tbuckley/cabot-search huggingface dataset:
Lupus Anticoagulants, Anticardiolipin Antibodies, and Fetal Loss: A Case–Control Study
Authors: Claire Infante-Rivard, Michèle David, Robert Gauthier, Georges-Etienne Rivard
Journal: New England Journal of Medicine (1991)

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies that have been associated with fetal loss, but they have not been shown unequivocally to be a risk factor for this event.
Bleeding Peptic Ulcer
Authors: Loren Laine, Walter L. Peterson
Journal: New England Journal of Medicine (1994)

Peptic ulcer is the most common cause of acute hemorrhage in the upper gastrointestinal tract, accounting for about 50 percent of cases114. There are approximately 150,000 hospitalizations per year in the United States for evaluation and treatment of bleeding ulcers (based on 1985 estimates and excluding federal hospitals)15. Although hospitalization and surgery for uncomplicated ulcers have decreased in the United States and Europe over the past 20 to 30 years, the number of hospital admissions for hemorrhage associated with ulcers has remained relatively unchanged1517. It is noteworthy that the incidence of bleeding ulcers appears to . . .
AB1428-HPR Fatigue in patients with quiescent systemic lupus erythematosus: The role of dehydroepiandrosterone sulfate
Authors: C.L. Overman, A. Hartkamp, E.R. Bossema, M. Bijl, G.L.R. Godaert, J.W.J. Bijlsma, R.H.W. Derksen, R. Geenen
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Fatigue is a major problem in systemic lupus erythematosus (SLE). In some patient groups, associations between fatigue and low levels of dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) have been found. Low levels of DHEA(S) may also play a role in SLE fatigue. <h3>Objectives</h3> To compare 1) serum DHEAS levels and fatigue between female patients with quiescent SLE and healthy women, and 2) fatigue between SLE patients with low and normal DHEAS levels. <h3>Methods</h3> Included were 60 female patients with quiescent SLE (31 using prednisone and 29 not using prednisone) and 60 age-matched healthy women. Serum DHEAS levels were determined using an Advantage Chemiluminescense System. Fatigue was measured with the Multidimensional Fatigue Inventory (MFI). Groups were compared on DHEAS and fatigue using Chi<sup>2</sup> and Mann-Whitney <i>U</i> tests. <h3>Results</h3> Compared to healthy women, SLE patients were more fatigued (<i>p</i>≤0.001) and more often had DHEAS levels below the lower limit of normal (<i>p</i>&lt;0.001), in particular those using prednisone. Compared to SLE patients with normal DHEAS levels, patients not using prednisone reported less fatigue on four out of five fatigue dimensions (<i>p</i>≤0.03). SLE patients using prednisone with low and normal DHEAS levels reported a similar level of fatigue (<i>p</i>≥0.39). <h3>Conclusions</h3> Although in patients with quiescent SLE low serum DHEAS levels are more frequent and fatigue levels are higher than in healthy people, low DHEAS levels are not - or even inversely - related to fatigue. After our previous finding that DHEA administration does not reduce fatigue, this result further indicates that low DHEA(S) levels alone do not offer an explanation for SLE fatigue. <h3>Disclosure of Interest</h3> None Declared
Abstract 2175: Role of p38 MAPK in regulating Cripto-1 expression and signaling in human embryonal carcinoma cells
Authors: Natalie Held, Cristina Rangel, Nadia Castro, Monica Gonzales, Tadahiro Nagaoka, Hideaki Karasawa, David S. Salomon, Caterina Bianco
Journal: Cancer Research (2011)

Abstract Cripto-1 (CR-1) is a cell-membrane protein that is overexpressed in several different types of human carcinomas. We have previously shown that TGFβ1 and Activins can enhance CR-1 expression while BMP2 and BMP4 can inhibit CR-1 expression in NTERA-2 embryonal carcinoma cells and in LS174T colon cancer cells. Nevertheless, there is still a very incomplete picture as to the nature of the epigenetic, transcriptional and hormonal factors that might be involved in regulating Cripto-1 expression under different conditions. Previous studies have demonstrated that activation of p38 MAPK can regulate expression of Nodal, a Cripto-1 ligand, during early embryogenesis and is necessary for the specification of mouse cardiomyocytes from embryonic stem cells, which depends upon a Nodal-dependent signaling pathway involving Cripto-1. We therefore evaluated if activation of p38 MAPK might be involved in regulating Cripto-1 expression and Cripto-1 dependent signaling in human embryonal carcinoma cells. In undifferentiated NTERA-2 and NCCIT embryonal carcinoma cells two p38 MAPK inhibitors PD169316 and SB20358 completely inhibited the basal levels of CR-1 mRNA and protein expression in both cell lines. A JNK inhibitor SP600125 had only minor effects on CR-1 mRNA and protein expression whereas the p44/42 MAPK inhibitor U0126 showed no effect. Transfection of specific siRNA against p38 MAPK was also able to significantly interfere with CR-1 mRNA and protein expression in NTERA2 and NCCIT embryonal carcinoma cells. In contrast, knockdown of p44/42 MAPK or JNK with specific siRNA did not significantly affect CR-1 expression in embryonal carcinoma cells. We therefore evaluated whether CR-1 might trigger activation of p38 MAPK in embryonal carcinoma cells and in mouse mammary epithelial cells. Recombinant CR-1 protein was found to stimulate in a delayed fashion (after 50-60 minutes) p38 MAPK phosphorylation in mouse mammary epithelial cells and in embryonal carcinoma cells suggesting a feed-forward activation loop. Whether p38 MAPK functions in undifferentiated embryonal carcinoma cells to regulate CR-1 expression and/or signaling involving regulation of invasion, migration and epithelial to mesenchymal transition in human embryonal carcinoma cells and in mouse mammary epithelial cells is under investigation. 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 2175. doi:10.1158/1538-7445.AM2011-2175
Exosomes in Human Breast Milk Promote EMT
Authors: Wenyi Qin, Yoshikazu Tsukasaki, Santanu Dasgupta, Nitai Mukhopadhyay, Mitsuo Ikebe, Edward R. Sauter
Journal: Clinical Cancer Research (2016)

Pregnancy increases breast cancer risk for all women for at least 5 years after parturition. During weaning and involution, the breast microenvironment becomes tumor promotional. Exosomes provide cell-cell communication during physiologic processes such as lactation, but also in breast cancer. We determined whether molecules in milk exosomes from healthy lactating women modulate the development and progression of breast cancer.Thirteen nursing women provided three (transitional, mature, and wean) milk samples. Exosomes were extracted and MCF7 and MCF10A breast cells labeled. The expression of six proteins linked to breast cancer was measured. On the basis of the findings, TGFβ2 concentration in exosome samples was measured, breast cells incubated with the exosomes and effect (epithelial-mesenchymal transition, EMT) on EMT-related proteins [E-cadherin, α-smooth muscle actin (α-SMA), filamentous (F)-actin and vimentin] measured.Human milk exosomes entered benign and malignant breast cells. The greatest change in wean milk protein was in TGFβ2 (P = 0.01). Exosomes with a high (but not low) level of TGFβ2 led to EMT in both cancer and benign cells, based on (i) change in cell morphology, actin cytoskeleton, and loss of cell-cell junction structure and (ii) increased α-SMA and vimentin and decreased E-cadherin.TGFβ2 is significantly upregulated in breast milk exosomes during weaning/early involution. Breast milk exosomes containing high levels of TGFβ2 induce changes in both benign and malignant breast epithelial cells, consistent with the development and progression of breast cancer, suggesting a role for high TGFβ2-expressing breast milk exosomes in influencing breast cancer risk. Clin Cancer Res; 22(17); 4517-24. ©2016 AACR.
PWE-173 Eligibility for Bariatric Surgery in England According to Nice Guidelines
Authors: A Ahmad, A Laverty, E Aasheim, A Majeed, C Millett, S Saxena
Journal: Gut (2013)

<h3>Introduction</h3> The number of people in England who are potentially eligible for bariatric surgery according to criteria set out in UK national guidance is not known. We used data from Health Survey for England (HSE) 2006, representative of the non-institutionalised English population, to determine the number of people eligible for bariatric surgery and their socio-demographic characteristics. The National Institute for Health and Clinical Excellence (NICE) criteria for eligibility are those with body mass index (BMI) 3540 kg/m<sup>2</sup> with at least one comorbidity that could be improved by losing weight, or a BMI &gt; 40 kg/m<sup>2</sup>. The comorbidities examined were hypertension, type 2 diabetes, stroke, coronary heart disease, and osteoarthritis. <h3>Methods</h3> Of 13,742 adult respondents in HSE 2006, we excluded participants with invalid data for BMI (N = 2103), comorbidities (N = 2187) or socio-demographic variables (N = 27), for a final study sample of 9,425 participants. <h3>Results</h3> 374 (4.0%) had BMI 3540 kg/m2 with at least one comorbid condition and 179 (1.9%) had BMI &gt; 40 kg/m2. 5.9% of the general adult population therefore fulfilled criteria for bariatric surgery in England. Those eligible were more likely than the general population to be women (60.1% vs 39.9% P &lt; 0.01), retired (22.4% vs 12.8% P &lt; 0.01), and have no educational qualifications (35.7% vs 21.3% P &lt; 0.01). <h3>Conclusion</h3> The number of adults potentially eligible for bariatric surgery in England (2,346,542 people based on census data) far exceeds provision. Greater investment may be required to ensure the National Health Service (NHS) and other health services internationally have the capacity to meet the needs of all those eligible for bariatric surgery under national guidance. In doing so, monitoring of implementation is essential to ensure access based on need. <h3>Disclosure of Interest</h3> None Declared.
A Controlled Trial of Prophylactic Granulocyte Transfusions during Initial Induction Chemotherapy for Acute Myelogenous Leukemia
Authors: Ronald G. Strauss, John E. Connett, Robert Peter Gale, Clara D. Bloomfield, Geoffrey P. Herzig, Jeffrey McCullough, Lawrence C. Maguire, Drew J. Winston, Winston Ho, David C. Stump, William V. Miller, John A. Koepke
Journal: New England Journal of Medicine (1981)

To evaluate the role of prophylactic granulocyte transfusions during remission-induction chemotherapy for acute myelogenous leukemia (AML) we randomized 102 infected patients either to receive daily granulocyte transfusions when blood granulocytes fell below 0.5 x 10(9) per liter (54 patients) or not to receive them (48). Although the percentage of patients acquiring any infection was similar in the transfusion and control groups (46 and 42 per cent, respectively), granulocyte transfusions decreased the proportion of patients with bacterial septicemia (9 per cent of those with transfusions vs. 27 per cent of the controls; P = 0.01). Granulocyte transfusions did not reduce the incidence of other infections or improve bone-marrow recovery, remission rate and duration, or survival. Seventy-two per cent of the patients given transfusions had transfusion reactions. Pulmonary infiltrates were more common in the transfusion group than in the control group (57 per cent vs. 27 per cent; P = 0.002). Thirty-five per cent of the patients with pulmonary filtrates died, as compared with 5 per cent of those without filtrates. We conclude that prophylactic granulocyte transfusions should not be used during remission-induction chemotherapy in AML because the risks outweigh the benefits.
SP0195 Measurement Considerations in Cross-National Studies: Translation and Assessment of Metric Equivalencies
Authors: L. Kwakkenbos
Journal: Annals of the Rheumatic Diseases (2014)

<h3></h3> Accurate measurement of outcomes relevant to patients living with rheumatic diseases is crucial to improve patient-centered care. The importance of well-validated measures is increasingly recognized in both research and clinical practice. Increasingly, research involves patients who complete outcomes in different languages. This occurs in countries with more than one common language, such as Canada (French/English) or Belgium (Flemish/French), as well as in international multi-centre collaborations. Multicenter collaborations are utilized frequently in the rheumatic diseases, in particular in rare diseases such as scleroderma. An important issue when pooling or comparing outcomes collected in different languages is that instruments should be measurement equivalent (invariant) across cultural or linguistic groups. This is because differences in the meaning of items due to translation or cultural differences in item interpretation can lead to responses that differ across groups even when levels of the outcome being measured are similar. Measurement differences between translated questionnaires can be a serious threat to the validity of cross-cultural comparisons, because when measures are not equivalent metrically, it is not possible to determine if any observed differences between groups reflect real differences or are a consequence of measurement artifacts (e.g., linguistic/cultural differences). Therefore, cross-cultural validity should be established if outcomes are to be pooled among study participants from different countries or used to compare results between patients from different cultural or linguistic groups. The objective of this presentation is to describe the rationale for and method by which measurement equivalent patient-reported outcome measures can be developed and evaluated. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6121
Interim estimates of 2014/15 influenza vaccine effectiveness in preventing laboratory-confirmed influenza-related hospitalisation from the Serious Outcomes Surveillance Network of the Canadian Immunization Research Network, January 2015
Authors: S A McNeil, M K Andrew, L Ye, F Haguinet, T F Hatchette, M ElSherif, J LeBlanc, A Ambrose, A McGeer, J E McElhaney, M Loeb, D MacKinnon-Cameron, R Sharma, G Dos Santos, V Shinde
Journal: Eurosurveillance (2015)

Binary file ES_Abstracts_Final_ECDC.txt matches
Pathogenesis of Hyperuricemia in Saturnine Gout
Authors: Gene V. Ball, Leif B. Sorensen
Journal: New England Journal of Medicine (1969)

Thirty-seven of 43 admissions for gout to the Birmingham Veterans Administration Hospital in 1967 were for gout of the "saturnine" variety secondary to prolonged consumption of moonshine contaminated with lead. Uric acid kinetic studies done on three typical patients on a purine deprivation diet yielded similar results. Mean values were: uric acid turnover, 550 mg per day; uric acid pool, 1308 mg per day; urinary uric acid in percentage of turnover, 25.7; and uric acid recovered from urine for seven days, as percentage of dose, 24.9. Glycine-14C incorporation into urinary uric acid expressed as percentage of dose and corrected for extrarenal disposal was 0.102. These results confirm the role of the kidney in the pathogenesis of hyperuricemia in this disorder and the susceptibility of these patients to the development of gout.
Abstract 2510: Increased Fc-FcR interaction of human phosphatidylserine targeting antibody enhances pro-inflammatory and ADCC anti-tumor mechanisms
Authors: Jeanette R. Doerr, Gary Larson, Rich Archer, Jian Gong, Van Nguyen, Aditi Iyengar, Amy E. Johnson, Mary Wakabayashi, Matthew Peacock, Christopher Hughes, Connie Chang, Bruce Freimark
Journal: Cancer Research (2012)

Abstract Anionic phospholipids, principally phosphatidylserine (PS), become exposed on the external surface of vascular endothelial cells in tumors, providing an excellent marker for tumor vascular targeting. Binding of antibodies targeting PS on the tumor endothelial cells and tumors recruits immune cells and engages the immune system to destroy tumor vasculature. The antibodies also enhance anti-tumor immunity by blocking the immunosuppressive action of PS. A chimeric anti-PS antibody, bavituximab, is being used in combination with chemotherapy to treat patients with solid tumors in Phase II trials. We have engineered mutations in the Fc region of fully human PS-targeting antibody PGN635 that enhance the interaction with FcRgammaIIIa and have characterized their ability to exert anti-tumor effects through various mechanisms, including ADCC and cytokine induction. Mutations that enhance Fc-FcR interaction of PS targeting antibodies enhance production of pro-inflammatory chemokines such as MCP-1 (CCL2), MIP-1alpha (CCL3) and MIP-1beta (CCL4). In addition, the same Fc mutations enhance ADCC of PS expressing tumor targets. Our data indicate that improvement of multiple immune effector functions via enhanced interaction of Fc-FcR interaction of PS-targeting antibodies may improve the treatment of 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 2510. doi:1538-7445.AM2012-2510
Dispersion of refractoriness in canine ventricular myocardium. Effects of sympathetic stimulation.
Authors: T Opthof, A R Misier, R Coronel, J T Vermeulen, H J Verberne, R G Frank, A C Moulijn, F J van Capelle, M J Janse
Journal: Circulation Research (1991)

In 18 dogs on total cardiopulmonary bypass, the average interval between local activations during artificially induced ventricular fibrillation (VF interval) was measured from extracellular electrograms, simultaneously recorded from up to 32 ventricular sites. VF intervals were used as an index of local refractoriness, based on the assumption that during ventricular fibrillation, cells are reexcited as soon as they have recovered their excitability. In support of this, microelectrode recordings in two hearts during ventricular fibrillation did not show a diastolic interval between successive action potentials. Refractory periods determined at a basic cycle length of 300 msec with the extrastimulus method correlated well with VF intervals measured at the same sites. Thus, this technique allows assessment of spatial dispersion of refractoriness during brief interventions such as sympathetic stimulation. The responses to left, right, and combined stellate ganglion stimulation varied substantially among individual hearts. This was observed both in dogs with an intact (n = 12) and decentralized (n = 6) autonomic nervous system. Individual ventricular sites could show effects of both left and right stellate ganglion stimulation (42% of tested sites) or show effects of left-sided stimulation only (31%) or right-sided stimulation only (14%). In 13% of sites, no effects of stellate stimulation were observed. Apart from these regional effects, the responses could be qualitatively different; that is, within the same heart, the VF interval prolonged at one site but shortened at another in response to the same intervention, although shortening was the general effect and prolongation the exception. Whenever sites responded to stellate ganglion stimulation with a shortening of VF interval, this shortening was approximately 10% for left, right, or combined stimulation, whether the autonomic nervous system was intact or decentralized. In six of 12 hearts in the intact group, there was a distinct regional effect of left stellate ganglion stimulation; in the other six hearts, the effects were distributed homogeneously over the ventricles. In three hearts, the effect of left stellate ganglion stimulation was strongest in the posterior wall, and in the other three hearts, in the anterior wall. The effects of right stellate ganglion stimulation were restricted to the anterior or lateral part of the left ventricle. Dispersion of VF intervals increased after left and combined stellate ganglion stimulation in the intact group and after right stellate ganglion stimulation in the decentralized group, but not significantly in every heart. This points to a marked individual variation with regard to the effects of sympathetic stimulation on electrophysiological properties of the heart.
Abstract 2644: In vivo and in vitro stem cell models suggest a role for LGR5 in regulating intestinal epithelial lineage specification.
Authors: Courtney M. Williams, Jessica L. Harper, Hui Huang, Pat Boland, Qing Zhang, George D. Yancopoulos, Zhe Li, O. Gavin Thurston
Journal: Cancer Research (2013)

Abstract The stem cell marker Leucine Rich Repeat Containing G-protein Coupled Receptor 5 (LGR5) is frequently upregulated in human colon cancer. Numerous observations implicate LGR5 in stem cell maintenance during intestinal development, tissue homeostasis and cancer, however the precise role of LGR5 in these processes is still unclear. To explore the role of LGR5, we generated mouse embryonic stem cells (ESCs) in which one or both alleles of Lgr5 were deleted and replaced with either β-galactosidase or green fluorescent protein (gfp) reporter genes, or the human LGR5 gene. These cell lines were used in three complimentary systems to differentiate and/or isolate cell lineages. The first system was an in vivo model in which subcutaneous xenografts of murine ESCs grew and formed tumors (teratomas) containing cellular structures from all three germ cell layers. Immunostaining showed that a subset of E-cadherin-positive epithelial cells also expressed Lgr5 reporter genes. Teratomas derived from Lgr5 null ESCs showed an increase in E-cadherin-positive epithelial structures, and gene expression profiling of Lgr5 null teratomas showed an upregulation of epithelial genes including Cdh1, Epcam, Cldn7, Krt5, and Krt14 compared with control teratomas. In contrast, ESCs constitutively overexpressing a secreted form of LGR5 ectodomain formed teratomas with fewer epithelial structures and reduced expression of epithelial genes compared to control teratomas. The second system used in vitro differentiation of ESCs towards an intestinal epithelial lineage, followed by 3D culturing, to derive intestinal organoids. Lgr5+/+ (WT), Lgr5lacZ/+ (Het), or Lgr5lacZ/gfp (Null) ESCs are being examined for their ability to adopt an intestinal fate and form organoids in vitro. A third system used ex vivo culture of murine intestinal crypts isolated from humanized LGR5 heterozygous mice to form intestinal organoids. In summary, the morphological and gene expression changes observed in teratomas implicate a role of LGR5 in regulating epithelial tissue homeostasis. The ability to grow and manipulate organoid cultures ex vivo/in vitro will allow us to use various soluble reagents and detailed microscopy to further assess the role of the Lgr5 pathway in intestinal cell lineage specification as well as tumorigenesis. Citation Format: Courtney M. Williams, Jessica L. Harper, Hui Huang, Pat Boland, Qing Zhang, George D. Yancopoulos, Zhe Li, O. Gavin Thurston. In vivo and in vitro stem cell models suggest a role for LGR5 in regulating intestinal epithelial lineage specification. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2644. doi:10.1158/1538-7445.AM2013-2644
A Comparison of Transurethral Surgery with Watchful Waiting for Moderate Symptoms of Benign Prostatic Hyperplasia
Authors: John H. Wasson, Domenic J. Reda, Reginald C. Bruskewitz, Jack Elinson, Adam M. Keller, William G. Henderson
Journal: New England Journal of Medicine (1995)

Transurethral resection of the prostate is the most common surgical treatment for benign prostatic hyperplasia. We conducted a multicenter randomized trial to compare this surgery with watchful waiting in men with moderate symptoms of benign prostatic hyperplasia.