tbuckley/cabot-search huggingface dataset:
Non-CPAP therapies in obstructive sleep apnoea: mandibular advancement device therapy
Authors: Marie Marklund, Johan Verbraecken, Winfried Randerath
Journal: European Respiratory Journal (2011)

Mandibular advancement devices (MADs) represent the main non-continuous positive airway pressure (non-CPAP) therapy for patients with obstructive sleep apnoea (OSA). The aim of the European Respiratory Society Task Force was to review the evidence in favour of MAD therapy. Effects of tongue-retaining devices are not included in this report. Custom-made MADs reduce apnoea/hypopnoea index (AHI) and daytime sleepiness compared with placebo devices. CPAP more effectively diminishes AHI, while increasing data suggest fairly similar outcomes in relation to symptoms and cardiovascular health from these treatments. Patients often prefer MADs to CPAP. Milder cases and patients with a proven increase in upper airway size as a result of mandibular advancement are most likely to experience treatment success with MADs. A custom-made device titrated from an initial 50% of maximum mandibular advancement has been recommended. More research is needed to define the patients who will benefit from MAD treatment compared with CPAP, in terms of the effects on sleep-disordered breathing and on other diseases related to OSA. In conclusion, MADs are recommended for patients with mild to moderate OSA (Recommendation Level A) and for those who do not tolerate CPAP. The treatment must be followed up and the device adjusted or exchanged in relation to the outcome.
Survey of synovial fluid cryoprecipitates.
Authors: C L Ludivico, A R Myers
Journal: Annals of the Rheumatic Diseases (1980)

Synovial fluid cryoproteins from various inflammatory and noninflammatory arthritides were examined for the presence of immunoglobulin, fibrinogen, antiglobulin activity, and third component of complement and correlated with the synovial fluid leucocyte count. The majority of rheumatoid synovial fluid cryoproteins contained either IgG-IgM complexes or IgG alone. Contrary to previous reports, many synovial fluid cryoproteins from psoriasis, Reiter's syndrome, nonspecific acute polyarthritis, gout, and gonococcal arthritis also contained IgG and occasionally IgG-IgM complexes. Noninflammatory synovial fluids were less likely to contain any immunoglobulin. The highest concentration of cryoprotein was found in Reiter's syndrome. There was a significant (P < 0.05) correlation between the presence of immunoglobulin and the concentration of the synovial fluid cryoprotein with the synovial fluid leucocyte count. Since synovial fluid cryoproteins containing immunoglobulin are present in the synovial fluids of many diverse rheumatic diseases not postulated to be immune complex mediated, they may be a nonspecific phenomenon related to the degree of inflammation.
Circulating CD34<sup>+</sup>, CD133<sup>+</sup>, and Vascular Endothelial Growth Factor Receptor 2–Positive Endothelial Progenitor Cells in Myelofibrosis With Myeloid Metaplasia
Authors: Margherita Massa, Vittorio Rosti, Isabella Ramajoli, Rita Campanelli, Alessandro Pecci, Gianluca Viarengo, Valentina Meli, Monia Marchetti, Ronald Hoffman, Giovanni Barosi
Journal: Journal of Clinical Oncology (2005)

Endothelial progenitor cells (EPCs) are present in circulation and contribute to vasculogenesis in adults. We measured the number of circulating EPCs in patients with myelofibrosis with myeloid metaplasia (MMM), and we examined the relationship between the number of EPCs and severity of the MMM disease process.The number of EPCs was measured by assaying the CD34+CD133+ vascular endothelial growth factor receptor 2 (VEGFR2) -positive cell phenotype in 110 MMM patients, 16 patients with other Philadelphia-negative chronic myeloproliferative disorders (Ph-negative CMPDs), and 14 healthy participants. In four MMM patients, the capacity of selected CD34+ cells to form endothelial colonies (CFU-End) in vitro was tested.CD34+, CD133+, and VEGFR2-positive EPCs were detectable in unselected peripheral-blood cells of 50.9% MMM patients, 37.5% control patients, and 21% healthy participants. Patients with MMM had a median of 0.26% EPCs, significantly higher than that in healthy controls (median, 0%) and in patients with other Ph-negative CMPDs (median, 0.1%). In 14.5% of MMM patients, the numbers of EPCs were greater than the highest value found in patients with other Ph-negative CMPDs. CD34+ selected cells produced colony-forming unit-endothelial (CFU-End), which were vascular endothelial (VE) -cadherin positive, CD31+, von Willebrand factor positive, and CD45-. In MMM patients, the larger the number of EPCs, the smaller the number of circulating immature myeloid cells and circulating CD45+CD34+ hematopoietic progenitor cells. Increased numbers of EPCs were associated with younger age and a diagnosis of prefibrotic MMM.Circulating EPCs are elevated in MMM patients in the early stage of the disease. Heightened mobilization of EPCs may represent an important mechanism for development of neoangiogenesis in MMM.
Paracrine Signaling Through MYCN Enhances Tumor-Vascular Interactions in Neuroblastoma
Authors: Yvan H. Chanthery, W. Clay Gustafson, Melissa Itsara, Anders Persson, Christopher S. Hackett, Matt Grimmer, Elise Charron, Slava Yakovenko, Grace Kim, Katherine K. Matthay, William A. Weiss
Journal: Science Translational Medicine (2012)

PI3K/mTOR inhibitors inhibit angiogenesis by blocking MYCN-dependent paracrine signaling between tumor and endothelial cells.
Disclosure of Researcher Contributions: A Study of Original Research Articles in The Lancet
Authors: Veronica Yank
Journal: Annals of Internal Medicine (1999)

Background: Authorship disputes and abuses have increased in recent years. In response to a proposal that researcher contributions be specified for readers, The Lancet began disclosing such contributions at the end of original articles. Objective: To analyze the descriptions researchers use for their contributions and to determine how the order of names on the byline corresponds to these contributions, whether persons listed on the byline fulfill a lenient version of the criteria for authorship specified by the International Committee of Medical Journal Editors (the Vancouver Group), and whether the contributions of persons listed as contributors overlap with the contributions of those who are acknowledged. Design: Descriptive study. Measurements: A taxonomy of researchers' contributions was developed and applied to researchers' self-reported contributions to original research articles published in The Lancet from July to December 1997. Results: Contributors lists occupied little page space (mean, 2.5 cm of column length). Placement on the byline did not indicate the specific category of task performed, although the first-contributor position corresponded to a significantly greater number of contributions (mean numbers of contributions: first-contributor position, 3.23; second-contributor position, 2.51; third-contributor position, 2.20; and fourth-contributor position, 2.51) (P < 0.01). Forty-four percent of contributors on the byline did not fulfill a lenient version of the Vancouver Group's criteria for authorship. Sixty percent of the most common categories of activities described on contributors lists overlapped with those on acknowledgments lists. Conclusions: Publication of lists that specify contributions to research articles is feasible and seems to impart important information. The criteria for authorship outlined by the Vancouver Group do not seem to be congruent with the self-identified contributions of researchers.
Fish oil increases antioxidant enzyme activities in macrophages and reduces atherosclerotic lesions in apoE-knockout mice
Authors: H Wang
Journal: Cardiovascular Research (2003)

The molecular and cellular mechanisms that fish oil (FO) exerts its physiological function are complicated. The present study brings evidence on the in vivo effect of FO on the development of atherosclerosis in apolipoprotein E knockout (apoE(-/-)) mice. We also test the hypothesis that the modulation of the cellular oxidative stress and antioxidant status contributes to the anti-atherosclerotic effect of FO.ApoE(-/-) mice were fed a diet rich either in FO or corn oil (CO) for 10 weeks. Both FO and CO had a plasma triacylglycerol-raising effect in apoE(-/-) mice, whereas aortic atherosclerotic lesions were significantly reduced in the mice that had consumed a high FO diet compared to those fed a high CO diet. The levels of hepatic superoxide dismutase (SOD) and catalase (CAT) activities were remarkably higher in the mice fed the FO diet than in mice fed the CO diet and the control diet. We then investigated the effects of FO and CO on the production of superoxide anion (O2*-)) and reactive oxygen species (ROS) in cultured J774 macrophages. Antioxidant status was assessed by the determination of antioxidant enzyme activities. Both FO and CO induced high levels of O2*-) and total ROS at a short time in macrophages. However, only the FO group restored the induction of O2*-) and ROS to near basal levels after oil treatment for 24 h. Throughout the time course experiments, antioxidant enzyme activities in the FO group mostly displayed a greater increase than in the corresponding CO group after the same time period of oil treatment.In the present study, FO reduced the formation of atherosclerotic lesions in the aortic arteries of apoE(-/-) mice not through any lipid-lowering effect. The protective role of FO in the development of atherosclerosis may result from its antioxidative defense mechanism through the induction of antioxidant enzyme activities.
Increased concentrations of proteoglycan components in the synovial fluids of patients with acute but not chronic joint disease.
Authors: A Ratcliffe, M Doherty, R N Maini, T E Hardingham
Journal: Annals of the Rheumatic Diseases (1988)

Synovial fluid samples (139) from 121 patients with rheumatoid arthritis, osteoarthritis, pseudogout, chronic pyrophosphate arthritis, gout, and reactive arthritis were analysed for cartilage proteoglycan components. Keratan sulphate (KS) epitope was determined by a competitive radioimmunoassay, and total sulphated glycosaminoglycans (S-GAG) were determined after papain digestion by a specific dye binding assay. Increased concentration of both KS epitope and S-GAG were found in synovial fluid from joints with acute inflammatory arthropathy (gout, pseudogout, and reactive arthritis). Analysis of consecutive samples from the same joint at different stages showed that the concentration of KS epitope or total S-GAG varied with acute inflammatory activity. In samples from patients with chronic conditions during active and inactive inflammatory phases concentrations were much lower and not distinguishable among these disease groups. The detection of raised concentration of proteoglycan components may reflect the rapid depletion or greatly increased turnover of proteoglycan in the articular cartilage during acute inflammation in the joint. This did not appear to be sustained in most patients with chronic joint diseases.
Luminal distension as a possible consequence of experimental intestinal perfusion
Authors: D. Wingate, A. Hyams, S. Phillips
Journal: Gut (1974)

In an experimental jejunal perfusion study, distress in healthy subjects occurred during eight out of 16 perfusions in which intestinal secretion was provoked. Calculation demonstrates the volumetric consequences of inadequate recovery of secretory perfusates, and analysis of the perfusion studies shows that distress was significantly associated with poor recovery of the perfusate. These observations are pertinent to increasing interest in the phenomenon of intestinal fluid secretion.
P2Y6 receptor mediates colonic NaCl secretion via differential activation of cAMP-mediated transport
Authors: Michael Köttgen, Thomas Löffler, Christoph Jacobi, Roland Nitschke, Hermann Pavenstädt, Rainer Schreiber, Sebastian Frische, Søren Nielsen, Jens Leipziger
Journal: Journal of Clinical Investigation (2003)

Extracellular nucleotides are important regulators of epithelial ion transport. Here we investigated nucleotide-mediated effects on colonic NaCl secretion and the signal transduction mechanisms involved. Basolateral UDP induced a sustained activation of Cl(-) secretion, which was completely inhibited by 293B, a specific inhibitor of cAMP-stimulated basolateral KCNQ1/KCNE3 K(+) channels. We therefore speculated that a basolateral P2Y(6) receptor could increase cAMP. Indeed UDP elevated cAMP in isolated crypts. We identified an epithelial P2Y(6) receptor using crypt [Ca(2+)](i) measurements, RT-PCR, and immunohistochemistry. To investigate whether the rat P2Y(6)elevates cAMP, we coexpressed the P2Y(1) or P2Y(6) receptor together with the cAMP-regulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel in Xenopus oocytes. A two-electrode voltage clamp was used to monitor nucleotide-induced Cl(-) currents. In oocytes expressing the P2Y(1) receptor, ATP transiently activated the endogenous Ca(2+)-activated Cl(-) current, but not CFTR. In contrast, in oocytes expressing the P2Y(6)receptor, UDP transiently activated the Ca(2+)-activated Cl(-) current and subsequently CFTR. CFTR Cl(-) currents were identified by their halide conductance sequence. In summary we find a basolateral P2Y(6) receptor in colonic epithelial cells stimulating sustained NaCl secretion by way of a synergistic increase of [Ca(2+)](i) and cAMP. In support of these data P2Y(6) receptor stimulation differentially activates CFTR in Xenopus oocytes.
Improvements in Transcatheter Aortic Valve Implantation Outcomes in Lower Surgical Risk Patients
Authors: Ruediger Lange, Sabine Bleiziffer, Domenico Mazzitelli, Yacine Elhmidi, Anke Opitz, Marcus Krane, Marcus-Andre Deutsch, Hendrik Ruge, Gernot Brockmann, Bernhard Voss, Christian Schreiber, Peter Tassani, Nicolo Piazza
Journal: Journal of the American College of Cardiology (2011)
Digital ischaemia due to vascular anomalies
Authors: NEVILLE ROWELL
Journal: British Journal of Dermatology (1977)

Journal Article Digital ischaemia due to vascular anomalies Get access NEVILLE ROWELL NEVILLE ROWELL Department of Dermatology, General Infirmary at Leeds Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 96, Issue 6, 1 June 1977, Pages 615–621, https://doi.org/10.1111/j.1365-2133.1977.tb05205.x Published: 01 June 1977
Duration of Adjuvant Chemotherapy for Colon Cancer and Survival Among the Elderly
Authors: Alfred I. Neugut, Matthew Matasar, Xiaoyan Wang, Russell McBride, Judith S. Jacobson, Wei-Yann Tsai, Victor R. Grann, Dawn L. Hershman
Journal: Journal of Clinical Oncology (2006)

In randomized trials, patients with stage III colon cancer who received 6 months of fluorouracil (FU)-based adjuvant chemotherapy had better survival than patients who did not. However, little is known about the predictors of, or the survival associated with, duration of chemotherapy in the community.The linked Surveillance, Epidemiology, and End Results-Medicare database was used to identify individuals > or = 65 years of age diagnosed with stage III colon cancer between 1995 and 1999. We used logistic and Cox proportional hazards regression models to analyze factors associated with early discontinuation of FU-based chemotherapy among these elderly colon cancer patients.Among 1,722 patients who received 1 to 7 months of FU-based chemotherapy, older age, being unmarried, and having comorbid conditions were associated with receiving less than 5 months of treatment. Among the 1,579 patients who survived > or = 8 months, the 1,091 (69.1%) who received 5 to 7 months of treatment had lower overall (hazard ratio [HR], 0.59; 95%, CI 0.49 to 0.71) and colon cancer-specific (HR, 0.53; 95% CI, 0.43 to 0.66) mortality than the 488 (30.9%) who received 1 to 4 months of treatment.More than 30% of elderly patients who initiated FU-based chemotherapy for stage III colon cancer and survived for at least 8 months discontinued treatment early. Mortality rates among such patients were nearly twice as high as among patients who completed 5 to 7 months of treatment. If the association we observed between duration of treatment and survival is confirmed, additional investigation is warranted to determine whether dose-intensity, cumulative dose, or other factors related to receipt of full adjuvant treatment are responsible.
Mechanisms of Synapse and Dendrite Maintenance and Their Disruption in Psychiatric and Neurodegenerative Disorders
Authors: Yu-Chih Lin, Anthony J. Koleske
Journal: Annual Review of Neuroscience (2010)

Emerging evidence indicates that once established, synapses and dendrites can be maintained for long periods, if not for the organism's entire lifetime. In contrast to the wealth of knowledge regarding axon, dendrite, and synapse development, we understand comparatively little about the cellular and molecular mechanisms that enable long-term synapse and dendrite maintenance. Here, we review how the actin cytoskeleton and its regulators, adhesion receptors, and scaffolding proteins mediate synapse and dendrite maintenance. We examine how these mechanisms are reinforced by trophic signals passed between the pre- and postsynaptic compartments. We also discuss how synapse and dendrite maintenance mechanisms are compromised in psychiatric and neurodegenerative disorders.
Guidelines of care for cutaneous squamous cell carcinoma
Authors: Lynn A. Drake, Roger I. Ceilley, Raymond L. Cornelison, William A. Dobes, William Dorner, Robert W. Goltz, Charles W. Lewis, Stuart J. Salasche, Maria L. Chanco Turner, Stuart Salasche, Scott M. Dinehart, Sheldon V. Pollack, John W. Skouge
Journal: Journal of the American Academy of Dermatology (1993)
Role of cysteinyl leukotrienes in the proliferation and the migration of murine vascular smooth muscle cells in vivo and in vitro
Authors: Y KAETSU, Y YAMAMOTO, S SUGIHARA, T MATSUURA, G IGAWA, K MATSUBARA, O IGAWA, C SHIGEMASA, I HISATOME
Journal: Cardiovascular Research (2007)

Objective Cysteinyl leukotrienes (Cys-LTs) are proinflammatory lipid mediators generated from arachidonic acid through 5-lipoxygenase (5-LO). It was reported that the 5-LO pathway is associated with vascular smooth muscle cell (VSMC) proliferation and migration; however, the relationship between Cys-LTs and VSMC proliferation and migration remains unclear.
Cetuximab-Induced Anaphylaxis and IgE Specific for Galactose-α-1,3-Galactose
Authors: Christine H. Chung, Beloo Mirakhur, Emily Chan, Quynh-Thu Le, Jordan Berlin, Michael Morse, Barbara A. Murphy, Shama M. Satinover, Jacob Hosen, David Mauro, Robbert J. Slebos, Qinwei Zhou, Diane Gold, Tina Hatley, Daniel J. Hicklin, Thomas A.E. Platts-Mills
Journal: New England Journal of Medicine (2008)

Cetuximab, a chimeric mouse-human IgG1 monoclonal antibody against the epidermal growth factor receptor, is approved for use in colorectal cancer and squamous-cell carcinoma of the head and neck. A high prevalence of hypersensitivity reactions to cetuximab has been reported in some areas of the United States.We analyzed serum samples from four groups of subjects for IgE antibodies against cetuximab: pretreatment samples from 76 case subjects who had been treated with cetuximab at multiple centers, predominantly in Tennessee, Arkansas, and North Carolina; samples from 72 control subjects in Tennessee; samples from 49 control subjects with cancer in northern California; and samples from 341 female control subjects in Boston.Among 76 cetuximab-treated subjects, 25 had a hypersensitivity reaction to the drug. IgE antibodies against cetuximab were found in pretreatment samples from 17 of these subjects; only 1 of 51 subjects who did not have a hypersensitivity reaction had such antibodies (P<0.001). IgE antibodies against cetuximab were found in 15 of 72 samples (20.8%) from control subjects in Tennessee, in 3 of 49 samples (6.1%) from northern California, and in 2 of 341 samples (0.6%) from Boston. The IgE antibodies were shown to be specific for an oligosaccharide, galactose-alpha-1,3-galactose, which is present on the Fab portion of the cetuximab heavy chain.In most subjects who had a hypersensitivity reaction to cetuximab, IgE antibodies against cetuximab were present in serum before therapy. The antibodies were specific for galactose-alpha-1,3-galactose.
Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
Authors: Manali S. Bendre, Aaron G. Margulies, Brandon Walser, Nisreen S. Akel, Sudeepa Bhattacharrya, Robert A. Skinner, Frances Swain, Vishnu Ramani, Khalid S. Mohammad, Lisa L. Wessner, Alfredo Martinez, Theresa A. Guise, John M. Chirgwin, Dana Gaddy, Larry J. Suva
Journal: Cancer Research (2005)

Abstract Bone is a common site of cancer metastasis. Breast, prostate, and lung cancers show a predilection to metastasize to bone. Recently, we reported that the chemokine interleukin 8 (IL-8) stimulates both human osteoclast formation and bone resorption. IL-8 mRNA expression was surveyed in a panel of human breast cancer lines MDA-MET, MDA-MB-231, MDA-MB-435, MCF-7, T47D, and ZR-75, and the human lung adenocarcinoma cell line A549. IL-8 mRNA expression was higher in cell lines with higher osteolytic potential in vivo. Human osteoclast formation was increased by MDA-MET or A549 cell-conditioned medium, but not by MDA-MB-231. Pharmacologic doses of receptor activator of nuclear factor-κB (RANK)-Fc or osteoprotogerin had no effect on the pro-osteoclastogenic activity of the conditioned medium; however, osteoclast formation stimulated by conditioned medium was inhibited 60% by an IL-8-specific neutralizing antibody. The data support a model in which tumor cells cause osteolytic bone destruction independently of the RANK ligand (RANKL) pathway. Tumor-produced IL-8 is a major contributor to this process. The role of secreted IL-8 isoforms was examined by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry, which detected distinct IL-8 isoforms secreted by MDA-MET and MDA-231 cells, suggesting different pro-osteoclastogenic activities of the two IL-8-derived peptides. These data indicate that (a) osteoclast formation induced by MDA-MET breast cancer cells and A549 adenocarcinoma cells is primarily mediated by IL-8, (b) cell-specific isoforms of IL-8 with distinct osteoclastogenic activities are produced by tumor cells, and (c) tumor cells that support osteoclast formation independent of RANKL secrete other pro-osteoclastogenic factors in addition to IL-8.