tbuckley/cabot-search huggingface dataset:
Association between obstructive sleep apnea and serum uric acid levels in obese women
Authors: Luca Viglietta, Anna Filomena Ferravante, Alessandro Di Marco Berardino, Esmeralda Capristo, Flaminio Mormile
Journal: European Respiratory Journal (2014)

INTRODUCTION Controversial data exist on association of hyperuricemia both with increased cardiovascular risk, particularly in obese patients, and with the presence and severity of obstructive sleep apnea (OSA).

AIM We correlated acid uric (AU) levels with metabolic and polygraphic parameters in obese patients with suspected OSA.

METHODS We studied 86 patients (44M) aged 44.3+9.7 yr, BMI 43.9+6.7), all CPAP naive. At the cardiorespiratory monitoring AHI was >5, >15 and >30 in 90,70,and 46% of them.

RESULTS Mean UA was greater in men (7.30+1.7 vs 5.6+0.12, p 0,003) and in the upper versus lowest AHI quartiles (7+1.5vs 5.5+1.6, p 0.007). Men showed also greater values of AHI, ODI, creatinine, haemoglobin and lower HDL cholesterol levels than women, with similar age and BMI.

UA was directly correlated with AHI and ODI (r 0.33-0.36, p 0.005), time spent with SpO2<90% (r 0.25, p 0.013), serum creatinine (r 0.29, p 0.014) and triglycerides (0.36, p=0.003), but not with age or BMI, and inversely with HDL cholesterol (r -0.36,p=0.001). Multiple linear regression demonstrated a significant association with AHI independent of age and BMI only in women and with glycated haemoglobin (HbA1c) in both sex subgroups.

The correlations with nocturnal OSA parameters were even stronger among women (r 0.46-0.52, p<0.004) but not significant in men.

CONCLUSION Our results support the hypothesis of a significant association between UA and OSAS in obese women, both for number of events and for induced hypoxemia, while in obese men the more complex interaction between OSA, UA and classical cardiovascular risk factors requires further clarification.
Impact of postmenopausal hormone therapy on cardiovascular events and cancer
Authors: S. Singleton, K. Bailey, S. Shah, L. Rhodes, V. Seagroatt, T. Sundkvist, F. Al-Azzawi, J. Thompson, A. Halligan, N. F Col, J. B Wong, S. G Pauker, R. Karas, E. Hemminki
Journal: BMJ (1997)

Accurate calibration of sensory estimators is critical for maintaining accurate estimates of the environment. Classically, it was assumed that sensory calibration occurs by one sense changing to become consistent with vision; this is visual dominance. Recently, it has been proposed that changes in estimators occur according to their relative reliabilities; this is the reliability-based model. We show that if cue combination occurs according to relative reliability, then reliability-based calibration assures minimum-variance sensory estimates over time. Recent studies are qualitatively consistent with the reliability-based model, but none have shown that the predictions are quantitatively accurate. We conducted an experiment in which the model could be assessed quantitatively. Subjects indicated whether visual, haptic, and visual–haptic planar surfaces appeared slanted positively or negatively from frontoparallel. In preadaptation, we determined the visual and haptic slants of perceived frontoparallel, and measured visual and haptic reliabilities. We varied visual reliability by adjusting the size of the viewable stimulus. Haptic reliability was fixed. During adaptation, subjects were exposed to visual–haptic surfaces with a discrepancy between the visual and haptic slants. After adaptation, we remeasured the visual and haptic slants of perceived frontoparallel. When vision was more reliable, haptics adapted to match vision. When vision was less reliable, vision adapted to match haptics. Most importantly, the ratio of visual and haptic adaptation was quantitatively predicted by relative reliability. The amount of adaptation of one sensory estimator relative to another depends strongly on the relative reliabilities of the two estimators.
Abstract 2612: ljm716, an anti her3 antibody that inhibits her3 dimerization, displays anti-tumor activity in esophageal squamous cell cancer
Authors: Qing Sheng, Hui-Qin Wang, rita das, yan chen, jinsheng liang, Fiona Xu, zongyao Wang, Z. Alexander Cao, youzhen Wang, alan huang
Journal: Cancer Research (2014)

Abstract Background: Esophageal cancer is the eighth most common cancer and the sixth most common cause of cancer related death in the world. Squamous cell carcinoma is the predominant histologic subtype of esophageal cancer, particularly in Asia. Currently, no targeted therapy has been approved for treating this type of disease. Platinum-based combination chemotherapy remains to be the standard care for first line treatment of advanced or metastatic esophageal cancer with limited efficacy. Activation of EGFR/HER3/PI3K pathway is frequently observed in esophageal cancer, however, their therapeutic value remains to be further tested. Methods: In this study, we evaluated the anti-tumor activity of LJM716, a fully human anti-HER3 antibody, either alone or in combination with anti-EGFR antibody cetuximab or PI3K alpha subunit inhibitor BYL719 in esophageal squamous cancer. LJM716, cetuximab and BYL719 single agent as well as their pair-wised combination activity were assessed in 24 esophageal squamous cancer cell (ESCC) lines using the CellTiter-Glo® Luminescent Cell Viability Assay. Single agent and combination anti-tumor activities of these reagents were also tested in selected cell line xenograft and patient derived xenograft mouse models. Results: NRG1 expression (60%), PIK3CA mutation (8%), moderate PIK3CA (30%) and EGFR (30%) amplification were detected in a panel of 24 ESCC lines. Anti-HER3 antibody LJM716 potently inhibited HER3 phosphorylation and decreased pAKT level in these cell lines. In vitro, LJM716 inhibited proliferation of a sub-set of ESCC lines. LJM716 further enhanced and broadened the anti-tumor activities of both BYL719 and cetuximab in ESCC lines. In mouse xenograft models, LJM716 single agent treatment induced tumor stasis while combination with either BYL719 or cetuximab induced model dependent tumor regression. Conclusion: NRG1-HER3-PI3K pathway activation is commonly observed in esophageal squamous cell cancer. Activation of HER3 is a potential mechanism leading to resistance to EGFR or PI3K targeted therapies, and combining anti-HER3 therapies with therapies targeting PI3K/EGFR may provide new therapeutic strategy for patients with esophageal squamous cell cancer. Citation Format: Qing Sheng, Hui-Qin Wang, rita das, yan chen, jinsheng liang, Fiona Xu, zongyao Wang, Z. Alexander Cao, youzhen Wang, alan huang. ljm716, an anti her3 antibody that inhibits her3 dimerization, displays anti-tumor activity in esophageal squamous cell cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2612. doi:10.1158/1538-7445.AM2014-2612
Important factors are hard to measure
Authors: E. Wilkes
Journal: BMJ (1995)

Evaluation of palliative careRecruitment figures may be low EDrroR,-In response to the paper by Ian R McWhinney and colleagues' we wish to report our experience of recruitment into trials in the palliative care setting.The trials were not of a palliative care service but of palliative therapeutic interventions in a specialist cancer hospital.These included randomised studies of pharmacological and non-pharmacological strategies in the manage- ment of bowel obstruction, hypercalcaemia, nausea induced by opiates, anorexia, pain, and dyspnoea as well as non-randomised studies in patients in pain.In the 12 months to October 1994, 344 patients were referred to one of two research sisters in palliative care as being suitable for entry to one of the above studies.Both inpatients and outpatients were referred by medical and nursing staff throughout the hospital.Of the 344 patients, 109 were not approached as they did not fulfil the criteria for inclusion in the studies.Thus after full discussion regarding the implications of entering the trial 235 patients were asked if they would agree to participate in one of the studies.Only 142 patients gave informed consent.The remainder were not entered into the studies because they were too unwell or their condition had deteriorated (27), they were eligible but declined to consent (38), they lived too far away from the hospital ( 16), or for unknown reasons (12).Thus 41% of the patients initially referred and 60% of the patients who were approached were entered into studies.These figures are low but are likely to be higher than those achieved in other palliative care settings since the patients were recruited in a specialist cancer hospital with a high research profile, where the role of the research sister is well established.We agree with Henry McQuay and Andrew Moore that palliative care should not be excused from conducting randomised controlled trials simply because they are difficult to do,2 but our recruitment data show several of the inherent difficulties.
Interleukin-13 in Combination With CD40 Ligand Potently Inhibits Apoptosis in Human B Lymphocytes: Upregulation of Bcl-xL and Mcl-1
Authors: Jon Lømo, Heidi Kiil Blomhoff, Sten Eirik Jacobsen, Stanislaw Krajewski, John C. Reed, Erlend B. Smeland
Journal: Blood (1997)
Efficacy of a Sexual Assault Resistance Program for University Women
Authors: Charlene Y. Senn, Misha Eliasziw, Paula C. Barata, Wilfreda E. Thurston, Ian R. Newby-Clark, H. Lorraine Radtke, Karen L. Hobden
Journal: New England Journal of Medicine (2015)

Young women attending university are at substantial risk for being sexually assaulted, primarily by male acquaintances, but effective strategies to reduce this risk remain elusive.
Abstract 274: Pulse Detection with Photoplethysmography (PPG) in Hemodynamic Instability
Authors: Pia Hubner, James K Russel, Andreas Schober, Christian Wallmueller, Fritz Sterz
Journal: Circulation (2013)

Pulse detection could guide therapy but noninvasive methods accurate in emergencies remain elusive. We investigated feasibility of noninvasive pulse detection in hemodynamic instability in an emergency department. Hypothesis: Pulse detection in hemodynamic instability may be feasible using PPG. Methods: An algorithm detected pulses in signals from commercial oximeters (NICO, Oxypleth - Philips) applied to a peripheral (fingertip) and two central (nasal septum, ear pinna) sites and pressure catheters in radial arteries (Intellivue - Philips). Heart rates from average interpulse intervals in 3 s periods, were updated each second. Data was classified by systolic pressure. Rates from each oximeter site were compared to the arterial rate. Results: We recorded over 140 hours of PPG signals from 30 patients during CPR, post-resuscitation care, shock and syncope from October 2012 to May 2013. Technical difficulties excluded 3 patients from analysis. Even weak pulses were evident in PPG waveforms (figure). Pulse detection was accurate for all sensors at all sites and pressures (table). Central sites tended to be more accurate than the finger at low pressures. Conclusions: A noninvasive pulse detector using PPG appears feasible and may be useful in initial patient assessment, during pauses in CPR and during chest compressions.
Abstract 16202: Changes in Hemoglobin After Pulmonary Artery Catheterization: Results From the ESCAPE Trial
Authors: Abdulla Damluji, Conrad Macon, Mohammed Al-Damluji, Arieh Fox, George R Marzouka, Ian C Gilchrist, Mauricio G Cohen, Mauro Moscucci
Journal: Circulation (2014)

Introduction: We sought to investigate the association between hemoglobin (Hgb) changes in patients with ADHF (with and without PACs) to mortality and clinical outcomes. Methods: We examined 433 patients enrolled in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial. Change of Hgb (g/dL) was defined as at least 1 (g/dL) drop by hospital discharge. Quartiles of % change of Hgb (g/dL) were calculated. We used multivariable Cox regression analysis to evaluate the effect Hgb change on mortality and composite end points of death, cardiac re-hospitalization, or cardiac transplant. Results: Of the 433 patients, 324 (75%) had baseline and discharge Hgb available for analysis. Of those, 64 (20%) had at least 1 (g/dL) drop of Hgb by time of discharge. Patients in the Hgb drop group were older than those without Hgb changes (59 vs. 55, p = 0.011). There were no baseline differences in gender, race, and etiology of HF between groups. Compared to patients without Hgb changes, patients with Hgb drop had lower systolic BP (99 vs. 106, p = 0.017), lower sodium (136 vs. 137, p =0.025), higher BUN (37 vs. 26, p &lt;0.001), and higher Creatinine (1.6 vs. 1.3, p &lt;0.001), respectively. Higher Hgb drop was observed in the PACs (vs. no PACs) randomized arm of the trial (2 g/dL: PACs 10% versus 3%, p =0.010; 3 g/dL: PACs 5% versus 0%, p =0.005). After adjustments, higher in-hospital Hgb was associated with lower mortality (HR 0.79, p =0.003). In addition, patients in the Hgb drop group had increased risk of mortality (Adjusted HR 2.38, p =0.003) and composite endpoints (Adjusted HR 1.43, p =0.055). PACs insertion was not associated with adverse clinical outcomes by quartiles of % change of hemoglobin (Mortality: Q1: HR 0.80, p 0.601, Q2 HR 0.79, p = 0.706, Q3 HR 0.34, p =0.101, Q4 HR 2.23, p =0.357). Conclusion: In-hospital decrease in Hgb is independently associated with increased long-term mortality and adverse cardiovascular events in severe HF. The ideal Hgb levels in ADHF patients should be investigated and the insertion of PACs to direct therapy should be weighed against bleeding risks.
PTU-044 Trends in rates of ileocolonic resection for Crohn's disease 2003–2008: experience from the TOPPIC trial
Authors: J M Thomson, I D R Arnott, C Mowat, A Cahill, J Satsangi
Journal: Gut (2010)

<h3>Introduction</h3> The TOPPIC trial is a UK based randomised control trial of 6-mercaptopurine vs placebo in the prevention of post operative Crohn9s disease originally conceived, designed and powered in 2003, but recruiting its first patient in 2008. During this period there has been a substantial increase in the availability and use of biologic agents for the treatment of Crohn9s disease. <h3>Methods</h3> As recruitment to the TOPPIC trial proceeded, it became apparent that actual recruitment did not match that projected. Therefore prior to an expansion of the centres to include sites across the UK, analysis of the resection figures from the initial sites (Aberdeen, Dundee, Edinburgh and Glasgow) was undertaken by retrospective review of data held by each centre regarding the number of ileocolonic resections with primary anastamosis performed for the 6-year period 2003–2008. <h3>Results</h3> Complete data for this period were available from two of the five initiating sites (Dundee and Glasgow) representing a total of 237 resections and a median number of resections of 43.5 per year (range 40–56). Across the 6 years there was an overall reduction in the number of resections with a linear correlation coefficient of R<sup>2</sup>=0.47 representing a 26% reduction in the number of resections from 2003 to 2008. This downward trend was more pronounced in Dundee with a median number of resections of 27.5 per year and a linear correlation coefficient R<sup>2</sup>=0.47 comprising an increase in the first 3 years and then a significant reduction from 2005 to 2008 (p=0.025). Glasgow with a median number of resections of 18.5 per year also had an overall downward trend with a linear correlation coefficient of R<sup>2</sup>=0.03 which consisted of a marked initial reduction that then stabilised at the reduced rate. <h3>Conclusion</h3> The reduction in surgical resection rates is likely to be multifactorial but the concurrent increase in the use of biological therapies in the UK is further circumstantial evidence that these therapies alter the natural history of Crohn9s disease. The TOPPIC trial continues to recruit across the UK and will be in a position to report further on this important observation regarding the number of ileocolonic resections in addition to the trial primary endpoint.
Breathing pattern and load compensatory responses in young scoliotic patients
Authors: M Ramonatxo, J Milic-Emili, C Prefaut
Journal: European Respiratory Journal (1988)

The breathing pattern and mouth occlusion pressure developed in 0.1 seconds (P0.1) were measured at rest in sixteen young scoliotic patients in whom the blood gases were within the normal limits. The patients exhibited rapid and shallow breathing. P0.1 was increased above normal, indicating a compensatory increase of neuromuscular inspiratory drive in the face of a stiffer respiratory system. P0.1 (% predicted) correlated positively with the angle of scoliosis. Both duration of inspiration and inspiratory duty cycle correlated negatively with angle of scoliosis and P0.1 (% predicted). On theoretical grounds we show that these changes in breathing pattern are beneficial, both in terms of reducing the energy cost of breathing and preventing the development of inspiratory muscle fatigue.
Kronik Hepatit B: Tedaviye Güncel Yaklaşımların Kritik Bir Değerlendirmesi
Authors: Robert P. Perrillo, Robert G. Gish, Marion Peters, Emmet B. Keeffe, Alfredo Alberti, Maria Buti, W. Graham E. Cooksley, Michael W. Fried, Stephanos J. Hadziyannis, sup> Yun-Fan Liaw, Nikolai V. Naoumov, Eugene R. Schiff, Chloe L. Thio, Naoky Tsai, sup> ve Solko Schalm §§§<
Journal: Clinical Gastroenterology and Hepatology (2006)
Cytokinesis defects, polyploidy and premature senescence in SSeCKS/Gravin/AKAP12-null mouse embryo fibroblasts
Authors: Peter Nochajski, Shin Akakura, Irwin Gelman
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

2696 

SSeCKS/Gravin/AKAP12 (“SSeCKS”) regulates a number of proliferative and cytoskeletal signaling events by scaffolding a number of key mediators of G1→S progression, such as protein kinase (PK) A and C, cyclins and calmodulin. SSeCKS expression is suppressed by Src and Ras oncogenes and in many cancer cell lines and human cancer tissues. Moreover, the re-expression of SSeCKS to physiologic levels can suppress oncogenic growth by disengaging active Src from MEK-ERK and PI3K proliferation pathways and by re-establishing a normalized actin cytoskeletal architecture through the inhibition of Rho-family GTPases (1-3). Although the overexpression of SSeCKS in untransformed cells is known to induce G1 arrest through the suppression of cyclin D1 expression (4), the precise mechanism of how SSeCKS controls normal cell cycle progression is not known. In this study, we have examined a role of SSeCKS on cellular functions by using SSeCKS-null mouse embryonic fibroblasts (KO-MEF). KO-MEF exhibit premature-senescence (between passages 6 and 7), coincident with the expression of senescence-associated β-galactosidase and with a very high level of multi-nucleation and/or tetraploidy. Preliminary evidence suggests that the senescence in KO-MEF is both Rb- and p53-dependent. Using a combination of live cell imaging and immunofluorescence staining, we show that SSeCKS is enriched around nascent segregated daughter chromosomes in anaphase cells and that KO cells are defective in both the polarity of anaphase spindles and the ability of late-stage cytokinetic plates to septate. Evidence will be shown suggesting that SSeCKS controls normal cell cycle progression by attenuating RhoA-mediated late-stage events in cytokinesis.
Abstract 5535: Gcn5 modulates the cellular response to oxidative stress induced by histone deacetylase inhibitors
Authors: Ann-Christin Gaupel, Thomas J. Begley, Martin P. Tenniswood
Journal: Cancer Research (2014)

Abstract Aberrant histone post-translational modifications including acetylation are common in human cancers and result in dysregulation of gene expression. Our laboratory has focused on studying the effects of hydroxamic acid based HDAC inhibitors (HDACis) including TSA, SAHA and CG-1521. We have employed a whole genome yeast deletion library screen to gain insight into the mechanism of the HDAC inhibitor CG-1521 and identify potential combinatorial drug targets. Gene ontology enrichment analysis shows that sensitive strains are highly enriched in processes regulating chromatin remodeling and transcription. Deletions of components of the SAGA HAT complex are highly overrepresented in the sensitive strains, including the catalytic subunit Gcn5. The gcn5 deletion strain displays increased sensitivity to CG-1521 induced cell death compared to the wild type strain, suggesting that the SAGA complex is required to reduce the effect of CG-1521 on cell growth. Gene expression analysis indicates that CG-1521 elicits an oxidative stress response in both the wild type and the gcn5 deletion strain. Gcn5 deletion substantially increases the level of oxidative stress induced by CG-1521 as measured by flow cytometry. In the colorectal cancer cell line HT29, treatment with CG-1521 is accompanied by an increase in oxidative stress and co-treatment with the Gcn5 specific inhibitor MB-3 or RNAi-mediated knockdown of the human Gcn5 homologs, Gcn5 and PCAF, enhances the growth-inhibitory effect of CG-1521. These studies have shown that disruption of the SAGA HAT complex with MB-3 or RNAi-mediated knockdown sensitizes tumor cells to CG-1521. Taken together, our work suggests that the combination of selective HAT and HDAC inhibitors may be an effective treatment of cancer. Citation Format: Ann-Christin Gaupel, Thomas J. Begley, Martin P. Tenniswood. Gcn5 modulates the cellular response to oxidative stress induced by histone deacetylase inhibitors. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5535. doi:10.1158/1538-7445.AM2014-5535
Association between upper airway diseases and bronchial asthma
Authors: Leonardo Antonicelli, Pierpaolo Marchetti, Massimiliano Bugiani, Lucio Casali, Maria Grazia Panico, Pietro Pirina, Virginia Ferretti, Caterina Bucca, Giuseppe Verlato, Marcello Ferrari, Roberto de Marco
Journal: European Respiratory Journal (2012)

Few studies investigated the association between allergic rhinitis (AR) with sinusitis (S), polyposis (P) and bronchial asthma.  The aim of the study was to evaluate the associations between different upper airway diseases and bronchial asthma in the general population and their impact on asthma exacerbation.  In the frame of the Gene Environment Interactions in Respiratory Diseases study (GEIRD), a postal screening questionnaire including questions about self reported symptoms of asthma, AR, S and P was administered. A random sample of subjects (n=5162) aged 20-44 years was selected in 4 Italian centres (Pavia, Sassari, Torino, Verona). The association among AR, AR plus S, AR plus S and P, and bronchial asthma was estimated by the relative risk ratio (RRR) using multinomial regression models adjusted for sex, age, smoking habits and design confounders.  The prevalence of AR in the sample was 25% (95%CI: 24-26). Among subjects with AR, 73% had AR only, 22% had AR with S and 5% had AR with S and P. The risk of current asthma was higher in subjects with AR+S and AR+S+P (RRR=1.38; 95%CI:1.01-1.90 and RRR=2.16; 95%CI:1.24-3.76, respectively) than subjects with AR only. There were no statistically significant differences in the number of asthma exacerbations among the three groups. The percentage of subjects with diagnosed asthma, who were treated with drugs for asthma, was 50%, 62% and 79% in AR only, AR+S and AR+S+P respectively.  In conclusion, the type of upper airway diseases seems to be a risk factor for current asthma but not for the asthma exacerbations.