tbuckley/cabot-search huggingface dataset:
Disappearance of Hyperplastic Polyps in the Stomach after Eradication of<i>Helicobacter pylori</i>
Authors: Toshifumi Ohkusa
Journal: Annals of Internal Medicine (1998)

Background: Helicobacter pylori infection is common in patients with hyperplastic gastric polyps. Objective: To study the effect of eradication of H. pylori on the clinical course of patients with hyperplastic gastric polyps. Design: Single-blind, randomized, controlled trial. Setting: University-based gastroenterology outpatient clinic. Patients: 35 patients with H. pylori infection and hyperplastic gastric polyps at least 3 mm in diameter. Intervention: Patients were randomly assigned to a treatment group (n = 17), which received a proton-pump inhibitor (omeprazole or lansoprazole), amoxicillin, and either clarithromycin or ecabet sodium, or to a control group (n = 18), which received no treatment. Measurements: Patients underwent endoscopy before enrollment and 12 to 15 months after the end of treatment. Serum gastrin levels and titers of IgG to H. pylori were measured. Results: In the treatment group, the polyps had disappeared by 3 to 15 months (average, 7.1 ± 1.2 months) after the end of treatment in 12 of all 17 patients (71%) and in 12 of the 15 patients (80%) in whom H. pylori was eradicated. However, 12 to 15 months after the start of the study, no change in polyps or H. pylori status was seen in any controls (P < 0.001). Histologic findings of inflammation and activity, serum gastrin levels, and titers of IgG to H. pylori showed significant regression in the treatment group compared with the control group (P < 0.01). Conclusions: Most hyperplastic polyps disappeared after eradication of H. pylori. Thus, eradication should be attempted before endoscopic removal is done in patients with hyperplastic gastric polyps and H. pylori infection.
Rationale, secondary outcome scores and 1-year follow-up of a randomised trial of platelet-rich plasma injections in acute hamstring muscle injury: the Dutch Hamstring Injection Therapy study
Authors: Gustaaf Reurink, Gert Jan Goudswaard, Maarten H Moen, Adam Weir, Jan A N Verhaar, Sita M A Bierma-Zeinstra, Mario Maas, Johannes L Tol
Journal: British Journal of Sports Medicine (2015)

Background Platelet-rich plasma (PRP) injections are an experimental treatment for acute muscle injuries. We examined whether PRP injections would accelerate return to play after hamstring injury. The methods and the primary outcome measure were published in the New England Journal of Medicine ( NEJM ) as ‘Platelet-rich plasma injections in acute muscle injury’ (2014). This article shares information not available in the NEJM letter or online supplement, especially the rationale behind the study and the secondary outcome measures including 1 year re-injury data. Methods We performed a multicentre, randomised, double-blind, placebo-controlled trial in 80 competitive and recreational athletes with acute hamstring muscle injuries. Details can be found in the NEJM ( http://www.nejm.org/doi/full/10.1056/NEJMc1402340 ). The primary outcome measure was the time needed to return to play during 6 months of follow-up. Not previously reported secondary outcome scores included re-injury at 1 year, alteration in clinical and MRI parameters, subjective patient satisfaction and the hamstring outcome score. Results In the earlier NEJM publication, we reported that PRP did not accelerate return to play; nor did we find a difference in the 2-month re-injury rate. We report no significant between-group difference in the 1-year re-injury rate (HR=0.89; 95% CI, 0.38 to 2.13; p=0.80) or any other secondary outcome measure. Conclusions At 1-year postinjection, we found no benefit of intramuscular PRP compared with placebo injections in patients with acute hamstring injuries in the time to return to play, re-injury rate and alterations of subjective, clinical or MRI measures.
Threshold Dose For Peanut Allergy During Peanut Oral Immunotherapy Procedure In Children
Authors: L. Christie, K.A. Althage, A.M. Scurlock, T.T. Perry, L. Pons, P. Steele, J. Kamilaris, S.M. Jones, A.W. Burks
Journal: Journal of Allergy and Clinical Immunology (2009)
Differential Effects of B Cell Receptor and B Cell Receptor–FcγRIIB1 Engagement on Docking of Csk to GTPase-activating Protein (GAP)-associated p62
Authors: Milena Vuica, Stephen Desiderio, Jonathan P. Schneck
Journal: The Journal of Experimental Medicine (1997)

The stimulatory and inhibitory pathways initiated by engagement of stimulatory receptors such as the B cell receptor for antigen (BCR) and inhibitory receptors such as Fcγ receptors of the IIB1 type (FcγRIIB1) intersect in ways that are poorly understood at the molecular level. Because the tyrosine kinase Csk is a potential negative regulator of lymphocyte activation, we examined the effects of BCR and FcγRIIB1 engagement on the binding of Csk to phosphotyrosine-containing proteins. Stimulation of a B lymphoma cell line, A20, with intact anti-IgG antibody induced a direct, SH2-mediated association between Csk and a 62-kD phosphotyrosine-containing protein that was identified as RasGTPase-activating protein–associated p62 (GAP-A.p62). In contrast, stimulation of A20 cells with anti-IgG F(ab′)2 resulted in little increase in the association of Csk with GAP-A.p62. The effect of FcγRIIB1 engagement on this association was abolished by blockade of FcγRIIB1 with the monoclonal antibody 2.4G2. Furthermore, the increased association between Csk and GAP-A.p62 seen upon stimulation with intact anti-Ig was abrogated in the FcγRIIB1-deficient cell line IIA1.6 and recovered when FcγRIIB1 expression was restored by transfection. The differential effects of BCR and BCR-FcγRIIB1–mediated signaling on the phosphorylation of GAP-A.p62 and its association with Csk suggest that docking of Csk to GAP-A.p62 may function in the negative regulation of antigen receptor–mediated signals in B cells.
CRAC: an integrated approach to the analysis of RNA-seq reads
Authors: Nicolas Philippe, Mikaël Salson, Thérèse Commes, Eric Rivals
Journal: Genome biology (2013)

Abstract A large number of RNA-sequencing studies set out to predict mutations, splice junctions or fusion RNAs. We propose a method, CRAC, that integrates genomic locations and local coverage to enable such predictions to be made directly from RNA-seq read analysis. A k -mer profiling approach detects candidate mutations, indels and splice or chimeric junctions in each single read. CRAC increases precision compared with existing tools, reaching 99:5% for splice junctions, without losing sensitivity. Importantly, CRAC predictions improve with read length. In cancer libraries, CRAC recovered 74% of validated fusion RNAs and predicted novel recurrent chimeric junctions. CRAC is available at http://crac.gforge.inria.fr .
The natural immune response to inhaled soluble protein antigens involves major histocompatibility complex (MHC) class I-restricted CD8+ T cell-mediated but MHC class II-restricted CD4+ T cell-dependent immune deviation resulting in selective suppression of immunoglobulin E production.
Authors: C McMenamin, P G Holt
Journal: The Journal of Experimental Medicine (1993)

The immunological basis for atopy is currently ascribed to an inherent bias in the CD4+ T cell response to nonreplicating antigens presented at mucosal surfaces, resulting in dominance of the T helper 2 (Th2) interleukin 4 (IL-4)-producing phenotype, which favors IgE production. In contrast, the "normal" response to such antigens involves a predominance of interferon gamma (IFN-gamma)-producing Th1 clones. This difference has been suggested to be the result of active selection in atopics for Th2 (and hence against Th1) clones at the time of initial antigen presentation. In the study below, we demonstrate that the natural immune response to inhaled protein antigens, particularly in animals expressing the low immunoglobulin E (IgE) responder phenotype, includes a major histocompatibility complex (MHC) class I-restricted CD8+ T cell component, the appearance of which is associated with active suppression of IgE antibody production. Thus, continued exposure of rats to aerosolized ovalbumin (OVA) antigen elicits a transient IgE response, that is terminated by the onset of a state of apparent "tolerance" to further challenge, and this tolerant state is transferable to naive animals with CD8+ T cells. Kinetic studies on in vitro T cell reactivity in these aerosol-exposed rats demonstrated biphasic CD4+ Th2 responses which terminated, together with IgE antibody production, and coincident with the appearance of MHC class I-restricted OVA-specific IFN-gamma-producing CD8+ T cells. However, the latter were not autonomous in vitro and required a source of exogenous IL-2 for initial activation, which in CD(8+)-enriched splenocyte cultures could be provided by small numbers of contaminating OVA-specific CD4+ T cells. This represents the first formal evidence for the induction of an MHC class I-restricted T cell response to natural mucosal exposure to an inert protein antigen, and is consistent with a growing literature demonstrating sensitization of MHC class I-restricted CD8+ T cells by deliberate immunization with soluble proteins. We suggest that crossregulation of MHC class II-restricted CD4+ T cells via cytokine signals generated in parallel CD8+ T cell responses represents a covert and potentially important selection pressure that can shape the nature of host responses to nonreplicating antigens presented at mucosal surfaces.
Enthusiasm for Cancer Screening in the United States
Authors: Lisa M Schwartz, Steven Woloshin, Floyd J Fowler, H Gilbert Welch
Journal: JAMA (2004)

Public health officials, physicians, and disease advocacy groups have worked hard to educate individuals living in the United States about the importance of cancer screening.To determine the public's enthusiasm for early cancer detection.Survey using a national telephone interview of adults selected by random digit dialing, conducted from December 2001 through July 2002. Five hundred individuals participated (women aged > or =40 years and men aged > or =50 years; without a history of cancer).Responses to a survey with 5 modules: a general screening module (eg, value of early detection, total-body computed tomography); and 4 screening test modules: Papanicolaou test; mammography; prostate-specific antigen (PSA) test; and sigmoidoscopy or colonoscopy.Most adults (87%) believe routine cancer screening is almost always a good idea and that finding cancer early saves lives (74% said most or all the time). Less than one third believe that there will be a time when they will stop undergoing routine screening. A substantial proportion believe that an 80-year-old who chose not to be tested was irresponsible: ranging from 41% with regard to mammography to 32% for colonoscopy. Thirty-eight percent of respondents had experienced at least 1 false-positive screening test; more than 40% of these individuals characterized that experience as "very scary" or the "scariest time of my life." Yet, looking back, 98% were glad they had had the initial screening test. Most had a strong desire to know about the presence of cancer regardless of its implications: two thirds said they would want to be tested for cancer even if nothing could be done; and 56% said they would want to be tested for what is sometimes termed pseudodisease (cancers growing so slowly that they would never cause problems during the persons lifetime even if untreated). Seventy-three percent of respondents would prefer to receive a total-body computed tomographic scan instead of receiving 1000 dollars in cash.The public is enthusiastic about cancer screening. This commitment is not dampened by false-positive test results or the possibility that testing could lead to unnecessary treatment. This enthusiasm creates an environment ripe for the premature diffusion of technologies such as total-body computed tomographic scanning, placing the public at risk of overtesting and overtreatment.
Candida infection of the oesophagus.
Authors: J M Holt
Journal: Gut (1968)

<h3>Abstract</h3> Cultural processes of change bear many resemblances to biological evolution. Identifying underlying units of evolution, however, has remained elusive in non-biological domains, especially in music, where music evolution is often considered to be a loose metaphor. Here we introduce a general framework to jointly identify underlying units and their associated evolutionary processes using a latent modeling approach. Musical styles and principles of organization in dimensions such as harmony, melody and rhythm can be modeled as partly following an evolutionary process. Furthermore, we propose that such processes can be identified by extracting latent evolutionary signatures from musical corpora, analogous to the analysis of mutational signatures in evolutionary genomics, particularly in cancer. These latent signatures provide a generative code for each song, which allows us to identify broad trends and associations between songs and genres. To provide a test case, we analyze songs from the McGill Billboard dataset, in order to find popular chord transitions (k-mers), associate them with music genres and identify latent evolutionary signatures related to these transitions. First, we use a generalized singular value decomposition to identify associations between songs, motifs and genres, and then we use a deep generative model based on a Variational Autoencoder (VAE) framework to extract a latent code for each song. We tie these latent representations together across the dataset by incorporating an energy-based prior, which encourages songs close in evolutionary space to share similar codes. Using this framework, we are able to identify broad trends and genre-specific features of the dataset. Further, our evolutionary model outperforms non-evolutionary models in tasks such as period and genre prediction. To our knowledge, ours is the first computational approach to identify and quantify patterns of music evolution <i>de novo</i>.
It's About Time: Scheduling Alters Effect of Histone Deacetylase Inhibitors on Camptothecin-Treated Cells
Authors: Robert L. Bevins, Stephen G. Zimmer
Journal: Cancer Research (2005)

Abstract Chemotherapeutic treatment with combinations of drugs is front-line therapy for many types of cancer. Combining drugs which target different signaling pathways often lessens adverse side effects while increasing the efficacy of treatment and reducing patient morbidity. A defined scheduling protocol is described by which histone deacetylase inhibitors (HDIs) facilitate the cytotoxic effectiveness of the topoisomerase I inhibitor camptothecin in the killing of tumor cells. Breast and lung cancer cell lines were treated with camptothecin and sodium butyrate (NaB) or suberoylanilide hydroxamic acid on the day of, the day before, or the day after camptothecin addition. Depending on the time of addition, NaB-treated cells displayed a spectrum of responses from protection to sensitization, indicating the critical nature of timing in the use of HDIs. The IC80 (72-hour assay) dose of 100 nmol/L camptothecin could be lowered to 15 nmol/L camptothecin while maintaining or surpassing cell killing of the single agent if combined with an HDI added 24 to 48 hours after camptothecin. Experiments determined that cells arrested in G2-M by camptothecin were most sensitive to subsequent HDI addition. Western blot analysis indicated that in camptothecin-arrested cells, NaB decreases cyclin B levels, as well as the levels of the antiapoptotic proteins XIAP and survivin. These findings suggest that reducing the levels of these critical antiapoptotic factors may increase the efficacy of topoisomerase I inhibitors in the clinical setting if given in a sequence that does not prevent or inhibit tumor cell progression through the S phase.
Responsiveness of iliac collateral vessels to constrictor stimuli in atherosclerotic primates.
Authors: J A Lopez, M L Armstrong, D G Harrison, D J Piegors, D D Heistad
Journal: Circulation Research (1988)

This study was performed to examine, first, the protective effects and responses of collateral vessels of the hind limb in normal and atherosclerotic monkeys and, second, the effects of chronic arterial occlusion on the development of atherosclerosis. The iliac artery was ligated on one side in cynomolgus monkeys. Sixteen months later, we recorded the pressure gradient across the limb collaterals and measured blood flow with microspheres. Collateral conductance was fivefold greater after chronic ligation of the iliac artery than after acute ligation. Despite dilatation or growth of collateral vessels after chronic ligation, iliac pressure was reduced distal to the ligation. Blood flow to the limb was normal after chronic ligation in both normal and atherosclerotic monkeys. Collateral vessels constricted in response to infusion of phenylephrine and serotonin in normal and atherosclerotic monkeys. Thus, one conclusion of this study is that collateral vessels restore limb blood flow to normal after chronic vascular occlusion in both normal and atherosclerotic monkeys, but the protective effects of collateral vessels may be compromised by vasoconstrictor stimuli. Morphometric measurements indicated that occlusion of the iliac artery reduced proliferation of atherosclerotic intima distal to the occlusion in the cholesterol-fed monkeys. Thus, a second conclusion of this study is that atherosclerosis is attenuated below an arterial occlusion.
Study of large bowel peristalsis.
Authors: J D Hardcastle, C V Mann
Journal: Gut (1968)

<b>Rationale:</b> The response characteristics of the six-minute walk test (6MWT) in studies of idiopathic pulmonary fibrosis (IPF) are only poorly understood, and the change in walk distance that constitutes the minimum important difference (MID) over time is unknown. <b>Objectives: </b>To examine changes over time in distance walked (i.e., 6MWD) during the 6MWT and to estimate the change in distance that constitutes the MID in patients with IPF. Methods: We used data from a recently completed trial in IPF that included subjects who completed the 6MWT, Baseline/Transition Dyspnea Index (BDI/TDI), and forced vital capacity (FVC) at six and twelve months to examine longitudinal changes in 6MWD over. We used both anchor- and distribution-based approaches as well as linear regression analysis to determine the MID for 6MWD. The BDI/TDI9s Magnitude of Task (MTA) domain score and FVC were used as clinical anchors. <b>Main results: </b>Among 123 subjects alive and able to complete the 6MWT at both follow-up time points, 6MWD did not to change significantly over time (378.1m at baseline vs. 376.8m at six months vs. 361.3m at twelve months, p = NS). The point estimate for the 6MWD MID was 30m with a range of 14.6-58.5m. <b>Conclusion:</b> In a group of IPF patients with moderate physiologic impairment, for those alive and able to complete a 6MWT at six and twelve months, 6MWD does not change significantly over time. At the population level, the MID for 6MWD appears to be around 30 meters. Further investigation using other anchors and derivation methods is required to refine estimates of the MID for 6MWD in this patient population.
Hot and cold biopsy: implications of study design on outcomes
Authors: A. Nath, R. Srinivas, R. Agarwal
Journal: European Respiratory Journal (2007)

To the Editors: 

We read with interest the article in the European Respiratory Journal by Tremblay et al . 1, wherein the authors conclude that the use of hot biopsy forceps for endobronchial biopsy does not appear to have a negative impact on the pathological samples, and that there was a statistically significant (albeit clinically insignificant) reduction in bleeding score with hot biopsy forceps. However, many …
Deletion of neuronal NOS prevents impaired vasodilation in septic mouse skeletal muscle
Authors: D LIDINGTON, F LI, K TYML
Journal: Cardiovascular Research (2007)

Sepsis-stimulated nitric oxide (NO) production impairs arteriolar responsiveness in skeletal muscle. Using wild type (WT), eNOS(-/-), iNOS(-/-) and nNOS(-/-) mice, we aimed to determine the key nitric oxide synthase (NOS) isoenzyme(s) responsible for the arteriolar hyporesponsiveness to acetylcholine (ACh) in septic skeletal muscle.Sepsis was induced by the cecal ligation and perforation procedure (24 h model). We measured the post-ACh increase in red blood cell velocity (V(RBC)) in a capillary fed by the stimulated arteriole as an index of vasodilation. NOS activity and protein expression in the muscle were measured by standard procedures.In all non-septic mice, ACh increased V(RBC) by approximately 150% from baseline. Sepsis impaired this response in WT, eNOS(-/-) and iNOS(-/-) mice, but not in nNOS(-/-) mice. Accordingly, pharmacological inhibition of nNOS with 7-nitroindazole reversed this impairment in WT mice. cNOS (eNOS+nNOS) activity was elevated in septic WT mice; Western blots indicated that this occurred through a post-translational mechanism. iNOS protein activity/expression was negligible. ACh caused dilation via endothelial-derived relaxing factor (EDRF) in WT mice and via endothelial-derived hyperpolarizing factor (EDHF) in eNOS(-/-) mice. Although exogenous NO reduced EDHF-mediated dilation in eNOS(-/-) mice, NOS inhibition did not reverse the sepsis-impaired dilation in these mice.In our 24-h mouse model of sepsis, NO in skeletal muscle is primarily derived from nNOS. Sepsis impairs both EDRF- and EDHF-mediated dilation in response to ACh. Both genetic deletion and inhibition of nNOS protect against this impairment when the dilation occurs via the EDRF but not EDHF pathway.
Psychological Stress and Disease
Authors: Sheldon Cohen, Denise Janicki-Deverts, Gregory E. Miller
Journal: JAMA (2007)

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