tbuckley/cabot-search huggingface dataset:
AB0836 Serum Uric Acid Level and Severity of Arterial Hypertension in A Treatment-Naive Hypertensive Population in Sub-Saharan Africa
Authors: M. Doualla, G. Ashuntantang, H. Luma, F. Kamdem
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> There is a known association between elevated serum uric acid (SUA) and incident hypertension (HTN) especially in Black males but the data is scarce in Africa. <h3>Objectives</h3> We aimed at evaluating the relationship between the severity of HTN and SUA in a population of newly diagnosed and untreated HTN <h3>Methods</h3> A cross sectional study conducted in Douala from January to December 2012. Participants were newly diagnosed untreated hypertensives recruited during a community based screening in an urban area of Cameroon. Patients with a history of gout were excluded. HTN was diagnosed after three consecutive blood pressure readings on 3 separate occasions following the screening exercise. SUA assays were performed on fasting blood samples. <h3>Results</h3> Of the 839 participants included, 412 (49%) were males. Mean age was 50 years (range 29-81); mean BMI was 26.8; Mean SUA was 60.47±16.53 mg/l, with 65.1±16.54 mg/l (29- 112) in males and 55.98±15.26 mg/l (26- 108) in females 267 (31.8%) participants had elevated SUA levels. Among the participants with elevated SUA, 51% were males, 12.7% had a family history of HTN, 5.7% were smokers, and 8.2% had a fasting plasma glucose level ≥1.26g/L. 202 (75.6%) patients had stage 2 HTN and SUA levels were significantly higher compared to the other stages of HTN (p=0.001 <h3>Conclusions</h3> Stage 2 hypertension was strongly associated with elevated SUA levels in newly diagnosed and untreated hypertensives of indigenous black Africans. More studies are required to characterize this association. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5596
Abstract 1298: Mechanisms of endothelial trophic support of genitourinary tumors
Authors: June Liang, Derya Tilki, Hideki Kobayashi, Shahin Rafii, Marco Seandel
Journal: Cancer Research (2010)

Abstract Background: Classically, principal roles of the vascular endothelium have been considered to be support of oxygenation, nutrient delivery, waste product removal, and cellular trafficking. But the endothelium may also release paracrine signals to neighboring cells. Targeting such interactions could lower the threshold for sensitivity to conventional therapies, if pro-survival signals are blocked. We hypothesize that a subset of tumor cells are protected by endothelial-derived NF-kappa B (NF-KB)-mediated trophic signals that enhance tumor growth. Due to the confounding effects of circulating signals, it has been difficult to address these hypotheses using animal models. In contrast, in vitro models are limited by the requirement of primary endothelial cells (PECs) for serum and/or growth factors (GFs), complicating efforts to identify novel secreted factors. We employed a strategy to maintain PECs without serum by expressing the non-transforming adenoviral E4ORF1 gene. Under these conditions, E4ORF1-expressing (E4) PECs retain features of native tumor endothelium, including responsiveness to endothelial GFs and the ability to form functional vessels in vivo. Using solid tumor cell lines, including testicular germ cell tumor (GCT) and prostate cancer (PC) lines, we tested the ability of E4 PECs to support solid tumor progression. Methods: Constitutive expression of E4ORF1 in primary human umbilical vein endothelial cells (HUVECs) was achieved using lentivirus. Co-culture assays in serum-free media were used to test the effect of E4 PECs on cancer cell survival, proliferation and clonagenicity. Xenografts were performed by delivering cancer cells subcutaneously in the presence or absence of E4 PECs. Results: We first identified minimal media in which significant cancer cell proliferation was not observed in the absence of feeders. Under these conditions, we observed massive expansion of cell numbers for certain lines (e.g., 27×1) in the presence of E4 PECs (62.6+/-3.1 fold [mean+/-s.d.] for 27×1) vs. feeder-free control (2.2+/-0.1 fold) over 4 days. Changes in expression of stem cell-related genes in tumor cells during exposure to E4 PECs were examined to determine the frequency of stem-like cells in the culture. Results of co-inoculation studies using tumor cells in NOD-SCID mice will be discussed. Interventions to address the role of endothelial inside-out NF-KB signaling are on-going. Conclusions: Under stressful microenvironmental conditions, some but not all solid tumor cell lines require endothelial-derived growth and survival signals. Targeting these signals may lead to alternate strategies for eliminating residual tumor present after optimal therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1298.
S12 Interstitial lung disease multidisciplinary discussion: six years of data from a tertiary service
Authors: A Wright, J Helm, L Spencer, C Leonard, P Bishop, M Greaves, N Chaudhuri
Journal: Thorax (2013)

<h3>Introduction</h3> Accurate diagnosis in Interstitial Lung Disease (ILD) is vital in optimising patient management. An integrated approach involving a multidisciplinary team (MDT) of physicians, radiologists and pathologists is strongly advised in ATS/ERS guidelines.<sup>1</sup> This has been shown to improve diagnostic confidence.<sup>2</sup> Consensus diagnosis post multidisciplinary team discussion often differs from that reached by individual clinicians. Our centre, which provides a tertiary interstitial lung disease service in the North of England, implemented multidisciplinary discussion in 2005. Our patient cohort is larger than series previously presented at both national and international respiratory meetings. Literature search also did not identify any published data with either an equal or greater patient population. <h3>Aims</h3> To review interstitial lung disease MDT outcomes and to determine if discussion resulted in a change of diagnosis and whether this impacted on subsequent patient management. <h3>Methods</h3> Retrospective review of both patient clinical notes and MDT outcomes from 2005 to 2013 was performed. Data from 2009 and 2010 was unavailable as it was not stored electronically. <h3>Results</h3> 385 patients were referred for MDT review from 2005 to 2008 (n = 167) and 2011 to 2013 (n = 218). Usual Interstitial Pneumonia (UIP) was the pre-MDT diagnosis in 144 (37%) cases. Post-MDT 71 (49%) individuals had their diagnosis altered, leading to a change of treatment in 37 (52%) cases. A further 3 patients were referred for biopsy. One individual died pre-MDT and therefore was not discussed. Of the 68 cases referred with no diagnosis multidisciplinary consensus was reached in 60 (88%) cases. The remaining 172 were referred with a range of aetiologies. <h3>Conclusion</h3> Our findings support ARS/ERS consensus guidelines<sup>1</sup> which strongly advise the implementation of multidisciplinary discussion in the care of the individual with interstitial lung disease. <h3>References</h3> Flaherty K <i><i>et al</i>. <i>Am J Crit Care Med</i> Vol 170. pp904–910, 2004</i> Raghu G <i>et al. Am J Crit Care Med</i> Vol 183. pp788–824, 2011
INCIDENCE OF TEMPORARY TRANSVENOUS PACEMAKER PLACEMENT WITH CORONARY ORBITAL ATHERECTOMY COMPARED TO ROTATIONAL ATHERECTOMY
Authors: Evan Shlofmitz, Jeffrey Chambers, Michael Lee, Jeffrey Moses, Brad Martinsen, Perwaiz Meraj, Rajiv Jauhar, Richard Shlofmitz
Journal: Journal of the American College of Cardiology (2016)
The Mechanism of Respiratory Failure in Paraneoplastic Pemphigus
Authors: Hossein C. Nousari, Robin Deterding, Henry Wojtczack, Sirpa Aho, Jouni Uitto, Takashi Hashimoto, Grant J. Anhalt
Journal: New England Journal of Medicine (1999)

Paraneoplastic pemphigus1 is an autoimmune disease that accompanies an overt or occult neoplasm and causes blisters. It is characterized by the presence of IgG autoantibodies that react against desmosomal and hemidesmosomal plakin proteins,2–5 desmosomal transmembrane proteins (desmogleins),6 and an unidentified 170-kd antigen. Blistering of stratified squamous epithelium results from acantholysis, the loss of cell–cell adhesion, induced by pathogenic antibodies against the desmogleins.6 The most commonly associated neoplasms are, in decreasing order of frequency, non-Hodgkin's lymphoma, chronic lymphocytic leukemia, Castleman's disease, thymoma, retroperitoneal sarcomas, and Waldenstrom's macroglobulinemia. Progressive respiratory failure with clinical features of bronchiolitis obliterans is frequently the cause . . .
Abstract 5347: Inhibition of Notch3 signaling reduces tumorigenic properties of human rhabdomyosarcoma cells
Authors: Lavinia Raimondi, Roberta Ciarapica, Federica Verginelli, Marie Gueguen, Renata Boldrini, Luigi De Sio, Alessandro Inserra, Giancarlo Cortese, Mattia Locatelli, Thao P. Dang, Lucio Miele, Stefano Stifani, Isabelle Limon, Franco Locatelli, Rossella Rota
Journal: Cancer Research (2011)

Abstract Rhabdomyosarcoma is a soft tissue sarcoma of childhood arising from impaired developmental processes involving skeletal muscle progenitors. Notch signaling is strictly implicated in muscle tissue determination and has been reported to be abnormally activated in rhabdomyosarcoma. The expression of a dominant negative form of the Notch target gene HES1 or the inhibition of the γ-secretase has been shown to arrest rhabdomyosarcoma cell growth and trigger differentiation in vitro. Nevertheless, the mechanism underlying the deregulation of Notch signaling in rhabdomyosarcoma remains unclear. Here, we show that Notch3 and Notch1 are aberrantly activated in primary rhabdomyosarcomas and cell lines compared to skeletal muscle tissues or cultured myoblasts. In the present study we provide evidence that Notch3 targeted down-regulation restrains cell proliferation in both alveolar and embryonal subtypes of rhabdomyosarcoma cell lines. This phenomenon is paralleled by a transcriptional down-regulation of HES1 and an increase in both the cell cycle inhibitor p21cip1 and the under-phosphorylated pRb. Further, cells in which Notch3 has been silenced are capable to form differentiated multinucleated fibers showing de novo expression of late markers of myogenesis. In addition, down-regulation of Notch3 results in p38 and Akt hyper-phosphorylation and over-expression of PTEN. Finally, sustained silencing of Notch3 in rhabdomyosarcoma cells hampers their tumorigenic properties in vitro and in vivo. These results support a pathogenetic role for Notch3 in rhabdomyosarcoma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5347. doi:10.1158/1538-7445.AM2011-5347
RIGHT VENTRICULAR FDG-PET UPTAKE SUGGESTS A SHIFT TO GLYCOLYTIC METABOLISM IN THE SETTING OF RIGHT VENTRICULAR DYSFUNCTION RELATED TO PULMONARY ARTERIAL HYPERTENSION
Authors: Margaret M. Park, Didem Uzunaslan, Srisakul Chirakarnjanakorn, Emir C. Roach, Kristin B. Highland, Samar Farha, Serpil Erzurum, James Thomas, Christine Jellis, Donald Neumann, Frank DiFilippo, W.H. Wilson Tang
Journal: Journal of the American College of Cardiology (2016)
A third of general practices in England's first wave of inspections failed on essential standards
Authors: G. Iacobucci
Journal: BMJ (2013)

England’s healthcare regulator has published its blueprint for inspecting general practice services under a new regime from April 2014. The Care Quality Commission will appoint new expert inspection teams to visit and measure practices against simplified standards of care. 

Meanwhile it said that about a third of inspections carried out under the present regime showed failure of practices to meet at least one of 16 essential standards.

From 2014 a greater focus will be placed on how practices provide care for specific groups of patients, such as vulnerable older people and mothers and children, while tougher action will be taken in response to unacceptable care, including closing down unsafe practices where necessary.

Each new inspection team will …
Abstract 798: Measuring TK1 autoantibodies in the serum of cancer and non-cancer patients
Authors: Wesley LaPorte, Taylor Abegg-Lawrence, Melissa M. Alegre, Richard A. Robison, Kim L. O'Neill
Journal: Cancer Research (2011)

Abstract One of the foremost problems in cancer is lack of a convenient, early detection method. Often malignancies are discovered too late, at stages that are so evolved that treatment becomes painful, expensive, or ineffective. Thymidine Kinase 1 (TK1) is an important nucleotide salvage pathway enzyme involved in DNA synthesis and repair. It has been shown that TK1 levels increase under normal cellular conditions typically during cell proliferation. However under malignant conditions, TK1 is over-expressed both in the cytosol of cancer cells and the serum of cancer patients. Consequently, serum TK1 levels (sTK1) are often used in cancer diagnosis and prognosis. We hypothesized that there may be autoantibodies against sTK1 in cancer patients because TK1 is generally intercellular and usually sequestered from the immune system. In order to investigate this hypothesis, we developed an ELISA in a 96 well plate format specifically to detect and measure the presence of autoantibodies against sTK1. Using purified TK1 as a capture antigen, we added serum from both pre-treatment cancer patients and age matched normal patients to detect any autoantibodies that interact with sTK1. Using two different types of primary, HRP conjugated antibodies, (Goat Anti-Human-HL &amp; Goat Anti-Human-Fc) we were able to determine that there are antibodies to TK1 in the serum of both cancer and non-cancer patients. We eliminated the possibility that we were only detecting fragments of autoantibodies that were not true autoantibodies since our GAH-Fc antibody is specific to only intact antibodies. Furthermore, when we added TCEP (A common reducing agent which we used to remove the antibodies from the serum) to the serum, we saw a measurable signal reduction. Preliminary data suggest there are autoantibodies to TK1 in both cancer serum and normal serum. Further research is underway to elucidate the mechanisms responsible. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 798. doi:10.1158/1538-7445.AM2011-798
Europeans Say Screen Only Women Age 50 and Older
Authors: C. Vanchieri
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Europeans Say Screen Only Women Age 50 and Older Get access Cori Vanchieri Cori Vanchieri Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 5, 3 March 1993, Page 350, https://doi.org/10.1093/jnci/85.5.350 Published: 03 March 1993
Abstract 504: Epithelial-mesenchymal transition confers stem-like properties and migratory ability to lung tumor cells
Authors: Giulia Bertolini, Luca Roz, Monica Tortoreto, Mattia Boeri, Ugo Pastorino, Gabriella Sozzi
Journal: Cancer Research (2011)

Abstract We previously demonstrated that lung cancer CD133+ cells are highly tumorigenic, display stem-like features and are spared by cisplatin treatment. Recent studies proposed that the process of EMT could generate cancer cells endowed with migratory and invasive abilities and with characteristics of cancer stem cells (CSCs) To test this hypothesis in lung cancer we induced EMT by transforming growth factor β (TGFβ1) in a lung cancer cell line established from primary tumor (LT73). EMT program activation in LT73 cell line resulted in cellular morphological changes, repression of E-cadherin expression and up-regulation of EMT-related genes, as evaluated by Real Time PCR. We also demonstrated that EMT-induced cells expressed high levels of stemness genes, similarly to mesenchymal stem cells. We furthermore found that LT73 cells undergone EMT exhibited an enhanced migrating potential and an increased drug resistance to cisplatin treatment than parental cell line, indicating that EMT activation provided cells with mesenchymal traits as well as stem-like properties. FASC analysis revealed an enrichment of CD133+ lung cancer initiating cells in EMT-induced LT73 cells. Interestingly in EMT-generated CD133+ cells we identified a fraction of CD133+ /ESA− cells, not detectable in parental cell line, that express high level of pro-metastatic chemokine receptor CXCR4. To validate the results obtained in the in vitro model, we analyzed primary lung cancer and corresponding lymph nodes metastasis, as well as spontaneous lung metastasis generated from subcutaneous xenografts tumor of H460 cell line. Preliminary results confirmed the existence of CD133+/ESA− /CXCR4High cells also in some primary lung cancer. Interestingly we found that lymph node metastasis contained a higher amount of this subpopulation of cells compared to corresponding primary tumors. Moreover the phenotypic analysis of spontaneous lung metastasis, derived from subcutaneous H460 xenograft tumor, demonstrated an enrichment for CD133/CXCR4 double positive population compared to parental tumors. In conclusion these data indicate that EMT process could generate a subpopulation of CD133+/ESA− /CXCR4High cells, endowed with the potential to initiate tumor and disseminate, that possibly may represent the migrating-CSC fraction, involved in metastatic process. The existence of EMT-generated cancer cells could provide new insights into the tumor metastatic progression and lead to novel approaches for selective targeting of CSC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 504. doi:10.1158/1538-7445.AM2011-504
P259 Tiotropium Handihaler(R) And Respimat(R) In Copd: A Safety Analysis On Pooled Data
Authors: D. Halpin, R. Dahl, C. Hallmann, I. Leimer, A. Mueller, D. Tashkin
Journal: Thorax (2014)

<h3>Rationale</h3> Tiotropium has been approved and marketed via HandiHaler® (18 µg once daily [qd]) since 2002 and via Respimat® (5 µg qd) since 2007. The recent TIOSPIR™ (TIOtropium Safety and Performance In Respimat®) study demonstrated that both products had comparable safety profiles; the objective of this analysis was to provide an updated safety evaluation of tiotropium in both formulations. <h3>Methods</h3> Analysis of pooled adverse events (AEs) from randomised, double-blind, parallel-group, placebo-controlled clinical trials of ≥4 weeks' duration where either tiotropium HandiHaler® 18 µg or tiotropium Respimat® 5 µg was indicated for chronic obstructive pulmonary disease (COPD). Rate ratios (RRs), incidence rates (IRs) and 95% confidence intervals (CIs) were determined for HandiHaler® and Respimat® trials together and separately. <h3>Results</h3> This analysis of 28 HandiHaler® and seven Respimat® studies provided 14,909 (12,469 and 2440 with HandiHaler® and Respimat®, respectively) patient-years' exposure to tiotropium. Mean age was 65 years and mean forced expiratory volume in 1 second was 1.16 L (41% predicted). The risk (RR [95% CI]) of AEs (0.90 [0.87, 0.93]) and serious AEs (0.94 [0.89, 0.99]) was significantly lower with a numerically lower risk of death (0.90 [0.79, 1.01]) in the tiotropium group (pooled results) (Table). When separated by device, the risk of AEs and serious AEs remained lower in the tiotropium groups than placebo: RR 0.88 and 0.94 for HandiHaler® and 0.94 and 0.94 for Respimat® for AEs and serious AEs, respectively. Risks for cardiac events (0.93 [0.85, 1.02]) and major adverse cardiovascular events (MACE) (0.87 [0.75, 1.01]) were numerically lower and risk for respiratory, thoracic and mediastinal disorders (0.76 [0.61, 0.96]) was significantly reduced in the tiotropium group. The typical anticholinergic effects of dry mouth (2.39 [2.01, 2.84]), constipation (1.28 [1.06, 1.54]), intestinal obstruction (3.80 [1.42, 10.12]), dysuria (2.16 [1.31, 3.57]) and urinary retention (1.93 [1.21, 3.09]) were higher in the tiotropium group. <h3>Conclusions</h3> The results from this safety review do not indicate an increased overall risk for fatal or cardiovascular events during tiotropium treatment, given via HandiHaler® or Respimat®, in patients with COPD.
S79 Cough Prevalence And Frequency In Pulmonary Tuberculosis
Authors: R. Turner, A. Repossi, S. Matos, S. Birring, G. Bothamley
Journal: Thorax (2014)

<h3>Introduction</h3> Patterns of cough in tuberculosis influence transmission of disease yet have been little studied. We report the prevalence, duration, severity and frequency of coughing in tuberculosis. <h3>Method</h3> The first part was a retrospective review of the medical records of all individuals diagnosed with pulmonary tuberculosis (PTB) at our hospital during 2012–3. The reported presence and duration of coughing was noted. In the second part of the study, successive patients with an ultimate diagnosis of PTB wore the Leicester Cough Monitor for 24 h prior to commencing treatment. Controls had latent TB infection (LTBI). Participants rated their cough severity from 0–100 with a visual analogue scale (VAS). Cough characteristics were compared with other clinical variables. <h3>Results</h3> 108 cases of PTB from 2012–3 were included. 82 reported cough of median (IQR) duration 4 (1–8) weeks. There was a significant association of the presence of cough with TB sputum culture positivity (odds ratio, 11.0; 95% confidence interval, 2.5–50.0) but not gender, smoking, smear positivity, cavitary disease or extent of radiographic change. No clear predictor of the duration of cough was identified and there were too few patients to estimate the effect of TB strain. Cough frequency was measured in subjects with sputum smear positive PTB (S+; n = 20), smear negative PTB (S-; n = 10) and LTBI (n = 11). Variability was high: median (IQR) cough rates were 238 (121–701), 126 (15–395) and 11 (7–56) coughs/24 h, respectively, and not significantly different for S+ vs. S- (figure). For active TB, cough rates were reduced overnight (2.8 [0.2–12.4] vs. 12.7 [3.3–23.4] coughs/h for night vs. day, respectively; p = 0.01). No effect of smoking was detected, nor was there a correlation between cough frequency and radiographic extent of disease, cavities or time to sputum culture positivity. Cough severity was higher for S+ than S- but also variable and the difference not statistically significant (VAS: 60 [13–94] vs. 22 [1.5–70] respectively; p = 0.41). Severity correlated with cough frequency in active tuberculosis (Spearman's r = 0.60, p = 0.001). <h3>Conclusion</h3> Cough in TB reduces overnight and is related to culture positivity. Bacterial burden and extent of disease may not be important. Other determinants of cough await characterisation.