tbuckley/cabot-search huggingface dataset:
SAT0515 Brucellosis: Clinical Manifestations Complications and Treatment (42 CASES)
Authors: I. Gharsallah, A. Laanani, R. Dhahri, F. Ajili, L. Metoui, N. Boussetta, N. Ben Abdelhafidh, B. Louzir, S. Othmani
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Brucellosis is the most common zoonotic infection worldwide. It is caused by intracellular gram-negative bacteria, <i>Brucella</i> spp. InTunisia, human brucellosis was reported in the first time in 1909. It represents a notifiable disease that occurs as an endemic evolution. The physical findings depend on the duration of illness, and the disease may be attended by various complications. <h3>Methods</h3> This is a retrospective study in the internal medicine department (from 2000 to 2013). The aim of this study was to evaluate the clinical, laboratory findings and therapeutic features of patients with brucellosis. <h3>Results</h3> We have studied 42 cases of brucellosis (29 men and 13 women9s), they were 46-year-old on an average (16-78 years). Most came from country areas, and only 7 came from the city. The source of infection was attributable to the consumption of contaminated milk or cheese, except in 3 cases of workplace exposure (veterinarian=1 case, laboratories=2 cases). Brucellosis is acute in 30 patients (71%) and focused in 12 patient cases (29%): (spondylodiscitis=8 cases, coxite=2 cases, sacroiliitis=3 cases, splenic abscess=1 case). The clinical profile was made of: fever (100%), articular and muscular pains (70%), sweats (50%) and spinal symptoms (19%). The clinical diagnosis of brucellosis was made by serology in 100% of patients (rose Bengal and/or Wright). The only organism identified was <i>brucellosis melitensis</i> in 18 cases (42%). All of patients had medical treatment (rifampicin and tetracycline) associated to corticosteroids in one case (spondylodiscitis with epiduritis). <h3>Conclusions</h3> Brucellosis presents with a wide clinical spectrum. Brucellosis melitensis is the species most incriminated. Eradication of the disease in humans can only be achieved by the control of the disease in animals. This necessitates a multidisciplinary approach involving both humans and animals. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5770
FRI0532 Effect of rheumatic diseases on long-term survival of cancer patients.
Authors: J. A. Yang, J. K. Park, S. H. Chang, E. B. Lee
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Patients with rheumatic diseases (RD) have underlying immune dysregulation and receive long-term immunosuppressive mediations which might negatively affect the outcome of a cancer in those patients. Conversely, autoimmune cells might help eliminate the cancer cells with a better outcome in RD patients. <h3>Objectives</h3> This study was aimed at systematically investigating effects of RD on the long term outcome of four most common cancers in a retrospective cohort study. <h3>Methods</h3> A total of 167 patients with RD and cancer and 501 age-, sex-, and cancer-matched controls without RD (1:3 ratio)who received their medical care at Seoul National University Hospital from 1992 to 2012 were included in this study. Survival curves were generated using the Kaplan-Meier plots and compared using log-ranks tests. <h3>Results</h3> The mean age of patients with RD was 57.2±11.5 years old. Female was dominant (75.0%). Rheumatoid arthritis was most common with 114 (68.4%) cases, followed by dermatomyositis/polymyositis (10.8%), systemic lupus erythematosus (10.8%), systemic sclerosis (10.2%). There were 42 (25.1%) gastric, 28 (16.8%) colon, 49 (29.3%) lung, and 48 (28.7%) breast cancers. One patient had 2 cancers. There was no significant difference in 5-year (90.0 % vs. 91.2%) and 10-year survival rates (84.3% vs. 85.0%, P=0.983) between the cancer patients with RD and the controls (Figure 1). In a subgroup analysis by cancer types, 5-year (100% vs. 92.2%) and 10-year cancer survival of gastric cancer were significantly better in the RD group as compared to the control group (100%, vs. 82.8%, P=0.026), whereas those of colon, lung, and breast cancer did not differ between them. <h3>Image/graph</h3> <h3>Conclusions</h3> This study clearly demonstrates that the cancer survival was not worse in patients with rheumatic diseases despite the additional presence of underlying defective immune system and concurrent use of immunosuppressive medications. <h3>Disclosure of Interest</h3> None Declared
Esophageal perforation during endoscopic removal of food impaction in eosinophilic esophagitis: stent well spent?
Authors: Bram van Rhijn, Wouter Curvers, Jacques Bergman, Joanne Verheij, Albert Bredenoord
Journal: Endoscopy (2014)

A 31-year-old man with an allergic constitution who had previously undergone endoscopic removal of impacted food in 2008 was referred to the outpatient clinic for chronic intermittent dysphagia of solid food. An upper endoscopy performed after administration of high-dose proton pump inhibitors showed linear furrows. Examination of mid and proximal esophageal biopsy specimens showed mild basal hyperplasia, moderate spongiosis, and a peak of 120 intraepithelial eosinophils per high power field ([Fig. 1]). The patient was diagnosed with eosinophilic esophagitis [1]. The patient showed a partial response to swallowed fluticasone aerosol and subsequently to budesonide, and was referred to the outpatient clinic of our hospital.
SP0208 Mri Comes of AGE for Clinical Trials in Rheumatoid Arthritis
Authors: C. Peterfy
Journal: Annals of the Rheumatic Diseases (2014)

<h3></h3> The past two decades have seen unprecedented advances in therapy for rheumatoid arthritis (RA), with several effective biologics introduced since 1998. Radiography played a central role in validating each of these novel agents. However, recent developments have undermined the practicality if not the feasibility of using radiography in clinical trials. Firstly, the availability of effective structure-modifying therapy has made extended placebo control unethical, and thus non-responders are offered rescue therapy or withdrawn by 12-16 weeks. Unfortunately, demonstrating treatment efficacy in less than 24 weeks with radiography is difficult. Another factor reducing radiography9s utility has been the recent conversion of most clinical facilities from film-based radiography to digital radiography. While this has been a positive change for image archival, patient throughput and environmental impact, it has added complexity and variability to multicenter clinical trials. This combination of ethical, technical and practical challenges has fueled an urgent need for more sensitive and rapid ways of imaging joint damage and its inflammatory causes in RA. Of the medical imaging alternatives currently available, MRI provides the most viable solution for multi-center trials. Numerous methodological and observational studies have established the construct validity of MRI depiction of bone erosions and cartilage loss in RA. Not only has MRI been repeatedly shown to be more sensitive than radiography for detecting these classical features of joint damage in RA, MRI is able to visualize the upstream inflammatory drivers of bone erosion and cartilage loss, namely synovitis and osteitis, as well as other important features of the disease, such as tenosynovitis. To date, a total of 10 randomized clinical trials have provided direct evidence of MRI9s ability to discriminate progression and treatment effect in RA in less than six months – in some cases even less than three months – using very few patients. In light of this evidence and the ethical imperative to limit the time that patients are exposed to ineffective treatment, it is important that regulatory authorities now consider accepting MRI data as an alternative to radiographic data to support claims of inhibition of progression of structural damage in RA. <h3>Disclosure of Interest</h3> C. Peterfy Shareholder of: Spire Sciences, Consultant for: AbbVie, Amgen, Articulinx, AstraZeneca, Bayer, BioClinica, Bristol Myers-Squibb, Celgene, Five Prime, Genentech/Roche, Icon Medical Imaging, Janssen, Lilly, Medimmune, Merck/Schering-Plough, Moximed, Novartis, PAREXEL Informatics, Pfizer, Salix-Santarus, Xoma, Employee of: Spire Sciences, Conflict with: Amgen <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6213
Abstract 3273: A robust transgenic mouse model to study male breast cancer
Authors: Silva Krause, Heather Tobin, Heidi L. Lurvey, Donald E. Ingber
Journal: Cancer Research (2012)

Abstract Male breast cancer accounts for about 1% of all breast cancers and even though it is a rare disease, the incidence rate has increased steadily during the past 20 years. Study of the male form of the disease has been hampered by a lack of relevant animal models as it is commonly believed that male mammary glands do not contain ducts. Female FVB C3(1)-SV40Tag transgenic mice spontaneously develop hyperplastic mammary lesions that progress to invasive mammary tumors, whereas most of the transgenic males develop prostatic hyperplasia that progresses to adenocarcinoma. However, upon closer examination, we discovered that approximately 55% of transgenic males develop mammary tumors by 40 weeks of age, often prior to developing prostate tumors. The course of male mammary development is similar to that observed in the females but with a later onset. Hyperplastic ducts form as early as 15 weeks of age and progress into DCIS-resembling tumors before developing into invasive tumors that invade locally into adipose tissue and muscle and occasionally form metastases to lung and other organs. We then examined male mammary development in the FVB background strain (wild type) and showed that all males develop mammary ducts that continue to grow and branch throughout adulthood. The morphology of these ducts was similar to that of females with a central lumen surrounded by concentric layers of luminal epithelium, myoepithelium, a basement membrane and surrounding stroma. A study of CD1 male mice confirmed that male mammary development was not specific to the FVB strain but that CD1 males showed similar mammary ductal development. Male mammary development in FVB wild type animals and tumor progression in the transgenic males was characterized in terms of cell proliferation, apoptosis and expression of various markers of differentiation including hormone receptor status. In summary, our results demonstrate that FVB C3(1)-SV40Tag transgenic males represent a highly robust and reproducible model for the study male breast cancer. Our long-term goal is to leverage the information we uncovered through this effort to design novel therapies for breast cancer treatment in men. 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 3273. doi:1538-7445.AM2012-3273
The Effects of Pancreas Transplantation on the Glomerular Structure of Renal Allografts in Patients with Insulin-Dependent Diabetes
Authors: Rudolf W. Bilous, S. Michael Mauer, David E.R. Sutherland, John S. Najarian, Frederick C. Goetz, Michael W. Steffes
Journal: New England Journal of Medicine (1989)

The microvascular complications of diabetes mellitus may be caused, in part, by poor glycemic control. Diabetic patients who have received renal allografts may have new glomerular lesions that are manifested structurally by increases in mesangial and glomerular volume. Successful pancreas transplantation produces long-term normoglycemia and provides a unique opportunity to evaluate the impact of the normalization of the blood glucose level on the development of the renal lesions typical of diabetes mellitus in transplanted kidneys. We obtained biopsy specimens from the functioning renal allografts of 12 patients with insulin-dependent (Type I) diabetes before successful pancreas transplantation (performed one to seven years after renal transplantation) and repeated the biopsy at least 1.9 years later. In renal biopsy specimens obtained before pancreas transplantation, the mesangial volume was normal or modestly increased and the glomerular basement membrane was moderately thickened. At follow-up, no progression could be detected in any structural measure in the glomerulus. Furthermore, the recipients of pancreas transplants had smaller glomerular volumes than 13 matched diabetic patients who were recipients of renal allografts but who did not undergo pancreas transplantation (means ±SD, 1.80±0.55 vs. 2.47±0.73x106 μm3; P = 0.02) and showed markedly less mesangial expansion (mesangial-volume fraction, 0.19±0.07 vs. 0.31 ±0.10 μm3 per cubic micrometer; P = 0.004). We conclude that successful pancreas transplantation is associated with significantly less severe diabetic glomerulopathy in kidneys previously transplanted into diabetic patients. These data support the hypothesis that normoglycemia can prevent the progression of diabetic glomerulopathy in humans. (N Engl J Med 1989; 321: 80–5.)
Clinical Importance of Lymphoblasts with T Markers in Childhood Acute Leukemia
Authors: Luisa Sen, Luis Borella
Journal: New England Journal of Medicine (1975)

Of 48 children with acute lymphocytic leukemia 11 had blast cells with receptors for sheep erythrocytes in their initial bone-marrow aspirates and 37 did not. A comparison of selected clinical features indicated striking differences between the two groups. Leukemia with the receptors was associated with a high proportion of older children, predominantly boys, a thymic mass, and a high white-cell count at diagnosis. In contrast, the 37 children with leukemia without the receptors were generally less than five years of age, with a nearly equal distribution of boys and girls; all but one had normal chest roentgenograms, and only one had a white-cell count greater than 100,000. Thus, the presence or absence of lymphoblasts with sheep erythrocyte receptors--a T-cell marker--distinguishes two forms of childhood acute lymphocytic leukemia, each with a distinct distribution of age and sex as well as other characteristic clinical features.
Abstract 5569: Tumor Treating Fields inhibit the growth of pancreatic and ovarian cancer in preclinical models .
Authors: Moshe Giladi, Rosa S. Schneiderman, Yaara Porat, Mijal Munster, Aviran Itzhaki, Daniel Mordechovich, Shay Cahal, Uri Weinberg, Eilon D. Kirson, Yoram Palti
Journal: Cancer Research (2013)

Abstract Tumor Treating Fields (TTFields) therapy is an established anti-mitotic treatment modality. The Novo TTF-100A system, which delivers TTFields to the brain received FDA approval for the treatment of patients with Recurrent Glioblastoma (GBM) Brain Tumors. The goal of the present study is to test whether TTFields therapy is effective as a treatment in pre-clinical models of pancreatic and ovarian cancer. TTFields of various frequencies were applied for 72h to cancerous tumor cells using two pairs of perpendicular insulated electrodes. Pancreatic adenocarcinoma and ovarian carcinoma culture growth was significantly reduced compared to controls (65%+10% and 21%+13%, respectively) with a maximal inhibitory effect seen at 150 and 200 kHz (respectively). The surviving cells exhibited increased cell volume (35%+11% and 61%+43% for pancreatic and ovarian cell lines, respectively) and a reduced viability. Fluorescence microscopy and FACS analysis revealed abnormal mitotic figure in the treated cells cultures and an increase in the 4N population, suggesting these cells failed to complete mitosis. Yet, the increase in the 4N cells fraction was too small to explain for the observed increase in cell volume in the entire remaining cell population. Combining TTFields with gemcitabine and paclitaxel commonly used for the treatment of pancreatic and ovarian cancer, enhanced treatment efficacy and led to a further increase in cell volume. The efficacy of TTFields either alone or in combination with 5FU or gemcitabine was tested in hamsters bearing syngeneic, orthotopic pancreatic tumors. In vivo imaging as well as post mortem analysis demonstrated a significant decrease in tumor weight and volume. Compared to chemotherapy treatment alone, TTF had a sensitizing effect and increased tumor response to chemotherapy. Based on previous reports, the observed increase in cell volume is expected to shift the peak response to TTFields to a lower frequency, allowing some of the cells to escape the effect of TTFields. While this is the first proposed mechanism of resistance to TTFields it also opens the possibility of overcoming that resistance using serial application of several frequencies. Citation Format: Moshe Giladi, Rosa S. Schneiderman, Yaara Porat, Mijal Munster, Aviran Itzhaki, Daniel Mordechovich, Shay Cahal, Uri Weinberg, Eilon D. Kirson, Yoram Palti. Tumor Treating Fields inhibit the growth of pancreatic and ovarian cancer in preclinical models . [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 5569. doi:10.1158/1538-7445.AM2013-5569
Serial Changes of FDG Uptake and Diagnosis of Suspected Lung Malignancy
Authors: Gang Cheng, Abass Alavi, Thomas J. Werner, Catherine V. Del Bello, Scott R. Akers
Journal: Clinical Nuclear Medicine (2013)

This study prospectively evaluates the serial change of FDG uptake and its diagnostic value in malignant versus benign lung lesions in patients with suspected lung cancer.Patients with suspected lung malignancy underwent whole-body FDG PET/CT at 1, 2, and 3 hours after an IV injection of F-FDG. The SUVs of FDG in lung nodules and hilar/mediastinal nodes at each time point were correlated with biopsy/surgical pathologic findings.There were a total of 45 malignant lesions and 80 benign lesions from 43 patients with pathologic diagnosis that were included for analysis. The SUVmax had an average of 25.5% increase in all tumor-positive lesions from 1 to 2 hours (vs 1.6% decrease in all tumor-negative lesions, P < 0.0001) and an average of 39.1% increase from 1 to 3 hours (vs 4.5% increase in all tumor-negative lesions, P < 0.0001). The receiver operating characteristic analysis showed that the 2-hour and 3-hour SUVmax had similar area under the curve and outperformed the SUVmax on the 1-hour initial imaging or retention index (RI). The optimal cutoff values to differentiate malignancy from benign lesions were 3.24 for 1-hour SUVmax, 3.67 for 2-hour SUVmax, and 4.21 for 3-hour SUVmax, with 11.6% for 1- to 2-hour RI and 23.9% for 1- to 3-hour RI. The 3-hour delayed SUVmax of 4.21 provided the best overall performance (accuracy of 88.8%). The analysis of the lesion-to-background ratio revealed that delayed imaging improved the image quality significantly, leading to much easier detection of either malignant or benign lesions.Multiple time point FDG PET/CT imaging moderately improves the diagnostic accuracy of lung cancer and significantly improves the image quality.
More than modularity and metaphor: The power of preadaptation and access
Authors: Paul Rozin
Journal: Behavioral and Brain Sciences (2010)

Abstract Neural reuse demonstrates preadaptation. In accord with Rozin (1976), the process is an increase in accessibility of an originally dedicated module. Access is a dimension that can vary from sharing by two systems to availability to all systems (conscious access). An alternate manifestation is to reproduce the genetic blueprint of a program. The major challenge is how to get a preadaptation into a “position” so that it can be selected for a new function.
Abstract 5147: Tumor angiogenesis-promoting activity of a hypoxia-inducible cytokine, growth differentiation factor-15 (GDF-15)
Authors: Jaeseob Lee, Hansoo Lee, Jeongsuk Choi, Iha Park, Jeong-Hyung Lee, Young-Myeong Kim
Journal: Cancer Research (2011)

Abstract Angiogenesis, growth of new blood vessels from pre-existing capillary blood vessels, is a marker of cancer and various ischemic and inflammatory diseases. Tumor growth depends on new blood vessel formation because tumor cells require oxygen and nutrients for their survival and proliferation. GDF-15, also known as MIC-1, NAG-1 and PTGF-beta, is a divergent member of the TGF-beta super family. GDF-15, like other TGF-beta family members, has shown janus-faced function in tumor development: pro-apoptotic and anti-tumorigenic vs. tumorigenic activity. Previously, we and others found that hypoxia-condition induced GDF-15 expression in various cancer cell types, leading to increased secretion from the cancer cells. Here, we present the tumor-promoting activity of GDF-15, along with pro-angiogenic activity. In in vivo mouse xenograft model using human melanoma cells, we found that tumors from GDF-15-expressing melanoma cells show higher degree of vessel formation with larger tumor volume than control tumors. Blood vessel inducing activity of GDF-15 was also observed when using human umbilical vein endothelial cells (HUVECs). GDF-15 treatment induced tube formation of HUVECs. Moreover, treatment of GDF-15 enhanced the growth and migration of HUVECs. Blood vessel inducing activity of GDF-15 was further confirmed by CAM and aortic ring sprouting assays, intravital microscopic analysis and matrigel plug assay. Furthermore, GDF-15 transgenic mice showed increased blood vessel development than wild type mice while lymphatic vessel development was no different. Interestingly, although angiogenic activity of GDF-15 was comparable to that of VEGF, its inflammatory activity was less significant than VEGF. Taken together, we show that GDF-15 functions as a potential angiogenic factor for tumor development with seemingly little inflammatory activity. Key words: Cytokine, GDF-15, Tumor, Angiogenesis, Inflammation 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 5147. doi:10.1158/1538-7445.AM2011-5147
Shock Reduction With Long-Term Quinidine in Patients With Brugada Syndrome and Malignant Ventricular Arrhythmia Episodes
Authors: Ignasi Anguera, Arcadio García-Alberola, Paolo Dallaglio, Jorge Toquero, Luisa Pérez, Juan Gabriel Martínez, Rafael Peinado, José M. Rubín, Josep Brugada, Angel Cequier
Journal: Journal of the American College of Cardiology (2016)
Cancer Evolution Constrained by Mutation Order
Authors: Charles Swanton
Journal: New England Journal of Medicine (2015)

In Wonderful Life: The Burgess Shale and the Nature of History, Gould1 pondered the existence of species, focusing on biologic diversity in the Cambrian period more than 500 million years ago that led to the major body plans known today. He argued that the subsequent chapters of the evolutionary book of life were constrained by embedded developmental pathways. Evolution is dependent on antecedent steps that influence or constrain future evolutionary routes.As analyses of the cancer genome deepen, parallels between ecological evolution and tumor evolution are apparent.2,3 These parallels suggest that the order of genetic events in tumors influences . . .