tbuckley/cabot-search huggingface dataset:
Mitral stenosis in Whipple's disease.
Authors: A G Rose
Journal: Thorax (1978)

A patient who died of Whipple9s disease had moderate mitral stenosis with large firm yellow vegetations on the contact area of the mitral leaflets. Light microsocopy showed PAS positive macrophages within the thickened cusps and overlying vegetations. Negative images of rod-shaped bodies were visible in the cytoplasm of the histiocytes. No Aschoff bodies were seen, and there was no history of rheumatic fever. The findings in this patient lend support to the concept that chronic rheumatic type valvar deformity may result from a persistent intrinsic infectious agent.
Dose-response study of nebulised nedocromil sodium in exercise induced asthma.
Authors: M K Albazzaz, M G Neale, K R Patel
Journal: Thorax (1989)

Ten patients with exercise induced asthma, in whom inhaled nedocromil sodium 4 mg by metered dose inhaler attenuated the exercise fall in forced expiratory volume in one second (FEV1) by at least 40%, participated in a double blind dose response study to compare the protective effect of nedocromil sodium given 15 minutes before exercise challenge via a nebuliser (Wright) in concentrations of 0.5, 5, 10, and 20 mg/ml with that of placebo (saline). Response was assessed as the maximum fall in FEV1 after the patient had run on a treadmill for six to eight minutes. Plasma concentrations of nedocromil sodium were measured at the time of challenge. After exercise challenge the mean (SEM) maximum percentage falls in FEV1 were 30.3 (1.6) for the control run and 28.0 (4.1) after placebo. The percentage fall was attenuated by pretreatment with all concentrations of nedocromil sodium to 12.8 (2.8), 11.2 (2.1), 12.8 (2.1), and 14.1 (3.5) for the 0.5, 5, 10, and 20 mg/ml concentrations respectively (p less than 0.001). There were no significant differences between the different nedocromil concentrations. Mean plasma concentrations of nedocromil were proportional to dose. Thus concentrations of nebulised nedocromil sodium that ranged from 0.5 to 20 mg/ml gave a similar degree of protection (50-60%) against exercise induced asthma. This appears to be the maximum protection that can be achieved with nedocromil sodium and is similar to the protection obtained with 4 mg nedocromil administered by metered dose aerosol.
Ephrin-B1 Is a Novel Specific Component of the Lateral Membrane of the Cardiomyocyte and Is Essential for the Stability of Cardiac Tissue Architecture Cohesion
Authors: Gaël Genet, Céline Guilbeau-Frugier, Benjamin Honton, Etienne Dague, Michael D. Schneider, Christelle Coatrieux, Denis Calise, Christelle Cardin, Cécile Nieto, Bruno Payré, Caroline Dubroca, Pauline Marck, Christophe Heymes, Alexandre Dubrac, Dina Arvanitis, Fabien Despas, Marie-Françoise Altié, Marie-Hélène Seguelas, Marie-Bernadette Delisle, Alice Davy, Jean-Michel Sénard, Atul Pathak, Céline Galés
Journal: Circulation Research (2012)

Cardiac tissue cohesion relying on highly ordered cardiomyocytes (CM) interactions is critical because most cardiomyopathies are associated with tissue remodeling and architecture alterations.Eph/ephrin system constitutes a ubiquitous system coordinating cellular communications which recently emerged as a major regulator in adult organs. We examined if eph/ephrin could participate in cardiac tissue cyto-organization.We reported the expression of cardiac ephrin-B1 in both endothelial cells and for the first time in CMs where ephrin-B1 localized specifically at the lateral membrane. Ephrin-B1 knock-out (KO) mice progressively developed cardiac tissue disorganization with loss of adult CM rod-shape and sarcomeric and intercalated disk structural disorganization confirmed in CM-specific ephrin-B1 KO mice. CMs lateral membrane exhibited abnormal structure by electron microscopy and notably increased stiffness by atomic force microscopy. In wild-type CMs, ephrin-B1 interacted with claudin-5/ZO-1 complex at the lateral membrane, whereas the complex disappeared in KO/CM-specific ephrin-B1 KO mice. Ephrin-B1 deficiency resulted in decreased mRNA expression of CM basement membrane components and disorganized fibrillar collagen matrix, independently of classical integrin/dystroglycan system. KO/CM-specific ephrin-B1 KO mice exhibited increased left ventricle diameter and delayed atrioventricular conduction. Under pressure overload stress, KO mice were prone to death and exhibited striking tissue disorganization. Finally, failing CMs displayed downregulated ephrin-B1/claudin-5 gene expression linearly related to the ejection fraction.Ephrin-B1 is necessary for cardiac tissue architecture cohesion by stabilizing the adult CM morphology through regulation of its lateral membrane. Because decreased ephrin-B1 is associated with molecular/functional cardiac defects, it could represent a new actor in the transition toward heart failure.
Coenzyme A Glutathione Disulfide
Authors: Hartmut Schlüter, Michael Meissner, Marcus van der Giet, Martin Tepel, Jürgen Bachmann, Isolde Groß, Eckhard Nordhoff, Michael Karas, Claus Spieker, Herbert Witzel, Walter Zidek
Journal: Circulation Research (1995)

Abstract The adrenal gland is involved in the regulation of vascular tone by secretion of vasoactive agents such as catecholamines, neuropeptide Y, or endogenous ouabain. A further potent vasoconstrictor is isolated from bovine adrenal glands and is identified by chromatography, mass spectrometry, UV spectroscopy, and enzymatic cleavage as coenzyme A glutathione disulfide (CoASSG). CoASSG is found in chromaffin granules of adrenal glands and is released from adrenal medulla slices by carbachol. At a concentration of 10 −12 mol/L CoASSG increases renal vascular resistance. Intra-aortic injection of 5×10 −10 mol CoASSG increases blood pressure in the intact animal. Besides its vasopressor properties, this substance potentiates the effects of angiotensin II on vascular tone. It is concluded that CoASSG could play a role in blood pressure regulation not only by direct effects but also by modulation of the action of angiotensin II.
Are there independent lexical and nonlexical routes in word processing? An evaluation of the dual-route theory of reading
Authors: Glyn W. Humphreys, Lindsay J. Evett
Journal: Behavioral and Brain Sciences (1985)

Abstract One of the most popular and influential theories of word processing, dual-route theory, proposes that there are two functionally independent means of processing words, one involving access to lexical knowledge and the other involving nonlexical grapheme-to-phoneme conversion. Three topics germane to this theory are the processing of nonwords, spelling regularity effects, and the manner in which reading may be impaired following selective damage to either route. This paper evaluates evidence on these topics, and in each case the claims of the theory for an independent nonlexical processing route are called into question. This conclusion is further supported by a discussion of the linguistic constraints that limit any nonlexical grapheme—phoneme conversion process. Some alternative approaches to visual word processing, which share the assumption that lexical knowledge can guide the assembly of phonological information, are discussed. It is argued that these approaches should direct future research.
Alcohol not a predictor of peripheral oedema in chronic bronchitis.
Authors: P McKee
Journal: BMJ (1993)

standard that centres could embellish as they wished.This advanced life support course was piloted in 1992 and is now available to centres that conform with the requirements.Advertisements often state that courses conform to the guide- lines of the European and British Resuscitation Councils.However, some centres fail to satisfy the standards laid down for the new advanced life support course.The Resuscitation Council (UK) has therefore agreed to approve on request every course that satisfies the advanced life support requirements.These courses will be given a number that can be checked with the coordinator at our London office and successful participants on the courses will be entitled to receive a certificate from the Resuscitation Council.
Leukocyte counts and macrophage phenotypes in induced sputum and bronchoalveolar lavage fluid from normal subjects
Authors: C Lensmar, G Elmberger, P Sandgren, CM Skold, A Eklund
Journal: European Respiratory Journal (1998)

It is unclear whether leukocytes in induced sputum (IS) and bronchoalveolar lavage (BAL) represent the same cell populations. To compare leukocyte counts and macrophage phenotypes and investigate any measurable dithiothreitol (DTT)-mediated effect on macrophage immunocytochemical staining results, IS and BAL samples from nine healthy smokers and seven nonsmokers were examined. BAL and IS samples were processed and cell viability and cell counts were assessed. The macrophages were characterized by seven monoclonal antibodies (RFD1, RFD7, CD11b, CD54, CD68, CD71 and HLA-DR) using an indirect immunoalkaline phosphatase method. Intraindividual comparison of IS and BAL showed that IS samples from smokers and nonsmokers contained a lower total cell count (p&lt;0.01 smokers, p&lt;0.05 nonsmokers), a lower percentage of macrophages (both p&lt;0.05) and a higher percentage of neutrophils (both p&lt;0.05) than BAL samples. In addition, nonsmokers sputum samples contained a lower proportion of lymphocytes (p&lt;0.05) than BAL. The macrophage expression of RFD7 and CD71 was higher in smokers sputum samples (both p&lt;0.05) than in BAL, while nonsmokers sputum macrophages showed a higher expression of CD54 and CD71 (both p&lt;0.05) than BAL macrophages. DTT-incubated BAL samples showed no difference in macrophage antigen expression from BAL samples not exposed to DTT. In conclusion, the relative proportions of leukocytes and the macrophage phenotypes differed between induced sputum and bronchoalveolar lavage suggesting that the methods provide samples from different lung compartments, inhabited by cells with different phenotypes.
Impaired insulin-stimulated muscle glycogen synthase activation in vivo in man is related to low fasting glycogen synthase phosphatase activity.
Authors: D Freymond, C Bogardus, M Okubo, K Stone, D Mott
Journal: Journal of Clinical Investigation (1988)

Insulin-mediated glycogen synthase activity in skeletal muscle correlates with the rate of insulin-mediated glycogen deposition and is reduced in human subjects with insulin resistance. To assess the role of glycogen synthase phosphatase as a possible mediator of reduced glycogen synthase activity, we studied 30 Southwestern American Indians with a broad range of insulin action in vivo. Percutaneous biopsies of the vastus lateralis muscle were performed before and during a 440-min euglycemic clamp at plasma insulin concentrations of 89 +/- 5 and 1,470 +/- 49 microU/ml (mean +/- SEM); simultaneous glucose oxidation was determined by indirect calorimetry. After insulin stimulation, glycogen synthase activity was correlated with the total and nonoxidative glucose disposal at both low (r = 0.73, P less than 0.0001; r = 0.68, P less than 0.0001) and high (r = 0.75, P less than 0.0001; r = 0.74, P less than 0.0001) plasma insulin concentrations. Fasting muscle glycogen synthase phosphatase activity was correlated with both total and nonoxidative glucose disposal rates at the low (r = 0.48, P less than 0.005; r = 0.41, P less than 0.05) and high (r = 0.47, P less than 0.05; r = 0.43, P less than 0.05) plasma insulin concentrations. In addition, fasting glycogen synthase phosphatase activity was correlated with glycogen synthase activity after low- (r = 0.47, P less than 0.05) and high- (r = 0.50, P less than 0.01) dose insulin stimulations. These data suggest that the decreased insulin-stimulated glucose disposal and reduced glycogen synthase activation observed in insulin resistance could be secondary to a low fasting glycogen synthase phosphatase activity.
HCMOGT-1 Is a Novel Fusion Partner to <b> <i>PDGFRB</i> </b> in Juvenile Myelomonocytic Leukemia with t(5;17)(q33;p11.2)
Authors: Cristina Morerio, Maura Acquila, Cristina Rosanda, Annamaria Rapella, Carlo Dufour, Franco Locatelli, Emanuela Maserati, Francesco Pasquali, Claudio Panarello
Journal: Cancer Research (2004)

Abstract PDGFRB, a transmembrane tyrosine kinase receptor for plateletderived growth factor, is constitutively activated by gene fusion with different partners in myeloproliferative/myelodysplastic disorders with peculiar clinical characteristics. Six alternative partner genes have been described thus far. In this study, we report the molecular cloning of a novel translocation t(5;17)(q33;p11.2) in a case of juvenile myelomonocytic leukemia. The novel partner gene was identified as HCMOGT-1 using 5′-rapid amplification of cDNA ends; fluorescence in situ hybridization and reverse transcriptase-PCR analyses confirmed that the translocation resulted in PDGFRB/HCMOGT-1 fusion. We show that the breakpoint of PDGFRB occurred at the same site of all previously reported PDGFRB translocations.
Treatment with an Inhibitory Monoclonal Antibody to Mouse Factor B Protects Mice from Induction of Apoptosis and Renal Ischemia/Reperfusion Injury
Authors: Joshua M. Thurman, Pamela A. Royer, Danica Ljubanovic, Belda Dursun, Amanda M. Lenderink, Charles L. Edelstein, V. Michael Holers
Journal: Journal of the American Society of Nephrology (2006)

Complement activation in the kidney after ischemia/reperfusion (I/R) seems to occur primarily via the alternative complement pathway. The ability of an inhibitory mAb to mouse factor B, a necessary component of the alternative pathway, to protect mice from ischemic acute renal failure was tested. Treatment with the mAb prevented the deposition of C3b on the tubular epithelium and the generation of systemic C3a after renal I/R. Treated mice had significantly lower increases in serum urea nitrogen and developed significantly less morphologic injury of the kidney after I/R. For gaining insight into potential mechanisms of protection, the activity of caspases within the kidney also was measured, and it was found that caspases-2, -3, and -9 increased in a complement-dependent manner after renal I/R. Apoptotic cells were detected by terminal deoxynucleotidyl transferase catalyzed labeling of DNA fragments, and mice in which the alternative pathway was inhibited demonstrated significantly less apoptosis than control mice. Thus, use of an inhibitory mAb to mouse factor B effectively prevented activation of complement in the kidney after I/R and protected the mice from necrotic and apoptotic injury of the tubules.
Optical Coherence Tomography for Optical Biopsy
Authors: Mark E. Brezinski, Guillermo J. Tearney, Brett E. Bouma, Joseph A. Izatt, Michael R. Hee, Eric A. Swanson, James F. Southern, James G. Fujimoto
Journal: Circulation (1996)

Background Optical coherence tomography (OCT) is a recently developed medical diagnostic technology that uses back-reflected infrared light to perform in situ micron scale tomographic imaging. In this work, we investigate the ability of OCT to perform micron scale tomographic imaging of the internal microstructure of in vitro atherosclerotic plaques. Methods and Results Aorta and relevant nonvascular tissue were obtained at autopsy. Two-dimensional cross-sectional imaging of the exposed surface of the arterial segments was performed in vitro with OCT. A 1300-nm wavelength, superluminescent diode light source was used that allows an axial spatial resolution of 20 μm. The signal-to-noise ratio was 109 dB. Images were displayed in gray scale or false color. Imaging was performed over 1.5 mm into heavily calcified tissue, and a high contrast was noted between lipid- and water-based constituents, making OCT attractive for intracoronary imaging. The 20-μm axial resolution of OCT allowed small structural details such as the width of intimal caps and the presence of fissures to be determined. The extent of lipid collections, which had a low backscattering intensity, also were well documented. Conclusions OCT represents a promising new technology for imaging vascular microstructure with a level of resolution not previously achieved with the use of other imaging modalities. It does not require direct contact with the vessel wall and can be performed with a catheter integrated with a relatively inexpensive optical fiber. The high contrast among tissue constituents, high resolution, and ability to penetrate heavily calcified tissue make OCT an attractive new imaging technology for intracoronary diagnostics.
CONTROLLED TRIAL OF ACUPUNCTURE FOR DISABLING BREATHLESSNESS
Authors: Kim Jobst, Klim Mcpherson, Vivienne Brown, HilaryJ. Fletcher, Peter Mole, Jing Hua Chen, Jill Arrowsmith, John Efthimiou, Giovanni Maciocia, Ken Shifrin, DonaldJ. Lane
Journal: The Lancet (1986)
Randomized Trial of Breast self-examination in Shanghai: Methodology and Preliminary Results
Authors: D. B. Thomas, S. G. Self, C. J. Allison, Y. Tao, J. Mahloch, R. Ray, Q. Qin, R. Presley, P. Porter, D. L. Gao
Journal: JNCI Journal of the National Cancer Institute (1997)

The efficacy of breast self-examination in helping to reduce mortality from breast cancer has not been rigorously demonstrated.To assess efficacy, a large, randomized trial was initiated in Shanghai, China.From October 1989 to October 1991, 267040 current and retired female employees associated with 520 factories in the Shanghai Textile Industry Bureau were randomly assigned on the basis of factory to either a self-examination instruction group (133375 women) or a control group (133665 women). The women were born within the period from 1925 through 1958. Women in the instruction group were given intensive training in breast self-examination, including the use of silicone breast models and personalized instruction, plus two subsequent reinforcement sessions and multiple reminders to practice the technique. Women in the control group were asked to attend training sessions on the prevention of low back pain. All women have been followed for the development of breast diseases and for death from breast cancer.A high level of participation during the first 4-5 years of the trial was documented among women in the instruction group. Randomly sampled women in this group demonstrated greater proficiency in detecting lumps in breast models than did randomly sampled women in the control group. Approximately equal numbers of breast cancers were detected in the two groups (331 in the instruction group and 322 in the control group) through 1994, which is the last year for which case-finding efforts have been completed. The breast cancers detected in the instruction group were not diagnosed at an appreciably earlier stage or smaller size than those in the control group. More benign breast lesions were detected in the instruction group than in the control group (1457 versus 623, respectively), suggesting a higher index of suspicion for women who received training. Cumulative breast cancer mortality rates through 5 years from entry into the study were nearly equivalent for the two groups.Breast self-examination has not led to a reduction in mortality from breast cancer in this study cohort in the first several years since the trial began. A shift toward the diagnosis of disease at a less advanced stage in women given instruction has also not been demonstrated. Longer follow-up of participants in this trial is required before final assessment can be made of the efficacy of breast self-examination.At this time, there is insufficient evidence to recommend for or against the teaching of breast self-examination.
Low-density lipoprotein receptor-related protein 1 mediates hypoxia-induced very low density lipoprotein-cholesteryl ester uptake and accumulation in cardiomyocytes
Authors: Roi Cal, José Castellano, Elena Revuelta-López, Rosa Aledo, Montse Barriga, Jordi Farré, Gemma Vilahur, Laura Nasarre, Leif Hove-Madsen, Lina Badimon, Vicenta Llorente-Cortés
Journal: Cardiovascular Research (2012)

The myocardium accumulates intracellular lipids under ischaemic conditions, and myocardial fat deposition is closely associated with cardiac dysfunction. Our aims were to analyse the effect of hypoxia on low-density lipoprotein receptor-related protein 1 (LRP1) expression in neonatal rat ventricular myocytes (NRVM) and cardiac-derived HL-1 cells and the molecular mechanisms involved in this effect, to determine the role of LRP1 in the very low density lipoprotein (VLDL) uptake by hypoxic cardiomyocytes, and to study the effect of hypoxia on lipoprotein receptor expression and myocardial lipid profile in an in vivo porcine experimental model of acute myocardial infarction. Thin-layer chromatography after lipid extraction showed that VLDL exposure leads to cholesteryl ester (CE) and triglyceride (TG) accumulation in a dose-dependent manner and that hypoxic conditions further increased VLDL-derived intracellular lipid accumulation in HL-1 cells. Knockdown of LRP1 through lentiviral-mediated interfering RNA specifically prevented hypoxia-induced VLDL-CE internalization in HL-1 cells and NRVM. Lipopolysaccharide (LPS)-induced LRP1 overexpression specifically increased VLDL-CE accumulation in NRVM. In addition, using double-radiolabelled [3H]CE-[14C]TG-VLDL, we found that LRP1 deficiency specifically prevented hypoxia-induced VLDL-[3H]CE uptake. Finally, in an in vivo porcine model of infarcted myocardium, ischaemic areas exhibited LRP1 protein up-regulation and intramyocardial CE overaccumulation. Our results demonstrate that hypoxia increases LRP1 expression through HIF-1α and that LRP1 overexpression mediates hypoxia-induced VLDL-CE uptake and accumulation in cardiomyocytes.