tbuckley/cabot-search huggingface dataset:
Abstract 3857: Cost-effectiveness of Aspirin for the Primary Prevention of Coronary Heart Disease
Authors: Nicolas Rodondi, Andrew Moran, Pamela G Coxson, James Lightwood, Lawrence W Williams, Jacques Cornuz, Lee Goldman
Journal: Circulation (2006)

Background:  Major trials have shown that aspirin was beneficial for primary prevention of coronary heart disease (CHD) but increased the risk of hemorrhagic strokes and gastrointestinal bleeding. These benefits and harms of aspirin may vary between men and women. We assessed the cost effectiveness of increased use of aspirin for primary prevention of CHD in men and women in the US population.   Methods:  We used the CHD Policy Model, a validated, state-transition model of CHD events in the US population, to estimate the incremental cost effectiveness of increased aspirin as primary prevention in all eligible adults (not allergic or intolerant to aspirin) aged 35 to 84 years from 2007 to 2037 over and above the maximal use of aspirin as secondary prevention for all eligible patients with CHD. Baseline aspirin use, CHD events, and case fatality rates were derived from US national surveys and the Framingham Heart Study. Benefits and risks of aspirin were based on a gender-specific meta-analysis of major trials of aspirin in primary prevention. Cost estimates, health-related quality-of-life, and population rates of strokes and gastrointestinal bleeding were based on Medicare data and observational studies. Using a societal perspective, we examined quality-adjusted life-years (QALYs), costs, and incremental cost-effectiveness ratios.   Results:  Aspirin as primary prevention for all eligible adults without CHD would result in 1.5 million fewer deaths, save 10,000,000 QALYs, and save $270 billion over 30 years, over and above the benefits of maximal secondary prevention in patients with CHD. Reductions in CHD events, ischemic strokes in women, and costs outweighed the side-effects and costs of aspirin. Benefits were derived mainly from increased QALYs and reduced costs in men aged ≥ 55 and women ≥ 65. The reduction in death rates was greatest in women ≥ 65, because of the reduction in both CHD and ischemic strokes by aspirin.   Conclusions:  The increased use of aspirin for primary prevention especially in men aged 55– 84 and women aged 65– 84 without CHD would lead to important gains in health and would be potentially cost saving, above and beyond the benefits of maximal use of aspirin for secondary prevention.
Spliceosome Gene Mutations Are Frequently Found In JAK2 Negative Myelofibrosis and Associated With Worse Clinical Outcomes
Authors: Ali Tabarroki, Valeria Visconte, Heesun J. Rogers, Juraj Bodo, Li Zhang, Edy Hasrouni, John Barnard, Alan E. Lichtin, Mikkael A. Sekeres, Ramon V. Tiu
Journal: Blood (2013)
Phosphatase PP2A is requisite for the function of regulatory T cells
Authors: Sokratis A Apostolidis, Noé Rodríguez-Rodríguez, Abel Suárez-Fueyo, Nikolina Dioufa, Esra Ozcan, José C Crispín, Maria G Tsokos, George C Tsokos
Journal: Nature Immunology (2016)
A Randomized, Double‐Blind, Active‐ and Placebo‐Controlled Efficacy and Safety Study of Arhalofenate for Reducing Flare in Patients With Gout
Authors: Jeffrey Poiley, Alexandra S. Steinberg, Yun‐Jung Choi, Charles S. Davis, Robert L. Martin, Charles A. McWherter, Pol F. Boudes
Journal: Arthritis & Rheumatology (2016)

Objective Arhalofenate is a novel antiinflammatory uricosuric agent. The objective of this study was to evaluate its antiflare activity in patients with gout. Methods This was a 12‐week, randomized, double‐blind, controlled phase IIb study. Eligible patients had had ≥3 flares of gout during the previous year, had discontinued urate‐lowering therapy and colchicine, and had a serum uric acid (UA) level of 7.5–12 mg/dl. Patients were randomly assigned at a 2:2:2:2:1 ratio to receive 600 mg arhalofenate, 800 mg arhalofenate, 300 mg allopurinol, 300 mg allopurinol plus 0.6 mg colchicine, or placebo once a day. The primary outcome measure was the flare incidence (number of flares divided by time of exposure). The serum UA level was a secondary outcome measure. Results A total of 239 gout patients were randomized and took at least 1 dose of study medication. The primary outcome measure comparing flare incidence between 800 mg arhalofenate and 300 mg allopurinol was achieved, with a 46% decrease in the 800 mg arhalofenate group (0.66 versus 1.24; P = 0.0056). Treatment with 800 mg arhalofenate was also significantly better than placebo ( P = 0.049) and not significantly different from treatment with 300 mg allopurinol plus 0.6 mg colchicine ( P = 0.091). Mean changes in serum UA level were −12.5% with 600 mg arhalofenate and −16.5% with 800 mg arhalofenate ( P = 0.001 and P = 0.0001, respectively, versus −0.9% with placebo). There were no meaningful differences in adverse events (AEs) between groups, and there were no serious AEs related to arhalofenate. Urinary calculus occurred in 1 patient receiving 300 mg allopurinol. No abnormal serum creatinine values &gt;1.5‐fold the baseline value were observed in the arhalofenate‐treated groups. Conclusion Arhalofenate at a dosage of 800 mg decreased gout flares significantly compared to allopurinol at a dosage of 300 mg. Arhalofenate was well tolerated and appeared safe. Arhalofenate is the first urate‐lowering antiflare therapy.
Podocyte injury and its consequences
Authors: Michio Nagata
Journal: Kidney International (2016)

Podocytes maintain the glomerular filtration barrier, and the stability of this barrier depends on their highly differentiated postmitotic phenotype, which also defines the particular vulnerability of the glomerulus. Recent podocyte biology and gene disruption studies in vivo indicate a causal relationship between abnormalities of single podocyte molecules and proteinuria and glomerulosclerosis. Podocytes live under various stresses and pathological stimuli. They adapt to maintain homeostasis, but excessive stress leads to maladaptation with complex biological changes including loss of integrity and dysregulation of cellular metabolism. Podocyte injury causes proteinuria and detachment from the glomerular basement membrane. In addition to "sick" podocytes and their detachment, our understanding of glomerular responses following podocyte loss needs to address the pathways from podocyte injury to sclerosis. Studies have found a variety of glomerular responses to podocyte dysfunction in vivo, such as disruption of podocyte-endothelial cross talk and activation of podocyte-parietal cell interactions, all of which help us to understand the complex scenario of podocyte injury and its consequences. This review focuses on the cellular aspects of podocyte dysfunction and the adaptive or maladaptive glomerular responses to podocyte injury that lead to its major consequence, glomerulosclerosis.
Abstract 15189: Creation of Nonischemic Functional Mitral Regurgitation by Annular Dilatation in an in vivo Swine Model
Authors: Haruo Yamauchi, Nikolay V Vasilyev, Eric N Feins, Pedro J del Nido
Journal: Circulation (2012)

Background: Mechanisms and treatments of nonischemic functional mitral regurgitation (NIMR) remain to be fully established because of a lack of proper large animal models. We developed a novel tech...
Ethical debate : why are doctors ambivalent about patients who misuse alcohol? (The case history and survey of doctors' attitudes)
Authors: R. Dale, R. Barton
Journal: BMJ (1997)

Why are doctors ambivalent about patients who misuse alcohol?It is not unusual for doctors to see patients who they strongly suspect are misusing alcohol.Should they ignore it or try to intervene?And what should they do if the patient's alcohol misuse puts other people at risk?In this ethical debate a lawyer, two psychiatrists, and an oral and maxillofacial surgeon give their views.
Intestinal Interleukin-17 Receptor Signaling Mediates Reciprocal Control of the Gut Microbiota and Autoimmune Inflammation
Authors: Pawan Kumar, Leticia Monin, Patricia Castillo, Waleed Elsegeiny, William Horne, Taylor Eddens, Amit Vikram, Misty Good, Alexi A. Schoenborn, Kyle Bibby, Ronald C. Montelaro, Dennis W. Metzger, Ajay S. Gulati, Jay K. Kolls
Journal: Immunity (2016)
New Strategies to Treat High Cholesterol
Authors: Conrad B. Blum, Neil J. Stone
Journal: JAMA (2016)

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
Funding the Cancer Moonshot
Authors: Rebecca Voelker
Journal: JAMA (2016)

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
Risk of Locoregional Recurrence After Mastectomy By Hormone Receptor Status and Her2 Status in Breast Cancer Patients with 1-3 Positive Nodes
Authors: T. Fujita, M. Sawaki, M. Hattori, N. Kondou, A. Yoshimura, N. Gondou, M. Ichikawa, H. Kotani, Y. Adachi, T. Hisada, J. Ishiguro, H. Iwata
Journal: Annals of Oncology (2014)
Abstract 16249: Acute Right Ventricular Pressure Overload Disrupts Organization of the Focal Adhesion Protein Talin
Authors: Clifford R Greyson, Shuyu Ye, Li Lu, Ya Xu, Gregory G Schwartz, Hasan Ahmad
Journal: Circulation (2010)

Right heart failure from acute right ventricular pressure overload (RVPO) is an important cause of morbidity and mortality, and currently has no specific therapy. We previously showed that RV dysfu...
Re: Hiury S. Andrade, Homayoun Zargar, Peter A. Caputo, et al. Five-year Oncologic Outcomes After Transperitoneal Robotic Partial Nephrectomy for Renal Cell Carcinoma. Eur Urol 2016;69:1149–54
Authors: Tae Young Shin, Ali Abdel Raheem, Koon Ho Rha
Journal: European Urology (2016)
Efficient multi-scale 3D CNN with fully connected CRF for accurate brain lesion segmentation
Authors: Konstantinos Kamnitsas, Christian Ledig, Virginia F.J. Newcombe, Joanna P. Simpson, Andrew D. Kane, David K. Menon, Daniel Rueckert, Ben Glocker
Journal: Medical Image Analysis (2016)

We propose a dual pathway, 11-layers deep, three-dimensional Convolutional Neural Network for the challenging task of brain lesion segmentation. The devised architecture is the result of an in-depth analysis of the limitations of current networks proposed for similar applications. To overcome the computational burden of processing 3D medical scans, we have devised an efficient and effective dense training scheme which joins the processing of adjacent image patches into one pass through the network while automatically adapting to the inherent class imbalance present in the data. Further, we analyze the development of deeper, thus more discriminative 3D CNNs. In order to incorporate both local and larger contextual information, we employ a dual pathway architecture that processes the input images at multiple scales simultaneously. For post-processing of the network's soft segmentation, we use a 3D fully connected Conditional Random Field which effectively removes false positives. Our pipeline is extensively evaluated on three challenging tasks of lesion segmentation in multi-channel MRI patient data with traumatic brain injuries, brain tumours, and ischemic stroke. We improve on the state-of-the-art for all three applications, with top ranking performance on the public benchmarks BRATS 2015 and ISLES 2015. Our method is computationally efficient, which allows its adoption in a variety of research and clinical settings. The source code of our implementation is made publicly available.
Aryl Hydrocarbon Hydroxylase Induction in Rat Tissues by Naturally Occurring Indoles of Cruciferous Plants&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;
Authors: W D Loub, L W Wattenberg, D W Davis
Journal: JNCI Journal of the National Cancer Institute (1975)

A phytochemical investigation to identify inducers of increased aryl hydrocarbon hydroxylase (AHH) activity from three cruciferous vegetables, Brussels sprouts, cabbage, and cauliflower, resulted in the identification of indole-3-acetonitrile, indole-3-carbinol, and 3,3'-diindolylmethane as naturally occurring inducers. These compounds are produced during the hydrolysis of indolyl-methyl glucosinolate by the plant enzyme myrosinase.
Acute myeloid leukemia-type chemotherapy for myelodysplasia.
Authors: P Anderlini, S Pierce, H Kantarjian, E Estey
Journal: Journal of Clinical Oncology (1996)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1996.14.4.1404 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 8648402 Acute myeloid leukemia-type chemotherapy for myelodysplasia. P AnderlinixP AnderliniSearch for articles by this author , S PiercexS PierceSearch for articles by this author , H KantarjianxH KantarjianSearch for articles by this author , E EsteyxE EsteySearch for articles by this author https://doi.org/10.1200/JCO.1996.14.4.1404 PDF "Acute myeloid leukemia-type chemotherapy for myelodysplasia.." Journal of Clinical Oncology, 14(4), pp. 1404–1405© 1996 by American Society of Clinical Oncology
Subgroup Analyses of a Phase 3, Multicenter, Double-Blind, Placebo-Controlled Trial of Lenvatinib (E7080) in Patients with 131I-Refractory Differentiated Thyroid Cancer
Authors: R. Elisei, M. Schlumberger, M. Tahara, B. Robinson, M. Brose, C. Dutcus, B.D.L. Heras, J. Zhu, M.A. Habra, K. Newbold, M. Shah, A.O. Hoff, A. Gianoukakis, N. Kiyota, M.H. Taylor, S. Kim, M.K. Krzyzanowska, S. Sherman, L.J. Wirth
Journal: Annals of Oncology (2014)
WITHDRAWN: Programmed hydrolysis in designing paclitaxel prodrug for nanocarrier assembly
Authors: Qiang Fu, Yan Ma, John KFallon, Dan Liu, Zhonggui He, Feng Liu
Journal: Asian Journal of Pharmaceutical Sciences (2015)

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.
ACOSOG Z05031: Report on a multicenter, phase II trial for adjuvant therapy of resected pancreatic cancer using cisplatin, 5- FU, and alpha-interferon
Authors: V. J. Picozzi, R. A. Abrams, L. W. Traverso, E. M. O’Reilly, E. Greeno, R. C. Martin, L. S. Wilfong, P. A. Decker, P. W. Pisters, M. C. Posner
Journal: Journal of Clinical Oncology (2008)

4505 Background: In 2003, ACOSOG began a multicenter phase II trial (Z05031) using novel chemoradiation with radiotherapy (XRT), cisplatin (C), 5-FU (F) and alpha-interferon (INT). Initial trial results (abs #125 Proc ASCO GI 2008) are now reported after further follow- up (f/u). Methods: Patient (pt) eligibility requirements included 1) head of pancreas primary, 2) R0/R1 resection, 3) ECOG 0/1 performance status, and 4) chemoradiation initiation within 56 days of surgery. Therapy included XRT 5,040 cGy d 1–38, C 30mg/m2 d 1, 8, 15, 22, 29,36, F 175 mg/m2 IV CI/d d 1–38, and INT 3x106 U sq q M,W,F during XRT (cycle 1). Therapy was completed with F 200mg/m2 IV CI/d weeks 11–16 and 19 -24 post chemoradiation (cycles 2 and 3). The primary study endpoint was 18 month (mo) median OS from registration (20 mos from surgery); > 65% OS was considered a positive result. Results: Target accrual of 93 pts was halted at 89 pts due to toxicity concerns. 81/84 pts (96%) had grade 3+ toxicity. No long-term toxicity or toxicity-related deaths were noted. 64/80 pts ( 80%) received at least 4,500 cGy XRT; 45/80 pts (56%) began cycle 3.Median f/u is 28 mo. 18 mo OS from registration is 66% (95% CI 55%-77%). 2-year and median OS from surgery are 55% (95% CI 43%-66%), and 27.1 mo (95% CI 23.4–33.6 mo). Pts who began all treatment cycles had a median survival of 31.8 months. Median disease-free survival from surgery is 14.1 mo (95% CI 12.2–21.4 mo). Local/systemic recurrence rates are 46%/35%. Surgical margin (75% (-) vs. 25% (+), 31.8 vs. 18.8 mo, p=0.022) and tumor grade (grade 1/2 vs. grade 3, 31.7 vs. 22.3 mo, p=0.047) were prognostically significant for OS; tumor size and nodal status were not. Conclusions: 1) The study achieved a positive primary endpoint with respect to OS and supports the success of an earlier single-center report using this regimen (abs#1061 Proc ASCO 2003) in a multicenter setting. 2) Inability to receive intended treatment may have a significant negative impact on OS. 3) Margin status and tumor grade were prognostically significant. 4) OS for margin (+) pts was superior to prior reports for this circumstance. 5) Improved success of treatment delivery with preservation/enhancement of treatment effect are important to further development of this promising regimen. No significant financial relationships to disclose.
Cell aggregation and apoptosis induced by hemodialysis membranes.
Authors: J Carracedo, R Ramirez, O Pintado, J C Gomez-Villamandos, A Martin-Malo, M Rodríguez, P Aljama
Journal: Journal of the American Society of Nephrology (1995)

During hemodialysis, circulating mononuclear cells can be stimulated to different degrees, depending on membrane biocompatibility. Cell activation usually leads to aggregation and proliferation. It may also result in apoptosis if cells are subjected to abnormal activation. This may be the case of cells exposed to bioincompatible hemodialysis membranes. The study presented here evaluates the effects of two hemodialysis membranes, with different degrees of biocompatibility, (Cuprophan (CU; Lundia IC 5N; GAMBRO, Sweden) and polyacrylonitrile (AN69; Biospal 3000S, Hospal, France)) on aggregation and apoptosis of circulating human mononuclear cells and the human mononuclear cell line (THP-1). The results showed that 2-h incubation with CU, a bioincompatible membrane, produces cell aggregation of both peripheral mononuclear cells and THP-1 cells (35% and 54%, respectively). After 48 h of incubation with a CU membrane, apoptotic death was observed in 32% of THP-1 cells and in 45% of normal peripheral mononuclear cells. Neither cell aggregation nor apoptosis was observed after incubation with the AN69 membrane. CU membrane-induced apoptosis was inhibited by Staurosporrin (Sigma, St. Louis, MO) a protein kinase C (PKC)-inhibitor, suggesting that cell apoptosis induced by the CU membrane is mediated by a PKC-dependent cell activation. Furthermore, cell prestimulation with phorbol 12-myristate 13-acetate, an activator of PKC, results in a increase in the percentage of THP-1 cell death by apoptosis after CU exposure (53%). Our study indicates that CU membranes induce mononuclear cell activation, leading to cell apoptosis.
Phase I/II trial of nemorubicin hydrochloride in combination with cisplatin is supported by new preclinical evidences of its mechanism of action
Authors: M. A. Pacciarini, C. Geroni, M. A. Sabatino, M. Ciomei, O. Valota, D. Ballinari, L. Capolongo, M. Broggini
Journal: Journal of Clinical Oncology (2006)

14116 Background: Nemorubicin hydrochloride (nemorubicin) is a non-conventional anthracycline in Phase II evaluation in hepatocellular carcinoma (HCC). Its mechanism of action is not fully elucidated. Although structurally related to doxorubicin, nemorubicin is a topoisomerase I inhibitor, overcomes anthracyclines resistance, is minimally cardiotoxic and is biotransformed by hepatic CYP3A4 into hundred times more cytotoxic metabolite. Phase I and II trials were conducted in Europe and China to test nemorubicin by hepatic intra-arterial (IHA) infusion in HCC patients (pts). The drug was well tolerated up to 600 mcg/m 2 q4–6w; DLT was transient liver transaminase elevations. Overall, 57 HCC pts were evaluable for efficacy, with 11/57 confirmed liver CR/PRs (RR = 19.3%; 95% ci 10–31.9%) lasting 1–54+ months. Stable disease ≥ 3 months was observed in 17/57 (29.8%) pts, most with AJCC Stage III, IIIA and IVA. These data supported new trials of nemorubicin in HCC. Methods: To further characterize the mechanism of action of the drug, we generated cells (L1210) resistant to nemorubicin. Since resistant cells were more sensitive than the parental ones to UV irradiation, we reasoned that the nucleotide excision repair (NER) system might be involved in mediating the activity of nemorubicin. To test this hypothesis we used isogenic CHO cells proficient or deficient in excision repair cross-complementing (ERCC) genes, namely ERCC1 and ERCC6 genes. Results: In contrast with what is observed for most DNA damaging drugs that show resistance in the presence of high NER activity, nemorubicin is more cytotoxic in NER proficient than in deficient cells. This suggests that NER pathway plays a role in the cytotoxic effect of nemorubicin. Also, cells resistant to nemorubicin are NER-deficient and are highly sensitive to platinum derivatives and alkylating agents and synergism was found combining cisplatin with nemorubicin. Conclusions: Nemorubicin has a peculiar mechanism of action through the NER system providing the rationale for clinical combination studies with platinum derivatives. A Phase I/II trial of nemorubicin with cisplatin in HCC patients started in Italy at the end of 2005. No significant financial relationships to disclose.