tbuckley/cabot-search huggingface dataset:
Abstract 1820: Patterns of hematopoietic cancers in Egypt from a population-based registry
Authors: Catherine M. Herzog, Amr S. Soliman, Ibrahim A. Seif Eldein, Ahmed Hablas, Mohamed Ramadan, Mark Wilson
Journal: Cancer Research (2010)

Abstract Objectives: Rates of lymphoma are rising by 4% annually in the United States. Globally, lymphoma incidence rates are also on the rise with about 342,000 new cases per year. Egypt, where hematopoietic (blood and lymphatic) cancer is considered common, has one of the highest age-standardized incidence rates of lymphoma in the world (16.3/100,000), greater than that of the United States (15.3/100,000). Risk factors for hematopoietic cancers include radiation, viral and bacterial infections, occupational and environmental exposures, family history, and genetic mutations. We evaluated the incidence of these cancers in Egypt and analyzed them in relation to select risk factors to better understand their etiology. Methods: Hematopoietic cancer case data for 1999-2005 from the Gharbiah Population-Based Cancer Registry in Tanta, Egypt, the only population-based registry in Egypt, were analyzed. Crude and age- and gender-specific rates were calculated for 4,260 cases, and evaluated by REAL Malignancy type, morphology, topology, and stage. Potential risk factor variables included age, gender, date of diagnosis, and district of residence, and urban/rural setting. Descriptive and multivariable statistics were calculated and space-time patterns were investigated. Results: Overall, incidence was greater among males and among residents of urban areas. More than half of cases were diagnosed at Stage III or IV. Leukemia and Hodgkin lymphoma predominated in cases under 18 years of age whereas mature B-cell neoplasms were the most common in those older than 18. Average annual crude incidence varied by district, ranging from 10.21 to 20.34 per 100,000, and generally rose during the seven year period. This rise was most prominent in the crude incidence of mature B cell neoplasms, mostly due to diffuse B cell lymphoma. Conclusions: This study provides numerical evidence of the impact of hematopoietic cancer, especially Non-Hodgkin lymphoma, on the Egyptian population. It also appears to follow the rising trend in Non-Hodgkin lymphoma cases seen worldwide. Further comparison of the distribution of incidence and alternative risk factors may lead to a novel understanding of the etiology of hematopoietic cancers and improvements in current treatment. 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 1820.
TCT-352 Validation of High Speed Pullback of a Novel High-Definition Intravascular Ultrasound System
Authors: Kaori Nakagawa, Shigemitsu Tanaka, Hideki Kitahara, Yuhei Kobayashi, Kozo Okada, Kyuhachi Otagiri, Paul Yock, Peter J. Fitzgerald, Yasuhiro Honda, Alan Yeung, Fumiaki Ikeno
Journal: Journal of the American College of Cardiology (2014)
Spatial and temporal analysis of human infection with avian influenza A(H7N9) virus in China, 2013
Authors: W Liu, K Yang, X Qi, K Xu, H Ji, J Ai, A Ge, Y Wu, Y Li, Q Dai, Q Liang, C Bao, R Bergquist, F Tang, Y Zhu
Journal: Eurosurveillance (2013)

Binary file ES_Abstracts_Final_ECDC.txt matches
IL-17F Promotes Tissue Injury in Autoimmune Kidney Diseases
Authors: Jan-Hendrik Riedel, Hans-Joachim Paust, Sonja Krohn, Jan-Eric Turner, Malte A Kluger, Oliver M Steinmetz, Christian F Krebs, Rolf A K Stahl, Ulf Panzer
Journal: Journal of the American Society of Nephrology (2016)

The T H 17 immune response has a central role in the pathogenesis of autoimmune diseases, implicating the T H 17 master cytokine, IL-17A, as the critical mediator of diseases such as human and experimental crescentic GN. However, the relative importance of additional T H 17 effector cytokines, including IL-17F, in immune-mediated tissue injury remains to be fully elucidated. Here, using a mouse model of acute crescentic GN (nephrotoxic nephritis), we identified CD4 + T cells and γδ T cells as the major cellular source of IL-17F in the inflamed kidney. Interventional studies using IL-17F gene–deficient mice, IL-17F–neutralizing antibodies, and adoptive transfer experiments into Rag1 −/− mice demonstrated that CD4 + T cell–derived IL-17F drives renal tissue injury in acute crescentic GN. Notably, IL-17F–deficient nephritic mice had fewer renal infiltrating neutrophils than wild-type nephritic mice, and neutrophil depletion did not affect the course of GN in IL-17F–deficient mice. Moreover, in the chronic model of pristane-induced SLE, IL-17F–deficient mice developed less severe disease than wild-type mice, with respect to survival and renal injury. Finally, we show that IL-17F induced expression of the neutrophil-attracting chemokines CXCL1 and CXCL5 in kidney cells. The finding that IL-17F has a nonredundant function in the development of renal tissue injury in experimental GN might be of great importance for the development of anti–IL-17 cytokine therapies in T H 17-mediated human autoimmune diseases.
Dysregulation of proinflammatory versus anti-inflammatory human TH17 cell functionalities in the autoinflammatory Schnitzler syndrome
Authors: Rebecca Noster, Heleen D. de Koning, Elisabeth Maier, Martina Prelog, Elke Lainka, Christina E. Zielinski
Journal: Journal of Allergy and Clinical Immunology (2016)

TH17 cells have so far been considered to be crucial mediators of autoimmune inflammation. Two distinct types of TH17 cells have been described recently, which differed in their polarization requirement for IL-1β and in their cytokine repertoire. Whether these distinct TH17 phenotypes translate into distinct TH17 cell functions with implications for human health or disease has not been addressed yet.We hypothesized the existence of proinflammatory and anti-inflammatory human TH17 cell functions based on the differential expression of IL-10, which is regulated by IL-1β. Considering the crucial role of IL-1β in the pathogenesis of autoinflammatory syndromes, we hypothesized that IL-1β mediates the loss of anti-inflammatory TH17 cell functionalities in patients with Schnitzler syndrome, an autoinflammatory disease.To assess proinflammatory versus anti-inflammatory TH17 cell functions, we performed suppression assays and tested the effects of IL-1β dependent and independent TH17 subsets on modulating proinflammatory cytokine secretion by monocytes. Patients with Schnitzler syndrome were analyzed for changes in TH17 cell functions before and during therapy with IL-1β-blocking drugs.Both TH17 cell subsets differ in their ability to suppress T-cell proliferation and their ability to modulate proinflammatory cytokine production by antigen-presenting cells because of their differential IL-10 expression properties. In patients with Schnitzler syndrome, systemic overproduction of IL-1β translates into a profound loss of anti-inflammatory TH17 cell functionalities, which can be reversed by anti-IL-1β treatment.IL-1β signaling determines the differential expression pattern of IL-10, which is necessary and sufficient to induce proinflammatory versus anti-inflammatory TH17 cell functions. Our data introduce TH17 cell subsets as novel players in autoinflammation and thus novel therapeutic targets in autoinflammatory syndromes including other IL-1β mediated diseases. This demonstrates for the first time alterations in the adaptive immune system in patients with autoinflammatory syndromes.
Abstract P1-01-17: The impact of triple negativity on lymph node positivity in breast cancer.
Authors: JJ Weber, LS Bellin, DE Milbourn, J Wong
Journal: Cancer Research (2012)

Abstract Introduction: Triple negative breast cancer (TNBC), defined as estrogen, progesterone, and HER2/Neu receptor-negative is biologically more aggressive than non-TNBC. Whether TNBC presents at a more advanced local/regional stage is controversial. We sought to determine whether TNBC had more frequent lymph node positivity. Methods: ER and PR status was determined by routine immunohistochemical analysis. HER2/Neu status was determined by immunohistochemistry; if 2+ equivocal status was noted, fluorescence in situ hybridization was performed for confirmation. Patients with a clinically negative axilla underwent sentinel lymph node biopsy, and if the sentinel node was positive, underwent immediate completion axillary node dissection. Lymph node positivity was determined by hematoxlyn-eosin staining. The main outcome measures were lymph node status and pathologic tumor size. Statistical differences were compared by means of paired t-test and chi-squared test where appropriate. Results: Between January 1, 2004 and December 31, 2010, 501 women with invasive breast cancer were treated at our institution. These patients ranged in age from 25 to 93 years (mean 57.6 yr), with 53.1% of patients self-reported as non-Hispanic white and 43.7% non-Hispanic black. TNBC patients were younger (mean 55.0 yr vs. 58.3 yr, p = 0.005), and were more often non-Hispanic black (52.7% vs. 41.1%, p = 0.03). The mean pathological tumor size of the entire population was 1.86 cm (range 0 to 18 cm). One hundred twelve patients (22.4%) were TNBC. The mean pathological tumor size for TNBC compared to non-TNBC patients was 2.07 cm (range 0 to 8.7 cm) and 1.80 cm (range 0 to 18 cm) (p = 0.068). There was a statistically significant difference in the T-stage at presentation between TNBC and non-TNBC tumors (T1, 58.9% TNBC vs. 72.0% non-TNBC; T2, 34.8% TNBC vs. 22.4% non-TNBC; T3/T4, 6.3% TNBC vs. 5.6% non-TNBC, p = 0.02). One hundred sixty patients (31.9%) were node positive. The number of positive lymph nodes in the TNBC patients ranged from 1–18, and the non-TNBC ranged from 1–35 (TNBC mean 2.94 vs. non-TNBC mean 3.94, p = 0.09). TNBC patients were more often node positive than non-TNBC (39.3% vs. 29.3%, p &amp;lt; 0.05). However, when stratified by T-stage, the differences did not achieve statistical significance (T1, 31.8% TNBC vs. 21.8% non-TNBC, p = 0.11; T2, 51.3% vs. 46.0%, p = 0.70; T3/T4, 57.1% vs. 59.1%, p = 1.0), despite a trend toward greater node positivity in earlier T-stage TNBC tumors. Conclusions: TNBC is more frequently lymph node positive than non-TNBC. This is largely attributable to more node positivity in early T-stage tumors. These data provide further evidence for the poor prognosis of TNBC and the increased likelihood of nodal metastases in early T-stage tumors. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-01-17.
Symptoms and Suffering at the End of Life in Children with Cancer
Authors: Joanne Wolfe, Holcombe E. Grier, Neil Klar, Sarah B. Levin, Jeffrey M. Ellenbogen, Susanne Salem-Schatz, Ezekiel J. Emanuel, Jane C. Weeks
Journal: New England Journal of Medicine (2000)

Cancer is the second leading cause of death in children, after accidents. Little is known, however, about the symptoms and suffering at the end of life in children with cancer.In 1997 and 1998, we interviewed the parents of children who had died of cancer between 1990 and 1997 and who were cared for at Children's Hospital, the Dana-Farber Cancer Institute, or both. Additional data were obtained by reviewing medical records.Of 165 eligible parents, we interviewed 103 (62 percent), 98 by telephone and 5 in person. The interviews were conducted a mean (+/-SD) of 3.1+/-1.6 years after the death of the child. Almost 80 percent died of progressive disease, and the rest died of treatment-related complications. Forty-nine percent of the children died in the hospital; nearly half of these deaths occurred in the intensive care unit. According to the parents, 89 percent of the children suffered "a lot" or "a great deal" from at least one symptom in their last month of life, most commonly pain, fatigue, or dyspnea. Of the children who were treated for specific symptoms, treatment was successful in 27 percent of those with pain and 16 percent of those with dyspnea. On the basis of a review of the medical records, parents were significantly more likely than physicians to report that their child had fatigue, poor appetite, constipation, and diarrhea. Suffering from pain was more likely in children whose parents reported that the physician was not actively involved in providing end-of-life care (odds ratio, 2.6; 95 percent confidence interval, 1.0 to 6.7).Children who die of cancer receive aggressive treatment at the end of life. Many have substantial suffering in the last month of life, and attempts to control their symptoms are often unsuccessful. Greater attention must be paid to palliative care for children who are dying of cancer.
THU0235 Global Tenderness and Anxiety/Depression as a Component of the DAS28
Authors: A. Pervez, S. Kelly, B. Kidd
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The DAS28 (disease activity score 28) was created for the purpose of quantifying and comparing inflammatory processes for patients with Rheumatoid Arthritis. One of the four components measured is a 28 joint tender count. The objectivity of this marker is unclear. <h3>Objectives</h3> To assess the disease activity of patients with tender joints and compare this to joint ultrasound scans. Can patients be globally tender despite absent joint inflammation on US? And furthermore, is there any correlation between a high tender count and patient anxiety/depression levels? <h3>Methods</h3> 47 patients with inflammatory arthritis had their routine DAS28 assessment, as well as joint ultrasound scans to identify Para Doppler activity. Along with the 28 joint counts, 10 reference points were used to identify patients who were globally tender. And finally each patient was asked to complete a HAD (hospital anxiety/depression) questionnaire to assess levels of anxiety and depression. <h3>Results</h3> Of the patients with moderate-high DAS28 scores, a subgroup (37-44%) was identified to have no activity on joint US scan. The high DAS28 (&gt;5.1) scoring patients with no disease activity on US scan appeared to have on average a high tender count (26/28 joints) and were globally very tender (8/10 reference points). This subgroup of patients also scored either as a case or borderline for anxiety/depression on the HAD score. <h3>Conclusions</h3> Global tenderness and anxiety/depression can result in a misleadingly high DAS28 score in a subgroup of patients with high DAS28 scores, despite absent joint US activity. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5716
Abstract 2865: Cytoplasmic deacetylase HDAC6 confers tumor suppressive potential through autophagic cell death in human hepatocellular carcinoma
Authors: Kwang Hwa Jung, Ji Heon Noh, Jung Woo Eun, Jeong Kyu Kim, Hyun Jin Bae, Hongjian Xie, Eliel Nam, Won Sang Park, Jung Young Lee, Suk Woo Nam
Journal: Cancer Research (2011)

Abstract The histone modification and acetylation by histone acetyltransferases (HATs) and histone deacetylases (HDACs) have been associated with chromatin decondensation and transcriptional activation and silencing. HDAC6, one of class II HDAC isotypes, is a cytosolic protein and microtubule-associated deacetylase that interacts with non-histone protein, including α-tubulin. HDAC6 is involved in autophagic degradation of the cells, but the underlying mechanism associated with carcinogenesis in solid tumors remains unclear. In this study, we investigated the expression levels of HDAC6 in human liver cancer cell lines and tissues. HDAC6 expression was analyzed by Western blot analysis in nine selected hepatocellular carcinomas (HCCs) and immunohistochemical staining was performed in paraffin-embedded samples from 32 liver cancers. HDAC6 expression was significantly down-regulated in the HCCs compared to corresponding normal tissues in nine selected tissue samples. Immunohistochemical analysis also showed commonly down-regulated HDAC6 expression in the HCCs. Thus, to investigate the HDAC6-induced anti-neoplastic potentials on liver cancer progression, we restored HDAC6 expression using gene transfection in human Hep3B liver cancer cell line. Over-expression of HDAC6 suppressed proliferation of liver cancer cells with decreased acetylation status of α-tubulin and exhibited the characteristics of autophagic degradation (autophagosome formation and the LC3-II generation) in Western blot and Electron Microscopy (EM) analysis. In addition, we found that over-expression of HDAC6 induced expression of autophagy-related gene Beclin 1, a key molecule of autophagosome formation. In contrast, knock-down of HDAC6 over-expressed cells could reduce the expression level of increased Beclin 1 and LC3-II with restoration of acetylated α-tubulin. Furthermore, in the xenograft mouse models, over-expression of HDAC6 significantly suppressed tumor growth and incidence of tumor formation. In conclusion, our results suggest that HDAC6-indued autophagic cell death provide a novel mechanism for the regulation of beclin1 and LC3 expression in liver cancer development and progression providing new therapeutic intervention in human hepatocellular carcinoma 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 2865. doi:10.1158/1538-7445.AM2011-2865
Preparedness for admission of patients with suspected Ebola virus disease in European hospitals: a survey, August-September 2014
Authors: M D de Jong, C Reusken, P Horby, M Koopmans, M Bonten, J D Chiche, C Giaquinto, T Welte, F Leus, J Schotsman, H Goossens
Journal: Eurosurveillance (2014)

Binary file ES_Abstracts_Final_ECDC.txt matches
Abstract 2487: CONSERTING: an accurate method for detecting focal and gross somatic copy number alterations in cancer genome by next generation sequencing
Authors: Xiang Chen, Jianmin Wang, Kathryn Roberts, Stanley Pounds, Michael Dyer, Charles Mullighan, James Downing, Jinghui Zhang
Journal: Cancer Research (2012)

Abstract The Identification of somatically acquired DNA copy number alterations (CNA) is extremely important for finding causal genes in cancer. Although next-generation sequencing (NGS) can assay a genome at base-pair resolution, accurate identification of CNA from NGS data has been hindered by sequencing artifacts, coverage bias and paralogous genomic duplication. As a result, existing algorithms tend to generate many CNA segments that are not corroborated by an alternative assay such as SNP array, suggesting high false discovery rate. To improve CNA analysis for NGS data, we developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), a novel copy number detection method that integrates read depth analysis with structural variation (SV) detection and adjustment for sequencing artifacts. Analysis of simulated data shown that CONSERTING outperforms existing methods by achieving high sensitivity of focal copy number detection (CONSERTING: 0.80, CNV-Seq: 0.26, SegSeq: 0.19, FREEC: 0.02) at a low false discovery rate (CONSERTING: 0.09, CNV-Seq: 0.19, SegSeq: 0.46, FREEC: 0.07). When applied to matching tumor/normal samples of hematopoietic malignancies and solid tumors, CONSERTING showed a high concordance with SNP array, with a mean of 18 uncorroborated CNA segments compared with 104 by CNVSeq, 182 by SegSeq and 63 by FREEC. In addition, CONSERTING is able to discover bona fide focal CNAs in genes of biological importance that were not detectable by SNP array, such as a 36 kb homozygous deletion in SH2B3 and a 20 kb deletion in CDK6. Finally, CONSERTING is able to find CNAs and SVs present in tumor subclone that are missed by SNP array or SV analysis of NGS data. The novel CNAs and SVs reported here were experimentally validated, demonstrating that the high sensitivity and accuracy of CONSERTING enable discovery of key genetic lesions in cancer. 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 2487. doi:1538-7445.AM2012-2487
Endoloop application for the removal of a self-expandable metallic stent (SEMS) in an esophagocolonic anastomotic stricture
Authors: B. Gonçalves, A. Ferreira, A. Caetano, P. Bastos, C. Rolanda
Journal: Endoscopy (2013)

Anastomotic strictures occur in 3 % – 46.2 % of patients after colonic reconstruction of the esophagus [1]. Self-expanding metal stents (SEMS) are increasingly considered for refractory or complex benign strictures of the esophagus [2]. Migration is a common complication and the stent should be removed to avoid gastrointestinal complications.
INCREASED RATE OF POSTOPERATIVE PERICARDITIS WITH CONTACT FORCE SENSING CATHETERS IN ATRIAL FIBRILLATION ABLATION
Authors: Cilomar Martins de Oliveira Filho, Roderick Tung, Jason Bradfield, Marmar Vaseghi, Olujimi Ajijola, Carlos Macias, Noel Boyle, Kalyanam Shivkumar, Eric Buch
Journal: Journal of the American College of Cardiology (2016)
Association of an Inversion of Chromosome 16 with Abnormal Marrow Eosinophils in Acute Myelomonocytic Leukemia
Authors: Michelle M. Le Beau, Richard A. Larson, Mitchell A. Bitter, James W. Vardiman, Harvey M. Golomb, Janet D. Rowley
Journal: New England Journal of Medicine (1983)

We identified 18 patients with an inversion of chromosome 16, inv(16)(p13q22), among 308 patients with newly diagnosed acute nonlymphocytic leukemia. Each of these 18 patients had acute myelomonocytic leukemia (M4 subtype) and eosinophils with distinctly abnormal morphology, cytochemical staining, and ultrastructure. These eosinophils constituted from 1 to 33 per cent of the nucleated marrow cells. In our series, every patient with acute myelomonocytic leukemia and abnormal eosinophils also had an abnormal chromosome 16. This subgroup of M4 patients had a good response to intensive therapy designed to induce remission; 13 of 17 treated patients entered a complete remission, and 10 remain in first remission. Thus, patients with an inversion of chromosome 16 appear to represent a unique cytogenetic–clinicopathological subtype of acute nonlymphocytic leukemia with a favorable prognosis. (N Engl J Med 1983; 309:630–6.)