tbuckley/cabot-search huggingface dataset:
PTU-056 Highly Successful, Minimally Invasive Enteral Access By Double-balloon Enteroscopy (dbe) And Laparoscopic-assisted Dbe
Authors: TC Shepherd, O Epstein, A Khan, ET Pring, M Varcada, S Rahman, EJ Despott
Journal: Gut (2014)

<h3>Introduction</h3> Patients with chronic gastroparesis frequently require prolonged enteral feeding via the jejunal route. This is often achieved through the placement of a percutaneous endoscopic gastrostomy with jejunal extension (PEG-J) or a surgically placed jejunostomy (SJ). Direct percutaneous endoscopic jejunostomy (DPEJ) is increasingly used as an alternative to these modalities: Avoiding the intrinsic problems associated with the narrow calibre PEG-J and the tendency of displacement and retrograde migration; and is less invasive than SJ insertion, which also requires an enterotomy and enteropexy. Although progress with deep enteroscopy over the last decade has facilitated DPEJ placement, the presence of post-surgical intra-abdominal adhesive disease may still reduce success rates and procedure safety. In this setting, miniport laparoscopic-assisted DBE (lap-DBE) has the potential to provide safe and successful placement while maintaining the relatively minimally invasive approach of the endoscopic pull-through technique. <h3>Methods</h3> Prospective assessment of outcomes of DPEJ placement by DBE and lap-DBE placed at our tertiary referral institution since June 2012. <h3>Results</h3> 10 patients (6 [60%] female, median age 40 years [range: 27–43 years]) with chronic gastroparesis underwent DBE or lap-DBE facilitated DPEJ placement. Miniport laparoscopic assistance was only required in patients with a history of abdominal surgery (30% [3/10]) and allowed us to identify and divide any underlying adhesions laparoscopically, facilitating DPEJ placement under direct endoscopic and laparoscopic vision, without the need for an enterotomy or surgical enteropexy. In this series DPEJ placement was successful in all 10 patients: Estimated depth of insertion [mean±SD] 66 ± 12 centimetres post-pylorus and procedure time [mean±SD] 49 ± 114 min. There were no immediate procedure-related complications and no delayed complications, morbidity or mortality at a mean follow-up of 339 days [range: 175–576 days]. <h3>Conclusion</h3> DPEJ placement by DBE is successful and safe. In patients with a history of abdominal surgery and underlying adhesive disease, lap-DBE should be considered, as it may enhance procedure success and safety. <h3>Disclosure of Interest</h3> None Declared.
THU0417 Exposure, latent tuberculosis, or disseminated infection? The role of tst, quantiferon, and multisite cultures in high risk patients on TNF-inhibitors
Authors: D. Cooray, R. Moran, P.P.C. Chen, J.A. Louie, G.A. Karpouzas
Journal: Annals of the Rheumatic Diseases (2013)

There is no detailed and practical description of how to identify the adrenal glands at necropsy. A simple technique is described, based on anatomical location. After removing the aorta by the Rokitansky method, the inferior vena cava is opened. The orifice of the right adrenal vein is identified just above the right renal vein, and a probe is inserted into it as a marker. The right adrenal gland is identified at the centre above the line of the probe after separation of the diaphragm, which is attached to the liver. The left adrenal vein arises as the first bifurcation of the left renal vein after its origin from the inferior vena cava. A probe is inserted into it and the vein is opened along the probe. The left adrenal gland is identified at the left side of the left adrenal vein, embedded in fat. This method is also useful in cases with severe adhesion, fibrosis, or metastases.
The Characteristic and Diagnosis of Chronic Pancreatitis in Endoscopic Ultrasound
Authors: X Xie, J Zheng, Y Cui, Z Xu, C Li
Journal: Endoscopy (2006)

Purpose: The purpose of our study was to character the feature of CP and to diagnosis of CP by EUS (endoscopic ultrasound) with good resolution and whole pancreas scanning potential. Material and methods: 30 cases of CP patients were examined by EUS from 9 2003 to 9 2004 with the Olympus EU-M30 and GF-UM200. The size of pancreas, the boundary, echo, pancreatic ducts, the diameter of common bile duct, side ducts, pancreas stone, pancreas albumen thrombosis, cysts were recorded. The control group was 30 cases with small polyps of stomach and esophagus.
AB0746 Diagnostic autoantibody signatures of rheumatoid arthritis patients identified with a bead-based assay approach
Authors: P. I. Budde, B. Ostendorf, A. Lueking, M. von Darl, A. Sörgel, C. Theek, H. Goehler, J. Schwermann, M. Gamer, K. Marquardt, A. Telaar, D. Chamrad, S. Vordenbäumen, P. Schulz-Knappe, M. Schneider
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoid arthritis (RA) is an autoimmune disease typically characterized by chronic inflammation, accumulation of self-reactive B-cells and production of autoantibodies of which anti–cyclic citrullinated peptide (anti-CCP) antibodies and rheumatoid factor (RF) have diagnostic utility. Despite these two well established markers up to 30% of RA patients remain sero-negative making an early diagnosis of RA more difficult. Although progress has been made to characterize risk factors for anti-CCP negative RA, studies on autoantibody profiles in CCP-negative RA are so far lacking. <h3>Objectives</h3> To improve the current diagnosis of RA, we aimed to determine whether the group of anti-CCP negative RA patients can be identified based on specific autoantibody profiles. Our major goal is to develop a novel autoantibody-based diagnostic test that allows to correctly diagnosing CCP- and RF-negative early RA patients. <h3>Methods</h3> In order to identify novel autoantigens characteristic for CCP-negative RA patients we performed a large-scale screen of 5800 proteins in a total of 150 serum samples of patients with stable RA and healthy volunteers. The major technology platform employed in this study is an automated bead-based Luminex xMAP technology which enables to measure the reactivity of autoantibodies to up to 500 different antigens in one single serum sample. All proteins are produced from E.<i>coli</i>, are highly purified by affinity capturing, sequenced by mass spectrometry, and each protein is coupled in optimised concentration to individual colour coded Luminex beads. <h3>Results</h3> Using both univariate and multivariate statistical algorithms we identified 144 novel antigens in RA patients. Furthermore, our data indicated heterogeneity in the autoantibody profile of RA patients and some overlap between the group of CCP-positive and CCP-negative patients. To address this complexity and heterogeneity we developed biomarker panels comprising five to ten antigens to identify CCP-negative RA patients. Notably, one panel with six antigens showed high specificity comparable to CCP. Another panel was able to detect about 60% of CCP-negative patients for whom currently no diagnostic marker is available. <h3>Conclusions</h3> CCP sero-negative RA patients can be identified based on specific set of autoantibodies. Further studies are currently conducted to validate the biomarker panels in early RA patients. <h3>Disclosure of Interest</h3> None Declared
Association Between Weight Gain and the Prevalence and Severity of Wheezing and Asthma in the First Year of Life
Authors: Gustavo Wandalsen, Leila Borges, Nathalia Barroso, Fabiola Suano, Elaine Prestes, Herberto J. Chong Neto, Nelson A. Rosario, Ana Carolina Dela Bianca, Carolina Aranda, Decio Medeiros, Emanuel Sarinho, Lillian Sanchez Lacerda Moraes, Javier Mallol, Dirceu Sole
Journal: Journal of Allergy and Clinical Immunology (2013)
Promoting male partner HIV testing and safer sexual decision making through secondary distribution of self-tests by HIV-negative female sex workers and women receiving antenatal and post-partum care in Kenya: a cohort study
Authors: Harsha Thirumurthy, Samuel H Masters, Sue Napierala Mavedzenge, Suzanne Maman, Eunice Omanga, Kawango Agot
Journal: The Lancet HIV (2016)
Abstract SY20-01: CHD5: Chromosome engineering, chromatin dynamics and cancer
Authors: Alea A. Mills
Journal: Cancer Research (2012)

Abstract Although 1p36 loss has been documented for decades and a variety of malignancies have this particular lesion, the tumor suppressor mapping to this genomic interval had not been identified. Using chromosome engineering to create models with gain and loss of the region of the mouse genome corresponding to human 1p36, we pinpointed a potent tumor suppressive interval, identified Chromodomain Helicase DNA-binding domain protein 5 (CHD5) as the causative gene in the region, elucidated molecular pathways induced by CHD5, and demonstrated that CHD5 is frequently deleted in human cancer. The discovery of CHD5 as a tumor suppressor has had a major impact in the cancer field. Indeed, it is now appreciated that CHD5 is mutated in cancers of the breast, ovary, colon, and prostate, as well as in melanoma, glioma, and neuroblastoma. Furthermore, CHD5 status is a prognostic indicator of patient survival following anti-cancer therapy. Still, the mechanism by which CHD5 exerts its tumor suppressive role is barely understood. CHD5 belongs to the CHD family of SWI-SNF-like ATP dependent-chromatin remodeling proteins; however, the role of CHD5 in modulating chromatin dynamics has not been reported. Here, we show that CHD5's tumor suppressive function is dependent on its tandem plant homeodomains (PHDs)—modules that in several other chromatin-remodeling proteins regulate transcription by binding to specific covalent modifications on histone tails. Each of the two PHDs of CHD5 preferentially bind unmethylated H3K4 (H3K4me0), an interaction abrogated by methylation of H3K4 but unaffected by modification of H3K9. Consistent with its binding specificity in vitro, genome-wide ChIP-sequencing indicates that CHD5 binds loci lacking highly methylated H3K4 marks in vivo. Both loss- and gain-of-function studies reveal that CHD5 modulates transcription, and furthermore, that CHD5 is a potent inhibitor of cellular proliferation. Mutation of residues within the PHDs of CHD5 that abolish H3K4me0 binding effectively abrogate the ability of CHD5 to modulate expression of target genes as well as to inhibit proliferation, leading to tumorigenesis in vivo. These findings identify CHD5 as a member of a newly appreciated class of H3K4me0-binding PHD containing proteins and reveal a critical role for this interaction in facilitating CHD5's cellular function, providing new insight into the molecular mechanism responsible for the tumor suppressive role of CHD5. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY20-01. doi:1538-7445.AM2012-SY20-01
<i>Méta-analyse en médecine</i>: the first book on systematic reviews in medicine
Authors: Milos Jenicek
Journal: Journal of the Royal Society of Medicine (2015)

Interest in systematic reviews and meta-analysis in medicine began in the late 1970s. During the 1980s, these methods began to be adopted more widely by medical researchers, and in the late 1980s, expository journal articles began to appear, and the first book about meta-analysis in medicine was published. The book was published in 1987 by Milos Jenicek, a professor at the Universite de Montreal. Too often, the anglophone world remains unaware of important contributions to science and other fields which have been published in languages other than English. So it was with this book, which was published in French. A bilingual friend – Michael Kramer, a professor of epidemiology at McGill University in Montreal – obtained a copy of the book for me in 1994. After reading and greatly enjoying it, I visited Montreal in October of that year and asked Milos to sign my copy. He wrote: ‘To Dr Iain Chalmers, with compliments and astonishment that he still believes that this book is worth reading’. Meta-analyse en medecine was and remains wellworth reading, even for someone whose knowledge of French is not very strong. I regard the book as an important and insufficiently acknowledged milestone in the development of methods to assess the effects of medical treatments. Even if I or others had cited the book appropriately, however, it would have been difficult and probably impossible for our readers to have accessed copies of it, as its stock was shredded by the publisher not all that long after it had been published. It is for this reason that fairly long excerpts from the book, with translations, have been added to the James Lind Library. Because of the importance of the book in the history of research synthesis in medicine, I wanted to find out from Milos Jenicek how he came to write it. What follows takes the form of an interview, although it is not a verbatim account of our conversations and communications. IC: How far back does one have to go to identify the origins of the ideas that led to the book?
Abstract 318: NAD(P)H: quinone oxidoreductase 1 possesses a strong regulatory role in MAPK signaling pathways
Authors: Brad A. Patrick, Labanyamoy Kole, Anil K. Jaiswal
Journal: Cancer Research (2010)

Abstract NAD(P)H: quinone oxidoreductase (NQO1) is a cytosolic redox-regulating enzyme modulated by Nrf2-mediated stress signaling pathways, with an established role in regulation of stress-related transcription factors. In these studies we investigate the role of NQO1 in regulation of mitogen-activated protein kinase (MAPK) signaling pathways. Quantitative PCR and western blot studies showed that constitutive levels of several MAPK members are upregulated in NQO1-null mouse skin as well as in skin-derived keratinocytes, relative to wild type. However, though total protein levels are increased, inducibility of these kinases by known MAPK inducers such as EGF and benzo[a]pyrene (BP) is significantly decreased in NQO1-null cells. NQO1 regulation of MAPK signaling was confirmed by studies showing that NQO1 knockdown by siRNA led to decreased MAPK activation, and overexpression of NQO1 protein led to increased MAPK activation by EGF. Similarly, downregulation of activity via dicoumarol caused loss of ERK phosphorylation, while NQO1 activation via t-BHQ caused increased ERK phosphorylation, which was blocked by MAPK pathway-specific inhibitors. To investigate the functional role of MAPK deactivation in skin-derived keratinocytes, studies with BP and menadione showed that lack of NQO1 expression led to increased susceptibility to ROS generation, and that this ROS generation causes increased toxicity. Taken together, these results show a significant role for NQO1 in regulation of MAPK signaling pathways, which ultimately leads to protection against ROS-mediated apoptosis. 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 318.
551Effects of interleukin-33 on tissue factor in human endothelial cells in vitro
Authors: S Stojkovic, C Kaun, I Huk, W Eppel, K Huber, J Wojta, S Demyanets
Journal: Cardiovascular Research (2014)

Background: Interleukin (IL)-33 is a member of the IL-1 cytokine family. IL-33 was previously shown to induce angiogenesis and the expression of inflammatory cytokines and adhesion molecules in endothelial cells. Tissue factor (TF) is a primary trigger of coagulation. Elevated levels of TF are found in atherosclerotic plaques, and TF leads to thrombus formation, when released upon plaque rupture. Aim: Here we investigated the impact of IL-33 on TF expression in human endothelial cells, as a new possible mechanism for IL-33 to regulate their thrombotic potential. Methods and Results: Human umbilical vein endothelial cells (HUVEC) and human coronary artery endothelial cells (HCAEC) were treated with 100, 10 and 1ng/ml recombinant human IL-33. Expression of mRNA specific for TF was determined by RT-PCR. TF protein levels were measured by specific enzyme-linked immunosorbent assays (ELISAs). We found that IL-33 significantly induced TF mRNA up to 200-fold and protein expression up to 145-fold in a time- and concentration-dependent manner in HUVEC and HCAEC. ST2-siRNA-mediated gene knockdown inhibited IL-33-induced TF expression, suggesting that this effect of IL-33 is facilitated through its receptor ST2. Preincubation of HUVEC with 100μM of the NFkB-inhibitor dimethyl-fumarate abrogated IL-33-induced TF protein synthesis. IL-1 receptor antagonist had no effect on IL-33-induced increase of TF expression. In human carotid atherosclerotic plaques (n=16), TF mRNA positively correlated with IL-33 mRNA expression (r=0.86, p<0.001). Conclusion: Our results showed that IL-33 increases TF expression in human endothelial cells, and that this effect is ST2/NFkB-dependent, but IL-1-independent. Furthermore, we supported our in vitro data in human atherosclerotic tissue where we found a strong positive correlation of IL-33 and TF expression. Thus, IL-33-induced changes in TF expression could affect the thrombotic potential of endothelial cells, as well as potentiate thrombotic events in the setting of ruptured human atherosclerotic plaques.
MS-09 * PROGNOSTIC IMPLICATIONS OF HISTOLOGICAL CLEAR CELLS IN HIGH GRADE INTRACRANIAL EPENDYMAL TUMORS: A RETROSPECTIVE ANALYSIS FROM A TERTIARY CARE HOSPITAL IN PAKISTAN
Authors: F. A. Hashmi, S. A. Khan, M. E. Bari, A. Ahmed
Journal: Neuro-Oncology (2014)

Clear Cell variant in Ependymal tumors is rare. We aim to compare the features & clinical outcomes of Clear Cell variant with the Classic pathology of high grade intracranial Ependymal tumors in Pakistan. A retrospective cohort study conducted at the Department of Neurosurgery, Aga Khan University. The medical record files from 2003 - 2013 were reviewed, MRI/C.T scans and Histopathological slides of WHO grade III Ependymal tumors were reviewed. Patients lost to follow-up were contacted. Analysis was done on SPSS 20.There were 10 cases of clear cell variant and 23 cases of classic Anaplastic Ependymoma. The median age of Clear Cell variant was 52 years (range 24years-72 years),whereas of Anaplastic Ependymoma was 37 years (range 3 months to 65 years). Symptoms included Headache 66% in CCE and 63% in AE, Seizures 30% in CCE and 22% in AE, and raised ICP in 30% in CCE and 54% of AE. CCE was Supratentorial in 70% cases, intracranial Anaplastic Ependymoma was supratentorial in 58% of cases. Gross Total Resection was achieved in 55% cases in CCE and 26% cases in AE. Subtotal resection was done in 45% cases in CCE and 65% in AE. Radiotherapy was given in 60% patients in CCE and in 50% in AE. Recurrence was there in 80% cases of CCE and 55% in AE. Repeat Surgery was done in 30% cases of CCE and 34% cases of AE. Median Progression free survival was 8 months(range 3-28 months), and Overall survival was 10 months(range 3-41 months) in CCE. Median Progression free survival was 4 months (range 0.5-53 months), Overall survival was 14 months (range 1.5- 36 months) in AE. The median Progression free survival was better in Clear Cell variant than Anaplastic Ependymoma, this could be explained by a higher Gross total resection in CCE, whereas the median Overall survival was worse in Clear Cell variant group.
The Mask of Sanity
Authors: M. S. Rahman
Journal: BMJ (2012)

It would be an understatement to say that The Mask of Sanity is one of the most important books in the discipline of psychopathy. This book not only inspired clinicians, but provided momentum for research into people whom before its publication had mostly been neglected by researchers.

The public is fascinated by so called psychopaths; a quick peek at the bestseller list will attest to this. Yet this book is much more entertaining than these novels of murder and mayhem. In addition, readers benefit from the clinical observations of one of the foremost psychiatrists of his …
Abstract 1890: Human papillomavirus serology and the risk of lung cancer
Authors: Devasena Anantharaman, Michael Pawlita, Tim Waterboer, David Zaridze, Anush Mukeria, Dana Mates, Neonila Szeszenia-Dabrowska, Peter Rudnai, Jolanta Lissowska, Vladimir Bencko, Ghislaine Scelo, Paolo Boffetta, Paul Brennan
Journal: Cancer Research (2011)

Abstract A role for HPV in lung cancer has been suggested by several case series. We examined further the role of HPV and lung cancer in a case-control study involving 1633 lung cancer cases and 2729 matched controls from six central European countries. HPV infection status was ascertained for several low-risk and high-risk HPV types by bead-based multiplex serology. Unconditional logistic regression models were used to examine the risk of lung cancer associated with specific HPV types. Overall, low prevalence (&amp;lt;5%) of antibodies for early proteins (E6 and E7) of all HPV types were observed among controls. Seropositivity for both E6 and E7 proteins (for any HPV type) was very rare (&amp;lt;0.3%). We observed a significantly increased risk of lung cancer in the presence of antibodies to HPV6L1, HPV11L1, HPV16L1, HPV18L1, HPV11E6, HPV11E7, HPV16E7 and HPV18E7 after adjustment for potential confounders including age, gender and smoking (Table 1). Similar effects were observed for never, former and current smokers. These results indicate that HPV antibodies are substantially increased in lung cancer cases compared to controls. Whether this indicates a causal relationship is yet to be determined. 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 1890. doi:10.1158/1538-7445.AM2011-1890
Abstract LB-197: Tumor vasculature associated marker as a target for recombinant DNA based vaccines
Authors: Andrea Facciabene, John Facciponte, George Coukos
Journal: Cancer Research (2010)

Abstract Discussion 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 LB-197.
P41 Pulmonary Rehabilitation (PR) endurance shuttle walk test distances: Differences between Interstital Lung Disease (ILD) and Chronic Obstructive Pulmonary Disease (COPD): Abstract P41 Table 1.
Authors: A Lewis, L Cornish, F Dyer, K Cheema, J Bott
Journal: Thorax (2013)

<h3>Background</h3> There is evidence to suggest that Pulmonary Rehabilitation (PR) is beneficial for patients with chronic lung diseases other than COPD (AACP/AACVPR guidelines 2007, ILD consultation document 2013). However, there is little evidence to suggest that PR provides exercise tolerance benefits comparable to COPD patients who participate in the same PR programmes. <h3>Aim</h3> To determine whether walking distance improvements differ significantly between ILD and COPD patients following PR. <h3>Method</h3> Retrospective data of PR Endurance Shuttle Walk Test distances (ESWTD) pre- to post-PR were analysed and compared between 55 Interstitial Lung Disease (ILD) and 440 COPD patients from February 2005 to December 2012. Patients participated in a PR programme run by the same clinical team. Independent sample two-tailed t-tests were performed on data for pre-PR ESWTD, post-PR ESWTD and ESWTD change. <h3>Results</h3> There were no significant differences between group ESWTD prior to PR (t = -0.049, p = 0.961), following PR (t = -0.227, p = 0.820) or change in ESWTD (t = -0.228, p = 0.820). <h3>Conclusions</h3> These data indicate there is no significant difference between ILD and COPD patients’ walking distances. ILD patients with a reduced exercise tolerance should be included and referred to PR programmes.