tbuckley/cabot-search huggingface dataset:
Bone Scintigraphy of Elephantiasis Neuromatosa in Von Recklinghausen’s Disease
Authors: MORDECHAI LORBERBOYM, LEONARDO TREJO, YAIR LAMPL
Journal: Clinical Nuclear Medicine (2000)

A 35-year-old man with a history of neurofibromatosis had a soft tissue mass and enlargement of the right thigh. A bone scan was requested before surgical intervention to assess the extent of soft tissue and osseous involvement. The bone scan showed marked soft tissue swelling and Tc-99m MDP uptake in the soft tissues of the right thigh and the sacral region. No abnormal bony uptake was noted in the femur or tibia.
PM-08 * INVESTIGATING THE DETERMINANTS OF GBM SUBTYPES USING NOVEL MOUSE MODELS
Authors: S. Lawn, R. Dixit, J. Chan
Journal: Neuro-Oncology (2014)

Molecular characterization of glioblastoma multiforme (gbm) has shown adult gbms to comprise a number of subtypes based on their gene expression signatures. While these subtypes are somewhat associated with distinct genetic alterations, the relative contributions of oncogenic driver, cell of origin and developmental stage are not fully understood. Using a novel and highly versatile modeling platform based on in vivo electroporation mediated transfer of transposon based plasmids to ventricular neural progenitors, we have generated high grade gliomas in mice using PDGFA, EGFRVIII or RasV12 expression in combination with p53 loss. These tumours show complete penetrance by 5 weeks post electroporation and bear key features of gbm such as necrosis and prevalent vascularisation. Gene expression analysis by Nanostring and subsequent unsupervised clustering shows each oncogenic driver to result in tumours of distinct gene expression profiles, with the PDGFA and RasV12 driven tumours showing similarity to the proneural and mesenchymal subclasses respectively. Modification of our plasmid system to incorporate selective promoters, floxed stop cassettes and tamoxifen inducible cre recombinase grants us precise spatiotemporal control over induction of gliomagenesis and allows us to probe the influence of developmental stage, cell of origin, brain region and gene expression level to the resulting tumour gene expression profiles.
Disappearing pancreatic arteriovenous malformation
Authors: Hiroyuki Matsubayashi, Toru Matsui, Kimihiro Igarashi, Kinichi Hotta, Kenichiro Imai, Hideyuki Kanemoto, Hiroyuki Ono
Journal: Endoscopy (2014)

Arteriovenous malformation (AVM) of the pancreas is a rare disorder for which treatment is recommended as it may cause development of portal hypertension and increase the risk of gastrointestinal bleeding [1] [2] [3].
The Bench Press Mark Revisited
Authors: ANDREW J. MEHOLIC, RICK G. HODGE, MICHAEL F. HARTSHORNE
Journal: Clinical Nuclear Medicine (1998)

Extensive soft-tissue uptake after strenuous physical exercise and/or trauma has been observed with bone scanning agents. Reports since 1984 suggest that muscle damage secondary to strenuous exertion is more common than realized, an observation that has assumed an important role in the last decade because of the evolution of sports medicine practices. Furthermore, although localization of the phosphate bone scanning agents following exercise has been recognized since 1978, there is no one explanation for the exact mechanism by which these bone-seeking agents are concentrated in injured skeletal tissues and muscles.
THU0108 Associations Between TRAF1-C5 Gene Polymorphisms and Rheumatoid Arthritis: A Meta-Analysis
Authors: Y. H. Lee, J.-H. Kim, S. J. Choi, J. D. Ji, G. G. Song
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The tumor necrosis factor receptor-associated factor 1 (TRAF1) gene encodes TRAF1, which acts in association with TNF receptor family members and regulates cytokine signaling networks. Complement 5 (C5) is a pivotal member of the complement system. Product of TRAF1 and C5 is a potent chemo-attractant complement component and an essential effector of the TNF signaling cascade. <h3>Objectives</h3> The aim of this study was to determine whether TRAF1-C5 polymorphisms confer susceptibility to rheumatoid arthritis (RA) in different populations. <h3>Methods</h3> We conducted a meta-analysis of associations between the TRAF1-C5 rs10818488, rs3761847, rs2900180 and rs10760130 polymorphisms and RA susceptibility, using fixed and random effects models. <h3>Results</h3> A total of 24 comparative studies were included in this meta-analysis, including 22,682 patients with RA and 23,493 controls. The meta-analysis showed an association between the second allele of rs10818488 and RA in all study subjects (OR 1.170, 95% CI 1.082-1.266, <i>p</i> = 8.2 x 10<sup>-6</sup>). Analysis after stratification by population indicated that the second allele of rs10818488 were associated with RA in Europeans, but not in Asians (OR 1.229, 95% CI 1.094-1.381, <i>p</i> = 0.001; OR 1.060, 95% CI 0.930-1.335, <i>p</i> = 0.092). The meta-analysis also indicated an association between the second allele of rs3761847 and RA in all study subjects (OR 1.098, 95% CI 1.019-1.184, <i>p</i> = 0.015). The second allele of rs3761847 was associated with RA in Europeans, but not in Asians (OR 1.156, 95% CI 1.006-1.327, <i>p</i> = 0.041; OR 1.049, 95% CI 0.952-1.156, <i>p</i> = 0.333). The meta-analysis revealed an association between the second allele of the rs2900180 polymorphism and the risk of developing RA in all study subjects and Europeans (OR 1.180, 95% CI 1.031-1.350, <i>p</i> = 0.016; OR 1.224, 95% CI 1.065-1.405, <i>p</i> = 0.004). An association between the second allele of rs10760130 and RA in Europeans (OR 1.072, 95% CI 1.002-1.147, <i>p</i> = 0.042) was also noted. <h3>Conclusions</h3> This meta-analysis confirms that the TRAF1-C5 rs10818488, rs3761847, rs2900180 and rs10760130 polymorphisms are associated with RA susceptibility in Europeans. However, the TRAF1-C5 rs10818488 and rs3761847 polymorphisms are not associated with RA in Asians. <h3>References</h3> Kurreeman FA, Goulielmos GN, Alizadeh BZ, Rueda B, Houwing-Duistermaat J, Sanchez E, Bevova M, Radstake TR, Vonk MC, Galanakis E, Ortego N, Verduyn W, Zervou MI, Roep BO, Dema B, Espino L, Urcelay E, Boumpas DT, van den Berg LH, Wijmenga C, Koeleman BP, Huizinga TW, Toes RE, Martin J (2010) The TRAF1-C5 region on chromosome 9q33 is associated with multiple autoimmune diseases. Ann Rheum Dis 69:696-699 <h3>Disclosure of Interest</h3> None Declared
Survival in Lung Cancer
Authors: Katharine R. Boucot, Utako Horie, Martin J. Sokoloff
Journal: New England Journal of Medicine (1959)

DESPITE a marked improvement in operative mortality1 2 3 five-year survival rates for primary lung cancer range between 4.1 and 9.6 per cent.4 , 5 This may be due to an inherent biologic tendency to early metastasis, to late diagnosis or to inadequacy of current therapeutic measures. Little is known about the natural history of bronchogenic carcinoma. Tumors vary in rates of growth and in invasive and metastasizing qualities.A major difficulty in the whole field of prognosis is the lack of a classification of lung cancer that would permit comparison of different series in the same manner in which cases of tuberculosis can . . .
SP0128 Is Therapeutic Drug Monitoring Useful? A Review of the Literature
Authors: D. Mulleman
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objectives</h3> 1) Outline the structure and the pharmacology of TNF inhibitors (full lenth monoclonal antibodies, Fc-TNFR fusion protein, PEGylated Fab) that are currently used 2) Discuss the dose-response relationship and the sources of pharmacokinetics and pharmacokinetic-pharmacodynamic variability 3) Focus on the effect of inflammation on pharmacokinetics of TNF inhibitors and the potential interest to adapt the dosage of TNF inhibitors according to the patient9s disease activity Denis Mulleman, M.D., Ph.D., is professor of rheumatology at the University of Tours. He is member of the CNRS research unit 7292 (team 1: "Antibodies, Fc receptors and clinical responses"). His main research interest is to characterize the concentration-response relationship of anti-TNF monoclonal antibodies and Fc-containing fusion proteins to help clinicians personalize drug administration (therapeutic drug monitoring). <h3>Disclosure of Interest</h3> D. Mulleman Grant/Research support from: Abbott, Consultant for: MSD, Pfizer <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6302
Transient Monocular Blindness Caused by Vasospasm
Authors: Stephen K. Burger, Robert F. Saul, John B. Selhorst, Stephen E. Thurston
Journal: New England Journal of Medicine (1991)

SPORADIC transient monocular loss of vision (amaurosis fugax) lasting a few seconds to several minutes has fascinated and perplexed clinicians for years. In the mid-19th century, von Graefe1 and later Gowers2 proposed an embolic pathogenesis. Temporary vasospasm, however, was later invoked to account for this type of visual loss.3 , 4 In 1959, Fisher5 observed platelet–fibrin emboli passing through the retinal vasculature during an episode of monocular blindness. This report helped establish the platelet–fibrin theory as an explanation of many transient and fixed ischemic visual deficits. We describe two patients with vasospastic transient monocular blindness, as demonstrated by photography of the fundus. . . .
DELAYED COMPLICATIONS OF ECT – "CRUSH SYNDROME"
Authors: RONALD MCNICHOL
Journal: American Journal of Psychiatry (1958)

A case of crush syndrome following ECT is reported. It emphasizes the need to anticipate such complications. There are probably other delayed complications in which the relationship to ECT has not yet been recognized. An increased awareness of their potential occurrence is essential if earlier and more adequate management of them is to result. Careful autopsy studies are necessary for the broadening of our knowledge in these areas. "Was man weiss, man sieht."
Diphtheria toxin fused to human interleukin-3 is toxic to blasts from patients with myeloid leukemias
Authors: AE Frankel, JA McCubrey, MS Miller, S Delatte, J Ramage, M Kiser, GL Kucera, RL Alexander, M Beran, EP Tagge, RJ Kreitman, DE Hogge
Journal: Leukemia (2000)
The Economics of Dying -- The Illusion of Cost Savings at the End of Life
Authors: Ezekiel J. Emanuel, Linda L. Emanuel
Journal: New England Journal of Medicine (1994)

For more than a decade, health policy analysts have noted -- and some have decried -- the high cost of dying1–7. With the acceleration of pressures on health care costs and calls for reform, considerably more attention has been focused on proposals to control costs at the end of life8. One proposal would require persons enrolling in a health care plan to complete an advance directive9,10. Others would require hospitals to establish guidelines to identify and reduce futile care11–13. Similar ideas have been expressed by members of President Bill Clinton's Health Care Task . . .
2-(4-Hydroxyphenyl)-Benzo[b]thiophen-6-ol, an Estrogen-Like Compound, Induces Apoptosis in T47D/PKCα Breast Cancer Cells.
Authors: M. Molloy, G. Thatcher, J. Bolton, D. Tonetti
Journal: Cancer Research (2009)

Abstract Background: Tamoxifen (TAM) treatment failure is a major obstacle encountered in the clinical setting. Our lab has previously shown that constitutive overexpression of PKCα imparts a TAM resistant/ hormone independent phenotype in the T47D:A18 breast cancer cell line. Furthermore 17β-estradiol (E2) inhibits tumor growth in vivo as well as inhibits colony formation when cells are grown in 3D Matrigel (Zhang, 2009). Before TAM treatment was introduced, breast cancer patients received high-dose E2 and diesthystilbesterol (DES) treatment. DES treated patients may have a survival advantage over TAM treated patients in the long term (Peethambaram,1999). Others have shown that E2 can have inhibitory effects on MCF-7 cells both in vitro and in vivo (Lewis-Wambi, 2009). Taken together, this suggests an estrogenic compound may be efficacious for TAM-resistant breast cancer. The present study was designed to evaluate the effect of an estrogenic compound, 2-(4-hydroxyphenyl)-benzo[b]thiophen-6-ol (BTC), related to the SERMs raloxifene and arzoxifene, on the T47D:A18/PKCα breast cancer cell line.Methods: To determine if BTC can activate estrogen regulated genes we preformed an ERE-luciferase reporter assay 24 hours after BTC treatment. 3D Matrigel colony formation assay was performed to determine if BTC could inhibit colony formation. Colonies were stained and counted on day 10. To determine if apoptosis was occurring, cells were grown in Matrigel and the TUNEL Assay was performed on Day 6.Results: T47D:A18/PKCα cells showed a 31-fold induction in ERE-luciferase reporter activity when treated with BTC (10-7M) compared to 7-fold induction when treated with E2. In the T47D:A18/Neo parental cell line, BTC induced a 40-fold induction whereas estradiol induced a 96-fold induction. In the Matrigel colony formation assay T47D:A18/PKCα cells formed significantly fewer colonies when treated with BTC. Conversely, in the T47D:A18/Neo parental cell line BTC enhanced colony formation similar to E2 treatment. Our results indicate that BTC was able to induce significant apoptosis on day 6 (P= 0.038) as determined by the TUNEL Assay. Therefore BTC acts similarly to estradiol by inhibiting T47D:A18/PKCα colony formation and inducing apoptosis when cells are grown in Matrigel.Conclusion: These findings suggest that BTC is a potential lead compound in the treatment of PKCα overexpressing breast cancer. Furthermore, BTC was shown to be a potent inducer of the cytoprotective enzyme NQO1 in the Hepa 1c1c7 cell system as well as a strong activator of antioxidant responsive elements (Yu, 2007) indicating it may have the added benefit of chemoprotective effects which are absent in estradiol treatment. Further understanding of the mechanism in which BTC induces apoptosis in the T47D:A18/PKCα cell line may result in a clinical advantage to estradiol treatment including fewer side effects. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 5140.
EFFICACY AND SAFETY OF TICAGRELOR FOR LONG-TERM SECONDARY PREVENTION OF ATHEROTHROMBOTIC EVENTS IN PATIENTS WITH PRIOR MI AND MULTIVESSEL CORONARY DISEASE: INSIGHTS FROM THE PEGASUS-TIMI 54 TRIAL
Authors: Sameer Bansilal, Marc Bonaca, J.H. Cornel, Robert Storey, Deepak Bhatt, Philippe Steg, Kelly Im, Peter Held, Eva Jensen, Eugene Braunwald, Marc Sabatine, Ton Oude Ophuis
Journal: Journal of the American College of Cardiology (2016)
PTU-043 Diagnostic Yield and Safety of Small Bowel Capsule Endoscopy
Authors: E Houston, R Rivera-Forrester, N Haslam, A Morris, P Reid, P Collins
Journal: Gut (2013)

<h3>Introduction</h3> Small bowel capsule endoscopy (CE) is a minimally-invasive, established tool for the detection of small bowel lesions. <h3>Methods</h3> All capsule endoscopy reports from Jan 2007 to Aug 2012 performed at the Royal Liverpool University Hospital were reviewed. <h3>Results</h3> A total of 311 examinations were performed during the period of review. Patients undergoing CE had a median age of 53 years (range 15 – 88) and a male:female ratio of 48.6%:57%. The commonest indication for examination was unexplained iron deficiency anaemia (IDA) (48.6%). Other indications included assessment for suspected Crohn’s disease (23.5%), obscure overt GI blood loss (11.9%), polyposis syndrome (3.9%), diarrhoea (2.6%)and investigation of refractory coeliac disease (1.6%). The median gastric transit time was 19 mins (range 0 – 276 mins). The median small bowel transit time was 245 mins (range 61–533 mins). The capsule failed to reach the colon in 17.4% of cases. 41.8% of examinations were normal. The commonest finding in patients with IDA was angioectasia (19.9%). 59.5% of patients with obscure overt GI blood loss had positive findings. (Active bleeding (24.3%), Vascular lesion (5.4%), polyp (10.8%), NSAID enteropathy (2.7%), and gastritis (2.7%)). Crohn’s disease was identified in 5.8% of all cases and in 13.8% of cases referred for assessment of suspected Crohn’s disease. 4.6% of patients with IDA had findings consistent with Crohn’s disease. Further investigation was advised in 36.7%. In 35.9% of those patients, the major abnormality identified for which a further procedure was required was located within the reach of a gastroscope. In those with IDA, gastroscopy was recommended in 22.7% of cases. Gastroscopy was recommended in a smaller proportion of patients (4.4%) having CE for other indications. A repeat procedure with bowel cleansing agents was required because of poor views in 1.6% of procedures. Capsule retention occurred in 2 of 186 patients (1.1%) for whom retention data was available. Prior small bowel imaging had not demonstrated a stricture in either case. Endoscopic removal of the capsule was successful in both patients. The cause of capsule retention was crohn’s disease in one and NSAID enteropathy in the other. <h3>Conclusion</h3> Adequate diagnostic images were obtained in &gt; 98% of patients without the administration of bowel cleansing agents. The yield of positive findings from capsule endoscopy is high, but a significant proportion of lesions are within the range of a gastroscope, especially in patients with IDA. We recommend that patients undergo at least two gastroscopies prior to CE. CE is a safe procedure. Capsule retention was reported with a similar frequency to that reported in other case series. Patients should be advised that normal small bowel radiology may not exclude a significant stricture. <h3>Disclosure of Interest</h3> None Declared
AB0185 A case control study of the presence and patterns of the shared epitope (SE) in 150 egyptian rheumatoid arthritis patients and comparison to control subjects
Authors: W.A.A. Mohamed, R. Abdel Kader, M.Y. Tayel, A.F. Elkoraie, I. Ibrahim, M.W. Ayad
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoid Arthritis (RA) is one of the commonest forms of inflammatory arthritis affecting 0.5-1% of population worldwide. One of the poor prognostic features (PPFs) that has been set by the American College of Rheumatology in 2008 is the presence of specific sequence of amino acids at positions 70-74 in the third hypervariable region of the beta chain which is one of the constituents of the second class HLA haplotypes; DR. This sequence is called Shared Epitope (SE) and it facilitates the citrullination or deamination (i.e. post-translational modification) of Arginine into Citrulline and the formation of Anti-citrullinated peptides antibodies (ACPAs) which are the main pathogenic factor in RA.<sup>(1)</sup> <h3>Objectives</h3> The aim of this case-control study was to detect the presence and patterns of Shared epitope in 150 Egyptian Rheumatoid arthritis patients admitted to the Alexandria Main University Hospital between June 2010 &amp; May 2011. We then compared these patterns to those encountered in 200 control subjects who resided in the same city during the same period. <h3>Methods</h3> We assigned study subjects into 2 groups; RA group (150 RA patients diagnosed based on the ACR/EULAR criteria 2010) and Control group (200 healthy subjects who were prepared to be living organ donors by our Transplantation Unit). We then used Dynal RELI TM SSO HLA-DRB Test and polymerase Chain Reaction (PCR) to detect the amino acid sequence at positions 70-74 on the DRB1 chain (shared epitope;SE) in both groups. We then tabulated and compared the data with proper methods. <h3>Results</h3> We found that DR15 (with 70-74 sequence of QARAA) was the commonest allele (95/150=63.3%) among RA group when compared to control group with Odds Ratio (OR) of 8.45, while alleles other than the recognized shared epitopes (e.g. DR1, DR4, DR10, DR14) were more prevalent in control group and were even protective. <h3>Conclusions</h3> DRB*1 1501/1502 (QARAA)was the commonest epitope among Egyptian RA patients included in our study and we concluded that it might be a new Shared Epitope (SE) in our population as it differs racially from other populations in which SE had been detected. <h3>References</h3> Gregersen PK et al. The shared epitope hypothesis. Arthritis Rheum 1987,30:2642-6. <h3>Disclosure of Interest</h3> None Declared
Case 9-1978
Authors: Richard C. Cabot, Robert E. Scully, James J. Galdabini, Betty U. McNeely, W. Hardy Hendren, Karl H. Proppe
Journal: New England Journal of Medicine (1978)

Presentation of CaseA two-year-old boy was admitted to the hospital because of recurrent vomiting.The child was born of the second pregnancy of a 23-year-old woman at 42 weeks of gestation. The pregnancy was uneventful; no medicines were taken. The duration of labor was 36 hours, and vaginal delivery was performed. The birth weight was 3.24 kg. His growth and development were normal, and he walked at one year. At about that time he had a brief illness characterized by abdominal cramps, without vomiting; no diarrhea or bleeding was observed.Two months before entry he suddenly began to vomit, . . .
THU0158 Six year follow-up study of bone mineral density in patients with systemic lupus erythematosus
Authors: J. Jacobs, L.-A. Korswagen, A. Schilder, L. van Tuyl, B. Dijkmans, W. Lems, A. Voskuyl, I. Bultink
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Low bone mineral density (BMD) is highly prevalent in patients with systemic lupus erythematosus (SLE). However, the determinants of long-term BMD changes in SLE are still largely unknown, since the majority of studies performed had a cross-sectional design and the few longitudinal studies had a small sample size (maximum 36) and short follow-up duration (≤3 years). <h3>Objectives</h3> The aim of this study was to assess the long-term BMD changes in patients with SLE and to identify the associated factors. <h3>Methods</h3> We prospectively studied 126 SLE patients. Demographic and clinical data were collected and BMD measurements of the lumbar spine and total hip were performed by dual energy x-ray absorptiometry at baseline and at follow-up. Statistical analyses were performed using repeated measures t-test, Mann-Whitney U-test, univariate and multivariate regression analyses. <h3>Results</h3> At baseline, osteopenia was present in 39.7% of the patients (90% female, mean age 39±12.2 years) and osteoporosis in 6.3%. After a median follow-up duration of 6.7 years (range 1.9 - 9.3 years), mean changes in BMD at the lumbar spine (-0.08%/year) and at the hip (-0.20%/year) were not significant. During follow-up, 70% of the patients used glucocorticoids. The mean ± SD daily glucocorticoid dose was 5.0±5.0 mg. In multiple regression analysis, BMD loss at the spine was significantly associated with higher daily glucocorticoid dose (<i>p</i>=0.004) and lower baseline 25-hydroxyvitamin D levels (<i>p</i>=0.030) whereas BMD gain at the spine was significantly associated with use of immunosuppressive medication other than glucocorticoids (<i>p</i>=0.016). BMD loss at the hip was associated with lower 25-hydroxyvitamin D levels (<i>p</i>=0.030), reduction of body mass index (<i>p</i>=0.040), and baseline use of antimalarials (<i>p</i>=0.006). <h3>Conclusions</h3> In this 6-year follow-up study - thus far the largest study conducted -, bone loss was remarkably low. A dose-dependent relationship between glucocorticoid use and spine bone loss was found. In addition, use of antimalarials and lower 25-hydroxyvitamin D levels were associated with bone loss whereas use of immunosuppressive medication other than glucocorticoids was associated with bone gain at the spine. These findings underline the importance of prevention and treatment of vitamin D deficiency and osteoporosis in SLE, especially in patients using glucocorticoids or antimalarials. Moreover, the importance of treatment with immunosuppressive medication to improve disease-control and to reduce glucocorticoid dosages was highlighted. <h3>Disclosure of Interest</h3> None Declared