tbuckley/cabot-search huggingface dataset:
Atrioverter: An Implantable Device for the Treatment of Atrial Fibrillation
Authors: Hein J. J. Wellens, Chu-Pak Lau, Berndt Lüderitz, Masood Akhtar, Albert L. Waldo, A. John Camm, Carl Timmermans, Hung-Fat Tse, Werner Jung, Luc Jordaens, Gregory Ayers
Journal: Circulation (1998)

During atrial fibrillation, electrophysiological changes occur in atrial tissue that favor the maintenance of the arrhythmia and facilitate recurrence after conversion to sinus rhythm. An implantable defibrillator connected to right atrial and coronary sinus defibrillation leads allows prompt restoration of sinus rhythm by a low-energy shock. The safety and efficacy of this system, called the Atrioverter, were evaluated in a prospective, multicenter study.The study included 51 patients with recurrent atrial fibrillation who had not responded to antiarrhythmic drugs, were in New York Heart Association Heart failure class I or II, and were at low risk for ventricular arrhythmias. The atrial defibrillation threshold had to be </=240 V during preimplant testing. Atrial fibrillation detection, R-wave shock synchronization, and defibrillation threshold were tested at implantation and during follow-up. Shock termination of spontaneous episodes of atrial fibrillation was performed under physician observation. Results are given after a minimum of 3 months of follow-up. During a follow-up of 72 to 613 days (mean, 259+/-138 days), 96% of 227 spontaneous episodes of atrial fibrillation in 41 patients were successfully converted to sinus rhythm by the Atrioverter. In 27% of episodes, several shocks were required because of early recurrence of atrial fibrillation. Shocks did not induce ventricular arrhythmias. Most patients received antiarrhythmic medication during follow-up. In 4 patients, the Atrioverter was removed: in 1 because of infection, in 1 because of cardiac tamponade, and in 1 because of frequent episodes of atrial fibrillation requiring His bundle ablation.With the Atrioverter, prompt and safe restoration of sinus rhythm is possible in patients with recurrent atrial fibrillation.
Total prosthetic replacement of atrioventricular valves in the dog: Part II. Development of tilting cone mitral prosthesis
Authors: G. Den Otter
Journal: Thorax (1968)

The free-floating cone and cage valve, described in a previous study as being successful as a substitute for the right atrioventricular valve, does not perform well when it is inserted in the mitral ostium. A tilting cone or disc was constructed and tested in a series of 15 dogs. This prosthesis gave excellent results in 12 animals. The reasons for its failure in the remaining three is discussed. The prosthesis presented has advantages over any ball and cage valve, mainly because of its smaller volume.
Tumor angiogenesis and progression are enhanced by Sema4D produced by tumor-associated macrophages
Authors: Jose Rafael Sierra, Simona Corso, Luisa Caione, Virna Cepero, Paolo Conrotto, Alessandro Cignetti, Wanda Piacibello, Atsushi Kumanogoh, Hitoshi Kikutani, Paolo Maria Comoglio, Luca Tamagnone, Silvia Giordano
Journal: The Journal of Experimental Medicine (2008)

Increased evidence suggests that cancer-associated inflammation supports tumor growth and progression. We have previously shown that semaphorin 4D (Sema4D), a ligand produced by different cell types, is a proangiogenic molecule that acts by binding to its receptor, plexin B1, expressed on endothelial cells (Conrotto, P., D. Valdembri, S. Corso, G. Serini, L. Tamagnone, P.M. Comoglio, F. Bussolino, and S. Giordano. 2005. Blood. 105:4321–4329). The present work highlights the role of Sema4D produced by the tumor microenvironment on neoplastic angiogenesis. We show that in an environment lacking Sema4D, the ability of cancer cells to generate tumor masses and metastases is severely impaired. This condition can be explained by a defective vascularization inside the tumor. We demonstrate that tumor-associated macrophages (TAMs) are the main cells producing Sema4D within the tumor stroma and that their ability to produce Sema4D is critical for tumor angiogenesis and vessel maturation. This study helps to explain the protumoral role of inflammatory cells of the tumor stroma and leads to the identification of an angiogenic molecule that might be a novel therapeutic target.
Pathophysiology of Psoriasis
Authors: J J Voorhees
Journal: Annual Review of Medicine (1977)

Psoriasis is a disease characterized by benign but unrestricted epithelial growth. The molecular pathophysiology of this unregulated growth has been discussed. A better understanding of the role of the cell surface, cyclic nucleotides, arachidonic acid-prostaglandin metabolism, and polyamines in psoriasis may clarify our understanding of this disease and produce clues pertinent to a general understanding of growth regulation.
Can diaphragmatic contractility be assessed by airway twitch pressure in mechanically ventilated patients?
Authors: S E Cattapan
Journal: Thorax (2003)

<b>Background:</b> In critically ill patients inspiratory muscle function may be assessed by measurements of maximal inspiratory airway pressure and the response of twitch transdiaphragmatic pressure (Pdi tw) to bilateral phrenic nerve stimulation. The first is limited by its total dependence on patient cooperation. Although the second approach is independent of patient volition, it is impractical because it requires oesophageal and gastric balloons. Because airway pressure is easily and non-invasively recorded in patients with artificial airways, we hypothesised that twitch airway pressure (Paw tw) reliably predicts Pdi tw and twitch oesophageal pressure (Poes tw) in mechanically ventilated patients. <b>Methods:</b> Thirteen mechanically ventilated patients recovering from an episode of acute respiratory failure received phrenic nerve stimulation at end exhalation. The rapid occlusion technique was used to record respiratory system mechanics. <b>Results:</b> Stimulations were well tolerated. Mean (SE) Paw tw at end exhalation was –8.2 (1.2) cm H<sub>2</sub>O and Poes tw and Pdi tw were –7.3 (1.1) and 10.4 (1.8) cm H<sub>2</sub>O, respectively. Stimulations produced a good correlation between Paw tw and Pdi tw (p&lt;0.001), although the limits of agreement were wide. The results were similar for Poes tw. No relationship was found between the Paw tw/Poes tw ratio and respiratory system compliance or airway resistance. Paw tw reproducibility was excellent (mean coefficient of variation 6%, range 3–9%). <b>Conclusions:</b> Despite a good correlation between Paw tw and Poes tw, Paw tw did not reliably predict Poes tw or Pdi tw in mechanically ventilated patients. Nevertheless, the excellent reproducibility of Paw tw suggests that it may be a useful means of monitoring inspiratory muscle contractility in the routine care of mechanically ventilated patients.
Autoimmune serological studies in chronic gastritis and pernicious anaemia
Authors: I. R. Mackay
Journal: Gut (1964)

EDITORIAL SYNOPSIS These serological observations provide further support for the concept of autoimmunization as an aetiological factor in these clinico-pathological conditions.This paper describes the incidence of positive serological tests for autoantibodies to gastric mucosal antigen and to thyroglobulin in patients with chronic gastritis, pernicious anaemia, and post- gastrectomy gastritis.The results support the recent concept (British Medical Journal, 1962) that diffuse atrophic gastritis, which is the essential lesion in most cases of pernicious anaemia, may have an autoimmune basis.The findings of an increased incidence of antithyroglobulin antibodies in patients with atrophic gastritis adds further evidence for the suggested association between chronic disease of the stomach and thyroid gland. METHODSTests for complement-fixing antibodies to tissue extracts were performed as described by Gajdusek (1958); the gastric mucosal antigen was made up as a 10% saline extract of mucosa from the pars media of a freshly resected human stomach.Titres of 16 or greater were regarded as significantly positive.Antibodies to thyro- globulin were titrated by tanned red cell haemagglutina- tion as described by Mackay and Perry (1960); titres of 100 or greater were regarded as significantly positive.Chronic gastritis was diagnosed by histological examination of a blind biopsy specimen of gastric mucosa.The criteria for gastritis were glandular dis- organization and atrophy with lymphocytic and plasma cell proliferation in the mucosa: however, lymphocytic on August 20,
A Case of Meigs's Syndrome
Authors: E. L. Thomson
Journal: BMJ (1960)

A Case of Meigs's SyndromeThe following case is reported because of the relative rarity of the condition.The presenting symptom was breathlessness, the immediate finding was gross right- sided pleural effusion, and the cause of the trouble was a right-sided ovarian carcinoma.The essential features of Meigs's (1934) syndrome are hydrothorax and ascites, associated with disease of the ovary.The patients are relieved of their serous fluids by removal of the tumour. CASE REPORTOn February 7, 1958, I was consulted by a woman aged 41, the mother of two children, who found it difficult even to walk; she had to be supported by two relatives.She looked extremely ill.Marked dyspnoea was at once obvious
Characterisation of cell adhesion in airway epithelial cell types using electric cell–substrate impedance sensing
Authors: I. H. Heijink, S. M. Brandenburg, J. A. Noordhoek, D. S. Postma, D-J. Slebos, A. J. M. van Oosterhout
Journal: European Respiratory Journal (2009)

Research on epithelial cell lines and primary epithelium is required to dissect the mechanisms underlying the structural abnormalities in airway epithelium observed for respiratory diseases, including asthma and chronic obstructive pulmonary disease. The novel electric cell–substrate impedance sensing technique was used to monitor cell adhesion/spreading, barrier function and wound healing. Primary bronchial epithelium was compared with airway epithelial cell lines 16HBE14o-, BEAS-2B, NCI-H292 and A549. BEAS-2B, A549 and primary cells form a confluent monolayer more rapidly than do 16HBE14o- cells. In contrast, 16HBE14o- cells form stronger intercellular contacts, with a 10-fold higher resistance than BEAS-2B, A549 and NCI-H292 cells and a five-fold increase over primary cells. Accordingly, expression of the adhesion molecules zona occludens-1 and E-cadherin was highest in 16HBE14o- cells. These molecules were localised in intercellular junctions in both 16HBE14o- and primary cells. Finally, restoration of barrier function upon injury was impaired in BEAS-2B compared to 16HBE14o- cells. In conclusion, epithelial cell types display remarkable phenotypic differences and should, accordingly, be used to address specific research questions. 16HBE14o- cells appear most suitable for studies on barrier formation, whereas resemblance in attachment of primary and BEAS-2B and A549 cells makes the latter more important for translational research on cell–matrix contact.
Peroxiredoxin II is essential for sustaining life span of erythrocytes in mice
Authors: Tae Hoon Lee, Sun Uk Kim, Seong Lan Yu, Sue Hee Kim, Do Sim Park, Hyung Bae Moon, So Hee Dho, Ki Sun Kwon, Hyun Jeong Kwon, Ying Hao Han, Sangkyun Jeong, Sang Won Kang, Hee Sup Shin, Kyung Kwang Lee, Sue Goo Rhee, Dae Yeul Yu
Journal: Blood (2003)
Syndecan-4 protects against osteopontin-mediated acute hepatic injury by masking functional domains of osteopontin
Authors: Shigeyuki Kon, Masahiro Ikesue, Chiemi Kimura, Momoe Aoki, Yosuke Nakayama, Yoshinari Saito, Daisuke Kurotaki, Hongyan Diao, Yutaka Matsui, Tatsuya Segawa, Masahiro Maeda, Tetsuhito Kojima, Toshimitsu Uede
Journal: The Journal of Experimental Medicine (2007)

Osteopontin (OPN) is a T helper type 1 immunoregulatory cytokine that plays a critical role in various inflammatory disorders. OPN exerts proinflammatory reactions through interaction with integrin receptors. OPN function can be modulated by protease digestion. However, the molecular mechanisms that regulate OPN function in vivo have not been elucidated. There are two putative heparin-binding domains (HBDs) within the OPN molecule, which may bind both heparin and heparin-like glycosaminoglycans such as syndecan. We show that expression of OPN and syndecan-4 is significantly up-regulated after concanavalin-A (ConA) injection. Syndecan-4 binds to one of the HBDs of OPN, which overlaps with the thrombin cleavage site of OPN. When OPN is associated with syndecan-4, syndecan-4 masks both the thrombin cleavage and the integrin binding sites within OPN. Importantly, syndecan-4–deficient (Syn4KO) mice are more susceptible to hepatic injury, and the thrombin-cleaved form of OPN is significantly elevated in Syn4KO mice as compared with wild-type mice after ConA injection. Finally, we demonstrate that administration of purified syndecan-4 protects mice from ConA-induced hepatic injury. Thus, syndecan-4 is a critical intrinsic regulator of inflammatory reactions via its effects on OPN function and is a potential novel therapeutic tool for treating inflammatory diseases.
Molecular Profiling of Laser-Microdissected Matched Tumor and Normal Breast Tissue Identifies Karyopherin α2 as a Potential Novel Prognostic Marker in Breast Cancer
Authors: Edgar Dahl, Glen Kristiansen, Kathrin Gottlob, Irina Klaman, Elke Ebner, Bernd Hinzmann, Klaus Hermann, Christian Pilarsky, Matthias Dürst, Monika Klinkhammer-Schalke, Hagen Blaszyk, Ruth Knuechel, Arndt Hartmann, André Rosenthal, Peter J. Wild
Journal: Clinical Cancer Research (2006)

The aim of the present study was to identify human genes that might prove useful in the diagnosis and therapy of primary breast cancer.Twenty-four matched pairs of invasive ductal breast cancer and corresponding benign breast tissue were investigated by a combination of laser microdissection and gene expression profiling. Differential expression of candidate genes was validated by dot blot analysis of cDNA in 50 pairs of matching benign and malignant breast tissue. Cellular expression of candidate genes was further validated by RNA in situ hybridization, quantitative reverse transcription-PCR, and immunohistochemistry using tissue microarray analysis of 272 nonselected breast cancers. Multivariate analysis of factors on overall survival and recurrence-free survival was done.Fifty-four genes were found to be up-regulated and 78 genes were found to be down-regulated. Dot blot analysis reduced the number of up-regulated genes to 15 candidate genes that showed at least a 2-fold overexpression in >15 of 50 (30%) tumor/normal pairs. We selected phosphatidic acid phosphatase type 2 domain containing 1A (PPAPDC1A) and karyopherin alpha2 (KPNA2) for further validation. PPAPDC1A and KPNA2 RNA was up-regulated (fold change >2) in 84% and 32% of analyzed tumor/normal pairs, respectively. Nuclear protein expression of KPNA2 was significantly associated with shorter overall survival and recurrence-free survival. Testing various multivariate Cox regression models, KPNA2 expression remained a highly significant, independent and adverse risk factor for overall survival.Gene expression profiling of laser-microdissected breast cancer tissue revealed novel genes that may represent potential molecular targets for breast cancer therapy and prediction of outcome.
Diagnostic Yield Improves With Collection of 2 Samples in Fecal Immunochemical Test Screening Without Affecting Attendance
Authors: Aafke H.C. van Roon, Janneke A. Wilschut, Lieke Hol, Marjolein van Ballegooijen, Jacqueline C.I.Y. Reijerink, Hans 't Mannetje, Laura J.C. Kranenburg, Katharina Biermann, Anneke J. van Vuuren, Jan Francke, Alexandra C.M. van der Togt, Dik J.F. Habbema, Monique E. van Leerdam, Ernst J. Kuipers
Journal: Clinical Gastroenterology and Hepatology (2010)
Surface Structure of Fetal Rat Brain Cells During Neoplastic Transformation in Cell Culture&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Åge Haugen, Ole Didrik Laerum
Journal: JNCI Journal of the National Cancer Institute (1978)

The surface microstructure of fetal rat brain cells undergoing neoplastic transformation in long-term cell culture after a single transplacental pulse of 75 microgram N-ethyl-N-nitrosourea/g body weight to the fetal (18th day of gestation) BD IX rat was investigated by scanning electron microscopy. After about 3 weeks of culture, N-ethyl-N-nitrosourea-pretreated fetal rat brain cells showed focal proliferation of neural cells on an underlayer of flat, epithelioid cells. The neural cells exhibited varying forms of numerous dorsal ruffles and an increased number of other surface microprojections. Between the 40th and the 100th day, nodules of bipolar and multipolar neural cells were observed with a complex surface microstructure including many blebs and ruffles and an increased number of microvilli. After 100-210 days, more rapidly proliferating, morphologically altered cells formed "piled-up" foci, which resulted in a homogeneous population of cells with numerous long microvilli, large ruffles, and blebs over the whole surface. The cells retained the same altered surface structure until tumorigenicity after reimplantation into the syngeneic host was first observed (approximately 273 days). Surface alterations characteristic of the neoplastic cells were thus observable more than 100 days before the cells became tumorigenic.
Anti–Tumor Necrosis Factor-α Treatment Improves Endothelial Function in Patients With Rheumatoid Arthritis
Authors: David Hürlimann, Adrian Forster, Georg Noll, Frank Enseleit, Rémy Chenevard, Oliver Distler, Markus Béchir, Lukas E. Spieker, Michel Neidhart, Beat A. Michel, Renate E. Gay, Thomas F. Lüscher, Steffen Gay, Frank Ruschitzka
Journal: Circulation (2002)

Background— Rheumatoid arthritis (RA) is associated with accelerated atherosclerosis and increased cardiovascular morbidity and mortality. Striking similarities exist in the inflammatory and immunologic response in RA and atherosclerosis. Indeed, adhesion molecules and cytokines, tumor necrosis factor (TNF)-α in particular, are key mediators of joint inflammation and of vascular dysfunction and progression of atherosclerotic vascular disease. Hence, the aim of the present study was to assess the effect of chronic antiinflammatory treatment with the anti-TNF-α antibody infliximab on disease activity and endothelial function in patients with active RA. Methods and Results— Eleven RA patients (mean age 46±5 years; disease duration 9±2 years) with high disease activity despite treatment with stable doses of methotrexate (≤25 mg/wk) and prednisone (≤10 mg/d) were investigated. Clinical status and endothelium-dependent and -independent vasodilation of the brachial artery as assessed by high-resolution ultrasound were measured before and after 12 weeks of infliximab therapy. Flow-mediated vasodilation improved from 3.2±0.4% to 4.1±0.5% ( P =0.018), whereas endothelium-independent vasodilation with nitroglycerin and baseline diameter remained unchanged (13.6±1.2% versus 12.8±1.4%, P =0.98, and 3.74±0.15 versus 3.66±0.11 mm, P =0.54, respectively). Disease activity score (DAS28) was significantly reduced, from 5.6±0.3 to 3.5±0.6 ( P =0.002). Erythrocyte sedimentation rate and C-reactive protein were lowered from 34±7 to 19±5 mm/h ( P =0.04) and from 38±11 to 15±10 mg/L ( P =0.08), respectively. Conclusions— This is the first study to show that anti-TNF-α treatment improves endothelial function in RA. The data suggest that in RA, endothelial dysfunction is part of the disease process and is mediated by TNF-α.
Randomized Trial of Folic Acid for Prevention of Cardiovascular Events in End-Stage Renal Disease
Authors: Elizabeth M. Wrone, John M. Hornberger, James L. Zehnder, Linda M. McCann, Norman S. Coplon, Stephen P. Fortmann
Journal: Journal of the American Society of Nephrology (2004)

ABSTRACT. High serum total homocysteine (tHcy) is gaining scrutiny as a risk factor for cardiovascular disease in the general population. The relationship between tHcy and mortality and cardiovascular events in patients with end-stage renal disease (ESRD) is unsettled. This randomized trial evaluates the efficacy of high-dose folic acid in preventing events in ESRD. A total of 510 patients on chronic dialysis were randomized to 1, 5, or 15 mg of folic acid contained in a renal multivitamin with a median follow-up of 24 mo. Mortality, cardiovascular events, and homocysteine levels were assessed. There were 189 deaths, and 121 patients experienced at least one cardiovascular event. Composite rates of mortality and cardiovascular events among the folic acid groups did not differ (at 24 mo: 43.7% in 1 mg group, 38.6% in 5 mg group, 47.1% in 15 mg group; log-rank P = 0.47). Unexpectedly, high baseline tHcy was associated with lower event rates. From lowest to highest quartile, event rates at 24 mo were 54.5% for Q1, 41.8% for Q2, 41.2% for Q3, and 34.7% for Q4 (log-rank P = 0.033). In contrast to some studies describing tHcy as a risk factor for mortality and cardiovascular events, this study found a reverse relationship between tHcy and events in ESRD patients. Administration of high-dose folic acid did not affect event rates.
Abstract B28: Histone methylation-mediated silencing of mir-139 enhances an aggressive phenotype of non-small cell lung cancer.
Authors: Kousuke Watanabe, Mitsuhiro Sunohara, Yosuke Amano, Rie Ishikawa, Junji Ichinose, Jun Nakajima, Masashi Fukayama, Yutaka Yatomi, Takahide Nagase, Nobuya Ohishi, Daiya Takai
Journal: Clinical Cancer Research (2014)

Abstract MicroRNA expression is frequently altered in human cancers, and some microRNAs act as oncogenes or tumor suppressors. Mir-139 has recently been reported to function as a tumor suppressor in hepatocellular carcinoma and gastric cancer, but its function in non-small cell lung cancer (NSCLC) and the mechanism of its suppression have not been studied in detail. Mir-139 was suppressed frequently in lung cancer cell lines and primary NSCLCs. Mir-139 was silenced with its host gene PDE2A by histone methylation, which was independent of DNA methylation. In primary NSCLCs, decreased expression of mir-139 was significantly associated with distant lymph node metastasis and histological invasiveness (lymphatic invasion and vascular invasion) on both univariate and multivariate analyses. Overexpression of mir-139 suppressed the proliferation of lung cancer cells. Collectively, these results suggest that histone methylation-mediated silencing of mir-139 enhances an aggressive phenotype of lung cancer. Citation Format: Kousuke Watanabe, Mitsuhiro Sunohara, Yosuke Amano, Rie Ishikawa, Junji Ichinose, Jun Nakajima, Masashi Fukayama, Yutaka Yatomi, Takahide Nagase, Nobuya Ohishi, Daiya Takai. Histone methylation-mediated silencing of mir-139 enhances an aggressive phenotype of non-small cell lung cancer. [abstract]. In: Proceedings of the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer; 2014 Jan 6-9; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2014;20(2Suppl):Abstract nr B28.