tbuckley/cabot-search huggingface dataset:
Abstract CSF1-1: Breast Cancer Screening: The Radiology Perspective
Authors: CI Flowers
Journal: Cancer Research (2010)

Abstract Rightly or wrongly, radiologists ‘own’ breast cancer screening, as it is a radiological procedure, administered by the radiology departments. As a result in the USA, radiologists are outraged at what is seen as misuse of published data showing the effectiveness of mammographic screening. In the USA, we do not have true population screening, and rely on women being informed, and having insurance coverage, to enable them to have an annual screening exam. There is no call/recall system, and we do not collect national statistics on breast screening and outcomes. Many low income women are not offered, what to many is a ‘life saving’ test, as a result of State budget cuts. In comparison with other countries, some of which have National Screening Programs (like the UK NHS BSP, the Netherlands and Sweden), there is support from epidemiology and public health departments, as screening is population based, and therefore a public health measure. The downsides with these programs are funding issues, with Cost-Benefit analysis being used, and QALYs (Quality Adjusted Life Years), to assist committees deciding affordable health policy for the nation. There are differences between Europe and the USA in recommendations for screening as a result, especially in terms of starting at 50 years and having a longer screening interval of 2 years. In late 2009, the US Preventive Services Task Force recommendations to abandon the guideline to start at age 40 for all women, and to recommend routine screening, unless high risk), until the age of 50 years, met with a storm of criticism by interested parties. The recommendations have largely been largely ignored, except by internists. However, in the current economic climate, it is becoming increasingly clear that decisions may have to be made on cost-benefit if health-care dollars are limited. The acknowledgment that health policy may have to change, is shown when compromises have to be made. This is demonstrated when screening policy is altered, for example, in the UK, where a decision was made to alter the screening target age, rather than reduce the interval between screens. (The NHS BSP is being extended in 2012 to cover women aged between 47 and 73). I will be concentrating on the screening guidelines and the different approaches taken between the USA and Europe. I will cover the screening of ‘Normal Risk’ women, and uphold the recommendations of the Society of Breast Imaging, American College of Radiology and the American Cancer Society. I will explain the ‘harms’ of screening and argue that screening recommendations should be made on evidence rather than on the numbers of lives saved. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr CSF1-1.
SAT0517 Automated Ultrasound for the Detection of Joint Swelling in Arthritic Diseases
Authors: M. Grünke, J. Wendler, F. Schuch, R. Jakobs, H. Schulze-Koops, J. von Kempis, R. B. Mueller
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The detection of joint swelling is a key feature in the diagnosis and assessment of arthritic diseases. Ultrasound and MRI have proven to be more sensitive and reliable than clinical examination, but a comprehensive examination of the small joints with these techniques is either time consuming or expensive. The automated breast volume scanner (ABVS) was developed to acquire series of consecutive B-mode pictures of the female breast and these data can be analysed in all three dimensions. <h3>Objectives</h3> To analyse the value of ABVS in detecting swelling of the finger joints compared to clinical examination and manual ultrasound. <h3>Methods</h3> 19 consecutive patients suffering from psoriatic (n=4) or rheumatoid (n=15) arthritis with at least 1 swollen MCP (metacarpophalangeal) or PIP (proximal interphalangeal) joint were included. ABVS and manual ultrasound were conducted using the ACUSON S2000™ (Siemens Medical Solutions, Mountain View, USA). The ABVS transducer was equipped with a linear array (5 – 14 MHz band width); the frequency was set at 11 MHz. Each automatic sweep of the scanner generated 15.4 x 16.8 cm x maximum 3 cm volume data sets. The system was set to perform an automatic scanning time of 65 s per scan with a slice thickness of 0.5 mm. The dorsal and palmar side of each hand were scanned separately. Multiplanar reconstruction enabled examination of the images at multiple levels for the presence of lesions or joint swelling (figure) <h3>Results</h3> Clinical examination of MCP, PIP, and DIP joints detected in average 4.1 swollen joints, manual ultrasound 13.7 joints, and ABVS 10.6 joints per patient. The interobserver reliability for detection of joint swelling were 73.3%, 72.5% and 85.9% for manual ultrasound, ABVS, and clinical examination, respectively. The sensitivities and specificities were 30.7% and 91.3% for clinical examination and 59.9% and 63.4% for ABVS using manual ultrasound as gold standard. <h3>Image/graph</h3> <h3>Conclusions</h3> ABVS is a simple and time sparing option for effective detection of joint swelling in patients suffering from arthritis with good sensitivity and specificity compared to manual ultrasound. <h3>Disclosure of Interest</h3> None Declared
THU0360 Small Bowel Mucosal Findings in Familial Mediterranean Fever
Authors: A. Demir, F. Akyüz, S. Gokturk, S. Evirgen, M. Gulluoglu, B. Erer, S. Kamali, A. Gul
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Familial Mediterranean fever (FMF), the most common form of autoinflammatory disorders, is characterized by recurrent episodes of serositis or arthritis. Abdominal pain due to peritoneal inflammation is the most common manifestation of FMF. However, other gastrointestinal manifestations including diarrhea can also be observed. No detailed investigation by endoscopic examination of small and large bowels has been reported so far in FMF. <h3>Objectives</h3> This study aimed to investigate the gastrointestinal tract by endoscopy in FMF patients with peritoneal attacks and abdominal findings. <h3>Methods</h3> The study group consisted of 41 patients with FMF, all fulfilling Tel-Hashomer criteria and followed-up at the Rheumatology Division. All of the patients were taking colchicine at highest tolerable doses of 1 to 2 mg/day. A standard questionnaire was used to record the gastrointestinal symptoms, other clinical findings, MEFV mutations, and history of medications including non-steroid anti-inflammatory drugs (NSAIDs). Gastroscopy, colonoscopy and small bowel capsule endoscopy (OMOM, Jinshan Science and Technology Company, China) were performed in all patients, and biopsies were taken from terminal ileum and duodenum. <h3>Results</h3> The mean age of the patients was 34±11 years, 63% of them were female, and 67.7% of them were carrying MEFV exon 10 mutations. All patients had a history of abdominal attacks and experienced at least one peritonitis episode within the last two months. Only one patient used NSAIDs in addition to colchicine. In endoscopic investigations, gastric erosion was detected in only one patient, and no significant findings were detected in colonoscopy. Pathologic examination of the terminal ileum specimens revealed nonspecific chronic inflammation in 70% of the patients. Capsule endoscopy showed small bowel mucosal defects in 44% (erosions in 26.8%, ulcer in 17.1%) and edema in 29.3% of the patients. Most (64%) of the ulcer and erosions were localized to jejunum, and only 24% were in ileum. In one patient, images were compatible with infiltration in the distal jejunum, and reactive amyloidosis was confirmed by biopsy. No correlation was found between small bowel mucosal defects and MEFV variations, and no predictor was detected by multivariate analysis for mucosal defects. <h3>Conclusions</h3> Capsule endoscopic investigations revealed small bowel mucosal defects in almost half of the patients with FMF, and it was mainly localized to jejunum. Those mucosal changes may result from underlying autoinflammatory condition or chronic exposure to colchicine. Further investigations are warranted for the characterization of small bowel findings and to rule out the possibility of colchicine toxicity. <h3>Acknowledgements</h3> Funded by Istanbul University, Scientific Research Projects, IUBAP No: 27107. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5964
Aspergillus Fungus Balls on the Mitral Valve
Authors: Franca Gori, Gabriella Nesi, Elena Pedemonte
Journal: New England Journal of Medicine (2001)

Irinotecan plus Fluorouracil and Leucovorin for Metastatic Colorectal CancerTo the Editor: The study by Saltz et al. (Sept.28 issue) 1 leaves unanswered questions regarding the toxicity and dose intensity of the combination of irinotecan, fluorouracil, and leucovorin for the treatment of metastatic colorectal cancer.The authors indicate that "the median relative intensity of the dose of irinotecan . . .was similar in the group given irinotecan alone and the group given irinotecan, fluorouracil, and leucovorin."However, the median relative intensity of the dose of fluorouracil was lower in the tripledrug combination than in the two-drug combination.These points lead us to ask the following: During cycle 1 of therapy, what proportion of patients in the triple-drug group received all four weekly treatments?What proportion of patients receiving the triple-drug combination had a reduction in the dose during cycle 1 -that is, how many received treatment during all four weeks but at reduced doses?What percentage of patients who received the tripledrug combination during cycle 2 had dose reductions as a result of dose-limiting toxicity during cycle 1?What proportion of patients had dose reductions in cycle 3 because of dose-limiting toxicity in cycle 2? C
Abstract 483: CXCR6, a newly defined biomarker of tissue-specific stem cell asymmetric self-renewal, identifies more aggressive human melanoma cancer stem cells
Authors: Rouzbeth Taghizadeh, Minsoo Noh, Yang Hoon Huh, Beatrice Arosio, James Sherley, Caterina AM LaPorta
Journal: Cancer Research (2011)

Abstract Background- A fundamental problem in cancer research is identifying the cell type that is capable of sustaining neoplastic growth and its origin from normal tissue cells. Recent investigations of a variety of tumor types have shown that phenotypically identifiable and isolable subfractions of cells possess the tumor-forming ability. In the present paper, using two lineage-related human melanoma cell lines, primary melanoma line IGR39 and its metastatic derivative line IGR37, two main contributes are reported. The first one is the first phenotypic evidence to support the origin of melanoma CSCs from mutated tissue-specific stem cells and the second one is the identification of a more aggressive subpopulation CXCR6+ in melanoma. Methods/Findings- We defined CXCR6 as a new biomarker for tissue-specific stem cell asymmetric self-renewal. Thus, the relationship between melanoma formation and ABCG2 and CXCR6 expression was investigated. Consistent with their non-metastatic character, unsorted IGR39 cells formed significantly smaller tumors than unsorted IGR37 cells. In addition, ABCG2+ tumors gave a 2-fold greater mass than tumors from unsorted cells or ABCG2- cells. Furthermore, CXCR6+ cells produced more aggressive tumors. These findings show that CXCR6 identifies a more discrete subpopulation of cultured human melanoma cells with a more aggressive melanoma cancer stem cell phenotype than cells selected on the basis of ABCG2, and CXCR6+/ABCG2+ expression. Conclusions/Significance- The association of more aggressive tumor phenotype with asymmetric self-renewal phenotype reveals a previously unrecognized aspect of tumor cell physiology. Namely, the retention of some tissue-specific stem cell attributes, like the ability to preserve self-phenotype, impacts the natural history of human tumor development. Knowledge of this new aspect of tumor progression may provide new targets for cancer prevention and treatment. 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 483. doi:10.1158/1538-7445.AM2011-483
Abstract A10: L1236, a Hodgkin and Reed-Sternberg cell line, stimulates monocytes in vitro to differentiate into M2-like macrophages
Authors: Kim Yee Lee, Siew Meng Chong, Yaw Chyn Lim
Journal: Cancer Research (2011)

Abstract The microenvironment of classical Hodgkin lymphoma (cHL) is characterized by a small number of malignant Hodgkin and Reed-Sternberg (HRS) cells embedded in a background rich with infiltrating immune cells. HRS cells and the surrounding cellular infiltrates are believed to produce soluble and membrane-bound factors that are essential for the survival and proliferation of HRS cells. Steidl et al (2010) have reported that an increase in the number of tumor associated macrophages in cHL correlates with poor prognosis. However, little is known about the molecular crosstalk between macrophages and HRS cells in cHL. This study aims to examine in-vitro the influence of HRS cells on monocyte activation and differentiation. Freshly isolated human monocytes were co-cultured with L1236 cells, a HRS cell-line, under standard culture conditions. At the end of 8 days in culture, we examined the influence of HRS cells on monocyte survival and differentiation. In addition, we determined the activation and differentiation status of the co-cultured monocyte by assessing the cells for CD206 and IL-10 expression. The role of IL-4Rα and Macrophage colony-stimulating factor (M-CSF) receptor on HRS cell-induced monocyte differentiation was examined using antibody blocking assay. We also examined consented cHL patient samples for the presence of CD206/CD68 double positive macrophages by immunofluorescent staining. Our data showed that L1236 cells are able to enhance the survival of monocytes in vitro. In the presence of L1236 cells, monocytes differentiated into alternatively activated, M2-like macrophages which expressed CD206 and IL-10. The observed enhanced survival, and differentiation to M2-like macrophages, was mediated by soluble factors secreted by the L1236 cells. The survival of co-cultured monocytes is enhanced by signalling through the M-CSF receptor. In contrast, the differentiation to M2-like macrophages is in part, regulated by signals generated via IL-4Rα. Finally, the presence of CD68/CD206 double positive macrophages was detected in three out of four cHL patient samples. We conclude that HRS cells secrete soluble factors that can in vitro directly modulate monocyte survival and differentiation to a CD206+ M2 macrophage phenotype. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr A10.
Abstract 2649: Maternal and offspring folate metabolic genes and the risk of childhood acute lymphoblastic leukemia (ALL)
Authors: Philip J. Lupo, Darryl Nousome, Kala Y. Kamdar, Mehmet F. Okcu, Melissa L. Bondy, Michael E. Scheurer
Journal: Cancer Research (2012)

Abstract Introduction: Childhood ALL is the most common type of cancer in children. Although the survival rate is relatively high, there are significant clinical sequelae associated with treatment and little is known about the etiology of this condition. Family studies suggest a genetic component to ALL, and the peak incidence between 2 and 4 years of age indicates factors during pregnancy may influence risk. The folate metabolic pathway is a strong candidate for genetic epidemiologic studies due to its role in DNA synthesis and methylation. Objective: The purpose of this study was to conduct a case-parent triad analysis to assess both maternal and offspring genetic effects of the folate metabolic pathway on childhood ALL risk. Methods: We recruited pediatric ALL case-parent triads (n = 120) from Texas Children's Hospital. DNA samples were genotyped in the Human Genetics Center at The University of Texas School of Public Health using the Sequenom iPLEX MassARRAY for 80 tagSNPs in six folate metabolic pathway genes (MTHFR, MTRR, MTR, DHFR, BHMT, and TYMS). Log-linear modeling was used to examine the associations between ALL and both maternal and offspring genotypes. Results: After controlling for the false discovery rate (&amp;lt;0.10), there were 19 significant maternal effects in the following genes: BHMT (n = 3), MTR (n = 12), and TYMS (n = 4). For instance, maternal genotypes for BHMT rs558133 (RR = 0.51, 95% CI: 0.30-0.88, p = 0.008, q = 0.08), MTR rs2282369 (RR = 0.46, 95% CI: 0.26-0.79, p = 0.003, q = 0.08), and TYMS rs699517 (RR = 1.92, 95% CI: 1.17-3.17, p = 0.006, q = 0.08) were all associated with ALL. There were no significant offspring effects after controlling for the false discovery rate. Conclusions: This is one of the few studies conducted to evaluate maternal genetic effects in the context of pediatric ALL risk. Furthermore, we employed a family-based design (i.e., case-parent triad) that is robust to confounding due to population structure and allows for the evaluation of both maternal and offspring genotypes. These results provide additional evidence that the risk of pediatric ALL is influenced by variation within folate pathway genes and indicate that studies to explore these relationships further are warranted. We plan to extend these analyses to the evaluate folate pathway haplotypes, as well as other relevant genetic pathways (e.g., DNA repair). 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 2649. doi:1538-7445.AM2012-2649
Increase in Lipoprotein Lipase during Clofibrate Treatment of Hypertriglyceridemia in Patients on Hemodialysis
Authors: Andrew P. Goldberg, Deborah M. Applebaum-Bowden, Edwin L. Bierman, William R. Hazzard, Linda B. Haas, Donald J. Sherrard, John D. Brunzell, Jussi K. Huttunen, Christian Ehnholm, Esko A. Nikkila
Journal: New England Journal of Medicine (1979)

In 11 hypertriglyceridemic patients on hemodialysis, clofibrate (1 to 1.50 g per week) reduced plasma triglyceride (-40 +/- 20%, P less than 0.001), very-low-density-lipoprotein triglyceride (-44 +/- 20%, P less than 0.001) and very-low-density lipoprotein cholesterol (-39 +/- 25%, P less than 0.01), and it increased high-density-lipoprotein cholesterol (82 +/- 106%, P less than 0.005). Low pretreatment lipoprotein-lipase activity in adipose-tissue specimens and postheparin plasma increased to normal with clofibrate, whereas low hepatic triglyceride lipase activity did not change. The reduced very-low-density-lipoprotein triglyceride correlated with the increased lipoprotein-lipase activity in adipose tissue (rs = 0.792, P less than 0.02, n = 8) and postheparin plasma (rs = 0.851, P less than 0.02, n = 8), whereas increased high-density-lipoprotein cholesterol correlated with changes in this activity in adipose tissue (rs = 0.696, P less than 0.06) and post-heparin plasma (rs = 0.679, P less than 0.10). There was no correlation between changes in hepatic triglyceride lipase activity and plasma lipids during treatment. Reduced lipoprotein-lipase activity may cause hypertriglyceridemia and decreased high-density-lipoprotein cholesterol in patients on hemodialysis; clofibrate may correct these abnormalities by increasing lipoprotein-lipase activity to normal.
Pathways to abnormal revenge and forgiveness
Authors: Pat Barclay
Journal: Behavioral and Brain Sciences (2012)

Abstract The target article's important point is easily misunderstood to claim that all revenge is adaptive. Revenge and forgiveness can overstretch (or understretch) the bounds of utility due to misperceptions, minimization of costly errors, a breakdown within our evolved revenge systems, or natural genetic and developmental variation. Together, these factors can compound to produce highly abnormal instances of revenge and forgiveness.
Abstract 2211: Array-comparative genomic hybridization identifies important recurrent copy number alterations in non-small cell lung cancer
Authors: Bajee K. Sriram, Jill E. Larsen, Santiyagu M. Savarimuthu Francis, Casey M. Wright, Belinda E. Clarke, Edwina E. Duhig, Hayward K. N, Rayleen V. Bowman, Ian A. Yang, Kwun M. Fong
Journal: Cancer Research (2010)

Abstract Comprehensive knowledge of the genomic aberrations involved in NSCLC may deliver improved therapies, diagnostic and prognostic biomarkers. Recurrent copy number alterations (CNA) found in the same locus across a set of tumour samples are assumed to be the site of “driver” cancer genes. We hypothesize that whole genome array comparative genomic hybridization (aCGH) will identify recurrent regions of gains and loss in NSCLC containing candidate “driver” genes. Methods: DNA from fresh-frozen tumor tissue of 133 NSCLCs were obtained from The Prince Charles Hospital lung tumour bank. aCGH was performed using Agilent CGH 44B microarrays (Agilent Technologies). Recurrent CNAs were identified using the Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm, controlling for false discovery rates (q≤0.005). Focal (&amp;lt;50% of chromosome arm) regions of amplification and deletion were identified by applying GISTIC with thresholds of log2 0.848 and −0.747, respectively, corresponding to 3.6 copies and 1.2 copies with stromal contamination of 30%. Results: Regions of amplification occurred in 3q26.33, 5p15.33, 8p11.23, 11q13.3 and 19q13.2 and deletions occurred in 3p11.2, 4p15.1, 4q34.3, 5q14.1, 6q22.31, 8p23.1, 9p21.3, 10q23.31, 11q25, 13q14.3, 15q14, 16q23.3, 17p12, 18q22.3, 21q21.3 and 22q13.33. The most significant CNA regions were deletion in 9p21.3 (q=1.20E-40) and amplification in 3q26.33 (q=1.13E-10). These regions contain known tumor suppressor genes (TSGs) (CDKN2A in 9p21.3) and oncogenes (SOX2 in 3q23.33). Conclusion: We have identified regions with recurrent CNAs in NSCLC many of which harbor known oncogenes and TSGs. Further validation will be performed using public datasets and independent test cohorts. Supported by: NHMRC Medical Postgraduate Scholarship 569762. 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 2211.
FIELD ACTIVATION OF THE CARDIAC CATHETERIZATION LAB WITH A DEDICATED UNIT AND STAFF IN THE EMERGENCY DEPARTMENT REDUCES DOOR TO BALLOON TIME IN THE TREATMENT OF ST-ELEVATION MYOCARDIAL INFARCTION: A SINGLE CENTER LEAN PROCESS EXPERIENCE
Authors: Leif Christianson, Marc Kaufman, Edward Keshishian, Amit Mitra, Michael Berlowitz
Journal: Journal of the American College of Cardiology (2016)