tbuckley/cabot-search huggingface dataset:
Esophageal and Esophagogastric Junction Cancers
Authors: Jaffer A. Ajani, James S. Barthel, David J. Bentrem, Thomas A. D'Amico, Prajnan Das, Crystal S. Denlinger, Charles S. Fuchs, Hans Gerdes, Robert E. Glasgow, James A. Hayman, Wayne L. Hofstetter, David H. Ilson, Rajesh N. Keswani, Lawrence R. Kleinberg, W. Michael Korn, A. Craig Lockhart, Mary F. Mulcahy, Mark B. Orringer, Raymond U. Osarogiagbon, James A. Posey, Aaron R. Sasson, Walter J. Scott, Stephen Shibata, Vivian E. M. Strong, Thomas K. Varghese, Graham Warren, Mary Kay Washington, Christopher Willett, Cameron D. Wright
Journal: Journal of the National Comprehensive Cancer Network (2011)

Overview Upper gastrointestinal tract cancers originating in the esophagus, esophagogastric junction (EGJ), and stomach constitute a major health problem around the world. An estimated 37,640 new cases of and 25,070 deaths from upper gastrointestinal cancers occurred in the United States in 2010.1 A dramatic shift in the location of upper gastrointestinal tumors has occurred in the United States.2,3 Changes in hisNCCN
Hepatic veno-occlusive disease due to tacrolimus in a single-lung transplant patient
Authors: S. Shah, M. Budev, H. Blazey, K. Fairbanks, A. Mehta
Journal: European Respiratory Journal (2006)

Hepatic veno-occlusive disease is defined as nonthrombotic fibrous obliterative endophlebitis of small centrilobular hepatic venules. Clinically, patients present with elevated liver enzymes and a triad of jaundice, hepatomegaly and ascites. Although reported as a complication of other solid organ and stem cell transplantation, there have been no reported cases to date of veno-occlusive disease following lung transplantation. The present authors report a case of veno-occlusive disease following single-lung transplantation in a patient on a triple-drug immunosuppressive regimen composed of tacrolimus, mycophenolate mofetil and prednisone. The diagnosis was established by transjugular liver biopsy and by discontinuing tacrolimus; there was clinical regression of symptoms and serological return to baseline.
The impact of cardiovascular events in hospitalized patients with community-acquired pneumonia (CAP): Preliminary results from the FAILCAP study
Authors: Letizia Morlacchi, Stefano Aliberti, Andrea Gramegna, Antonio Voza, Lisa Pancini, Cornelia Baumgartner, Fabio Giuliani, Riccardo Fantini, Anna Lasagni, Elisabetta Lavezzi, Simona Perossi, Paula Peyrani, Valter Monzani, Alberto Pesci, Julio Ramirez, Francesco Blasi
Journal: European Respiratory Journal (2011)

Cardiovascular events (CVEs) could be detected during the management of hospitalized patients with CAP because of the concomitant hypoxemia and systemic inflammation. The aim of our study was to evaluate incidence, risk factors and outcomes of hospitalized patients with CAP undergoing CVEs. An international, multicenter, prospective, observational study was performed on consecutive CAP patients hospitalized from October 2009 to December 2010 in 8 Respiratory Dpts (ClinicalTrials: NCT01143155). CVEs were recorded both on hospital admission and during hospitalization. Among the 431 patients enrolled (56% males; mean±SD age:73±16 years), incidence of CVEs was 20%. The type of CVEs and their incidence is depicted in table.  Risk factors independently associated with the presence of CVEs were age, ventilatory support, thrombocytosis and a low diastolic blood pressure on admission, as well as a clinical failure during hospitalization. Mortality among patients who experienced CVEs was higher in comparison to the rest of the population (21% vs. 10%, p=0.004), as well as mortality at 30 days (28% vs. 11%, p
Comparative study of automatic blood-gas analysers and their use in analysing arterial and capillary samples.
Authors: P Rubin, S Bradbury, K Prowse
Journal: BMJ (1979)

Three automatic blood-gas analysers were compared for ease of use; calibration; reproducibility and accuracy of results; maintenance; fault-finding; and use of expert technician time. Results obtained from arterial and capillary blood were compared with duplicate values obtained with a semi-automatic analyser controlled and calibrated with tonometered blood. No analyser was fully automatic, and all three needed maintenance by expert technicians. Difficulties were encountered when inexperienced operators used the machines. One automatic blood-gas analyser gave aberrant values for oxygen pressure (PO2) due to electrode dysfunction that was not indicated by the fault-finding system. A second analyser gave significantly lower values for blood pH than the standard machine. A comparison of pH, carbon dioxide pressure (PCO2), and PO2 measured in 40 simultaneous paired samples of arterial and arterialised capillary blood showed no significant difference for pH or PCO2, but the PO2 values were significantly lower in the capillary samples over the range studied. We conclude that all machines perform satisfactorily in terms of blood-gas analysis, but none may be regarded as fully automatic. Some degree of technical supervision is essential, as is proper training for all potential users.
Antiangiogenic Actions of Vascular Endothelial Growth Factor-A <sub>165</sub> b, an Inhibitory Isoform of Vascular Endothelial Growth Factor-A, in Human Obesity
Authors: Doan T.M. Ngo, Melissa G. Farb, Ryosuke Kikuchi, Shakun Karki, Stephanie Tiwari, Sherman J. Bigornia, David O. Bates, Michael P. LaValley, Naomi M. Hamburg, Joseph A. Vita, Donald T. Hess, Kenneth Walsh, Noyan Gokce
Journal: Circulation (2014)

Background— Experimental studies suggest that visceral adiposity and adipose tissue dysfunction play a central role in obesity-related cardiometabolic complications. Impaired angiogenesis in fat has been implicated in the development of adipose tissue hypoxia, capillary rarefaction, inflammation, and metabolic dysregulation, but pathophysiological mechanisms remain unknown. In this study, we examined the role of a novel antiangiogenic isoform of vascular endothelial growth factor-A (VEGF-A), VEGF-A 165 b, in human obesity. Methods and Results— We biopsied paired subcutaneous and visceral adipose tissue in 40 obese subjects (body mass index, 45±8 kg/m 2 ; age, 45±11 years) during bariatric surgery and characterized depot-specific adipose tissue angiogenic capacity using an established ex vivo assay. Visceral adipose tissue exhibited significantly blunted angiogenic growth compared with subcutaneous fat ( P &lt;0.001) that was associated with marked tissue upregulation of VEGF-A 165 b ( P =0.004). The extent of VEGF-A 165 b expression correlated negatively with angiogenic growth ( r =−0.6, P =0.006). Although recombinant VEGF-A 165 b significantly impaired angiogenesis, targeted inhibition of VEGF-A 165 b with neutralizing antibody stimulated fat pad neovascularization and restored VEGF receptor activation. Blood levels of VEGF-A 165 b were significantly higher in obese subjects compared with lean control subjects ( P =0.02), and surgical weight loss induced a marked decline in serumVEGF-A 165 b ( P =0.003). Conclusions— We demonstrate that impaired adipose tissue angiogenesis is associated with overexpression of a novel antiangiogenic factor, VEGF-A 165 b, that may play a pathogenic role in human adiposopathy. Moreover, systemic upregulation of VEGF-A 165 b in circulating blood may have wider-ranging implications beyond the adipose milieu. VEGF-A 165 b may represent a novel area of investigation to gain further understanding of mechanisms that modulate the cardiometabolic consequences of obesity.
Testisin, a Glycosyl-Phosphatidylinositol–Linked Serine Protease, Promotes Malignant Transformation <i>In vitro</i> and <i>In vivo</i>
Authors: Tenny Tang, Muriel Kmet, Laura Corral, Steffan Vartanian, Andreas Tobler, Jackie Papkoff
Journal: Cancer Research (2005)

Human testisin, a serine protease, is highly expressed in ovarian cancer and premeiotic spermatocytes with relatively little expression in other normal tissues. We first showed that testisin was localized on the surface of cultured tumor cells as a glycosyl-phosphatidylinositol-linked protein. We next explored the biological function of testisin in malignant transformation through manipulation of testisin expression in cell culture model systems. Small interfering RNA-mediated knockdown of endogenous testisin mRNA and protein expression in tumor cell lines led to increased apoptosis and diminished growth in soft agar. Conversely, overexpression of testisin in an epithelial cell line induced colony formation in soft agar as well as s.c. tumor growth in severe combined immunodeficient mice. A catalytic domain mutant was unable to induce soft-agar growth indicating that testisin protease activity is required for transformation. Ectopic expression of testisin in a human ovarian cancer cell line without endogenous testisin expression, led to the formation of larger tumors in severe combined immunodeficient mice. Data presented here provide the first demonstration that testisin can promote cellular processes that drive malignant transformation. Our functional data coupled with the restricted normal tissue distribution of testisin and its overexpression in a majority of ovarian cancers validates this cell surface protein as a target for therapeutic intervention.
Deletion of p120-Catenin Results in a Tumor Microenvironment with Inflammation and Cancer that Establishes It as a Tumor Suppressor Gene
Authors: Douglas B. Stairs, Lauren J. Bayne, Ben Rhoades, Maria E. Vega, Todd J. Waldron, Jiri Kalabis, Andres Klein-Szanto, Ju-Seog Lee, Jonathan P. Katz, J. Alan Diehl, Albert B. Reynolds, Robert H. Vonderheide, Anil K. Rustgi
Journal: Cancer Cell (2011)
Increased Proximal Reflux in a Hypersensitive Esophagus Might Explain Symptoms Resistant to Proton Pump Inhibitors in Patients With Gastroesophageal Reflux Disease
Authors: Wout O. Rohof, Roelof J. Bennink, Hugo de Jonge, Guy E. Boeckxstaens
Journal: Clinical Gastroenterology and Hepatology (2013)
Ischemic Mononeuropathy and Mononeuropathy Multiplex in Diabetes Mellitus
Authors: Martin C. Raff, Arthur K. Asbury
Journal: New England Journal of Medicine (1968)

Abstract Seven cases of mononeuropathy multiplex occurring in association with diabetes  are described, including a case previously reported in which numerous small infarcts in the peripheral nerve trunks proved to be the basis for the neuropathy. It is suggested that all the asymmetric types of diabetic neuropathy, including the cranial-nerve palsies, mononeuropathies and mononeuropathy multiplex, are caused by infarcts within nerve. Diabetic amyotrophy is a proximal mononeuropathy multiplex and should not be separated from the other asymmetric neuropathies. Because these asymmetrical neuropathic syndromes do not seem to be unique to diabetes and the role of diabetes in their pathogenesis is still uncertain, the term ischeic mononeuropathy or mononeuropathy multiplex associated with diabetes mellitus is recommended.
Sarcolemmal permeability changes during ischaemia and reperfusion: release of survival factors
Authors: A. Lochner
Journal: Cardiovascular Research (2008)

Enzyme release by ischaemic myocardium has been used as a hallmark of the infarction process for several decades: in the clinical setting, deterioration of cell membrane integrity, as evidenced by the release of macromolecules such as creatine kinase and lactate dehydrogenase, has been used as quantitative indication of myocardial infarction. Leakage of membrane-impermeable molecules due to sarcolemmal rupture is considered to be the most prominent feature of irreversible injury, and the main mechanisms proposed to underlie this phenomenon are energy deficiency and calcium overload.1,2 However, changes in sarcolemmal permeabililty have been demonstrated to occur after exposure of the heart to relatively short periods of ischaemia. Using NMR spectroscopy, Askenasy et al. 3 showed that sarcolemmal integrity deteriorated as a function of the duration of ischaemia and that even after as short a period as 10 min ischaemia cellular membrane permeability to osmolytes increased, although myocytes remained impermeable to polar and large molecules. Interestingly, before the onset of irreversible injury, enzyme release by the ischaemic perfused heart can be manipulated by the substrate present: for example, glucose reduces fatty acid-induced enzyme release, possibly via provision of glycolytic ATP.4,5 With the discovery of the phenomenon of ischaemic pre-conditioning, attention was again drawn to the potential of the myocardium to release a variety of substances (autocoids) after exposure to very short periods of ischaemia and reperfusion (e.g. 5 min), which may have either beneficial or detrimental effects on the heart. However, the causal stimulus for and the … 

*Corresponding author. Tel: +27 21 938 9391; fax: +27 21 938 9476. E-mail address : alo{at}sun.ac.za
Informed consent for upper gastrointestinal endoscopy.
Authors: S P Pereira, S H Hussaini, M L Wilkinson
Journal: Gut (1995)

Informed consent for upper gastrointestinal endoscopy requires that the patient understands the nature of, and reason for, the proposed procedure, and that he or she is given adequate time to deliberate and ask questions. In a prospective study, 200 outpatients completed questionnaires immediately before, and one day after, endoscopy, which assessed satisfaction with information provided by: (a) the referring doctor, (b) a standard information sheet sent out two to four weeks before endoscopy, and (c) the endoscopist. The first 100 patients were asked to read and sign a standard consent form immediately before the endoscopy. In the second 100 patients, a new endoscopy consent form that was simpler and easier to read than the standard form was sent out with the information sheet. Patients were directed to sign the new consent form before arriving at the unit only if they had no further questions. Overall, the indication for the endoscopy, and how it would be done, were explained clearly by the referring doctor in 79% and 68% of cases, respectively. Of the first 100 patients, only 54% had read the standard consent form in the endoscopy unit before signing it. In contrast, of the second 100 patients, the new form sent with the information sheet was read by 95%, and signed by 88% before coming to the unit. Furthermore, 84% found the new form easier to read and understand than the standard form. In our unit, roughly one quarter of patients referred for endoscopy are not adequately informed about the procedure. In contrast with the standard consent form, a simple endoscopy consent form sent out with the information sheet is preferred by most patients, and safeguards against patients undergoing endoscopy without informed consent.
Development of the bronchial epithelial reticular basement membrane: relationship to epithelial height and age
Authors: L. Tsartsali, A. A. Hislop, K. McKay, A. L. James, J. Elliot, J. Zhu, M. Rosenthal, D. N. Payne, P. K. Jeffery, A. Bush, S. Saglani
Journal: Thorax (2011)

<h3>Background</h3> The bronchial epithelium and underlying reticular basement membrane (RBM) have a close spatial and functional inter-relationship and are considered an epithelial–mesenchymal trophic unit (EMTU). An understanding of RBM development is critical to understanding the extent and time of appearance of its abnormal thickening that is characteristic of asthma. <h3>Methods</h3> RBM thickness and epithelial height were determined in histological sections of cartilaginous bronchi obtained postmortem from 47 preterm babies and infants (median age 40 weeks gestation (22 weeks gestation–8 months)), 40 children (2 years (1 month–17 years)) and 23 adults (44 (17–90) years) who had died from non-respiratory causes, and had no history of asthma. <h3>Results</h3> The RBM was visible by light microscopy at 30 weeks gestation. RBM thickness increased in successive age groups in childhood; in infants (r=0.63, p&lt;0.001) and in children between 1 month and 17 years (r=0.82, p&lt;0.001). After 18 years, RBM thickness decreased with increasing age (r=−0.42, p&lt;0.05). Epithelial height showed a similar relationship with age, a positive relationship from preterm to 17 years (r=0.50, p&lt;0.001) and a negative relationship in adulthood (r=−0.84, p&lt;0.0001). There was a direct relationship between epithelial height and RBM thickness (r=0.6, p&lt;0.001). <h3>Conclusions</h3> The RBM in these subjects was microscopically identifiable by 30 weeks gestation. It thickened during childhood and adolescence. In adults, there was either no relationship with age, or a slow reduction in thickness in older age. Developmental changes of RBM thickness were accompanied by similar changes in epithelial height, supporting the close relationship between RBM and epithelium within the EMTU.
Structural cardiac disease diagnosed by echocardiography in asymptomatic young male soccer players: implications for pre-participation screening
Authors: Marta Rizzo, Antonio Spataro, Cristiano Cecchetelli, Federico Quaranta, Simona Livrieri, Fabio Sperandii, Barbara Cifra, Paolo Borrione, Fabio Pigozzi
Journal: British Journal of Sports Medicine (2011)

To evaluate the prevalence of structural cardiac lesions using echocardiography in apparently healthy boys referred for pre-participation screening (PPS).3100 male soccer players were evaluated by echocardiography in addition to the standard PPS.In 56 subjects (1.8%), a structural cardiac lesion with potential future complication was detected. Specifically, hypertrophic cardiomyopathy (HCM) was found in two boys; bicuspid aortic valve (BAV) in 24; mitral valve prolapse in 10 and atrial septal defects (ASDs) in 20. Resting physical examination (PE) failed to identify any abnormalities in the majority of the subjects. All the boys presented an uncomplicated echocardiography, except two boys with HCM, one with BAV associated with aortic dilatation and one with a large ASD.Asymptomatic young athletes may have a structural cardiac alteration with the potential of present or future haemodynamic and arrhythmic consequences. A majority of mild cardiac lesions are difficult to diagnose or suspect by the current screening based on medical history, PE and ECG. Transthoracic echocardiography significantly improves the diagnostic power of screening in the detection of both mild and serious cardiac conditions in the athletic population.
Transcendental self-organization
Authors: Carl N. Johnson, Melanie Nyhof
Journal: Behavioral and Brain Sciences (2006)

Bering makes a good case for turning attention to an organized system that provides the self with transcendental meaning. In focusing on the evolutionary basis of this system, however, he overlooks the self-organizing properties of cognitive systems themselves. We propose that the illusory system Bering describes can be more generally and parsimoniously viewed as an emergent by-product of self-organization, with no need for specialized “illusion by design.”
The PSGL-1–L-selectin signaling complex regulates neutrophil adhesion under flow
Authors: Anika Stadtmann, Giulia Germena, Helena Block, Mark Boras, Jan Rossaint, Prithu Sundd, Craig Lefort, Charles I. Fisher, Konrad Buscher, Bernadette Gelschefarth, Ana Urzainqui, Volker Gerke, Klaus Ley, Alexander Zarbock
Journal: The Journal of Experimental Medicine (2013)

Neutrophils are recruited from the blood to sites of inflammation, where they contribute to immune defense but may also cause tissue damage. During inflammation, neutrophils roll along the microvascular endothelium before arresting and transmigrating. Arrest requires conformational activation of the integrin lymphocyte function–associated antigen 1 (LFA-1), which can be induced by selectin engagement. Here, we demonstrate that a subset of P-selectin glycoprotein ligand-1 (PSGL-1) molecules is constitutively associated with L-selectin. Although this association does not require the known lectin-like interaction between L-selectin and PSGL-1, the signaling output is dependent on this interaction and the cytoplasmic tail of L-selectin. The PSGL-1–L-selectin complex signals through Src family kinases, ITAM domain–containing adaptor proteins, and other kinases to ultimately result in LFA-1 activation. The PSGL-1–L-selectin complex–induced signaling effects on neutrophil slow rolling and recruitment in vivo demonstrate the functional importance of this pathway. We conclude that this is a signaling complex specialized for sensing adhesion under flow.
BRCAPRO Validation, Sensitivity of Genetic Testing of <i>BRCA1/BRCA2</i>, and Prevalence of Other Breast Cancer Susceptibility Genes
Authors: Donald A. Berry, Edwin S. Iversen, Daniel F. Gudbjartsson, Elaine H. Hiller, Judy E. Garber, Beth N. Peshkin, Caryn Lerman, Patrice Watson, Henry T. Lynch, Susan G. Hilsenbeck, Wendy S. Rubinstein, Kevin S. Hughes, Giovanni Parmigiani
Journal: Journal of Clinical Oncology (2002)

PURPOSE: To compare genetic test results for deleterious mutations of BRCA1 and BRCA2 with estimated probabilities of carrying such mutations; to assess sensitivity of genetic testing; and to assess the relevance of other susceptibility genes in familial breast and ovarian cancer. PATIENTS AND METHODS: Data analyzed were from six high-risk genetic counseling clinics and concern individuals from families for which at least one member was tested for mutations at BRCA1 and BRCA2. Predictions of genetic predisposition to breast and ovarian cancer for 301 individuals were made using BRCAPRO, a statistical model and software using Mendelian genetics and Bayesian updating. Model predictions were compared with the results of genetic testing. RESULTS: Among the test individuals, 126 were Ashkenazi Jewish, three were male subjects, 243 had breast cancer, 49 had ovarian cancer, 34 were unaffected, and 139 tested positive for BRCA1 mutations and 29 for BRCA2 mutations. BRCAPRO performed well: for the 150 probands with the smallest BRCAPRO carrier probabilities (average, 29.0%), the proportion testing positive was 32.7%; for the 151 probands with the largest carrier probabilities (average, 95.2%), 78.8% tested positive. Genetic testing sensitivity was estimated to be at least 85%, with false-negatives including mutations of susceptibility genes heretofore unknown. CONCLUSION: BRCAPRO is an accurate counseling tool for determining the probability of carrying mutations of BRCA1 and BRCA2. Genetic testing for BRCA1 and BRCA2 is highly sensitive, missing an estimated 15% of mutations. In the populations studied, breast cancer susceptibility genes other than BRCA1 and BRCA2 either do not exist, are rare, or are associated with low disease penetrance.
DDD pacing with optimal AV delay versus AAI pacing in patients with AV block I degree
Authors: I. Illiev, S. Yamachika, K. Muta, Y. Shin, T. Ishimatsu, N. Kornya, K. Nakao, T. Hirata, M. Hayano, K. Yano
Journal: Journal of the American College of Cardiology (1998)
Liver biopsy under ultrasound control: implications for training Reply
Authors: S Y CHUAH;
Journal: Gut (2000)

Editor,—As a gastroenterologist/hepatologist, I appreciate the anxiety expressed by Shah et al ( Gut 1999; 45 :628–629) about having to surrender liver biopsy samples to radiologists as a result of reduced training opportunities. The desire of an overwhelming number of gastroenterology trainees to become proficient in ultrasound techniques1should send a loud and clear message to the relevant regulatory training bodies. Once ultrasound has been introduced into gastroenterology training programmes in the United Kingdom, such as in Europe2 or … Professor Playford Professor Playford Professor Playford