tbuckley/cabot-search huggingface dataset:
BELGRADE
Journal: JAMA (1934)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
<i>ERJ</i>Podcast November 2017: ERS statement on the diagnosis and treatment of pulmonary disease caused by α<sub>1</sub>-antitrypsin deficiency
Journal: European Respiratory Journal (2017)

As part of the November issue, the European Respiratory Journal presents the latest in its series of podcasts. Chief editor Marc Humbert discusses the ERS statement on the diagnosis and treatment of pulmonary disease caused by α1-antitrypsin deficiency with Task Force chairs Marc Miravitlles (Hospital Universitari Vall d'Hebron, Barcelona, Spain) and Robert A. Stockley (Queen Elizabeth Hospital, Birmingham, UK).
1735P SARS-CoV-2 infection induces EMT-like molecular changes, including ZEB1-mediated repression of the viral receptor ACE2, in lung cancer models
Authors: C.A. Stewart, C. Gay, K. Ramkumar, K.R. Cargill, R. Cardnell, M. Nilsson, S. Heeke, E.M. Park, S. Kundu, L. Diao, Q. Wang, L. Shen, Y. Xi, C.M. Della Corte, K. Kundu, D.L. Gibbons, J. Wang, J.V. Heymach, L.A. Byers
Journal: Annals of Oncology (2020)
Clinical impact of vivax malaria: A collection review
Authors: Aung Pyae Phyo, Prabin Dahal, Mayfong Mayxay, Elizabeth A. Ashley
Journal: PLoS Medicine (2022)

Background Plasmodium vivax infects an estimated 7 million people every year. Previously, vivax malaria was perceived as a benign condition, particularly when compared to falciparum malaria. Reports of the severe clinical impacts of vivax malaria have been increasing over the last decade. Methods and findings We describe the main clinical impacts of vivax malaria, incorporating a rapid systematic review of severe disease with meta-analysis of data from studies with clearly defined denominators, stratified by hospitalization status. Severe anemia is a serious consequence of relapsing infections in children in endemic areas, in whom vivax malaria causes increased morbidity and mortality and impaired school performance. P . vivax infection in pregnancy is associated with maternal anemia, prematurity, fetal loss, and low birth weight. More than 11,658 patients with severe vivax malaria have been reported since 1929, with 15,954 manifestations of severe malaria, of which only 7,157 (45%) conformed to the World Health Organization (WHO) diagnostic criteria. Out of 423 articles, 311 (74%) were published since 2010. In a random-effects meta-analysis of 85 studies, 68 of which were in hospitalized patients with vivax malaria, we estimated the proportion of patients with WHO-defined severe disease as 0.7% [95% confidence interval (CI) 0.19% to 2.57%] in all patients with vivax malaria and 7.11% [95% CI 4.30% to 11.55%] in hospitalized patients. We estimated the mortality from vivax malaria as 0.01% [95% CI 0.00% to 0.07%] in all patients and 0.56% [95% CI 0.35% to 0.92%] in hospital settings. WHO-defined cerebral, respiratory, and renal severe complications were generally estimated to occur in fewer than 0.5% patients in all included studies. Limitations of this review include the observational nature and small size of most of the studies of severe vivax malaria, high heterogeneity of included studies which were predominantly in hospitalized patients (who were therefore more likely to be severely unwell), and high risk of bias including small study effects. Conclusions Young children and pregnant women are particularly vulnerable to adverse clinical impacts of vivax malaria, and preventing infections and relapse in this groups is a priority. Substantial evidence of severe presentations of vivax malaria has accrued over the last 10 years, but reporting is inconsistent. There are major knowledge gaps, for example, limited understanding of the underlying pathophysiology and the reason for the heterogenous geographical distribution of reported complications. An adapted case definition of severe vivax malaria would facilitate surveillance and future research to better understand this condition.
HDAC Inhibition in the Heart
Authors: Thomas G. Gillette
Journal: Circulation (2021)

Alterations in the transcriptional profile of cells govern downstream events fundamental to both physiology and pathology.Central in this control of transcription are changes in chromatin structure elicited by post-translational modifications of histone proteins. 1The protein machinery that act to add, remove, or detect these modifications are known colloquially as writers, erasers, and readers of histone modifications. 2 There is great interest in the clinical application of small molecules that alter the activity of these proteins in the hope of fostering clinical benefit.Small molecule inhibitors of a class of "erasers" known as histone deacetylases (HDACs) have made their way to the clinic. 3s the name implies, HDAC proteins remove acetyl groups from histone protein tails, but they can also target nonhistone proteins.HDACs fall into 4 different classes (I, II, III, and IV).Class I, II, and IV share a conserved zinc-dependent functional domain and most small molecule inhibitors in use target that domain. 3 number of HDAC inhibitors (HDACis) have been approved by the US Food and Drug Administration for the treatment of various cancers, with >60 clinical trials reported as currently active on clinicaltrials.gov.The list of approved drugs includes the pan-HDACis vorinostat, panobinostat, and belinostat, which inhibit class I, II, and IV HDACs, and the more specific class I HDACi romidepsin.3 The safety and efficacy of these drugs in treating cancers have spurred preclinical testing for use in a variety of other diseases including heart disease.2,3 Early indications of the potential of HDACi to treat heart disease emerged from results using a mouse model of aortic constriction.4,5 This model of pressure overload-induced hypertrophy is marked by development of pathologic ventricular hypertrophy progressively leading to cardiac dilation and emergence of the phenotype of heart failure with reduced ejection fraction.Treatment with a pan-HDACi resulted in a blunting of the hypertrophic response and a slowing of progression to failure.4,5 Markers of cardiac fibrosis were also decreased in the ventricle, and HDACi blunted collagen production in isolated cardiac fibroblasts.5 HDACi was also capable of promoting regression of established hypertrophy.4 These fundamental cardioprotective findings have been replicated in a number of studies, including a study using cardiomyocyte-specific inactivation of the class I HDACs (HDAC1 and HDAC2).2,6 In contrast, genetic studies using cardiomyocyte-specific deletions of specific class II HDACs reported an enhanced hypertrophic response.7 These opposing data suggest that class I HDAC activity may dominate class II-dependent events in the response to hypertrophic stress.HDACi can protect the ischemic heart both by limiting the extent of cell death at reperfusion and by reducing the pathologic remodeling that occurs subsequently.In both a murine and rabbit model of ischemia/reperfusion, a single dose of HDACi administered HDAC Inhibition in the HeartErasing Hidden Fibrosis
Assessment of coronary flow velocity with transthoracic doppler echocardiography during dobutamine stress echocardiography Masaaki Takeuchi, Hidetoshi Yoshitani, Chinami Miyazaki, Shinichirou Otani, Kazuo Sakamoto, Junichi Yoshikawa. Tane General hospital, Osaka, Japan, Graduate School of Medicine, Osaka City University, Osaka, Japan
Journal: Journal of the American College of Cardiology (2001)
An intravascular ultrasound classification of angiographic coronary artery aneurysms Akiko Maehara, Gary S. Mintz, Javed M. Ahmed, Shmuel Fuchs, Neil J. Weissman, August D. Pichard, Lowell F. Satler, Ron Waksman, John R. Laird, Jr., Kenneth M. Kent, Stephen E. Epstein. Washington Hospital Center, Washington DC, DC
Journal: Journal of the American College of Cardiology (2001)
α‐thalassemia carrier identification by DNA analysis in the screening for thalassemia
Authors: Renzo Galanello, Carla Sollaino, Elisabetta Paglietti, Susanna Barella, Chiara Perra, Ilaria Doneddu, Maria G. Pirroni, Liliana Maccioni, Antonio Cao
Journal: American Journal of Hematology (1998)

Differentiation between heterozygous α-thalassemia and several phenotypically resembling alleles at the β-globin gene cluster such as coinherited δ- and β-thalassemia or γδβ-thalassemia is a critical step in genetic counseling. In this paper we report our experience in the identification of the α-thalassemia carrier state using polymerase chain reaction (PCR)-based methods, and the feasibility and simplification of screening for thalassemia using this approach. α-Globin genotype was determined by PCR-based method in 526 adult subjects with reduced mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH), normal hemoglobin A2 and F, and normal serum iron. To verify the reliability of the protocol used, in 68 of these subjects we performed globin chain synthesis analysis and in 101 we determined α-globin genotype by Southern blot analysis. Five hundred twenty-one (99%) of 526 subjects examined were identified as carriers of one or two α-thalassemia alleles. The identification of the α-thalassemia carrier state may be fast and accurate by PCR-based method, avoiding other cumbersome and expensive methods such as globin chain synthesis and Southern blot analysis. Am. J. Hematol. 59:273–278, 1998. © 1998 Wiley-Liss, Inc.
Gossypol: A Potential Antifertility Agent for Males
Authors: S-Z Qian
Journal: The Annual Review of Pharmacology and Toxicology (1984)

Over the past two decades, deadly coronaviruses, with the most recent being the severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2) 2019 pandemic, have majorly challenged public health. The path for virus invasion into humans and other ...Read More
Die Hormonforschung und ihre Methoden
Journal: JAMA (1935)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Long-term treatment with pravastatin reduces coronary heart disease mortality in women with prior coronary heart disease and average cholesterol levels Wendy Hague, Jennifer Johns, Peta Young, David Hunt, Robyn Bradfield, Mary Denton, Jan Garrett, Phil Aylward, Andrew Tonkin, John Simes, For the LIPID Investigators. NHMRC Clinical Trials Centre, University of Sydney, Australia, National Heart Foundation of Australia, Melbourne, Australia
Journal: Journal of the American College of Cardiology (2001)
ABC of health informatics: Improving services with informatics tools
Journal: BMJ (2006)

likely to be promoted may in part reflect this.Investigating this point would require complete data on employment history since graduation.The data will also include doctors in the training grades who may not want to become a consultant, and the results may be partly reflecting the preferences of this group, who are more likely to be female and work part time.However, this group is likely to be small. ConclusionsThe achievement of current government targets for the numbers of consultants are influenced by the promotion process and the quality control exercised by the royal colleges.As the proportion of female doctors increases, it will be difficult to meet government targets unless the promotion process is re-examined.This should focus on the weight given to individuals' skills and ability and the flexibility of contracts and working conditions.Safeguards will need to be in place to ensure that factors less likely to be related to ability or performance (such as sex, place of graduation, or part time working) will not influence promotion chances.Since 2000, when the data used in this paper finish, several changes have been intro-duced that have altered the career structures of hospital doctors.These include the Calman reforms, Modernising Medical Careers, further proposals for reform of the staff or associate specialist grades, and new contracts for junior doctors and consultants.It is unclear what impact these changes will have on the issues discussed in this paper.
Age as a confounding factor on helicobacter pylori infection and the risk of coronary artery disease Jianhui Zhu, Joseph B. Muhlestein, Julian P. J. Halcox, Javier F. Nieto, Benjamin D. Horne, Alexandra Zalles-Ganley, Stephen E. Epstein. Washington Hospital Center, Washington, DC
Journal: Journal of the American College of Cardiology (2001)
Table of Contents
Authors: C Bailleux, L Lacroix, E Barranger, S Delaloge, J Nabi, D Friedlander, Aron Goldhirsch, R Gelber, A Coates, S Gelber, R Orecchia, P Veronesi, A Leo, M Colleoni, E Winer, H Burstein, G Viale, H.-J Senn, M Piccart, G Curigliano, S Paluch-Shimon, F Cardoso, A Partridge, O Abulkhair, H Azim, G Bianchi-Micheli, M.-J Cardoso, K Gelmon, N Harbeck, J Merschdorf, P Poortmans, G Pruneri, E Senkus, T Spanic, V Stearns, Y Wengström, F Peccatori, O Pagani, M Heuser, Y Ofran, N Boissel, S Mauri, C Craddock, A Fabi, R Bhargava, S Fatigoni, M Guglielmo, M Horneber, F Roila, J Weis, K Jordan, C Ripamonti, J Haanen, Y Ernstoff, A Wang, I Menzies, P Puzanov, J Grivas, S Larkin, J Peters, M Thompson, M Liu, G Oxnard, E Klein, C Swanton, M Seiden, Y Jiang, H Wang, J Wu, C Chen, Q Yuan, W Huang, T Li, S Xi, Y Hu, Z Zhou, Y Xu, G Li, & Li, E Hui, W Li, B Ma, W Lam, K Chan, F Mo, Q Ai, A King, C Wong, R Guo, D Poon, M Tong, L Li, T Lau, K Wong, D Lam, Y Lo, J Ma, A Chan, V Moreno, J Sepulveda, M Vieito, T Hernández-Guerrero, B Doger, O Saavedra, O Ferrero, R Sarmiento, M Arias, J De Alvaro, J Martino, M Zuraek, T Sanchez-Pérez, I Aronchik, E Filvaroff, M Lamba, B Hanna, Z Nikolova, I Braña, M Schuler, R Berardi, W.-T Lim, M De Jonge, T Bauer, A Azaro, M Gottfried, J.-Y Han, D Lee, M Wollner, D Hong, A Vogel, A Delmonte, M Akimov, S Ghebremariam, X Cui, N Nwana, M Giovannini, T Kim
Journal: Annals of Oncology (2020)
Commentaire de travail de C. Luigiano et al., pp. 829
Journal: Endoscopy (2009)

See also:Endoscopic mucosal resection for large and giant sessile and flat colorectal polyps: a single-center experience with long-term follow-upEndoscopy 2009; 41(10): 829-835DOI: 10.1055/s-0029-1215091
The role of genetic variants involved with ferroptosis regulator genes in predicting outcomes in patients (pts) with RAS-mutant metastatic colorectal cancer (mCRC): Data from MAVERICC and TRIBE trials.
Authors: Jingyuan Wang, Joshua Millstein, Hiroyuki Arai, Francesca Battaglin, Natsuko Kawanishi, Priya Jayachandran, Shivani Soni, Zhang Wu, Christoph Mancao, Chiara Cremolini, Volker Heinemann, Alfredo Falcone, Heinz-Josef Lenz
Journal: Journal of Clinical Oncology (2022)

197 Background: Ferroptosis, an iron-dependent programmed cell death, is one of the anti-tumor mechanisms of anti-angiogenesis drugs. RAS mutation can confer ferroptosis in colorectal cancer (CRC). Previous studies suggested that polymorphisms of ferroptosis regulator genes are associated with the increased risk of CRC. Therefore, we hypothesized that genetic variants in the ferroptosis regulator genes may predict first-line treatment outcome in RAS-mutant mCRC pts treated with bevacizumab (bev)-based chemotherapy. Methods: Genomic DNA from blood samples of mCRC pts enrolled in two independent randomized trials, MAVERICC (FOLFIRI+bev arm: discovery cohort, RAS-mutant, n = 56; control-1: RAS-wildtype, n = 87) and TRIBE (FOLFOXIRI+bev arm: validation cohort, RAS-mutant, n = 57; control-2: RAS-wildtype, n = 34), was genotyped through the OncoArray, a customized array manufactured by Illumina including approximately 530K SNP markers. The impact on outcome of 13 selected SNPs in 5 main ferroptosis regulator genes (ACSL4, LPCAT3, SLC3A2, SLC7A11, ALOX15) was analyzed. Results: In the MAVERICC bev cohort, pts with RAS-mutant tumors carrying ALOX15 rs7217186 any C allele (n = 35) showed significant longer overall survival (OS) than carrier of T/T allele (n = 5) in both univariate (24.97 vs. 12.22 months, hazard ratio [HR] = 0.23; 95% confidence interval [CI]: 0.06-0.9; p = 0.02) and multivariate (HR = 0.06; 95%CI 0.007-0.5; p = 0.009) analysis. In the TRIBE bev cohort, RAS-mutant carriers of any C allele (n = 30) showed numerically longer progression-free survival (PFS), compared to carriers of T/T allele (n = 13) in both univariate (11.91 vs. 9.47 months, HR = 0.45; 95%CI 0.2-1.02; p = 0.05) and multivariate (HR = 0.42; 95%CI 0.16-1.1; p = 0.09) analysis. Conversely, RAS-wildtype carriers of any C allele (n = 17) showed significant shorter PFS than T/T carriers in the TRIBE bev cohort (8.91 vs. 15.59 months, univariate HR = 3.39, 95%CI: 1.03-11.18, p = 0.04). Conclusions: Our study demonstrated for the first time that ALOX15 polymorphisms may have different predictive values for the bev-based treatment in mCRC patients based on RAS mutational status. These findings may provide novel insights for the combination of ferroptosis inducers and anti-VEGF treatment.
Manuscripts Approved for JNCI, June 1 to July 1, 1968
Journal: JNCI Journal of the National Cancer Institute (1968)

Manuscripts Approved for JNCI, June 1 to July 1, 1968 JNCI: Journal of the National Cancer Institute, Volume 41, Issue 2, August 1968, Pages 617–618, https://doi.org/10.1093/jnci/41.2.617-b Published: 01 August 1968
The rocky road to universal COVID-19 vaccination
Authors: None The Lancet Infectious Diseases
Journal: The Lancet Infectious Diseases (2021)

As of May 9, 2021, the COVID-19 pandemic has caused 3 277 272 deaths and disrupted the lives of billions of people. Global equitable access to COVID-19 vaccines is the only way to mitigate the public health and economic impact of the pandemic. That is why 1 year ago the COVAX scheme, co-led by the Coalition for Epidemic Preparedness Innovations, Gavi, the Vaccine Alliance, and WHO, was set up to try to ensure fair access to vaccines, by guaranteeing that each country would receive vaccine doses for at least 20% of its population.
Dose-dependent blockade of the angiotensin II type 1 receptor in normal volunteers: Incomplete and transient blockade by losartan 50 mg Michael S. Berlowitz, Pierre V. Ennezat, Farhana Latif, Stacie Lauro, Jiong-Ming Hu, Suman Tandon, Robert Moskowitz, Edmund H. Sonnenblick, Thierry H. Le Jemtel. Albert Einstein College of Medicine, Bronx, NY
Journal: Journal of the American College of Cardiology (2001)
Temozolomide treatment duration and secondary hematological neoplasms: A review of the literature and implications for patients with neuroendocrine tumors.
Authors: Robin Park, Manik A. Amin, Nikolaos A. Trikalinos
Journal: Journal of Clinical Oncology (2022)

510 Background: Evidence-based recommendations for the optimal duration of temozolomide-based treatment in advanced neuroendocrine neoplasms are lacking. Because of the relatively long median survival of NEN and the potential long-term myelotoxicities of temozolomide, suggestions have been made to optimize the duration of temozolomide-based therapy. Here, we have conducted a systematic review of the literature for a descriptive analysis of temozolomide-associated myelodysplasias and leukemias to guide treatment planning. Methods: A database search of PubMed and Embase was conducted to identify case reports and/or case series reporting secondary myelodysplasias or leukemias in the setting of temozolomide therapy. Key data items extracted from the studies were the temozolomide dose and duration, latency to hematologic disorder, type of secondary malignancy and cytogenetics. Reported cases were summarized graphically and descriptively analyzed. Results: A total of 14 studies with 25 patient cases of therapy-related hematologic neoplasms were identified, all of which were case reports or case series. The median treatment duration and cumulative dose were 15 months and 18000 mg/m 2 respectively. Most patients (20/25) were diagnosed on or after 12 months while only one patient was diagnosed before 6 months of treatment. Majority of the patients were diagnosed while still on treatment with temozolomide. Graphically, cases clustered around a cumulative dose of 10,000 to 30,000 mg/m 2 and a latency period of 10 to 40 months which translates to an approximate treatment duration of 12.5 – 37.5 months. Conclusions: Taken together, treatment-related hematologic neoplasms appear to develop beyond the 12-month mark while still on treatment with temozolomide. We suggest an approach to optimizing treatment duration by establishing disease response at 6 months before continuing further treatment and restricting treatment to 12 months or establishing closer vigilance beyond 12 months.