tbuckley/cabot-search huggingface dataset:
Abstract 3919: Potential roles of oncogenic ΔNP63α during bone and bone cancer formation
Authors: Sam Abbassi, Ming Ding, Feifei Li, Yaojuan Lu, Guojun Wu, Qiping Zheng
Journal: Cancer Research (2010)

Abstract P63 belongs to the P53 tumor suppressor gene family. Due to its alternative promoter usage and splicing, p63 consists of two major subtypes (TAp63 and ΔNp63) and six different isoforms (TAp63α, β, or γ and ΔNp63α, β, or γ). These isoforms have been shown to play distinct biological functions in cancer and development. P63, especially the ΔNp63α variant, has been suggested to play an oncogenic role in cancer progression, including bone-related tumors such as giant cell tumor of bone and osteosarcoma. Interestingly, P63 has previously been shown to be an essential player for limb development. This raises the possibility that there might be a specific mechanism linking P63 regulation of bone and bone cancer formation. The type X collagen gene (Col10a1) is a specific marker of hypertrophic chondrocytes during endochondral bone formation. As a matrix protein, type X collagen also functions as a regulatory molecule that affects chondrocyte mineralization, apoptosis, and angiogenesis. Therefore, transcriptional regulators critical for Col10a1 expression are also expected to affect the apoptotic pathway that occurs during bone cancer formation. By real-time RT-PCR and proteomic approaches using a MCT cell model, we demonstrate here that P63 contributes to regulation of Col10a1 expression in vitro. We also have data which supports that Runx2 regulates cell-specific Col10a1 expression via the Runx2 binding sites found within the Col10a1 cis-enhancer. This is intriguing since p63 was previously shown to interact with Runx2 by yeast two-hybrid approach. Moreover, we have generated a mouse model in which Runx2 was driven by the cell-specific Col10a1 control element. Our preliminary results showed that these Col10a1-Runx2 transgenic mice have enhanced Runx2 and Col10a1 expression, a longer hypertrophic zone, altered chondrocyte maturation, apoptosis, and disturbed ossification. These results suggest the decreased apoptotic activity mediated by Runx2, whereas elevated Runx2 expression has been associated with osteosarcoma development and chondrosarcoma progression. To address the potential in vivo relevance of P63 on bone and cancer formation, we have established Col10a1-ΔNp63α transgenic mouse lines using the same Col10a1 control element. Characterization of these transgenic mice will allow us to study if this oncogenic P63 isoform regulates Col10a1 expression in vivo and if this regulation is within the network regulating both bone and bone cancer formation. 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 3919.
The Long Term Incidence and Predictors of Radial Artery Occlusion Following a Transradial Coronary Procedure
Authors: Ali Buturak, Sevket Gorgulu, Tugrul Norgaz, Nuray Voyvoda, Yusuf Sahingoz, Alex Degirmencioglu, Yasemin Demirci, Sinan Dagdelen
Journal: Journal of the American College of Cardiology (2013)
An Eruptive Fever Involving the Skin and Mucous Membranes (Stevens–Johnson Disease)
Authors: Arnall Patz
Journal: New England Journal of Medicine (1947)

IN 1866 von Hebra1 first described erythema multiforme as a generalized skin eruption without marked systemic symptoms; a rare type with fever, malaise, prostration and an accompanying severe stomatitis and purulent conjunctivitis was mentioned. Kaposi,2 in 1893, described an infrequent form with involvement of the mucous membranes. More recently, reports of erythema multiforme with occasional involvement of the mucous membranes of the eyes, mouth and genitalia have been presented.3 4 5 6 7 8 In 1922 Stevens and Johnson9 reported 2 cases of "a new eruptive fever associated with stomatitis and ophthalmia." They believed that the features of their cases, although previously described as a . . .
A2.6 Cell-Specific Type I IFN Signatures in Autoimmunity and Viral Infection: What Makes the Difference?
Authors: Chieko Kyogoku, Biljana Smiljanovic, Joachim R Grün, Tobias Alexander, Robert Biesen, Falk Hiepe, Thomas Häupl, Andreas Radbruch, Andreas Grützkau
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Gene expression profiling experiments using peripheral blood mononuclear cells (PBMCs) revealed a crucial role of type I interferon (IFN) in the pathogenesis of systemic lupus erythematosus (SLE). However, it is almost unknown how particular leukocyte subsets contribute to the overall type I IFN signature described for PBMCs. Furthermore, a detailed analysis of how IFN signatures differ in autoimmune disease from that observed after viral infection is missing so far. Therefore, we compared expression levels of 2442 IFN signature genes in peripheral CD4+ T helper cells and monocyte (Mo) subsets isolated from patients with SLE, healthy donors (ND) and ND vaccinated against yellow fever by global gene expression profiling. <h3>Materials and Methods</h3> Peripheral blood from 8 patients with SLE and 4 ND were recruited. Same ND were examined before and after immunisation by yellow fever vaccine. After sorting cells, isolated RNA were applied to Affymetrix Human Genome U133 Plus 2.0 Array. Data analysis was done using BioRetis database, Genesis Software and Ingenuity Pathway Analysis (IPA). <h3>Results</h3> 98/165/173 probe sets (CD4+ T cells/CD16– inflammatory Mo/CD16+ resident Mo, respectively, fold change ≥ 2, ≤ –2) were detected as a "common" IFN signature observed both in autoimmunity and in immunised ND. 111/164/120 probe sets were detected as an "autoimmune-specific" IFN signature, whereas only 0/8/5 probe sets were detected to be specific for the "virus-induced" IFN signature. Expression pattern of these IFN signature genes clearly distinguished patients with SLE from immunised ND by hierarchical cluster analysis. Although major IFN signature genes were commonly expressed in CD4+ T cells and Mo of patients with SLE and immunised ND, expression magnitudes of them were higher in patients with SLE compared to immunised ND. In SLE, in addition to the typical "viral-induced" IFN signature, genes that are involved in apoptosis signalling, antiviral PKR signalling, Fcγ receptor-mediated phagocytosis and IL-10-/IL-9-/IL-15-mediated JAK/Stat signalling pathways were identified by IPA. <h3>Conclusions</h3> This study demonstrated that IFN signature in autoimmunity and that in viral infection are quite different in the number of IFN-related genes activated and their expression magnitudes. Autoimmunity is characterised by a much stronger expression of IFN signature genes and is obviously modulated by a separate set of co-regulated genes defining the "autoimmune-specific" IFN signature. "Common" and "autoimmune-specific" IFN signature genes can be applied as a clinical biomarker to diagnose SLE flare discriminating from viral infection.
FRONTAL BONE HYPEROSTOSIS IN PSYCHOSES
Authors: J. NOTKIN
Journal: American Journal of Psychiatry (1953)

Frontal bone hyperostosis in psychoses was observed in 9 women. Certain laboratory changes, especially in blood cholesterol content and blood sugar tolerance, were noted. Obesity was not observed as a characteristic feature. Five cases began with functional types of psychosis, later showing evidence of organic mental deterioration. Four patients had organic mental reactions from the beginning, one showing pronounced neurologic signs.
A10.6 Dissecting Disease-Specific Differences in RA and OA by Transcriptome Analyses of Synovial Tissue, Blood and Bone Marrow Monocytes
Authors: Biljana Smiljanovic, Bruno Stuhlmüller, Wlodzimierz Maslinski, Gerd-R Burmester, Andreas Radbruch, Andreas Grützkau, Thomas Häupl
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with joint destruction. Joint inflammation is characterised by infiltration and activation of various immune cells. To avoid difficulties in sampling synovial tissue and to avoid fluctuation in cellular composition of leukocytes, which accompanies inflammation both in synovial tissue and blood, this study was focused on transcriptome analyses of synovial tissues, blood and bone marrow monocytes. The main aim was to analyse potential of blood monocytes in dissecting inflammation in RA and in reflecting inflammation that is evident in synovial tissue. Osteoarthritis (OA), which represents a non-inflammatory disease was used as control in this study. <h3>Materials and Methods</h3> Synovial tissues from 10 RA and 10 OA patients were used for gene-expression profiling by Affymetrix HG-U133A arrays. Blood and bone marrow monocytes, obtained from 8 RA and 8 OA patients undergoing hip replacement surgery, were utilised for gene-expression profiling by Affymetrix HG-U133Plus arrays. The BioRetis database was used for microarray analyses and generation of RA profiles. <h3>Results</h3> Transcriptome analyses of synovial tissues from RA and OA patients revealed more than 1000 differentially expressed genes. Increased expression of genes involved in chemotaxis (CCL13, CCL18, CXCL9, CXCL10, CXCL13), cell adhesion and activation (ICAM1, PECAM1, ITGAL, ITGB2, CD40, CD86) indicate to inflammation but also to infiltration of various cell types like monocytes/macrophages, NK, T- and B-cells. By comparing transcriptome of RA and OA monocytes, both from blood and bone marrow, it was obvious that monocytes were able to disclose differences between these two diseases. The RA disease-specific gene-expression profile was evident both in blood and bone marrow and it demonstrated only a minor overlap between these two bodies compartments. Altogether, a typical RA inflammatory profile disclosed in synovial tissues was greatly silenced in blood monocytes, and almost completely absent in bone marrow derived monocytes. <h3>Conclusions</h3> The RA gene-expression profile was the most specific and robust in synovial tissue, demonstrating the dominance of the inflammatory process in the joints. Nevertheless, the systemic nature of RA was also evident at the level of blood and bone marrow monocytes. Concerning that blood is a favourable and easily accessible material for diagnosis and that monocytes are able to exhibit disease-specific alterations, understanding monocyte response in different rheumatic diseases seems to be advantageous approach for biomarkers discovery. This approach should be essential for identifying the objective criteria relevant for disease and therapeutic stratification of patients with RA.
Indium-111 Platelet Scintigraphy in a Patient with Chronic Disseminated Intravascular Coagulation
Authors: ETSUKO NAKANISHI, YOSHINARI ISAKA, HIDEKI ETANI, SATOSHI FURUKAWA, YOSUKE OOE, MASATOSHI IMAIZUMI
Journal: Clinical Nuclear Medicine (2000)

The authors describe a relation between the in vivo localized consumption of In-111 platelets and results of laboratory tests in a 82-year-old man with an aortic graft prosthesis who had chronic disseminated intravascular coagulation. In-111 platelets accumulated markedly over the abdominal aortic graft with a shortened platelet survival time and reflected changes in hematologic studies, which showed low platelet counts and a high concentration of fibrinogen degradation products in the plasma. If a strong clinical likelihood of local disseminated intravascular coagulation exists, then In-111 platelets may be valuable in localizing the focus of platelet consumption.
PWE-037 “Bear-Claw” or Over-The-Scope -Clip System (Otsc); a Breakthrough, Surgery Sparing, Endoscopic Device
Authors: J Toshniwal, L Fry, K Vormbrock, M Zabielski, K Mönkemüller
Journal: Gut (2013)

<h3>Introduction</h3> The “bear-claw” or over-the-scope clip system, OTSC (Ovesco Endoscopy, Tübingen, Germany) is a new clipping device developed for closure of large luminal gastrointestinal (GI) defects. <h3>Methods</h3> To evaluate the clinical outcomes of patients treated with the OTSC a prospective, single-arm, pilot study was conducted in a regional hospital with tertiary care endoscopy. This study involved 11 clip applications in 10 patients (median age 76.2 years [range 52–89 years], 5 women) with GI defects from fistulas and anastomotic dehiscence and peptic ulcer bleeding. <h3>Results</h3> Bleeding posterior duodenal wall ulcers (n = 4), bleeding gastric ulcer (n = 2), three fistulas or anastomotic dehiscences (n = 4) were treated using the OTSC-system. In addition a self-expanding metal stent was anchored securely in place with an OTSC-system. The diameter of ulcers and/or leaks ranged between 12 and 20 mm. A complete sealing of leaks was achieved in 3/4 patients. There were no clip complications. However, during introduction of the loaded clip on the tip of the endoscope, the hood tended to migrate over the scope, i.e. retracting, thus diminishing the exposed hood. This leads to diminished tissue suction and closure. Thus we modified the technique by tightly taping the hood on the tip of the scope. This trick may explain why all our cases were successful. <h3>Conclusion</h3> The OTSC system is a useful device in a variety of clinical scenarios including the management of larger GI leaks, GI bleeding and stent anchoring, even in very old and frail patients. <h3>Disclosure of Interest</h3> None Declared.
P2-05-07: Combined Antiangiogenic and Anti-Estrogen Therapy in Breast Cancer. Molecular Mechanisms Involved.
Authors: la Haba J de, M Berciano, M Cañabate, I Porras, A Valverde, A Cañas, A Rodriguez, E Aranda
Journal: Cancer Research (2011)

Abstract Background: Much is known about the mechanisms involved in the response to anti-hormonal treatment or those involved in the response to antiangiogenic therapy. It is also known the association between angiogenesis and hormonal status, both in physiological and pathological settings. However, the molecular and cellular mechanisms contributing to the efficacy of combined antiangiogenic-antihormonal therapy in breast cancer are still unknown. This combination is currently in clinical trials, but unfortunately there are scarce preclinical studies contributing to the rationale of combining antiangiogenic and antihormonal therapies. Aims: To define the mechanisms involved in the response to combined antiangiogenic-antihormonal treatments in breast cancer cells. Methods: Breast cancer cell lines with different estrogen dependence (MCF-7, BT-474, MDA-MB-231) were subjected to an estrogen gradient (estradiol), and treated with fulvestrant (antiestrogen), plus bevacizumab (anti-angiogenic). Cellular proliferation and apoptosis were determined using the corresponding kits. Proliferation and survival intracellular signaling pathways, estrogen alpha and VEGF receptors activation and COX-2 expression were analyzed by western-blot using specific antibodies. Results: In estrogen-dependent breast cancer cells (MCF-7 and BT-474) the pro-proliferative effect of estradiol decreased after bevacizumab treatment. Furthermore, the combination of the antiangiogenic with an antiestrogen enhanced this antiproliferative effect, that was also related to the reduction in the levels of VEGF-A in the culture medium and to diminished ER alpha phosphorylation. The combined treatment also altered the phosphorylation of Akt and Erk1/2 signaling kinases. Interestingly, bevacizumab treatment augmented COX-2 activity in MCF-7. Conclusions: Our results suggest that in estrogen dependent breast cancer cells the anti-proliferative effect of bevacizumab depends on estradiol concentration, that in turn affects VEGF production levels, using a different mechanism to apoptosis. The combination of bevacizumab with antiestrogens enhances this antitumoral effect, altering intracellular signaling pathways of proliferation and survival. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-05-07.
EFFECTS OF SIMULATED MICROGRAVITY ON PROLIFERATION AND CHEMOSENSITIVITY IN MALIGNANT GLIOMA CELLS
Authors: K. Kurisu, M. Takeda, T. Okazaki, Y. Kawahara, L. Yuge
Journal: Neuro-Oncology (2014)

BACKGROUND: Everything on the earth can be affected by gravity of the earth. So, microgravity, as small as 10 minus 3 times G, can make some effects to the growth or maturation of cells. Under this hypothesis we examined cell proliferation and chemosensitivity after exposure to simulated microgravity using the malignant glioma cell lines. We exposed cells to simulated microgravity using a 3D-clinostat which is a type of rotating culture system that has two independent axes of rotation to disperse the gravity vector throughout the whole steric angle. METHODS: D54MG, U251MG and T98G cell lines were used in this study. All samples were identically treated before the start of the experiment and randomized for clinorotation (CL group) or culturing at 1G (C group). The Opticell cell culture system, mounted in a 3D-clinostat, was used for culture under simulated microgravity. Cells were cultured under a 1G environment for 24 h before using the 3D-clinostat to achieve adhesion. Morphological changes in glioblastoma cells during culture were examined using an inverted phase-contrast microscope. We analyzed the viability of the CL group and the C group cells by Trypan-blue exclusion method. The mitochondrial membrane potential was measured using the fluorescent dye Rhodamine123. Cell cycle distribution was measured with a FACS Caliber flow cytometer. Immunoblotting and sensitivity to CDDP was examined. RESULTS: Proliferation was significantly lower in all cell lines in the CL group compared to the C group on day three. The percentage of living cells in the CL group showed no significant differences compared to the C group. Cell cycles indicated by flow cytometry showed no differences between the CL and C groups. In both groups, FACS analysis also showed there was no significant proportion of apoptotic cells in any of the cell lines. In the CL group, significant deterioration of mitochondrial activity was shown in all malignant glioma cell lines compared to the C group. CONCLUSIONS: This is the first study to examine the effect of simulated microgravity on the proliferation, mitochondrial activity, and chemosensitivity of human malignant glioma cells. Our data suggests that simulated microgravity induces growth inhibition through reduction of mitochondrial activity, and enhances the chemosensitivity of malignant glioma cells to CDDP. Our findings using 3D-clinorotation provide new insight into the responses to simulated microgravity of malignant glioma cells. SECONDARY CATEGORY: Tumor Biology.
207 DIAGNOSTIC PERFORMANCE OF C-REACTIVE PROTEIN AND NEUTROPHIL-TO-LYMPHOCYTE RATIO FOR INFECTION IN PATIENTS WITH DECOMPENSATED CIRRHOSIS
Authors: J.H. Kwon, J.W. Jang, Y.W. Kim, M.J. Kim, B.S. Oh, C.R. You, S.W. Nam, K.W. Chung, S.H. Bae, S. Lee
Journal: Journal of Hepatology (2013)
Colon capsule endoscopy as possible filter test for colonoscopy selection in a screening population with positive fecal immunology
Authors: Grainne Holleran, Ronan Leen, Colm O’Morain, Deirdre McNamara
Journal: Endoscopy (2014)

<b>Background and study aims:</b> Stool tests are highly useful in colorectal cancer (CRC) screening programs; however, they are not as specific as users would like, and place a major burden on resources and subject a number of patients to the risks of invasive optical colonoscopy unnecessarily. Colon capsule endoscopy (CCE) has the potential to reduce the need for optical colonoscopy. To date, the role of CCE in a fecal immunological test (FIT)-based CRC screening program has not been formally evaluated. The aims of this study were to assess the sensitivity, specificity, and negative and positive predictive values of CCE compared with optical colonoscopy in an FIT-positive CRC screening cohort. <b>Patients and methods:</b> A prospective comparison study of CCE compared with optical colonoscopy was undertaken within the second round of a FIT-based bowel screening pilot. Participants with a positive FIT result were invited to undergo both CCE and optical colonoscopy. CCE was performed on Day 1 and optical colonoscopy was performed the following morning. <b>Results:</b> A total of 62 participants were recruited. Optical colonoscopy detected at least one polyp in 36 participants (58 %), significant lesions in 18 (29 %), and cancer in 1 (2 %). There was good correlation between CCE and optical colonoscopy for any lesion and for significant lesions (r = 0.62 and 0.84, respectively). The negative predictive value of CCE was high both for any polyp (90 %) and for significant lesions (96 %). <b>Conclusions:</b> CCE is a safe and effective means of detecting cancer and polyps in a positive FIT screening cohort. The results suggest that CCE would be a useful "filter test" in this situation, and would reduce the number of colonoscopies performed by 71 %.
Abstract LB-39: Kidney cancer association fighting back togethe
Authors: Maria T. Fahy
Journal: Cancer Research (2012)

Abstract The Kidney Cancer Association's (KCA) vision since its creation by founder Eugene P. Schonfeld, PhD has been The Elimination of Death and Suffering from Renal Cancers and to pursue A World Without Kidney Cancer. The Kidney Cancer Association has grown in the last 21 years to be an amazing organization that included over 55,000 people in more than 100 countries, The KCA is organization that pursues its worldwide vision through education, research and advocacy with a three person staff which is assisted by a dedicated group of professionals and other individuals who serve on a governing board, or a medical advisory board, or performs a host of other duties that allows the KCA to play an important role in the advances that have made in the diagnosis, treatment and follow up of renal cancers during the past two decades. As an independent advocate and daughter who lost her father to kidney cancer, Team Chema was born. With the help and support of KCA, Team Chema will be involved in bringing information about the latest research and best practices to the places that have cultural and language barriers that hinder cancer prevention and treatment. Team Chema is dedicated to supporting patients, organizing fundraising events and creating awareness. 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 LB-39. doi:1538-7445.AM2012-LB-39