tbuckley/cabot-search huggingface dataset:
Effects of Glucagon on Myocardial Metabolism in Patients With and Without Coronary Artery Disease
Authors: MARTIAL G. BOURASSA, JOSÉ EIBAR, LUCIEN CAMPEAU
Journal: Circulation (1970)

The metabolic effects of glucagon on the heart were studied in subjects with and without coronary artery disease. In both groups, a moderate rise in the arterial glucose level occurred with practically unchanged glucose uptake by the myocardium. Myocardial oxygen extraction was also unchanged in both groups of subjects. In individuals with normal coronary arteries, myocardial extraction ratio of lactate was normal before and unchanged after glucagon administration. In patients with significant coronary artery disease, mean extraction ratio of lactate was very low before glucagon and increased markedly following its administration. Seven of 18 patients had production of lactate by the myocardium before glucagon, and this reverted to lactate extraction 5 min after glucagon administration. Left ventricular work index was found to increase more than indices of myocardial contractility and oxygen consumption, and improved aerobic lactate utilization during glucagon action may be partly related to the lower oxygen cost of work performance or improved cardiac efficiency. Arterial serum potassium level decreased in both groups of subjects after glucagon administration, with the appearance of a slightly negative potassium balance across the myocardium. The possible relationship of the cardiac inotropism induced by glucagon to intramyocardial ionic exchanges is discussed.
Abstract 4681: Urothelial gene expression signatures aid bladder cancer detection
Authors: Charles Rosser, Yijun Sun, Virginia Urquidi, Steve Goodison
Journal: Cancer Research (2010)

Abstract Bladder cancer is the fifth most commonly diagnosed malignancy in the United States and one of the most prevalent worldwide. It harbors a probability of recurrence of &amp;gt;50%, thus rigorous, long-term surveillance of patients is advocated, so improvements in non-invasive urinalysis assessment strategies would benefit patients. We applied gene expression microarray analysis to exfoliated urothelia recovered from bladder washes obtained prospectively from 102 patients with subsequently confirmed presence or absence of bladder cancer. Data from microarrays containing 56,000 targets was subjected to a panel of statistical analyses to identify bladder cancer-associated gene signatures. Hierarchical clustering and supervised learning algorithms were used to classify samples on the basis of tumor burden. A differentially expressed set of 323 gene probes was associated with the presence of bladder cancer (P&amp;lt;0.01). Supervised machine learning and a cross-validation approach were used to build a 55-gene molecular classifier that was able to classify patients with and without bladder cancer with an overall accuracy of &amp;gt;75%. Our results show that it is possible to achieve the detection of bladder cancer using molecular signatures present in exfoliated tumor urothelia. Further investigation and validation of the cancer-associated profiles may reveal important biomarkers for the non-invasive detection and surveillance of bladder cancer. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4681.
Association between tobacco smoking and response to tumour necrosis factor α inhibitor treatment in psoriatic arthritis: results from the DANBIO registry
Authors: Pil Højgaard, Bente Glintborg, Merete Lund Hetland, Torben Højland Hansen, Philip Rask Lage-Hansen, Martin H Petersen, Mette Holland-Fischer, Christine Nilsson, Anne Gitte Loft, Bjarne Nesgaard Andersen, Thomas Adelsten, Jørgen Jensen, Emina Omerovic, Regitse Christensen, Ulrik Tarp, René Østgård, Lene Dreyer
Journal: Annals of the Rheumatic Diseases (2014)

Objectives To investigate the association between tobacco smoking and disease activity, treatment adherence and treatment responses among patients with psoriatic arthritis (PsA) initiating the first tumour necrosis factor α inhibitor therapy (TNFi) in routine care. Methods Observational cohort study based on the Danish nationwide DANBIO registry. Kaplan–Meier plots, logistic and Cox regression analyses by smoking status (current/previous/never smoker) were calculated for treatment adherence, ACR20/50/70-responses and EULAR-good-response. Additional stratified analyses were performed according to gender and TNFi-subtype (adalimumab/etanercept/infliximab). Results Among 1388 PsA patients included in the study, 1148 (83%) had known smoking status (33% current, 41% never and 26% previous smokers). Median follow-up time was 1.22 years (IQR 0.44–2.96). At baseline, current smokers had lower Body Mass Index (27 kg/m 2 (23–30)/28 kg/m 2 (24–31)) (median (IQR)), shorter disease duration (3 years (1–8)/5 years (2–10)), lower swollen joint count (2 (0–5)/3 (1–6)), higher visual-analogue-scale (VAS) patient global (72 mm (54–87)/68 mm (50–80)), VAS fatigue (72 mm (51–86)/63 mm (40–77)) and Health Assessment Questionnaire (HAQ) score (1.1 (0.7 to 1.5)/1.0 (0.5 to 1.5)) than never smokers (all p&lt;0.05). Current smokers had shorter treatment adherence than never smokers (1.56 years (0.97 to 2.15)/2.43 years (1.88 to 2.97), (median (95% CI)), log rank p=0.02) and poorer 6 months’ EULAR-good-response rates (23%/34%), ACR20 (24%/33%) and ACR50 response rates (17%/24%) (all p&lt;0.05), most pronounced in men. In current smokers, the treatment adherence was poorer for infliximab (HR) 1.62, 95% CI 1.06 to 2.48) and etanercept (HR 1.74, 1.14 to 2.66) compared to never smokers, but not for adalimumab (HR 0.80, 0.52 to 1.23). Conclusion In PsA, smokers had worse baseline patient-reported outcomes, shorter treatment adherence and poorer response to TNFi's compared to non-smokers. This was most pronounced in men and in patients treated with infliximab or etanercept.
P170 Long-term effectiveness of omalizumab in patients with severe persistent allergic (IgE-mediated) asthma: UK centre real-life experience
Authors: AH Mansur, V Mitchell, L Alfridi, J Sullivan, I Kasujee
Journal: Thorax (2013)

<h3></h3> Omalizumab has been shown to be an effective add-on therapy for patients with uncontrolled severe persistent allergic (IgE-mediated) asthma. There has been a steady accumulation of evidence on long-term effectiveness of omalizumab; however, data on real-life outcomes beyond one year of treatment in a UK clinical setting is limited. In this analysis, data were compared for a number of patients from the Heartlands Hospital (Birmingham, UK), to determine if improvements were sustained with longer-term treatment. Patients (n = 45, mean age 44.9 years, range: 19–69) received omalizumab for a mean duration of 49.3 months (range: 23–96). All patients with available data (n = 18/45) showed a clinically relevant improvement in asthma control questionnaire (ACQ) scores post-omalizumab (mean ?ACQ: 2.27, range: 0.5–4.1; mean baseline ACQ: 4.1, range: 3.7–4.7). In patients on oral corticosteroids (OCS) <i>vs</i> patients not on OCS (at baseline), improvements were greater: ACQ of patients on OCS at baseline was 4.1 and 1.6 post treatment <i>vs</i> 4.0 at baseline and 2.7 post treatment. Mean OCS dose reduced pre- to post-omalizumab: 30.5 to 7 mg/day. Reductions in hospital admissions/bed days were seen post-treatment (figure). There were also reductions in work/school days missed in 17/19 patients; the other 2 patients showing no change. Overall mean FEV<sub>1</sub> was improved in the majority of patients with available data (17/20). Results from this real-life follow-up study demonstrate that improved outcomes in patients with severe allergic asthma are sustained with longer-term omalizumab therapy.
Management of Ventricular Tachycardia in the Setting of a Dedicated Unit for the Treatment of Complex Ventricular Arrhythmias
Authors: Paolo Della Bella, Francesca Baratto, Dimitris Tsiachris, Nicola Trevisi, Pasquale Vergara, Caterina Bisceglia, Francesco Petracca, Corrado Carbucicchio, Stefano Benussi, Francesco Maisano, Ottavio Alfieri, Federico Pappalardo, Alberto Zangrillo, Giuseppe Maccabelli
Journal: Circulation (2013)

We investigated the impact of catheter ablation on ventricular tachycardia (VT) recurrence and survival in a large number of patients with structural heart disease treated in the setting of a dedicated multiskilled unit.Since January 2007, we have implemented a multidisciplinary model, aiming for a comprehensive management of VT patients. Programmed ventricular stimulation was used to assess acute outcome. Primary end points were VT recurrence and the occurrence of cardiac and sudden cardiac death. Overall, 528 patients were treated by ablation (634 procedures; 1-4 procedures per patient). Among 482 tested with programmed ventricular stimulation after the last procedure, a class A result (noninducibility of any VT) was obtained in 371 patients (77%), class B (inducibility of nondocumented VT) in 12.4%, and class C (inducibility of index VT) in 10.6%. After a median follow-up time of 26 months, VT recurred in 164 (34.1%) of 472 patients. VT recurrence was documented in 28.6% of patients with a class A result versus 39.6% of patients with class B and 66.7% with class C result (log-rank P<0.001). The incidence of cardiac mortality was lower in class A patients than in those with class B and class C (8.4% versus 18.5% versus 22%, respectively; log-rank P=0.002). On the basis of multivariate analysis, postprocedural inducibility of index VT was independently associated both with VT recurrence (hazard ratio, 4.030; P<0.001) and with cardiac mortality (hazard ratio, 2.099; P=0.04).Within a dedicated VT unit, catheter ablation prevents long-term VT recurrences, which may favorably affect survival in a large number of patients who have VT.
The Lieutenant’s Story
Authors: Ted McMahon
Journal: JAMA (2011)

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
Neuroethics and National Security
Authors: Turhan Canli, Susan Brandon, William Casebeer, Philip J. Crowley, Don DuRousseau, Henry T. Greely, Alvaro Pascual-Leone
Journal: The American Journal of Bioethics (2007)

Click to increase image sizeClick to decrease image size Acknowledgement: This paper grew out of a daylong meeting held at Tufts University in September 2006 ("The Neuroethics of Homeland Security", Tufts University, Medford, MA, September 29, 2006). The authors gratefully acknowledge the support in funding and organizing the meeting by the Institute for Global Leadership (IGL) at Tufts University, a unique interdisciplinary cross school program (http://www.tuftsgloballeadership.org), the Office of the Tufts University Provost, Jamshed Bharucha, and the Merrin Family Foundation. We would like to acknowledge the contributions of the IGL Director, Sherman Teichman, the IGL Associate Director, Heather Barry, and its key staffers, Lily Bayat, Ben Mann, and especially Erica Levine.
Dialysis Accelerates Medial Vascular Calcification in Part by Triggering Smooth Muscle Cell Apoptosis
Authors: Rukshana C. Shroff, Rosamund McNair, Nichola Figg, Jeremy N. Skepper, Leon Schurgers, Ashmeet Gupta, Melanie Hiorns, Ann E. Donald, John Deanfield, Lesley Rees, Catherine M. Shanahan
Journal: Circulation (2008)

Vascular calcification is associated with increased morbidity and mortality in stage V chronic kidney disease, yet its early pathogenesis and initiating mechanisms in vivo remain poorly understood. To address this, we quantified the calcium (Ca) load in arteries from children (10 predialysis, 24 dialysis) and correlated it with clinical, biochemical, and vascular measures.Vessel Ca load was significantly elevated in both predialysis and dialysis and was correlated with the patients' mean serum Ca x phosphate product. However, only dialysis patients showed increased carotid intima-media thickness and increased aortic stiffness, and calcification on computed tomography was present in only the 2 patients with the highest Ca loads. Importantly, predialysis vessels appeared histologically intact, whereas dialysis vessels exhibited evidence of extensive vascular smooth muscle cell (VSMC) loss owing to apoptosis. Dialysis vessels also showed increased alkaline phosphatase activity and Runx2 and osterix expression, indicative of VSMC osteogenic transformation. Deposition of the vesicle membrane marker annexin VI and vesicle component mineralization inhibitors fetuin-A and matrix Gla-protein increased in dialysis vessels and preceded von Kossa positive overt calcification. Electron microscopy showed hydroxyapatite nanocrystals within vesicles released from damaged/dead VSMCs, indicative of their role in initiating calcification.Taken together, this study shows that Ca accumulation begins predialysis, but it is the induction of VSMC apoptosis in dialysis that is the key event in disabling VSMC defense mechanisms and leading to overt calcification, eventually with clinically detectable vascular damage. Thus the identification of factors that lead to VSMC death in dialysis will be of prime importance in preventing vascular calcification.
Editorial: Somatostatin, hormone inhibitor
Authors: H. T. Ricketts
Journal: JAMA (1975)

For many years, the anterior lobe of the pituitary has been known as the master gland in the endocrine constellation. The appellation was appropriate, for as everyone knows, it was the little nubbin riding in the sella turcica that drove the peripheral slave glands to secrete all manner of hormones, without which we would sicken and, in some cases, die. With the discovery of the feedback system, however, it became plain that this ostensibly powerful regulator sometimes had to yield to the command of its subordinate glands. When, for example, an exuberant thyroid gland poured out too much thyroxin, the feedback told the pituitary in no uncertain terms to shut down on its secretion of thyroidstimulating hormone (TSH). In the sixties, the pituitary's autonomy was, apparently, further undermined. It was established gradually that many anterior pituitary hormones require the presence of an active hypothalamic "releasing factor," specific for each hormone,
Storm over Statins — The Controversy Surrounding Pharmacologic Treatment of Children
Authors: Sarah de Ferranti, David S. Ludwig
Journal: New England Journal of Medicine (2008)

In July, the American Academy of Pediatrics released revised recommendations for the management of hypercholesterolemia in children, and within days, it had elicited a firestorm of controversy. Drs. Sarah de Ferranti and David Ludwig discuss the inclusion of statins as potential first-line pharmacologic agents.
Respiratory disease trends in the Pulmonary Complications of HIV Infection Study cohort. Pulmonary Complications of HIV Infection Study Group.
Authors: J M Wallace, N I Hansen, L Lavange, J Glassroth, B L Browdy, M J Rosen, P A Kvale, B T Mangura, L B Reichman, P C Hopewell
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

We examined trends in the incidence of specific respiratory disorders in a multicenter cohort with progressive human immunodeficiency virus (HIV) disease during a 5-yr period. Individuals with a wide range of HIV disease severity belonging to three transmission categories were evaluated at regular intervals and for episodic respiratory symptoms using standard diagnostic algorithms. Yearly incidence rates of respiratory diagnoses were assessed in the cohort as a whole and according to CD4 count or HIV transmission category. The most frequent respiratory disorders were upper respiratory tract infections, but the incidence of lower respiratory tract infections increased as CD4 counts declined. Specific lower respiratory infections followed distinctive patterns according to study-entry CD4 count and transmission category. Acute bronchitis was the predominant lower respiratory infection of cohort members with entry CD4 counts > or = 200 cells/mm3. In cohort members with entry CD4 counts of 200 to 499 cells/mm3, the incidence of bacterial and Pneumocystis carinii pneumonia each increased an average of 40% per year. In members with entry CD4 counts < 200 cells/mm3, acute bronchitis, bacterial pneumonia, and P. carinii pneumonia occurred at high rates without discernible time trends, despite chemoprophylaxis in more than 80% after Year 1, and the rate of other pulmonary opportunistic infections increased over time. Each year, injecting drug users had a higher incidence of bacterial pneumonia than did homosexual men. The yearly rate of tuberculosis was < 3 episodes/100 person-yr in each entry CD4 and HIV-transmission group. We conclude that the time trends of HIV-associated respiratory disorders are determined by HIV disease stage and influenced by transmission category. Whereas acute bronchitis is prevalent during all stages of HIV infection, incidence rates of bacterial pneumonia and P. carinii pneumonia rise continuously during progression to advanced disease. In advanced disease, the incidence of acute bronchitis, bacterial pneumonia and P. carinii pneumonia is high despite widespread chemoprophylaxis.
A multiplex one-step real-time RT-PCR assay for influenza surveillance
Authors: I Huber, H Campe, D Sebah, C Hartberger, R Konrad, M Bayer, U Busch, A Sing
Journal: Eurosurveillance (2011)

For surveillance purposes real-time PCR assays for influenza viruses had to be adapted to the pandemic influenza A(H1N1)2009 strain. We combined published primers and probes for influenza A, influenza B and an internal amplification control with a detection system for influenza A(H1N1)2009 to set up a rapid, reliable, simple and cost-effective high-throughput multiplex one-step real-time RT-PCR. The workflow also includes automated sample preparation for high-throughput screening. The lower limit of detection of the multiplex assay was 3.5x10(2) RNA copies per PCR reaction. The diagnostic sensitivity of the multiplex assay was 87.7%, but increased to 99.4% for influenza-positive samples yielding C(t) values of less than 34 cycles in the respective diagnostic assay. High specificity was confirmed by sequencing and correct detection of 15 reference samples from two quality assurance studies. The multiplex PCR was introduced for surveillance of samples from a network of general practitioners and paediatricians in Bavaria, Germany during the influenza pandemic of 2009. Comparison with surveillance data from reported cases proved the reliability of the multiplex assay for influenza surveillance programmes.
Clinical and radiological study of vagotomy and gastric drainage in the treatment of pyloric stenosis due to duodenal ulceration.
Authors: H Ellis, F Starer, C Venables, C Ware
Journal: Gut (1966)

EDITORIAL COMMENT Twenty-one patients with pyloric stenosis treated by vagotomy and gastric drainage have been followed up clinically and radiologically for periods of between nine months and five years from operation.Results are uniformly good and the method is advocated as the surgical treatment of choice for this condition.
Targeted Gene Delivery to Vascular Tissue In Vivo by Tropism-Modified Adeno-Associated Virus Vectors
Authors: Stephen J. White, Stuart A. Nicklin, Hildegard Büning, M. Julia Brosnan, Kristen Leike, Emmanuel D. Papadakis, Michael Hallek, Andrew H. Baker
Journal: Circulation (2004)

Gene therapy offers an unprecedented opportunity to treat diverse pathologies. Adeno-associated virus (AAV) is a promising gene delivery vector for cardiovascular disease. However, AAV transduces the liver after systemic administration, reducing its usefulness for therapies targeted at other sites. Because vascular endothelial cells (ECs) are in contact with the bloodstream and are heterogeneous between organs, they represent an ideal target for site-specific delivery of biological agents.We isolated human venous EC-targeting peptides by phage display and genetically incorporated them into AAV capsids after amino acid 587. Peptide-modified AAVs transduced venous (but not arterial) ECs in vitro, whereas hepatocyte transduction was significantly lower than with native AAV. Intravenous infusion of engineered AAVs into mice produced reduced vector accumulation in liver measured 1 hour and 28 days after injection and delayed blood clearance rates compared with native AAV. Peptide-modified AAVs produced enhanced uptake of virions in the vena cava with selective transgene expression. Retargeting was dose dependent, and coinfusion of either heparin or free competing peptides indicated that uptake was principally independent of native AAV tropism and mediated via the peptide.AAV tropism can be genetically engineered by use of phage display-derived peptides to generate vectors that are selective for the vasculature.
p56lck Signals for Regulating Thymocyte Development Can Be Distinguished by Their Dependency on Rho Function
Authors: Stefan W. Henning, Doreen A. Cantrell
Journal: The Journal of Experimental Medicine (1998)

The tyrosine kinase p56lck regulates the differentiation and proliferative expansion of pre-T cells. However, nothing is known about other signaling molecules that operate with p56lck to mediate the pleiotropic changes that occur at this stage of thymocyte development. We used a genetic strategy to examine the requirement for the GTPase Rho in p56lck-mediated signals in the thymus. By generating mice double transgenic for a constitutively activated form of p56lck (p56lckF505) and the Rho inhibitor C3 transferase we were able to compare thymocyte development in mice expressing active p56lck on a wild-type or Rho− background. Thymocytes expressing active p56lck show enhanced proliferation of pre-T cells resulting in increased numbers of late pre-T cells, however, this dramatic effect on pre-T cell proliferation is lost when the p56lck transgene is expressed in thymocytes lacking endogenous Rho GTPase function. Expression of active p56lck also generates double positive (DP) thymocytes with low levels of CD2 antigen expression. Again, p56lck cannot prevent expression of CD2 when expressed on a Rho− background. CD4+CD8+ DP cells expressing active p56lck have been shown to lack functional α/β–T cell receptor (TCR) complexes due to p56lck-mediated inhibition of TCR gene Vβ-Dβ rearrangement. This inhibition of TCR expression by active p56lck is unimpaired in the absence of Rho function. The signaling pathways that are mediated by p56lck and control thymocyte proliferation, α/β-TCR and CD2 antigen expression can thus be distinguished by their dependency on Rho function.