tbuckley/cabot-search huggingface dataset:
Abstract 1165: A tissue-engineered bone mimetic in vitro model for monitoring metastatic PCa growth and therapy response
Authors: Claudia Paindelli, Dietmar Hutmacher, Peter Friedl, Eleonora Dondossola
Journal: Cancer Research (2018)

Abstract Despite recent advances in prostate cancer (PCa) treatment, the outcome of metastatic disease remains frequently fatal and the underlying biology poorly understood. Thus, the development of clinically relevant in vitro models to monitor PCa biology in organotypic bone-like environment is critical to uncover mechanisms of therapy resistance and identify more effective treatments. To establish a bone-mimetic culture, we combined the following components: (i) bioactive osteoblasts depositing bone-like calcified extracellular matrix, (ii) complex 3D surface geometries, (iii) multicellular tumor application as spheroids/organoids, and (iv) applicability for live-cell microscopy to monitor the development of lesions over time. Calcified polycaprolactone (PCL) scaffolds were functionalized with bone-derived human mesenchymal stem cells (hMSCs) differentiated to osteoblasts, to generate a 3D niche-like calcified scaffold. PCa spheroids (PC3, C4-2B, patient-derived xenografts) were on-planted and their growth and invasion longitudinally monitored by advanced microscopy. PCa spheroids seeded on the organotypic bone model could be maintained and expanded over weeks, sufficient for monitoring therapy response to docetaxel, a first-line therapy for advanced PCa. The bone mimetic culture further revealed resistance to docetaxel mainly at the invasive edges, through a mechanism depending on the presence of osteoblasts. Thus, this 3D in vitro organotypic model will be suitable for dissecting the physical and molecular PCa cell-osteoblast interaction involved in PCa growth and therapy resistance. Citation Format: Claudia Paindelli, Dietmar Hutmacher, Peter Friedl, Eleonora Dondossola. A tissue-engineered bone mimetic in vitro model for monitoring metastatic PCa growth and therapy response [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1165.
Abstract P265: Association of Dietary Fatty Acid Intake with Serum High-density Lipoprotein Particle Concentration
Authors: MaryamZaid, KatsuyukiMiura, AkiraFujiyoshi, AkiraOkayama, HideakiNakagawa, KiyomiSakata, ShigeyukiSaito, NagakoOkuda, KatsushiYoshita, SohelChoudhury, BeatrizRodriguez, KamalMasaki, BradleyWillcox, NaokoMiyagawa, JeremiahStamler, HirotsuguUeshima
Journal: Circulation (2014)

Background: Studies have found that HDL particle (HDL-P) concentration is inversely associated with risk of CVD, independent of HDL cholesterol (HDL-C). Dietary factors (such as fatty acid intake) have been found to affect levels of HDL-C and influence risk of CVD. However, little is known about the associations of dietary fatty acid with serum HDL-P levels. Hypothesis: We hypothesized that dietary fatty acid associations with HDL-P are independent of HDL-C in men. Methods: Data were from 463 male participants in the 1996-98 cross-sectional INTERLIPID Study, ages 40-59 years, randomly selected from five populations; four in Japan (n=386) and one in Hawaii (n=77). Fatty acid intake was estimated from the mean of four in-depth 24-hour dietary recalls (% kcal per day). Individuals were excluded due to missing data on HDL-P or HDL-C and use of lipid lowering medication. Serum HDL-P was measured using nuclear magnetic resonance and HDL-C was measured using standard methods. Multiple linear regression models we...
Cardiac Actions of Methoxamine
Authors: Shoichiimai, Tatsuroshigei, Korokuhashimoto
Journal: Circulation Research (1961)

The cardiac action of large doses of methoxamine and its antagonistic action to epinephrine were studied, using a dog heart-lung preparation. In doses of 4 mg. and above, methoxamine showed a marked negative inotropic action, while it produced only a slight decrease in the heart rate. Pretreatment of animals with 0.1 mg./Kg. of reserpine did not modify the inotropic action, but the decrease in the heart rate disappeared. Simultaneous with these changes, a decrease in the coronary flow and a rise of the pulmonary arterial pressure were observed. Methoxamine in doses of 1 mg. and more abolished both the positive inotropic and the positive chronotropic actions of epinephrine. The negative inotropic action of methoxamine was ascribed to a nonspecific, as yet undetermined mechanism, and the antagonistic action was ascribed to the competitive antagonism at the receptor site (thus methoxamine may be looked upon as a blocking agent of adrenergic β receptor). The weak negative chronotropic action was taken to be a...
Abstract 2520: FGFR2 and miR-671-5p as key participants involved in the progression of human esophageal squamous cell carcinoma
Authors: Xiaojia Chen, Xiaoyan Li, Baoqing Tian, Xuan Tan, Wei Han, Jiakang Wang, An Hong
Journal: Cancer Research (2018)

Abstract Esophageal cancer is the world's tenth common malignant tumor. Esophageal cancer is divided into esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (ECA). ESCC is the dominant histological subtype. The overall 5-year survival rate for people with advanced-stage of ESCC is only about 10%-20%, but ESCC is still not well-studied. Therefore, it is very important to study the mechanism of cancer progression in ESCC in order to develop new therapies for this deadly disease. Fibroblast growth factor receptor2 (FGFR2) is one of the RTK members and generally regarded as an oncogene, but little is known about its function in ESCC. In our study, we proved FGFR2 played the key role in ESCC progression. From In vitro studies, overexpression of FGFR2 promoted the ESCC cells' migration, invasion, and proliferation, which was confirmed through knocking down FGFR2 in ESCC cells. In vivo xenograft tumor mouse model studies showed the tumor size from ESCC cells with FGFR2 over-expression larger than that of the control group. Conversely, the tumor size from ESCC cells with FGFR2 knock-down was significantly smaller compared with the control group. Molecular mechanism studies showed that overexpression of FGFR2 activated the ERK and AKT signal pathways and altered the cell cycle in ESCC. In addition, decreased expression of miR-671-5p was identified by microRNA array and QPCR verify assay in ESCC–FGFR2+ tissue. Using a dual influence report system, we confirmed miR-671-5p could regulate expression of FGFR2. It was also found that FGFR2 was highly expressed whereas miR-671-5p was expressed at a low level in most of the FGFR2-positive ESCC clinic samples. Furthermore, we demonstrated that miR-671-5p could inhibit the proliferation and metastasis of ESCC cells in vitro and it could suppress growth of ESCC in vivo. The miR-671-5p suppressed MAPK and PI3K signal pathways through down-regulation of phosphorylation of FGFR2. Therefore, miR-671-5p was seen as a tumor suppressor in ESCC. Our results demonstrated that FGFR2 and miR-671-5p are potential therapeutic targets in ESCC. They both participate in the progression of ESCC, but also play the contrasting roles. Antagonists of FGFR2 or activators of miR-671-5p could be therapeutics against ESCC. Citation Format: Xiaojia Chen, Xiaoyan Li, Baoqing Tian, Xuan Tan, Wei Han, Jiakang Wang, An Hong. FGFR2 and miR-671-5p as key participants involved in the progression of human esophageal squamous cell carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2520.
Challenges in Open Access Publishing
Authors: Nishant Ganesh Kumar, Keith G. Meador, Brian C. Drolet
Journal: JAMA Surgery (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA 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
Outcomes of Cardiac Screening in Adolescent Soccer Players
Authors: Aneil Malhotra, Harshil Dhutia, Gherardo Finocchiaro, Sabiha Gati, Ian Beasley, Paul Clift, Charlotte Cowie, Antoinette Kenny, Jamil Mayet, David Oxborough, Kiran Patel, Guido Pieles, Dhrubo Rakhit, David Ramsdale, Leonard Shapiro, John Somauroo, Graham Stuart, Amanda Varnava, John Walsh, Zaheer Yousef, Maite Tome, Michael Papadakis, Sanjay Sharma
Journal: New England Journal of Medicine (2018)

Reports on the incidence and causes of sudden cardiac death among young athletes have relied largely on estimated rates of participation and varied methods of reporting. We sought to investigate the incidence and causes of sudden cardiac death among adolescent soccer players in the United Kingdom.
Maternal dietary antioxidant intake in pregnancy and childhood respiratory and atopic outcomes: birth cohort study
Authors: Annabelle Bédard, Kate Northstone, John W. Holloway, A. John Henderson, Seif O. Shaheen
Journal: European Respiratory Journal (2018)

Evidence for a possible protective effect of maternal dietary antioxidant intake during pregnancy on childhood asthma and other atopic outcomes is conflicting, and associations with childhood lung function have been little studied. In the Avon Longitudinal Study of Parents and Children, we analysed associations between maternal intake of fruits, vegetables, vitamins C and E, carotene, zinc, and selenium in pregnancy and current doctor-diagnosed asthma, atopy and lung function in 8915 children at age 7–9 years. Potential modification of associations by maternal smoking and common maternal antioxidant gene polymorphisms was explored to strengthen causal inference. After controlling for confounders, positive associations were observed between maternal intake of zinc and childhood forced expiratory volume in 1 s and forced vital capacity (difference in age-, height- and sex-adjusted sd units per quartile increase in maternal dietary zinc intake β 0.05 (95% CI 0.01–0.08); p trend =0.01 and 0.05 (95% CI 0.02–0.09); p trend =0.005, respectively). Weak evidence was found for an interaction between maternal zinc intake and maternal glutathione S -transferase GSTM1 genotype on childhood forced vital capacity (p interaction =0.05); association among the GSTM1 null group β 0.11 (95% CI 0.05–0.17); p trend =0.001. Our results suggest that a higher maternal intake of zinc during pregnancy may be associated with better lung function in the offspring.
Long-Term Prognosis of Patients With Takotsubo Syndrome
Authors: Jelena R. Ghadri, Ken Kato, Victoria L. Cammann, Sebastiano Gili, Stjepan Jurisic, Davide Di Vece, Alessandro Candreva, Katharina J. Ding, Jozef Micek, Konrad A. Szawan, Beatrice Bacchi, Rahel Bianchi, Rena A. Levinson, Manfred Wischnewsky, Burkhardt Seifert, Susanne A. Schlossbauer, Rodolfo Citro, Eduardo Bossone, Thomas Münzel, Maike Knorr, Susanne Heiner, Fabrizio D’Ascenzo, Jennifer Franke, Annahita Sarcon, L. Christian Napp, Milosz Jaguszewski, Michel Noutsias, Hugo A. Katus, Christof Burgdorf, Heribert Schunkert, Holger Thiele, Johann Bauersachs, Carsten Tschöpe, Burkert M. Pieske, Lawrence Rajan, Guido Michels, Roman Pfister, Alessandro Cuneo, Claudius Jacobshagen, Gerd Hasenfuß, Mahir Karakas, Wolfgang Koenig, Wolfgang Rottbauer, Samir M. Said, Ruediger C. Braun-Dullaeus, Adrian Banning, Florim Cuculi, Richard Kobza, Thomas A. Fischer, Tuija Vasankari, K.E. Juhani Airaksinen, Grzegorz Opolski, Rafal Dworakowski, Philip MacCarthy, Christoph Kaiser, Stefan Osswald, Leonarda Galiuto, Filippo Crea, Wolfgang Dichtl, Klaus Empen, Stephan B. Felix, Clément Delmas, Olivier Lairez, Ibrahim El-Battrawy, Ibrahim Akin, Martin Borggrefe, John Horowitz, Martin Kozel, Petr Tousek, Petr Widimský, Ekaterina Gilyarova, Alexandra Shilova, Mikhail Gilyarov, David E. Winchester, Christian Ukena, Jeroen J. Bax, Abhiram Prasad, Michael Böhm, Thomas F. Lüscher, Frank Ruschitzka, Christian Templin
Journal: Journal of the American College of Cardiology (2018)
Enhanced Cardiac Contractility After Gene Transfer of V2 Vasopressin Receptors In Vivo by Ultrasound-Guided Injection or Transcoronary Delivery
Authors: Hans-JörgWeig, Karl-LudwigLaugwitz, AlessandraMoretti, KaiKronsbein, ChristianStädele, StefanBrüning, MelchiorSeyfarth, ThomasBrill, AlbertSchömig, MartinUngerer
Journal: Circulation (2000)

Background—Systemic levels of arginine vasopressin (AVP) are increased in congestive heart failure, resulting in vasoconstriction and reduced cardiac contractility via V1 vasopressin receptors. V2 vasopressin receptors (V2Rs), which promote activation of adenylyl cyclase, are physiologically expressed only in the kidney and are absent in the myocardium. Heterologous expression of V2Rs in the myocardium could result in a positive inotropic effect by using the endogenous high concentrations of AVP in heart failure. Methods and Results—We tested gene transfer with a recombinant adenovirus for the human V2R (Ad-V2R) to stimulate contractility of rat or rabbit myocardium in vivo. Ultrasound-guided direct injection or transcoronary delivery of adenovirus in vivo resulted in recombinant receptor expression in the myocardial target area, leading to a substantial increase in [3H]AVP binding. In 50% of the cardiomyocytes isolated from the directly injected area, single-cell shortening measurements detected a signif...
Influence of an Oscillating Bed on Cutaneous Temperature and Oxygen Tension of Ischemic Toes
Authors: Carlosforno, Hughmontgomery, Orvillehorwitz
Journal: Circulation (1958)

Measurements of temperature and oxygen tension of the skin demonstrated that treatment with an oscillating bed increases the circulation to ischemic toes. When the angle and duration of the dependent position of the foot of the bed were increased, further increments in circulation resulted.
Protein Kinase A as Another Mediator of Ischemic Preconditioning Independent of Protein Kinase C
Authors: ShojiSanada, HiroshiAsanuma, OsamuTsukamoto, TetsuoMinamino, KoichiNode, SeijiTakashima, TomiFukushima, AkikoOgai, YoshiroShinozaki, MasashiFujita, AkioHirata, HirokoOkuda, HiroakiShimokawa, HitonobuTomoike, MasatsuguHori, MasafumiKitakaze
Journal: Circulation (2004)

Background— We and others have reported that transient accumulation of cyclic AMP (cAMP) in the myocardium during ischemic preconditioning (IP) limits infarct size independent of protein kinase C (PKC). Accumulation of cAMP activates protein kinase A (PKA), which has been demonstrated to cause reversible inhibition of RhoA and Rho-kinase. We investigated the involvement of PKA and Rho-kinase in the infarct limitation by IP. Methods and Results— Dogs were subjected to 90-minute ischemia and 6-hour reperfusion. We examined the effect on Rho-kinase activity during sustained ischemia and infarct size of (1) preischemic transient coronary occlusion (IP), (2) preischemic activation of PKA/PKC, (3) inhibition of PKA/PKC during IP, and (4) inhibition of Rho-kinase or actin cytoskeletal deactivation during myocardial ischemia. Either IP or dibutyryl-cAMP treatment activated PKA, which was dose-dependently inhibited by 2 PKA inhibitors (H89 and Rp-cAMP). IP and preischemic PKA activation substantially reduced infar...
Abstract 1492: High-efficiency, strand-specific, low-bias library preparation method for transcriptome profiling of low-input RNA
Authors: Anetta Nowosielska-Vecchietti
Journal: Cancer Research (2018)

Abstract RNA Sequencing (RNA-seq) is a powerful technique for transcriptome analysis. It is widely used for gene expression analysis, detection of mutations, fusion transcripts, alternative splicing, and the study of post transcriptional modifications. RNA-seq is emerging as a powerful tool for molecular diagnostics as well, providing insights into the biological pathways and molecular mechanisms associated with disease progression including cancer. Recent improvements in next generation sequencing technologies (NGS) and sample barcoding strategies have resulted in significant cost reduction. As RNA-seq is increasingly adopted for molecular diagnostics, the quality and reproducibility of library preparation methods become more important. In addition, demand for library preparation methods that produce successful NGS libraries from very low input RNA or precious clinical samples is increasing. To achieve these goals, we have developed an RNA-seq library preparation method which can be used across a wide range of input RNA (5-1000 ng total RNA). GC content analysis, gene body coverage and gene expression correlation show that these important parameters remain consistent across varying inputs, even though input amounts vary by two orders of magnitude. As a result, our method has increased sensitivity and specificity for low-abundance transcripts, and reduced PCR duplicates and sequence bias, delivering high quality strand-specific data. Our method is compatible with poly A-tail enriched and ribosomal RNA depleted samples as well as RNA extracted from FFPE (formaldehyde fixed paraffin embedded) tissue samples. Citation Format: Anetta Nowosielska-Vecchietti. High-efficiency, strand-specific, low-bias library preparation method for transcriptome profiling of low-input RNA [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1492.
Adventitial Mast Cells Contribute to Pathogenesis in the Progression of Abdominal Aortic Aneurysm
Authors: ToshihiroTsuruda, JohjiKato, KintaHatakeyama, KazushiKojima, MitsuhiroYano, YoshikazuYano, KunihideNakamura, FukumiNakamura-Uchiyama, YoshibumiMatsushima, TakurohImamura, ToshioOnitsuka, YujiroAsada, YukifumiNawa, TanenaoEto, KazuoKitamura
Journal: Circulation Research (2008)

Abdominal aortic aneurysm (AAA) is histologically characterized by medial degeneration and various degrees of chronic adventitial inflammation, although the mechanisms for progression of aneurysm are poorly understood. In the present study, we carried out histological study of AAA tissues of patients, and interventional animal and cell culture experiments to investigate a role of mast cells in the pathogenesis of AAA. The number of mast cells was found to increase in the outer media or adventitia of human AAA, showing a positive correlation between the cell number and the AAA diameter. Aneurysmal dilatation of the aorta was seen in the control (+/+) rats following periaortic application of calcium chloride (CaCl2) treatment but not in the mast cell–deficient mutant Ws/Ws rats. The AAA formation was accompanied by accumulation of mast cells, T lymphocytes and by activated matrix metalloproteinase 9, reduced elastin levels and augmented angiogenesis in the aortic tissue, but these changes were much less in ...
Abstract 2287: Precise common and rare germline CNV calling with GATK
Authors: Mehrtash Babadi, Samuel K. Lee, Andrey Smirnov, Lee Lichtenstein, Laura D. Gauthier, Daniel P. Howrigan, Timothy Poterba
Journal: Cancer Research (2018)

Abstract We propose, implement, and evaluate a novel method (GATK gCNV) for accurate discovery of rare and common copy-number variations (CNVs) from read-depth data obtained from whole genome sequencing (WGS), whole exome sequencing (WES), or custom gene panels. GATK gCNV utilizes a sophisticated Bayesian model to learn bias factors arising from sequencing and library preparation. This model accounts for ploidy of sex chromosomes and autosomal aneuploidies, treats GC bias probabilistically, and automatically determines the necessary level of model complexity in a data-driven manner. Unlike most existing read-depth methods, GATK gCNV maintains a high level of sensitivity in common CNV regions, due to a hierarchical hidden Markov model used for accurate genotyping of multi-allelic loci. Furthermore, GATK gCNV performs bias modeling and CNV discovery simultaneously and self-consistently, resulting in significantly improved sensitivity and precision. Our implementation utilizes the PyMC3/Theano framework for performing automatic differentiation variational inference (ADVI). In addition, GATK gCNV automatically scatters large tasks across multiple machines using the Cromwell/WDL framework, enabling the scalable processing of large cohorts. We use GATK gCNV to compute copy-number transmission and de novo rates in a cohort of WES trios and observe consistency with observed population metrics. Furthermore, we benchmark GATK gCNV for sensitivity, precision, and reproducibility of both rare and common CNV calls. Using a cohort of WES blood normal samples from The Cancer Genome Atlas (TCGA), we show that GATK gCNV calls are in remarkable concordance with Genome STRiP calls on matched WGS data and gCNV substantially outperforms XHMM and CODEX. We also validate GATK gCNV calls on WGS data against calls made using PacBio long reads. Citation Format: Mehrtash Babadi, Samuel K. Lee, Andrey Smirnov, Lee Lichtenstein, Laura D. Gauthier, Daniel P. Howrigan, Timothy Poterba. Precise common and rare germline CNV calling with GATK [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2287.