bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sensitivity of Medicaid Claims Data for Identifying Opioid Use Disorder in Patients Admitted to 6 New York City Public Hospitals
Authors: McNeely Jennifer , Gallagher Shane D. , Mazumdar Medha , Appleton Noa , Fernando Jasmine , Owens Elizabeth , Bone Emmeline , Krawczyk Noa , Dolle Johanna , Marcello Roopa Kalyanaraman , Billings John , Wang Scarlett 
Published: October 2022

Objectives
Behavioral health diagnoses are frequently underreported in administrative health data. For a pragmatic trial of a hospital addiction consult program, we sought to determine the sensitivity of Medicaid claims data for identifying patients with opioid use disorder (OUD).

Methods
A structured review of electronic health record (EHR) data was conducted to identify patients with OUD in 6 New York City public hospitals. Cases selected for review were adults admitted to medical/surgical inpatient units who received methadone or sublingual buprenorphine in the hospital. For cases with OUD based on EHR review, we searched for the hospitalization in Medicaid claims data and examined International Classification of Diseases, Tenth Revision discharge diagnosis codes to identify opioid diagnoses (OUD, opioid poisoning, or opioid-related adverse events). Sensitivity of Medicaid claims data for capturing OUD hospitalizations was calculated using EHR review findings as the reference standard measure.

Results
Among 552 cases with OUD based on EHR review, 465 (84.2%) were found in the Medicaid claims data, of which 418 (89.9%) had an opioid discharge diagnosis. Opioid diagnoses were the primary diagnosis in 49 cases (11.7%), whereas in the remainder, they were secondary diagnoses.

Conclusion
In this sample of hospitalized patients receiving OUD medications, Medicaid claims seem to have good sensitivity for capturing opioid diagnoses. Although the sensitivity of claims data may vary, it can potentially be a valuable source of information about OUD patients.
Circ_0026123 promotes cisplatin resistance and progression of ovarian cancer by upregulating RAB1A through sequestering miR-543
Authors: Wei Lei , He Weicai , Zhao Hua , Zhao Peixi 
Published: October 2022

Background
Circular RNAs can act as critical regulators in the tumorigenesis and chemoresistance of ovarian cancer (OC). Herein, this work aimed to probe the function and mechanism of circ_0026123 in the cisplatin (DDP) resistance and progression of OC and its potential value in the clinic.

Methods
The quantitative real-time PCR and western blotting were used to detect the levels of RNAs and proteins. In vitro experiments were conducted using CCK-8, EdU, transwell, tube formation assays and flow cytometry. Mouse subcutaneous xenograft model was used for in vivo experiments. The interaction between circ_0026123 or RAB1A (Ras-related protein Rab-1A) and miR-543 was confirmed using dual-luciferase reporter and RNA immunoprecipitation assays.

Results
Circ_0026123 expression was higher in DDP-resistant OC tissues and cells. Silencing of circ_0026123 dramatically boosted the sensitivity of DDP-resistant OC cells to DDP, as well as inhibited cell growth, angiogenesis, invasion and migration abilities in vitro. Circ_0026123 functionally targeted miR-543, and knockdown of miR-543 reversed the impacts of circ_0026123 deficiency on DDP sensitivity and the malignant behaviors of DDP-resistant OC cells. RAB1A was a target of miR-543, RAB1A overexpression attenuated the inhibitory functions of miR-543 on DDP resistance and the malignant phenotypes of DDP-resistant OC cells. Preclinically, lentivirus-mediated circ_0026123 downregulation also suppressed OC growth and enhanced DDP cytotoxicity in vivo.

Conclusion
Our study demonstrated that circ_0026123 acted as a sponge for miR-543 to elevate RAB1A expression, thus promoting cisplatin resistance and tumorigenesis in ovarian cancer.
Effect of the use of prediagnosis hormones on breast cancer prognosis: MCC-Spain study
Authors: Alonso-Molero Jéssica , Gómez-Acebo Inés , Llorca Javier , Lope-Carvajal Virginia , Amiano Pilar , Guevara Marcela , Martín Vicente , Castaño-Vinyals Gemma , Fernández-Ortiz María , Obón-Santacana Mireia , Alguacil Juan , Fernandez-Tardon Guillermo , Molina-Barceló Ana , Marcos-Gragera Rafael , Pérez-Gómez Beatriz , Aizpurua Amaia , Ardanaz Eva , Molina Antonio J. , Rodríguez-Cundín Paz , Moreno Víctor , Rodríguez-Reinado Carmen , Aragonés Nuria , Kogevinas Manolis , Pollán Marina , Dierssen-Sotos Trinidad 
Published: October 2022

Abstract

Objective
To extend knowledge about the long-term use of hormones in hormone therapy or oral contraception as prognostic factors in breast cancer.

Methods
The MCC-Spain project is a cohort of 1,685 women with incident breast cancer recruited in Spain. Recruitment was carried out between 2007 and 2010, and the follow-up finished in December 2017. The impact of hormone therapy or oral contraception on breast cancer prognosis was analyzed considering year of birth and menopausal status (1,095 women [65%] were postmenopausal). Hazard ratios (HRs) were estimated using Cox regression models. Death by any cause was considered as the event, and hormone therapy or oral contraception were analyzed as regressors.

Results
Oral contraception use for less than 5 years shows an HR of 1.10 (95% CI, 0.75 to 1.62), whereas use for 5 or more years shows an HR of 1.46 (95% CI, 0.95 to 2.25), with a P trend of 0.01, showing a dose-dependent response. Regarding hormone therapy and restricting the analysis to postmenopausal women born between1940 and 1959, where most hormone therapy (consumption) is concentrated, the results did not show any trend.

Conclusion
Concerning oral contraception use, our results demonstrate that their use is related to poor prognosis in breast cancer. However, research in this field is limited and controversial, indicating the need for more research in this area. Regarding hormone therapy consumption, our results indicate no association with better prognosis, which contradicts what has previously been published.
Workplace Injuries and Receipt of Benefits From Workers’ Compensation and Social Security Disability Insurance
Authors: Ladd Daniel , Neumark David 
Published: October 2022

Objective
We examine whether workers who experience permanently disabling injuries covered by workers’ compensation (WC) end up on Social Security Disability Insurance (SSDI) and whether Social Security Administration (SSA) seems to offset WC payments for permanently disabling injuries against SSDI benefits, when appropriate. Methods: We capture data on WC benefit receipt from the Health and Retirement Study and link it to SSA data on WC and SSDI recipients to study descriptive information on these questions. Results: We find that SSA seems to be missing data on WC benefits for a sizable share of recipients of WC benefits and that the frequency with which SSDI benefits are reduced because of the WC offset seems surprisingly low. Conclusions: For a variety of reasons, WC benefits for permanently disabling injuries may not be appropriately offset against SSDI benefits, possibly shifting the cost of these workplace injuries to SSDI.
A Systematic Review of Strategies to Enhance Response Rates and Representativeness of Patient Experience Surveys
Authors: Anhang Price Rebecca , Quigley Denise D. , Hargraves J. Lee , Sorra Joann , Becerra-Ornelas Alejandro U. , Hays Ron D. , Cleary Paul D. , Brown Julie , Elliott Marc N. 
Published: October 2022

Background:
Data from surveys of patient care experiences are a cornerstone of public reporting and pay-for-performance initiatives. Recently, increasing concerns have been raised about survey response rates and how to promote equity by ensuring that responses represent the perspectives of all patients.

Objective:
Review evidence on survey administration strategies to improve response rates and representativeness of patient surveys.

Research Design:
Systematic review adhering to the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines.

Study Selection:
Forty peer-reviewed randomized experiments of administration protocols for patient experience surveys.

Results:
Mail administration with telephone follow-up provides a median response rate benefit of 13% compared with mail-only or telephone-only. While surveys administered only by web typically result in lower response rates than those administered by mail or telephone (median difference in response rate: −21%, range: −44%, 0%), the limited evidence for a sequential web-mail-telephone mode suggests a potential response rate benefit over sequential mail-telephone (median: 4%, range: 2%, 5%). Telephone-only and sequential mixed modes including telephone may yield better representation across patient subgroups by age, insurance type, and race/ethnicity. Monetary incentives are associated with large increases in response rates (median increase: 12%, range: 7%, 20%).

Conclusions:
Sequential mixed-mode administration yields higher patient survey response rates than a single mode. Including telephone in sequential mixed-mode administration improves response among those with historically lower response rates; including web in mixed-mode administration may increase response at lower cost. Other promising strategies to improve response rates include in-person survey administration during hospital discharge, incentives, minimizing survey language complexity, and prenotification before survey administration.
Nocardia Infection With Adrenal Gland Abscess Mimicking Metastatic Lung Cancer on FDG PET/CT
Authors: Kesim Selin , Oksuzoglu Kevser , Ozguven Salih 
Published: October 2022

Abstract
We present FDG PET/CT findings of a human immunodeficiency virus–positive patient suspicious for lung cancer with a solitary metastasis to the adrenal gland. Wedge resection of the pulmonary nodules revealed Nocardia infection and a repeat FDG PET/CT imaging after the antibiotic treatment demonstrated complete metabolic response of the adrenal lesion and pulmonary nodules. It should be kept in mind that nocardiosis may present with FDG-avid lesions masquerading as malignancies in immunocompromised patients.
Complete Metabolic Response in Adenocarcinoma Lung With Lymphangitic Carcinomatosis
Authors: Goyal Harish , Kishore Sai , Ganesan Prasanth , Halanaik Dhanapathi 
Published: October 2022

Abstract
Pulmonary lymphangitic carcinomatosis refers to the tumor spread into the lymphatic system of the lungs and is considered a poor prognostic marker. We present an interesting case of adenocarcinoma of right lung evaluated with 18F-FDG PET/CT for baseline staging, with extensive bilateral lung involvement and lymphangitic carcinomatosis pattern. Subsequently, the patient received 3 cycles of carboplatin- and pemetrexed-based chemotherapy regimen along with oral ceritinib. Complete metabolic response and significant reduction in size of the primary lung lesion was noted on response evaluation with 18F-FDG PET/CT, which is a rare phenomenon.
High-throughput screening identifies small molecule inhibitors of thioesterase superfamily member 1: Implications for the management of non-alcoholic fatty liver disease
Authors: Krumm Christopher S. , Ramos-Espiritu Lavoisier , Landzberg Renée S. , Adura Carolina , Liu Xu , Acuna Mariana , Xie Yang , Xu Xu , Tillman Matthew C. , Li Yingxia , Glickman J. Fraser , Ortlund Eric A. , Ginn John D. , Cohen David E. 
Published: October 2022

ABSTRACTThioesterase superfamily member 1 (Them1; synonyms Acyl-CoA thioesterase 11 (Acot11) and steroidogenic acute regulatory protein-related lipid transfer (START) domain 14 (StarD14) is a long chain acyl-CoA thioesterase comprising two N-terminal hot-dog fold enzymatic domains linked to a C-terminal lipid-sensing START domain, which allosterically modulates enzymatic activity. Them1 is highly expressed in thermogenic adipose tissue, where it functions to suppress energy expenditure by limiting rates of fatty acid oxidation. Its expression is also induced markedly in liver in response to high fat feedings, where it suppresses fatty acid oxidation and promotes hepatic glucose production. Mice lacking the gene (Them1-/-) are protected against diet-induced non-alcoholic fatty liver disease (NAFLD), suggesting Them1 as a therapeutic target. The current study was designed to develop small molecule inhibitors of Them1 and to establish their activitiesin vitroand in cell culture. High-throughput screening combined with counter screening assays were leveraged to identify two lead allosteric inhibitors that selectively inhibited Them1 by binding the START domain. In primary mouse brown adipocytes, these inhibitors promoted fatty acid oxidation, as evidence by increased rates of oxygen consumption. In primary mouse hepatocytes, they similarly promoted fatty acid oxidation, but also reduced glucose production. Optimized Them1 inhibitors could provide an attractive modality for the pharmacologic management of NAFLD and obesity-associated metabolic disorders.
Vitamin B2 enables peroxisome proliferator-activated receptor α regulation of fasting glucose availability
Authors: Masschelin Peter M. , Saha Pradip K. , Ochsner Scott A. , Cox Aaron R. , Kim Kang Ho , Felix Jessica B. , Sharp Robert , Li Xin , Tan Lin , Park Jun Hyoung , Wang Liping , Putluri Vasanta , Lorenzi Philip L. , Nuotio-Antar Alli M. , Sun Zheng , Kaipparettu Benny , Putluri Nagireddy , Moore David D. , Summers Scott A. , McKenna Neil J. , Hartig Sean M. 
Published: October 2022

AbstractFlavin adenine dinucleotide (FAD) interacts with flavoproteins to mediate oxidation-reduction reactions required for cellular energy demands. Not surprisingly, mutations that alter FAD binding to flavoproteins cause rare inborn errors of metabolism (IEMs) that disrupt liver function and render fasting intolerance, hepatic steatosis, and lipodystrophy. In our study, depleting FAD pools in mice with a vitamin B2 deficient diet (B2D) caused phenotypes associated with organic acidemias and other IEMs, including reduced body weight, hypoglycemia, and fatty liver disease. Integrated discovery approaches revealed B2D tempered fasting activation of target genes for the nuclear receptor PPARα, including those required for gluconeogenesis. Treatment with the PPARα agonist fenofibrate activated the integrated stress response and refilled amino acid substrates to rescue fasting glucose availability and overcome B2D phenotypes. Overall, these findings reveal PPARα governs metabolic responses to FAD availability and nominate its pharmacologic activation as strategies for organic acidemias.
Benign-Ex: Delineating Regions of the Human Genome Benign to Copy Number Variation
Authors: Wetzel Alyssa S. , Major Heather , Parida Mrutyunjaya , Manak J. Robert , Darbro Benjamin W. 
Published: October 2022

AbstractWhile copy number variants (CNVs) have been identified as an important cause of rare genetic disorders, they have also been identified in unaffected control populations, making clinical interpretation of these lesions challenging. Discriminating benign CNVs from those pathogenic for rare genetic disorders, therefore, relies on understanding what regions of the human genome are tolerant to copy number variation. Benign-Ex is a python-based program that uses information from databases of CNVs to generate one or more benign interval map(s) and then identifies the optimal map by computing the overlap with known pathogenic regions. We utilized Benign-Ex to identify the optimal set of benign intervals from two distinct CNV databases: Database of Genomic Variants (DGV) and Clinical Genome Resource (ClinGen). Benign-Ex called 41.1% of the genome benign using data from DGV and 37.6% of the genome benign using data from ClinGen. The benign regions from DGV and ClinGen werenotspatially correlated, underscoring the importance of integrating both research and clinical databases for determining CNV benignity.
Enhancing pain care with the American Pain Society Patient Outcome Questionnaire for use in the Emergency Department (APS-POQ-RED): validating a patient-reported outcome measure
Authors: Hughes James A , Hazelwood Sarah , Lyrstedt Anna-Lisa , Jones Lee , Brown Nathan J , Jarugula Rajeev , Douglas Clint , Chu Kevin 
Published: October 2022

AbstractPain is the most common symptom experienced when presenting to the emergency department (ED). Estimates indicate over half of all patients will present in pain. EDs typically focus on care process measures, such as time to first analgesic medication. Process-based metrics remove the patient from their own experience. Unfortunately, when patient-reported measures of pain care are used in the ED for quality improvement or research, they vary widely and often lack validation. Previous work has demonstrated that a modified version of the American Pain Society – Patient Outcome Questionnaire – Revised Edition (APS-POQ-R) may provide an ideal patient-reported outcome measure for the adult ED population. However, previous work has left validation incomplete. In this multi-site, multistage research, we demonstrate the construct, convergent and divergent validity and the internal consistency of a modified version of the APS-POQ-R in adult patients presenting to two large, inner-city EDs with moderate to severe acute pain. After three stages of psychometric testing in 646 patients, we present a nine-question, three construct patient-reported outcome measure for moderate to severe pain in the adult emergency department, now known as the American Pain Society – Patient Outcome Questionnaire – Revised for the ED (APS-POQ-RED).PerspectiveThis article presents the psychometric properties of a revised version of the APS-POQ-R for use in the adult ED. This shortened, ED-specific patient-reported outcome measure (APS-POQ-RED) seeks to provide a standardised, validated measure of patient-reported outcomes of acute pain care in the ED for quality and research purposes.
Soluble VE-cadherin disrupts endothelial barrier function via VE-PTP/RhoA signalling
Authors: Knop Juna-Lisa , Burkard Natalie , Danesh Mahshid , Dandekar Thomas , Srivastava Mugdha , Hiermaier Matthias , Waschke Jens , Flemming Sven , Schlegel Nicolas 
Published: October 2022

AbstractAimIncreased levels of soluble Vascular endothelial (VE)-cadherin fragments (sVE-cadherin) have previously been linked with inflammation-induced loss of endothelial barrier function. We tested whether sVE-cadherin is critically involved in the onset of endothelial barrier dysfunction.Methods and ResultsApplication of recombinant human sVE-cadherin (extracellular domains EC1-5) on human microvascular endothelial cellsin vitroand in a rat modelin vivoinduced loss of endothelial barrier function and reduced microcirculatory flow. sVE-cadherinEC1-5led to decreased localization of VE-cadherin at cell borders. Additionally, sVE-cadherinEC1-5perturbed VE-protein tyrosine phosphatase (VE-PTP)/VE-cadherin interaction. VE-PTP inhibitor AKB9778 blunted all sVE-cadherinEC1-5-induced effectsin vitroandin vivo. Downstream effects involve VE-PTP-dependent RhoA activation which was attenuated by AKB9778. Rho-kinase inhibitor Y27632 blocked sVE-cadherinEC1-5-induced loss of endothelial barrier function.ConclusionsVE-cadherin disrupts endothelial barrier function by dismantling the VE-cadherin complex at cell borders via VE-PTP-dependent RhoA activation. This uncovers a novel pathophysiological role of sVE-cadherin in the context of endothelial barrier dysfunction in inflammation.
A marmoset brain cell census reveals influence of developmental origin and functional class on neuronal identity
Authors: Krienen Fenna M. , Levandowski Kirsten M. , Zaniewski Heather , del Rosario Ricardo C.H. , Schroeder Margaret E. , Goldman Melissa , Wienisch Martin , Lutservitz Alyssa , Beja-Glasser Victoria F. , Chen Cindy , Zhang Qiangge , Chan Ken Y. , Li Katelyn X. , Sharma Jitendra , McCormack Dana , Shin Tay Won , Harrahill Andrew , Nyase Eric , Mudhar Gagandeep , Mauermann Abigail , Wysoker Alec , Nemesh James , Kashin Seva , Vergara Josselyn , Chelini Gabriele , Dimidschstein Jordane , Berretta Sabina , Deverman Benjamin E. , Boyden Ed , McCarroll Steven A. , Feng Guoping 
Published: October 2022

AbstractThe mammalian brain is composed of many brain structures, each with its own ontogenetic and developmental history. Transcriptionally-based cell type taxonomies reveal cell type composition and similarity relationships within and across brain structures. We sampled over 2.4 million brain cells across 18 locations in the common marmoset, a New World monkey primed for genetic engineering, and used single-nucleus RNA sequencing to examine global gene expression patterns of cell types within and across brain structures. Our results indicate that there is generally a high degree of transcriptional similarity between GABAergic and glutamatergic neurons found in the same brain structure, and there are generally few shared molecular features between neurons that utilize the same neurotransmitter but reside in different brain structures. We also show that in many cases the transcriptional identities of cells are intrinsically retained from their birthplaces, even when they migrate beyond their cephalic compartments. Thus, the adult transcriptomic identity of most neuronal types appears to be shaped much more by their developmental identity than by their primary neurotransmitter signaling repertoire. Using quantitative mapping of single molecule FISH (smFISH) for markers for GABAergic interneurons, we found that the similar types (e.g.PVALB+ interneurons) have distinct biodistributions in the striatum and neocortex. Interneuron types follow medio-lateral gradients in striatum but form complex distributions across the neocortex that are not described by simple gradients. Lateral prefrontal areas in marmoset are distinguished by high relative proportions ofVIP+ neurons. We further used cell-type-specific enhancer driven AAV-GFP to visualize the morphology of molecularly-resolved interneuron classes in neocortex and striatum, including the previously discovered novel primate-specificTAC3+striatal interneurons. Our comprehensive analyses highlight how lineage and functional class contribute to the transcriptional identity and biodistribution of primate brain cell types.One-Sentence SummaryAdult primate neurons are imprinted by their region of origin, more so than by their functional identity.
MLL1 regulates cytokine-driven cell migration and metastasis
Authors: Nair Praful R. , Danilova Ludmila , Gómez-de-Mariscal Estibaliz , Kim Dongjoo , Fan Rong , Muñoz-Barrutia Arrate , Fertig Elana J. , Wirtz Denis 
Published: October 2022

AbstractCell migration is a critical requirement for cancer metastasis. Cytokine production and its role in cancer cell migration have been traditionally associated with immune cells in the tumor microenvironment. MLL1 is a histone methyltransferase that controls 3D cell migration via the secretion of cytokines, IL-6 and TGF-β1, by the cancer cells themselves.In vivo, MLL1 depletion reduced metastatic burden and prolonged survival. MLL1 exerts its effects with its scaffold protein, Menin. Mechanistically, the MLL1-Menin interaction controls actin filament assembly via the IL-6/pSTAT3/Arp3 axis and acto-myosin contractility via the TGF-β1/Gli2/ROCK1/2/pMLC2 axis, which regulate dynamic protrusion generation and 3D cell migration. MLL1 also regulates cell proliferation via mitosis-based and cell cycle-related pathways. Combining an MLL1-Menin inhibitor with Paclitaxel, a standard chemotherapeutic, abrogated tumor growth and metastasis in a syngeneic model. These results highlight the potential of targeting the MLL1 in metastasis prevention and its potential to be combined with currently administered chemotherapeutics.Statement of SignificanceWe identify MLL1 as being vital to metastasis, which causes the vast majority of cancer-related deaths. MLL1 controls cell migration, a requirement for metastasis, by regulating the secretion of cytokines. MLL1 inhibition lowers metastatic burden independent of its impact on primary tumor growth, highlighting its anti-metastatic potential in TNBC.