tbuckley/cabot-search huggingface dataset:
Sex-related differences in emphysema progression
Authors: Saher B. Shaker, Mathilde W. Wille, Asger Dirksen, Laura H. Thomsen, Jesper H. Pedersen
Journal: European Respiratory Journal (2014)

Background:  Lung density measured from CT is a surrogate for emphysema. Several factors influence lung density and its decline with the progression of emphysema. We previously found that the decline is faster in women. In the current analysis, the reason for this sex-related difference was investigated.   Material and methods:  2,042 current or ex-smokers aged 50-70 years underwent annual CT scans in the Danish Lung Cancer Screening Trial for 5 years. CT lung density was measured as the volume-adjusted 15 th  percentile density (PD15). Two mixed effects models were used: one to study the influence of sex, age, smoking and airflow obstruction (AFO) on PD15; and a second in which height and BMI were added as covariates. Former smoking men without AFO aged 60, with less than 30 pack-years at entry was chosen as reference group.   Results:  Data were analysed for all subjects throughout the study although censored after they changed their smoking habit. There were 900 women and 1142 men at baseline. In the first model, lung density was significantly higher in women (Δ17.28 g/L, SE 0.62, p   Conclusion:  Lung density should be adjusted for height and BMI, which partially explain the difference in lung density between men and women. We found no sex-related difference in the progression of emphysema in smokers.
Nodular Lymphoid Hyperplasia
Authors: Vishal Sharma, Arvind Ahuja
Journal: New England Journal of Medicine (2016)

An 18-year-old woman presented with recurrent episodes of diarrhea associated with epigastric discomfort and bloating. Examination of the stool revealed trophozoites of the species Giardia lamblia. Gastroduodenoscopy revealed multiple nodules in the duodenum.
The Complicated Calculus of Publicly Reporting Mortality After Percutaneous Coronary Intervention
Authors: Ajay J. Kirtane, Brahmajee K. Nallamothu, Jeffrey W. Moses
Journal: JAMA Cardiology (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 Cardiology 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 Cardiology journal
P1166 : Decreased serum DNase1 activity in patients with autoimmune liver diseases
Authors: N.K. Gatselis, A.G. Vakrakou, K. Zachou, T. Androutsakos, K. Azariadi, G. Hatzis, M.N. Manoussakis, G.N. Dalekos
Journal: Journal of Hepatology (2015)
Abstract 1225: NVP-HDM201: cellular and in vivo profile of a novel highly potent and selective PPI inhibitor of p53-Mdm2
Authors: Sébastien Jeay, Patrick Chène, Stéphane Ferretti, Pascal Furet, Bjoern Gruenenfelder, Vito Guagnano, Nelson Guerreiro, Ensar Halilovic, Francesco Hofmann, Joerg Kallen, Michelle Léonard, Robert Mah, Keiichi Masuya, Rita Ramos, Caroline Rynn, Stephan Ruetz, Thérèse Stachyra-Valat, Stefan Stutz, Andrea Vaupel, Jens Wuerthner, Philipp Holzer
Journal: Cancer Research (2016)

Abstract Stabilization of p53 protein by preventing its interaction with the negative regulator Mdm2 leads to selective induction of the p53 pathway, thus offering a promising cancer therapeutic strategy in p53 wild-type tumors. In the present study, we show the identification of NVP-HDM201, a novel, highly optimized, and selective inhibitor of the p53-Mdm2 interaction. NVP-HDM201 activates p53 in human cells and induces robust p53-dependent cell cycle arrest and apoptosis, selectively in p53 wild-type tumor cells. Its activity and selectivity has been tested and confirmed across a large panel of cancer cell lines from the Cancer Cell Line Encyclopedia. In vivo, NVP-HDM201 shows a dose-proportional pharmacokinetic (PK) profile and a clear PK/PD relationship, resulting in tumor growth inhibition and regression in SJSA-1 tumor-bearing rats at well-tolerated oral (p.o.) doses. The validation and understanding of its mechanism of action, the overall favorable drug-like properties and the characterization of its on-target toxicological profile in preclinical species strongly supported the initiation of Phase I clinical trials with NVP-HDM201 in pre-selected patients with p53 wild-type tumors. Citation Format: Sébastien Jeay, Patrick Chène, Stéphane Ferretti, Pascal Furet, Bjoern Gruenenfelder, Vito Guagnano, Nelson Guerreiro, Ensar Halilovic, Francesco Hofmann, Joerg Kallen, Michelle Léonard, Robert Mah, Keiichi Masuya, Rita Ramos, Caroline Rynn, Stephan Ruetz, Thérèse Stachyra-Valat, Stefan Stutz, Andrea Vaupel, Jens Wuerthner, Philipp Holzer. NVP-HDM201: cellular and in vivo profile of a novel highly potent and selective PPI inhibitor of p53-Mdm2. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1225.
Plasma fibrinogen and fibrinogen genotypes in 4685 cases of myocardial infarction and in 6002 controls: Test of causality by "Mendelian randomisation"
Authors: L D Youngman, B D Keavney, A Palmer, S Parish, S Clark, J Danesh, M Delepine, M Lathrop, R Peto, R Collins
Journal: Circulation (2000)
Phase I Study of Bortezomib, (BTZ) Followed by High-Dose Melphalan, (HD Mel) and BTZ as Conditioning Regimen for Tandem Peripheral Blood Stem Cell Transplants (TanPSCT) in Patients with Primary Refractory Multiple Myeloma (MM) and Plasma Cell Leukemia (PCL).
Authors: Todd Alekshun, Christine Mcisaac-Simonelli, Mohamed Kharfan-Dabaja, William Dalton, Benjamin Djulbegovic, Hugo Fernandez, Daniel M. Sullivan, Ernesto Ayala, Teresa L. Field, Dawn Garrett, William E. Janssen, Beth Maddox, Lia Perez, Dawn Kettner, Janelle Perkins, Jyoti Raychaudhuri, Claudio Anasetii, Melissa Alsina
Journal: Blood (2007)
A phase II study of bevacizumab (B) and high-dose aldesleukin (IL-2) in patients (p) with metastatic renal cell carcinoma (mRCC): A Cytokine Working Group Study (CWGS).
Authors: U. B. Dandamudi, M. S. Ghebremichael, J. A. Sosman, M. M. Regan, M. B. Atkins, J. Clark, J. P. Dutcher, B. D. Curti, U. N. Vaishampayan, M. S. Ernstoff
Journal: Journal of Clinical Oncology (2010)

4530 Background: Overexpression of VEGF in RCC leads to angiogenesis and inhibition of immune function. We conducted a multicenter phase II study designed to estimate the efficacy of the addition of B to standard IL-2 therapy in mRCC patients. The primary objective of the study was to estimate progression-free survival (PFS) and response rate (RR). Methods: Patients with histologically confirmed mRCC, predominantly clear cell histology, measurable disease, KPS of ≥ 80%, adequate end organ function for IL-2, and no underlying coagulopathy or thrombotic event were eligible. IL-2 (600,000 IU/kg) IV Q8 hours (maximum 28 doses) was given during two 5-day courses starting on day 15 and 29 of each 84 day cycle. B (10 mg/kg) IV was given every 2 wks beginning on day 1. Results: 49 of 51 evaluable patients (33M: 18F) from 8 institutions (median age 55yrs: range 29-74) were enrolled. For evaluable patients, median PFS was 9.0 months (90% CI: 5.7 -13.0) and 2 year PFS was 15% (90% CI: 5-24%). Responses include complete (8%; 4p), partial (20%; 10p), and stable disease (42%; 21p). Median baseline serum VEGF (pg/ml) concentrations were 459 (range: 181-1873) among responders and 383 (range: 32-1340) in non-responders. Toxicities appeared to be no different from single agent IL-2 or B alone. Conclusions: The combination of HD IL-2 +B is a safe and active treatment for mRCC. B appears to increase the PFS of IL-2. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Dartmouth-Hitchcock Medical Center Biovex, Genentech, Novartis, Pfizer, Vical Genentech, Novartis, Pfizer Abbott Laboratories, Bristol-Myers Squibb, Genentech, Mannkind Corporation, Novartis, Pfizer
Risk-Reduction Program for Cardiovascular and Limb Events in Patients With Peripheral Arterial Disease
Authors: Tomoyuki Kawada
Journal: JAMA Surgery (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 Surgery 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 Surgery journal
Colonic Pro-inflammatory Macrophages Cause Insulin Resistance in an Intestinal Ccl2/Ccr2-Dependent Manner
Authors: Yoshinaga Kawano, Jun Nakae, Nobuyuki Watanabe, Tetsuhiro Kikuchi, Sanshiro Tateya, Yoshikazu Tamori, Mari Kaneko, Takaya Abe, Masafumi Onodera, Hiroshi Itoh
Journal: Cell Metabolism (2016)
Pericytes for the treatment of orthopedic conditions
Authors: Aaron W. James, Paul Hindle, Iain R. Murray, Christopher C. West, Tulyapruek Tawonsawatruk, Jia Shen, Greg Asatrian, Xinli Zhang, Vi Nguyen, A. Hamish Simpson, Kang Ting, Bruno Péault, Chia Soo
Journal: Pharmacology & Therapeutics (2016)
Abstract 403: Performance assessment of highly sensitive NGS assay for TP53
Authors: Johannes Fredebohm, Daniel Mehnert, Ann-Kathrin Löber, Hiroyuki Shimizu, Frank Holtrup, Frank Diehl
Journal: Cancer Research (2016)

Abstract We have designed a highly sensitive assay based on the Safe-Sequencing technology(1) to detect de novo mutations in the TP53 gene. A custom panel was designed to cover 95% of all reported mutations in TP53. To demonstrate assay performance, we assessed LoD, LoB, reproducibility, and repeatability and evaluated concordance with BEAMing(2). A customized data analysis pipeline for ultra-deep sequencing runs was developed that includes extensive quality control and advanced mutation calling. This highly sensitive NGS-based workflow can be applied to monitor recurrent or minimal residual disease in cancer patients after surgery or chemotherapy. References: (1) Kinde I, Wu J, Papadopoulos N, Kinzler KW, Vogelstein B. Detection and quantification of rare mutations with massively parallel sequencing. Proc Natl Acad Sci U S A. 2011 Jun 7; 108(23): 9530-9535 (2) Diehl F, Li M, He Y, Kinzler KW, Vogelstein B, Dressman D. BEAMing: single-molecule PCR on microparticles in water-in-oil emulsions. Nat Methods. 2006 Jul;3(7):551-9. Citation Format: Johannes Fredebohm, Daniel Mehnert, Ann-Kathrin Löber, Hiroyuki Shimizu, Frank Holtrup, Frank Diehl. Performance assessment of highly sensitive NGS assay for TP53. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 403.
Text Messaging and Medication Adherence—Do We Have a Missed Call?
Authors: Alireza Ahmadvand, Lisa Nissen
Journal: JAMA Internal Medicine (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 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
A Phase III Study of Enoxaparin Versus Low-Dose Warfarin Versus Aspirin as Thromboprophylaxis for Patients with Newly Diagnosed Multiple Myeloma Treated up-Front with Thalidomide-Containing Regimens
Authors: Michele Cavo, Antonio Palumbo, Sara Bringhen, Antonietta Falcone, Pellegrino Musto, Fabio Ciceri, Mariella Grasso, Renato Zambello, Maria Concetta Petti, Fabrizio Ciambelli, Giovanni De Sabbata, Stefano Rocco, Luigi Gugliotta, Filippo Gherlinzoni, Alfonso D’Arco, Massimo Martelli, Tommasina Guglielmelli, Paola Tacchetti, Michele Baccarani, Mario Boccadoro
Journal: Blood (2008)
Abstract 3655: Suppression of Plk3 expression by nickel may contribute to lung carcinogenesis
Authors: Cen Li, Soyoung Park, Wei Dai, Dazhong Xu
Journal: Cancer Research (2016)

Abstract Exposure to nickel (Ni) compounds is known to induce human lung malignancies. Research shows that Ni induces lung cancer mainly through epigenetic and metabolic pathways. Polo-like kinase 3 (Plk3) is a multifunctional protein kinase that involves in tumor initiation and progression. Plk3−/− mice tend to develop highly vascularized lung tumors at an advanced age. Reduced expression of Plk3 was reported in human lung cancers. In this study, we examined the effect of Ni on Plk3 expression in A549 lung carcinoma cells. Western blot showed that NiCl2 reduced the Plk3 protein level in a time- and dose-dependent manner. We then treated A549 cells with cycloheximide for various times to examine the effect of NiCl2 on the half-life of Plk3 protein. We observed a shortened half-life of Plk3 in the presence of NiCl2. A reduced level of Plk3 protein was also found in hypoxia-treated A549 cells. In addition, MG132, a specific proteasome inhibitor, could partially reverse the effect of NiCl2 or hypoxia on the Plk3 protein level. Our cell fractionation experiments showed that majority of the endogenous Plk3 protein is located in the cytoplasm where degradation of Plk3 likely occurs. Transfection of A549 cells with FLAG-tagged ubiquitin (FLAG-Ub) followed by treatment with NiCl2 and/or MG132, immunoprecipitation (IP) with an anti-FLAG antibody, and Western blot with an anti-Plk3 antibody showed that Plk3 was poly-ubiquitinated and that the ubiquitination was significantly enhanced by NiCl2 and/or MG132 treatments. The elevated ubiquitination of Plk3 in response to NiCl2 was further confirmed in 293T cells with co-transfection of Plk3 and FLAG-Ub. Furthermore, overexpression of USP28, a deubiquitinase known to be inhibited by Ni or hypoxia, partially restored the protein level of Plk3 suppressed by NiCl2. Moreover, real-time PCR analysis showed that NiCl2 also reduced the Plk3 mRNA level, in a time- and dose-dependent pattern. Taken together, our data show that NiCl2 suppresses Plk3 expressions by lowering the Plk3 mRNA level and promoting proteasome-mediated degradation of the Plk3 protein. Given the potential role of Plk3 as a tumor suppressor in the lung, suppression of Plk3 expression likely contributes to Ni-induced lung carcinogenesis and tumor progression. Citation Format: Cen Li, Soyoung Park, Wei Dai, Dazhong Xu. Suppression of Plk3 expression by nickel may contribute to lung carcinogenesis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3655.
Abstract 5096: Development of a decellularized tumor model for the evaluation of breast carcinomas
Authors: Elizabeth Martin, Nicholas Pashos, Jeffrey Gimble, Bruce Bunnell, Matthew Burow, Bridgette Collins-Burow
Journal: Cancer Research (2016)

Abstract Breast cancer recurrence is a clinical manifestation of tumor progression in patients which has been shown to significantly increase mortality rates. While up to one-fifth of breast cancer patients will experience recurrence, the mechanisms underlying this process remain poorly understood. Recently, gene expression profiling of human tumor metastasis and recurrence demonstrated that the extracellular matrix (ECM)-receptor interactions pathway was enhanced. In breast carcinomas, the ECM is known to vary with cancer progression. The ECM acts as a chemical reservoir, structural component, and mediator of tumorigenesis to tumors. To date, the ECM of breast carcinomas has been evaluated within the context of a seeded cellular population, i.e. intact tumor. Here we demonstrate for the first time a mechanism to evaluate the ECM devoid of breast cancer cells. We have employed a model of tissue decellularization to breast cancer cell line derived tumors and demonstrate that tumor ECM architecture remains intact when devoid of cells. Validation of loss of cell content is evident through DNA quantification, nuclear DAPI stain, and H&amp;E stain. Furthermore we demonstrate that structural proteins, fibronectin, collagen, and elastin are still retained within the decellularized scaffold. Applications of the tumor decellularization model will aid in the evaluation of ECM structural and molecular characteristics independent of cancer cell populations. The data presented here will enhance methods used to evaluate the cancer microenvironment and further our understanding of breast cancer recurrence, altering existing treatment strategies to extend survival. Citation Format: Elizabeth Martin, Nicholas Pashos, Jeffrey Gimble, Bruce Bunnell, Matthew Burow, Bridgette Collins-Burow. Development of a decellularized tumor model for the evaluation of breast carcinomas. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5096.
18F-FDG Uptake in Neurosarcoid Dural Plaque on PET/CT
Authors: Iman Khodarahmi, Roger E. Turbin, Larry P. Frohman, Nasrin Ghesani
Journal: Clinical Nuclear Medicine (2016)

While the imaging modality of choice to diagnose neurosarcoidosis is gadolinium-enhanced MRI, F-FDG PET/CT maybe used to stage the disease or target the optimal biopsy site. Few cases have described intense F-FDG uptake at the sites of active neurosarcoidosis in the midbrain and pituitary gland, cerebellar hemispheres, and temporal lobes. Here, we present a case of neurosarcoidosis whose PET/CT examination demonstrated F-FDG avidity in a dural plaque.
Abstract 5181: Dual inhibition of RNA Pol I transcription and PIM kinase as a new therapy to treat prostate cancer
Authors: Richard J. Rebello, Eric Kusnadi, Don Cameron, Analia Lesmana, Denis Drygin, Ashlee K. Clark, Laura Porter, Shahneen Sandhu, Gail P. Risbridger, Richard B. Pearson, Ross D. Hannan, Luc Furic
Journal: Cancer Research (2016)

Abstract Background: The MYC oncogene is commonly over-expressed in prostate cancer (PC). Upregulation of ribosome biogenesis and function is a characteristic feature of MYC-driven tumors. Accordingly, inhibition of ribosomal RNA (rRNA) synthesis with CX-5461, a potent, selective and orally bioavailable inhibitor of RNA polymerase I (Pol I) transcription has been successfully exploited therapeutically in models of hematological malignancy characterized by elevated MYC expression. Additionally, PIM kinases activate MYC signaling and mRNA translation in PC and cooperate with MYC to accelerate tumorigenesis. Here we investigate the efficacy of a dual approach targeting ribosome biogenesis and function to treat PC by combining CX-5461 with the pan-PIM kinase inhibitor CX-6258 in murine and human models Methods: The efficacy of CX-5461 and CX-6258, alone and in combination, was tested in PC cell lines, in the Hi-MYC mouse model of PC (n = 8-11 per group) and in PC metastatic tissues. Primary cell lines derived from Hi-MYC mice were used to analyze signaling events underpinning therapeutic efficacy. Triplicate experiments were analyzed with ANOVA followed by Dunnett's post hoc test. All statistical tests were two-sided. Results: CX-5461 reduced anchorage independent growth and induced cell cycle arrest in human PC cell lines and in primary prostatic epithelial cells from Hi-MYC mice (P&amp;lt;0.001). CX-5461 treatment of Hi-MYC mice induced p53 expression and activity and significantly reduced prostate epithelial cell proliferation (P = 0.02) and invasion. While CX-6258 showed little effect alone, its combination with CX-5461 further suppressed proliferation (P = 0.01), dramatically reduced the incidence of large invasive lesions from 64% to 9% and preserved prostate ductal architecture. This promising combination strategy prevented the growth of PDX tissue characterized by elevated MYC and resistance to conventional therapy (P = 0.04). Conclusions: Our results demonstrate preclinical efficacy of combination therapies targeting the ribosome at multiple levels and provide a new approach for treatment of PC with high MYC activity. Citation Format: Richard J. Rebello, Eric Kusnadi, Don Cameron, Analia Lesmana, Denis Drygin, Ashlee K. Clark, Laura Porter, Shahneen Sandhu, Gail P. Risbridger, Richard B. Pearson, Ross D. Hannan, Luc Furic. Dual inhibition of RNA Pol I transcription and PIM kinase as a new therapy to treat prostate cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 5181.