TY - JOUR A1 - Reimer, Georg A1 - Rose, Kathleen M. A1 - Scheer, Ulrich A1 - Tan, Eng M. T1 - Autoantibody to RNA polymerase I in scleroderma sera N2 - Autoantibodies to components of the nucleolus are a unique serological feature of patients with scleroderma. There are autoantibodies of several specificities; one type produces a speckled pattern of nucleolar staining in immunofluorescence. In actinomycin D and 5,6-dichloro-{j-D-ribofuranosylbenzimidazoletreated Vero cells, staining was restricted to the fibrillar and not the granular regions. By double immunofluorescence, specific rabbit anti-RNA polymerase I antibodies stained the same fibrillar structures in drug-segregated nucleoli as scleroderma sera. Scleroderma sera immunoprecipitated 13 polypeptides from (35S)methionine-labeled HeLa cell extract with molecular weights ranging from 210,000 to 14,000. Similar polypeptides were precipitated by rabbit anti-RNA polymerase I antibodies, and their common identities were confirmed in immunoabsorption experiments. Microinjection of purified IgG from a patient with speckled nucleolar staining effectively inhibited ribosomal RNA transcription. Autoantibodies to RNA polymerase I were restricted to certain patients with scleroderma and were not found in other autoimmune diseases. Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-34294 ER - TY - JOUR A1 - Reimer, Georg A1 - Raska, Ivan A1 - Tan, Eng M. A1 - Scheer, Ulrich T1 - Human autoantibodies: probes for nucleolus structure and function N2 - No abstract available Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-41410 ER - TY - JOUR A1 - Reimer, Georg A1 - Raska, Ivan A1 - Scheer, Ulrich A1 - Tan, Eng M. T1 - Immunolocalization of 7-2-ribonucleoprotein in the granular component of the nucleolus N2 - Certain autoimmune sera contain antibodies against a nucleolar ribonucleoprotein particle associated with 7-2-RNA (R. Reddy et al. (1983) J. Bioi. Chem . 258, 1383; C. Hashimoto and J. A. Steitz (1983) J. Bioi. Chem. 258, 1379). In this study, we showed by immunofluorescence microscopy that antibodies reactive with 7-2-ribonucleoprotein immunolocalized in the granular regions of actinomycin D and 5,6-dichloro-I-j3-D-ribofuranosylbenzimidazole (DRB)-segregated nucleoli from Vero cells. By electron microscopic immunocytochemistry, antigen-antibody complexes were located in the granular component of transcriptionally active nucleoli from rat liver hepatocytes and HeLa cells. Anti-7- 2-RNP antibodies from two autoimmune sera immunoprecipitated a major protein of Mr 40,000 from e5S] methionine-Iabeled HeLa cell extract. The immunolocalization data suggest that 7-2-ribonucleoprotein may be involved in stages of ribosome biogenesis which take place in the granular component of the nucleolus, i.e., assembly, maturation, and/or transport of preribosomes Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-33890 ER - TY - JOUR A1 - Reimer, Georg A1 - Scheer, Ulrich A1 - Peters, Jan-Michael A1 - Tan, Eng M. T1 - Immunolocalization and partial characterization of a nucleolar autoantigen (PM-Scl) associated with polymyositis / scleroderma overlap syndromes. N2 - Precipitating anti-PM-Sel antibodies are present in sera from patients with polymyositis. scleroderma. and polymyositis/scleroderma overlap syndromes. By indirect immunofluorescence microscopy. anti-PM-Scl antibodies stained the nucleolus in cells of different tissues and species. suggesting that the antigen is highly conserved. By electron microscopy, anti-PM-Scl antibodies reacted primarily with the granular component of the nuc1eolus. Drugs that inhibit rRNA synthesis had a marked effect on the expression of PM-Scl antigen. In actinomycin D-treated cells, immunofluorescence staining by anti-PM-Scl was signüicantly reduced with residual staining restricted to the granular regions of nuc1eoli. Treatment with 5,6-dichloro-beta-D- ribofuranosylbenzimidazole (DRB) also selectively reduced nuc1eolar staining. On a molecular level, anti-PM-Sel antibodies precipitated 11 polypeptides with molecular weights (Mr) ranging from 110,000 to 20,000. The Mr 80,000 and 20.000 polypeptides were phosphorylated. Evidence suggests that the PM-Scl antigen complex may be related to a prerlbosomal particle. Y1 - 1986 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-33191 ER - TY - JOUR A1 - Fruchart, Jean-Charles A1 - Davignon, Jean A1 - Hermans, Michael P. A1 - Al-Rubeaan, Khalid A1 - Amarenco, Pierre A1 - Assmann, Gerd A1 - Barter, Philip A1 - Betteridge, John A1 - Bruckert, Eric A1 - Cuevas, Ada A1 - Farnier, Michel A1 - Ferrannini, Ele A1 - Fioretto, Paola A1 - Genest, Jacques A1 - Ginsberg, Henry N. A1 - Gotto Jr., Antonio M. A1 - Hu, Dayi A1 - Kadowaki, Takashi A1 - Kodama, Tatsuhiko A1 - Krempf, Michel A1 - Matsuzawa, Yuji A1 - Núñez-Cortés, Jesús Millán A1 - Monfil, Calos Calvo A1 - Ogawa, Hisao A1 - Plutzky, Jorge A1 - Rader, Daniel J. A1 - Sadikot, Shaukat A1 - Santos, Raul D. A1 - Shlyakhto, Evgeny A1 - Sritara, Piyamitr A1 - Sy, Rody A1 - Tall, Alan A1 - Tan, Chee Eng A1 - Tokgözoğlu, Lale A1 - Toth, Peter P. A1 - Valensi, Paul A1 - Wanner, Christoph A1 - Zambon, Albertro A1 - Zhu, Junren A1 - Zimmet, Paul T1 - Residual macrovascular risk in 2013: what have we learned? JF - Cardiovascual Diabetology N2 - Cardiovascular disease poses a major challenge for the 21st century, exacerbated by the pandemics of obesity, metabolic syndrome and type 2 diabetes. While best standards of care, including high-dose statins, can ameliorate the risk of vascular complications, patients remain at high risk of cardiovascular events. The Residual Risk Reduction Initiative (R(3)i) has previously highlighted atherogenic dyslipidaemia, defined as the imbalance between proatherogenic triglyceride-rich apolipoprotein B-containing-lipoproteins and antiatherogenic apolipoprotein A-I-lipoproteins (as in high-density lipoprotein, HDL), as an important modifiable contributor to lipid-related residual cardiovascular risk, especially in insulin-resistant conditions. As part of its mission to improve awareness and clinical management of atherogenic dyslipidaemia, the R(3)i has identified three key priorities for action: i) to improve recognition of atherogenic dyslipidaemia in patients at high cardiometabolic risk with or without diabetes; ii) to improve implementation and adherence to guideline-based therapies; and iii) to improve therapeutic strategies for managing atherogenic dyslipidaemia. The R(3)i believes that monitoring of non-HDL cholesterol provides a simple, practical tool for treatment decisions regarding the management of lipid-related residual cardiovascular risk. Addition of a fibrate, niacin (North and South America), omega-3 fatty acids or ezetimibe are all options for combination with a statin to further reduce non-HDL cholesterol, although lacking in hard evidence for cardiovascular outcome benefits. Several emerging treatments may offer promise. These include the next generation peroxisome proliferator-activated receptor alpha agonists, cholesteryl ester transfer protein inhibitors and monoclonal antibody therapy targeting proprotein convertase subtilisin/kexin type 9. However, long-term outcomes and safety data are clearly needed. In conclusion, the R(3)i believes that ongoing trials with these novel treatments may help to define the optimal management of atherogenic dyslipidaemia to reduce the clinical and socioeconomic burden of residual cardiovascular risk. KW - phospholipid fatty acids KW - term fenofibrate therapy KW - cardiovascular munster procam KW - residual cardiovascular risk KW - atherogenic dyslipidaemia KW - type 2 diabetes KW - therapeutic options KW - high denisty lipoprotein KW - randomized controlled-trial KW - coronary artery disease KW - type-2 diabetes mellitus KW - triglyceride-rich lipoproteins KW - alpha/delta agonist GFT505 KW - placebo-controlled trial Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-117546 SN - 1475-2840 VL - 13 IS - 26 ER -