena, metabolism, and nutrition, Article
Abstract

As the SARS-CoV-2 pandemic enters its third year, vaccines that not only prevent disease, but also prevent transmission are needed to help reduce global disease burden. Currently approved parenteral vaccines induce robust systemic immunity, but poor immunity at the respiratory mucosa. Here we describe the development of a novel vaccine strategy, Prime and Spike, based on unadjuvanted intranasal spike boosting that leverages existing immunity generated by primary vaccination to elicit mucosal immune memory within the respiratory tract. We show that Prime and Spike induces robust T resident memory cells, B resident memory cells and IgA at the respiratory mucosa, boosts systemic immunity, and completely protects mice with partial immunity from lethal SARS-CoV-2 infection. Using divergent spike proteins, Prime and Spike enables induction of cross-reactive immunity against sarbecoviruses without invoking original antigenic sin.One-sentence summaryBroad sarbecovirus protective mucosal immunity is generated by unadjuvanted intranasal spike boost in preclinical model.

Published
2022

35. Role of Nitric Oxide Isoforms in Vascular and Alveolar Development and Lung Injury in Vascular Endothelial Growth Factor Overexpressing Neonatal Mice Lungs.

Author

Mansoor A Syed, Rayman Choo-Wing, Robert J Homer, and Vineet Bhandari

Subjects
Medicine, Science
Abstract

The role of vascular endothelial growth factor (VEGF)-induced 3 different nitric oxide synthase (NOS) isoforms in lung development and injury in the newborn (NB) lung are not known. We hypothesized that VEGF-induced specific NOS pathways are critical regulators of lung development and injury.We studied NB wild type (WT), lung epithelial cell-targeted VEGF165 doxycycline-inducible overexpressing transgenic (VEGFTG), VEGFTG treated with a NOS1 inhibitor (L-NIO), VEGFTG x NOS2-/- and VEGFTG x NOS3+/- mice in room air (RA) for 7 postnatal (PN) days. Lung morphometry (chord length), vascular markers (Ang1, Ang2, Notch2, vWF, CD31 and VE-cadherin), cell proliferation (Ki67), vascular permeability, injury and oxidative stress markers (hemosiderin, nitrotyrosine and 8-OHdG) were evaluated.VEGF overexpression in RA led to increased chord length and vascular markers at PN7, which were significantly decreased to control values in VEGFTG x NOS2-/- and VEGFTG x NOS3+/- lungs. However, we found no noticeable effect on chord length and vascular markers in the VEGFTG / NOS1 inhibited group. In the NB VEGFTG mouse model, we found VEGF-induced vascular permeability in the NB murine lung was partially dependent on NOS2 and NOS3-signaling pathways. In addition, the inhibition of NOS2 and NOS3 resulted in a significant decrease in VEGF-induced hemosiderin, nitrotyrosine- and 8-OHdG positive cells at PN7. NOS1 inhibition had no significant effect.Our data showed that the complete absence of NOS2 and partial deficiency of NOS3 confers protection against VEGF-induced pathologic lung vascular and alveolar developmental changes, as well as injury markers. Inhibition of NOS1 does not have any modulating role on VEGF-induced changes in the NB lung. Overall, our data suggests that there is a significant differential regulation in the NOS-mediated effects of VEGF overexpression in the developing mouse lung.

Published
2016
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36. A Coaching Model to Promote Economic Mobility and Child Developmental Outcomes

Author

Charles J. Homer, Ashley Winning, and Kevin Cummings

Subjects
Adult, Employment, Parents, Washington, Psychosocial Support Systems, Mentoring, Articles, Career Mobility, Executive Function, Child Development, Pediatrics, Perinatology and Child Health, Humans, Child, Poverty
Abstract

OBJECTIVES Children growing up in poverty experience worse developmental outcomes than their more economically advantaged peers. Whether Mobility Mentoring, a program focused on building parent executive function to promote economic mobility, results in improved child developmental outcomes is not known. METHODS This study population was drawn from children enrolled in Washington State’s public, income-qualified prekindergarten program and their families. We used a quasi-experimental, preintervention-postintervention design with 2 contemporaneous comparison groups: children in the same settings whose families did not receive the intervention and children in settings in which the intervention was not offered. Primary outcomes are improvement in each of the 6 dimensions of the Teaching Strategies GOLD (TSG) measure (social-emotional, physical, cognitive, language, literacy, and mathematics) and meeting or exceeding “widely held expectations” in all of these 6 dimensions. RESULTS Within sites that offered the coaching program, children whose parents received the program (n = 2609) showed gains in 2 of 6 TSG dimensions compared with children (n = 440) whose parents did not, and also met or exceeded widely held expectations. TSG outcomes of all children in sites offering the intervention (n = 3049) did not differ from those of children in sites that did not (n = 7216). CONCLUSIONS Findings provide sufficient evidence of a positive impact of Mobility Mentoring on child development to merit further study. If substantiated, building parental executive function may improve child outcomes as well as enhance progress toward economic self-sufficiency, and potentially be more engaging than traditional family support programs.

Published
2021

37. Case Report: Bullous Lung Disease Following COVID-19

Author

Prachi Pednekar, Changwan Ryu, Kwesi Amoah, Robert J. Homer, and Denyse D. Lutchmansingh

Subjects
medicine.medical_specialty, Medicine (General), Bullous lung disease, Bronchiectasis, post-acute COVID-19, Coronavirus disease 2019 (COVID-19), business.industry, Pulmonary disease, COVID-19, SARS CoV-2, Case Report, General Medicine, medicine.disease, bullous lung disease, Dermatology, R5-920, post-COVID “Long Haulers”, Radiological weapon, medicine, Medicine, Symptom onset, Respiratory system, business, Complication
Abstract

More than 87% of patients report the persistence of at least one symptom after recovery from Coronavirus disease 2019 (COVID-19). Dyspnea is one of the most frequently reported symptoms following severe acute respiratory syndrome coronavirus-2 infection (SARS CoV-2) with persistent chest radiological abnormalities up to three months after symptom onset. These radiological abnormalities are variable and most commonly include ground-glass opacities, reticulations, mosaic attenuation, parenchymal bands, interlobular septal thickening, bronchiectasis, and fibrotic like changes. However, in this case report, we describe findings of bullous lung disease as a complication of severe acute respiratory syndrome coronavirus-2 infection. As the pandemic continues there is a need to understand the multiple respiratory manifestations of post-acute sequelae of COVID-19. We, therefore, present this case to add to the current body of literature describing pulmonary disease as a consequence of SARS CoV-2 infection.

Published
2021

39. Differences in Pathology, Staging, and Treatment between HIV+ and Uninfected Patients with Microscopically Confirmed Hepatocellular Carcinoma

Author

Rajni Mehta, Amy C. Justice, Xuchen Zhang, Norbert Bräu, Darshana Jhala, Dena M. Carbonari, Farah Kidwai-Khan, Lesley S. Park, Tamar H. Taddei, Kisha Mitchell Richards, Vincent Lo Re, Kathryn D'Addeo, Michael J. Kallan, Melissa Skanderson, Robert J. Homer, and Jessie Torgersen

Subjects
0301 basic medicine, Pathology, medicine.medical_specialty, Epidemiology, business.industry, Lymphovascular invasion, Proportional hazards model, Hazard ratio, Retrospective cohort study, medicine.disease, Tumor Pathology, BCLC Stage, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Oncology, 030220 oncology & carcinogenesis, Hepatocellular carcinoma, Carcinoma, medicine, business
Abstract

Background: The incidence of hepatocellular carcinoma (HCC) is substantially higher among HIV-infected (HIV+) than uninfected persons. It remains unclear if HCC in the setting of HIV infection is morphologically distinct or more aggressive. Methods: We evaluated differences in tumor pathology in a cohort of HIV+ and uninfected patients with microscopically confirmed HCC in the Veterans Aging Cohort Study from 2000 to 2015. We reviewed pathology reports and medical records to determine Barcelona Clinic Liver Cancer stage (BCLC), HCC treatment, and survival by HIV status. Multivariable Cox regression was used to determine the hazard ratio [HR; 95% confidence interval (CI)] of death associated with HIV infection after microscopic confirmation. Results: Among 873 patients with HCC (399 HIV+), 140 HIV+ and 178 uninfected persons underwent liver tissue sampling and had microscopically confirmed HCC. There were no differences in histologic features of the tumor between HIV+ and uninfected patients, including tumor differentiation (well differentiated, 19% vs. 28%, P = 0.16) and lymphovascular invasion (6% vs. 7%, P = 0.17) or presence of advanced hepatic fibrosis (40% vs. 39%, P = 0.90). There were no differences in BCLC stage (P = 0.06) or treatment (P = 0.29) by HIV status. After adjustment for risk factors, risk of death was higher among HIV-infected than uninfected patients (HR = 1.37; 95% CI, 1.02–1.85). Conclusions: We found no differences in HCC tumor characteristics or background hepatic parenchyma by HIV status, yet HIV was associated with poorer survival. Of note, pathology reports often omitted these characteristics. Impact: Systematic evaluation of HCC pathology by HIV status is needed to understand tumor characteristics associated with improved survival.

Published
2020
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40. Broadband optical mammography: chromophore concentration and hemoglobin saturation contrast in breast cancer.

Author

Pamela G Anderson, Jana M Kainerstorfer, Angelo Sassaroli, Nishanth Krishnamurthy, Marc J Homer, Roger A Graham, and Sergio Fantini

Subjects
Medicine, Science
Abstract

This study reports the optical characterization and quantitative oximetry of human breast cancer using spectrally-resolved images collected with a broadband, continuous-wave optical mammography instrument. On twenty-six cancer patients, we collected two-dimensional optical mammograms and created maps of the concentrations of hemoglobin, water, and lipids, as well as the oxygen saturation of hemoglobin. For each cancerous breast, we analyzed the difference between the tumor region (as identified by x-ray and optical mammography) and the remainder of breast tissue. With respect to the surrounding tissue, we found that cancer regions have significantly higher concentrations of total hemoglobin (+2.4 ± 0.4 μM) and water (+7 ± 1% v/v), and significantly lower lipid concentration (8 ± 2% v/v) and oxygen saturation of hemoglobin (5 ± 1%). We also found a significant correlation between the tumor optical contrast and the grade of breast cancer as quantified by the Nottingham histologic score; this demonstrates how optical signatures may be representative of metabolic and morphological features, as well as the aggressive potential of the tumor.

Published
2015
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41. A Semiquantitative Scoring System May Allow Biopsy Diagnosis of Pulmonary Large Cell Neuroendocrine Carcinoma

Author

John H. Sinard, Marina K. Baine, Robert J. Homer, and Guoping Cai

Subjects
0301 basic medicine, Pathology, medicine.medical_specialty, Lung, Scoring system, Tissue microarray, medicine.diagnostic_test, Proliferative index, business.industry, General Medicine, Large cell neuroendocrine carcinoma of the lung, medicine.disease, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Biopsy, Carcinoma, Medicine, business, Cutoff score
Abstract

ObjectivesThe aim of this study was to devise reproducible biopsy criteria for distinguishing pulmonary large cell neuroendocrine carcinoma (LCNEC) from non-small cell lung carcinoma (NSCLC).MethodsTissue microarrays of LCNEC and NSCLC were generated from resection specimens and used as biopsy surrogates. They were stained for neuroendocrine markers, Ki-67, napsin-A, and p40, and independently analyzed by standardized morphologic criteria by four pathologists. Tumors were scored based on morphology, neuroendocrine marker expression, and Ki-67 proliferative index.ResultsThe average total score for LCNEC was significantly higher than for NSCLC (5.65 vs 0.51, P < .0001). Utilizing a cutoff score of 4 or higher showed 100% sensitivity and 99% specificity for LCNEC diagnosis, with an excellent agreement among four pathologists (98%).ConclusionsThe proposed semiquantitative approach based on a combination of specific morphologic and immunophenotypic features may be a useful tool for biopsy diagnosis of LCNEC.

Published
2019
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42. Voice burden in teachers and non‐teachers in a UK population: A questionnaire‐based survey

Author

Frances M. Ascott, Catherine Fullwood, Jarrod J Homer, and Chaitanya Gadepalli

Subjects
Adult, Male, medicine.medical_specialty, Voice Quality, education, Population, behavioral disciplines and activities, Occupational safety and health, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Surveys and Questionnaires, Intervention (counseling), mental disorders, Epidemiology, medicine, Humans, 030223 otorhinolaryngology, Phoniatrics, education.field_of_study, Voice Disorders, business.industry, Questionnaire, Speech Therapist, Faculty, England, Otorhinolaryngology, 030220 oncology & carcinogenesis, Family medicine, Female, business
Abstract

OBJECTIVE To characterise the burden of voice disorders in teachers in a UK population, compare it with non-teachers and identify groups of teachers who may be particularly at risk of developing a voice problem. DESIGN Questionnaire-based survey of primary and secondary school teachers and non-teachers. Questions consisted of general demographics, VHI-10 and questions relating to voice problems. METHODS Distribution of questionnaires to teachers and non-teachers and statistical analysis of the responses. SETTING University teaching hospital. PARTICIPANTS Teachers and non-teachers in a region of North West England. MAIN OUTCOME MEASURES Identification of risk factors for voice problems in teachers, compared to non-teachers. RESULTS A total of 210 primary and 244 secondary school teachers and 304 non-teachers participated in the questionnaire survey. Response rates were 67.9% from primary schools, 41.2% from secondary schools and 40.0% from the non-teachers. 30.0% of teachers and 9.0% of non-teachers had reported problems with their voice. 12.8% of teachers and 2.0% of non-teachers had missed work due to voice problems. 14.1% of teachers and 5.3% non-teachers had seen a general practitioner for voice-related problems, whilst 7.1% of teachers and 6.3% of non-teachers had been referred to an otolaryngologist or speech therapist for voice problems. Factors related to VHI-10 (P

Published
2019
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43. False-positive pathology: improving reproducibility with the next generation of pathologists

Author

Benjamin L. Mazer, David L. Rimm, and Robert J. Homer

Subjects
0301 basic medicine, Pathology, medicine.medical_specialty, MEDLINE, Cell Biology, Scientific literature, Pathology and Forensic Medicine, External validity, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Incentive, 030220 oncology & carcinogenesis, medicine, False positive paradox, Observational study, Overdiagnosis, Inefficiency, Psychology, Molecular Biology
Abstract

The external validity of the scientific literature has recently come into question, popularly referred to as the "reproducibility crisis." It is now generally acknowledged that too many false positive or non-reproducible results are being published throughout the biomedical and social science literature due to misaligned incentives and poor methodology. Pathology is likely no exception to this problem, and may be especially prone to false positives due to common observational methodologies used in our research. Spurious findings in pathology contribute inefficiency to the scientific literature and detrimentally influence patient care. In particular, false positives in pathology affect patients through biomarker development, prognostic classification, and cancer overdiagnosis. We discuss possible sources of non-reproducible pathology studies and describe practical ways our field can improve research habits, especially among trainees.

Published
2019
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44. Low ambient humidity impairs barrier function and innate resistance against influenza infection

Author

Akiko Iwasaki, Patrick Wong, Tasfia Rakib, Eriko Kudo, Laura J. Yockey, Robert J. Homer, and Eric Song

Subjects
Mucociliary clearance, Mice, Transgenic, Respiratory Mucosa, 010501 environmental sciences, Biology, medicine.disease_cause, 01 natural sciences, Virus, Mice, Mice, Congenic, 03 medical and health sciences, Immunology and Inflammation, Orthomyxoviridae Infections, Interferon, Influenza, Human, medicine, Flu season, Influenza A virus, Animals, Humans, Respiratory system, Immunity, Mucosal, disease tolerance, 030304 developmental biology, 0105 earth and related environmental sciences, 0303 health sciences, Multidisciplinary, Humidity, interferon, Biological Sciences, respiratory tract, Immunity, Innate, humanities, 3. Good health, Disease Models, Animal, medicine.anatomical_structure, flu season, Immunology, mucosal immunity, Disease Susceptibility, Viral load, medicine.drug, Respiratory tract
Abstract

Significance Influenza virus causes seasonal outbreaks in temperate regions, with an increase in disease and mortality in the winter months. Dry air combined with cold temperature is known to enable viral transmission. In this study, we asked whether humidity impacts the host response to influenza virus infections. Exposure of mice to low humidity conditions rendered them more susceptible to influenza disease. Mice housed in dry air had impaired mucociliary clearance, innate antiviral defense, and tissue repair function. Moreover, mice exposed to dry air were more susceptible to disease mediated by inflammasome caspases. Our study provides mechanistic insights for the seasonality of the influenza virus epidemics, whereby inhalation of dry air compromises the host’s ability to restrict influenza virus infection., In the temperate regions, seasonal influenza virus outbreaks correlate closely with decreases in humidity. While low ambient humidity is known to enhance viral transmission, its impact on host response to influenza virus infection and disease outcome remains unclear. Here, we showed that housing Mx1 congenic mice in low relative humidity makes mice more susceptible to severe disease following respiratory challenge with influenza A virus. We find that inhalation of dry air impairs mucociliary clearance, innate antiviral defense, and tissue repair. Moreover, disease exacerbated by low relative humidity was ameliorated in caspase-1/11–deficient Mx1 mice, independent of viral burden. Single-cell RNA sequencing revealed that induction of IFN-stimulated genes in response to viral infection was diminished in multiple cell types in the lung of mice housed in low humidity condition. These results indicate that exposure to dry air impairs host defense against influenza infection, reduces tissue repair, and inflicts caspase-dependent disease pathology.

Published
2019
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45. The need for dried plasma – a national issue

Author

Mary J Homer, Michael R. Davis, Ernest E. Moore, Jason L. Sperry, W. Keith Hoots, Stacy Shackelford, Frank K. Butler, Andrew P. Cap, Anthony E. Pusateri, Audra L Taylor, and Richard B. Weiskopf

Subjects
Immunology, Blood Component Transfusion, Shock, Hemorrhagic, 030204 cardiovascular system & hematology, Disaster Medicine, Plasma, 03 medical and health sciences, 0302 clinical medicine, Drug approval, Humans, Immunology and Allergy, Medicine, In patient, Military Medicine, Drug Approval, Mass disaster, National health, United States Food and Drug Administration, business.industry, Hematology, medicine.disease, United States, Severe trauma, Plasma products, Disaster preparedness, Hemorrhagic shock, Medical emergency, business, 030215 immunology
Abstract

Recent studies have demonstrated that early transfusion of plasma or RBCs improves survival in patients with severe trauma and hemorrhagic shock. Time to initiate transfusion is the critical factor. It is essential that transfusion begin in the prehospital environment when transport times are longer than approximately 15 to 20 minutes. Unfortunately, logistic constraints severely limit the use of blood products in the prehospital setting, especially in military, remote civilian, and mass disaster circumstances, where the need can be most acute. US military requirements for logistically supportable blood products are projected to increase dramatically in future conflicts. Although dried plasma products have been available and safely used in a number of countries for over 20 years, there is no dried plasma product commercially available in the United States. A US Food and Drug Administration-approved dried plasma is urgently needed. Considering the US military, disaster preparedness, and remote civilian trauma perspectives, this is an urgent national health care issue.

Published
2019
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46. Civilian walking blood bank emergency preparedness plan

Author

Eugene E. Moore, Elizabeth Waltman, Marisa B. Marques, Kevin C. O'Connor, Heidi Doughty, Andrew P. Cap, Kevin R. Ward, Audra L. Taylor, Donald H. Jenkins, Philip C. Spinella, Torunn Oveland Apelseth, Paul M. Ness, Jeremy W. Cannon, John B. Holcomb, Sara F. Goldkind, Martin A. Schreiber, Steve Sloan, Mark H. Yazer, Eilat Shinar, James R. Stubbs, Sarah J. Ilstrup, Mary J. Homer, Jan O. Jansen, Jason B. Corley, Jennifer M. Gurney, Geir Strandenes, Frank K Butler, and Michael Fitzpatrick

Subjects
medicine.medical_specialty, Blood transfusion, Civil defense, medicine.medical_treatment, Immunology, Plan (drawing), Blood Banks/methods, Blood Preservation/methods, Multidisciplinary approach, Pandemic, medicine, Immunology and Allergy, Humans, Blood Transfusion, Pandemics, transfusion, COVID-19/epidemiology, Emergency management, business.industry, emergency, whole blood, COVID-19, Civil Defense, Transfusion medicine, Hematology, medicine.disease, walking blood bank, Blood Preservation, Blood Transfusion/methods, Blood Banks, Medical emergency, business, Emergency Service, Hospital, Blood bank
Abstract

Background: The current global pandemic has created unprecedented challenges in the blood supply network. Given the recent shortages, there must be a civilian plan for massively bleeding patients when there are no blood products on the shelf. Recognizing that the time to death in bleeding patients is less than 2 h, timely resupply from unaffected locations is not possible. One solution is to transfuse emergency untested whole blood (EUWB), similar to the extensive military experience fine-tuned over the last 19 years. While this concept is anathema in current civilian transfusion practice, it seems prudent to have a vetted plan in place. Methods and Materials: During the early stages of the 2020 global pandemic, a multidisciplinary and international group of clinicians with broad experience in transfusion medicine communicated routinely. The result is a planning document that provides both background information and a high-level guide on how to emergently deliver EUWB for patients who would otherwise die of hemorrhage. Results and Conclusions: Similar plans have been utilized in remote locations, both on the battlefield and in civilian practice. The proposed recommendations are designed to provide high-level guidance for experienced blood bankers, transfusion experts, clinicians, and health authorities. Like with all emergency preparedness, it is always better to have a well-thought-out and trained plan in place, rather than trying to develop a hasty plan in the midst of a disaster. We need to prevent the potential for empty shelves and bleeding patients dying for lack of blood.

Published
2021
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