tbuckley/cabot-search huggingface dataset:
The Effect of Finasteride on the Risk of Acute Urinary Retention and the Need for Surgical Treatment among Men with Benign Prostatic Hyperplasia
Authors: John D. McConnell, Reginald Bruskewitz, Patrick Walsh, Gerald Andriole, Michael Lieber, H. Logan Holtgrewe, Peter Albertsen, Claus G. Roehrborn, J. Curtis Nickel, Daniel Z. Wang, Alice M. Taylor, Joanne Waldstreicher
Journal: New England Journal of Medicine (1998)

Finasteride is known to improve urinary symptoms in men with benign prostatic hyperplasia, but the extent to which the benefit is sustained and whether finasteride reduces the incidence of related events, including the need for surgery and the development of acute urinary retention, are not known.
High Mobility Group Box‐1 Drives Fibrosis Progression Signaling via the Receptor for Advanced Glycation End Products in Mice
Authors: Xiaodong Ge, Elena Arriazu, Fernando Magdaleno, Daniel J. Antoine, Rouchelle dela Cruz, Neil Theise, Natalia Nieto
Journal: Hepatology (2018)

High‐mobility group box‐1 (HMGB1) is a damage‐associated molecular pattern (DAMP) increased in response to liver injury. Because HMGB1 is a ligand for the receptor for advanced glycation endproducts (RAGE), we hypothesized that induction of HMGB1 could participate in the pathogenesis of liver fibrosis though RAGE cell‐specific signaling mechanisms. Liver HMGB1 protein expression correlated with fibrosis stage in patients with chronic hepatitis C virus (HCV) infection, primary biliary cirrhosis (PBC), or alcoholic steatohepatitis (ASH). Hepatic HMGB1 protein expression and secretion increased in five mouse models of liver fibrosis attributed to drug‐induced liver injury (DILI), cholestasis, ASH, or nonalcoholic steatohepatitis (NASH). HMGB1 was up‐regulated and secreted mostly by hepatocytes and Kupffer cells (KCs) following CCl 4 treatment. Neutralization of HMGB1 protected, whereas injection of recombinant HMGB1 promoted liver fibrosis. Hmgb1 ablation in hepatocytes ( Hmgb1 ΔHep ) or in myeloid cells ( Hmgb1 ΔMye ) partially protected, whereas ablation in both ( Hmgb1 ΔHepΔMye ) prevented liver fibrosis in vivo . Coculture with hepatocytes or KCs from CCl 4 ‐injected wild‐type (WT) mice up‐regulated Collagen type I production by hepatic stellate cells (HSCs); yet, coculture with hepatocytes from CCl 4 ‐injected Hmgb1 ΔHep or with KCs from CCl 4 ‐injected Hmgb1 ΔMye mice partially blunted this effect. Rage ablation in HSCs ( Rage ΔHSC ) and RAGE neutralization prevented liver fibrosis. Last, we identified that HMGB1 stimulated HSC migration and signaled through RAGE to up‐regulate Collagen type I expression by activating the phosphorylated mitogen‐activated protein kinase kinase (pMEK)1/2, phosphorylated extracellular signal‐regulated kinase (pERK)1/2 and pcJun signaling pathway. Conclusion: Hepatocyte and KC‐derived HMGB1 participates in the pathogenesis of liver fibrosis by signaling through RAGE in HSCs to activate the pMEK1/2, pERK1/2 and pcJun pathway and increase Collagen type I deposition.
Best Evidence Supports Annual Surveillance for Resected Colorectal Cancer
Authors: Hanna K. Sanoff
Journal: JAMA (2018)

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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Use of Outpatient Rehabilitation Among Adult Stroke Survivors — 20 States and the District of Columbia, 2013, and Four States, 2015
Authors: Carma Ayala, Jing Fang, Cecily Luncheon, Sallyann Coleman King, Tiffany Chang, Matthew Ritchey, Fleetwood Loustalot
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

Stroke is a leading cause of mortality and disability in the United States (1,2). Approximately 800,000 American adults experience a stroke each year (2,3). Currently, approximately 6 million stroke survivors live in the United States (2). Participation in stroke rehabilitation (rehab), which occurs in diverse settings (i.e., in-hospital, postacute care, and outpatient settings), has been determined to reduce stroke recurrence and improve functional outcomes and quality of life (3,4). Despite longstanding national guidelines recommending stroke rehab, it remains underutilized, especially in the outpatient setting. Professional associations and evidence-based guidelines support the increasing stroke rehab use in health systems and are promoted by the public health community (3-6). An analysis of 2005 Behavioral Risk Factor Surveillance System (BRFSS) data revealed that 30.7% of stroke survivors reported participation in outpatient rehab for stroke after hospital discharge in 21 states and the District of Columbia (DC) (7). To update these estimates, 2013 and 2015 BRFSS data were analyzed to assess outpatient rehab use among adult stroke survivors. Overall, outpatient rehab use was 31.2% (20 states and DC) in 2013 and 35.5% (four states) in 2015. Disparities were evident by sex, race, Hispanic origin, and level of education. Focused attention on system-level interventions that ensure participation is needed, especially among disparate populations with lower levels of participation.
Blaschkoid Acute Graft-vs-Host Disease
Authors: Vishal Gupta, Sudheer Arava, M. Ramam
Journal: JAMA Dermatology (2018)

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 Dermatology 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 Dermatology journal
As-Needed Budesonide–Formoterol versus Maintenance Budesonide in Mild Asthma
Authors: Eric D. Bateman, Helen K. Reddel, Paul M. O’Byrne, Peter J. Barnes, Nanshan Zhong, Christina Keen, Carin Jorup, Rosa Lamarca, Agnieszka Siwek-Posluszna, J. Mark FitzGerald
Journal: New England Journal of Medicine (2018)

Patients with mild asthma often rely on inhaled short-acting β2-agonists for symptom relief and have poor adherence to maintenance therapy. Another approach might be for patients to receive a fast-acting reliever plus an inhaled glucocorticoid component on an as-needed basis to address symptoms and exacerbation risk.We conducted a 52-week, double-blind, multicenter trial involving patients 12 years of age or older who had mild asthma and were eligible for treatment with regular inhaled glucocorticoids. Patients were randomly assigned to receive twice-daily placebo plus budesonide-formoterol (200 μg of budesonide and 6 μg of formoterol) used as needed or budesonide maintenance therapy with twice-daily budesonide (200 μg) plus terbutaline (0.5 mg) used as needed. The primary analysis compared budesonide-formoterol used as needed with budesonide maintenance therapy with regard to the annualized rate of severe exacerbations, with a prespecified noninferiority limit of 1.2. Symptoms were assessed according to scores on the Asthma Control Questionnaire-5 (ACQ-5) on a scale from 0 (no impairment) to 6 (maximum impairment).A total of 4215 patients underwent randomization, and 4176 (2089 in the budesonide-formoterol group and 2087 in the budesonide maintenance group) were included in the full analysis set. Budesonide-formoterol used as needed was noninferior to budesonide maintenance therapy for severe exacerbations; the annualized rate of severe exacerbations was 0.11 (95% confidence interval [CI], 0.10 to 0.13) and 0.12 (95% CI, 0.10 to 0.14), respectively (rate ratio, 0.97; upper one-sided 95% confidence limit, 1.16). The median daily metered dose of inhaled glucocorticoid was lower in the budesonide-formoterol group (66 μg) than in the budesonide maintenance group (267 μg). The time to the first exacerbation was similar in the two groups (hazard ratio, 0.96; 95% CI, 0.78 to 1.17). The change in ACQ-5 score showed a difference of 0.11 units (95% CI, 0.07 to 0.15) in favor of budesonide maintenance therapy.In patients with mild asthma, budesonide-formoterol used as needed was noninferior to twice-daily budesonide with respect to the rate of severe asthma exacerbations during 52 weeks of treatment but was inferior in controlling symptoms. Patients in the budesonide-formoterol group had approximately one quarter of the inhaled glucocorticoid exposure of those in the budesonide maintenance group. (Funded by AstraZeneca; SYGMA 2 ClinicalTrials.gov number, NCT02224157 .).
HIV Preexposure Prophylaxis in the U.S. Military Services — 2014–2016
Authors: Jason M. Blaylock, Shilpa Hakre, Jason F. Okulicz, Eric Garges, Kerry Wilson, Jenny Lay, Ellen A. Roska, Nelson L. Michael, Charmagne G. Beckett, Steven B. Cersovsky, Sheila A. Peel, Paul T. Scott
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

Human immunodeficiency virus (HIV) infection is a substantial health concern for the U.S. Department of Defense (DoD) and for service members stationed throughout the world. Each year, approximately 350 new HIV infections are diagnosed in members of the U.S. military services, with most infections acquired within the United States (1). The DoD populations most affected by HIV mirror those in the U.S. civilian population; the highest rates of new military diagnoses are in men and blacks or African Americans (blacks) (1). Blacks are disproportionally affected, and most new diagnoses occur among men who have sex with men (MSM). HIV preexposure prophylaxis (PrEP) is approximately 90% effective in preventing HIV infection when used properly (2), and an increasing number of active duty personnel have used HIV prevention services and PrEP in the military health system since the repeal of "Don't Ask, Don't Tell"* in 2011 (3). Military health system and service records were reviewed to describe HIV PrEP use among military personnel, and military health care providers were surveyed to assess HIV PrEP knowledge and attitudes. Among 769 service members prescribed PrEP during February 1, 2014-June 10, 2016, 60% received prescriptions from an infectious disease provider, 19% were black men, and 42% were aged >28 years. Half of surveyed military health care providers self-rated their PrEP knowledge as poor. DoD is developing new policy to address access to care challenges by defining requirements and establishing pathways for universal patient access to PrEP.
Endoscopic closure of a chronic tracheo-esophageal fistula with an over-the-scope suturing technique
Authors: Marco Bustamante Bernal, Srinidhi Bhat, Antonio Mendoza-Ladd
Journal: Endoscopy (2018)

A 47-year-old Hispanic woman developed a tracheo-esophageal fistula (TEF) secondary to prolonged intubation for septic shock with multiple organ dysfunction. Upon extubation, the patient complained of persistent dysphagia, and a barium swallow showed a TEF, for which a temporary percutaneous gastrostomy tube was placed to prevent aspiration until surgical closure was performed. Unfortunately, the patient was lost to follow-up. A year later, she was admitted to our institution for leakage around the gastrostomy site and for closure evaluation of the TEF.
Abstract 17483: Tert-butylhydroquinone Induces Gene Expression of Anti-oxidant Enzymes in Human Coronary Artery Endothelial Cells After Cyclosporine Treatment
Authors: Arash Ghashghai, David Banner, Roberto Ribeiro, Maja Degan, Mitesh Badiwala, Vivek Rao
Journal: Circulation (2016)

Introduction:  Cyclosporine (CsA) is an important immunosuppressant; however it may lead to oxidative stress in coronary vasculature and subsequently cardiac allograft vasculopathy (CAV). We previously demonstrated that CsA impairs kinematics of the master antioxidant gene regulator - nuclear factor erythroid 2–related factor 2 (Nrf2) in Human Coronary Artery Endothelial Cells (HCAECs).   Hypothesis:  We assessed the hypothesis that tert-hydroquinone (tBHQ), an Nrf2 agonist, rescues CsA-mediated downregulation of antioxidant enzymes via increase in gene expression of Nrf2.   Methods:  HCAECs (n=6) were treated with 50μg/ml CsA ± 20μM tBHQ or tBHQ alone for 2 hours. Control (CON) groups received 0.1% DMSO. Quantitative-real time polymerase chain reaction was performed to assess gene expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), superoxide dismutase 1 (SOD1), and -2 (SOD2) at 2 hours. We also assessed Nrf2 gene expression at 2 hours.   Results:  Compared to control, CsA decreased the expression of NQO1, SOD1, and SOD2, but not HO-1. Exposure to tBHQ alone resulted in increased expression of NQO1, SOD2, and Nrf2, but not HO-1, and SOD1 compared to control. When cells were exposed to both tBHQ and CsA, we determined that expressions of NQO1, HO-1, SOD2 and Nrf2 were synergistically upregulated. Concomitant exposure to tBHQ partially restored the downregulated expression of SOD1 compared to CsA alone, but did not achieve control levels.   Conclusion:  Oxidative stress is increasingly known as a key component in pathogenesis of post-heart transplant coronary vasculopathy which is associated with morbidity and mortality. In conclusion, heart transplant patients who receive CsA therapy, may benefit from exposure to tBHQ since tBHQ-CsA co-therapy may mitigate coronary artery oxidative stress.
Enhanced Cardiomyocyte NLRP3 Inflammasome Signaling Promotes Atrial Fibrillation
Authors: Chunxia Yao, Tina Veleva, Larry Scott, Shuyi Cao, Luge Li, Gong Chen, Prince Jeyabal, Xiaolu Pan, Katherina M. Alsina, Issam Abu-Taha, Shokoufeh Ghezelbash, Corey L. Reynolds, Ying H. Shen, Scott A. LeMaire, Wilhelm Schmitz, Frank U. Müller, Ali El-Armouche, N. Tony Eissa, Christine Beeton, Stanley Nattel, Xander H.T. Wehrens, Dobromir Dobrev, Na Li
Journal: Circulation (2018)

Atrial fibrillation (AF) is frequently associated with enhanced inflammatory response. The NLRP3 (NACHT, LRR, and PYD domain containing protein 3) inflammasome mediates caspase-1 activation and interleukin-1β release in immune cells but is not known to play a role in cardiomyocytes (CMs). Here, we assessed the role of CM NLRP3 inflammasome in AF.
Response by Good et al to Letter Regarding Article, “Pannexin-1 Channels as an Unexpected New Target of the Antihypertensive Drug Spironolactone”
Authors: Miranda E. Good, Yu-Hsin Chiu, Ivan K.H. Poon, Iris Z. Jaffe, Douglas A. Bayliss, Brant E. Isakson, Kodi S. Ravichandran
Journal: Circulation Research (2018)
Abstract 10512: Does integration of Personalized Ultrasound into Ward Rounds Influence Patient Management?
Authors: Marco Campo dell’ Orto, Florian Seeger, Peter Zechner, Christain Hamm, Raoul Breitkreutz
Journal: Circulation (2013)

Background:  Point-of-care ultrasound has become more popular in the environment of acute and critical care medicine. There is an ongoing debate as to whether miniaturization of ultrasound devices can improve patient care. The potential personalized usage opens up the field of ultrasound in acute and critical care medicine for a large group of new users. Our aim, therefore, was the frequency of use, decision-making, and time consumption of personalized ultrasound (PersUS) implementation in the daily routine.   Methods:  In a cardiological and nephrological speciality care unit a PersUS (VscanTM; GE Healthcare, Wauwatsoa, WI, USA) device was randomized between two wards by switching presence or absence on alternating calendar days. The ward rounds teams were blinded to the study aims and differed from day to day. They were instructed to use PersUS whenever it was available and note the times and indications of use. All data was then sorted into Group A (control group) or Group B (PersUS). Exam time per patient per ward round was calculated. Our null hypothesis was that the exam time per patient would not change significantly by using PersUS on ward rounds.   Results:  Patients were enrolled between July 2010 and September 2011 after approval of the local Ethics Comittee. The PersUS was integrated into 53 regular ward rounds with a total of 1007 patients on two wards. Mean ward round operation time was 142±33 minutes with 18±3 patients per ward. In 194 of 1007 (19 %) patient visits an ultrasound exam was requested. The average PersUS examination time was 3.6±2 minutes per patient. Interestingly, this PersUS integration into the ward rounds management effected a significant reduction of the time needed per patient from a mean of 8.9 minutes to 7.2 minutes. Patient referral to the echo lab for further examination was deemed necessary for 95 of 473 patients (20,1 %) in group A, only 12 of 534 patients (2,2 %) in group B ).   Conclusion:  PersUS markedly reduced both contact times per patient in ward rounds and request for patient referral to an echo lab. It thus may optimize patient process management.
Abstract B11: Foxm1 mediates maintenance and progression of mouse lung tumor driven by oncogenic Kras
Authors: Sheng-Yang Chao, Chien-Cheng Li, Sheng-Kai Liang, Yi-Shiuan Chiu, Yi-Kai Lin, Chia-Chan Hsu, Jen-Kun Chen, Tsui-Chun Tsou, I-Ching Wang
Journal: Cancer Research (2018)

Abstract Oncogenic mutation of Kras gene is one of the major causes of non-small cell lung cancer (NSCLC), and there is no effective chemotherapy agent available for targeting cancers harboring oncogenic Kras mutations. Hence, identifying new downstream molecular targets of KRAS signaling is critical for improving current therapeutic outcomes. Previous research has demonstrated that increased activity and expression of Forkhead box M1 (FOXM1) transcription factor are associated with poor prognosis in NSCLC patients. We and others have reported that FOXM1 regulates gene transcription network of cell cycle, angiogenesis, epithelial-to-mesenchymal transition (EMT), cell migration, and cancer stemness. Deletion of Foxm1 alleles in respiratory epithelial cells diminished the lung tumor initiation in SPC-rtTA/tetO-KrasG12D/Foxm1-/- mice; however, whether Foxm1 is critical for Kras mutant tumor maintenance and progression remains unclear. Herein, we report that intratracheal (IT) injected adenoviral Ad-Cre to CCSP-rtTA/tetO-KrasG12D/Foxm1fl/fl mice that bear induced KRAS mutant lung tumors, causing 75% of preexisting lung tumor regression as detected by micro-computed tomography (μCT). IT treatment with Ad-Cre that mediated genetically deletion of Foxm1 alleles in lungs, resulted in reduced proliferation of tumor cells. Moreover, in vitro disruption of FOXM1 expression by shRNA diminished cell proliferation on plate and anchorage-independent growth in soft agar of KRAS-mutated lung cancer NCI-H23 as well as KRASG12D-transformed BEAS-2B cells. Accordingly, these results demonstrated that Foxm1 is critical for oncogenic KRAS signaling pathway in both maintenance and progression of lung adenocarcinoma, suggesting that Foxm1 could be a potential therapeutic target to improve the outcome of KRAS mutant lung cancer treatment. Citation Format: Sheng-Yang Chao, Chien-Cheng Li, Sheng-Kai Liang, Yi-Shiuan Chiu, Yi-Kai Lin, Chia-Chan Hsu, Jen-Kun Chen, Tsui-Chun Tsou, I-Ching Wang. Foxm1 mediates maintenance and progression of mouse lung tumor driven by oncogenic Kras [abstract]. In: Proceedings of the AACR Special Conference: Advances in Modeling Cancer in Mice: Technology, Biology, and Beyond; 2017 Sep 24-27; Orlando, Florida. Philadelphia (PA): AACR; Cancer Res 2018;78(10 Suppl):Abstract nr B11.
Photo-excitable hybrid nanocomposites for image-guided photo/TRAIL synergistic cancer therapy
Authors: Gan Lin, Yang Zhang, Congqing Zhu, Chengchao Chu, Yesi Shi, Xin Pang, En Ren, Yayun Wu, Peng Mi, Haiping Xia, Xiaoyuan Chen, Gang Liu
Journal: Biomaterials (2018)
Serious Infections in Rheumatoid Arthritis Offspring Exposed to Tumor Necrosis Factor Inhibitors
Authors: Évelyne Vinet, Cristiano De Moura, Christian A. Pineau, Michal Abrahamowicz, Jeffrey R. Curtis, Sasha Bernatsky
Journal: Arthritis & Rheumatology (2018)

To evaluate the risk of serious infections in rheumatoid arthritis (RA) offspring exposed to tumor necrosis factor inhibitors (TNFi) in the gestational period compared to unexposed RA offspring, as well as to children from the general population.We used US claim data (2011-2015) to identify 2,989 offspring born to women who have RA and a randomly selected group of 14,596 control children, matched ≥4:1 for maternal age, year of delivery, and state of residence. We defined TNFi exposure based on ≥1 filled prescription during pregnancy. We ascertained serious infections based on ≥1 hospitalization, with infection as a primary diagnosis, at ≤12 months of life. We performed multivariable analyses, adjusting for maternal demographics, comorbidities, pregnancy complications, and drugs.Among RA offspring, 380 (12.7%) were exposed to TNFi during pregnancy. The percentage of serious infections in RA offspring with no TNFi exposure (2.0%; 95% confidence interval [95% CI] 1.5, 2.6) was similar to that in non-RA offspring (1.9%; 95% CI 1.9, 2.2), while the percentage of serious infections in RA offspring with TNFi exposure was 3.2% (95% CI 1.5, 5.6). In multivariable analyses, we were unable to establish an increased risk of serious infections in RA offspring exposed to TNFi versus both non-RA offspring (odds ratio [OR] 1.7, 95% CI 0.8, 3.7) and RA offspring unexposed to TNFi (OR 1.4, 95% CI 0.7, 2.8).We did not demonstrate a marked excess risk for serious infections in RA offspring exposed to TNFi during pregnancy versus unexposed RA offspring or general population controls.
Tumor immune evasion arises through loss of TNF sensitivity
Authors: Conor J. Kearney, Stephin J. Vervoort, Simon J. Hogg, Kelly M. Ramsbottom, Andrew J. Freeman, Najoua Lalaoui, Lizzy Pijpers, Jessica Michie, Kristin K. Brown, Deborah A. Knight, Vivien Sutton, Paul A. Beavis, Ilia Voskoboinik, Phil K. Darcy, John Silke, Joseph A. Trapani, Ricky W. Johnstone, Jane Oliaro
Journal: Science Immunology (2018)

Whole-genome CRISPR screens identify resistance to TNF-mediated killing by T and NK cells as a tumor immune evasion mechanism.