26 results on '"Hoischen S"'
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2. Einfluß einer veränderten extrazellulären K+- und Mg2+-Konzentration auf die intrazelluläre Ca2+-Homöostase, die Kontraktionskopplung und die Kraft-Frequenz-Beziehung am menschlichen Myokard
- Author
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Schwinger, R. H. G., Frank, K., Hoischen, S., Müller-Ehmsen, J., and Brixius, K.
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- 1997
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3. Riociguat for the treatment of pulmonary arterial hypertension
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Ghofrani, Ha, Galiè, N, Grimminger, F, Grünig, E, Humbert, M, Jing, Zc, Keogh, Am, Langleben, D, Kilama, Mo, Fritsch, A, Neuser, D, Rubin, Lj, 1 Study Group including Bortman G, Patent, Keogh, A, Kermeen, F, Feenstra, J, Williams, T, Reeves, G, Kilpatrick, D, Lang, I, Kahler, C, Mascherbauer Steringer, R, Vachiery, Jl, Delcroix, M, Meyer, G, Arakaki, J, Santana, M, Waetge, D, Granton, J, Helmersen, D, He, J, Jing, Z, Zhou, D, Huang, Y, Wang, C, Jansa, P, Neilsen Kudsk JE, Hachulla, E, De Groote, P, Frachon, I, Bourdin, A, Pison, C, Bauer, F, Dromer, C, Marquette, Ch, Degano, B, Neurohr, C, Wilkens, H, Hoffken, G, Hoeper, M, Ghofrani, A, Wirtz, H, Rosenkranz, S, Ewert, R, Orfanos, S, Kramer, M, Ben Gal, T, Scelsi, L, Vizza, C, Harari, S, Confalonieri, M, Albera, Carlo, Fukumoto, Y, Sano, M, Hatano, M, Saji, T, Tanaka, S, Takeda, Y, Takehara, K, Matsubara, H, Kihara, Y, Shiohira, Y, Kawai, H, Homma, S, Satoh, T, Tokunaga, T, Ishizaki, T, Diaz, C, Zamudio, T, De Los Rios, M, Estupian, S, Cacho, Jr, Gamba, M, Beckert, L, Torbicki, A, Castro, G, Reis, A, Agapito, A, Martins, S, Kim, H, Lee, S, Chang, H, Song, Y, Chazova, I, Moiseeva, O, Lim, S, Yip, J, Barbera, J, Roman, A, Palma Jdel, C, Reitan, O, Soderberg, S, Jansson, K, Speich, R, Hsu, Hh, Lin, Hy, Cheng, Cc, Phrommintikul, A, Jaimchariyatam, N, Sayin, T, Kultursay, H, Ongen, G, Pepke Zaba, J, Coghlan, G, Peacock, A, Gibbs, J, Wagoner, L, Badesch, D, Frost, A, Hill, N, Allen, R, Waxman, A, Sood, N, Torres, F, Minai, O, Shapiro, S, Klinger, J, Engel, P, Garcia, H, Schuller, D, Poch, D, Rosenzweig, E, Mcconnell, J, Rischard, F, Olschewski, H, Haverkamp, W, Lehmacher, W, Hoischen, S, Collamati, S, Dehay, J, Hallmann, M, Menezes, F., Ghofrani HA, Galiè N, Grimminger F, Grünig E, Humbert M, Jing ZC, Keogh AM, Langleben D, Kilama MO, Fritsch A, Neuser D, Rubin LJ, and PATENT-1 Study Group
- Subjects
medicine.medical_specialty ,business.industry ,General Medicine ,Placebo ,medicine.disease ,Pulmonary hypertension ,Riociguat ,law.invention ,Surgery ,Clinical trial ,chemistry.chemical_compound ,medicine.anatomical_structure ,Randomized controlled trial ,chemistry ,DRUG THERAPY ,law ,Anesthesia ,riociguat ,pulmonary arterial hypertension ,Clinical endpoint ,Vascular resistance ,Medicine ,business ,Macitentan ,medicine.drug - Abstract
Riociguat, a soluble guanylate cyclase stimulator, has been shown in a phase 2 trial to be beneficial in the treatment of pulmonary arterial hypertension. METHODS: In this phase 3, double-blind study, we randomly assigned 443 patients with symptomatic pulmonary arterial hypertension to receive placebo, riociguat in individually adjusted doses of up to 2.5 mg three times daily (2.5 mg-maximum group), or riociguat in individually adjusted doses that were capped at 1.5 mg three times daily (1.5 mg-maximum group). The 1.5 mg-maximum group was included for exploratory purposes, and the data from that group were analyzed descriptively. Patients who were receiving no other treatment for pulmonary arterial hypertension and patients who were receiving endothelin-receptor antagonists or (nonintravenous) prostanoids were eligible. The primary end point was the change from baseline to the end of week 12 in the distance walked in 6 minutes. Secondary end points included the change in pulmonary vascular resistance, N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, World Health Organization (WHO) functional class, time to clinical worsening, score on the Borg dyspnea scale, quality-of-life variables, and safety. RESULTS: By week 12, the 6-minute walk distance had increased by a mean of 30 m in the 2.5 mg-maximum group and had decreased by a mean of 6 m in the placebo group (least-squares mean difference, 36 m; 95% confidence interval, 20 to 52; P
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- 2013
4. Study of Heart and Renal Protection (SHARP): Randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease.
- Author
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Reaich R., Schouten D., Rashid H., Birtcher K., Cantu J., Tait C., Taun W., Fadem S., Das D., Khosla U., Brown C., Brown T., Buquing J., Cromwell H., Dickson N., Najimipour B., Robeson J., Tabibi W., Mulloy L., Bailey K., Burton B., Fall P., Jagadeesan M., Paulson W., Szerlip H., White J., Faulkner M., Adeleye O., Boatright D., Mensah D., Nwankwo U., Crutcher L., Cummings C., Floyd M., Putatunda B., Ross J., Sanford V., Thadani U., Haragsim L., Parker B., Rogan L., Thresher M., Turner J., Dworkin L., Mignano D., O'Mara A., Shemin D., Bakris G., Basta E., Chua D., Neri G., Ahmed I., Elliott W., Fondren L., Hasabou N., Khosla N., Mazin A., Riehle J., Kovesdy C., Mendoza J., Ahmadzadeh S., Iranmanesh A., Lewis M., Lu J., Benabe J., Gonzalez-Melendez E., Padilla B., Serrano J., Russ T., Athmann L., Funke L., Larson P., Roach D., Salveson B., Nogueira J., Hanes D., Hise M., Light P., Copland E., Fink J., Hakim M., Hough K., McMinn S., Weir M., Young C., Kershaw G., Hill I., White B., Plumb T., Florescu M., Groggel G., Martin M., Rao V., Denu-Ciocca C., Candiani C., Cooper J., Gordon B., Joy M., Kiser M., Lambeth C., Rosas S., Cochetti P., Robinson J., Schankel K., Teng H., Weise W., Geneidy A., Murray P., Solomon R., De Waal D., LaPointe S., Schoenknecht A., Campese V., Habashy M., Ananthakrisna R., Bedwani D., Fazli U., Fetrat M., Frampton Q., Kaldas B., Kazarian V., Pitts L., Sadeghi A., Yeasmin N., Young E., Fissell R., Belanger K., Ricci N., Farwell W., Bowman T., Dhingra R., Pesenson A., Ambrosino J., Chittamooru S., Kaufman J., Ramos M., Yap C., Nakhle S., Aligaen L., Duren D., Laine B., Moore S., Tuazon H., Coyne D., Audrain J., Bryant B., Dombek S., Freeman S., Klein P., Germain M., Berkowitz A., Bokhari A., Braden G., Diaz A., Greco B., Mulhern J., O'Shea M., Poindexter A., Poppel D., Ryan M., Sweet S., Ye J., Osterman J., Lin T., Mays B., Rizvi A., Sonnier C., Twining C., Wang S., Hix M., Schenck J., Baigent C., Landray M., Reith C., Dasgupta T., Emberson J., Herrington W., Lewis D., Mafham M., Collins R., Bray C., Chen Y., Baxter A., Young A., Hill M., Knott C., Cass A., Feldt-Rasmussen B., Fellstrom B., Grobbee R., Gronhagen-Riska C., Haas M., Holdaas H., Hooi L.S., Jiang L., Kasiske B., Krairittichai U., Levin A., Massy Z., Tesar V., Walker R., Wanner C., Wheeler D., Wiecek A., Majoni W., Simpson D., Strony J., Musliner T., Agodoa L., Armitage J., Chen Z., Craig J., De Zeeuw D., Gaziano M., Grimm R., Krane V., Neal B., Ophascharoensuk V., Pedersen T., Sleight P., Tobert J., Tomson C., Sandercock P., Keech A., Whelton P., Yusuf S., Peto R., Parish S., Dolph L., Bahu T., Booth-Davey E., Brewster A., Yau F., Denis E., Frederick K., Haywood D., Heineman J., Howard S., Jayne K., Madgwick Z., Michell S., Murphy K., Ning L., Nolan J., Nunn M., Roberts J., Wickman M., Bowman L., Bulbulia R., Haynes R., Rahimi K., Rahman N., Ait-Sadi R., Barton I., Zhu W., Clark S., Kourellias K., Radley M., Brown K., Worthing D., Coates G., Goodenough B., Lucas N., Carreras A., Currie R., Donaldson O., Fjalling E., Gallagher M., Gibson K., Goddard J., Healy J., Hones L., Jardine M., Kwong I., Merai M., Murray S., Perkovic V., Rendina A., Gallo K., Caron S., Carlson K., Foley K., Matzek S., Mewhort L., O'Donoghue S., Perel-Winkler A., Terins T., Nie Q., Yu H., Ge L., Hao D., Li L., Pang X., Wei X., Yan G., Certikova Chabova V., Holst H., Molvadgaard T., Munksgaard D., Peltonen Y., Liabeuf S., Lebel C., Ouabou L., Bauer B., Bergmann K., Beusch M., Cavitt D., Drechsler C., Dulau I., Hugen K., Kempf S., Kuchenmeister B., Pscheidl V., Schmiedeke D., Schwarz M., Speerschneider K., Stahl B., Lim B.C., Nadia H., Zishareena M.F., Vasuthavan S., Ganesapillai A.T., Yuen S., Grobbee D., Bobbink I., Groot K., Sikking I., Raley J., Colban M., Smerud K., Trygg N., Waagaard E., Westad H., Rotkegel S., Spiechowicz U., Domoradzka M., Gawlowska M., Flygar A., Odmark I., Pettersson A., Blackwood S., Barclay J., Benham J., Brown R., Cureton L., Jackson D., Kennedy I., Leaper C., Taylor A., Winter C., Wise C., Nash M., Taylor Bennett A., Donaldson D., Chalmers K., Corderoy H., Bartkoske M., Bjerk C., Camarena A., Herskovitz L., Heuer C., Levin J., Robinson R., Wicklund B., Bentzel D., Cohen S., Costa C., Scranton R., Auwardt R., Boyer M., Cogdell P., Menahem S., Sheldrake J., Mount P., Fraenkel M., Bisscheroux P., Dempester J., Gleeson P., Harris G., Holmes C., Hyett K., Linton A., Miach P., Booth D., Druce L., Mantha M., Borg E., Green S., Killen J., Lynch Y., Colquhoun D., Herzig K., Row G., Addison J., Asa J., Beatson G., Calvird D., Edmunds J., Ferreira-Jardim A., Gwynne A., Mackay D., McLoughlin L., Wightwick C., Williams L., Ferrari P., Barry J., Hodson S., Zakrzewska W., Meagher E., Mulcahy M., Parnham A., Carney S., Garvey L., Gillies A., Hayes S., Mathew M., Fassett R., Anderson L., Clingeleffer C., Curnock A., Mayne L., Richardson D., Smith M., Smith S., Suranyi M., Howlin K., Chow J., Cleland B., Rayment G., Spicer T., Wong J., Wong M., Packham D., Alison C., Fraser I., Mitchell J., Nagle J., Brown F., Ellery C., Monkhouse J., Nandkumar J., Reith-Myers L., Gray N., Cocks C., Courtney M., Hollett P., Johnston C., Larsen H., Pollock A., Stewart S., Styles G., Wyndham R., Fanning M., Gibson W., Jackson S., Mannering M., Mercado E., Oliphant R., Sud K., Ubera N., Wood C., Karrasch J., Brinkley T., Estensen K., Moroney A., Sutton J., Warren R., Saltissi D., Jahke H., Roach H., Saltissi J., Wiederroth O'Brien M., Johnson D., Bali V., Evans M., Franzen K., Halbish S., Helyar J., Martin A., Mudge D., Sonnenburg K., Sudak J., Roger S., Almeida S., Andrews H., Bohringer L., Bouwhuis L., Brady L., Carpenter A., Warren S., Elias T., Bannister K., Chew G., Clarke J., Faull R., Hooper A., Jeffs L., Napier A., Peh C., Pirone K., Skilton F., Ranganathan D., Best J., Hart L., Healy H., Morgan C., Ratanjee S., Salisbury A., Jose M., Freeman J., Hamilton R., Kirkland G., Read G., Anderson H., Boekel K., Farrell M., Foreman A., Iliev K., Pedagogos E., Raspudic T., Pollock C., Cooper B., Kesselhut J., Macadam C., Pearse J., Rowland C., Tully H., Irish A., Dogra G., Coutts P., Hayes L., Khoo D., Nathoo B., Shakespeare K., Warger A., Gillin A., Burman J., George C., Sherwood S., Snelling P., Stevens C., Hutchison B., Luxton G., Devenny N., Herson H., Pellicano S., Kelly J., Coutelas J., Garlinge C., McClelland A., Pirabhahar S., Saleh H., Langham R., Englebright B., Giang M., Lanteri M., Mullins K., Turner C., Collett P., Stokoe S., Sutherland K., Talafua D., Talaulikar G., Clarkson A., Rees C., Carney G., Falk M., Gracey D., Jadeer A., Johnson P., Karpe K., Singer R., Walters G., McDonald S., Burgess J., Fischer K., Gentgall M., Hockley M., Veitch D., De Jersey P., Gillam A., Hartig V., Holland K., McArdle J., Washington W., Rangan G., Mikaheal M., Murie P., Perez N., Punnoose N., Smolonogov T., Taler N., Williams G., Wen C., Kohlhagen J., Wessels J., Johnson S., Reid A., Ryan J., Taprell D., Auinger M., Eigner M., Kodras K., Leithner C., Magpantay L., Marterer C., Prager R., Prinz C., Seiringer E., Kramar R., Mitter E., Stummvoll H., Dieplinger G., Wenzel R., Stolz G., Drose S., Edlinger E., Headlam-Leitner E., Miska H., Then M., Weninger S., Lhotta K., Neyer U., Dickie H., Smodek S., Sprenger-Mahr H., Rosenkranz A., Zitt E., Mayr B., Schinner A., Soltys G., Begin V., Brunet S., Cournoyer S., Gelinas M., Giroux C., Martineau J., Roy M., Savoie L., Agharazii M., Blouin J., Desmeules S., Langlois S., Samson F., Wong G., Constantini L., Jing J., Malko J., Rivers C., Rochester D., Skilling C., Wadgymar A., Wu G., Kates D., Husch J., Mantle M., Turri L., Barrett B., Curtis B., Greeley B., Hannaford M., Harnett J., Kelly M., Langille E., Morgan J., Murphy S., Karim M., Arbo T., Carpenito G., Chan V., DaRoza G., Friesen M., Kraus D., Lam S., Lange B., Minhas S., Starko R., Torng S., Vela K., Madore F., Roy P., Troyanov S., Bonnardeaux A., Lauzon L., Pichette V., Yeates K., Mahoney K., Myers C., Pilkey R., Moist L., Edgar M., House A., Kortas C., Mindorff S., Tam P., Chow S., Fung J., Nagai G., Ng P., Sikaneta T., Ting R., Forzley B., Clouatre Y., Cooper S., DaCosta H., Granger S., Valley S., Karunakaran S., Abdulhadi M., Altwasser C., Anderson S., Bergquist L., Wijeyesinghe C., Berst L., Horgan K., Coles K., Lotter T., Robson L., Barre P., Golden J., Golden M., Tanguay N., Rigatto C., Armstrong S., Fine A., Fontaine B., Friesen D., Henry S., Kraushar M., Reslerova M., Verrelli M., Rabbat C., Clase C., Suva G., Winegard N., Goldstein M., Curvelo S., Donnelly S., Huckle J., Marticorena R., Chan-Yan C., Chiu A., DeLuca L., Flamer D., Gill J., Jamal A., Jung B., Kiaii M., Landsberg D., Rozen N., Taylor P., Werb R., Pylypchuk G., Ahmed A., Barton J., Hundseth M., Kappel J., Keindel I., Klassen J., Pylypchuk S., Rindall M., Tobe S., Naimark D., Agelopoulos M., Chessman M., Hladunewich M., Perkins N., Sainsbury S., McCready W., Adams B., Tonelli M., Caldwell S., Kumar U., McMahon A., Nikitin S., Restall J., Treit S., Wysocki Y., Duncan J., Copland M., Jastrzebski J., Keown P., Kwan S., Rogers D., Shapiro J., Singh S., Sioson L., Yee K., Yeung C., Zacharias J., Bueti J., Dizon B., Lam H., Miller L., Ross M., Zarrillo M., Li Z., Wang C., Liu L., Hong M., Zheng H., Zuo W., Ge Z., Liu Q., Li Y., Sun K., Zhao R., Sun G., Wang F., Cui Z., Lou F., Du Y., Song L., Huang H., Song Z., Wang J., Zhou L., Wu R., Xiao R., Zhang Q., Duan N., Ju N., Wang A., Xu Z., Lu Z., Zhang Y., Zhao L., Zhang C., Mo Z., Xie Y., Xiong J., Chen J., Guo L., Zhao S., Peiskerova M., Jancova E., Kazderova M., Kobrova L., Gorun P., Kmentova T., Burgelova M., Lyerova L., Viklicky O., Berdych M., Nydlova Z., Jelinkova G., Moltas J., Pauzar T., Knetl P., Cahova J., Simkova J., Zakova M., Vankova S., Safarova R., Hruby M., Karlova R., Prikaska V., Sellenberg P., Vesela E., Malanova L., Vlasak J., Kaprova P., Novakova D., Kotherova K., Studenovska M., Christensen J., Solling J., Jepsen M., Kristensen V., Aerenlund H., Braemer-Jensen M., Kamper A., Raaschou S., Heaf J., Dreyer J., Freese P., Holm M., Munch M., Gade-Rasmussen E., Bredmose K., Daugaard H., Nielsen J., Friedberg M., Jensen D., Munk Plum M., Solling K., Dieperink H., Arp Nielsen L., Friborg E., Gloe-Jakobsen A., Thye Ronn P., Rasmussen K., Andersen C., Johansen A., Odum L., Ostergaard O., Pedersen L., Lykkegaard S., Aundal M., Faureholm Huess S., Danielsen H., Madsen J., Nyvang M., Ekstrand A., Boman H., Hartman J., Lipponen A., Lithovius R., Rauta V., Salmela A., Saloranta K., Forslund T., Koskiaho P., Jaaskelainen K., Kanninen M., Laine K., Asola M., Huhti J., Pentti M., Metsarinne K., Heiro M., Koivuviita N., Saarinen M., Tertti R., Choukroun G., Fournier A., Ducloux D., Marechal F., Simula Faivre D., Combe C., Douillet M., Lamblot T., Nardi H., Vendrely B., Bourbigot B., Ferlandin S., Zaoui P., Jouet C., Geffroy-Guiberteau S., Bugnazet L., Aldigier J., El Hamel-Belili C., Giraud S., Dussol B., Berland Y., Chollet M., Sichez H., Cristol J., Canaud B., Morena M., Rodriguez A., Kessler M., Mizejewski B., Risse B., Urena Torres P., Bou-Bekr M.A., Arezki C., Ras El Qdim P., Vela C., Borsato F., Talairach A., Normand M., Normand V., Rieu P., Gauthier B., Vigneron-Foy C., Wolak A., Menoyo V., Alos L., Caillette-Beaudoin A., Berger V., Al-Sarraf S., Konnerth I., Urban C., Weiner S., Boesken W., Jochum E., Kiefer C., Wagner A., Krumme B., Bohler J., Bonow B., Hohenstatt U., Mettang T., Rockel A., Langanke J., Lipponer H., Dunschen-Weimar G., Dunst R., Hubel E., Petrik R., Rengel R., Schmidgen M., Mayr H., Garschhammer C., Weirauch S., Anger H., Goock T., Mai A., Bast I., Suptitz C., Iwig B., Florschutz K., Hasselbacher R., Sauerbrey G., Delrieux S., Rau S., Poley M., Laux R., Schonfelder O., Kunowski G., Fuchs G., Hoffmann K., Schurger R., Brensing K., Guven Z., Immenkamp C., Kottmann C., Schmitt H., Schulz M., Arnold P., Knaup R., Schneider H., Siemsen H., Pyriki P., Korkemeyer F., Pyriki R., Siebrecht A., Schulz E., Krumwiede A., Kruse D., Lucke S., Keim H., Fink H., Fischer S., Klingbeil A., Kuhlmei K., Ortwein-Horn N., Merker L., Bayer B., Benamar K., Emmert S., Floten E., Holzheuer K., Lummer M., Ossendorf E., Scholz M., Oppitz M., Georgiew L., Tripps C., Wendehake M., Lange D., Pingel V., Brause M., Schanze W., Duygulu E., Dellanna F., Heinemann-Nieberding S., Sturmer C., Wieczorek K., Zarga O., Kullmer B., Kullmer S., Akin M., Gondolf M., Schutterle S., Walker G., Bertsch R., Seul M., Allendorff J., Siehler R., Stemmler S., Baldus M., Adler A., Harter S., Wurmell W., Moller M., Hame C., Muller M., Schreiber M., Schurfeld C., Millington-Herrmann M., Benschneider A., Gaffal J., Sprunken U., Bohling M., Wunderlich S., Schramm L., Kollenbrath C., Netzer K., Sieber T., Zimmermann J., Bellersen M., Uerkvitz M., David-Walek T., Hauschildt B., Leimenstoll G., Lonnemann G., Hilfenhaus M., Benedetto C., Stockmann S., Ichtiaris P., Jungmann A., Neumeier K., Stoof A., Bohmer K., Kirpal A., Knogl A., Flege F., Franke K., Groth P., Parensen E., Bockmann M., Przyklenk P., Piazolo L., Thinius-Jaudas L., Versen A., Hettich R., Arendt R., Geiger K., Hoppe H., Schwarting A., Beyer T., Faust J., Hazenbiller A., Tschirner S., Grupp C., Dorsch O., Eigner-Schmidtchen M., Michler K., Roth J., Schramm S., Waldmuller G., Riedl B., Vogele-Dirks H., Linz J., Biggar P., Hennemann H., Bauer G., Buchholz J., Fischer P., Bihlmaier W., Baumann A., Peichl B., Roser S., Ludewig S., Ricksgers M., Szendzielorz M., Baus A., Baust K., Schaller P., Schnellbacher G., Sorensen S., Buschges-Seraphin B., Hauenstein L., Hofmann B., Nikolay J., Merkel F., Nebel M., Petersen J., Schweb S., Zeissler H., Baumhackel K., Krauss A., Schafer R., Pastor A., Zielinski B., Strauss H., Theis H., Burkhardt K., Heckel M., Hussendorfer K., Bahner U., Brandl M., Hammerl-Kraus B., Herrmann D., Kramer H., Baudenbacher H., Blaser C., Buschmann G., Eckert G., Ehrich H., Hofmann K., Huller U., Geiger H., Becker B., Hoischen S., Bartel C., Hennig J., Obermuller N., Schulte C., Fischereder M., Burchardi F., Rupprecht H., Weidner S., Anders H., Andriaccio L., Lederer S., Ricken G., Strasser C., Lammert A., Schmitt W., Van Der Woude F., Langhauser B., Markau S., Osten B., Thiemicke D., Dorligschaw O., Weickert M., Breunig F., Denninger G., Osiek S., Rebstock W., Schulz P., Swoboda F., De Cicco D., Harlos J., Lebert A., Riegel M., Schmiedeke T., Hoffmann U., Nolle M., Jankrift P., Pfleiderer H., Witta J., Wittler B., Luth J., Dumann H., Habel U., Torp A., Sehland D., Tiess M., Etzold C., Friederiszik A., Morgenroth A., Dybala A., Suffel A., Leimbach T., Kron J., Sauer S., Meyer T., Meyer M., Lammers U., Bekman J., Holtz S., Kausler-Book B., Stobbe S., Hohage H., Heck M., Schulte F., Welling U., Zeh M., Seyfried J., De Heij T., Menzinger A., Weinreich T., Hopf M., Groll J., Kammholz K., Peters K., Schwietzer G., Kreft B., Weibchen U., Vosskuhler A., Hollenbeck M., Klaue K., Rzepucha E., Sperling K., Seeger W., Weyer J., Heine C., Kirste P., Zemann B., Alscher D., Rumpf D., Wullen B., Bengel A., Friedrich B., Kirschner T., Knodler U., Machleidt C., Niederstrasser K., Noack E., Wilhelm J., Heuer H., Dulea J., Piolot R., Rudke M., Treinen G., Elberg B., Hanke J., Nitschke T., Rosendahl C., Schmitz A., Schrader J., Kulschewski A., Lubcke C., Hammersen F., Luders S., Venneklaas U., Muhlfeld A., Arabi Al-Khanne F., Ketteler M., Politt D., Schuster C., Eitner F., Goretz U., Heidenreich S., Janssen U., Kranz A., Moormann E., Schneider B., Weber W., Frei U., Jovanovic T., Asmus H., Canaan-Kuhl S., Pannier L., Petersen S., Pluer M., Schaeffner E., Schafer C., Warncke S., Schmieder R., Donhauser C., Schulze B., Koziolek M., Bechtel W., Kurz B., Strutz F., Bramlage C., Dreyer S., Mommeyer E., Niemann J., Scheel A., Troche-Polzien I., Weber F., Heine G., Girndt M., Lizzi F., Rogacev K., Lindner T., Achenbach H., Peschel K., Beige J., Jentho S., Kreyssig C., Prill K., Renders L., Walcher J., Cerny S., Fulbier A., Kristen H., Nitschke M., Kramer J., Marek P., Meier M., Schlieter J., Heyne N., Bachmann F., Faber M., Klipp K., Kustner U., Risler T., Rath T., Ruf T., Budiman D., Seidel C., Weik S., Teo S.M., Lee L.Y., Azizah H., Faridunishah S.A., Foo S.M., Go K.W., Ghazali A., Koh K.H., Zaki M., Wong H.S., Bavanandan S., Boey L.M., Lily M., Wong S.L., Rosnawati Y., Zawawi N., Azimawati A., Hindun A., Hasnah J., Korina R., Yunaidah A., Noraidah P., Ong L.M., Noor Asma A., Liew Y.F., Rozina G., Cheong Y.H., Ang A.H., Dayang J., Lim L.S., Sukeri M., Ramli S., Zulkifli M., Wan Mahmood W.K., Goh B.L., Sarifah B., Bee B.C., Ramasamy C., Ruszarimah S., Liu W.J., Razali O., Haslinah S., Vaithilingam I., Jaaini A., Faridah L., Ng K.H., Krishnan P., Rosnah A.A., Nor Azizah A.S., Tam C.C., Tan S.H., Tan C.C., Shahnaz F.K., Wazir H., Munusamy P., Wan Shaariah M.Y., Chew T.F., Fuziah Z., Tan C.H.H., Maria L., Javelin P., Lim S.K., Nazatul S.B., Engkasan L.P., Tan S.Y., Wong M.G., Julita A.A., Ang 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Mathisen U., Pedersen M., Rumsfeld M., Toft I., Berget K., Landsverk K., Tveiten G., Wamstad H., Klinger M., Krajewska M., Golebiowski T., Kusztal M., Spiechowicz-Zaton U., Rutkowski B., Renke M., Tylicki L., Czekalski S., Koziol L., Wanic-Kossowska M., Wasik-Olejnik A., Nowicki M., Dryja P., Kurnatowska I., Zawiasa A., Ciszek M., Gomolka M., Mysliwiec M., Brzosko S., Mazerska M., Hruby Z., Koscielniak K., Stanek-Piotrowska M., Mesjasz J., Rudka R., Baranski M., Jupowiecki J., Klein D., Switalski M., Kuriga M., Ostrowski M., Lidman A., Linde T., Waltersson K., Weiss L., Andersson G., Lindell C., Welander G., Jacobson S., Edensjo P., Wallin J., Linder M., Karsberg M., Hellgren K., Lonn I., Frisenette-Fich C., Johansson A., Lundstrom A., Mauritz N., Stahl-Nilsson A., Tobafard N., Hellberg O., Ejemar E., Von Schmalensee N., Gunne T., Eriksson A., Ostberg S., Svensson C., Mulec H., Jacobsson A., Karlsson M., Onnermalm L., Osagie S., Ekengren U., Larsson M., Lindberger K., Olofsson A., Samuelsson O., Beagan L., Dezfoolian H., Just M., Ortegren L., Saeed A., Strand U., Ramsauer B., Hultstrom D., Nordlinder K., Sundberg I., Oqvist B., Green C., Fernstrom A., Cassel A., Goransson I., Gylling M., Jorgensen A., Sterner G., Christensson A., Hjelmstedt P., Nystrom A., Sundin P., Samuelsson I., Tidman M., Johansson M., Lofgren Andersson M., Ohman M., Andersson P., Hallberg Karlsson A., Ringstad L., Chittinandana A., Chailimpamontree W., Gojaseni P., Singprasert R., Tungsanga K., Amphun W., Intim P., Kanjanabuch T., Poowarattanakul D., Treratha C., Wongvan P., Jittikanont S., Suriya T., Indrasthitya P., Sumethkul V., Ingsathit A., Jansomwong J., Lertchalorarn K., Phachiyanukul V., Phiromkit T., Saengsri S., Vareesangthip K., Chawanasuntorapoj R., Kiattisunthorn K., Larpkitkachorn R., Webster J., Henderson J., Jayne D., Hollis J., Townsend K., Harron C., Bleakley N., Hanley N., Morgan S., Brittney L., Brown H., Maxwell P., Murtagh H., Thomas M., Burke E., Carmody M., Cox G., Dasgin J., Ali G., Whitehouse L., Williams V., Brown E., Dlelana G., Esson A., Fagerbrink S., Marshall F., Mazibuko B., Nelson C., Russell E., Williams R., Altmann P., McNichols-Thomas C., Parsons K., MacGregor M., McGowan J., Mead P., Gilbanks K., Sanderson M., Fluck R., Chandler G., Hulme L., Smith J., Tse Y., West C., Taylor J., Breakspear S., Burgess B., Isles C., Bell J., Duignan J., Gorman J., Swainson C., Beveridge C., Cairns A., Miller D., Paterson F., Smith L., Kumwenda M., Glover R., Geddes C., Gemmell C., Grieve I., Matthews E., McLaren B., Meyer B., Spiers A., Banks R., Apperley P., Patterson T., Paynter H., Scoble J., Thom D., Watkins J., Kalra P., Gowland S., Haydock L., Smart I., Bhandari S., Gillett P., James K., Lewis R., Melville H., Tamimi A., Williams P., Heath T., Small S., Paterson A., Gibson N., Laven C., Wilson T., Cairns H., Casley-Ready K., Warwick G., Fentum B., James J., Kumar T., Marshall R., Ratcliffe F., Shenton A., Warwicker P., Bowser M., Mumford C., 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Szymanski J., Almond M., Bourton L., Bromwich C., Dawson S., Mason S., Oliveira D., Ramkhelawon R., Tuazon J., Andrews P., Archer K., Moore A., Thomas G., Velazquez C., Mumtaz R., Roberts R., Farquhar F., Ott J., Fenwick S., Callaway A., Garrett P., Dees L., McDonagh U., Garner S., Zehnder D., Aldridge N., Dyer C., Gomez M., Hewins S., McCarthy K., Rush J., Spencer S., Harvey M., Mills H., Drew P., Henry M., Wilberforce S., Worth D., Adair Z., Hartley J., Jibani M., Jones D., Swan S., Shamp T., Alcorn H., Bookey J., Cannon C., Jarvis K., Muesing C., Murphy M., Muster H., Planting M., Strand C., Middleton J., Gitter K., Mace N., Schumm D., Pogue V., Alimohammadi B., Arora P., Herbert L., Cheng J., Dowie D., Mohan S., Peters G., Tuttle K., Albritton S., Benedetti R., Joshi S., Lund B., Shuler L., Trevino M., Mai K., Osborn T., Parekh R., Eustace J., Novak G., Patterson S., Lindsey C., Hill T., Liston M., Wiegmann T., Nagaria A., Hurd C., Hurst A., Omoscharka E., Parks S., Price V., 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N., Carreras A., Currie R., Donaldson O., Fjalling E., Gallagher M., Gibson K., Goddard J., Healy J., Hones L., Jardine M., Kwong I., Merai M., Murray S., Perkovic V., Rendina A., Gallo K., Caron S., Carlson K., Foley K., Matzek S., Mewhort L., O'Donoghue S., Perel-Winkler A., Terins T., Nie Q., Yu H., Ge L., Hao D., Li L., Pang X., Wei X., Yan G., Certikova Chabova V., Holst H., Molvadgaard T., Munksgaard D., Peltonen Y., Liabeuf S., Lebel C., Ouabou L., Bauer B., Bergmann K., Beusch M., Cavitt D., Drechsler C., Dulau I., Hugen K., Kempf S., Kuchenmeister B., Pscheidl V., Schmiedeke D., Schwarz M., Speerschneider K., Stahl B., Lim B.C., Nadia H., Zishareena M.F., Vasuthavan S., Ganesapillai A.T., Yuen S., Grobbee D., Bobbink I., Groot K., Sikking I., Raley J., Colban M., Smerud K., Trygg N., Waagaard E., Westad H., Rotkegel S., Spiechowicz U., Domoradzka M., Gawlowska M., Flygar A., Odmark I., Pettersson A., Blackwood S., Barclay J., Benham J., Brown R., Cureton L., Jackson D., Kennedy I., Leaper C., Taylor A., Winter C., Wise C., Nash M., Taylor Bennett A., Donaldson D., Chalmers K., Corderoy H., Bartkoske M., Bjerk C., Camarena A., Herskovitz L., Heuer C., Levin J., Robinson R., Wicklund B., Bentzel D., Cohen S., Costa C., Scranton R., Auwardt R., Boyer M., Cogdell P., Menahem S., Sheldrake J., Mount P., Fraenkel M., Bisscheroux P., Dempester J., Gleeson P., Harris G., Holmes C., Hyett K., Linton A., Miach P., Booth D., Druce L., Mantha M., Borg E., Green S., Killen J., Lynch Y., Colquhoun D., Herzig K., Row G., Addison J., Asa J., Beatson G., Calvird D., Edmunds J., Ferreira-Jardim A., Gwynne A., Mackay D., McLoughlin L., Wightwick C., Williams L., Ferrari P., Barry J., Hodson S., Zakrzewska W., Meagher E., Mulcahy M., Parnham A., Carney S., Garvey L., Gillies A., Hayes S., Mathew M., Fassett R., Anderson L., Clingeleffer C., Curnock A., Mayne L., Richardson D., Smith M., Smith S., Suranyi M., Howlin K., Chow J., Cleland B., Rayment G., Spicer T., Wong J., Wong M., Packham D., Alison C., Fraser I., Mitchell J., Nagle J., Brown F., Ellery C., Monkhouse J., Nandkumar J., Reith-Myers L., Gray N., Cocks C., Courtney M., Hollett P., Johnston C., Larsen H., Pollock A., Stewart S., Styles G., Wyndham R., Fanning M., Gibson W., Jackson S., Mannering M., Mercado E., Oliphant R., Sud K., Ubera N., Wood C., Karrasch J., Brinkley T., Estensen K., Moroney A., Sutton J., Warren R., Saltissi D., Jahke H., Roach H., Saltissi J., Wiederroth O'Brien M., Johnson D., Bali V., Evans M., Franzen K., Halbish S., Helyar J., Martin A., Mudge D., Sonnenburg K., Sudak J., Roger S., Almeida S., Andrews H., Bohringer L., Bouwhuis L., Brady L., Carpenter A., Warren S., Elias T., Bannister K., Chew G., Clarke J., Faull R., Hooper A., Jeffs L., Napier A., Peh C., Pirone K., Skilton F., Ranganathan D., Best J., Hart L., Healy H., Morgan C., Ratanjee S., Salisbury A., Jose M., Freeman J., Hamilton R., Kirkland G., Read G., Anderson H., Boekel K., Farrell M., Foreman A., Iliev K., Pedagogos E., Raspudic T., Pollock C., Cooper B., Kesselhut J., Macadam C., Pearse J., Rowland C., Tully H., Irish A., Dogra G., Coutts P., Hayes L., Khoo D., Nathoo B., Shakespeare K., Warger A., Gillin A., Burman J., George C., Sherwood S., Snelling P., Stevens C., Hutchison B., Luxton G., Devenny N., Herson H., Pellicano S., Kelly J., Coutelas J., Garlinge C., McClelland A., Pirabhahar S., Saleh H., Langham R., Englebright B., Giang M., Lanteri M., Mullins K., Turner C., Collett P., Stokoe S., Sutherland K., Talafua D., Talaulikar G., Clarkson A., Rees C., Carney G., Falk M., Gracey D., Jadeer A., Johnson P., Karpe K., Singer R., Walters G., McDonald S., Burgess J., Fischer K., Gentgall M., Hockley M., Veitch D., De Jersey P., Gillam A., Hartig V., Holland K., McArdle J., Washington W., Rangan G., Mikaheal M., Murie P., Perez N., Punnoose N., Smolonogov T., Taler N., Williams G., Wen C., Kohlhagen J., Wessels J., Johnson S., Reid A., Ryan J., Taprell D., Auinger M., Eigner M., Kodras K., Leithner C., Magpantay L., Marterer C., Prager R., Prinz C., Seiringer E., Kramar R., Mitter E., Stummvoll H., Dieplinger G., Wenzel R., Stolz G., Drose S., Edlinger E., Headlam-Leitner E., Miska H., Then M., Weninger S., Lhotta K., Neyer U., Dickie H., Smodek S., Sprenger-Mahr H., Rosenkranz A., Zitt E., Mayr B., Schinner A., Soltys G., Begin V., Brunet S., Cournoyer S., Gelinas M., Giroux C., Martineau J., Roy M., Savoie L., Agharazii M., Blouin J., Desmeules S., Langlois S., Samson F., Wong G., Constantini L., Jing J., Malko J., Rivers C., Rochester D., Skilling C., Wadgymar A., Wu G., Kates D., Husch J., Mantle M., Turri L., Barrett B., Curtis B., Greeley B., Hannaford M., Harnett J., Kelly M., Langille E., Morgan J., Murphy S., Karim M., Arbo T., Carpenito G., Chan V., DaRoza G., Friesen M., Kraus D., Lam S., Lange B., Minhas S., Starko R., Torng S., Vela K., Madore F., Roy P., Troyanov S., Bonnardeaux A., Lauzon L., Pichette V., Yeates K., Mahoney K., Myers C., 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A., Nikitin S., Restall J., Treit S., Wysocki Y., Duncan J., Copland M., Jastrzebski J., Keown P., Kwan S., Rogers D., Shapiro J., Singh S., Sioson L., Yee K., Yeung C., Zacharias J., Bueti J., Dizon B., Lam H., Miller L., Ross M., Zarrillo M., Li Z., Wang C., Liu L., Hong M., Zheng H., Zuo W., Ge Z., Liu Q., Li Y., Sun K., Zhao R., Sun G., Wang F., Cui Z., Lou F., Du Y., Song L., Huang H., Song Z., Wang J., Zhou L., Wu R., Xiao R., Zhang Q., Duan N., Ju N., Wang A., Xu Z., Lu Z., Zhang Y., Zhao L., Zhang C., Mo Z., Xie Y., Xiong J., Chen J., Guo L., Zhao S., Peiskerova M., Jancova E., Kazderova M., Kobrova L., Gorun P., Kmentova T., Burgelova M., Lyerova L., Viklicky O., Berdych M., Nydlova Z., Jelinkova G., Moltas J., Pauzar T., Knetl P., Cahova J., Simkova J., Zakova M., Vankova S., Safarova R., Hruby M., Karlova R., Prikaska V., Sellenberg P., Vesela E., Malanova L., Vlasak J., Kaprova P., Novakova D., Kotherova K., Studenovska M., Christensen J., Solling J., Jepsen M., Kristensen 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Samuelsson O., Beagan L., Dezfoolian H., Just M., Ortegren L., Saeed A., Strand U., Ramsauer B., Hultstrom D., Nordlinder K., Sundberg I., Oqvist B., Green C., Fernstrom A., Cassel A., Goransson I., Gylling M., Jorgensen A., Sterner G., Christensson A., Hjelmstedt P., Nystrom A., Sundin P., Samuelsson I., Tidman M., Johansson M., Lofgren Andersson M., Ohman M., Andersson P., Hallberg Karlsson A., Ringstad L., Chittinandana A., Chailimpamontree W., Gojaseni P., Singprasert R., Tungsanga K., Amphun W., Intim P., Kanjanabuch T., Poowarattanakul D., Treratha C., Wongvan P., Jittikanont S., Suriya T., Indrasthitya P., Sumethkul V., Ingsathit A., Jansomwong J., Lertchalorarn K., Phachiyanukul V., Phiromkit T., Saengsri S., Vareesangthip K., Chawanasuntorapoj R., Kiattisunthorn K., Larpkitkachorn R., Webster J., Henderson J., Jayne D., Hollis J., Townsend K., Harron C., Bleakley N., Hanley N., Morgan S., Brittney L., Brown H., Maxwell P., Murtagh H., Thomas M., Burke E., Carmody M., Cox G., 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- Abstract
Background: Lowering low-density lipoprotein (LDL) cholesterol with statin therapy has been shown to reduce the incidence of atherosclerotic events in many types of patient, but it remains uncertain whether it is of net benefit among people with chronic kidney disease (CKD). Method(s): Patients with advanced CKD (blood creatinine >=1.7 mg/dL [>= 150 mumol/L] in men or >=1.5 mg/dL [ >= 130 mumol/L] in women) with no known history of myocardial infarction or coronary revascularization were randomized in a ratio of 4:4:1 to ezetimibe 10 mg plus simvastatin 20 mg daily versus matching placebo versus simvastatin 20 mg daily (with the latter arm rerandomized at 1 year to ezetimibe 10 mg plus simvastatin 20 mg daily vs placebo). The key outcome will be major atherosclerotic events, defined as the combination of myocardial infarction, coronary death, ischemic stroke, or any revascularization procedure. Results A total of 9,438 CKD patients were randomized, of whom 3,056 were on dialysis. Mean age was 61 years, two thirds were male, one fifth had diabetes mellitus, and one sixth had vascular disease. Compared with either placebo or simvastatin alone, allocation to ezetimibe plus simvastatin was not associated with any excess of myopathy, hepatic toxicity, or biliary complications during the first year of follow-up. Compared with placebo, allocation to ezetimibe 10 mg plus simvastatin 20 mg daily yielded average LDL cholesterol differences of 43 mg/dL (1.10 mmol/L) at 1 year and 33 mg/dL (0.85 mmol/L) at 2.5 years. Follow-up is scheduled to continue until August 2010, when all patients will have been followed for at least 4 years. Conclusions SHARP should provide evidence about the efficacy and safety of lowering LDL cholesterol with the combination of ezetimibe and simvastatin among a wide range of patients with CKD.Copyright © 2010, Mosby, Inc. All rights reserved.
- Published
- 2010
5. Die Ca 2+ -Sensitizer CGP 48506 und EMD 57033, nicht aber der Na + -Kanal-Modulator BDF 9148, verlängern die Relaxation an isolierten Kardiomyocyten des Meerschweinchens
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Brixius, K., primary, Hoischen, S., additional, Zobel, C., additional, Lasek, K., additional, and Schwinger, R.H.G., additional
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- 2001
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6. Regional Expression and Functional Characterization of the L-type Ca2+-Channel in Myocardium from Patients with End-stage Heart Failure and in Non-failing Human Hearts
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Schwinger, R.H.G., primary, Hoischen, S., additional, Reuter, H., additional, and Hullin, R., additional
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- 1999
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7. Vorschlag einer MR-Stadieneinteilung der frühen rheumatoiden Arthritis an den Metakarpophalangeal- und proximalen Interphalangealgelenken
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Scheck, R., primary, Hoischen, S., additional, Willemsen, U., additional, Pfluger, T., additional, Küffer, G., additional, Krüger, K., additional, Schattenkirchner, M., additional, and Hahn, K., additional
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- 1997
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8. Einfluß einer veränderten extrazellulären K+- und Mg2+-Konzentration auf die intrazelluläre Ca2+-Homöostase, die Kontraktionskopplung und die Kraft-Frequenz-Beziehung am menschlichen Myokard
- Author
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Schwinger, R., Frank, K., Hoischen, S., Müller-Ehmsen, J., and Brixius, K.
- Abstract
Copyright of Herz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 1997
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9. Inotropic and coronary vasodilatory actions of the K-adenosine triphosphate channel modulator nicorandil in human tissue.
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Müller-Ehmsen, J, Brixius, K, Hoischen, S, and Schwinger, R H
- Abstract
The present study aimed to characterize the inotropic and vasodilatory properties of the K-ATP channel opener nicorandil (NIC) in isolated human cardiac tissue. For comparison, the Ca+2 channel blockers diltiazem (DIL) and nifedipine (NIF) have been studied. Concentration-dependent effects of NIC, DIL and NIF on the force of contraction (FOC) and the vascular tone have been studied on left ventricular papillary muscle strips (dilated cardiomyopathy, New York Heart Association Class IV, n = 20; nonfailing, donor hearts, n = 4), on right auricular trabeculae (nonfailing, n = 5) and on precontracted (prostaglandin F2 alpha: 0.3, 0.5 or 1 mumol/l) isolated human coronary artery rings (cardiac transplantation, n = 15). NIC, DIL and NIF concentration-dependently reduced the FOC of the papillary muscle preparations. However, the IC25 for the negative inotropic effect was significantly higher for NIC compared to DIL and NIF. The maximal negative inotropic effects of NIC, DIL and NIF (100 mumol/l) were -48.2 +/- 4.1, -92.9 +/- 0.9 and -93.4 +/- 1.4% of the basal FOC. The negative inotropic actions of NIC were similar in the human failing and the nonfailing ventricular and in the right atrial myocardium. Whereas pretreatment with methylene blue, an inhibitor of guanylyl cyclase, had no effect on the negative inotropic action of NIC, it was almost abolished by glibenclamide, a selective antagonist of the ATP-dependent K channels. NIC, DIL and NIF relaxed the coronary artery rings with 97.1 +/- 0.5, 90.7 +/- 0.9 and 96.4 +/- 0.7% of maximal relaxation (papaverine, 100 mumol/l). The rank order of vasodilatory potency was NIF > NIC > DIL. In conclusion, NIC is as effective as DIL and NIF in relaxing human coronary artery rings. However, NIC showed significantly lower negative inotropic effects when compared with the Ca+2 channel antagonists. The negative inotropic action of NIC is probably due to an interaction with the ATP-dependent K channels. In addition, activation of guanylyl cyclase does not seem to exert any negative inotropic action in the human myocardium.
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- 1996
10. Fruit and Vegetable Intake and Mortality in Adults undergoing Maintenance Hemodialysis.
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Saglimbene VM, Wong G, Ruospo M, Palmer SC, Garcia-Larsen V, Natale P, Teixeira-Pinto A, Campbell KL, Carrero JJ, Stenvinkel P, Gargano L, Murgo AM, Johnson DW, Tonelli M, Gelfman R, Celia E, Ecder T, Bernat AG, Del Castillo D, Timofte D, Török M, Bednarek-Skublewska A, Duława J, Stroumza P, Hoischen S, Hansis M, Fabricius E, Felaco P, Wollheim C, Hegbrant J, Craig JC, and Strippoli GFM
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- Aged, Cohort Studies, Diet Surveys, Female, Humans, Male, Middle Aged, Mortality, Renal Dialysis, Cardiovascular Diseases mortality, Diet statistics & numerical data, Fruit, Kidney Failure, Chronic therapy, Vegetables
- Abstract
Background and Objectives: Higher fruit and vegetable intake is associated with lower cardiovascular and all-cause mortality in the general population. It is unclear whether this association occurs in patients on hemodialysis, in whom high fruit and vegetable intake is generally discouraged because of a potential risk of hyperkalemia. We aimed to evaluate the association between fruit and vegetable intake and mortality in hemodialysis., Design, Setting, Participants, & Measurements: Fruit and vegetable intake was ascertained by the Global Allergy and Asthma European Network food frequency questionnaire within the Dietary Intake, Death and Hospitalization in Adults with ESKD Treated with Hemodialysis study, a multinational cohort study of 9757 adults on hemodialysis, of whom 8078 (83%) had analyzable dietary data. Adjusted Cox regression analyses clustered by country were conducted to evaluate the association between tertiles of fruit and vegetable intake with all-cause, cardiovascular, and noncardiovascular mortality. Estimates were calculated as hazard ratios with 95% confidence intervals (95% CIs)., Results: During a median follow up of 2.7 years (18,586 person-years), there were 2082 deaths (954 cardiovascular). The median (interquartile range) number of servings of fruit and vegetables was 8 (4-14) per week; only 4% of the study population consumed at least four servings per day as recommended in the general population. Compared with the lowest tertile of servings per week (0-5.5, median 2), the adjusted hazard ratios for the middle (5.6-10, median 8) and highest (>10, median 17) tertiles were 0.90 (95% CI, 0.81 to 1.00) and 0.80 (95% CI, 0.71 to 0.91) for all-cause mortality, 0.88 (95% CI, 0.76 to 1.02) and 0.77 (95% CI, 0.66 to 0.91) for noncardiovascular mortality and 0.95 (95% CI, 0.81 to 1.11) and 0.84 (95% CI, 0.70 to 1.00) for cardiovascular mortality, respectively., Conclusions: Fruit and vegetable intake in the hemodialysis population is low and a higher consumption is associated with lower all-cause and noncardiovascular death., (Copyright © 2019 by the American Society of Nephrology.)
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- 2019
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11. Dietary n-3 polyunsaturated fatty acid intake and all-cause and cardiovascular mortality in adults on hemodialysis: The DIET-HD multinational cohort study.
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Saglimbene VM, Wong G, Ruospo M, Palmer SC, Campbell K, Larsen VG, Natale P, Teixeira-Pinto A, Carrero JJ, Stenvinkel P, Gargano L, Murgo AM, Johnson DW, Tonelli M, Gelfman R, Celia E, Ecder T, Bernat AG, Del Castillo D, Timofte D, Török M, Bednarek-Skublewska A, Duława J, Stroumza P, Hoischen S, Hansis M, Fabricius E, Wollheim C, Hegbrant J, Craig JC, and Strippoli GFM
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- Cohort Studies, Europe epidemiology, Female, Humans, Male, Middle Aged, Prospective Studies, South America epidemiology, Cardiovascular Diseases epidemiology, Diet methods, Fatty Acids, Omega-3 administration & dosage, Renal Dialysis mortality
- Abstract
Background & Aims: Patients on hemodialysis suffer from high risk of premature death, which is largely attributed to cardiovascular disease, but interventions targeting traditional cardiovascular risk factors have made little or no difference. Long chain n-3 polyunsaturated fatty acids (n-3 PUFA) are putative candidates to reduce cardiovascular disease. Diets rich in n-3 PUFA are recommended in the general population, although their role in the hemodialysis setting is uncertain. We evaluated the association between the dietary intake of n-3 PUFA and mortality for hemodialysis patients., Methods: The DIET-HD study is a prospective cohort study (January 2014-June 2017) in 9757 adults treated with hemodialysis in Europe and South America. Dietary n-3 PUFA intake was measured at baseline using the GA
2 LEN Food Frequency Questionnaire. Adjusted Cox regression analyses clustered by country were conducted to evaluate the association of dietary n-3 PUFA intake with cardiovascular and all-cause mortality., Results: During a median follow up of 2.7 years (18,666 person-years), 2087 deaths were recorded, including 829 attributable to cardiovascular causes. One third of the study participants consumed sufficient (at least 1.75 g/week) n-3 PUFA recommended for primary cardiovascular prevention, and less than 10% recommended for secondary prevention (7-14 g/week). Compared to patients with the lowest tertile of dietary n-3 PUFA intake (<0.37 g/week), the adjusted hazard ratios (95% confidence interval) for cardiovascular mortality for patients in the middle (0.37 to <1.8 g/week) and highest (≥1.8 g/week) tertiles of n-3 PUFA were 0.82 (0.69-0.98) and 1.03 (0.84-1.26), respectively. Corresponding adjusted hazard ratios for all-cause mortality were 0.96 (0.86-1.08) and 1.00 (0.88-1.13), respectively., Conclusions: Dietary n-3 PUFA intake was not associated with cardiovascular or all-cause mortality in patients on hemodialysis. As dietary n-3 PUFA intake was low, the possibility that n-3 PUFA supplementation might mitigate cardiovascular risk has not been excluded., (Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.)- Published
- 2019
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12. The Association of Mediterranean and DASH Diets with Mortality in Adults on Hemodialysis: The DIET-HD Multinational Cohort Study.
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Saglimbene VM, Wong G, Craig JC, Ruospo M, Palmer SC, Campbell K, Garcia-Larsen V, Natale P, Teixeira-Pinto A, Carrero JJ, Stenvinkel P, Gargano L, Murgo AM, Johnson DW, Tonelli M, Gelfman R, Celia E, Ecder T, Bernat AG, Del Castillo D, Timofte D, Török M, Bednarek-Skublewska A, Duława J, Stroumza P, Hoischen S, Hansis M, Fabricius E, Felaco P, Wollheim C, Hegbrant J, and Strippoli GFM
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- Aged, Argentina epidemiology, Cohort Studies, Europe epidemiology, Female, Humans, Internationality, Male, Middle Aged, Mortality, Proportional Hazards Models, Renal Insufficiency, Chronic therapy, Turkey epidemiology, Cardiovascular Diseases mortality, Diet, Mediterranean, Dietary Approaches To Stop Hypertension, Renal Dialysis
- Abstract
Background Mediterranean and Dietary Approaches to Stop Hypertension (DASH) diets associate with lower cardiovascular and all-cause mortality in the general population, but the benefits for patients on hemodialysis are uncertain. Methods Mediterranean and DASH diet scores were derived from the GA
2 LEN Food Frequency Questionnaire within the DIET-HD Study, a multinational cohort study of 9757 adults on hemodialysis. We conducted adjusted Cox regression analyses clustered by country to evaluate the association between diet score tertiles and all-cause and cardiovascular mortality (the lowest tertile was the reference category). Results During the median 2.7-year follow-up, 2087 deaths (829 cardiovascular deaths) occurred. The adjusted hazard ratios (95% confidence intervals) for the middle and highest Mediterranean diet score tertiles were 1.20 (1.01 to 1.41) and 1.14 (0.90 to 1.43), respectively, for cardiovascular mortality and 1.10 (0.99 to 1.22) and 1.01 (0.88 to 1.17), respectively, for all-cause mortality. Corresponding estimates for the same DASH diet score tertiles were 1.01 (0.85 to 1.21) and 1.19 (0.99 to 1.43), respectively, for cardiovascular mortality and 1.03 (0.92 to 1.15) and 1.00 (0.89 to 1.12), respectively, for all-cause mortality. The association between DASH diet score and all-cause death was modified by age ( P =0.03); adjusted hazard ratios for the middle and highest DASH diet score tertiles were 1.02 (0.81 to 1.29) and 0.70 (0.53 to 0.94), respectively, for younger patients (≤60 years old) and 1.05 (0.93 to 1.19) and 1.08 (0.95 to 1.23), respectively, for older patients. Conclusions Mediterranean and DASH diets did not associate with cardiovascular or total mortality in hemodialysis., (Copyright © 2018 by the American Society of Nephrology.)- Published
- 2018
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13. Home versus in-centre haemodialysis for end-stage kidney disease.
- Author
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Palmer SC, Palmer AR, Craig JC, Johnson DW, Stroumza P, Frantzen L, Leal M, Hoischen S, Hegbrant J, and Strippoli GF
- Subjects
- Adult, Blood Pressure physiology, Humans, Quality of Life, Randomized Controlled Trials as Topic, Time Factors, Hemodialysis, Home adverse effects, Kidney Failure, Chronic therapy, Renal Dialysis adverse effects
- Abstract
Background: Home haemodialysis is associated with improved survival and quality of life in uncontrolled studies. However, relative benefits and harms of home versus in-centre haemodialysis in randomised controlled trials (RCTs) are uncertain., Objectives: To evaluate the benefits and harms of home haemodialysis versus in-centre haemodialysis in adults with end-stage kidney disease (ESKD)., Search Methods: The Cochrane Renal Group's Specialised Register was searched up to 31 October 2014., Selection Criteria: RCTs of home versus in-centre haemodialysis in adults with ESKD were included., Data Collection and Analysis: Data were extracted by two investigators independently. Study risk of bias and other patient-centred outcomes were extracted. Insufficient data were available to conduct meta-analyses., Main Results: We identified a single cross-over RCT (enrolling 9 participants) that compared home haemodialysis (long hours: 6 to 8 hours, 3 times/week) with in-centre haemodialysis (short hours: 3.5 to 4.5 hours, 3 times/weeks) for 8 weeks in prevalent home haemodialysis patients. Outcome data were limited and not available for the end of the first phase of treatment in this cross-over study which was at risk of bias due to differences in dialysate composition between the two treatment comparisons.Overall, home haemodialysis reduced 24 hour ambulatory blood pressure and improved uraemic symptoms, but increased treatment-related burden of disease and interference in social activities. Insufficient data were available for mortality, hospitalisation or dialysis vascular access complications or treatment durability., Authors' Conclusions: Insufficient randomised data were available to determine the effects of home haemodialysis on survival, hospitalisation, and quality of life compared with in-centre haemodialysis. Given the consistently observed benefits of home haemodialysis on quality of life and survival in uncontrolled studies, and the low prevalence of home haemodialysis globally, randomised studies evaluating home haemodialysis would help inform clinical practice and policy.
- Published
- 2014
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14. [Superselective occlusion of renal arteriovenous fistula with detachable spiral].
- Author
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Begemann PG, Hoischen SH, and Adam G
- Subjects
- Angiography, Arteriovenous Fistula diagnostic imaging, Creatinine blood, Equipment Design, Female, Humans, Kidney Function Tests, Middle Aged, Postoperative Complications diagnostic imaging, Treatment Outcome, Arteriovenous Fistula therapy, Embolization, Therapeutic instrumentation, Kidney blood supply, Kidney Failure, Chronic surgery, Kidney Transplantation, Postoperative Complications therapy
- Published
- 2003
- Full Text
- View/download PDF
15. Force/shortening-frequency relationship in multicellular muscle strips and single cardiomyocytes of human failing and nonfailing hearts.
- Author
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Brixius K, Hoischen S, Reuter H, Lasek K, and Schwinger RH
- Subjects
- Electric Stimulation, Female, Heart Ventricles cytology, Humans, Male, Middle Aged, Papillary Muscles physiology, Cardiomyopathy, Dilated physiopathology, Myocardial Contraction physiology, Myocardium cytology, Papillary Muscles cytology
- Abstract
Background: Force of contraction (FOC) frequency-dependently increases in multicellular muscle strip preparations of human nonfailing myocardium, whereas FOC declines in human failing myocardium with increasing stimulation frequency. We investigated whether these characteristics can be observed in single isolated myocytes., Methods and Results: Isolated multicellular muscle strip preparations and single isolated cardiomyocytes of failing (heart transplants, dilative cardiomyopathy; n = 11) and nonfailing (donor hearts; n = 11) human hearts were studied. The changes in contraction amplitude (cell shortening in micrometers) at increasing frequency of stimulation (0.5-2 Hz) were continuously recorded with a 1-dimensional high-speed camera that detected the cell edges and measured their distance during contraction. The increase in stimulation frequency was associated with a significant decrease in FOC (2 v 0.5 Hz; 68% basal) and a decrease in cell shortening of human left ventricular cardiomyocytes from failing hearts (2 v 0.5 Hz; 65% basal). In contrast, in human nonfailing myocardium, contraction increased at increasing stimulation frequencies (2 v 0.5 Hz; FOC, 180% basal; cell shortening, 129% basal)., Conclusions: The negative force-frequency relationship measured in multicellular preparations of failing human myocardium results from alterations at the single cell level.
- Published
- 2001
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16. [The Ca(2+) sensitizers CGP 48506 and EMD 57033, but not the Na(+) channel modulator BDF 9148, prolong relaxation in isolated cardiomyocytes of the guinea pig].
- Author
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Brixius K, Hoischen S, Zobel C, Lasek K, and Schwinger RH
- Subjects
- Animals, Cells, Cultured, Diastole drug effects, Dose-Response Relationship, Drug, Guinea Pigs, Male, Azetidines pharmacology, Azocines pharmacology, Calcium Channels drug effects, Cardiotonic Agents pharmacology, Myocardial Contraction drug effects, Quinolines pharmacology, Sodium Channels drug effects, Thiadiazines pharmacology
- Abstract
The sodium channel modulator DPI 201-106 has been described to posses Ca(2+)-sensitizing properties. Therefore, the present study investigated the inotropic effect of the Na(+)-channel modulator BDF 9148 (1 microM), a congener of DPI 201-106, in comparison with the Ca(2+)-sensitizers CGP 48506 (1-50 mumol/l) and EMD 57033 (1-30 mumol/l) in electrically driven left ventricular cardiomyocytes isolated from guinea pigs. The changes of the contraction amplitude in comparison to the basal cell shortening (cell shortening in micron and %) were continuously recorded with a one-dimensional high speed camera. BDF 9148, CGP 48506, and EMD 57033 exerted a significant increase in the contraction amplitude (p < 0.05 vs. control). The maximal positive inotropic effects of CGP 48506 (50 mumol/l) and EMD 57033 (30 mumol/l) were +249 +/- 30% and +226 +/- 28%, respectively. The corresponding value for BDF 9148 (1 mumol/l) was +176 +/- 16%. However, only the Ca(2+)-sensitizers CGP 48506 and EMD 57033, but not BDF 9148, prolonged the contractile twitch. Especially in patients with an already enhanced intracellular myocardial Ca(2+)-concentration, Ca(2+)-sensitizers, which impair relaxation, may be disadvantageous for therapeutical use despite their positive inotropic effect.
- Published
- 2001
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17. Human herpes virus 8 interleukin-6 homologue triggers gp130 on neuronal and hematopoietic cells.
- Author
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Hoischen SH, Vollmer P, März P, Ozbek S, Götze KS, Peschel C, Jostock T, Geib T, Müllberg J, Mechtersheimer S, Fischer M, Grötzinger J, Galle PR, and Rose-John S
- Subjects
- Amino Acid Sequence, Animals, Cell Differentiation drug effects, Cell Division drug effects, Cytokine Receptor gp130, GAP-43 Protein drug effects, GAP-43 Protein metabolism, Hematopoietic Stem Cells drug effects, Humans, Interleukin-6 genetics, Molecular Sequence Data, Neurons drug effects, PC12 Cells drug effects, Rats, Receptors, Interleukin metabolism, Receptors, Interleukin-6 metabolism, Recombinant Fusion Proteins metabolism, Recombinant Proteins genetics, Recombinant Proteins metabolism, Recombinant Proteins pharmacology, Viral Proteins genetics, Antigens, CD metabolism, Hematopoietic Stem Cells metabolism, Herpesvirus 8, Human, Interleukin-6 metabolism, Interleukin-6 pharmacology, Membrane Glycoproteins metabolism, Neurons metabolism, Viral Proteins metabolism, Viral Proteins pharmacology
- Abstract
Human herpes virus-8 (HHV8) encodes a cytokine named viral interleukin-6 (vIL-6) that shares 25% amino-acid identity with its human homologue. Human IL-6 is known to be a growth and differentiation factor of lymphatic cells and plays a potential role in the pathophysiology of various lymphoproliferative diseases. vIL-6 is expressed in HHV8-associated-diseases including Kaposi's sarcoma, Body-cavity-based-lymphoma and Castleman's disease, suggesting a pathogenetic involvement in the malignant growth of B-cell associated diseases and other malignant tumours. We expressed vIL-6 in Escherichia coli as a fusion protein with recombinant periplasmic maltose binding protein. After cleavage from the maltose binding protein moiety and purification, vIL-6 was shown to be correctly folded using circular dichroism spectroscopy. A rabbit antiserum was raised against the recombinant vIL-6 protein. vIL-6 turned out to be active on cells that expressed gp130 but no IL-6 receptor (IL-6-R) suggesting that, in contrast to human IL-6, vIL-6 stimulated gp130 directly. Accordingly, vIL-6 activity could be inhibited by a soluble gp130 Fc Fusion protein. vIL-6 was shown to induce neuronal differentiation of rat pheochromocytoma cells and to stimulate colony formation of human hematopoietic progenitor cells. Thus, vIL-6 exhibits biologic activity that has only been observed for the IL-6/soluble IL-6-R complex but not for IL-6 alone. These properties are important for the evaluation of the pathophysiological potential of vIL-6.
- Published
- 2000
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18. IL-6 receptor independent stimulation of human gp130 by viral IL-6.
- Author
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Müllberg J, Geib T, Jostock T, Hoischen SH, Vollmer P, Voltz N, Heinz D, Galle PR, Klouche M, and Rose-John S
- Subjects
- Aged, Animals, Antigens, CD biosynthesis, COS Cells, Chemical Precipitation, Cloning, Molecular, Cytokine Receptor gp130, DNA-Binding Proteins metabolism, Genetic Vectors, Growth Inhibitors pharmacology, Humans, Interleukin-6 genetics, Interleukin-6 metabolism, Male, Membrane Glycoproteins biosynthesis, Phosphorylation, Protein Binding, Receptors, Interleukin-6 metabolism, Recombinant Proteins isolation & purification, Recombinant Proteins pharmacology, STAT3 Transcription Factor, Sarcoma, Kaposi chemistry, Sarcoma, Kaposi immunology, Sarcoma, Kaposi pathology, Trans-Activators metabolism, Tumor Cells, Cultured, Viral Proteins genetics, Viral Proteins metabolism, Antigens, CD metabolism, Interleukin-6 physiology, Membrane Glycoproteins metabolism, Receptors, Interleukin-6 physiology, Signal Transduction immunology, Viral Proteins physiology
- Abstract
The genome of human herpes virus 8, which is associated with Kaposi's sarcoma, encodes proteins with similarities to cytokines and chemokines including a homologue of IL-6. Although the function of these viral proteins is unclear, they might have the potential to modulate the immune system. For viral IL-6 (vIL-6), it has been demonstrated that it stimulates IL-6-dependent cells, indicating that the IL-6R system is used. IL-6 binds to IL-6R, and the IL-6/IL-6R complex associates with gp130 which dimerizes and initiates intracellular signaling. Cells that only express gp130 but no IL-6R cannot be stimulated by IL-6 unless a soluble form of the IL-6R is present. This type of signaling has been shown for hematopoietic progenitor cells, endothelial cells, and smooth muscle cells. In this paper we show that purified recombinant vIL-6 binds to gp130 and stimulates primary human smooth muscle cells. IL-6R fails to bind vIL-6 and is not involved in its signaling. A Fc fusion protein of gp130 turned out to be a potent inhibitor of vIL-6. Our data demonstrate that vIL-6 is the first cytokine which directly binds and activates gp130. This property points to a possible role of this viral cytokine in the pathophysiology of human herpes virus 8.
- Published
- 2000
- Full Text
- View/download PDF
19. The enhanced contractility in phospholamban deficient mouse hearts is not associated with alterations in (Ca2+)-sensitivity or myosin ATPase-activity of the contractile proteins.
- Author
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Schwinger RH, Brixius K, Savvidou-Zaroti P, Bölck B, Zobel C, Frank K, Kranias EG, Hoischen S, and Erdmann E
- Subjects
- Animals, Female, Male, Mice, Mice, Mutant Strains, Calcium metabolism, Calcium-Binding Proteins deficiency, Calcium-Transporting ATPases deficiency, Muscle Proteins physiology, Myocardial Contraction physiology, Myosins metabolism
- Abstract
Work performing heart preparations from hypercontractile, phospholamban deficient mouse hearts showed no change in parameters of contraction or relaxation in response to isoproterenol stimulation. Thus, the aim of the present study was to investigate whether or not changes at the level of the contractile apparatus occur in addition to the altered expression of Ca2+-regulating proteins observed in these mouse models, e.g., phospholamban, ryanodine receptors. Triton-X skinned fiber preparations from phospholamban deficient (n = 9) and wild-type (n = 10) mice were used and the Ca2+-activated force as well as the myosin ATPase-activity were simultaneously measured. The tension dependent ATPase-activity was unchanged in phospholamban deficient animals when compared to controls. The SERCA 2a-inhibitor cyclopiazonic acid did not affect myosin ATPase-activity in this system. The Ca2+-sensitivity of Ca2+-activated force and myosin ATPase were unchanged as well. Comparison of the concentrations needed to achieve half maximal activation of the myosin ATPase-activity and force demonstrated that the Ca2+-sensitivity of the myosin ATPase was higher compared to the Ca2+-sensitivity of tension development. This holds true for phospholamban deficient mice (EC50 ATPase: 0.9 +/- 0.2 micromol/l; tension: 1.7 +/- 0.3 micromol/l; p < 0.001) and wild-type controls (1.1 +/- 0.01 micromol/l; 2.2 +/- 0.4 micromol/l; p < 0.01). The myosin ATPase-activity and force were correlated to each other in both, phospholamban deficient mice and controls and did not change at submaximal Ca2+ concentrations. The ATPase/ force-ratio, as a parameter of tension cost, was similar in either phospholamban deficient mice or controls. Thus, the present study provides evidence that at the level of the contractile proteins regulation of Ca2+-activated force and energy demand of force development are not altered in phospholamban deficient mice with enhanced myocardial performance. At the level of the regulation of crossbridge interaction, no adaptive or compensatory mechanisms have been initiated by ablation of phospholamban.
- Published
- 2000
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- View/download PDF
20. Potent vasodilatory with minor cardiodepressant actions of mibefradil in human cardiac tissue.
- Author
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Brixius K, Mohr V, Müller-Ehmsen J, Hoischen S, Münch G, and Schwinger RH
- Subjects
- Adult, Aged, Arteries drug effects, Arteries physiology, Calcium metabolism, Diltiazem pharmacology, Fluorescent Dyes, Fura-2, Humans, Mibefradil, Middle Aged, Myocardium metabolism, Nifedipine pharmacology, Benzimidazoles pharmacology, Calcium Channel Blockers pharmacology, Heart drug effects, Tetrahydronaphthalenes pharmacology, Vasodilator Agents pharmacology
- Abstract
1. The present study compared the cardiovascular effects of mibefradil (MIB), a novel Ca2+-channel antagonist with high selectivity for T-type Ca2+-channels to the effect of the L-type Ca2+-channel-antagonists nifedipine (NIF) and diltiazem (DIL) in left ventricular myocardium and coronary arteries of hearts obtained from patients suffering from dilated cardiomyopathy (NYHA IV). Right atrial myocardium from patients undergoing aortocoronary bypass surgery without signs of cardiac failure was studied as well. 2. NIF and DIL (100 micromol l(-1)) completely depressed force of contraction (FOC) in electrically driven left ventricular myocardium (NIF 6.5+/-1.4% and DIL 7.1+/-1.2% of control), whereas a similar concentration of MIB only reduced force of contraction to 55.1+/-4.0% of the basal FOC. The negative inotropic potency as measured by the concentration needed to reduce basal FOC for 25% was NIF (0.0095 micromol l(-1))>DIL (0.041 micromol l(-1))>MIB (9.47 micromol l(-1)). 3. All three Ca2+-channel antagonists were more potent in human atrial compared to human left ventricular myocardium to reduce FOC. 4. The rank order of Ca+-antagonistic moiety as measured by the decrease of the intracellular Ca2+-transient (fura-2 ratio method) was NIF>DIL>MIB. 5. All Ca2+-channel antagonists completely relaxed human coronary arteries (% of papaverine effect: MIB 81.7+/-5.5%, DIL 91.3+/-0.9%, NIF 96.4+/-3.7%) precontracted with PGF2alpha (0.3 micromol l(-1)). The rank order of vasodilatory potency was NIF (EC50; 0.02 micromol l(-1))>DIL (0.13 micromol l(-1))>MIB (2.05 micromol l(-1)). 6. The vasoselectivity measured by the ratio of the concentration needed to achieve a 25% decrease in force and the concentration needed for 25% vasodilatation was 316 for MIB, 1.5 for NIF and 1.0 for DIL. 7. The present study provides evidence that blockade of T-type Ca2+-channels (e.g. mibefradil) results in potent vasodilatory properties with only minor cardiodepressant effects.
- Published
- 1998
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21. T- and L-type Ca2+-channel antagonists reduce contractility in guinea pig cardiac myocytes.
- Author
-
Hoischen S, Brixius K, and Schwinger RH
- Subjects
- Animals, Calcium metabolism, Calcium Channels metabolism, Calcium Channels, L-Type, Diltiazem pharmacology, Guinea Pigs, Male, Mibefradil, Myocardium metabolism, Benzimidazoles pharmacology, Calcium Channel Blockers pharmacology, Calcium Channels drug effects, Myocardial Contraction drug effects, Tetrahydronaphthalenes pharmacology
- Abstract
The aim of this study was to investigate the influence of L- and T-type Ca2+-channel blockade on myocardial contractility in guinea pig cardiomyocytes. Left ventricular myocardium from guinea pig contains both L- and T-type Ca2+ channels. The T-type Ca2+ influx was inhibited with mibefradil (1-100 microM), a novel compound with a threefold higher affinity for T- compared with L-type Ca2+ channels. In comparison, L-type Ca2+ influx was reduced by the benzodiazepine diltiazem (1-100 microM). The effect of mibefradil and diltiazem on electrically driven (0.5 Hz) isolated cardiomyocytes (n = 12) was studied in a concentration-dependent manner. The change of the contraction amplitude (percentage of cell shortening) was continuously recorded with an one-dimensional high-speed camera. Both mibefradil and diltiazem concentration-dependently reduced (p < 0.05 vs. control) the contraction amplitude in isolated myocytes from guinea pig. The concentration at which the contraction amplitude of guinea pig cardiomyocytes was reduced by 50% (EC50) was 31.6 microM for diltiazem and 6.3 microM for mibefradil, indicating that the T-type Ca2+-channel blocker mibefradil is more potent in reducing contractility in guinea pig cardiac myocytes in comparison with the L-type Ca2+-channel antagonist diltiazem. Mean values for cell shortening in percentage +/- SEM for mibefradil (0, 1, 10, 100 microM) were 100%, 78 +/- 9.2%, 36 +/- 5.4%, and 24 +/- 3.6%. The corresponding values for diltiazem were 100%, 92 +/- 12.5%, 79 +/- 8.9%, and 35 +/- 2.6%. In contrast, the increase of the extracellular Ca2+ concentration (2-7.5 mM) resulted in a significant increase of the contraction amplitude (+213 +/- 14%). Therefore, blockade of the Ca2+ influx through voltage-dependent T- or L-type Ca2+ channels decreases contraction in isolated cardiac myocytes from guinea pigs containing L- and T-type Ca2+ channels.
- Published
- 1998
- Full Text
- View/download PDF
22. Unchanged protein expression of sarcoplasmic reticulum Ca2+-ATPase, phospholamban, and calsequestrin in terminally failing human myocardium.
- Author
-
Münch G, Bölck B, Hoischen S, Brixius K, Bloch W, Reuter H, and Schwinger RH
- Subjects
- Adult, Aged, Blotting, Western, Cardiomyopathy, Dilated physiopathology, Female, Humans, Male, Microscopy, Electron, Middle Aged, Myocardial Contraction, Myocardium ultrastructure, Calcium-Binding Proteins biosynthesis, Calcium-Transporting ATPases biosynthesis, Calsequestrin biosynthesis, Cardiomyopathy, Dilated metabolism, Myocardium metabolism, Sarcoplasmic Reticulum metabolism
- Abstract
The enhanced diastolic Ca2+ levels observed in cardiac myocytes from patients with idiopathic dilated cardiomyopathy (DCM) may be either a consequence of functional impairment of sarcoplasmic reticulum calcium-ATPase (SERCA 2) and its regulator protein phospholamban or due to a reduction in the number of SERCA 2 proteins. As different myocardial membrane preparations may lead to different accumulation of proteins, the present study evaluated two different membrane preparations, in human failing and nonfailing myocardium for comparison of SERCA 2 activity and the protein expression of SERCA 2 and phospholamban. Crude membranes and tissue homo-genates without any centrifugation steps were prepared from human nonfailing hearts (donor hearts, NF, n=18) and terminally failing hearts (heart transplant, DCM, n=18). Calsequestrin protein expression was used as an internal control for overall protein expression. In both crude membranes and homogenates maximal SERCA 2 activity (Vmax) was significantly reduced in failing heart preparations (NF crude membranes, 130+/-8; DCM crude membranes, 102+/-5 nmol ATP/mg protein per minute). In contrast, the protein expression of SERCA 2 (NF crude membranes, 488+/-35; DCM crude membranes, 494+/-42; P=0.92), phospholamban (NF crude membranes, 497+/-51; DCM crude membranes, 496+/-45; P=0.98) and calsequestrin (NF crude membranes, 109+/-06; DCM crude membranes, 107+/-08; P=0.84) was unchanged in NF and DCM hearts in both preparation methods. This was also the case when the protein expression was normalized to calsequestrin protein levels. Preparation of sarcoplasmic reticulum in crude membranes led to enhanced purification and consequently higher SERCA 2, phospholamban, and calsequestrin protein levels in crude membranes than in the homogenates, which was paralleled by an increase in SERCA 2 enzyme activity. In conclusion, the altered Ca2+ handling in DCM may be a consequence of reduced SERCA 2 enzyme activity and not the result of differences in protein expression of the Ca2+ regulating proteins SERCA 2, phospholamban, and calsequestrin in human myocardium. The present study emphasizes the importance of different myocardial membrane preparations with respect to quantitative investigations of protein expression and function.
- Published
- 1998
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- View/download PDF
23. Effect of cyclopiazonic acid on the force-frequency relationship in human nonfailing myocardium.
- Author
-
Schwinger RH, Brixius K, Bavendiek U, Hoischen S, Müller-Ehmsen J, Bölck B, and Erdmann E
- Subjects
- Adult, Calcium metabolism, Calcium-Transporting ATPases antagonists & inhibitors, Dose-Response Relationship, Drug, Humans, In Vitro Techniques, Middle Aged, Sarcoplasmic Reticulum enzymology, Sodium-Calcium Exchanger analysis, Calcium-Transporting ATPases physiology, Enzyme Inhibitors pharmacology, Indoles pharmacology, Myocardial Contraction drug effects
- Abstract
The present study investigated the functional role of the sarcoplasmic reticulum Ca++-ATPase in contraction and relaxation, intracellular Ca++-transients, as well as on the force-frequency relationship in human myocardium. The Ca++-ATPase activity of membrane vesicles isolated from sarcoplasmic reticulum (SR) obtained from nonfailing donor hearts (n = 7) was measured in the presence of cyclopiazonic acid (CPA, 0-30 microM), a highly specific inhibitor of the Ca++-ATPase of the SR (SERCA). The effects of CPA on parameters of contraction and relaxation, force-frequency relationship and [Ca++]i transients (with fura-2) were studied on isolated left ventricular muscle strips from human nonfailing myocardium. CPA concentration-dependently inhibited SERCA activity of isolated SR vesicles. In the presence of CPA (30 microM) the former positive force-frequency relationship in human left ventricular nonfailing myocardium became negative. Especially at high frequencies of stimulation, CPA decreased developed tension, peak rate of tension rise and systolic fura-2-light emission, whereas time to peak tension, time to peak [Ca++]i, time to 95% relaxation, diastolic tension and diastolic Ca++ levels were increased. Peak rate of tension decay and time to half-relaxation and half-decay of [Ca++]i were not altered significantly after treatment with CPA. These findings provide evidence that the SERCA plays a functional role in the frequency-dependent increase in force of contraction in human myocardium. Because an impaired function of the SERCA is predominantly followed by alterations of inotropic and to a lesser degree of lusitropic function, other important factors to lower [Ca++]i and influence relaxation may be present in human myocardium to compensate for the reduced SERCA activity, e.g., Na+-Ca++ exchanger.
- Published
- 1997
24. Effect of inotropic interventions on contraction and Ca2+ transients in the human heart.
- Author
-
Brixius K, Pietsch M, Hoischen S, Müller-Ehmsen J, and Schwinger RH
- Subjects
- Adult, Aged, Calcium pharmacology, Female, Humans, Isometric Contraction, Isoproterenol pharmacology, Male, Middle Aged, Ouabain pharmacology, Quinolines pharmacology, Thiadiazines pharmacology, Calcium metabolism, Cardiotonic Agents pharmacology, Myocardial Contraction drug effects, Myocardium metabolism
- Abstract
The present study investigated the influences of inotropic intervention on the intracellular Ca2+ transient (intracellular Ca2+ concentration ([Ca2+]i)) and contractile twitch. Isometric twitch and [Ca2+]i (fura 2 ratio method) were measured simultaneously (1 Hz, 37 degrees C) after stimulation with Ca2+ (0.9-3.2 mM), the cardiac glycoside ouabain (Oua; 0.1 microM), the beta1- and beta2-adrenoceptor-agonist isoprenaline (Iso; 1-10 nM), and the Ca2+ sensitizer EMD-57033 (30 microM) by using isolated human nonfailing right auricular trabeculae (n = 19). Inotropic interventions increased force of contraction and peak rate of tension rise (+T) significantly. Only Iso stimulated peak rate of tension decay (-T) higher than +T (P < 0.05), thereby reducing time of contraction (Ttwitch). EMD-57033 increased +T more effectively than -T and prolonged Ttwitch (P < 0.05). Ca2+, Oua, and Iso, but not EMD-57033, increased systolic Ca2+. Diastolic Ca2+ increased after stimulation with Oua or Ca2+, but not in the presence of EMD-57033. Iso shortened the Ca2+ transient and did not influence diastolic Ca2+. In conclusion, positive inotropic agents differently affect force and [Ca2+]i depending on their mode of action. Inotropic interventions influence diastolic Ca2+ and thus may be less advantageous in a situation with altered intracellular Ca2+ homeostasis (e.g., heart failure due to dilated cardiomyopathy).
- Published
- 1997
- Full Text
- View/download PDF
25. [A proposal for the MR staging of early rheumatoid arthritis in the metacarpophalangeal and proximal interphalangeal joints].
- Author
-
Scheck RJ, Hoischen SH, Willemsen UF, Pfluger T, Küffer G, Krüger K, Schattenkirchner M, and Hahn K
- Subjects
- Adult, Aged, Arthritis, Rheumatoid classification, Contrast Media, Female, Gadolinium, Gadolinium DTPA, Humans, Male, Middle Aged, Organometallic Compounds, Pentetic Acid analogs & derivatives, Prospective Studies, Arthritis, Rheumatoid diagnosis, Finger Joint pathology, Magnetic Resonance Imaging instrumentation, Magnetic Resonance Imaging methods, Metacarpophalangeal Joint pathology
- Abstract
Purpose: MRI can demonstrate pathology of joint disease in the early course of rheumatoid arthritis prior to destructions seen on conventional radiographs. In a prospective study, we tried to develop a systematical classification of joint pathology demonstrated by MRI, which would be essential for scoring the course of the disease., Patients and Method: Metacarpophalangeal and interphalangeal joints of 48 patients suffering from early rheumatoid arthritis (mean disease duration: 6.4 months) were evaluated by MRI using a high-resolution transmitter-receiver coil. Examinations included 2 mm sliced T2-, T1- and gadolinium enhanced T1-SE sequences in coronal and axial orientation. In consideration of pathological findings on MRI and histopathogenetical pathways of destruction in rheumatoid arthritis a MR-score (0-5) was established., Results: This allowed to score each joint examined: score 0 (normal) in 47.8%/49.5%, score 1 in 35.5%/50.5%, score 2 in 4.2%/0%, score 3 in 10.8%/0%, score 4 in 1.5%/0% of the metacarpophalangeal/interphalangeal joints, respectively., Conclusions: Using the MR-score a relative individual destruction number can be calculated, which may be used to follow up patients in the early course of rheumatoid arthritis (e.g. drug therapy studies). The presented MR scoring system has to be evaluated further in longitudinal studies and must be correlated to radiographical and clinical findings.
- Published
- 1997
- Full Text
- View/download PDF
26. Genomic sequences and structural organization of the human nidogen gene (NID).
- Author
-
Zimmermann K, Hoischen S, Hafner M, and Nischt R
- Subjects
- Base Sequence, Chromosome Mapping, DNA chemistry, Epidermal Growth Factor genetics, Exons, Humans, Molecular Sequence Data, Protein Precursors genetics, RNA, Messenger chemistry, Receptors, LDL genetics, Sequence Homology, Amino Acid, Membrane Glycoproteins genetics
- Abstract
Nidogen/entactin is a ubiquitous 150-kDa multidomain basement membrane protein. Since in vitro binding studies indicated that nidogen may function as a major mediator in basement membrane organization and assembly, analysis of gene structure and regulation of gene expression will help us to understand many biological processes that involve degradation and reorganization of the basement membrane zone. An approximately 100-kb region of genomic DNA encoding the human nidogen gene (NID) including 5' and 3' flanking sequences has been cloned and characterized by restriction mapping and sequencing. The entire gene is more than 90 kb in length and contains 20 exons. All introns interrupt protein coding sequences. The size of individual introns varies significantly, ranging from 0.6 to 18 kb. Its exon/intron structure revealed that the protein domains of human nidogen are organized in a domain-specific manner with various subdomains being encoded by individual exons, indicating that exon duplication and shuffling have played an important role in determining the present structure of the protein. Comparison of the exon organization with the recently published ascidian nidogen amino acid sequence strongly suggests that vertebrate nidogen might have evolved from a common ancestral precursor resembling ascidian nidogen.
- Published
- 1995
- Full Text
- View/download PDF
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