tbuckley/cabot-search huggingface dataset:
Cardiac tamponade in left ventricular dysfunction.
Authors: B D Hoit, M Gabel, N O Fowler
Journal: Circulation (1990)

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.
Human Apolipoprotein A-II Enrichment Displaces Paraoxonase From HDL and Impairs Its Antioxidant Properties
Authors: Vicent Ribas, José Luis Sánchez-Quesada, Rosa Antón, Mercedes Camacho, Josep Julve, Joan Carles Escolà-Gil, Luís Vila, Jordi Ordóñez-Llanos, Francisco Blanco-Vaca
Journal: Circulation Research (2004)

Apolipoprotein A-II (apoA-II), the second major high-density lipoprotein (HDL) apolipoprotein, has been linked to familial combined hyperlipidemia. Human apoA-II transgenic mice constitute an animal model for this proatherogenic disease. We studied the ability of human apoA-II transgenic mice HDL to protect against oxidative modification of apoB-containing lipoproteins. When challenged with an atherogenic diet, antigens related to low-density lipoprotein (LDL) oxidation were markedly increased in the aorta of 11.1 transgenic mice (high human apoA-II expressor). HDL from control mice and 11.1 transgenic mice were coincubated with autologous very LDL (VLDL) or LDL, or with human LDL under oxidative conditions. The degree of oxidative modification of apoB lipoproteins was then evaluated by measuring relative electrophoretic mobility, dichlorofluorescein fluorescence, 9- and 13-hydroxyoctadecadienoic acid content, and conjugated diene kinetics. In all these different approaches, and in contrast to control mice, HDL from 11.1 transgenic mice failed to protect LDL from oxidative modification. A decreased content of apoA-I, paraoxonase (PON1), and platelet-activated factor acetyl-hydrolase activities was found in HDL of 11.1 transgenic mice. Liver gene expression of these HDL-associated proteins did not differ from that of control mice. In contrast, incubation of isolated human apoA-II with control mouse plasma at 37°C decreased PON1 activity and displaced the enzyme from HDL. Thus, overexpression of human apoA-II in mice impairs the ability of HDL to protect apoB-containing lipoproteins from oxidation. Further, the displacement of PON1 by apoA-II could explain in part why PON1 is mostly found in HDL particles with apoA-I and without apoA-II, as well as the poor antiatherogenic properties of apoA-II–rich HDL.
Integrative View of α2,3-Sialyltransferases (ST3Gal) Molecular and Functional Evolution in Deuterostomes: Significance of Lineage-Specific Losses
Authors: Daniel Petit, Elin Teppa, Anne-Marie Mir, Dorothée Vicogne, Christine Thisse, Bernard Thisse, Cyril Filloux, Anne Harduin-Lepers
Journal: Molecular Biology and Evolution (2014)

Sialyltransferases are responsible for the synthesis of a diverse range of sialoglycoconjugates predicted to be pivotal to deuterostomes' evolution. In this work, we reconstructed the evolutionary history of the metazoan α2,3-sialyltransferases family (ST3Gal), a subset of sialyltransferases encompassing six subfamilies (ST3Gal I–ST3Gal VI) functionally characterized in mammals. Exploration of genomic and expressed sequence tag databases and search of conserved sialylmotifs led to the identification of a large data set of st3gal-related gene sequences. Molecular phylogeny and large scale sequence similarity network analysis identified four new vertebrate subfamilies called ST3Gal III-r, ST3Gal VII, ST3Gal VIII, and ST3Gal IX. To address the issue of the origin and evolutionary relationships of the st3gal-related genes, we performed comparative syntenic mapping of st3gal gene loci combined to ancestral genome reconstruction. The ten vertebrate ST3Gal subfamilies originated from genome duplication events at the base of vertebrates and are organized in three distinct and ancient groups of genes predating the early deuterostomes. Inferring st3gal gene family history identified also several lineage-specific gene losses, the significance of which was explored in a functional context. Toward this aim, spatiotemporal distribution of st3gal genes was analyzed in zebrafish and bovine tissues. In addition, molecular evolutionary analyses using specificity determining position and coevolved amino acid predictions led to the identification of amino acid residues with potential implication in functional divergence of vertebrate ST3Gal. We propose a detailed scenario of the evolutionary relationships of st3gal genes coupled to a conceptual framework of the evolution of ST3Gal functions.
Acute exposure to sawdust does not alter airway calibre and responsiveness to histamine in asthmatic subjects
Authors: S De Luca, N Caire, Y Cloutier, A Cartier, H Ghezzo, JL Malo
Journal: European Respiratory Journal (1988)

We investigated the effects of particles of sawdust delivered through a special device at known concentrations (close to the threshold limit value-short term exposure limit (TLV-STEL) of 10 mg.m-3) on FEV1 and PC20 in 12 asthmatic subjects free of clinical sensitization to this product. Subjects were studied over two days (day 1: exposure to sawdust; day 2: sham exposure) in random order with a maximum interval of 1 week. On each day, after the assessment of spirometry and PC20, subjects underwent exposure to sawdust or sham exposure. Sawdust was inhaled for a total of 30 min at average concentrations varying from 8.0 to 19.3 mg.m-3 (mean = 11.5 mg.m-3). Twenty-five to 39.7% (mean = 34.6%) of inhaled particles had a diameter less than 10 mu (diameter allowing deposition in the trachea and lower respiratory tract). At the end of each period of exposure, FEV1 was assessed. After recovery, the second PC20 was obtained. Serial measurements of FEV1 were carried out every hour for up to 6 h after the end of exposure. At that time, PC20 was reassessed. Only one subject showed an acute bronchoconstriction immediately after exposure to sawdust (maximum fall of 14% in FEV1) with complete recovery 10 min later. Overall, inhalation of sawdust did not modify PC20 by comparing the mean result of the first test with the second and the third assessments. Also, the mean changes in PC20 at each interval after exposure to sawdust were not significantly different from the variations in PC20 on the sham day.(ABSTRACT TRUNCATED AT 250 WORDS)
Physical activity and health related physical fitness in children with juvenile idiopathic arthritis
Authors: T Takken
Journal: Annals of the Rheumatic Diseases (2003)

<b>Objective:</b> To obtain insight into the interaction between daily physical activity and components of health related physical fitness in children with juvenile idiopathic arthritis. <b>Methods:</b> Forty five patients (10 male/35 female; mean (SD) age 8.9 (2.2) years) participated in the study. Body mass, height, skinfold thickness, number of swollen joints, and joint range of motion were determined. The maximal oxygen consumption (Vo<sub>2peak</sub>) was assessed during a graded maximal bicycle exercise test. Daily physical activity levels were measured with a Caltrac activity monitor and a parental physical activity rating (PAL) on a five point Likert scale. <b>Results:</b> Partial correlation coefficients (to control for age) between physical activity and indices of health related physical fitness showed significant relationships between Caltrac motion counts and absolute Vo<sub>2peak</sub> (<i>r</i>=0.31) and relative Vo<sub>2peak</sub> (<i>r</i>=0.34), but not with the indices of body composition. There was also a significant correlation between PAL and relative Vo<sub>2peak</sub> (<i>r</i>=0.33). <b>Conclusions:</b> Physical activity was significantly related to cardiorespiratory fitness but not to body composition in children with juvenile idiopathic arthritis. A longitudinal follow up should show whether an active lifestyle protects for loss of aerobic fitness in this patient group.
Use of anti-inflammatory therapy and asthma mortality in Japan
Authors: S. Suissa, P. Ernst
Journal: European Respiratory Journal (2003)

Asthma treatment guidelines were introduced in Japan in the 1990s, insisting as elsewhere, on the importance of anti-inflammatory therapy. The present study assessed whether use of anti-inflammatory medications was associated with a decrease in asthma mortality in Japan, the first country to use leukotriene receptor antagonists. A population-based ecological study was conducted, spanning the period 1987–1999, among people aged 5–34 yrs in Japan. The association between the yearly rate of asthma death and sales of inhaled corticosteroids and leukotriene receptor antagonists was estimated using Poisson regression. The yearly asthma death rate was stable at 6–7 deaths per million before the introduction of leukotriene receptor antagonists in 1995 and decreased by 23% thereafter, reaching 3.5 per million in 1999. The rate of asthma death was found to decrease with increasing use of both leukotriene receptor antagonists and inhaled corticosteroids. The rate ratio of asthma death was 0.96 per 1 million 25-day treatment courses of inhaled corticosteroids and 0.80 for every 1 million 25-day treatment courses of leukotriene receptor antagonists, consumed per year in Japan. The increasing use of inhaled corticosteroids and leukotriene receptor antagonists may have contributed to the significant reduction in asthma mortality among young asthmatics in Japan.
ANTIGEN MODULATION OF THE IMMUNE RESPONSE
Authors: T. L. Feldbush, J. L. Gowans
Journal: The Journal of Experimental Medicine (1971)

Secondary immune responsiveness to dinitrophenylated bovine gamma globulin (DNP-BGG) was transferred to heavily irradiated rats by means of small lymphocytes from the thoracic duct of immunized syngeneic donors. Affinity of the antibody produced by the adoptive recipients when challenged immediately was the same as that seen in immunized controls and cell donors, suggesting that the performance of lymphocytes in the thoracic duct of immunized rats provide an accurate measure of the immunologic history of memory cells both in the intact animal and the lymphocyte-depleted donor. The relevance of this to cell cooperation in the production of antibody to hapten-protein complexes is discussed. Direct evidence on antigen modulation of the immune response was also obtained. When immune thoracic duct lymphocytes were transferred to adoptive recipients and challenged either immediately or after a delay of 6 wk, it was found that, although the amount of antibody decreased with this delay in challenge, the affinity remained constant. Thus it would seem that in control rats, the increase in the affinity of antibody with time after immunization is, in fact, due to the selection of new populations of cells by the progressively waning concentration of antigen.
A novel Hsp90 inhibitor AT13387 induces senescence in EBV-positive nasopharyngeal carcinoma cells and suppresses tumor formation
Authors: King Chi Chan, Choi Man Ting, Pui Shan Chan, Ming Chu Lo, Kwok Wai Lo, Jayne E Curry, Tomoko Smyth, Anne Wing Mui Lee, Wai Tong Ng, George Sai Wah Tsao, Ricky Ngok Shun Wong, Maria Li Lung, Nai Ki Mak
Journal: Molecular Cancer (2013)

Abstract Background Nasopharyngeal carcinoma (NPC) is an epithelial malignancy strongly associated with Epstein-Barr virus (EBV). AT13387 is a novel heat shock protein 90 (Hsp90) inhibitor, which inhibits the chaperone function of Hsp90 and reduces expression of Hsp90-dependent client oncoproteins. This study aimed to evaluate both the in vitro and in vivo antitumor effects of AT13387 in the EBV-positive NPC cell line C666-1. Results Our results showed that AT13387 inhibited C666-1 cell growth and induced cellular senescence with the downregulation of multiple Hsp90 client oncoproteins EGFR, AKT, CDK4, and restored the protein expression of negative cell cycle regulator p27. We also studied the ability of AT13387 to restore p27 expression by downregulation of AKT and the p27 ubiquitin mediator, Skp2, using AKT inhibitor and Skp2 siRNA. In the functional study, AT13387 inhibited cell migration with downregulation of a cell migration regulator, HDAC6, and increased the acetylation and stabilization of α-tubulin. We also examined the effect of AT13387 on putative cancer stem cells (CSC) by 3-D tumor sphere formation assay. AT13387 effectively reduced both the number and size of C666-1 tumor spheres with decreased expression of NPC CSC-like markers CD44 and SOX2. In the in vivo study, AT13387 significantly suppressed tumor formation in C666-1 NPC xenografts. Conclusion AT13387 suppressed cell growth, cell migration, tumor sphere formation and induced cellular senescence on EBV-positive NPC cell line C666-1. Also, the antitumor effect of AT13387 was demonstrated in an in vivo model. This study provided experimental evidence for the preclinical value of using AT13387 as an effective antitumor agent in treatment of NPC.
Concentration-Dependent Mutation by Alkylating Agents in Human Lymphoblasts and &lt;italic&gt;Salmonella typhimurium: N&lt;/italic&gt;-Methyl-&lt;italic&gt;N&lt;/italic&gt;-nitrosourethane and β-Propiolactone&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: B W Penman, H Hoppe, W G Thilly
Journal: JNCI Journal of the National Cancer Institute (1979)

The toxic and mutagenic effects of the alkylating agents N-methyl-N-nitrosourethane (MNUT) and beta-propiolactone (BPL) were quantitatively measured in human lymphoblasts and Salmonella typhimurium. Forward mutation to 6-thioguanine resistance was measured in the human lymphoblasts, and forward mutation to 8-azaguanine resistance was measured in the bacterial cells after equigenerational (1.5 doubling times) exposures. In both systems, the induced mutant fraction rose linearly as a function of concentration for BPL and was biphasic for MNUT. The responses of the two assay systems to eight alkylating agents were compared. The exposure of the cells to each alkylating agent was calculated as exposure concentration multiplied by the time of exposure, and allowance was made for the decomposition of the alkylating agents during exposure (integral exposure). Human cells were 2.5--13 times more sensitive than was S. typhimurium to the alkylating agents methyl methanesulfonate, ethyl methanesulfonate, propyl methanesulfonate, N-methyl-N'-nitro-N-nitrosoguanidine, methylnitrosourea, and MNUT. S. typhimurium cells were three times more sensitive to butyl methanesulfonate and 25 times more sensitive to BPL than were human cells.
Von Willebrand Factor and Platelet Function
Authors: R Moroose, L W Hoyer
Journal: Annual Review of Medicine (1986)

CD40 is a cell-surface member of the TNF (tumor necrosis factor) receptor superfamily. Upon activation, CD40 can license dendritic cells to promote antitumor T cell activation and re-educate macrophages to destroy tumor stroma. Numerous agonist CD40 ...Read More
An essential role for ΔFosB in the nucleus accumbens in morphine action
Authors: Venetia Zachariou, Carlos A Bolanos, Dana E Selley, David Theobald, Michael P Cassidy, Max B Kelz, Tamara Shaw-Lutchman, Olivier Berton, Laura J Sim-Selley, Ralph J Dileone, Arvind Kumar, Eric J Nestler
Journal: Nature Neuroscience (2006)
Annual Oncogene Meeting: Hot Weather and Hot Science
Authors: P. A. Newman
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article Annual Oncogene Meeting: Hot Weather and Hot Science Particia A. Newman Particia A. Newman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 12, 17 August 1988, Pages 888–889, https://doi.org/10.1093/jnci/80.12.888 Published: 17 August 1988
Rupture of major bronchi resulting from closed chest injuries
Authors: J. P. Collins, V. Ketharanathan, I. McConchie
Journal: Thorax (1973)

Four cases of ruptured bronchus following closed chest trauma are described. All injuries resulted from motor vehicle accidents and were diagnosed and treated within 24 hours of admission to the hospital. A satisfactory result followed early suture repair of the ruptured bronchus in three cases. One patient died during pneumonectomy. The early diagnosis and treatment of the condition are discussed.
How long should long be? Long-term trials in rheumatic diseases.
Authors: S N Ciccolunghi, H A Chaudri, B I Schubiger
Journal: Annals of the Rheumatic Diseases (1979)

In the interests of the safety of patients it is necessary to collect long-term clinical data. It is often assumed that the longer the trial the better. However, the longer the trial the more scientific compromises are necessary if it is to be carried out in a practical way. Because the therapeutic efficacy of and tolerance to the nonsteroidal anti-inflammatory drug diclofenac was established after 6 months' trial the optimal duration for a comparative long-term trial of this preparation is 6 months. The small amount of information gained from trials of diclofenac longer than this did not justify the reduction in quality of trial design and performance that they required. Thus it would appear that at least for 1 antirheumatic drug the assumption that 'the longer the trial the better' is not true.
CANCER EN CUIRASSE
Authors: LOUIS SAVATARD
Journal: British Journal of Dermatology (1943)

Journal Article CANCER EN CUIRASSE Get access LOUIS SAVATARD LOUIS SAVATARD Manchester Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 55, Issue 2, 1 February 1943, Pages 31–39, https://doi.org/10.1111/j.1365-2133.1943.tb10733.x Published: 01 February 1943
The Laboratory Evaluation of Opportunistic Pulmonary Infections
Authors: James H. Shelhamer
Journal: Annals of Internal Medicine (1996)

The patient population at risk for opportunistic pulmonary infections has increased during the last decade.The spectrum of organisms causing opportunistic infections has also grown. With an ever broader list of potential therapeutic options and a growing differential diagnosis, a specific diagnosis of the cause of pulmonary disease becomes more important. Recent microbiologic advances have helped to facilitate the laboratory diagnosis of some of these agents. Immunoassays are available for the detection of antigen in nasopharyngeal secretions (respiratory syncytial virus, influenza), in serum (Cryptococcus species), and in urine (Legionella or Histoplasma species). Rapid-culture techniques are available for the culture and detection of various viruses, including cytomegalovirus. Molecular probes can now assist in the rapid identification of Mycobacterium tuberculosis and some fungi. In the near future, polymerase chain reaction-based techniques may assist in the detection of Pneumocystis carinii and Legionella, Chlamydia, Mycoplasma, and mycobacteria species. An expeditious evaluation of pulmonary disease requires an understanding of the differential diagnosis of likely causes of pulmonary disease in specific immunosuppressed patient populations, an understanding of the most appropriate specimens to process for these diagnoses, and an understanding of the limitations (sensitivity and specificity) of these diagnostic tests. An understanding of the most appropriate specimens and tests in a given institution should allow for early, relatively specific treatment of many potentially life-threatening infections.
Pulmonary Artery Smooth Muscle Cell Senescence Is a Pathogenic Mechanism for Pulmonary Hypertension in Chronic Lung Disease
Authors: Hibo Noureddine, Guillaume Gary-Bobo, Marco Alifano, Elisabeth Marcos, Mirna Saker, Nora Vienney, Valérie Amsellem, Bernard Maitre, Ari Chaouat, Christos Chouaid, Jean-Luc Dubois-Rande, Diane Damotte, Serge Adnot
Journal: Circulation Research (2011)

Senescence of pulmonary artery smooth muscle cells (PA-SMCs) caused by telomere shortening or oxidative stress may contribute to pulmonary hypertension associated with chronic lung diseases.To investigate whether cell senescence contributes to pulmonary vessel remodeling and pulmonary hypertension in chronic obstructive pulmonary disease (COPD).In 124 patients with COPD investigated by right heart catheterization, we found a negative correlation between leukocyte telomere length and pulmonary hypertension severity. In-depth investigations of lung vessels and derived cultured PA-SMCs showed greater severity of remodeling and increases in senescent p16-positive and p21-positive PA-SMCs and proliferating Ki67-stained cells in 14 patients with COPD compared to 13 age-matched and sex-matched control subjects who smoke. Cultured PA-SMCs from COPD patients displayed accelerated senescence, with fewer cell population doublings, an increased percentage of β-galactosidase-positive cells, shorter telomeres, and higher p16 protein levels at an early cell passage compared to PA-SMCs from controls. Both in situ and in vitro PA-SMC senescence criteria correlated closely with the degree of pulmonary vessel wall hypertrophy. Because senescent PA-SMCs stained for p16 and p21 were virtually confined to the media near the Ki67-positive cells, which predominated in the neointima and hypertrophied media, we evaluated whether senescent cells affected normal PA-SMC functions. We found that senescent PA-SMCs stimulated the growth and migration of normal target PA-SMCs through the production and release of paracrine soluble and insoluble factors.PA-SMC senescence is an important contributor to the process of pulmonary vascular remodeling that underlies pulmonary hypertension in chronic lung disease.