tbuckley/cabot-search huggingface dataset:
FRI0212 What Are the Effects of Interventions Targetting Medication Adherence in Rheumatic Diseases: A Systematic Review: Table 1.
Authors: M.A. De Vera, J. Galo
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Recent medication adherence rates reported as low 30% in rheumatoid arthritis (RA),<sup>1</sup> 49% in systemic lupus erythematosus (SLE),<sup>1</sup> and 17% in gout<sup>2</sup> highlight the importance of understanding how health care providers can intervene and support patients. To date, there are no synthesis of the evidence on interventions targeting medication adherence and their effectiveness in rheumatology patients. <h3>Objectives</h3> To systematically review studies of interventions targeting medication adherence in rheumatic diseases <h3>Methods</h3> We searched Medline, Embase, PsycINFO, CINAHL, and Cochrane Central Register of Controlled Trials databases. We considered controlled, uncontrolled, prospective, retrospective, randomized, and non-randomized studies of interventions conducted among patients with rheumatic diseases (e.g., RA, SLE, psoriatic arthritis [PsA], gout). Medication adherence must be reported as a primary or secondary outcome. We classified interventions according to target (patient vs. provider), implementation (generalized vs. tailored), and focus (educational vs. behavioural vs. affective) and related these factors with reported effects. <h3>Results</h3> Few studies met inclusion criteria – 4 in RA, 1 in RA and PsA, 1 in RA, PsA and inflammatory polyarthritis, and 1 in SLE (Table). Three studies in RA patients showed significant effects of a group patient meeting, one-on-one patient meeting, and cognitive behavioural therapy, respectively. Similarities across interventions are patient-tailored approaches that combine educational and affective methods. Three studies in RA patients alone or in RA, PsA, and/or inflammatory polyarthritis showed non-significant effects. A single study in SLE showed positive effects of patient counselling. <h3>Conclusions</h3> Despite consistent data on medication non-adherence in rheumatic diseases, there is limited and inconsistent literature on adherence interventions. Further research on interventions to improve medication adherence among rheumatology patients is needed. <h3>References</h3> de Achaval S, Suarez-Almazor ME. Treatment adherence to disease-modifying antirheumatic drugs in patients with rheumatoid arthritis and systemic lupus erythematosus. International Journal of Clinical Rheumatology. 2010;5:313-326. Zandman-Goddard G, Amital H, Shamrayevsky N, Raz R, Shalev V, Chodick G. Rates of adherence and persistence with allopurinol therapy among gout patients in Israel. Rheumatology. Jun 2013;52(6):1126-1131. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4753
Accountable Care Organizations — The Fork in the Road
Authors: Thomas L. Greaney
Journal: New England Journal of Medicine (2010)

Despite the uncertainty and controversy it has generated, the Patient Protection and Affordable Care Act (ACA) has sown the seeds for a major reorganization of the U.S. health care delivery system. In almost every region of the country, hospitals and physicians are forming (or talking about forming) accountable care organizations (ACOs) and entering into other arrangements designed to integrate care, manage chronic conditions, and enable evidence-based practices. Critical to the achievement of these ends are the regulations and guidance soon to be issued by the Centers for Medicare and Medicaid Services (CMS) and the Federal Trade Commission (FTC). One of the . . .
FGF2-Targeted Adenovirus Encoding Platelet-Derived Growth Factor-B Enhances de Novo Tissue Formation
Authors: Lois A. Chandler, John Doukas, Ana Maria Gonzalez, Diana K. Hoganson, Dan-Ling Gu, Chenglie Ma, Mark Nesbit, Timothy M. Crombleholme, Meenhard Herlyn, Barbara A. Sosnowski, Glenn F. Pierce
Journal: Molecular Therapy (2000)

Gene therapy has yet to achieve reproducible clinical efficacy, due to inadequate gene delivery, inadequate gene expression, or dose-limiting toxicity. We have developed a gene therapy technology for tissue repair and regeneration that employs a structural matrix for DNA delivery. The matrix holds the DNA vector at the treatment site and provides a scaffolding for in-growth and accumulation of repair cells and efficient DNA transfection. We now report, for the first time, matrix-mediated delivery of targeted DNA vectors for soft tissue repair. A collagen matrix was used to deliver an adenoviral vector encoding platelet-derived growth factor-B (AdPDGF-B), resulting in efficient transgene expression in vitro and in vivo. Increases in the overall levels of expression and in the relative amounts of secreted PDGF-BB were achieved when AdPDGF-B was conjugated to fibroblast growth factor (FGF2) such that the virus was targeted for cellular uptake via FGF receptors. Matrix-mediated delivery of AdPDGF-B enhanced wound healing responses in vivo, and FGF2 targeting generated effects comparable to nontargeted vectors at significantly lower doses. Therefore, matrix-mediated delivery in combination with FGF2 targeting overcomes some of the safety and efficacy limitations of current gene therapy strategies and is an attractive therapeutic approach for tissue repair and regeneration.
Serum Levels of Sex Hormones in Vulvar Lichen Sclerosus, and the Effect of Topical Testosterone
Authors: Eduard G. Friedrich, Pushpa S. Kalra
Journal: New England Journal of Medicine (1984)

Lichen sclerosus is a chronic cutaneous disorder of unknown cause that most commonly occurs on the vulva in postmenopausal women. Earlier investigations suggested that the affected tissue is reversibly atrophic and that it has normal metabolic potential. The present study was designed to determine whether levels of sex steroid hormones in serum are altered in this disease and how they are affected by topical testosterone, a recognized form of therapy. As compared with normal values for age, serum levels of dihydrotestosterone, free testosterone, and androstenedione were significantly decreased in patients with untreated vulvar lichen sclerosus. Dihydrotestosterone and testosterone levels rose and exceeded normal values after therapy. These results suggest that abnormal enzymatic activity (5 alpha-reductase) may be responsible for this disease and indicate a need for similar studies of the disorder in other locations.
AB0164 Stromal cell-derived factor (SDF)-1 induces rankl in rheumaroid arthritis synovial fibroblasts and CD4+ T cells
Authors: J. Lee, S.-H. Lee, H.-R. Kim, J.-H. Woo, K.-W. Kim
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Stromal cell-derived factor (SDF)-1 (CXCL12) is a chemokine promoting the migration of inflammatory cells into the inflamed synovium in rheumatoid arthritis (RA). The expression of SDF-1 is elevated in serum, synovial fluid, and synovial tissues and it can promote joint destruction by inducing angiogenesis and MMP production. <h3>Objectives</h3> This study aims to determine the effect and mechanism of SDF-1 on bony destructive process in RA through RANKL regulation from synovial fibroblasts and CD4+ T cells. <h3>Methods</h3> Synovial fibroblasts were isolated from synovial tissues of RA patients and CD4+ T cells were isolated from PBMC of RA patients. After RA synovial fibroblasts and CD4+ T cells were treated with rhSDF-1, the expression of RANKL mRNA was determined using real-time PCR. After inhibition of pro-inflammatory cytokines or intracellular signal molecules, the change of the SDF-1-induced RANKL expression was analyzed. <h3>Results</h3> The expression of RANKL mRNA in RA synovial fibroblasts was increased after SDF-1 stimulation in a dose dependent manner. The expression of RANKL mRNA in RA CD4+ T cells was also increased after SDF-1 stimulation in a similar pattern with synovial fibroblasts. After RA synovial fibroblasts were cultured with neutralizing antibodies of TNF-a and IL-6, the expression of RANKL mRNA was decreased in RA synovial fibroblasts. The expression of RANKL mRNA was decreased after CD4+ T cells were cultured with SDF-1 in presence of IL-1b, TNF-a and IL-6. SDF-1-induced RANKL expression was also diminished after inhibition of PI3 kinase, p38 MAP kinase, and JNK. <h3>Conclusions</h3> This result suggests that SDF-1 could induce RANKL from RA synovial fibroblasts mediated by TNF-a and IL-6. In RA CD4+ T cells, SDF-1-induced RANKL expression is mediated by IL-1b as well as TNF-a and IL-6. <h3>Disclosure of Interest</h3> None Declared
PERSISTENT ALTERATIONS IN MYOCARDIAL INFARCTION CIRCADIAN RHYTHM AFTER HURRICANE KATRINA: NINE YEARS AFTER THE STORM
Authors: Holly Gonzales, John Lawrence, Matthew Peters, Kapil Yadav, Derar Albashaireh, Hassan Baydoun, Muhammad Raja, Christopher Westley, Henry Quevedo Diaz, Sudesh Srivastav, Anand Irimpen
Journal: Journal of the American College of Cardiology (2016)
Abstract 4279: Isolation of a high affinity, specific human monoclonal antibody that binds to FGFR-2 IIIc.
Authors: Ullrich S. Schwertschlag, Katherine J. Turner
Journal: Cancer Research (2013)

Abstract Fibroblast Growth Factor Receptor-2 (FGFR-2) expression and activation have been increasingly implicated in a number of human cancers, including prostate, ovarian, breast, gastric, bladder, pancreatic, endometrial and lung malignancies. Mechanisms include stimulation of angiogenesis, direct stimulation of tumor growth and promotion of tumor metastasis. Similar to other FGFRs, FGFR-2 binds a subset of FGF ligands with high affinity and consists of an extracellular region comprised of two or three immunoglobulin-like (Ig) domains, a single transmembrane region and an intracellular kinase domain. Variable splicing in the second half of the third Ig-like domain generates two isoforms, IIIb or IIIc, with different ligand binding specificity and expression patterns. An isoform switch from epithelial cell-expressed FGFR-2IIIb to mesenchymal cell-expressed FGFR2-IIIc has been shown to associate with an epithelial to mesenchymal transition (EMT), which increases cell migration and invasion and facilitates metastasis of epithelial carcinomas, such as prostate and bladder cancer. Several groups are developing antibodies to block FGFR-2 as therapeutics. Small molecule drugs that block FGFR-2 signaling are currently being evaluated in clinical trials. Recently, there have been reports of FGFR-2 IIIb-specific antibodies. In the same studies, monoclonal antibodies that bind both isoforms IIIb and IIIc were described, but, to date, no detailed studies describing the isolation of an FGFR-2 IIIc-specific antibody have been reported. The high degree of sequence conservation between the IIIb and IIIc exons is presumably the major reason why this has been technically challenging. In this study, we report the isolation of a high affinity, human monoclonal antibody, ATTO-1, and a murine mAb, 5H11, that bind to human and mouse FGFR-2 IIIc, but not FGFR2-IIIb, respectively. ATTO-1 binds to established mesenchymal tumor cell lines, such as AT3 and BT459 (FGFR-2 IIIc+), but not to MCF-7 or DT (FGFR-2 IIIb+). These antibodies may be valuable research tools for studying and developing novel therapies for blocking tumor invasion and metastasis. Citation Format: Ullrich S. Schwertschlag, Katherine J. Turner, Central Lab Naval Hospital Bejing. Isolation of a high affinity, specific human monoclonal antibody that binds to FGFR-2 IIIc. [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 4279. doi:10.1158/1538-7445.AM2013-4279
393 MMP REGULATION BY CD147 IN HEPATOCYTES DURING CHRONIC LIVER INJURY
Authors: A.J. Morgan, V.W. Wen, S.R. Calabro, A. Mridha, M. Lee, B. Roediger, B. Patkunanathan, W. d'Avigdor, S.A. Locarnini, G.W. McCaughan, F.J. Warner, S.V. McLennan, N.A. Shackel
Journal: Journal of Hepatology (2012)
Scintigraphic and Computed Tomographic Imaging of Isolated Peripancreatic Nodal Gastrinomas
Authors: BA D. NGUYEN
Journal: Clinical Nuclear Medicine (2003)

From the Department of Radiology, Mayo Clinic Scottsdale, Scottsdale, Arizona Received for publication April 22, 2002. Revision accepted August 9, 2002. Correspondence: Ba D. Nguyen, Department of Radiology, Mayo Clinic Scottsdale, 13400 E. Shea Boulevard, Scottsdale, Arizona 85259. E-mail: [email protected]
Abstract 4766: Negative control of glutaredoxin activity by Smad3 contributes to transforming growth factor-beta1-induced apoptosis of hepatoma cells
Authors: Byung-Chul Kim, Woo-Kwang Jeon, Seong-Ji Park, Hyung-Ju Jang
Journal: Cancer Research (2011)

Abstract Although reactive oxygen species (ROS) has been established as important signaling molecules in transforming growth factor-beta1 (TGF-β1)-mediated apoptosis, its underlying molecular mechanisms are not well understood. Here, we demonstrate that TGF-β1 induces apoptotic cell death through decreasing the expression and activity of glutaredoxin (Grx), a thiol antioxidant enzyme, in hepatoma cells. Down-regulation of Grx by TGF-β1 was highly dependent on Smad3, a major TGF-β signaling transducer. Western blot analysis and chromatin immunoprecipitation (ChIP) assay revealed that endogenous Smad3 physically interacts with histone deacetylase 1 (HDAC1) and its co-repressor, mSin3A in response to TGF-β1 stimulation and this complex binds to Grx1 promoter region -1872/-1662 bp containing two CAGA boxes. Deletion or mutation of these sites abolished binding of Smad3 to Grx1 promoter and subsequent down-regulation of Grx1 promoter activity in TGF-β1-stimulated hepatoma cells. Notably, hepatoma cells which stably express hepatitis B virus X (HBx) displayed increased Grx activity and level of Grx protein, and showed resistance to TGF-β1-induced apoptosis. Importantly, HBx inhibited binding of Smad3 to Grx1 promoter by inducing phosphoprylation of serine 208 in linker region of Smad3. Expression of a mutant Smad3 in which linker phosphorylation sites were ablated caused a marked attenuation in inhibition by HBx of TGF-β1-induced apoptosis. Finally, elevated levels of Grx and phosphorylated Smad3 at linker regions were observed in the hepatocellular carcinoma (HCC) tissues compared to normal tissues. Taken together, these findings suggest that Smad3 is a transcriptional repressor of Grx and increased Smad3 phosphorylation at linker regions in HCC may intercept the tumor suppressor function of TGF-β through transcriptional activation of Grx, thereby providing new mechanistic insight into the development of anti-cancer drug-resistant HCC. This work was supported by the “Human Resource Development Center for Economic Region Leading Industry” Project, the Ministry of Education, Science &amp; Technology (MEST), and the National Research Foundation of Korea (NRF). 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 4766. doi:10.1158/1538-7445.AM2011-4766
Abstract 749: Cancer stem cell vaccination confers significant anti-tumor immunity by selectively targeting cancer stem cells
Authors: Ning Ning, Seagal Teitz-Tennenbaum, Ji Yet, Mu Li, Jeffrey S. Moyer, Christophe Ginestier, Max S. Wicha, Yingxin Xu, Mark EP Prince, Alfred E. Chang, Qiao Li
Journal: Cancer Research (2011)

Abstract To date, the majority of cancer stem cell (CSC) studies have been confined to human tumors inoculated into severely immunosuppressed hosts (e.g. SCID mice), where adaptive immune responses are absent, and such hosts are therefore not suitable for immunologic evaluation. The lack of immunocompetent syngeneic animal tumor models where stem cells can be isolated has been the primary obstacle to evaluating the immunogenicity of CSCs. In this study, we identified CSC-enriched populations in two histologically distinct murine tumors (melanoma B16-D5 and squamous cell cancer SCC7). We found that a very small percentage (0.5-5%) of ALDEFLUOR/ALDH1+ cells exist in these tumors; as few as 500 sorted ALDEFLUOR+ cells could form tumors in syngeneic hosts. The stem cell nature of the ALDELFUOR+ cells was confirmed by their ability to form spheres in culture and to self-renew in vivo. We evaluated the protective anti-tumor responses induced by D5 cancer stem cell-based vaccination with dendritic cell in the syngeneic immunocompetent host (B6 mice) in a pulmonary metastatic setting. We found that enriched D5 CSCs are immunogenic and are significantly more effective as an antigen source compared with unselected D5 tumor cells in inducing protective anti-tumor immunity. CSC-induced protective antitumor immunity was confirmed in a second tumor model (SCC7) syngeneic to a genetically different immunocompetent host (C3H) in a subcutaneous tumor setting. Immune sera collected from D5 or SCC7 CSC-vaccinated hosts contain high levels of IgG and IgG2b which bound specifically to D5 CSCs or SCC7 CSCs, respectively. This binding resulted in the CSC lysis in the presence of complement. In addition, CTLs generated from PBMCs harvested from D5 or SCC7 CSC-vaccinated hosts selectively killed D5 or SCC7 CSCs efficiently. We provide the first direct experimental evidence that selective targeting of cancer stem cells by CSC-primed antibodies and T cells may represent the mechanisms involved in CSC vaccine-conferred anti-tumor immunity. The findings from these studies may help develop novel cancer stem cell-targeted immunological approaches for cancer treatment. 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 749. doi:10.1158/1538-7445.AM2011-749
Coil migration into the common bile duct as a cause of cholangitis
Authors: R. Altun, A. Yildirim, S. Ocal, E. Akbas, M. Korkmaz, H. Selcuk, U. Yılmaz
Journal: Endoscopy (2011)

Bile leakage is among the most common complications of cholecystectomy. This complication is successfully treated by either endoscopic or percutaneous interventions [1] [2] [3] [4]. We report a case of cholangitis secondary to migration of coils that were placed percutaneously into the cystic duct in a previous procedure for high-flow bile leakage after open cholecystectomy 5 years ago.
Insertion of an Intraosseous Needle in Adults
Authors: Shelly P. Dev, Raluca A. Stefan, Tomas Saun, Shirley Lee
Journal: New England Journal of Medicine (2014)

Intraosseous needle insertion is used as a temporary measure when intravascular access cannot be achieved through peripheral or central venous routes. The intraosseous needle may remain in situ for 72 to 96 hours, but it is best removed within 6 to 12 hours, as soon as an alternative site of intravascular access has been established. The intraosseous route provides fast and reliable vascular access in emergency medical situations. The use of the appropriate technique will ensure that the procedure is performed as safely and effectively as possible.
Modified peroral pyloromyotomy and placement of a covered stent for refractory gastric outlet obstruction following ingestion of sulfuric acid
Authors: Mingyan Zhang, Dongxin Hu, Chunqing Zhang, Yongjun Shi
Journal: Endoscopy (2016)

A 15-year-old boy accidentally ingested a mouthful of sulfuric acid (160 g/L). He presented 20 days later with complaints of postprandial epigastric distress, repeated nonbilious vomiting, and marked weight loss (about 15 kg). Barium swallow and endoscopy revealed antropyloric narrowing ([Fig. 1], [Fig. 2]). Endoscopic balloon dilation was performed, and the symptoms were relieved. However, 2 months later the symptoms recurred, and barium swallow again showed pyloric narrowing ([Fig. 3]).
Effect of melanoma intrinsic β-catenin signaling on immune exclusion and resistance to immunotherapies.
Authors: Stefani Spranger, Yuanyuan Zha, Thomas Gajewski
Journal: Journal of Clinical Oncology (2015)

9014 Background: A subset of metastatic melanoma patients shows evidence for a T cell-inflamed tumor microenvironment at baseline, which has prognostic value and is associated with clinical response to immunotherapies including anti-PD-1. However, the molecular mechanisms mediating the absence of T cell infiltration in a major subset of patients have not been defined. Methods: Exome sequencing and gene expression profiling of melanoma metastases (TCGA) was combined with mechanistic studies in genetically engineered mouse models. Results: Analysis of melanoma metastases samples using gene expression profiling and exome sequencing, revealed activation of Wnt/ß-catenin pathway in a major subset of non-T cell-inflamed tumors. Using genetically engineered mouse melanoma models (BrafV600E/PTEN-/-± active ß-catenin), we demonstrated a causal effect between tumor-intrinsic ß-catenin signaling and T cell exclusion from the tumor microenvironment. The mechanism was via failed production of the chemokine CCL4, which was associated with failed recruitment of Batf3-lineage dendritic cells. Mice with these non-T cell-inflamed melanomas failed to respond to anti-CTLA-4/anti-PD-L1 mAb therapy. Active Wnt/ß-catenin signature in human melanomas was associated with reduction of Batf3 dendritic cell transcripts. Clinically, a patient who responded to a melanoma vaccine then recurred showed selection for loss of the T cell signature and gain of the ß-catenin phenotype. Conclusions: We have for the first time identified an oncogenic pathway that directly mediates immune evasion, which is implicated in examples of both primary and acquired resistance to immunotherapies.
IN-HOSPITAL OUTCOMES OF MULTIVESSEL PERCUTANEOUS CORONARY INTERVENTION IN HEMODYNAMICALLY STABLE PATIENTS PRESENTING WITH ST ELEVATION MYOCARDIAL INFARCTION
Authors: Shilpkumar Arora, Sidakpal Panaich, Nilay Patel, Chirag Savani, Sopan Lahewala, Nishith Vayada, Ronak Bhimani, Rajesh Sonani, Sanskruti Patel, Emmanuel Valery, Nilesh Balar, Nileshkumar Patel, Carlos Gongora, Abhishek Deshmukh, Apurva Badheka
Journal: Journal of the American College of Cardiology (2016)
Iron-Chelation Therapy with Oral Deferiprone in Patients with Thalassemia Major
Authors: Nancy F. Olivieri, Gary M. Brittenham, Doreen Matsui, Matitiahu Berkovitch, Laurence M. Blendis, Ross G. Cameron, Robert A. McClelland, Peter P. Liu, Douglas M. Templeton, Gideon Koren
Journal: New England Journal of Medicine (1995)

To determine whether the orally active iron chelator deferiprone (1,2-dimethyl-3-hydroxypyridin-4-one) is efficacious in the treatment of iron overload in patients with thalassemia major, we conducted a prospective trial of deferiprone in 21 patients unable or unwilling to use standard chelation therapy with parenteral deferoxamine.