tbuckley/cabot-search huggingface dataset:
Outcome of domiciliary nasal intermittent positive pressure ventilation in restrictive and obstructive disorders.
Authors: A K Simonds, M W Elliott
Journal: Thorax (1995)

Nasal intermittent positive pressure ventilation (NIPPV) is a new technique which has rapidly supplanted other non-invasive methods of ventilation over the last 5-10 years. Data on its effectiveness are limited.The outcome of long term domiciliary NIPPV has been analysed in 180 patients with hypercapnic respiratory failure predominantly due to chest wall restriction, neuromuscular disorders, or chronic obstructive lung disease. One hundred and thirty eight patients were started on NIPPV electively, and 42 following an acute hypercapnic exacerbation. Outcome measures were survival (five year probability of continuing NIPPV), pulmonary function, and health status. A crossover study from negative pressure ventilation to NIPPV was carried out in a subgroup of patients.Five year acturial probability of continuing NIPPV for individuals with early onset scoliosis (n = 47), previous poliomyelitis (n = 30), following tuberculous lung disease (n = 20), general neuromuscular disorders (n = 29), and chronic obstructive pulmonary disease (n = 33) was 79% (95% CI 66 to 92), 100%, 94% (95% CI 83 to 100), 81% (95% CI 61 to 100), 43% (95% CI 6 to 80), respectively. Most of the patients with bronchiectasis died within two years. One year after starting NIPPV electively the mean (SD) PaO2 compared with the pretreatment value was +1.8 (1.9) kPa, mean PaCO2 -1.4 (1.3) kPa in patients with extrapulmonary restrictive disorders, and PaO2 +0.8 (1.0) kPa, PaCO2 -0.9 (0.8) kPa in patients with obstructive lung disease. Arterial blood gas tensions improved in patients transferred from negative pressure ventilation to NIPPV. Health status was ranked highest in patients with early onset scoliosis, previous poliomyelitis, and following tuberculous lung disease. In the group as a whole health perception was comparable to outpatients with other chronic disorders.The long term outcome of domiciliary NIPPV in patients with chronic respiratory failure due to scoliosis, previous poliomyelitis, and chest wall and pulmonary disease secondary to tuberculosis is encouraging. The results of NIPPV in patients with COPD and progressive neuromuscular disorders show benefit in some subgroups. The outcome in end stage bronchiectasis is poor.
Human Epicardial Adipose Tissue Is a Source of Inflammatory Mediators
Authors: Tomasz Mazurek, LiFeng Zhang, Andrew Zalewski, John D. Mannion, James T. Diehl, Hwyda Arafat, Lea Sarov-Blat, Shawn O’Brien, Elizabeth A. Keiper, Anthony G. Johnson, Jack Martin, Barry J. Goldstein, Yi Shi
Journal: Circulation (2003)

Inflammatory mediators that originate in vascular and extravascular tissues promote coronary lesion formation. Adipose tissue may function as an endocrine organ that contributes to an inflammatory burden in patients at risk of cardiovascular complications. In this study, we sought to compare expression of inflammatory mediators in epicardial and subcutaneous adipose stores in patients with critical CAD.Paired samples of epicardial and subcutaneous adipose tissues were harvested at the outset of elective CABG surgery (n=42; age 65+/-10 years). Local expression of chemokine (monocyte chemotactic protein [MCP]-1) and inflammatory cytokines (interleukin [IL]-1beta, IL-6, and tumor necrosis factor [TNF]-alpha) was analyzed by TaqMan real-time reverse transcription-polymerase chain reaction (mRNA) and by ELISA (protein release over 3 hours). Significantly higher levels of IL-1beta, IL-6, MCP-1, and TNF-alpha mRNA and protein were observed in epicardial adipose stores. Proinflammatory properties of epicardial adipose tissue were noted irrespective of clinical variables (diabetes, body mass index, and chronic use of statins or ACE inhibitors/angiotensin II receptor blockers) or plasma concentrations of circulating biomarkers. In a subset of samples (n=11), global gene expression was explored by DNA microarray hybridization and confirmed the presence of a broad inflammatory reaction in epicardial adipose tissue in patients with coronary artery disease. The above findings were paralleled by the presence of inflammatory cell infiltrates in epicardial adipose stores.Epicardial adipose tissue is a source of several inflammatory mediators in high-risk cardiac patients. Plasma inflammatory biomarkers may not adequately reflect local tissue inflammation. Current therapies do not appear to eliminate local inflammatory signals in epicardial adipose tissue.
Skeletal effects of exemestane on bone-mineral density, bone biomarkers, and fracture incidence in postmenopausal women with early breast cancer participating in the Intergroup Exemestane Study (IES): a randomised controlled study
Authors: Robert E Coleman, Linda M Banks, Samia I Girgis, Lucy S Kilburn, Eduard Vrdoljak, John Fox, Simon J Cawthorn, Ashraf Patel, Claire F Snowdon, Emma Hall, Judith M Bliss, R Charles Coombes
Journal: The Lancet Oncology (2007)
Dichloroacetate Prevents and Reverses Pulmonary Hypertension by Inducing Pulmonary Artery Smooth Muscle Cell Apoptosis
Authors: M. Sean McMurtry, Sebastien Bonnet, Xichen Wu, Jason R.B. Dyck, Alois Haromy, Kyoko Hashimoto, Evangelos D. Michelakis
Journal: Circulation Research (2004)

The pulmonary arteries (PA) in pulmonary arterial hypertension (PAH) are constricted and remodeled;. They have suppressed apoptosis, partly attributable to suppression of the bone morphogenetic protein axis and selective downregulation of PA smooth muscle cell (PASMC) voltage-gated K + channels, including Kv1.5. The Kv downregulation-induced increase in [K + ] i , tonically inhibits caspases, further suppressing apoptosis. Mitochondria control apoptosis and produce activated oxygen species like H 2 O 2 , which regulate vascular tone by activating K + channels, but their role in PAH is unknown. We show that dichloroacetate (DCA), a metabolic modulator that increases mitochondrial oxidative phosphorylation, prevents and reverses established monocrotaline-induced PAH (MCT-PAH), significantly improving mortality. Compared with MCT-PAH, DCA-treated rats (80 mg/kg per day in drinking water on day 14 after MCT, studied on day 21) have decreased pulmonary, but not systemic, vascular resistance (63% decrease, P &lt;0.002), PA medial thickness (28% decrease, P &lt;0.0001), and right ventricular hypertrophy (34% decrease, P &lt;0.001). DCA is similarly effective when given at day 1 or day 21 after MCT (studied day 28) but has no effect on normal rats. DCA depolarizes MCT-PAH PASMC mitochondria and causes release of H 2 O 2 and cytochrome c, inducing a 10-fold increase in apoptosis within the PA media (TUNEL and caspase 3 activity) and decreasing proliferation (proliferating-cell nuclear antigen and BrdU assays). Immunoblots, immunohistochemistry, laser-captured microdissection-quantitative reverse-transcription polymerase chain reaction and patch-clamping show that DCA reverses the Kv1.5 downregulation in resistance PAs. In summary, DCA reverses PA remodeling by increasing the mitochondria-dependent apoptosis/proliferation ratio and upregulating Kv1.5 in the media. We identify mitochondria-dependent apoptosis as a potential target for therapy and DCA as an effective and selective treatment for PAH.
Pulmonary hypertension in patients with chronic myeloproliferative disorders
Authors: Y. Adir, M. Humbert
Journal: European Respiratory Journal (2010)

Pulmonary hypertension (PH) is a severe haemodynamic disorder in which the pulmonary artery pressure is persistently elevated, leading to right-sided heart failure and death. Recently, chronic myeloproliferative diseases associated with pulmonary hypertension were included in the group 5 category, corresponding to PH for which the aetiology is unclear and/or multifactorial. In this review we will describe the distinct forms of PH in the context of the myeloproliferative diseases chronic thromboembolic pulmonary hypertension and pre-capillary PH mimicking pulmonary arterial hypertension. The epidemiology, mechanisms and treatment approaches will be discussed.
Corneal Confocal Microscopy
Authors: Mitra Tavakoli, Cristian Quattrini, Caroline Abbott, Panagiotis Kallinikos, Andrew Marshall, Joanne Finnigan, Philip Morgan, Nathan Efron, Andrew J.M. Boulton, Rayaz A. Malik
Journal: Diabetes Care (2010)

The accurate quantification of human diabetic neuropathy is important to define at-risk patients, anticipate deterioration, and assess new therapies.A total of 101 diabetic patients and 17 age-matched control subjects underwent neurological evaluation, neurophysiology tests, quantitative sensory testing, and evaluation of corneal sensation and corneal nerve morphology using corneal confocal microscopy (CCM).Corneal sensation decreased significantly (P = 0.0001) with increasing neuropathic severity and correlated with the neuropathy disability score (NDS) (r = 0.441, P < 0.0001). Corneal nerve fiber density (NFD) (P < 0.0001), nerve fiber length (NFL), (P < 0.0001), and nerve branch density (NBD) (P < 0.0001) decreased significantly with increasing neuropathic severity and correlated with NDS (NFD r = -0.475, P < 0.0001; NBD r = -0.511, P < 0.0001; and NFL r = -0.581, P < 0.0001). NBD and NFL demonstrated a significant and progressive reduction with worsening heat pain thresholds (P = 0.01). Receiver operating characteristic curve analysis for the diagnosis of neuropathy (NDS >3) defined an NFD of <27.8/mm(2) with a sensitivity of 0.82 (95% CI 0.68-0.92) and specificity of 0.52 (0.40-0.64) and for detecting patients at risk of foot ulceration (NDS >6) defined a NFD cutoff of <20.8/mm(2) with a sensitivity of 0.71 (0.42-0.92) and specificity of 0.64 (0.54-0.74).CCM is a noninvasive clinical technique that may be used to detect early nerve damage and stratify diabetic patients with increasing neuropathic severity.
Evolving concepts on the value of adenosine hyperresponsiveness in asthma and chronic obstructive pulmonary disease
Authors: R Polosa
Journal: Thorax (2002)

Adenosine is a purine nucleoside which mediates a variety of cellular responses relevant to asthma and COPD through interaction with specific receptors. Administration of adenosine by inhalation to patients with asthma and COPD is known to cause concentration related bronchoconstriction. Responses elicited by this purine derivative in asthma and COPD should not be considered as a mere reflection of non-specific airways hyperresponsiveness. Evaluation of airways responsiveness by adenosine induced bronchoconstriction may be valuable in differentiating asthma from COPD, monitoring of anti-inflammatory treatment in asthma, surveying disease progression, and assessing disease activity in relation to allergic airways inflammation.
Medulloblastomas and primitive neuroectodermal tumors rarely contain polyomavirus DNA sequences
Authors: John Y.H. Kim, Igor J. Koralnik, Mark LeFave, Rosalind A. Segal, Luz-Andrea Pfister, Scott L. Pomeroy
Journal: Neuro-Oncology (2002)

To address the hypothesis that medulloblastoma or supratentorial primitive neuroectodermal tumor (sPNET) can arise through infection by polyomaviruses, we examined genomic DNA isolated from 15 primary medulloblastoma and 5 sPNET biopsy specimens and from 2 medulloblastoma cell lines for the presence of DNA sequences from the polyomaviruses simian virus 40 (SV40), JC virus, and BK virus. These polyomaviruses have oncogenic potential in animals, and their DNA sequences have been detected in other surveys of various solid tumors, including childhood brain tumors. The tumor DNA samples were analyzed by Southern blot hybridization of polymerase chain reaction products that employed probes designed to detect specific polyomavirus sequences. Neither JC virus nor BK virus DNA sequences were detected in any of the specimens. None of the primary medulloblastoma or sPNET specimens contained SV40 sequences. However, SV40 DNA coding and noncoding sequences were detected in the D283-Med (medulloblastoma) cell line. Immunocytochemical studies of D283-Med revealed nuclear expression of SV40 large T antigen. In contrast to childhood ependymomas and choroid plexus tumors, medulloblastomas and sPNETs infrequently express evidence of polyomavirus infection.
Analysis of proteomic profiles and functional properties of human peripheral blood myeloid dendritic cells, monocyte-derived dendritic cells and the dendritic cell-like KG-1 cells reveals distinct characteristics
Authors: Claire Horlock, Farouk Shakib, Jafar Mahdavi, Nick S Jones, Herb F Sewell, Amir M Ghaemmaghami
Journal: Genome biology (2007)

Dendritic cells (DCs) are specialized antigen presenting cells that play a pivotal role in bridging innate and adaptive immune responses. Given the scarcity of peripheral blood myeloid dendritic cells (mDCs) investigators have used different model systems for studying DC biology. Monocyte-derived dendritic cells (moDCs) and KG-1 cells are routinely used as mDC models, but a thorough comparison of these cells has not yet been carried out, particularly in relation to their proteomes. We therefore sought to run a comparative study of the proteomes and functional properties of these cells. Despite general similarities between mDCs and the model systems, moDCs and KG-1 cells, our findings identified some significant differences in the proteomes of these cells, and the findings were confirmed by ELISA detection of a selection of proteins. This was particularly noticeable with proteins involved in cell growth and maintenance (for example, fibrinogen γ chain (FGG) and ubiquinol cytochrome c) and cell-cell interaction and integrity (for example, fascin and actin). We then examined the surface phenotype, cytokine profile, endocytic and T-cell-activation ability of these cells in support of the proteomic data, and obtained confirmatory evidence for differences in the maturation status and functional attributes between mDCs and the two DC models. We have identified important proteomic and functional differences between mDCs and two DC model systems. These differences could have major functional implications, particularly in relation to DC-T cell interactions, the so-called immunological synapse, and, therefore, need to be considered when interpreting data obtained from model DC systems.
Relation of titred peripheral pattern ANA to anti-DNA and disease activity in systemic lupus erythematosus.
Authors: R J Weitzman, S E Walker
Journal: Annals of the Rheumatic Diseases (1977)

This study compared the clinical usefulness of the peripheral pattern detected in immunofluorescent antinuclear antibody (ANA) testing with anti-DNA measured by the modified Farr technique. 48 patients with active or inactive systemic lupus erythematosus (SLE) were studied at one point in the course of their disease. There was no association between titres of serum giving a peripheral ANA pattern (tp-ANA) and anti-DNA values. Tp-ANA did not correlate with activity of SLE. In contrast with this finding, anti-DNA correlated with severity of renal disease, decreased serum complement, and number of SLE criteria. In a separate group of 9 patients with flare-ups of SLE, tp-ANA and anti-DNA fell as disease activity was controlled. Nevertheless, these two parameters were independent of one another. It was concluded that tp-ANA did not accurately reflect anti-DNA or activity of SLE.
POLYMORPHIC LIGHT ERUPTION.
Authors: DANILO V. STEVANOVIĆ
Journal: British Journal of Dermatology (1960)

Journal Article POLYMORPHIC LIGHT ERUPTION. Get access DANILO V. STEVANOVIĆ, M.D., M.Sc.(Cantab.). DANILO V. STEVANOVIĆ, M.D., M.Sc.(Cantab.). Department of Dermatology, University of Belgrade, Yugoslavia Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 72, Issue 7, 1 July 1960, Pages 261–270, https://doi.org/10.1111/j.1365-2133.1960.tb13889.x Published: 01 July 1960
Complications After Robot-assisted Radical Cystectomy: Results from the International Robotic Cystectomy Consortium
Authors: Raza S. Johar, Matthew H. Hayn, Andrew P. Stegemann, Kamran Ahmed, Piyush Agarwal, M. Derya Balbay, Ashok Hemal, Adam S. Kibel, Fred Muhletaler, Kenneth Nepple, John G. Pattaras, James O. Peabody, Joan Palou Redorta, Koon-Ho Rha, Lee Richstone, Matthias Saar, Francis Schanne, Douglas S. Scherr, Stefan Siemer, Michael Stökle, Alon Weizer, Peter Wiklund, Timothy Wilson, Michael Woods, Bertrum Yuh, Khurshid A. Guru
Journal: European Urology (2013)
TCT-692 Multicentre clinical study evaluating a novel resheatable self-expanding transcatheter aortic valve system
Authors: Ganesh Manoharan, Axel Linke, Helge Moellmann, Martyn Thomas, Ulrich Schäfer, Karl-Heinz Kuck, Stephen G. Worthley, Alexander Lauten, Gerhard Schymik, A.J. van Boven, Christian Butter, Lars Sondergaard, Thomas Walther
Journal: Journal of the American College of Cardiology (2014)
Novel Tumor-Specific Isoforms of BEHAB/Brevican Identified in Human Malignant Gliomas
Authors: Mariano S. Viapiano, Wenya Linda Bi, Joseph Piepmeier, Susan Hockfield, Russell T. Matthews
Journal: Cancer Research (2005)

Abstract Malignant gliomas are deadly brain tumors characterized by diffuse invasion into the surrounding brain tissue. Understanding the mechanisms involved in glioma invasion could lead to new therapeutic strategies. We have previously shown that BEHAB/brevican, an extracellular matrix protein in the central nervous system, plays a role in the invasive ability of gliomas. The mechanisms that underlie BEHAB/brevican function are not yet understood, due in part to the existence of several isoforms that may have different functions. Here we describe for the first time the expression of BEHAB/brevican in human brain and characterize two novel glioma-specific isoforms, B/bsia and B/bΔg, which are generated by differential glycosylation and are absent from normal adult brain and other neuropathologies. B/bsia is an oversialylated isoform expressed by about half the high- and low-grade gliomas analyzed. B/bΔg lacks most of the carbohydrates typically present on BEHAB/brevican and is the major up-regulated isoform of this protein in high-grade gliomas but is absent in a specific subset of low-grade, indolent oligodendrogliomas. B/bΔg is detected on the extracellular surface, where it binds to the membrane by a mechanism distinct from the other BEHAB/brevican isoforms. The glioma-specific expression of B/bΔg, its restricted membrane localization, and its expression in all high-grade gliomas tested to date suggest that it may play a significant role in glioma progression and make it an important new potential therapeutic target. In addition, its absence from benign gliomas prompts its use as a diagnostic marker to distinguish primary brain tumors of similar histology but different pathologic course.
Combination therapy with remote ischaemic conditioning and insulin or exenatide enhances infarct size limitation in pigs
Authors: Juan José Alburquerque-Béjar, Ignasi Barba, Javier Inserte, Elisabet Miró-Casas, Marisol Ruiz-Meana, Marcos Poncelas, Úrsula Vilardosa, Laura Valls-Lacalle, Antonio Rodríguez-Sinovas, David Garcia-Dorado
Journal: Cardiovascular Research (2015)

Remote ischaemic conditioning (RIC) has been shown to reduce myocardial infarct size in patients. Our objective was to investigate whether the combination of RIC with either exenatide or glucose–insulin–potassium (GIK) is more effective than RIC alone. Pigs were submitted to 40 min of coronary occlusion followed by reperfusion, and received (i) no treatment, (ii) one of the following treatments: RIC (5 min ischemia/5 min reperfusion × 4), GIK, or exenatide (at doses reducing infarct size in clinical trials), or (iii) a combination of two of these treatments (RIC + GIK or RIC + exenatide). After 5 min of reperfusion (n = 4/group), prominent phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) was observed, both in control and reperfused myocardium, in animals receiving GIK, and mitochondria from these hearts showed reduced ADP-stimulated respiration. 1H NMR-based metabonomics disclosed a shift towards increased glycolysis in GIK and exenatide groups. In contrast, oxidative stress (myocardial nitrotyrosine levels) and eNOS uncoupling were significantly reduced only by RIC. In additional experiments (n = 7–10/group), ANOVA demonstrated a significant effect of the number of treatments after 2 h of reperfusion on infarct size (triphenyltetrazolium, % of the area at risk; 59.21 ± 3.34, 36.64 ± 3.03, and 21.04 ± 2.38% for none, one, and two treatments, respectively), and significant differences between one and two treatments (P = 0.004) but not among individual treatments or between RIC + GIK and RIC + exenatide. GIK and exenatide activate cardioprotective pathways different from those of RIC, and have additive effects with RIC on infarct size reduction in pigs.
The Molecular Basis of Opioid Receptor Function
Authors: WILLIAM F. SIMONDS
Journal: Endocrine Reviews (1988)

An extensive body of pharmacological data demonstrates the existence of at least three opioid receptor subtypes mediating the diverse effects of opioids. Distinct binding and activity profiles of highly selective ligands, variable sensitivity to naloxone antagonisms, and selective protection and inactivation experiments strongly suggest that mu-, delta-, and kappa-opioid receptors represent recent discrete molecular entities. Purification and affinity labeling of receptor subunits are beginning to provide confirmation of this concept. The delta-opioid receptor affinity labeled and purified to homogeneity from NG108-15 cells comprises a glycoprotein subunit of Mr58,000 with one mol ligand bound/mol protein. Antibodies to this protein recognize native receptor in detergent solution and selectively bind to the Mr58,000 protein on immunoblots of partially purified preparations. Purification of the mu-opioid receptor from bovine striatum reveals a glycoprotein of Mr 65,000 which demonstrates opioid binding activity. Purification and affinity-labeling studies from other laboratories suggest a smaller size of Mr 58,000 for the mu-receptor however. The kappa-opioid receptor from guinea pig brain exhibits a unique mobility on sucrose density gradient centrifugation but has not been characterized in purified form. The primary structure of the opioid receptors, although unknown at present, will most likely reflect structural features of other inhibitory receptors coupled to G-proteins, with seven transmembrane helices and a large third cytoplasmic loop. Biochemical evidence clearly demonstrates the coupling of opioid receptors to Gi, accounting for opioid inhibition of adenylyl cyclase in neuronal cell culture and brain. Opioid inhibition of adenylyl cyclase has been reconstituted in IAP-treated NG108-15 cell membranes with a Gi preparation from brain. Electrophysiological evidence suggests that mu- and delta-opioid receptors can couple to a G-protein which mediates activation of inwardly rectifying potassium channels, perhaps to the same Gk mediating muscarinic potassium channel activation in heart. kappa-Opioid receptors are coupled to inhibition of voltage-dependent calcium channels in several neuronal systems. In NG108-15 cells opioid inhibition of calcium conductance is IAP sensitive and can be reconstituted with G-proteins purified from brain. Differences in the primary structure of mu-, delta-, and kappa-opioid receptors, as well as possible novel opioid receptor subtypes, will be defined by molecular cloning of recombinant DNA.(ABSTRACT TRUNCATED AT 400 WORDS)