tbuckley/cabot-search huggingface dataset:
Abstract PS9-56: High compliance with choosing wisely breast procedures at a safety net hospital
Authors: Annie Tang, Colin Mooney, Shannon Ugarte, Kevin Knopf, Amal Khoury
Journal: Cancer Research (2021)

Abstract The Choosing Wisely campaign has emerged recently in setting guidelines for surgical procedures of low utility and cost-ineffectiveness. Hospitals caring for underserved medical populations represent a unique opportunity to assess for quality of care and adherence to these guidelines. The Choosing Wisely campaign for breast surgery has highlighted: avoiding surgical re-excision for invasive cancer close to margins of excised breast tissue, avoiding double mastectomy in patients who have a single breast with cancer, avoidance of axillary lymph node dissection in women undergoing lumpectomy with limited nodal disease, and avoiding sentinel lymph node biopsy in patients ≥ 70 years of age with early stage breast cancer. Recent studies have shown variable adherence to these recommendations. In order to evaluate cost-effective surgery at our hospital serving a poorer patient population, we retrospectively analyzed patients who underwent surgery for breast cancer from 2015-2020. A total of 231 patients were identified. There were no patients who underwent re-excision for close margins of invasive cancer. Only 0.9% of patients (2/231) received contralateral mastectomy and only 1.6% of eligible patients (3/191) received axillary lymph node dissection instead of sentinel lymph node biopsy. Although 77.7% of patients ≥ 70 years of age with stage 1 hormone positive breast cancer (14/18) received sentinel lymph node biopsy, there was a downward trend during 2015 to 2020 from 100% to 50% of eligible patients receiving sentinel lymph node biopsy. De-implementation of traditional surgical practices, deemed as low-value care, towards newer cost-effective guidelines are achievable even at community hospitals serving a low socioeconomic community while preserving patient outcome and avoiding overtreatment. By avoiding overtreatment, cost savings can be achieved which allow for social distributive justice amongst breast cancer patients by ensuring careful utilization of scarce health economic resources. Citation Format: Annie Tang, Colin Mooney, Shannon Ugarte, Kevin Knopf, Amal Khoury. High compliance with choosing wisely breast procedures at a safety net hospital [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS9-56.
Oleic Acid and Eicosapentaenoic Acid Reverse Palmitic Acid-Induced Insulin Resistance in Human HepG2 Cells via the Reactive Oxygen Species/<i>JUN</i> Pathway
Authors: Yaping Sun, Jifeng Wang, Xiaojing Guo, Nali Zhu, Lili Niu, Xiang Ding, Zhensheng Xie, Xiulan Chen, Fuquan Yang
Journal: Genomics Proteomics & Bioinformatics (2021)

Abstract Oleic acid (OA), a monounsaturated fatty acid (MUFA), has previously been shown to reverse saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, its underlying molecular mechanism is unclear. In addition, previous studies have shown that eicosapentaenoic acid (EPA), a ω-3 polyunsaturated fatty acid (PUFA), reverses PA-induced muscle IR, but whether EPA plays the same role in hepatic IR and its possible mechanism involved need to be further clarified. Here, we confirmed that EPA reversed PA-induced IR in HepG2 cells and compared the proteomic changes in HepG2 cells after treatment with different free fatty acids (FFAs). A total of 234 proteins were determined to be differentially expressed after PA+OA treatment. Their functions were mainly related to responses to stress and endogenous stimuli, lipid metabolic process, and protein binding. For PA+EPA treatment, the PA-induced expression changes of 1326 proteins could be reversed by EPA, 415 of which were mitochondrial proteins, with most of the functional proteins involved in oxidative phosphorylation (OXPHOS) and tricarboxylic acid (TCA) cycle. Mechanistic studies revealed that the protein encoded by JUN and reactive oxygen species (ROS) play a role in OA- and EPA-reversed PA-induced IR, respectively. EPA and OA alleviated PA-induced abnormal adenosine triphosphate (ATP) production, ROS generation, and calcium (Ca2+) content. Importantly, H2O2-activated production of ROS increased the protein expression of JUN, further resulting in IR in HepG2 cells. Taken together, we demonstrate that ROS/JUN is a common response pathway employed by HepG2 cells toward FFA-regulated IR.
“Alongside-the-stiff-guidewire” – a novel variant technique for difficult sigmoid intubation using gastroscope-directed guidewire pre-insertion
Authors: Vincent Zimmer
Journal: Endoscopy (2021)

Colonoscopy completion may occasionally prove tricky, and many tricks of the trade have been reported to this end, albeit mostly on an individual basis [1]. Among the myriad rescue techniques when encountering difficult sigmoid intubation is gastroscope-directed guidewire insertion followed by over-the-wire scope insertion after wire backloading onto a colonoscope [2]. Here, a variant technique designated “alongside-the-stiff-guidewire” was pioneered and successfully applied without complications in five consecutive patients over the last 12 months (two patients referred and three in-patients, each with sigmoid intubation failures using the conventional colonoscopy approach) ([Table 1]).
Should spreading anti-vaccine misinformation be criminalised?
Authors: Melinda C Mills, Jonas Sivelä
Journal: BMJ (2021)

The spread of false health information casts a shadow over required vaccine coverage. <b>Melinda Mills</b> says that we must, reluctantly, consider criminalising people who deliberately spread false information—but <b>Jonas Sivelä</b> argues that the definitions are too murky and that criminalisation may do more harm than good
Association between ambient air pollution and development and persistence of atopic and non‐atopic eczema in a cohort of adults
Authors: Diego J. Lopez, Caroline J. Lodge, Dinh S. Bui, Nilakshi T. Waidyatillake, John C. Su, Jenny L. Perret, Luke D. Knibbs, Bircan Erbas, Paul S. Thomas, Garun S. Hamilton, Bruce R. Thompson, Michael J. Abramson, E. Haydn Walters, Shyamali C. Dharmage, Gayan Bowatte, Adrian J. Lowe
Journal: Allergy (2021)

Abstract Background There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. Methods Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO 2 ], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM 2.5 ]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years), and persistence were assessed from surveys, while IgE sensitization was assessed using skin prick tests. The presence or absence of eczema and sensitization was classified into four groups: no atopy or eczema, atopy alone, non‐atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. Results Of 3153 participants in both follow‐ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baselineNO 2 was associated with increased odds of prevalent eczema (OR = 1.15 [95% CI 0.98–1.36]) and prevalent atopic eczema (OR = 1.26 [1.00–1.59]). These associations were not seen in females ( p for interaction = 0.08, &lt;0.01). For both sexes, a 1.6 µg/m 3 increase in PM 2.5 exposure at follow‐up was associated with increased odds of aeroallergen sensitization (OR = 1.15 [1.03–1.30]). Conclusion Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders.
Experimental Designs to Optimize Treatments for Individuals
Authors: Karina W. Davidson, Michael Silverstein, Ken Cheung, Rocco A. Paluch, Leonard H. Epstein
Journal: JAMA Pediatrics (2021)

Conventional randomized clinical trials (RCTs) compare treatment effectiveness to provide support for evidence-based treatments that can be generalized to the average patient. However, the information obtained from RCTs may not always be useful for selecting the best treatment for individual patients. This article presents a complementary approach to identifying optimized treatments using experimental designs that focus on individuals. Personalized, or N-of-1, designs provide both a comparative analysis of treatments and a functional analysis demonstrating that changes in patient symptoms are likely because of the treatment implemented. This approach contributes to the zeitgeist of personalized medicine and provides clinicians with a paradigm for investigating optimal treatments for rare diseases for which RCTs are not always feasible, identifying personally effective treatments for patients with comorbidities who have historically been excluded from most RCTs, handling clinical situations in which patients respond idiosyncratically (either positively or negatively) to treatment, and shortening the time lag between identification and implementation of an evidence-based treatment. These designs merge experimental analysis of behavior methods used for decades in psychology with new methodological and statistical advances to assess significance levels of changes in individual patients, and they can be generalized to larger populations for meta-analytic purposes. This article presents a case for why these models are needed, an overview of how to apply personalized designs for different types of clinical scenarios, and a brief discussion of challenges associated with interpretation and implementation of personalized designs. The goal is to empower pediatricians to take personalized trial designs into clinical practice to identify optimal treatments for their patients.
Electrocardiographic Findings and Their Associations With Adverse Outcomes in Hospitalized Patients With COVID-19
Authors: M. Fatakdawala, J. Pang, R. Patel, T. Thannoun, C. Grable, S. Damaraju, S. B. Mawji, M. Folivi, S. Chauhan, C. Powell, M. A. Shabbir, R. Lyubarova, N. L. Palaskas, A. M. Deswal, H. Taegtmeyer, E. Garcia-Sayan, E. Koutroumpakis
Journal: Circulation (2020)
The Common Germline <i>TP53-R337H</i> Mutation Is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model
Authors: John R. Jeffers, Emilia M. Pinto, Jerold E. Rehg, Michael R. Clay, Jinling Wang, Geoffrey Neale, Richard J. Heath, Guillermina Lozano, Enzo Lalli, Bonald C. Figueiredo, Alberto S. Pappo, Carlos Rodriguez-Galindo, Wenan Chen, Stanley Pounds, Raul C. Ribeiro, Gerard P. Zambetti
Journal: Cancer Research (2021)

Abstract The TP53-R337H founder mutation exists at a high frequency throughout southern Brazil and represents one of the most common germline TP53 mutations reported to date. It was identified in pediatric adrenocortical tumors in families with a low incidence of cancer. The R337H mutation has since been found in association with early-onset breast cancers and Li–Fraumeni syndrome (LFS). To study this variability in tumor susceptibility, we generated a knockin mutant p53 mouse model (R334H). Endogenous murine p53-R334H protein was naturally expressed at high levels in multiple tissues and was functionally compromised in a tissue- and stress-specific manner. Mutant p53-R334H mice developed tumors with long latency and incomplete penetrance, consistent with many human carriers being at a low but elevated risk for cancer. These findings suggest the involvement of additional cooperating genetic alterations when TP53-R337H occurs in the context of LFS, which has important implications for genetic counseling and long-term clinical follow-up. Significance: A p53-R334H knockin mouse serves as an important model for studying the most common inherited germline TP53 mutation (R337H) that is associated with variable tumor susceptibility.
PPM1D mutations appear in complete remission after exposure to chemotherapy without predicting emerging AML relapse
Authors: Adil S. A. Al Hinai, Tim Grob, Melissa Rijken, François G. Kavelaars, Annelieke Zeilemaker, Claudia A. J. Erpelinck-Verschueren, Mathijs A. Sanders, Bob Löwenberg, Mojca Jongen-Lavrencic, Peter J. M. Valk
Journal: Leukemia (2021)
Abstract 14347: Biomechanical and Histological Analysis Supports Increased Stiffness and Fibrosis in Chronic versus Acute Aortic Dissection Flaps
Authors: Xiaoying Lou, Wei Sun, Minliang Liu, Fatiesa Sulejmani, Qing Zou, Muhammed Subhi Al Jabi, Edward P Chen, Bradley G Leshnower
Journal: Circulation (2019)

Introduction: Thoracic endovascular aortic repair (TEVAR) more effectively remodels the dissected aorta in acute vs chronic type B aortic dissection (TBAD). It has been hypothesized that this is du...
Pharmacological Interventions for Breathlessness—Absence of Effect or Absence of Evidence?
Authors: Hayley Barnes, Natasha Smallwood
Journal: JAMA Network Open (2021)

Josephine L. Feliciano, MD; Julie M. Waldfogel, PharmD, BCGP, CPE; Ritu Sharma, BSc; Allen Zhang, BS; Arjun Gupta, MD; Ramy Sedhom, MD; Jeff Day, MD, MA; Eric B. Bass, MD, MPH; Sydney M. Dy, MD, MS
Cultural mindsets shape what grounded procedures mean: Cleansing can separate or connect and separating can feel good or not so good
Authors: Daphna Oyserman
Journal: Behavioral and Brain Sciences (2021)

Are grounded procedures such as cleansing value-neutral main effects? Culture-as-situated-cognition theory suggests otherwise. Societies differ in how frequently they trigger membership and individualizing cultural mindsets and their linked mental-procedures - connecting and separating, respectively. Commonly triggered mindsets (and their linked mental-procedures) feel fluent. Fluency feels good. Cleansing can separate from but also connect to others in the form of membership-based rituals.
Asymptomatic Purpuric Eruption on the Scalp of a Middle-aged Man
Authors: Evgeniya Teterina Mohammed, Tejesh Patel
Journal: JAMA Oncology (2021)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
Sequelae in Adults at 6 Months After COVID-19 Infection
Authors: Jennifer K. Logue, Nicholas M. Franko, Denise J. McCulloch, Dylan McDonald, Ariana Magedson, Caitlin R. Wolf, Helen Y. Chu
Journal: JAMA Network Open (2021)

Many individuals experience persistent symptoms and a decline in health-related quality of life (HRQoL) after coronavirus disease 2019 (COVID-19) illness.1 Existing studies have focused on hospitalized individuals 30 to 90 days after illness onset2,3,4 and have reported symptoms up to 110 days after illness.3 Longer-term sequelae in outpatients have not been well characterized.
KDIGO 2021 Clinical Practice Guideline for the Management of Blood Pressure in Chronic Kidney Disease
Authors: Alfred K. Cheung, Tara I. Chang, William C. Cushman, Susan L. Furth, Fan Fan Hou, Joachim H. Ix, Gregory A. Knoll, Paul Muntner, Roberto Pecoits-Filho, Mark J. Sarnak, Sheldon W. Tobe, Charles R.V. Tomson, Johannes F.E. Mann
Journal: Kidney International (2021)

The Kidney Disease: Improving Global Outcomes (KDIGO) 2021 Clinical Practice Guideline for the Management of Blood Pressure in Chronic Kidney Disease (CKD) represents an update to the 2012 KDIGO guideline on this topic. The scope includes topics covered in the original guideline, such as optimal blood pressure targets, lifestyle interventions, and antihypertensive therapies in CKD patients not receiving dialysis, including special populations such as kidney transplant recipients and children. In addition, this guideline introduces a chapter dedicated to proper blood pressure measurement. The goal of the guideline is to serve as a useful resource for clinicians and patients by providing actionable recommendations with useful infographics based on a rigorous formal systematic review. Another aim is to propose research recommendations for areas in which there are gaps in knowledge. The guideline targets clinicians treating high blood pressure and CKD, while taking into account policy and resource implications. Development of this guideline update followed an explicit process of evidence review. Treatment approaches and guideline recommendations are based on systematic reviews of relevant studies, and appraisal of the quality of the evidence and the strength of recommendations followed the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Limitations of the evidence are discussed, and areas of future research are presented.
Impact of diabetes on promoting the growth of breast cancer
Authors: Ping‐Chieh Chou, Hyun Ho Choi, Yizhi Huang, Enrique Fuentes‐Mattei, Guermarie Velazquez‐Torres, Fanmao Zhang, Liem Phan, Jaehyuk Lee, Yanxia Shi, James A. Bankson, Yun Wu, Huamin Wang, Ruiying Zhao, Sai‐Ching Jim Yeung, Mong‐Hong Lee
Journal: Cancer Communications (2021)

Type II diabetes mellitus (DM2) is a significant risk factor for cancers, including breast cancer. However, a proper diabetic breast cancer mouse model is not well-established for treatment strategy design. Additionally, the precise diabetic signaling pathways that regulate cancer growth remain unresolved. In the present study, we established a suitable mouse model and demonstrated the pathogenic role of diabetes on breast cancer progression.We successfully generated a transgenic mouse model of human epidermal growth factor receptor 2 positive (Her2+ or ERBB2) breast cancer with DM2 by crossing leptin receptor mutant (Leprdb/+ ) mice with MMTV-ErbB2/neu) mice. The mouse models were administrated with antidiabetic drugs to assess the impacts of controlling DM2 in affecting tumor growth. Magnetic resonance spectroscopic imaging was employed to analyze the tumor metabolism.Treatment with metformin/rosiglitazone in MMTV-ErbB2/Leprdb/db mouse model reduced serum insulin levels, prolonged overall survival, decreased cumulative tumor incidence, and inhibited tumor progression. Anti-insulin resistance medications also inhibited glycolytic metabolism in tumors in vivo as indicated by the reduced metabolic flux of hyperpolarized 13 C pyruvate-to-lactate reaction. The tumor cells from MMTV-ErbB2/Leprdb/db transgenic mice treated with metformin had reprogrammed metabolism by reducing levels of both oxygen consumption and lactate production. Metformin decreased the expression of Myc and pyruvate kinase isozyme 2 (PKM2), leading to metabolism reprogramming. Moreover, metformin attenuated the mTOR/AKT signaling pathway and altered adipokine profiles.MMTV-ErbB2/Leprdb/db mouse model was able to recapitulate diabetic HER2+ human breast cancer. Additionally, our results defined the signaling pathways deregulated in HER2+ breast cancer under diabetic condition, which can be intervened by anti-insulin resistance therapy.
Abstract 14833: Which Vessel is Preferred to Initiate Spasm Provocation Test: Right or Left Coronary Artery?
Authors: Hiroki Teragawa, Chikage Oshita, Yuichi Orita
Journal: Circulation (2019)

Introduction: Although spasm provocation test (SPT) is a critical test for diagnosing vasospastic angina (VSA), it remains unclear which vessel is preferred to initiate SPT—the right coronary arter...
Abstract 15669: Serum Albumin and Incident Heart Failure: Insights From Epidemiological and Mendelian Randomization Studies
Authors: Xiaodong Zhuang, Lizhen Liao, Shaozhao Zhang, Xinxue Liao
Journal: Circulation (2019)

Introduction: To characterize the nature and magnitude of prospective association between serum albumin and incident heart failure (HF), and to investigate any causal relevance to the association u...
Transcription Factor MAFF (MAF Basic Leucine Zipper Transcription Factor F) Regulates an Atherosclerosis Relevant Network Connecting Inflammation and Cholesterol Metabolism
Authors: Moritz von Scheidt, Yuqi Zhao, Thomas Q. de Aguiar Vallim, Nam Che, Michael Wierer, Marcus M. Seldin, Oscar Franzén, Zeyneb Kurt, Shichao Pang, Dario Bongiovanni, Masayuki Yamamoto, Peter A. Edwards, Arno Ruusalepp, Jason C. Kovacic, Matthias Mann, Johan L.M. Björkegren, Aldons J. Lusis, Xia Yang, Heribert Schunkert
Journal: Circulation (2021)

Coronary artery disease (CAD) is a multifactorial condition with both genetic and exogenous causes. The contribution of tissue-specific functional networks to the development of atherosclerosis remains largely unclear. The aim of this study was to identify and characterize central regulators and networks leading to atherosclerosis.Based on several hundred genes known to affect atherosclerosis risk in mouse (as demonstrated in knockout models) and human (as shown by genome-wide association studies), liver gene regulatory networks were modeled. The hierarchical order and regulatory directions of genes within the network were based on Bayesian prediction models, as well as experimental studies including chromatin immunoprecipitation DNA-sequencing, chromatin immunoprecipitation mass spectrometry, overexpression, small interfering RNA knockdown in mouse and human liver cells, and knockout mouse experiments. Bioinformatics and correlation analyses were used to clarify associations between central genes and CAD phenotypes in both human and mouse.The transcription factor MAFF (MAF basic leucine zipper transcription factor F) interacted as a key driver of a liver network with 3 human genes at CAD genome-wide association studies loci and 11 atherosclerotic murine genes. Most importantly, expression levels of the low-density lipoprotein receptor (LDLR) gene correlated with MAFF in 600 CAD patients undergoing bypass surgery (STARNET [Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task]) and a hybrid mouse diversity panel involving 105 different inbred mouse strains. Molecular mechanisms of MAFF were tested in noninflammatory conditions and showed positive correlation between MAFF and LDLR in vitro and in vivo. Interestingly, after lipopolysaccharide stimulation (inflammatory conditions), an inverse correlation between MAFF and LDLR in vitro and in vivo was observed. Chromatin immunoprecipitation mass spectrometry revealed that the human CAD genome-wide association studies candidate BACH1 (BTB domain and CNC homolog 1) assists MAFF in the presence of lipopolysaccharide stimulation with respective heterodimers binding at the MAF recognition element of the LDLR promoter to transcriptionally downregulate LDLR expression.The transcription factor MAFF was identified as a novel central regulator of an atherosclerosis/CAD-relevant liver network. MAFF triggered context-specific expression of LDLR and other genes known to affect CAD risk. Our results suggest that MAFF is a missing link between inflammation, lipid and lipoprotein metabolism, and a possible treatment target.