tbuckley/cabot-search huggingface dataset:
Left Ventricular Volume and Hypertrophy in Outflow Obstruction
Authors: C. Grant, M. J. Raphael, R. E. Steiner, J. F. Goodwin
Journal: Cardiovascular Research (1968)

Journal Article Left Ventricular Volume and Hypertrophy in Outflow Obstruction Get access Colin Grant, Colin Grant † From the Departments of Radiodiagnosis and Clinical Cardiology, Royal Postgraduate Medical School and Hammersmith Hospital, London, and the Department of Medicine, Buffalo General Hospital and the State University of New York, Buffalo, New York, U.S.A. † Research Trainee supported by Training Grant HE-5508-03 from the U.S. Public Health Service. Search for other works by this author on: Oxford Academic PubMed Google Scholar M. J. Raphael, M. J. Raphael From the Departments of Radiodiagnosis and Clinical Cardiology, Royal Postgraduate Medical School and Hammersmith Hospital, London, and the Department of Medicine, Buffalo General Hospital and the State University of New York, Buffalo, New York, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar R. E. Steiner, R. E. Steiner From the Departments of Radiodiagnosis and Clinical Cardiology, Royal Postgraduate Medical School and Hammersmith Hospital, London, and the Department of Medicine, Buffalo General Hospital and the State University of New York, Buffalo, New York, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. F. Goodwin J. F. Goodwin From the Departments of Radiodiagnosis and Clinical Cardiology, Royal Postgraduate Medical School and Hammersmith Hospital, London, and the Department of Medicine, Buffalo General Hospital and the State University of New York, Buffalo, New York, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 2, Issue 4, October 1968, Pages 346–355, https://doi.org/10.1093/cvr/2.4.346 Published: 01 October 1968 Article history Received: 22 January 1968 Published: 01 October 1968
Upregulation of Nitric Oxide Production in Vascular Endothelial Cells by All- <i>trans</i> Retinoic Acid Through the Phosphoinositide 3-Kinase/Akt Pathway
Authors: Akira Uruno, Akira Sugawara, Hiroshi Kanatsuka, Hiroyuki Kagechika, Akiko Saito, Kazunori Sato, Masataka Kudo, Kazuhisa Takeuchi, Sadayoshi Ito
Journal: Circulation (2005)

Background— A natural retinoid all- trans retinoic acid (ATRA) contains various beneficial effects on vasculature, including suppression of neointima formation after balloon injury. However, little is known about the effects of ATRA on vascular endothelial function. We therefore studied its role in nitric oxide (NO) production of vascular endothelial cells (ECs). Methods and Results— Human dermal microvascular ECs, human umbilical vein ECs, and SV40-transformed rat lung vascular ECs were incubated with or without ATRA (1 μmol/L) for 48 hours. Their NO production was determined with the use of a fluorescent NO indicator, diaminofluorescein-2 diacetate. ATRA significantly increased their basal as well as acetylcholine-induced NO production. Treatment with N ω -nitro- l -arginine methyl ester or carboxy-PTIO suppressed their fluorescence. Increase of NO production was also observed by incubation with retinoic acid receptor (RAR) agonist Am580. ATRA-induced NO increase was abolished by coincubation with RAR antagonist LE540. Moreover, the NO increase was completely inhibited by the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin and LY294002. ATRA as well as Am580 enhanced endothelial NO synthase (eNOS) phosphorylation at Ser-1177 as well as Akt phosphorylation at Ser-473 without changing their protein expression. Overexpression of dominant-negative Akt inhibited the eNOS phosphorylation. Moreover, ATRA increased PI3K activity as well as PI3K catalytic subunit p110β protein expression, which was completely inhibited by LE540 treatment. Real-time polymerase chain reaction analyses demonstrated that ATRA increased PI3K catalytic subunit p110β mRNA expression without affecting its stability. Finally, ATRA-induced NO increase was observed in COS-1 cells transfected with wild-type eNOS and RARα, but not with mutated eNOS whose Ser-1177 was substituted. Conclusions— ATRA increases NO production by eNOS phosphorylation through RAR-mediated PI3K/Akt pathway activation in vascular ECs and possibly plays beneficial roles in vascular endothelium. Retinoids may therefore be candidates as novel therapeutic agents against vascular disorders with endothelial damage.
Standard reference values for musculoskeletal ultrasonography
Authors: W A Schmidt
Journal: Annals of the Rheumatic Diseases (2004)

<b>Objectives:</b> To determine standard reference values for musculoskeletal ultrasonography in healthy adults. <b>Methods:</b> Ultrasonography was performed on 204 shoulders, elbows, hands, hips, knees, and feet of 102 healthy volunteers (mean age 38.4 years; range 20–60; 54 women) with a linear probe (10–5 MHz; Esaote Technos MP). Diameters of tendons, bursae, cartilage, erosions, hypoechoic rims around tendons and at joints were measured with regard to established standard scans. Mean, minimum, and maximum values, as well as two standard deviations (2 SD) were determined. Mean values ±2 SD were defined as standard reference values. <b>Results:</b> Hypoechoic rims were normally present in joints and tendon sheaths owing to physiological synovial fluid and/or cartilage. Similarly, fluid was found in the subdeltoid bursa in 173/204 (85%), at the long biceps tendon in 56 (27%), in the suprapatellar recess in 158 (77%), in the popliteal bursae in 32 (16%), and in the retrocalcaneal bursa in 49 (24%). Erosions of &gt;1 mm were seen at the humeral head in 47 (23%). Values for important intervals were determined. The correlation between two investigators was 0.96 (0.78–0.99). The reliability of follow up investigations was 0.83 (0.52–0.99). <b>Conclusions:</b> Fluid in bursae as well as hypoechoic rims within joints and around tendons are common findings in healthy people. This study defines standard reference values for musculoskeletal ultrasonography to prevent misinterpretation of normal fluid as an anatomical abnormality.
Proteomics: from single molecules to biological pathways
Authors: Sarah R. Langley, Joseph Dwyer, Ignat Drozdov, Xiaoke Yin, Manuel Mayr
Journal: Cardiovascular Research (2012)

The conventional reductionist approach to cardiovascular research investigates individual candidate factors or linear signalling pathways but ignores more complex interactions in biological systems. The advent of molecular profiling technologies that focus on a global characterization of whole complements allows an exploration of the interconnectivity of pathways during pathophysiologically relevant processes, but has brought about the issue of statistical analysis and data integration. Proteins identified by differential expression as well as those in protein–protein interaction networks identified through experiments and through computational modelling techniques can be used as an initial starting point for functional analyses. In combination with other '-omics' technologies, such as transcriptomics and metabolomics, proteomics explores different aspects of disease, and the different pillars of observations facilitate the data integration in disease-specific networks. Ultimately, a systems biology approach may advance our understanding of cardiovascular disease processes at a 'biological pathway' instead of a 'single molecule' level and accelerate progress towards disease-modifying interventions.
Relationship between blood flow to ischemic regions and extent of myocardial infarction. Serial measurement of blood flow to ischemic regions in dogs.
Authors: F Rivas, F R Cobb, R J Bache, J C Greenfield
Journal: Circulation Research (1976)

This study was designed to measure early sequential changes in blood flow to ischemic regions after acute coronary occlusion and to determine the relationship between blood flow and the extent of subsequent myocardial infarction. Initial studies were carried out on five dogs which verified using radioisotope-labeled microspheres, 7-10 mum in diameter, to measure changes in blood flow in small myocardial regions after acute coronary artery occlusions. Studies then were carried out on 11 awake dogs chronically prepared with dwelling catheters in the aorta and left atrium and occluders on the left circumflex coronary artery. Microspheres were injected via the left atrial catheter 45 seconds and 2, 6, and 24 hours after complete circumflex coronary occlusion. Six days later myocardial blood flow and the extent of histological infarction were determined for multiple samples from four transmural layers of the entire ischemic zone. Average blood flow to the circumflex region was 0.25 +/- 0.03 (SE), 0.39 +/- 0.05, and 0.53 +/- 0.07 ml/min per g at 45 seconds, and 2, 6, and 24 hours, respectively. When samples from each transmuarl layer were grouped according to increasing ranges of blood flow, the extent of infarction in each layer was inversely related to blood flow. When samples in the same range of blood flow were compared, the extent of infarction in endocardial samples exceeded that in epicardial samples. These data indicate that the relationship between a given measurement of regional blood flow after acute coronary occlusion and the extent of subsequent myocardial infarction varies in different transmural layers and is a function of the time after occlusion that blood flow is measured.
Who Needs Cause-of-Death Data?
Authors: Peter Byass
Journal: PLoS Medicine (2007)

More than half of the world's deaths pass by undocumented as to cause [1]. Whilst the appropriate focus of health services may well be the care of the living, consistent and reliable cause-of-death data also constitute a crucial and major resource for health planning and prioritisation, and their lack in many settings is a major concern. Two new papers from Christopher Murray and colleagues in this issue of PLoS Medicine [2,3] report important methodological advances which should go some way towards filling these data gaps.
Reply to the Letter to the Editor from Schultes et al
Authors: Paul Sabbatini, Kunle Odunsi
Journal: Clinical Cancer Research (2007)

In Response: We wish to thank Drs. Schultes, Smith, and Nicodemus for their questions about our characterization of oregovomab as passive immunotherapy, the potential interference of human anti-mouse antibody (HAMA) in the Luminex assay used in our studies, and clarification on the induction of
Safe discharge of patients with low-risk upper gastrointestinal bleeding (UGIB): can use of Glasgow-Blatchford Bleeding Score (GBS) be extended?
Authors: I. R. Le Jeune, A. Gordon, D. Farrugia, R. Manwani, N. Guha, M. W. James
Journal: Gut (2011)

<h3>Introduction</h3> Risk stratification of patients with suspected UGIB using either Glasgow-Blatchford Bleeding Score or pre-endoscopy Rockall score to facilitate early safe discharge (GBS = 0, pre-Rockall = 1) has been reported.12 This observational study compared score utility and considered the impact of extending the range of GBS or pre-Rockall scores permitting safe discharge. <h3>Methods</h3> Consecutive adult patients presenting from September 2008-March 2009 with suspected UGIB to acute medicine and the emergency department had clinical history, vital signs, laboratory and endoscopy results prospectively recorded using electronic databases. GBS, pre-Rockall scores and a composite endpoint (blood transfusion, endoscopic therapy, interventional radiology and surgery or 30-day mortality) were calculated. <h3>Results</h3> 388 patients with suspected UGIB were identified of which 92.3% were admitted (median (range) GBS = 5 (0–19) and Pre-Rockall = 2 (0–11)), representing 2.4% of 14,809 medical admissions. 7.7% were discharged (GBS = 0 (0–4) and Pre-Rockall = 0 (0–4)). 47.9% underwent endoscopy. 151 (38.9%) patients had the composite endpoint; of these, 77.5% received blood transfusion, 45.7% endoscopic treatment and 8.0% died within 30 days. AUROC (95% CI) for 30-day composite endpoint was 0.92 (0.89–0.94) using GBS and 0.75 (0.70–0.80) using pre-Rockall. Sensitivity, specificity, NPV and PPV for different GBS and pre-Rockall score thresholds are listed in table 1. <h3>Conclusion</h3> GBS is superior to pre-Rockall in predicting patients with UGIB who can be safely discharged. Sensitivity analysis suggests that patients with GBS &lt;3 could be considered for early discharge doubling the number of eligible patients (from 15.2% to 32.5%). This has important patient safety and financial implications.
Evidence That Methylphenidate Enhances the Saliency of a Mathematical Task by Increasing Dopamine in the Human Brain
Authors: Nora D Volkow, Gene-Jack Wang, Joanna S Fowler, Frank Telang, Laurence Maynard, Jean Logan, Samuel J Gatley, Naomi Pappas, Christopher Wong, Paul Vaska, Wei Zhu, James M Swanson
Journal: American Journal of Psychiatry (2004)

Methylphenidate is the most commonly prescribed drug for attention deficit hyperactivity disorder (ADHD), yet its therapeutic mechanisms are poorly understood. The objective of this study was to assess if methylphenidate, by increasing dopamine (neurotransmitter involved in motivation) in brain, would enhance the saliency of an academic task, making it more interesting.Healthy subjects (N=16) underwent positron emission tomography with [(11)C]raclopride (dopamine D(2) receptor radioligand that competes with endogenous dopamine for binding) to assess the effects of oral methylphenidate (20 mg) on extracellular dopamine in the striatum. The authors compared the effects of methylphenidate during an academic task (solving mathematical problems with monetary reinforcement) and a neutral task (passively viewing cards with no remuneration). In parallel, the effects of methylphenidate on the interest that the academic task elicited were also evaluated.Methylphenidate, when coupled with the mathematical task, significantly increased extracellular dopamine, but this did not occur when coupled with the neutral task. The mathematical task did not increase dopamine when coupled with placebo. Subjective reports about interest and motivation in the mathematical task were greater with methylphenidate than with placebo and were associated with dopamine increases.The significant association between methylphenidate-induced dopamine increases and the interest and motivation for the task confirms the prediction that methylphenidate enhances the saliency of an event by increasing dopamine. The enhanced interest for the task could increase attention and improve performance and could be one of the mechanisms underlying methylphenidate's therapeutic effects. These findings support educational strategies that make schoolwork more interesting as nonpharmacological interventions to treat ADHD.
Sir Arbuthnot Lane, Chronic Intestinal Stasis, and Autointoxication
Authors: J. LACEY SMITH
Journal: Annals of Internal Medicine (1982)

In the early 1900s, a theory that constipation (stasis) led to systemic dysfunction became popular. Sir Arbuthnot Lane was largely responsible for the popularity of this theory, which was constructed entirely on unfounded hypotheses. As a result, colon bypass or colectomy was done for indications ranging from lassitude to epilepsy. The theory was accepted—although disputed—until the clinical futility of radical surgery was recognized. The favorable acceptance of stasis in its time exemplifies the dangers of medical practice by hypothesis.
Sleep-related Periodic Breathing Does Not Acclimatize to Chronic Hypobaric Hypoxia: A 1-Year Study at High Altitude in Antarctica
Authors: Helio Fernandez Tellez, Olivier Mairesse, Eoin Macdonald-Nethercott, Xavier Neyt, Romain Meeusen, Nathalie Pattyn
Journal: American Journal of Respiratory and Critical Care Medicine (2014)
Serum-based tracking of de novo initiated liver cancer progression reveals early immunoregulation and response to therapy
Authors: Jeff J. Subleski, Anthony J. Scarzello, W. Gregory Alvord, Qun Jiang, Jimmy K. Stauffer, Anthony Kronfli, Bahara Saleh, Timothy Back, Jonathan M. Weiss, Robert H. Wiltrout
Journal: Journal of Hepatology (2015)

Background & AimsLiver inflammatory diseases associated with cancer promoting somatic oncogene mutations are increasing in frequency. Preclinical cancer models that allow for the study of early tumor progression are often protracted, which limits the experimental study parameters due to time and expense. Here we report a robust inexpensive approach using Sleeping Beauty transposition (SBT) delivery of oncogenes along with Gaussia Luciferase expression vector GLuc, to assess de novo liver tumor progression, as well as the detection of innate immune responses or responses induced by therapeutic intervention.MethodsTracking de novo liver tumor progression with GLuc was demonstrated in models of hepatocellular carcinoma (HCC) or adenoma (HCA) initiated by hydrodynamic delivery of SBT oncogenes.ResultsRising serum luciferase levels correlated directly with increasing liver tumor burden and eventual morbidity. Early detection of hepatocyte apoptosis from mice with MET+CAT transfected hepatocytes was associated with a transient delay in HCC growth mediated by a CD8+ T-cell response against transformed hepatocytes. Furthermore, mice that lack B cells or macrophages had an increase in TUNEL+ hepatocytes following liver MET transfection demonstrating that these cells provide protection from MET-induced hepatocyte apoptosis. Treatment with IL-18+IL-12 of mice displaying established HCC decreased tumor burden which was associated with decreased levels of serum luciferase.ConclusionsHydrodynamic delivery of the SBT vector GLuc to hepatocytes serves as a simple blood-based approach for real-time tracking of pathologically distinct types of liver cancer. This revealed tumor-induced immunologic responses and was beneficial in monitoring the efficacy of therapeutic interventions.
Association of FOXP3 (rs3761548) promoter polymorphism with nondermatomal vitiligo: A study from India
Authors: Parveen Jahan, Rajeshwari Cheruvu, Surekha Tippisetty, Prasanna Latha Komaravalli, Vijayalakshmi Valluri, Mohammed Ishaq
Journal: Journal of the American Academy of Dermatology (2013)
Roles of Chemokine Receptor 4 (CXCR4) and Chemokine Ligand 12 (CXCL12) in Metastasis of Hepatocellular Carcinoma Cells
Authors: Hui Liu, Zeya Pan, Aijun Li, Siyuan Fu, Yin Lei, Hangyong Sun, Mengchao Wu, Weiping Zhou
Journal: Cellular and Molecular Immunology (2008)
C-Src is required for complex formation between the hepatitis C virus-encoded proteins NS5A and NS5B: A prerequisite for replication
Authors: Andreas Pfannkuche, Katrin Büther, Juliane Karthe, Marion Poenisch, Ralf Bartenschlager, Mirko Trilling, Hartmut Hengel, Dieter Willbold, Dieter Häussinger, Johannes Georg Bode
Journal: Hepatology (2011)

Hepatitis C virus (HCV) is a leading cause of chronic liver disease worldwide and establishes a persistent infection in more than 60% of infected individuals. This high frequency of persistent infection indicates that HCV has evolved efficient strategies to interfere with the adaptive and innate immune response and to occupy and use host cell infrastructure. The present study provides evidence that c-Src, a member of the Src family kinases that participates in many signal transduction pathways, represents an essential host factor exploited for viral replication. c-Src directly interacts with the viral RNA-dependent RNA polymerase (NS5B) via its SH3 domain and with the nonstructural phosphoprotein NS5A via its SH2 domain. Both interactions are required to maintain the protein-protein interaction of NS5A and NS5B, which has been previously demonstrated to be essential for viral replication. Accordingly, HCV genome replication and production of the viral proteins was strongly reduced upon small interfering RNA-mediated knockdown of c-Src or in the presence of the tyrosine kinase inhibitor herbimycin A. This effect could not be rescued by supplementation of the two other ubiquitously expressed Src family kinases Fyn or Yes. Conclusion: Our data suggest that c-Src participates in the formation of an NS5A/NS5B protein complex that is required for efficient replication of HCV. (HEPATOLOGY 2011;53:-)
Identification of mutation-specific tumor infiltrating lymphocytes from metastatic ovarian cancer
Authors: Drew C Deniger, Mini Bharathan, Pasetto Anna, Eric Tran, Jared J Gartner, Todd D Prickett, Paul F Robbins, Steven A Rosenberg
Journal: Journal for ImmunoTherapy of Cancer (2015)

Meeting abstracts Novel interventions are needed for the treatment of women with metastatic ovarian cancer that causes 14,000 deaths each year in the USA. Retrospective analysis of tumor infiltrating lymphocytes (TIL) infused into patients who achieved complete, durable regressions of metastatic
Correlation between epidermal growth factor receptor (EGFR) protein expression (PE) and gene amplification (GA) in non-small cell lung carcinoma (NSCLC)
Authors: S. Dacic, S. Ramalingam, M. Flanagan, K. Cieply, J. D. Luketich, C. P. Belani, S. Yousem
Journal: Journal of Clinical Oncology (2005)

7079 Background: Inhibition of EGFR pathway is an established strategy for the treatment of advanced NSCLC. In NSCLC, EGFR expression has been analyzed by immunohistochemistry (IHC) and has not shown any correlation with response to EGFR inhibitors. We evaluated 199 consecutive cases of newly diagnosed NSCLC to determine the correlation between EGFR PE and GA with various clinico-pathological characteristics and survival. Methods: IHC was performed and graded using anti-EGFR mouse monoclonal antibody (DakoCytomation, Carpenter, CA). For GA, FISH analysis was performed using the dual-color EGFR SpectrumOrange/CEP7 SpectrumGreeen probe (Vysis, Downers Grove, IL) and paraffin pretreatment reagent kit (Vysis, Inc., Downers Grove, IL). Average and maximum numbers of EGFR gene copies per cell, average ratio of EGFR gene to chromosome 7 centromere signals (CEP7) and amplification were determined by FISH for each tumor. Amplification was defined as a ratio of EGFR signals to CEP7 of ≥2.0. Results: EGFR PE was more frequent in squamous cell carcinoma (SCC) (26%) than in adenocarcinoma (ADC) (11%) (P=0.0076). EGFR GA was present in 10% of NSCLC. SCC had a higher ratio of CEP7 than ADC (mean ratio 1.95 vs 1.47) (P=0.0005). Of 34 cases with PE (18 SCC, 15 ADC) only 15 (44%) had EGFR GA, and 5 of those without PE demonstrated GA. There was no correlation between EGFR PE/GA with age, gender, stage or survival. Poorly differentiated carcinomas(PDC) demonstrated higher average number of EGFR gene copies/cell (mean 4.10, P=0.032). Higher ratio of EGFR gene to CEP7 was seen in PDC (mean ratio 1.839, P=0.0324) and stage pT1 (mean ratio 1.797, P=0.0243). Conclusions: EGFR PE or GA did not correlate with outcome for NSCLC. Our data indicate that expression of EGFR is regulated by gene amplification in only a small subset of NSCLC. No significant financial relationships to disclose.