tbuckley/cabot-search huggingface dataset:
Endoscopic ultrasound-guided fine needle biopsy of pancreatic metastasis from Merkel cell carcinoma
Authors: Antonella Maimone, Maria Bianchi, Paola Lorenzini, Annalisa de Leone, Luca De Luca
Journal: Endoscopy (2016)

Merkel cell carcinoma (MCC) is a rare and aggressive cutaneous neuroendocrine carcinoma. The incidence rate is approximately 0.3 – 0.6/100 000 per year [1] [2]. At initial presentation most patients with MCC (70 % – 80 %) have localized disease, and only a few (1 % – 4 %) have distant metastases [3]. Moreover, MCC rarely metastasizes to the pancreas, therefore this represents a challenge for the differential diagnosis of pancreatic masses [4].
FRI0504 TNF-Alpha Gene Polymorphisms and Juvenile Idiopathic Arthritis: Influence on Disease Outcome and Therapeutic Response
Authors: A. Scardapane, R. Ferrante, M. Nozzi, V. Marzetti, M. Lucantoni, M. Marsili, L. Stuppia, F. Chiarelli, L. Breda
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> One of the most important molecules involved in juvenile idiopathic arthritis (JIA) is the Tumor Necrosis Factor-α (TNF-α), since several studies have demonstrated increased TNF-α levels in both serum and synovial fluid of children with chronic arthritis. Moreover, the proven efficiency of anti TNF-α biologic drugs in JIA patients suggests a key role for this cytokine. Several single nucleotide polymorphisms (SNPs) have been identified within the promoter, exonic, intronic, and 39untranslated region of the TNF-α gene, but conflicting results about the role of these variants in JIA have been reported and only a very small minority of these genetic variants have proven to be correlated with disease phenotype and/or clinical outcome. <h3>Objectives</h3> To investigate the genetic contribution of TNF-α gene polymorphisms on the disease course and therapeutic response in patients with JIA. <h3>Methods</h3> 74 Caucasian patients with JIA were recruited with a control group of 77 healthy children. DNA was extracted for analysis of TNF-α gene promoter polymorphisms at position -163, -244, -238, -376 and -308. <h3>Results</h3> No SNPs at position -163 were observed while we observed only SNPs at position -244 and -376 in the controls. No differences were observed in the prevalence of SNPs at -238 and -308 between JIA and controls. In JIA patients no significant differences were observed between the -238 and -308 G/A genotypes and different disease phenotypes. We observed a significant lower disease activity expressed in the carriers of -308 GG genotype with respect to GA and AA genotypes after 6 (p=0.008 p=0.013 respectively) and 12 months of disease (p=0.02 p=0.08 respectively). Also the -238 GG genotypes showed a better disease course after12 months of disease. Moreover the -238/-308 GG genotypes presented the higher reduction of disease activity both after 6 (p&lt;0.01 vs GA and p&lt;0.01 vs AA) and 12months from baseline (p&lt;0.01 vs GA and p&lt;0.01 vs AA). After 12 months of biologic therapy, a significant higher disease activity was observed in patients with genotype -308AA respect to both GA (p=0.012) and GG (p=0.016). <h3>Conclusions</h3> JIA patients carrying the TNF-α -308 GA/AA and -238 GA genotypes are associated with a worse prognosis and with a lower response to anti-TNF-α drugs. <h3>References</h3> Field M. Tumour necrosis factor polymorphisms in rheumatic diseases. QJM 2001;94(5):237-46. Hajeer AH, Hutchinson IV. TNF-alpha gene polymorphism: clinical and biological implications. Microsc Res Tech 2000;50(3):216-28. <h3>Disclosure of Interest</h3> None declared
Fatal Bacterial Meningitis Possibly Associated with Substandard Ceftriaxone — Uganda, 2013
Authors: Jason W. Nickerson, Amir Attaran, Brian D. Westerberg, Sharon Curtis, Sean Overton, Paul Mayer
Journal: MMWR Morbidity and Mortality Weekly Report (2015)

annual reporting were excluded from this analysis.For 2012, data from all 50 states, DC, and Puerto Rico were summarized.To calculate the number of TB cases that were averted by treating LTBI diagnosed during contact investigations in 2012, an estimated 2.4% (95% confidence interval [CI] = 1.2%-4.7%)cumulative 5-year incidence without treatment (5) was used, discounted for an estimated 80% treatment effectiveness (based on findings of efficacy in clinical trials) (6).Incomplete treatment of LTBI was considered equivalent to no treatment.Missed opportunities for prevention were calculated by projecting the number of missed contacts from patients with no contact elicited or outcomes at each step of the contact investigation by the observed proportions.The projections for completing treatment were discounted by the observed proportions of patients not completing for reasons of death, adverse medication effects, health care provider decisions to discontinue treatment, and development of TB disease.During 2003-2012, the 44 states and Puerto Rico reported 114,003 TB cases in surveillance, accounting for 90.2% of all TB cases reported in the United States and Puerto Rico (1).During this time, the number of index patients in the 44 states and Puerto Rico decreased while the number of contacts listed per index patient with contacts elicited increased from 14.9 to 21.3 contacts for sputum smear-positive index patients (Table 1).The percentage of index patients with no contact elicited decreased overall, from 7.2% in 2003 to 5.1% in 2012 for smear-positive patients and from 18.6% to 11.3%
Conspiracy of silence: psychiatric counseling with students at high risk for academic failure
Authors: J K Kuehn, J L Kuehn
Journal: American Journal of Psychiatry (1975)

The authors examined the academic records and counseling histories of 132 freshman students at a state university who sought psychiatric counseling. They found that most students with poor previous academic performance were not helped academically by brief (crisis intervention) psychiatric counseling. They also found that many couselors resisted confronting such students with their academic inadequacies.
Safety of Nonanesthetist Sedation with Propofol for Outpatient Colonoscopy and Esophagogastroduodenoscopy
Authors: D Külling, R Rothenbühler, W Inauen
Journal: Endoscopy (2003)

Background and Study Aims: In our endoscopy service, nonanesthetists administered propofol sedation has been used in more than 8000 procedures during the past 3 years. This study prospectively assessed the safety of propofol sedation in outpatient colonoscopy and esophagogastroduodenoscopy (EGD). Patients and Methods: A total of 300 consecutive outpatients (mean age 53, range 14-94) were enrolled in the study (139 colonoscopies, 161 EGDs). After an initial dose of 0.5 mg/kg (ASA I-II and age ≤70) or 0.25 mg/kg (ASA >III or age >70 years), propofol was titrated in 10 mg boluses to a steady state of sedation by the endoscopy nurse under the endoscopist's supervision. Colonoscopy patients also received 25 mg pethidine (meperidine) and 20 mg butylscopolamine, whereas EGDs were performed with propofol sedation alone, without topical pharyngeal anesthesia. In addition to standard monitoring with pulse oximetry and automated sphygmomanometry, patients were also observed with sidestream capnography or measurement of electrocardiographic impedance changes, providing real-time graphic assessment of respiratory activity. All patients were given oxygen 2 L/min by nasal cannula during the entire procedure. Results: Mean dosages of 157 mg (range 70-340) and 180 mg (60-400) propofol were administered for colonoscopy and EGD procedures, respectively. No episodes of apnea occurred. The oxygen saturation fell below 90 % for short periods of time in 11 patients (3.7 %). Three patients required a temporary increase in oxygen delivery. No assisted ventilation was necessary. In 22 patients (7.3 %), the mean blood pressure temporarily decreased below 50 mmHg. Two patients received a 500-ml infusion of normal saline. Conclusions: Propofol can be safely administered for sedation during colonoscopy and esophagogastroduodenoscopy by nonanesthetists who are familiar with the pharmacological properties and use of this drug.
Infantile cortical hyperostosis (Caffey's disease)
Authors: A O Ogunmekan
Journal: JAMA (1973)

A case of infantile cortical hyperostosis (Caffey's disease) is presented with its usual clinical and radiological manifestations. The accompanying anaemia and thrombocytopenia as seen in our case is discussed. The possibility of autoantibodies secondary to an immunological defect is put forward to explain the cause of the anaemia and thrombocytopenia. This may be a new feature of the disease or a modification of the current concept.
Reduced Expression of Histone Methyltransferases KMT2C and KMT2D Correlates with Improved Outcome in Pancreatic Ductal Adenocarcinoma
Authors: Joshua B.N. Dawkins, Jun Wang, Eleni Maniati, James A. Heward, Lola Koniali, Hemant M. Kocher, Sarah A. Martin, Claude Chelala, Frances R. Balkwill, Jude Fitzgibbon, Richard P. Grose
Journal: Cancer Research (2016)

Genes encoding the histone H3 lysine 4 methyltransferases KMT2C and KMT2D are subject to deletion and mutation in pancreatic ductal adenocarcinoma (PDAC), where these lesions identify a group of patients with a more favorable prognosis. In this study, we demonstrate that low KMT2C and KMT2D expression in biopsies also defines better outcome groups, with median survivals of 15.9 versus 9.2 months (P = 0.029) and 19.9 versus 11.8 months (P = 0.001), respectively. Experiments with eight human pancreatic cell lines showed attenuated cell proliferation when these methyltransferases were depleted, suggesting that this improved outcome may reflect a cell-cycle block with diminished progression from G0-G1 RNA-seq analysis of PDAC cell lines following KMT2C or KMT2D knockdown identified 31 and 124 differentially expressed genes, respectively, with 19 genes in common. Gene-set enrichment analysis revealed significant downregulation of genes related to cell-cycle and growth. These data were corroborated independently by examining KMT2C/D signatures extracted from the International Cancer Genome Consortium and The Cancer Genome Atlas datasets. Furthermore, these experiments highlighted a potential role for NCAPD3, a condensin II complex subunit, as an outcome predictor in PDAC using existing gene expression series. Kmt2d depletion in KC/KPC cell lines also led to an increased response to the nucleoside analogue 5-fluorouracil, suggesting that lower levels of this methyltransferase may mediate the sensitivity of PDAC to particular treatments. Therefore, it may also be therapeutically beneficial to target these methyltransferases in PDAC, especially in those patients demonstrating higher KTM2C/D expression. Cancer Res; 76(16); 4861-71. ©2016 AACR.
PTU-080 Calprotectin predicts relapse of ibd even in the presence of a ‘normal’ colonoscopy
Authors: R Deberry, A Rahman, P Dubois, G Chung-Faye, B Hayee
Journal: Gut (2015)

<h3>Introduction</h3> Faecal calprotectin is a sensitive and reliable marker of mucosal inflammation and mucosal healing in IBD. It has always been compared against endoscopic appearance as the presumed gold standard for assessment of disease activity. Several strands of evidence – using magnifying or image-enhanced endoscopy as well as confocal laser endomicroscopy – highlight abnormalities in colonic mucosa reported as 'normal' by standard white light colonoscopy (WLC). This may be compounded by the difficulties in bowel preparation in IBD and the non-widespread use of high definition technology (although the latter has not been specifically studied in relation to IBD). We wished to determine whether an elevated FCALP could predict relapse even in the presence of an ostensibly normal WLC. <h3>Method</h3> As part of a larger study correlating FCALP to histologic assessment of disease activity, retrospective data was collected for consecutive patients with IBD on stable therapy undergoing colonoscopy for disease assessment. FCALP (Bühlmann ELISA) was collected as close as possible (prior) to the colonoscopy. When the colonoscopic appearances were reported as normal (Mayo endoscopic subscore 0 for ulcerative colitis, UC, and SES-CD = 0 for Crohn's disease, CD), patients were followed to determine if they relapsed, with time to relapse (or last recorded follow-up) taken from the date of colonoscopy. For the purposes of this study, relapse was defined generally as "continuous or worsening intestinal symptoms requiring an escalation in therapy". Switching between 5ASA classes was not included in this definition unless the specifically stated to be in response to uncontrolled symptoms. <h3>Results</h3> 46 patients with UC and 37 with CD were identified with the above criteria. Median time between FCALP measurement and colonoscopy was 0.70 (max 2.89) and 0.90 (max 1.5) months respectively. Normal FCALP was detected in 16 patients with UC and 12 with CD. Figures 1 and 2 below show relapse-free survival in those patients with a normal colonoscopy and normal FCALP (&lt;60 mcg/g faeces; green line) compared to those with elevated levels (red line). Median calprotectin in the 'high' group was 377 (229–794) in UC and 192 (118–247) in CD. At 12 months, survival proportions were 86% with UC and normal FCALP compared to 34% in those with high FCALP. In CD, these proportions were 50% and 12% respectively. <h3>Conclusion</h3> Elevated levels of FCALP predict relapse of IBD even in the presence of a macroscopically normal colonoscopy. <h3>Disclosure of interest</h3> None Declared.
American College of Cardiology clinical expert consensus document on standards for acquisition, measurement and reporting of intravascular ultrasound studies (ivus)31When citing this document, the American College of Cardiology would appreciate the following citation format: Mintz GS, Nissen SE, Anderson WD, Bailey SR, Erbel R, Fitzgerald PJ, Pinto FJ, Rosenfield K, Siegel RJ, Tuzcu EM, Yock PG. ACC Clinical Expert Consensus Document on Standards for the acquisition, measurement and reporting …
Authors: Gary S Mintz, Steven E Nissen, William D Anderson, Steven R Bailey, Raimund Erbel, Peter J Fitzgerald, Fausto J Pinto, Kenneth Rosenfield, Robert J Siegel, E.Murat Tuzcu, Paul G Yock, Robert A O’Rourke, Jonathan Abrams, Eric R Bates, Bruce R Brodie, Pamela S Douglas, Gabriel Gregoratos, Mark A Hlatky, Judith S Hochman, Sanjiv Kaul, Cynthia M Tracy, David D Waters, William L Winters
Journal: Journal of the American College of Cardiology (2001)
PTU-119 Outcomes of viraemic hepatitis c patients in chester: a 10 year district general hospital experience
Authors: W On, H Caldwell, S Dale, T Maheswaran, M Karmo
Journal: Gut (2015)

<h3>Introduction</h3> Poor access to appropriate healthcare services is implicated as one of the shortcomings of the Hepatitis C (HCV) treatment pathway in the UK and Public Health England has recommended improving accessibility to treatment centres as part of a national strategy to improve treatment uptake rates.<sup>1</sup>The Countess of Chester NHS Foundation Trust (COCH) is the main hospital serving a population of approximately 250,000 people from the town of Chester and surrounding rural areas. COCH does not provide treatment for HCV and patients are referred to the Royal Liverpool University Hospital NHS Trust (RLUH) for anti-viral therapy. We wanted to assess the impact of segregating HCV services between two separate hospitals on the treatment outcomes and follow-up rates. <h3>Method</h3> A retrospective analysis from January 2004 to July 2014 was done. 235 patients with positive HCV serology and a quantifiable viral load confirmed on polymerase chain reaction (PCR) testing were identified from the microbiology database at COCH. Data on treatment outcomes was obtained from the hepatology unit at RLUH. Analysis of patients’ case notes and clinic letters was done where appropriate. <h3>Results</h3> 87% (204/235) of patients were reviewed in a gastroenterology clinic at COCH. 71% (144/204) of patients seen in clinic were referred to RLUH for treatment. Of the 144 patients referred to RLUH, 28% (41/144) successfully completed treatment. The overall percentage of patients lost to follow-ups due to non-attendances (DNA) was 38% (78/204). The flowchart depicts the known outcomes of the 204 patients seen in clinic. <h3>Conclusion</h3> Our data illustrates a 10 year experience of the management of HCV in a district general hospital and supports the need to improve access to HCV treatment centres. Localisation of treatment centres would minimise the burden of travel for patients and improve adherence to treatment. Patients with HCV within a hospital catchment area should also have their care centralised to that hospital to prevent loss to follow-ups. This is particularly important to allow surveillance for complications of chronic HCV infections. <h3>Disclosure of interest</h3> None Declared. <h3>Reference</h3> Public Health England, Hepatitis C in the UK: 2014 report. (https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/337115/HCV_in_the_UK_2014_24_July.pdf)
Paraoxonase 1 Activity Is Modulated by the rs662 Polymorphism and IgG Anti–High‐Density Lipoprotein Antibodies in Patients With Rheumatoid Arthritis: Potential Implications for Cardiovascular Disease
Authors: Javier Rodríguez‐Carrio, Raquel López‐Mejías, Mercedes Alperi‐López, Patricia López, Francisco J. Ballina‐García, Miguel Á. González‐Gay, Ana Suárez
Journal: Arthritis & Rheumatology (2016)

Objective Paraoxonase 1 (PON‐1) is a high‐density lipoprotein (HDL)–associated antioxidant enzyme that plays an important role in HDL‐mediated cardioprotection. Although genetic polymorphisms are known to modulate PON-1 activity, its involvement in cardiovascular disease (CVD) in rheumatoid arthritis (RA) is controversial, suggesting that other factors may modulate its function. Since anti‐HDL antibodies have been found to be related to an impaired lipid profile and occurrence of CVD in RA, this study was undertaken to examine the associations between PON-1 activity, anti‐HDL antibodies, and CVD according to PON1 genetic variants in patients with RA. Methods Serum PON-1 activity, using paraoxon as substrate, and IgG anti‐HDL antibodies were quantified in 212 RA patients and 110 healthy controls. The PON1 rs662 genotype (Q&gt;R) was determined with TaqMan probes. An additional group of 13 biologics‐naive patients with RA was prospectively followed up for 3 months. Results PON‐1 activity was decreased in RA patients compared to healthy controls ( P = 0.005), and an effect of the rs662 genotype was noted in both groups, with Q/Q homozygotes exhibiting the lowest PON‐1 activity. The distribution of rs662 genotypes did not differ between RA patients and healthy controls ( P = 0.215). In patients carrying the Q/Q genotype, anti‐HDL antibodies were associated with impaired PON‐1 activity ( P = 0.010), and levels of anti‐HDL antibodies were associated with decreased HDL levels (r = −0.680, P &lt; 0.001) and higher prevalence of cardiovascular events, as determined in univariate and multivariate models. Furthermore, change in anti‐HDL antibody levels upon tumor necrosis factor blockade was an independent predictor of improved PON‐1 activity (β = −0.369, 95% confidence interval −0.669, −0.069; P = 0.024). Conclusion PON‐1 activity is impaired in RA in association with the rs662 genotype and anti‐HDL antibodies, the latter being recognized as a pivotal player in the link between rs662 and CVD in patients with RA.
FRI0582 Could MRI of the Hand Improve the Accuracy of the 2010 ACR/EULAR Criteria for Rheumatoid Arthritis?:
Authors: D. Marques, M.P. Lisbona, L. Orpinell, A. Solano, J. Ares, M. Almirall, T. Salman-Monte, J. Maymo
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Objectives</h3> To analyze whether the addition of inflammatory findings or erosions on hand MRI improve the accuracy of ACR/ EULAR 2010 RA classification criteria in early arthritis. <h3>Methods</h3> Cross-sectional study of patients with early arthritis (defined as the presence of at least one inflamed joint, less than a year since the start of the first symptoms and without meeting the ACR/EULAR 2010 criteria) referred to the Early Arthritis Clinic at Hospital Mar (PSMAR, Barcelona). At baseline, demographic (age, gender), disease-related (median of disease duration in months, serum levels of RF U/ml and ACPA U/ml, presence of radiological erosions on hands and feet) and previous treatments (NSAIDs, glucocorticoids (GCs) and synthetic DMARDs) were recorded. Clinical data, laboratory tests and functional disability were collected. MRI of the dominant hand (h-MRI) was performed and score according to the OMERACT RAMRIS recommendations (RAMRIS-synovitis (0-21), RAMRIS-bone edema (0-69) RAMRIS-erosions (0-230)), tenosynovitis (0-26) and total inflammation (sinovitis plus bone edema plus tenosynovitis, 0-116) in wrist and 2nd to 5th MCP joints were recorded. We used the presence of any lesion on h-MRI added 2010 RA criteria to improve the diagnostic accuracy of these criteria. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and diagnostic accuracy of the ACR/EULAR 2010 criteria alone and associated with h-MRI parameters were analyzed using fulfillment of the ACR 1987 criteria at one year follow-up as standard reference. All data was analyzed using the SPSS v.18. <h3>Results</h3> Sixty-one patients with early arthritis out of 199 (30.6%) who did not fulfilled the ACR/EULAR 2010 criteria for the diagnosis of RA at baseline and with avalaible data of h-MRI were included. Demographic, clinical and h-MRI data at baseline will be shown in an additional Table. The mean (±SD) RAMRIS score for synovitis was 4.86 (±2.61), for RAMRIS bone-edema was 6.81 (±3.61), for RAMRIS-erosions was 4.42 (±4.84), for tenosynovitis was 4.63 (±5.3), total inflammation was 10.6 (±13.11) and Total RAMRIS of 12.98±11.25). The table showed the sensitivity, specificity, PPV, NPV and diagnostic accuracy of the ACR/EULAR 2010 criteria alone or associated with MRI parameters using as reference standard fulfil the 1987 RA criteria at one year. <h3>Conclusions</h3> Our results suggest that including baseline inflammatory findings and erosions from h-MRI in the ACR/EULAR 2010 criteria using the 1987 ACR criteria as a reference at one year, does not improve the diagnostic accuracy in our patients with early arthritis. <h3>References</h3> Tamai M et al. Ann Rheum Dis 2014;73:2219-20. Nieuwenhuis WP et al. Ann Rheum Dis 2014;0:1-2. <h3>Disclosure of Interest</h3> None declared