@article{ReimerRoseScheeretal.1987, author = {Reimer, Georg and Rose, Kathleen M. and Scheer, Ulrich and Tan, Eng M.}, title = {Autoantibody to RNA polymerase I in scleroderma sera}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34294}, year = {1987}, abstract = {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.}, language = {en} } @misc{ReimerRaskaTanetal.1987, author = {Reimer, Georg and Raska, Ivan and Tan, Eng M. and Scheer, Ulrich}, title = {Human autoantibodies: probes for nucleolus structure and function}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-41410}, year = {1987}, abstract = {No abstract available}, language = {en} } @article{ReimerRaskaScheeretal.1988, author = {Reimer, Georg and Raska, Ivan and Scheer, Ulrich and Tan, Eng M.}, title = {Immunolocalization of 7-2-ribonucleoprotein in the granular component of the nucleolus}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-33890}, year = {1988}, abstract = {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}, language = {en} } @article{ReimerScheerPetersetal.1986, author = {Reimer, Georg and Scheer, Ulrich and Peters, Jan-Michael and Tan, Eng M.}, title = {Immunolocalization and partial characterization of a nucleolar autoantigen (PM-Scl) associated with polymyositis / scleroderma overlap syndromes.}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-33191}, year = {1986}, abstract = {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 sign{\"u}icantly 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.}, language = {en} } @article{FruchartDavignonHermansetal.2014, author = {Fruchart, Jean-Charles and Davignon, Jean and Hermans, Michael P. and Al-Rubeaan, Khalid and Amarenco, Pierre and Assmann, Gerd and Barter, Philip and Betteridge, John and Bruckert, Eric and Cuevas, Ada and Farnier, Michel and Ferrannini, Ele and Fioretto, Paola and Genest, Jacques and Ginsberg, Henry N. and Gotto Jr., Antonio M. and Hu, Dayi and Kadowaki, Takashi and Kodama, Tatsuhiko and Krempf, Michel and Matsuzawa, Yuji and N{\´u}{\~n}ez-Cort{\´e}s, Jes{\´u}s Mill{\´a}n and Monfil, Calos Calvo and Ogawa, Hisao and Plutzky, Jorge and Rader, Daniel J. and Sadikot, Shaukat and Santos, Raul D. and Shlyakhto, Evgeny and Sritara, Piyamitr and Sy, Rody and Tall, Alan and Tan, Chee Eng and Tokg{\"o}zoğlu, Lale and Toth, Peter P. and Valensi, Paul and Wanner, Christoph and Zambon, Albertro and Zhu, Junren and Zimmet, Paul}, title = {Residual macrovascular risk in 2013: what have we learned?}, series = {Cardiovascual Diabetology}, volume = {13}, journal = {Cardiovascual Diabetology}, number = {26}, issn = {1475-2840}, doi = {10.1186/1475-2840-13-26}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-117546}, year = {2014}, abstract = {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.}, language = {en} }