tbuckley/cabot-search huggingface dataset:
Association of the Usability of Electronic Health Records With Cognitive Workload and Performance Levels Among Physicians
Authors: Lukasz M. Mazur, Prithima R. Mosaly, Carlton Moore, Lawrence Marks
Journal: JAMA Network Open (2019)

<h3>Importance</h3> Current electronic health record (EHR) user interfaces are suboptimally designed and may be associated with excess cognitive workload and poor performance. <h3>Objective</h3> To assess the association between the usability of an EHR system for the management of abnormal test results and physicians’ cognitive workload and performance levels. <h3>Design, Setting, and Participants</h3> This quality improvement study was conducted in a simulated EHR environment. From April 1, 2016, to December 23, 2016, residents and fellows from a large academic institution were enrolled and allocated to use either a baseline EHR (n = 20) or an enhanced EHR (n = 18). Data analyses were conducted from January 9, 2017, to March 30, 2018. <h3>Interventions</h3> The EHR with enhanced usability segregated in a dedicated folder previously identified critical test results for patients who did not appear for a scheduled follow-up evaluation and provided policy-based decision support instructions for next steps. The baseline EHR displayed all patients with abnormal or critical test results in a general folder and provided no decision support instructions for next steps. <h3>Main Outcomes and Measures</h3> Cognitive workload was quantified subjectively using NASA–Task Load Index and physiologically using blink rates. Performance was quantified according to the percentage of appropriately managed abnormal test results. <h3>Results</h3> Of the 38 participants, 25 (66%) were female. The 20 participants allocated to the baseline EHR compared with the 18 allocated to the enhanced EHR demonstrated statistically significantly higher cognitive workload as quantified by blink rate (mean [SD] blinks per minute, 16 [9] vs 24 [7]; blink rate, –8 [95% CI, –13 to –2];<i>P</i> = .01). The baseline group showed statistically significantly poorer performance compared with the enhanced group who appropriately managed 16% more abnormal test results (mean [SD] performance, 68% [19%] vs 98% [18%]; performance rate, –30% [95% CI, –40% to –20%];<i>P</i> &lt; .001). <h3>Conclusions and Relevance</h3> Relatively basic usability enhancements to the EHR system appear to be associated with better physician cognitive workload and performance; this finding suggests that next-generation systems should strip away non–value-added EHR interactions, which may help physicians eliminate the need to develop their own suboptimal workflows.
Obesity alters oestrogen metabolism and contributes to pulmonary arterial hypertension
Authors: Kirsty M. Mair, Katie Y. Harvey, Alasdair D. Henry, Dianne Z. Hillyard, Margaret Nilsen, Margaret R. MacLean
Journal: European Respiratory Journal (2019)

Obesity is a common comorbidity for pulmonary arterial hypertension (PAH). Additionally, oestrogen and its metabolites are risk factors for the development of PAH. Visceral adipose tissue (VAT) is a major site of oestrogen production; however, the influence of obesity-induced changes in oestrogen synthesis and metabolism on the development of PAH is unclear. To address this we investigated the effects of inhibiting oestrogen synthesis and metabolism on the development of pulmonary hypertension in male and female obese mice. We depleted endogenous oestrogen in leptin-deficient ( ob / ob ) mice with the oestrogen inhibitor anastrozole (ANA) and determined the effects on the development of pulmonary hypertension, plasma oestradiol and urinary 16α-hydroxyestrone (16αOHE1). Oestrogen metabolism through cytochrome P450 1B1 (CYP1B1) was inhibited with 2,2′,4,6′-tetramethoxystilbene (TMS). ob / ob mice spontaneously develop pulmonary hypertension, pulmonary vascular remodelling and increased reactive oxygen species production in the lung; these effects were attenuated by ANA. Oestradiol levels were decreased in obese male mice; however, VAT CYP1B1 and 16αOHE1 levels were increased. TMS also attenuated pulmonary hypertension in male ob / ob mice. Intra-thoracic fat from ob / ob mice and VAT conditioned media produce 16αOHE1 and can contribute to oxidative stress, effects that are attenuated by both ANA and TMS. Obesity can induce pulmonary hypertension and changes in oestrogen metabolism, resulting in increased production of 16αOHE1 from VAT that contributes to oxidative stress. Oestrogen inhibitors are now in clinical trials for PAH. This study has translational consequences as it suggests that oestrogen inhibitors may be especially beneficial in treating obese individuals with PAH.
Noninvasive Follicular Thyroid Neoplasm with Papillary-Like Nuclear Features (NIFTP): Update and Diagnostic Considerations—a Review
Authors: Esther Diana Rossi, William C. Faquin, Zubair Baloch, Guido Fadda, Lester Thompson, Luigi Maria Larocca, Liron Pantanowitz
Journal: Endocrine Pathology (2019)
Effect of Collaborative Telerehabilitation on Functional Impairment and Pain Among Patients With Advanced-Stage Cancer
Authors: Andrea L. Cheville, Timothy Moynihan, Jeph Herrin, Charles Loprinzi, Kurt Kroenke
Journal: JAMA Oncology (2019)

<h3>Importance</h3> Most patients with advanced-stage cancer develop impairment and pain-driven functional losses that jeopardize their independence. <h3>Objective</h3> To determine whether collaborative telerehabilitation and pharmacological pain management improve function, lessen pain, and reduce requirements for inpatient care. <h3>Design, Setting, and Patients</h3> The Collaborative Care to Preserve Performance in Cancer (COPE) study was a 3-arm randomized clinical trial conducted at 3 academic medical centers within 1 health care system. Patient recruitment began in March 2013 and follow-up concluded in October 2016. Participants (N = 516) were low-level community or household ambulators with stage IIIC or IV solid or hematologic cancer. <h3>Interventions</h3> Participants were randomly assigned to the (1) control arm, (2) telerehabilitation arm, or (3) telerehabilitation with pharmacological pain management arm. All patients underwent automated function and pain monitoring with data reporting to their care teams. Participants in arms 2 and 3 received 6 months of centralized telerehabilitation provided by a physical therapist-physician team. Those in arm 3 also received nurse-coordinated pharmacological pain management. <h3>Main Outcomes and Measures</h3> Blinded assessment of function using the Activity Measure for Postacute Care computer adaptive test, pain interference and average intensity using the Brief Pain Inventory, and quality of life using the EQ-5D-3L was performed at baseline and months 3 and 6. Hospitalizations and discharges to postacute care facilities were recorded. <h3>Results</h3> The study included 516 participants (257 women and 259 men; mean [SD] age, 65.6 [11.1] years), with 172 randomized to 1 of 3 arms. Compared with the control group, the telerehabilitation arm 2 had improved function (difference, 1.3; 95% CI, 0.08-2.35;<i>P</i> = .03) and quality of life (difference, 0.04; 95% CI, 0.004-0.071;<i>P</i> = .01), while both telerehabilitation arms 2 and 3 had reduced pain interference (arm 2, −0.4; 95% CI, −0.78 to −0.09;<i>P</i> = .01 and arm 3, −0.4; 95% CI, −0.79 to −0.10;<i>P</i> = .01), and average intensity (arm 2, −0.4; 95% CI, −0.78 to −0.07;<i>P</i> = .02 and arm 3, −0.5; 95% CI, −0.84 to −0.11;<i>P</i> = .006). Telerehabilitation was associated with higher odds of home discharge in arms 2 (odds ratio [OR], 4.3; 95% CI, 1.3-14.3;<i>P</i> = .02) and 3 (OR, 3.8; 95% CI, 1.1-12.4;<i>P</i> = .03) and fewer days in the hospital in arm 2 (difference, −3.9 days; 95% CI, −2.4 to −4.6;<i>P</i> = .01). <h3>Conclusions and Relevance</h3> Collaborative telerehabilitation modestly improved function and pain, while decreasing hospital length of stay and the requirement for postacute care, but these outcomes were not enhanced with the addition of pharmacological pain management. <h3>Trial Registration</h3> ClinicalTrials.gov identifier:NCT01721343
Prognostic impact of circulating tumor DNA status post–allogeneic hematopoietic stem cell transplantation in AML and MDS
Authors: Sousuke Nakamura, Kazuaki Yokoyama, Eigo Shimizu, Nozomi Yusa, Kanya Kondoh, Miho Ogawa, Tomomi Takei, Asako Kobayashi, Mika Ito, Masamichi Isobe, Takaaki Konuma, Seiko Kato, Rika Kasajima, Yuka Wada, Tokiko Nagamura-Inoue, Rui Yamaguchi, Satoshi Takahashi, Seiya Imoto, Satoru Miyano, Arinobu Tojo
Journal: Blood (2019)
Programmable Therapeutic Nanodevices with Circular Amplification of H<sub>2</sub>O<sub>2</sub> in the Tumor Microenvironment for Synergistic Cancer Therapy
Authors: Jiong Li, Zuwu Wei, Xinyi Lin, Dongye Zheng, Ming Wu, Xiaolong Liu, Jingfeng Liu
Journal: Advanced Healthcare Materials (2019)

Abstract Tumor microenvironment activated nanodevices have remarkable superiority to enhance therapeutic efficacy and minimize side effects, but their practical applications are dramatically reduced by the low abundance and heterogeneous distribution of specific stimuli at the tumor site. Herein, programmable vesicular nanodevices based on the triblock copolymer containing poly(ethylene glycol) (PEG) and poly(caprolactone) (PCL) with peroxalate esters (PO) as hydrogen peroxide‐responsive linkage (PEG‐PO‐PCL‐PO‐PEG), are developed for co‐delivery of hypoxia‐activated prodrug (AQ4N) and glucose oxidase (GOD). The obtained nanodevices (PAG) can be activated by the high level of H 2 O 2 in tumor microenvironment to improve the permeability of membranes for glucose entrance. Afterward, the oxidation of glucose catalyzed by GOD produces amplified H 2 O 2 amounts which in turn induce complete destruction of PAG for fast release of AQ4N and GOD. Ultimately, the PAG can exert programmable therapeutic effects from the following aspects: 1) starvation therapy by cutting off the energy supply from glucose through GOD catalysis; 2) oxidative cytotoxicity after H 2 O 2 amplification; 3) chemotherapy of AQ4N activated by the intensified tumor hypoxia microenvironment after oxygen consumption. The stimuli amplification, controlled drug release, synergistic therapy, and corresponding mechanisms of PAG are demonstrated. Therefore, the presented work could provide significant new insights for cancer treatment.
Human BCR analysis of single-sorted, putative IgE+ memory B cells in food allergy
Authors: Rodrigo Jiménez-Saiz, Yosef Ellenbogen, Kelly Bruton, Paul Spill, Doron D. Sommer, Hermenio Lima, Susan Waserman, Sarita U. Patil, Wayne G. Shreffler, Manel Jordana
Journal: Journal of Allergy and Clinical Immunology (2019)
Traction strategy with clips and rubber band allows complete en bloc endoscopic submucosal dissection of sessile serrated adenoma/polyp invading the site of previous appendectomy
Authors: Borathchakra Oung, Edouard Chabrun, Clément Subtil, Elodie Cesbron-Metivier, Véronique Dumora-Ezponda, Jérémie Jacques, Mathieu Pioche
Journal: Endoscopy (2019)

Endoscopic submucosal dissection (ESD) is now the reference method for en bloc resection of colorectal neoplasia with fibrosis [1]. Nevertheless, ESD appears difficult when the lesion develops on the site of previous appendectomy with severe submucosal fibrosis, and surgery was the only option before the introduction of the full-thickness resection device [2]. However, clip and rubber band traction completely changed the ESD procedure by offering triangulation to reveal the submucosal cutting line, even in cases of submucosal fibrosis or when the lesion deeply invaded the appendix [3].
Control of tumor-associated macrophages and T cells in glioblastoma via AHR and CD39
Authors: Maisa C. Takenaka, Galina Gabriely, Veit Rothhammer, Ivan D. Mascanfroni, Michael A. Wheeler, Chun-Cheih Chao, Cristina Gutiérrez-Vázquez, Jessica Kenison, Emily C. Tjon, Andreia Barroso, Tyler Vandeventer, Kalil Alves de Lima, Sonja Rothweiler, Lior Mayo, Soufiene Ghannam, Stephanie Zandee, Luke Healy, David Sherr, Mauricio F. Farez, Alexandre Prat, Jack Antel, David A. Reardon, Hailei Zhang, Simon C. Robson, Gad Getz, Howard L. Weiner, Francisco J. Quintana
Journal: Nature Neuroscience (2019)
Environmental variables and family history of breast cancer
Authors: Chris D. Bajdik, Raymond Fang, Pierre R. Band, Nhu D. Le, Rick P. Gallagher
Journal: Cancer Research (2004)

1088  Background: Women with a family history are at twice the risk of developing breast cancer than are women in the general population. The family history might be caused by genetic or environmental variables, or it might occur by chance. Germline mutations in BRCA1 and BRCA2 account for about half of familial breast cancer cases. Some authors have proposed that there are other, yet unknown, forms of genetic susceptibility to explain many of the remaining family histories. Indeed, no one has produced evidence that a substantial fraction of family histories is due to a non-chance, non-genetic variable. Methods: We reviewed data from a large population-based case-control study of breast cancer in British Columbia (BC), Canada, and tested whether non-genetic variables predicted which women had a family history of the disease. Results: Our analysis included 658 pre-menopausal women (318 breast cancer cases and 340 healthy controls) and 1384 post-menopausal women (699 cases and 685 controls). About 11% of pre-menopausal women had a family history of breast cancer (16% of cases and 7% of controls); about 16% of post-menopausal women had a family history of breast cancer (20% of cases and 12% of controls). The post-menopausal controls with a family history were older on average than the post-menopausal cases (p=0.005) but otherwise there were no major differences in non-genetic factors between women with and without a family history. Interpretation: A family history of breast cancer might be due to genetic or environmental factors, but our analysis has not found any environmental factors that predict whether a woman has a family history of breast cancer.
Nuclear lncRNA HOXD-AS1 suppresses colorectal carcinoma growth and metastasis via inhibiting HOXD3-induced integrin β3 transcriptional activating and MAPK/AKT signalling
Authors: Min-Hui Yang, Li Zhao, Lan Wang, Wen Ou-Yang, Sha-Sha Hu, Wen-Lu Li, Mei-Ling Ai, Yi-Qing Wang, Yue Han, Ting-Ting Li, Yan-Qing Ding, Shuang Wang
Journal: Molecular Cancer (2019)

Long noncoding RNAs (lncRNAs) have been indicated to play critical roles in cancer development and progression. LncRNA HOXD cluster antisense RNA1 (HOXD-AS1) has recently been found to be dysregulated in several cancers. However, the expression levels, cellular localization, precise function and mechanism of HOXD-AS1 in colorectal carcinoma (CRC) are largely unknown.Real-time PCR and in situ hybridization were used to detect the expression of HOXD-AS1 in CRC tissue samples and cell lines. Gain- and loss-of-function experiments were performed to investigate the biological roles of HOXD-AS1 in CRC cell line. RNA pull down, RNA immunoprecipitation and chromatin immunoprecipitation assays were conducted to investigate the mechanisms underlying the functions of HOXD-AS1 in CRC.We observed that HOXD-AS1 was located in the nucleus of CRC cells and that nuclear HOXD-AS1 was downregulated in most CRC specimens and cell lines. Lower levels of nuclear HOXD-AS1 expression were associated with poor outcomes of CRC patients. HOXD-AS1 downregulation enhanced proliferation and migration of CRC cells in vitro and facilitated CRC tumourigenesis and metastasis in vivo. Mechanistic investigations revealed that HOXD-AS1 could suppress HOXD3 transcription by recruiting PRC2 to induce the accumulation of the repressive marker H3K27me3 at the HOXD3 promoter. Subsequently, HOXD3, as a transcriptional activator, promoted Integrin β3 transcription, thereby activating the MAPK/AKT signalling pathways.Our results reveal a previously unrecognized HOXD-AS1-HOXD3-Integrin β3 regulatory axis involving in epigenetic and transcriptional regulation constitutes to CRC carcinogenesis and progression.
Association Between Insurance Status and Access to Hospital Care in Emergency Department Disposition
Authors: Arjun K. Venkatesh, Shih-Chuan Chou, Shu-Xia Li, Jennie Choi, Joseph S. Ross, Gail D’Onofrio, Harlan M. Krumholz, Kumar Dharmarajan
Journal: JAMA Internal Medicine (2019)

Studies of public hospitals have reported increasing incidence of emergency department (ED) transfers of uninsured patients for hospitalization, which is perceived to be associated with financial incentives.To examine the differences in risk-adjusted transfer and discharge rates by patient insurance status among hospitals capable of providing critical care.A cross-sectional analysis of the 2015 National Emergency Department Sample was conducted, including visits between January 2015 and December 2015. Adult ED visits throughout 2015 (n = 215 028) for the 3 common medical conditions of pneumonia, chronic obstructive pulmonary disease, and asthma, at hospitals with intensive care capabilities were included. Only hospitals with advanced critical care capabilities for pulmonary care were included.The primary outcomes were patient-level and hospital-level risk-adjusted ED discharges, ED transfers, and hospital admissions. Adjusted odds of discharge or transfer compared with admission among uninsured patients, Medicaid and Medicare beneficiaries, and privately insured patients are reported. Hospital ownership status was used for the secondary analysis.Of the 30 542 691 ED visits to 953 hospitals included in the 2015 National Emergency Department Sample, 215 028 visits (0.7%) were for acute pulmonary diseases to 160 intensive care-capable hospitals. These visits were made by patients with a median (interquartile range [IQR]) age of 55 (40-71) years and who were predominantly female (124 931 [58.1%]). Substantial variation in unadjusted and risk-standardized ED discharge, ED transfer, and hospital admission rates was found across EDs. Compared with privately insured patients, uninsured patients were more likely to be discharged (odds ratio [OR], 1.66; 95% CI, 1.57-1.76) and transferred (adjusted OR [aOR], 2.41; 95% CI, 2.08-2.79). Medicaid beneficiaries had comparable odds of discharge (aOR, 1.00; 95% CI, 0.97-1.04) but higher odds of transfer (aOR, 1.19; 95% CI, 1.05-1.33).After accounting for hospital critical care capability and patient case mix, the study found that uninsured patients and Medicaid beneficiaries with common medical conditions appeared to have higher odds of interhospital transfer.
Cerebral Intraparenchymal Hemorrhage
Authors: Bradley A. Gross, Brian T. Jankowitz, Robert M. Friedlander
Journal: JAMA (2019)

<h3>Importance</h3> Although spontaneous intraparenchymal hemorrhage (IPH) accounts for less than 20% of cases of stroke, it continues to be associated with the highest mortality of all forms of stroke and substantial morbidity rates. <h3>Observations</h3> Early identification and management of IPH is crucial. Blood pressure control, reversal of associated coagulopathy, care in a dedicated stroke unit, and identification of secondary etiologies are essential to optimizing outcomes. Surgical management of hydrocephalus and space occupying hemorrhage in the posterior fossa are accepted forms of treatment. Modern advances in minimally invasive surgical management of primary, supratentorial IPH are being explored in randomized trials. Hemorrhagic arteriovenous malformations and cavernous malformations are surgically excised if accessible, while hemorrhagic dural arteriovenous fistulas and distal/mycotic aneurysms are often managed with embolization if feasible. <h3>Conclusions and Relevance</h3> IPH remains a considerable source of neurological morbidity and mortality. Rapid identification, medical management, and neurosurgical management, when indicated, are essential to facilitate recovery. There is ongoing evaluation of minimally invasive approaches for evacuation of primary IPH and evolution of surgical and endovascular techniques in the management of lesions leading to secondary IPH.
Macrophage-lineage TRAP+ cells recruit periosteum-derived cells for periosteal osteogenesis and regeneration
Authors: Bo Gao, Ruoxian Deng, Yu Chai, Hao Chen, Bo Hu, Xiao Wang, Shouan Zhu, Yong Cao, Shuangfei Ni, Mei Wan, Liu Yang, Zhuojing Luo, Xu Cao
Journal: Journal of Clinical Investigation (2019)

The periosteum, a thin tissue that covers almost the entire bone surface, accounts for more than 80% of human bone mass and is essential for bone regeneration. Its osteogenic and bone regenerative abilities are well studied, but much is unknown about the periosteum. In this study, we found that macrophage-lineage cells recruit periosteum-derived cells (PDCs) for cortical bone formation. Knockout of colony stimulating factor-1 eliminated macrophage-lineage cells and resulted in loss of PDCs with impaired periosteal bone formation. Moreover, macrophage-lineage TRAP+ cells induced transcriptional expression of periostin and recruitment of PDCs to the periosteal surface through secretion of platelet-derived growth factor-BB (PDGF-BB), where the recruited PDCs underwent osteoblast differentiation coupled with type H vessel formation. We also found that subsets of Nestin+ and LepR+ PDCs possess multipotent and self-renewal abilities and contribute to cortical bone formation. Nestin+ PDCs are found primarily during bone development, whereas LepR+ PDCs are essential for bone homeostasis in adult mice. Importantly, conditional knockout of Pdgfrβ (platelet-derived growth factor receptor beta) in LepR+ cells impaired periosteal bone formation and regeneration. These findings uncover the essential role of periosteal macrophage-lineage cells in regulating periosteum homeostasis and regeneration.