tbuckley/cabot-search huggingface dataset:
The STROCSS statement: Strengthening the Reporting of Cohort Studies in Surgery
Authors: Riaz Ahmed Agha, Mimi R. Borrelli, Martinique Vella-Baldacchino, Rachel Thavayogan, Dennis P. Orgill, Duilio Pagano, Prathamesh S. Pai, Somprakas Basu, Jim McCaul, Frederick Millham, Baskaran Vasudevan, Cláudio Rodrigues Leles, Richard David Rosin, Roberto Klappenbach, David A. Machado-Aranda, Benjamin Perakath, Andrew J. Beamish, Mangesh A. Thorat, M. Hammad Ather, Naheed Farooq, Daniel M. Laskin, Kandiah Raveendran, Joerg Albrecht, James Milburn, Diana Miguel, Indraneil Mukherjee, Michele Valmasoni, James Ngu, Boris Kirshtein, Nicholas Raison, Michael Boscoe, Maximilian J. Johnston, Jerome Hoffman, Mohammad Bashashati, Achilleas Thoma, Donagh Healy, Dennis P. Orgill, Salvatore Giordano, Oliver J. Muensterer, Hüseyin Kadioglu, Abdulrahman Alsawadi, Patrick J. Bradley, Iain James Nixon, Samuele Massarut, Ben Challacombe, Ashraf Noureldin, Mushtaq Chalkoo, Raafat Yahia Afifi, Riaz Ahmed Agha, Jeffrey K. Aronson, Thomas E. Pidgeon
Journal: International Journal of Surgery (2017)
Macitentan for the treatment of inoperable chronic thromboembolic pulmonary hypertension (MERIT-1): results from the multicentre, phase 2, randomised, double-blind, placebo-controlled study
Authors: Hossein-Ardeschir Ghofrani, Gérald Simonneau, Andrea M D'Armini, Peter Fedullo, Luke S Howard, Xavier Jaïs, David P Jenkins, Zhi-Cheng Jing, Michael M Madani, Nicolas Martin, Eckhard Mayer, Kelly Papadakis, Dominik Richard, Nick H Kim, Irene Lang, Christian Kähler, Marion Delcroix, Zoheir Bshouty, Pablo Sepulveda Varela, Zhi-Cheng Jing, Yuanhua Yang, Jinming Liu, Gangcheng Zhang, Nuofu Zhang, Yuhong Mi, Xianyang Zhu, Pavel Jansa, Xavier Jaïs, Grégoire Prévot, Hélène Bouvaist, Olivier Sanchez, Friedrich Grimminger, Matthias Held, Heinrike Wilkens, Stephan Rosenkranz, Ekkehard Grünig, Kristóf Karlócai, András Temesvári, Istvan Edes, Sigita Aidietienė, Skaidrius Miliauskas, Tomas Rene Pulido Zamudio, Carlos Jerjes Sanchez, Anton Vonk Noordegraaf, Jerzy Lewczuk, Piotr Podolec, Jarosław Kasprzak, Tatiana Mularek-Kubzdela, Ryszard Grzywna, Keertan Dheda, Olga Moiseeva, Alexander Chernyavskiy, Vladimir Shipulin, Olga Barbarash, Tamila Martynyuk, Hyung-Kwan Kim, Jun-Bean Park, Jae Seung Lee, Rudolf Speich, Silvia Ulrich, John-David Aubert, Arintaya Phrommintikul, Nattapong Jaimchariyatam, Suree Sompradeekul, Zeynep Pinar Onen, Gulfer Okumus, Lyubomyr Solovey, Volodymyr Gavrysyuk, Luke Howard, Joanna Pepke-Zaba, Robin Condliffe, John McConnell, Kim Kerr, Lan Hieu Nguyen, Nguyen Vinh Pham
Journal: The Lancet Respiratory Medicine (2017)
IgE autoreactivity in bullous pemphigoid: eosinophils and mast cells as major targets of pathogenic immune reactants
Authors: P.C. Freire, C.H. Muñoz, G. Stingl
Journal: British Journal of Dermatology (2017)

Bullous pemphigoid (BP) is an autoimmune disease characterized by tense blisters that are usually preceded by urticarial eruptions. Affected patients exhibit IgG and/or IgE autoantibodies against BP180 and/or BP230. Their relative importance in disease pathogenesis has not been fully elucidated.The aim of this study was to provide a better characterization of the circulating and tissue-resident IgE in patients with BP at the serological, structural and functional levels.Sera (n = 19) and skin (n = 33) from patients with BP were analysed via enzyme-linked immunosorbent assay (ELISA) and immunofluorescence, respectively.The results obtained show that many patients with BP exhibit elevated IgE levels in the serum and in the skin. In the skin, it is very rarely and only sparsely found along the basement membrane zone, but is prominently present on mast cells and eosinophils. At least a portion of these IgE antibodies are BP-specific, as evidenced by serum ELISA and by the colocalization of BP180 and FcεRI-bound IgE on mast cells and/or eosinophils. An important role of these immune reactants can be inferred from our additional finding that cross-linking of IgE, derived from BP sera, on FcεRI-expressing rat basophils with BP180 results in robust degranulation of these cells.We propose the existence of a disease pathway alternative to IgG and complement that may well be responsible for some of the clinical features of this autoimmune disease.
Therapeutic Targeting of Oncogenic Tyrosine Phosphatases
Authors: Rochelle Frankson, Zhi-Hong Yu, Yunpeng Bai, Qinglin Li, Ruo-Yu Zhang, Zhong-Yin Zhang
Journal: Cancer Research (2017)

Abstract Protein tyrosine phosphatases (PTP) are exciting and novel targets for cancer drug discovery that work in concert with protein tyrosine kinases (PTK) in controlling cellular homeostasis. Given the activating role that some PTKs play in initiating growth factor–mediated cellular processes, PTPs are usually perceived as the negative regulators of these events and therefore tumor suppressive in nature. However, mounting evidence indicate that PTPs do not always antagonize the activity of PTKs in regulating tyrosine phosphorylation, but can also play dominant roles in the initiation and progression of signaling cascades that regulate cell functions. It follows, therefore, that PTP malfunction can actively contribute to a host of human disorders, in particular, cancer, metabolic syndromes, and autoimmune diseases. The Src homology domain containing phosphatase 2 (SHP2) and the three-membered family of phosphatases of regenerating liver (PRL) are infamously oncogenic members of the PTP superfamily. Both are established regulators of major cancer pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-κB, and PTEN/PI3K/AKT. Furthermore, upregulation, mutation, or other dysregulation of these PTPs has been positively correlated with cancer initiation and progression. This review will provide topical coverage of target validation and drug discovery efforts made in targeting these oncogenic PTPs as compelling candidates for cancer therapy. Cancer Res; 77(21); 5701–5. ©2017 AACR.
Early and Delayed 99mTc-MDP SPECT/CT Findings in Rheumatoid Arthritis and Osteoarthritis
Authors: Yasser G. Abdelhafez, Rosalie J. Hagge, Ramsey D. Badawi, Siba P. Raychaudhuri, Abhijit J. Chaudhari
Journal: Clinical Nuclear Medicine (2017)

We report the case of a 74-year-old man with seropositive rheumatoid arthritis (RA) and radiographic osteoarthritis (OA) who underwent dual-phase high-resolution Tc-MDP SPECT/CT. Early radiotracer enhancement was noted in 2 RA joints of the right hand, both presenting with a ring-like uptake pattern around the joint, consistent with synovitis. Insignificant early enhancement was noted at the first carpometacarpal joint, despite presentation of CT features of OA. The delayed-phase enhancement patterns were distinct, showing asymmetry in RA joints, but a symmetric, joint-centered pattern for the OA joint.
Abstract P004: Cardiac Regeneration in Neonatal Mice Following Ischemic Injury
Authors: Enzo R Porrello, Ahmed I Mahmoud, Emma Simpson, Joseph A Hill, James A Richardson, Eric N Olson, Hesham A Sadek
Journal: Circulation Research (2011)

As a consequence of the adult mammalian heart's limited regenerative capacity, ischemic heart disease is the leading cause of morbidity and mortality in the developed world. We have recently identified a brief window during post-natal development when the mammalian heart retains significant cardiac regenerative potential. Similar to adult zebrafish, the 1 day-old neonatal mouse heart is capable of complete cardiac regeneration following amputation of the entire ventricular apex. One major unresolved question is whether the neonatal mouse heart can also regenerate in response to myocardial ischemia. Here, we demonstrate that the neonatal mouse heart is also capable of undergoing a cardiac regenerative response to replace lost cardiomyocytes following myocardial ischemia. Following permanent ligation of the left anterior descending (LAD) coronary artery of 1 day-old neonatal mice, we documented evidence of significant cardiac injury and myocyte death by histology and echocardiography at 1 and 4 days after LAD ligation (Ejection Fraction (MI vs. Sham) = 70.9±10.1% vs. 98.6±0.3%, P&lt;0.05). Remarkably, the 1 day-old neonatal mouse heart completely regenerated the necrotic myocardium within 21 days, with minimal fibrosis and full recovery of cardiac function (Ejection Fraction (MI vs. Sham) = 94.6±1.4% vs. 97.9±0.1%). Similar to the regenerative response of neonatal mice to apical resection, the regenerative response of the neonatal mouse heart to ischemic injury was associated with robust and widespread activation of cardiomyocyte proliferation (∼11-fold), which peaked at day 7 post-injury. In contrast, following LAD ligation at 7 days-of-age, the cardiac regenerative response of neonatal mice was significantly impaired and by 14 days-of-age, the cardiac injury response was characterized by a fibrotic repair process that was reminiscent of the adult heart's response to ischemic injury. Additionally, over-expression of miR-195, a potent inhibitor of cardiomyocyte proliferation, impaired the cardiac regenerative response of neonatal mice. Thus, the neonatal mammalian heart is capable of complete regeneration following ischemic myocardial necrosis and cardiomyocyte proliferation appears to play an important role in this process.
The Ideal Blood Pressure Target for Patients With Chronic Kidney Disease—Searching for the Sweet Spot
Authors: Csaba P. Kovesdy
Journal: JAMA Internal Medicine (2017)

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 Internal Medicine 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 Internal Medicine journal
Potential Cardiovascular and Total Mortality Benefits of Air Pollution Control in Urban China
Authors: Chen Huang, Andrew E. Moran, Pamela G. Coxson, Xueli Yang, Fangchao Liu, Jie Cao, Kai Chen, Miao Wang, Jiang He, Lee Goldman, Dong Zhao, Patrick L. Kinney, Dongfeng Gu
Journal: Circulation (2017)

Outdoor air pollution ranks fourth among preventable causes of China's burden of disease. We hypothesized that the magnitude of health gains from air quality improvement in urban China could compare with achieving recommended blood pressure or smoking control goals.The Cardiovascular Disease Policy Model-China projected coronary heart disease, stroke, and all-cause deaths in urban Chinese adults 35 to 84 years of age from 2017 to 2030 if recent air quality (particulate matter with aerodynamic diameter ≤2.5 µm, PM2.5) and traditional cardiovascular risk factor trends continue. We projected life-years gained if urban China were to reach 1 of 3 air quality goals: Beijing Olympic Games level (mean PM2.5, 55 μg/m3), China Class II standard (35 μg/m3), or World Health Organization standard (10 μg/m3). We compared projected air pollution reduction control benefits with potential benefits of reaching World Health Organization hypertension and tobacco control goals.Mean PM2.5 reduction to Beijing Olympic levels by 2030 would gain ≈241,000 (95% uncertainty interval, 189 000-293 000) life-years annually. Achieving either the China Class II or World Health Organization PM2.5 standard would yield greater health benefits (992 000 [95% uncertainty interval, 790 000-1 180 000] or 1 827 000 [95% uncertainty interval, 1 481 00-2 129 000] annual life-years gained, respectively) than World Health Organization-recommended goals of 25% improvement in systolic hypertension control and 30% reduction in smoking combined (928 000 [95% uncertainty interval, 830 000-1 033 000] life-years).Air quality improvement in different scenarios could lead to graded health benefits ranging from 241 000 life-years gained to much greater benefits equal to or greater than the combined benefits of 25% improvement in systolic hypertension control and 30% smoking reduction.
Ets-1 and tissue factor expression and regulation in PC3 cells in vitro and in prostate cancer in vivo
Authors: Varsha Kaushal, Paulette Mehta, Manish Kohli, Perkins Mukunyadzi, Richard A. Dennis, Louis M. Fink
Journal: Cancer Research (2005)

4630  The transcription factor Ets-1 promotes tumorigenesis by transactivating numerous genes required for angiogenesis and matrix degradation. In our previous study, we found Ets-1 to be present in the PC3 prostate cancer cell line expressing tissue factor (TF) but not in the TF-negative prostate cancer cell line, LNCaP. We have further studied the expression of Ets-1 mRNA in metastatic prostate cancer cell line PC3. Its expression was induced two-fold when PC3 cells were treated in vitro with active recombinant factor VII (rFVIIa). Treatment of PC3 cells with active site-inactivated FVIIa reduced the level of Ets-1 below basal level. To elucidate the mechanism of Ets-1 regulation, TF expression was knocked down in PC3 cells using shRNAs. Levels of TF RNA and protein were then measured using qRTPCR and flow cytometry. TF levels were reduced to less than 10% of parental PC3 cells and levels of Ets-1 mRNA also reduced proportionately in TF-deficient cells. These experiments suggest that Ets-1 expression is regulated by TF in prostate cancer cells. To determine if this pattern also occurs in vivo, we assessed Ets-1 expression in clinical specimens of prostate cancer. We measured mRNA and protein levels in prostate tissues from patients with localized (n=9) and metastatic (n=7) disease using real-time RTPCR and Western analysis. The average expression of Ets-1 in prostate cancer specimens from patients with localized disease was 1.96-fold greater than that of β-actin, an internal standard, while the expression of Ets-1 in prostate cancer specimens from patients with metastatic disease was 9.18-fold greater than that of β-actin (P= 0.0004). Similarly, only one of nine prostate specimens from patients with localized disease had any detectable Ets-1 protein band on the Western blot, while five of seven prostate specimens from patients with metastatic disease expressed high levels of Ets-1. Thus, the expression of Ets-1 correlates with metastatic disease in patients with prostate cancer. Further studies are needed to determine if Ets-1 is directly regulated by TF or is indirectly regulated via protease-activated receptors in PC3 cells. Further studies are also needed to evaluate Ets-1 and TF expression in patients with different stages of the disease to determine their prognostic value and role in dissemination of the disease.
Managing Conflicts of Interest in Practice Guidelines Panels
Authors: Yaolong Chen, Kehu Yang, Susan L. Norris
Journal: JAMA (2017)

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
マウスにおけるMRIモダリティを用いた肝インテグリンαvβ3発現視覚化による肝線維症の非侵襲的分化程度【Powered by NICT】
Authors: Li Feng, Yan Huihui, Wang Jiyao, Li Cong, Wu Jian, Wu Shengdi, Rao Shengxiang, Gao Xihui, Jin Qu
Journal: Biomaterials (2016)
MET–GRB2 Signaling-Associated Complexes Correlate with Oncogenic MET Signaling and Sensitivity to MET Kinase Inhibitors
Authors: Matthew A. Smith, Thomas Licata, Aliya Lakhani, Marileila Varella Garcia, Hans-Ulrich Schildhaus, Vincent Vuaroqueaux, Balazs Halmos, Alain C. Borczuk, Y. Ann Chen, Benjamin C. Creelan, Theresa A. Boyle, Eric B. Haura
Journal: Clinical Cancer Research (2017)

Purpose: Targeting MET in cancer is hampered by lack of diagnostics that accurately reflect high MET signaling and dependence. We hypothesized that assays reflecting MET signaling associated protein complexes could redefine tumors dependent on MET and could add additional precision beyond genomic assessments.Experimental Design: We used biochemical approaches, cellular viability studies, and proximity ligation assays to assess MET dependence. We examined MET signaling complexes in lung cancer patient specimens (N = 406) and patient-derived xenograft (PDX) models of solid tumors (N = 308). We evaluated response to crizotinib in a MET-amplified cohort of PDX models of lung cancer (N = 6) and provide a case report of a lung cancer patient harboring a Δexon14 MET splice variant.Results: We found the interaction of MET with the adaptor protein GRB2 is necessary for oncogenic survival signaling by MET. MET-GRB2 complexes were identified only within MET-amplified PDX models and patient specimens but exhibit substantial variability. Lack of MET-GRB2 complexes was associated with lack of response to MET TKI in cell lines and PDX models. Presence of MET-GRB2 complexes can further subtype tumors with Δexon14 MET splice variants. Presence of these complexes correlated with response to crizotinib in one patient with Δexon14 MET lacking MET gene amplification.Conclusions: Proximity assays measuring MET-GRB2 signaling complexes provide novel insights into MET-mediated signaling and could complement current clinical genomics-based assay platforms. Clin Cancer Res; 23(22); 7084-96. ©2017 AACR.
Gefitinib (G) versus vinorelbine+cisplatin (VP) as adjuvant treatment in stage II-IIIA (N1-N2) non-small-cell lung cancer (NSCLC) with <i>EGFR</i>-activating mutation (ADJUVANT): A randomized, Phase III trial (CTONG 1104).
Authors: Yi-Long Wu, Wenzhao Zhong, Qun Wang, Song-Tao Xu, Wei-Min Mao, Lin Wu, Yi Shen, Yong-Yu Liu, Chun Chen, Ying Cheng, Lin Xu, Jun Wang, Ke Fei, Xiao-Fei Li, Jian Li, Cheng Huang, Zhi-Dong Liu, Ke-Neng Chen, Hong-Hong Yan, Xue-Ning Yang
Journal: Journal of Clinical Oncology (2017)

8500 Background: Cisplatin-based adjuvant chemotherapy is standard of care for patients (pts) with stage II-IIIA non-small cell lung cancer (NSCLC). Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors have shown no benefits in the adjuvant setting for pts with unselected resected NSCLC in the BR19 and RADIANT trials. ADJUVANT (NCT01405079) is the first randomized trial to compare gefitinib (G) with vinorelbine+cisplatin (VP) in completely resected pathological stage II-IIIA (N1-N2) NSCLC with EGFR-activating mutation. Methods: Completely resected stage II-IIIA (N1-N2) NSCLC pts with EGFR-activating mutation were randomized 1:1 to receive G (250 mg once daily) for 24 months or vinorelbine (25 mg/m 2 Day 1 and Day 8) plus cisplatin (75 mg/m 2 Day 1) every 3 weeks for 4 cycles. Stratification factors were lymph node status (pN1/N2) and EGFRmutation status. The primary endpoint was disease-free survival (DFS) in the intent-to-treat population. Results: A total of 222 pts were randomly assigned (Sep 19 2011 to Apr 24 2014). Baseline characteristics were balanced. At the time of data cutoff, the median duration of treatment was 21.9 months in the G arm, and 4 cycles in the VP arm. The median follow-up period was 36.5 months (range 0.1 to 62.8). G had significantly longer median DFS (28.7 months, 95% confidence interval [CI] 24.9 to 32.5) than VP (18.0 months, 95% CI 13.6 to 22.3; hazard ratio 0.60; 95% CI 0.42 to 0.87; p= 0.005). 3-year DFS was significantly better with G (34.0% vs 27.0%; p= 0.013). The number of overall survival events was 76 (34.2%). In the subgroup analysis of patients treated with G, lymph node status (pN1/N2) demonstrated significant correlation with DFS ( p&lt; 0.05). Grade 3 or higher adverse events were less common with G than with VP (12.3% vs 48.3%; p&lt; 0.001). No interstitial lung disease was observed with G. Conclusions: Adjuvant G significantly prolonged DFS compared with VP in pts with resected stage II-IIIA (N1-N2) NSCLC with EGFR-activating mutation. Adjuvant gefitinib should be considered as an important option for stage II-IIIA lung cancer pts with EGFR mutation. Clinical trial information: NCT01405079.
Biomarker-Stratified Phase III Clinical Trials: Enhancement with a Subgroup-Focused Sequential Design
Authors: Shigeyuki Matsui, John Crowley
Journal: Clinical Cancer Research (2017)

Abstract Among various design approaches to phase III clinical trials with a predictive biomarker, the marker-stratified all-comers design is advantageous because it allows for establishing the utility of both treatment and biomarker, but it is often criticized for requiring large sample sizes, as the design includes both marker-positive and marker-negative patients. In this article, we propose a simple but flexible subgroup-focused design for marker-stratified trials that allow both sequential assessment across marker-defined subgroups and adaptive subgroup selection while retaining an assessment using the entire patient cohort at the final analysis stage, possibly using established marker-based multiple testing procedures. Numerical evaluations indicate that the proposed marker-stratified design has a robustness property in preserving statistical power for detecting various profiles of treatment effects across the subgroups while effectively reducing the number of randomized patients in the marker-negative subgroup with presumably limited treatment efficacy. In contrast, the traditional all-comers and sequential enrichment designs could suffer from low statistical power for some possible profiles of treatment effects. The latter also needs long study durations and a large number of marker-screened patients. We also provide an application to SWOG S0819, a trial to assess the role of cetuximab in treating non–small cell lung cancers. These evaluations indicate that the proposed subgroup-focused approach can enhance the efficiency of the marker-stratified design for definitive evaluation of treatment and biomarker in phase III clinical trials. Clin Cancer Res; 24(5); 994–1001. ©2017 AACR.
Enhanced plasmacytoid dendritic cell antiviral responses after omalizumab
Authors: Michelle A. Gill, Andrew H. Liu, Agustin Calatroni, Rebecca Z. Krouse, Baomei Shao, Allison Schiltz, James E. Gern, Alkis Togias, William W. Busse
Journal: Journal of Allergy and Clinical Immunology (2017)
Right Heart Thrombi in Pulmonary Embolism, Association of Pulmonary Embolism with Acute Exacerbations of Chronic Obstructive Pulmonary Disease, and Catheter-directed Therapies for Acute Pulmonary Embolism
Authors: Rajany V. Dy, Sumit Patel, Ken Burns, M. Jeffery Mador
Journal: American Journal of Respiratory and Critical Care Medicine (2017)