tbuckley/cabot-search huggingface dataset:
SP0122 Osteoporosis and bone disease
Authors: W.F. Lems
Journal: Annals of the Rheumatic Diseases (2013)

Osteoporosis can be divided in primary osteoporosis and secondary osteoporosis. In the field of primary osteoporosis, the new focus is the diagnostic and therapeutic follow-up of individuals 50 years and over with a fracture. One of the big issues is how to implement that DXA-measurements will be adequately performed in all individuals 50 years and over with a fracture. Since it is nowadays possible to detect vertebral deformities with VFA (Vertebral Fracture Assessment), a software technique imaging the heights of the thoracal and lumbar vertebral bodies that can be used in one session with a BMD measurement, it is attractive to combine VFA with DXA of the lumbar spine and hip(s). Other critical points are how to integrate fall risk with bone related risk factors, and secondary osteoporosis: new data have shown that roughly 50% of fracture patients do have one or more secondary causes of osteoporosis. For those patients who have already started with anti-osteoporotic therapy, one of the issues is how long to continue with anti-osteoporotic therapy (5 years? or more?), and what is the balance of the bisphosphonate related increased risk of subtrochanteric fractures versus the reduction in vertebral- and nonvertebral fractures. What about secondary osteoporosis? Recent data in the field of osteo-immunology, the crosstalk between cytokines and bone, have elucidated that activated inflammatory cells at the sites of inflammation produce a wide spectrum of cytokines which stimulate local and generalised bone resorption, and which inhibit (in RA) or stimulate (in AS) bone formation. Osteoporosis related fragility fractures represent one of the most important complications that may occur in patients with rheumatic diseases; obviously these fractures may contribute to an important decrease in quality of life. Disease activity (inflammation), immobility and treatment with glucocorticoids are the main factors that increase the risk of osteoporotic fractures, on top of the background fracture risk based on, amongst others, age, body mass index and gender. During the lecture, some topics will be discussed: –can both the local and generalised bone loss in RA be blocked with effective antirheumatic therapies? –the complex pathogenesis of bone loss and fractures in SLE; –the intriguing elevated loss of BMD and bone quality, with also local new bone formation in patients with ankylosing spondylitis. <h3>Disclosure of Interest</h3> W. Lems Speakers Bureau: MSD, Lilly, Amgen, Servier, Novartis, Procter and Gamble, Will Pharma
Biliary Tract Cancers
Authors: Piet C. de Groen, Gregory J. Gores, Nicholas F. LaRusso, Leonard L. Gunderson, David M. Nagorney
Journal: New England Journal of Medicine (1999)

In the United States, an estimated 20,000 new cases of liver and biliary tract cancer are diagnosed annually.1 Biliary tract cancer is the second most common primary hepatobiliary cancer, after hepatocellular cancer. Approximately 7500 new cases of biliary tract cancer are diagnosed per year; about 5000 of these are gallbladder cancer, and between 2000 and 3000 are bile-duct cancers.1 Biliary tract cancers have traditionally been divided into cancers of the gallbladder, the extrahepatic bile ducts, and the ampulla of Vater, whereas intrahepatic bile-duct cancers have been classified as primary liver cancers.2 The term "cholangiocarcinoma" was originally intended to refer only . . .
AB0480 Colchicine reduces relapse of acute neurological attacks in behcet’s disease
Authors: S. Hirohata, H. Kikuchi, T. Sawada, H. Nagafuchi, M. Kuwana, M. Takeno, Y. Ishigatsubo
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Acute neurolo-Behcet's disease (NBD) is characterized by acute attacks of meningoencephalitis with or without focal lesions, responding to corticosteroid therapy, and is usually self-limiting, although recurrence of the attacks is sometimes seen. <h3>Objectives</h3> In the current studies, we investigate the effects of various factors on the relapse rate in patients with acute NBD. Special attention has been paid to the influences of the cessation of cyclosporine A as well as the use of various immunosuppressants and colchicine. <h3>Methods</h3> In a retrospective cohort of 144 patients obtained from a multicenter retrospective survey on BD patients who met the international classification criteria for Behcet's disease and presented any neurological manifestations between 1988 and 2008, 61 patients had attacks of acute NBD. We assessed factors associated with relapses of acute neurological attacks in these 61 patients. <h3>Results</h3> Twenty of 61 patients were taking CyA at the onset of acute NBD. All the 20 CyA (+) patients and 34 of the 41 CyA (-) patients had eye involvement. There were no significant differences in demographic features, clinical symptoms, MRI findings, the need for and response to corticosteroid therapy including pulse therapy between CyA (+) patients and CyA (-) patients. Of note, CyA (+) patients showed significantly less relapse rates than CyA (-) patients (HR:0.1177, 95%CI:0.0064-0.6027, p=0.0064). Colchicine appeared to reduce the relapse rates in 61 patients with acute NBD, although it did not reach the statistical significance (HR:0.1177, 95%CI:0.0064-0.6027, p=0.0064). However, colchicine significantly reduced the relapse rates in 41 CyA (-) patients (HR:0.1758, 95%CI:0.0093-0.9728, p=0.0457 on multivariate analysis), whereas methotrexate (HR:1,2093, 95%CI:0.0628-7.2624, p=0.8653) and azathioprine (HR:1.8814, 95%CI:0.2845-7.4039, p=0.4532) did not show any significant effects on relapses in these patients. <h3>Conclusions</h3> These results indicate that CyA-related acute NBD is characterized by the paucity of relapse on discontinuation of CyA compared with CyA-unrelated acute NBD. The data also demonstrate that colchicine is effective to prevent relapses of acute neurological attacksespecially in patients who developed acute NBD in the absence of CyA. <h3>References</h3> Hirohata S, Kikuchi H, Sawada T, Nagafuchi H, Kuwana M, Takeno M, Ishigatsubo Y. Clinical characteristics of neuro-Behcet's disease in Japan: a multicenter retrospective analysis. Mod Rheumatol 22: 405-13, 2012. Akman-Demir G, Ayranci O, Kurtuncu M, Vanli EN, Mutlu M, Tugal-Tutkun I. Cyclosporine for Behçet's uveitis: is it associated with an increased risk of neurological involvement? Clin Exp Rheumatol. 2008; 26(Suppl 50): S84-90. <h3>Disclosure of Interest</h3> None Declared
GROUP THERAPY FOR PARENTS OF BEHAVIOR PROBLEM CHILDREN IN PUBLIC SCHOOLS
Authors: JANE KAHN, A. D. BUCHMUELLER, MARGARET C.-L. GILDEA
Journal: American Journal of Psychiatry (1951)

A group therapy project for parents of behavior problem children in public schools succeeded in several varied white school districts, but failed in a colored area. Reasons for failure lay in minority tensions and status anxieties between group members which made it impossible for the Negro mothers to face responsibility for their children. The behavior problems of their children could not be felt by them as clear-cut issues without contamination by ideas of discrimination. Also the educational-cultural level of the Negro population in this partially segregated area is not comparable to that in the white districts. Methods in mental health education for parents and school personnel are outlined. Preventive and therapeutic psychiatric methods must be specifically tailored to the population to be served if they are to be successful.
Abstract 87: Differential effects of JNK1 and JNK2 on cell death in hypoxic colon cancer cell lines
Authors: Irina A. Vasilevskaya, Muthu Selvakumaran, David Roberts, Peter J. O'Dwyer
Journal: Cancer Research (2010)

Abstract BACKGROUND: We previously showed that hypoxic colon cancer cell lines exhibit higher sensitivity to oxaliplatin when SEK1 function is impaired, and greater resistance when MKK7 is down regulated. The MKK7 mutant lines exhibit more profound inhibition of JNK activation than those lacking SEK1, and their effects on the activation of JNK1 and JNK2 differ. The HT29 cells do not die readily by apoptosis under these conditions, and both oxaliplatin and hypoxia induce autophagy in these cells. PURPOSE: The purpose of this study is to investigate further how modulation of signaling through JNK1 and JNK2 influences cell death pathways in hypoxic HT29 cells treated with oxaliplatin. For that, we employed HT29-derived cell lines stably expressing empty vector (HT.LX) and dominant negative constructs for JNK1 (HTJ1.3) and JNK2 (HTJ2.2). RESULTS: We observed higher induction and activation of c-Jun in cells with dnJNK1, while introduction of dnJNK2 caused the opposite effect. Resistance to oxaliplatin under hypoxic conditions was also higher in the cell line with lowest c-Jun activation level (IC50 of 2.1 μM for HT.LX, 3 μM for HTJ2.2 and 0.8 μM for HTJ1.3), suggesting a pro-survival role for JNK1 under these conditions. Both oxaliplatin- and hypoxia-induced formation of autophagosomes was reduced significantly in HT29 cells treated with the JNK inhibitor SP600125. We also found differential sensitivity of these cell lines to an inhibitor of autophagy, chloroquine (CQ): HTJ1.3 and HTJ2.2 cell lines were slightly more resistant to CQ under normal conditions, as compared to parental line, but under hypoxia all of the lines demonstrated higher sensitivity to the drug. Notably, in light of the role of JNK1 in activating autophagy, cells with diminished JNK1 activity were the most sensitive to CQ under hypoxia. Moreover, when we treated the cell lines with 5 μM of CQ under hypoxia/reoxygenation, inhibition of autophagy and induction of apoptosis were most significant in dnJNK1-expressing cells. This effect of JNK1 down-regulation is specific to hypoxia, since the constructs do not differ in sensitivity to CQ and oxaliplatin in combination. CONCLUSIONS: Our data demonstrate the differential effects of JNK1/JNK2 modulation on cell death of hypoxic HT29 cells treated with oxaliplatin or chloroquine, and imply pro-survival function for JNK1 versus JNK2 under these conditions. 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 87.
Charles John Henry Bland
Authors: T. Bloomberg
Journal: BMJ (2013)

Charles John Henry Bland was a talented and respected radiologist with a broad diagnostic practice, who, in his early days as a consultant, showed his skill in intervention, especially in uroradiology. In recent years his main interests were gastrointestinal radiology and uroradiology, and he was a popular and wise contributor at multidisciplinary team meetings of the gastrointestinal and genitourinary team and the care of the elderly team.

For all his clinical skills, Charles will be remembered most for his personal qualities. His …
IMPACT OF QUADRIPOLAR LEFT VENTRICULAR LEADS ON INTRAPROCEDURAL AND LONG TERM OUTCOMES: RESULTS FROM A PROSPECTIVE REGISTRY
Authors: Madhu Reddy, Arun Kanmanthareddy, Sampath Gunda, Jayasree Pillarisetti, Sandeep Koripelli, Sudharani Bommana, Donita Atkins, Dhanunjaya Lakkireddy
Journal: Journal of the American College of Cardiology (2015)
Abstract SY05-01: microRNAs: Micromanagers of human cancers
Authors: George A. Calin
Journal: Cancer Research (2012)

Abstract The newly discovered differential expression in numerous tissues, key cellular processes and multiple diseases for several families of long and short non-codingRNAs (ncRNAs, RNAs that do not codify for proteins but for RNAs with regulatory functions), including the already famous class of microRNAs (miRNAs) strongly suggest that the scientific and medical communities have significantly underestimated the spectrum of ncRNAs whose altered expression has significant consequences in diseases. MicroRNA and other short or long non-codingRNAs alterations are involved in the initiation, progression and metastases of human cancer. The main molecular alterations are represented by variations in gene expression, usually mild and with consequences for a vast number of target protein coding genes. The causes of the widespread differential expression of non-codingRNAs in malignant compared with normal cells can be explained by the location of these genes in cancer-associated genomic regions, by epigenetic mechanisms and by alterations in the processing machinery. MicroRNA and other short or long non-codingRNAs expression profiling of human tumors has identified signatures associated with diagnosis, staging, progression, prognosis and response to treatment. In addition, profiling has been exploited to identify non-codingRNAs that may represent downstream targets of activated oncogenic pathways or that are targeting protein coding genes involved in cancer. Recent studies proved that miRNAs and non-coding ultraconserved genes are main candidates for the elusive class of cancer predisposing genes and that other types of non-codingRNAs participate in the genetic puzzle giving rise to the malignant phenotype. Last, but not least, the shown expression correlations of these new ncRNAs with cancer metastatic potential and overall survival rates suggest that at least some member of these novel classes of molecules could potentially find use as biomarkers or novel therapeutics in cancers and other diseases. 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 SY05-01. doi:1538-7445.AM2012-SY05-01
PATIENT-REPORTED SYMPTOMS AND REVASCULARIZATION STATUS AFTER CORONARY ARTERY BYPASS GRAFT SURGERY IN DIABETICS AND NON-DIABETICS
Authors: Brack Hattler, Brendan M. Carr, John Spertus, John Messenger, John Rumsfeld, Ramin Ebrahimi, Muath Bishawi, Hossein Almassi, Joseph F. Collins, Frederick Grover, Annie Laurie Shroyer
Journal: Journal of the American College of Cardiology (2015)
Functional Retention of Tc-99m MIBI in Mediastinal Lymphomas As a Predictor of Chemotherapeutic Response Demonstrated by Consecutive Thoracic SPECT Imaging
Authors: WEI-JEN SHIH, AMITA RASTOGI, VIKIE STIPP, SYLVIA MAGOUN, JOHN COUPAL
Journal: Clinical Nuclear Medicine (1998)

Tc-99m MIBI is used as a tumor imaging agent and has been proposed to measure p-glycoprotein function, which plays an important role in tumor multidrug resistance to chemotherapy. It has been reported that lung cancer and breast cancer with a high retention of Tc-99m MIBI have been more responsive to chemotherapy than tumors with low retention. Thus Tc-99m MIBI SPECT could be used as a measure of p glycoprotein function and consequently may serve as a predictor of the tumor's responsiveness to chemotherapeutic agents. Described here are two patients with lymphomas, one with non-Hodgkin's lymphoma and the other with Hodgkin's disease, who underwent Tc-99m MIBI thoracic SPECT before and after chemotherapy. The sequential studies demonstrated a reduction in tumor size and diminished tumor uptake in one patient and disappearance of tumor uptake after a course of chemotherapy in the other patient. The data suggest that elevated Tc-99m MIBI uptake in a tumor as a result of retention by p glycoprotein not only demonstrates mediastinal involvement of lymphomas but also may be used to forecast responsiveness to chemotherapy.
SP0202 How to Measure Bone Quality in Daily Practice?
Authors: J. van den Bergh
Journal: Annals of the Rheumatic Diseases (2014)

<h3></h3> In recent years a number of new imaging techniques have been developed in order to evaluate components of bone quality in-vivo, in particular advanced three-dimensional Quantitative Computer Tomography (QCT), high resolution peripheral QCT (HRpQCT) and Finite Element Analysis (FEA). There is growing evidence that spine fracture prediction can be improved with these techniques, that age-related changes are larger than for BMD and that QCT and FEA provide additional information regarding treatment effects. HR-pQCT enables the analysis of cortical and trabecular bone properties separately and for calculating bone biomechanical competence at the distal sites of the skeleton (distal radius and distal tibia). In addition recent research expands to in-vivo assessment of fracture healing of the distal radius and of cortical bone erosions, periarticular cortical and trabecular microarchitecture, and 3D joint-space volume of the finger joints and wrists. In this presentation these novel developments will be discussed. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6343
Abstract 1699: Suppressor of cytokine signaling 6 (SOCS6) promotes mitochondrial fission through E3 ubiquitin ligase complex activity.
Authors: Huan-Yu Lin, Shiu-Ting Lin, Mei-June Wang, Jeou-Yuan Chen
Journal: Cancer Research (2013)

Abstract Mitochondria are highly motile organelles that constantly undergo fission and fusion. Impairment of mitochondrial dynamics is associated with mitochondrial dysfunction and is frequently linked to the pathogenesis of neurodegenerative diseases and cancer. We have previously shown that biallelic inactivation of the suppressor of cytokine signaling 6 (SOCS6) is a frequent event in human gastric cancer, and that overexpression of SOCS6 inhibits cell growth as well as colony formation in soft agar, suggesting a potential role of SOCS6 as a tumor suppressor. We also showed that SOCS6 is targeted to mitochondria, and induces mitochondrial fragmentation accompanied with intrinsic apoptosis. SOCS6 induces mitochondrial fragmentation is in part mediated through its interaction with DRP1 and regulation of DRP1 fission activity. In this study, we further showed that SOCS6 interacts with the Elongin B/C and Cullin 5 forming an ECS E3 ubiquitin ligase complex, and that formation of an intact ECS E3 ligase complex is important for SOCS6-mediated mitochondrial fragmentation. First, the interaction of SOCS6 with Elongin B/C and/or Cullin 5 prolonged SOCS6 stability. Second, mutations of the conserved Leu500 and Cys504 residues in SOCS6 BC-box which are critical for Elongin B/C binding yielded a SOCS6 mutant failed to induce mitochondrial fragmentation and apoptosis. Most importantly, ablation of Elongin C activity protected cells from SOCS6-mediated mitochondrial fission. Taken together, our data suggest an important role of SOCS6 in modulating mitochondrial dynamics that is dependent on ECS E3 ubiquitin ligase complex activity. Citation Format: Huan-Yu Lin, Shiu-Ting Lin, Mei-June Wang, Jeou-Yuan Chen. Suppressor of cytokine signaling 6 (SOCS6) promotes mitochondrial fission through E3 ubiquitin ligase complex activity. [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 1699. doi:10.1158/1538-7445.AM2013-1699
713 INSULIN-LIKE GROWTH FACTOR II MRNA-BINDING PROTEIN 3 EXPRESSION ASSOCIATES WITH FASCIN 1 AND CK19 EXPRESSION, INVOLVING IN PROGRESSION OF HEPATOCELLULAR CARCINOMA
Authors: S.Y. Han, M.H. Ju, Y.H. Paik, S.W. Lee, J.S. Jeong
Journal: Journal of Hepatology (2012)
Long-Term Results of Stenting versus Endarterectomy for Carotid-Artery Stenosis
Authors: Thomas G. Brott, George Howard, Gary S. Roubin, James F. Meschia, Ariane Mackey, William Brooks, Wesley S. Moore, Michael D. Hill, Vito A. Mantese, Wayne M. Clark, Carlos H. Timaran, Donald Heck, Pierre P. Leimgruber, Alice J. Sheffet, Virginia J. Howard, Seemant Chaturvedi, Brajesh K. Lal, Jenifer H. Voeks, Robert W. Hobson
Journal: New England Journal of Medicine (2016)

In the Carotid Revascularization Endarterectomy versus Stenting Trial, we found no significant difference between the stenting group and the endarterectomy group with respect to the primary composite end point of stroke, myocardial infarction, or death during the periprocedural period or any subsequent ipsilateral stroke during 4 years of follow-up. We now extend the results to 10 years.Among patients with carotid-artery stenosis who had been randomly assigned to stenting or endarterectomy, we evaluated outcomes every 6 months for up to 10 years at 117 centers. In addition to assessing the primary composite end point, we assessed the primary end point for the long-term extension study, which was ipsilateral stroke after the periprocedural period.Among 2502 patients, there was no significant difference in the rate of the primary composite end point between the stenting group (11.8%; 95% confidence interval [CI], 9.1 to 14.8) and the endarterectomy group (9.9%; 95% CI, 7.9 to 12.2) over 10 years of follow-up (hazard ratio, 1.10; 95% CI, 0.83 to 1.44). With respect to the primary long-term end point, postprocedural ipsilateral stroke over the 10-year follow-up occurred in 6.9% (95% CI, 4.4 to 9.7) of the patients in the stenting group and in 5.6% (95% CI, 3.7 to 7.6) of those in the endarterectomy group; the rates did not differ significantly between the groups (hazard ratio, 0.99; 95% CI, 0.64 to 1.52). No significant between-group differences with respect to either end point were detected when symptomatic patients and asymptomatic patients were analyzed separately.Over 10 years of follow-up, we did not find a significant difference between patients who underwent stenting and those who underwent endarterectomy with respect to the risk of periprocedural stroke, myocardial infarction, or death and subsequent ipsilateral stroke. The rate of postprocedural ipsilateral stroke also did not differ between groups. (Funded by the National Institutes of Health and Abbott Vascular Solutions; CREST ClinicalTrials.gov number, NCT00004732.).