tbuckley/cabot-search huggingface dataset:
Pharmacotherapy Relapse Prevention in Body Dysmorphic Disorder: A Double-Blind, Placebo-Controlled Trial
Authors: Katharine A. Phillips, Aparna Keshaviah, Darin D. Dougherty, Robert L. Stout, William Menard, Sabine Wilhelm
Journal: American Journal of Psychiatry (2016)

Body dysmorphic disorder is common, distressing, and often severely impairing. Serotonin reuptake inhibitors appear efficacious, but the few existing pharmacotherapy studies were short term (≤4 months), and no relapse prevention studies or continuation phase studies have been conducted to the authors' knowledge. The authors report results from the first relapse prevention study in body dysmorphic disorder. Adults (N=100) with DSM-IV body dysmorphic disorder received open-label escitalopram for 14 weeks (phase 1); 58 responders were then randomized to double-blind continuation treatment with escitalopram versus switch to placebo for 6 months (phase 2). Reliable and valid outcome measures were utilized. In phase 1, 67.0% of treated subjects and 81.1% of subjects who completed phase 1 responded to escitalopram. Body dysmorphic disorder severity (in both the intent-to-treat and the completer groups) and insight, depressive symptoms, psychosocial functioning, and quality of life significantly improved from baseline to end of phase 1. In phase 2, time to relapse was significantly longer with escitalopram than with placebo treatment (hazard ratio=2.72, 95% CI=1.01-8.57). Phase 2 relapse proportions were 18% for escitalopram and 40% for placebo. Among escitalopram-treated subjects, body dysmorphic disorder severity significantly decreased over time during the continuation phase, with 35.7% of subjects showing further improvement. There were no significant group differences in body dysmorphic disorder severity or insight, depressive symptoms, psychosocial functioning, or quality of life. Continuation-phase escitalopram delayed time to relapse, and fewer escitalopram-treated subjects relapsed than did placebo-treated subjects. Body dysmorphic disorder severity significantly improved during 6 additional months of escitalopram treatment following acute response; more than one-third of escitalopram-treated subjects experienced further improvement.
Anicteric Viral Hepatitis
Authors: William C. Cooper, Richard K. Gershon, Shieh-Chien Sun, James W. Fresh
Journal: New England Journal of Medicine (1966)

ANICTERIC viral hepatitis is a widely discussed but little studied entity. Its existence has been acknowledged for many years on the basis of epidemiologic and clinical data, mostly indirect and inferential. For example, during epidemics when the hepatitis infection rate is high, cases in which clinical evidence of hepatitis develops without jaundice are often diagnosed as anicteric hepatitis.1 2 3 In addition, clinicopathological studies have been done on patients in whom chronic liver disease developed without jaundice or with the late appearance of jaundice; the diagnosis of anicteric hepatitis was made retrospectively.4 5 6 The military population of Taiwan offers advantages to the study . . .
FRI0256 Risk of Relapse after Discontinuing Tumor Necrosis Factor Inhibitors in Rheumatoid Arthritis Patients with Low Disease Activity: A Systematic Review and Meta-Analysis
Authors: N. Filippi, J. Morel, B. Combe, C. Lukas
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Clinical remission or low disease activity (LDA) are now realistic targets in the management of patients with rheumatoid arthritis (RA), especially in early disease and thanks to biologic treatments. The subsequent handling of biologic therapy after remission or LDA has been achieved however remains unclear, and possibility of discontinuation of tumor necrosis factor (TNF) inhibitors may become an important issue with relevant safety and economy issues. <h3>Objectives</h3> To assess the currently available data on the risk of relapse after TNF inhibitors withdrawal in patients with LDA. <h3>Methods</h3> We conducted a systematic literature review and assessed available articles published (up to December 2013) in Medline/Pubmed, and presented at ACR and EULAR congresses from 2010 to 2013. The primary endpoint was the comparison in proportions of patients who had relapsed at 52 weeks after either discontinuation or maintain of TNF inhibitors, in RA patents who had achieved at least LDA state with anti-TNF agents. Relapse was defined as DAS28&gt;3.2 or DAS28CRP&gt;2.7. The Mantel-Haenszel method was used to provide a pooled odds-ratio (OR) estimate and a 95% confidence interval (CI) in “discontinuation” versus “maintain the treatment” groups. Statistical heterogeneity was assessed by χ<sup>2</sup> test. <h3>Results</h3> The literature search identified 81 articles and 7 congress abstracts, of which 5 articles and 3 abstracts could be included in the study according to predefined requirements. Among these, 3 articles (BRIGHT [1], PRESERVE [2], OPTIMA [3]) and 1 abstract (DOSERA [4]) met the criteria to allow meta-analysis. After discontinuing TNF inhibitors, the proportion of relapse ranged across the studies from 19% to 87% in “discontinuation” group, and from 9% to 48% in “maintain the treatment”. The meta-analysis showed a significantly increased risk of relapse after drug withdrawal (OR 1.97 (95%CI 1.12-3.48), with substantial heterogeneity due to study OPTIMA, which differed from others by disease duration (i.e. including patients with earlier disease). <h3>Conclusions</h3> This meta-analysis shows a significantly increased risk of relapse after discontinuation of TNF inhibitors in RA patients who had achieved LDA under this treatment. Further evaluation of other options, especially progressive tapering of the biologic drug, might be a more efficient option to decrease drug exposure. <h3>References</h3> BRIGHT: Harigai and al, Mod Rheumatol. 2012; 22(6):814-22. PRESERVE: Smolen and al, Lancet. 2013; 381(9870):918-29. OPTIMA: Smolen and al, Lancet. 2014; 383:321–32 DOSERA: Van Vollenhoven [abstract]. Arthritis Rheum 2012; 64:4171. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5498
Analysis of Risk Factors for Stroke in a Cohort of Men Born in 1913
Authors: Lennart Welin, Kurt Svärdsudd, Lars Wilhelmsen, Bo Larsson, Gösta Tibblin
Journal: New England Journal of Medicine (1987)

We analyzed parental death from stroke and other potential risk factors in relation to the incidence of stroke among 789 men, all 54 years old at the base-line examination. During 18.5 years of follow-up, 57 men (7.2 percent) had strokes. In univariate analyses, the following characteristics correlated significantly with the incidence of stroke: increased systolic (P = 0.004) and diastolic blood pressure (P = 0.0001), larger waist circumference (P = 0.007), higher waist:hip ratio (P = 0.0004), increased plasma fibrinogen level (P = 0.01), and lower vital capacity (P = 0.03). In addition, men whose mothers had died of stroke had a threefold increase in their incidence of stroke as compared with men without such a maternal history (P = 0.0005). Potential risk factors for stroke that were not confirmed were body-mass index, serum cholesterol level, hematocrit, blood glucose level, smoking, coronary heart disease, electrocardiographic signs of left ventricular hypertrophy, and a paternal history of death from stroke. In multivariate analyses, increased blood pressure, abdominal obesity, increased plasma fibrinogen level, and maternal history still correlated significantly with the risk of stroke. A maternal history of stroke should probably be added to the list of risk factors for stroke among middle-aged men.
Abstract 1320: Estrogen as a modulator of thyroid proliferative disease: Implications for disease etiology and therapy
Authors: Shilpi Rajoria, Andrea George, Arulkumaran Shanmugam, Ameet Kamat, Stimson P. Schantz, Jan Geliebter, Robert Suriano, Raj K. Tiwari
Journal: Cancer Research (2011)

Abstract Metastasis of cancer is a multifactorial disease and is responsible for over 90% of all cancer related deaths. Thyroid cancer is the most common endocrine related cancer with well differentiated thyroid cancer metastasizing to the nearby lymph nodes in upto 50% of the cases. Interestingly, according to American Thyroid Association (ATA), the incidences of thyroid cancer are four to five times more in women than in men with one in eight women developing thyroid disorder at least once in her lifetime. In this study, we explored the possible etiological contribution of estrogen in thyroid proliferative disease using an in vitro experimental model system. We observed that thyroid cancer cells express functionally active estrogen receptors (ER), ER-α and ER-β. Furthermore, estrogen enhances the metastatic propensity of thyroid cells as evidenced by increased migration, adhesion and invasion, which is reversed by anti-estrogens. These observations were further supported by ER-α down-regulation (siRNA) studies. Western blot and zymography analyses provide direct evidence for this estrogen mediated enhancement of metastasis associated events by enhanced secretion of the proteolytic enzymes, matrix metalloproteinases (MMP), MMP-2 and MMP-9. We also observed that conditioned medium from estrogen treated thyroid cells contains enhanced levels of vascular endothelial growth factor (VEGF) and modulates angiogenesis associated events, such as migration, proliferation and tubulogenesis of endothelial cells. Our studies provide evidence that the higher incidence of thyroid cancer in females is potentially attributed to the presence of a functional ER that participates in cellular processes contributing to enhanced mitogenic, migratory, invasive and angiogenic properties of thyroid cells, which is responsive to anti-estrogens. Our findings formed the basis of an ongoing clinical trial in patients with thyroid proliferative diseases using dietary anti- estrogenic compound, 3, 3’-diindolylmethane (DIM). 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 1320. doi:10.1158/1538-7445.AM2011-1320
Partial Liquid Ventilation with Perflubron in Premature Infants with Severe Respiratory Distress Syndrome
Authors: Corinne Lowe Leach, Jay S. Greenspan, S. David Rubenstein, Thomas H. Shaffer, Marla R. Wolfson, J. Craig Jackson, Robert DeLemos, Bradley P. Fuhrman
Journal: New England Journal of Medicine (1996)

The intratracheal administration of a perfluorocarbon liquid during continuous positive-pressure ventilation (partial liquid ventilation) improves lung function in animals with surfactant deficiency. Whether partial liquid ventilation is effective in the treatment of infants with severe respiratory distress syndrome is not known.
Abstract 1399: CCN3 enhances migration and ICAM-1 upregulation via avb3 integrin, ILK, Akt, and NF-kB-dependent pathway in human prostate cancer cells
Authors: Po-Chun Chen, Chih-Hsin Tang, Hsu-Chen Cheng
Journal: Cancer Research (2011)

Abstract Nephroblastoma overexpressed (NOV/CCN3), from the CCN gene family, is a secreted and matrix-associated protein, which is involved in many cellular functions such as growth, differentiation and adhesion. However, the effect of CCN3 in human prostate cancer is still unclear. Here, we found that CCN3 and intercellular adhesion molecule-1 (ICAM-1) expression level were related to cell migration ability in prostate cancer cells. In addition, CCN3 increased the migration and expression of ICAM-1 in human prostate cancer cells. RGD peptide, αvβ3 monoclonal antibody, integrin-linked kinase (ILK) and Akt inhibitors but not RAD peptide inhibited the CCN3-induced increase of the migration and ICAM-1 upregulation of prostate cancer cells. CCN3 stimulation activated the ILK/Akt/ NF-κB pathway. Moreover, CCN3 increased the binding of p65 to the NF-κB element on the ICAM-1 promoter. Finally, knock down of CCN3 expression markedly inhibited cell migration ability, tumor growth and bone destruction. Taken together, our results indicated that CCN3 enhances the migration of prostate cancer cells by increasing ICAM-1 expression through the αvβ3 integrin receptor/ ILK/ Akt and NF-κB signal transduction pathway. Therefore, CCN3 may be developed as alternate therapy of prostate cancer cells. 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 1399. doi:10.1158/1538-7445.AM2011-1399
GLOBAL LONGITUDINAL STRAIN BY ECHOCARDIOGRAPHY PREDICTS LONG TERM RISK OF CARDIOVASCULAR MORBIDITY AND MORTALITY IN A LOW RISK GENERAL POPULATION: THE COPENHAGEN CITY HEART STUDY
Authors: Tor Biering-Sorensen, Sofie R. Biering-Sørensen, Flemming Javier Olsen, Morten Sengeløv, Amil Shah, Jan Jensen
Journal: Journal of the American College of Cardiology (2016)
Abstract 2206: Molecular interaction of HIF-1α and the androgen receptor in prostate cancer
Authors: Douglas K. Price, Kelie M. Reece, Sarah M. Troutman, Heather M. Pressler, Stephen T. Pisle, William D. Figg
Journal: Cancer Research (2012)

Abstract Background: Prostate cancer is the most common noncutaneous cancer among men in the United States, and its progression is largely controlled by the androgen receptor (AR). Androgen deprivation therapy (ADT) is an initially effective treatment for prostate cancer, but most tumors eventually become castrate resistant. Tumor hypoxia also appears to be associated with a poor prognosis in prostate cancer. HIF-1α regulates the transcription of genes that allow tumor survival and growth in low oxygen conditions. Our laboratory has data showing that in response to castration and anti-androgen therapy in mice, there was a strong transcriptional relationship between HIF-1α and AR, as measured by quantitative RT-PCR, suggesting an interaction between the two proteins. Thus, the purpose of this study was to determine if there is a molecular interaction between HIF-1α and AR in prostate cancer cells. Methods: We used Western blot analysis to examine the expression levels of HIF-1α and AR in LNCaP prostate cancer cells to determine if they are upregulated together at the protein level. Four experimental conditions were tested: control (no treatment), DHT for induction of AR expression, CoCl2 for induction of HIF-1α, and a combination treatment of DHT and CoCl2. Immunoprecipitation experiments were carried out to determine if there is an association between HIF-1α and AR. In addition, cells were fractionated into nuclear and cellular cells extracts, followed by Western blot analysis to determine where in the cells this interaction occurs. Results: Western blot analysis of cell lysates showed synergistic upregulation of both HIF-1α and AR expression only under combined CoCl2 and DHT treatment conditions. In addition, immunoprecipitation experiments showed that HIF-1α and AR exist in a complex with one another, and fractionation experiments indicated this complex occurs in the nucleus. Conclusions: Our results demonstrate that HIF-1α and AR associate with one another in cells. Binding assays are in progress to determine the nature of this interaction. In addition, we are examining the cellular consequences of this protein interaction, as it is possible that upregulation of HIF-1α in response to low androgen contributes to the development of tumor resistance to ADT. 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 2206. doi:1538-7445.AM2012-2206
Abstract 1727: Evidence that E2F1-mediated upregulation of Bim, a proapoptotic BH3-only protein, functions as a prosurvival molecule in cancer.
Authors: Neelu Yadav, Raghu Gogada, Junwei Liu, Shaohua Tang, Dianmu Zhang, C Marcelo Aldaz, Dean Tang, Dhyan Chandra
Journal: Cancer Research (2013)

Abstract Proapoptotic BH3-only protein Bim plays an important role in Bax/Bak-mediated cytochrome c release and apoptosis. Here we provide evidence for a novel prosurvival function of Bim in cancer cells. Bim was constitutively overexpressed in multiple prostate and breast cancer cells as well as in primary tumor cells. Quantitative real time PCR analysis showed that Bim was transcriptionally upregulated. We have identified eight endogenous E2F1-binding sites on the Bim promoter using in silico analysis. Luciferase assay demonstrated that Bim expression was E2F1-dependent as mutation of E2F1-binding sites on the Bim promoter inhibited luciferase activities. In support, E2F1 silencing led to the loss of Bim expression in cancer cells. Bim primarily localized to mitochondrial and cytoskeleton-associated fractions. Bim-silencing or microinjection of anti-Bim antibodies into the cell cytoplasm resulted in cell rounding, detachment, and subsequent apoptosis. We observed upregulation of prosurvival proteins Bcl-xL and Mcl-1, which sequester Bim in cancer cells. In addition, phosphorylated form of Bim was also elevated in cancer cells. These findings suggest that the constitutively overexpressed Bim may function as a prosurvival molecule in epithelial cancer cells, and phosphorylation and association with Bcl-xL/Mcl-1 block its proapoptotic functions. The prosurvival functions associated with multiple proapoptotic proteins raise the possibility that anticancer agents that only harness proapoptotic function of Bim or other BH3-only proteins may not be an efficient approach for the permeabilization of mitochondria. Our findings demonstrate that in order to induce efficient apoptosis, inhibition of prosurvival function of Bim may provide a new approach for efficient cancer therapy. Citation Format: Neelu Yadav, Raghu Gogada, Junwei Liu, Shaohua Tang, Dianmu Zhang, C Marcelo Aldaz, Dean Tang, Dhyan Chandra. Evidence that E2F1-mediated upregulation of Bim, a proapoptotic BH3-only protein, functions as a prosurvival molecule in cancer. [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 1727. doi:10.1158/1538-7445.AM2013-1727
PML in a Patient Treated with Dimethyl Fumarate from a Compounding Pharmacy
Authors: Bob W. van Oosten, Joep Killestein, Frederik Barkhof, Chris H. Polman, Mike P. Wattjes
Journal: New England Journal of Medicine (2013)

Two cases of progressive multifocal leukoencephalopathy (PML) are reported in patients with psoriasis who were treated with fumarates, one with Fumaderm and the other with a compound containing dimethyl fumarate. The manufacturer of Fumaderm comments on the reports.
Potential Predictive Markers of Efficacy of Dacomitinib in Patients with Recurrent/Metastatic Scchn from a Phase 2 Trial
Authors: D. Soulieres, G. Allo, M.-L. Audet, L. Kim, X. Weng, O. Gologan, S. Quinn, I. Taylor, P.A. English, L.L. Siu
Journal: Annals of Oncology (2013)
The need to research refractory breathlessness
Authors: David C. Currow, Amy P. Abernethy, Peter Allcroft, Robert B. Banzett, Claudia Bausewein, Sara Booth, Virginia Carrieri-Kohlman, Patricia Davidson, Rebecca Disler, DorAnne Donesky, Deborah Dudgeon, Magnus Ekstrom, Morag Farquhar, Irene Higginson, Daisy Janssen, Dennis Jensen, Caroline Jolley, Malgorzata Krajnik, Pierantonio Laveneziana, Christine McDonald, Matthew Maddocks, Capucine Morelot-Panzini, John Moxham, Richard A. Mularski, Simon Noble, Denis O'Donnell, Mark B. Parshall, Kyle Pattinson, Jane Phillips, Joy Ross, Richard M. Schwartzstein, Thomas Similowski, Steffen T. Simon, Tracy Smith, Athol Wells, Patsy Yates, Janelle Yorke, Miriam J. Johnson
Journal: European Respiratory Journal (2015)

The joint American Thoracic Society (ATS)/European Respiratory Society (ERS) statement "An official American Thoracic Society/European Respiratory Society statement: research questions in COPD" by Celli et al. [1] is a timely summary of the current evidence and the questions that arise directly from where that evidence reaches its limits. Such documents are crucial in framing research strategies for researchers and research funders. High-quality research is needed to improve quality of life for people with chronic refractory breathlessness in COPD <http://ow.ly/Q2GDY>
AB0087 Higher levels of th17/23, TH2 and proinflammatory cytokines levels in synovial fluid of rheumatoid arthritis compared with psoriatic arthritis
Authors: J.D. Cañete, R. Celis, J. Ramirez, J.L. Fernández-Sueiro, V. Ruiz-Esquide, M.V. Hernández, R. Sanmartí
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoid arthritis (RA) and Psoriatic arthritis (PsA) are two chronic inflamatory diseases mediated by the immune system with joints as main targets. Both diseases seem to exhibit a Th1/Th17 pattern, but studies including joint cytokines and clinical variables are scarse and inconclusive. <h3>Objectives</h3> To compare concentrations of Th1, Th2, Th17/23 and other proinflammatory cytokines in Synovial fluid, as well as their relation with disease activity, between RA and PsA patients. <h3>Methods</h3> Synovial fluid was obtained from a inflammed knee joint of RA and PsA patients. SF concentrations of Th1, Th2, Th17 and proinflammatory cytokines were determined by Quantibody® Human Th17 Array (RayBiotech, GA, USA). Clinical and biological data were collected at inclusion. <h3>Results</h3> 82 RA and 48 PsA patients were included. 78% and 21% of them were women; mean age was 57 and 47.6 years; disease duration 10.2 and 9.3 years; DAS28 4.94 and 3.80 (p&lt;0.001), respectively. No significant differences were found in systemic (CRP and ESR) and synovial (SF IL-6 levels and ST CD68+ macrophages/mm<sup>2</sup>) between both groups. IL-17F, IL-21, IL-22 and IL-23 SF levels were significantly higher (p&lt;0.001, p=0.01, p=0.02 and p&lt;0.001, respectively) in RA patients compared with PsA patients. Also SF levels of IL-12p70, IL-10, TGFb1, IL-1 beta, TNFalpha, TNF-beta and CCL20 were significantly higher (p=0.03, p&lt;0.001, p&lt;0.001, p&lt;0.001, p=0.04 and p&lt;0.001, respectively) in RA than in PsA patients. In RA, DAS28 correlated with IL-21 (p=0.008) and CCL20 (p=0.001) levels; CRP with IL-10 (p=0.043) and CCL-20 (p&lt;0.001); ESR with IL-10 (p=0.006), IL-17 (p=0.006) and CCL20 (p&lt;0.001); TJC and SJC correlated with IL-21 (p=0.041 and p=0.028) and CCL20 (p=0.021 and p=0.02); RF levels was correlated with IL-2 (p=0.034), IL-4 (p=0.044), IL-10 (p=0.048) and CCL20 (p=0.019), and CCP levels with IL-4 (p=0.025) and CCL20 (p=0.026). In PsA, SF IL-17 levels correlated with SJC (p=0.026) and CRP levels (p=0.001), and IL-10 and CCL 20 levels with erosive disease (p=0.020 and p=0.006, respectively). <h3>Conclusions</h3> SF Th17/23, CCL20 (a chemoskine attracting CCR6+ Th17 cells), Th2, and proinflammatory cytokines levels are all higher in RA patients compared with PsA patients matched by systemic and Synovial inflammation. IL-21 and CCL20 levels correlated with disease activity in RA, while in PsA IL-17 levels correlated with markers of systemic inflammation. <h3>Disclosure of Interest</h3> None Declared
FDG PET/CT of Intercostal Schwannoma
Authors: Si-Yun Wang, Dong-Lan Luo, Gang Chen, En-Tao Liu, Shu-Xia Wang
Journal: Clinical Nuclear Medicine (2016)

Intercostal schwannoma is rare. We report FDG PET/CT findings of intercostal schwannoma in a 66-year-old woman. The tumor contains both solid and cystic components with intense FDG activity in the solid component. Postsurgical pathology diagnosis revealed schwannoma.