13 results on '"Studer, R."'
Search Results
2. Glycerol therapy of experimental cerebral microembolism.
- Author
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Welch, D M, Studer, R K, and Siegel, B A
- Published
- 1974
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3. Decreased cytosolic calcium and prostaglandin synthesis in prehypertensive rats.
- Author
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Craven, Patricia A., Studer, Rebecca K., DeRubertis, Frederick R., Craven, P A, Studer, R K, and DeRubertis, F R
- Published
- 1990
4. Concerns about the purported safety of elective flexible bronchoscopic-assisted intubation.
- Author
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Cooper RM, Heidegger T, Starzyk L, Villiger CR, Schumacher S, Studer R, Peter B, Nuebling M, Gerig HJ, and Schnider TW
- Published
- 2008
- Full Text
- View/download PDF
5. Regarding fiberoptic intubation and laryngeal morbidity.
- Author
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Cowles CE, Heidegger T, Starzyk L, Villiger C, Schumacher S, Studer R, Peter B, Nuebling M, Gerig HJ, and Schnider TW
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- 2008
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- View/download PDF
6. In vitro and in vivo testing of a novel regulatory system for gene therapy for intervertebral disc degeneration.
- Author
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Sowa G, Westrick E, Pacek C, Coelho P, Patel D, Vadala G, Georgescu H, Vo N, Studer R, and Kang J
- Published
- 2011
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7. Comparison of Macitentan and Bosentan on Right Ventricular Remodeling in a Rat Model of Non-vasoreactive Pulmonary Hypertension.
- Author
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Iglarz M, Landskroner K, Bauer Y, Vercauteren M, Rey M, Renault B, Studer R, Vezzali E, Freti D, Hadana H, Schläpfer M, Cattaneo C, Bortolamiol C, Weber E, Whitby BR, Delahaye S, Wanner D, Steiner P, Nayler O, Hess P, and Clozel M
- Subjects
- Animals, Bleomycin, Bosentan, Disease Models, Animal, Gene Expression Regulation, Heart Ventricles metabolism, Heart Ventricles physiopathology, Hypertension, Pulmonary chemically induced, Hypertension, Pulmonary genetics, Hypertension, Pulmonary metabolism, Hypertension, Pulmonary physiopathology, Hypertrophy, Right Ventricular chemically induced, Hypertrophy, Right Ventricular genetics, Hypertrophy, Right Ventricular metabolism, Hypertrophy, Right Ventricular physiopathology, Male, Pulmonary Artery drug effects, Pulmonary Artery metabolism, Pulmonary Artery physiopathology, Rats, Wistar, Time Factors, Vascular Remodeling drug effects, Endothelin Receptor Antagonists pharmacology, Heart Ventricles drug effects, Hypertension, Pulmonary drug therapy, Hypertrophy, Right Ventricular prevention & control, Pyrimidines pharmacology, Sulfonamides pharmacology, Ventricular Function, Right drug effects, Ventricular Remodeling drug effects
- Abstract
Aims: We compared the efficacy of macitentan, a novel dual endothelin A/endothelin B receptor antagonist, with that of another dual endothelin receptor antagonist, bosentan, in a rat model of non-vasoreactive pulmonary hypertension (PH) with particular emphasis on right ventricular (RV) remodeling., Methods and Results: Unlike monocrotaline or hypoxic/sugen rats, bleomycin-treated rats presented a non-vasoreactive PH characterized by the absence of pulmonary dilatation to adenosine. We therefore chose the bleomycin rat model to compare the effects of the maximally effective doses of macitentan and bosentan on pulmonary vascular and RV remodeling. Macitentan (100 mg·kg(-1)·d(-1)), but not bosentan (300 mg·kg(-1)·d(-1)), significantly prevented pulmonary vascular remodeling, RV hypertrophy, and cardiomyocyte diameter increase. Cardiac protection by macitentan was associated with a significant attenuation of genes related to cell hypertrophy and extracellular matrix remodeling. Microautoradiography and high performance liquid chromatography analysis showed greater distribution of macitentan than bosentan in the RV and pulmonary tissue., Conclusions: Macitentan was more efficacious than bosentan in preventing the development of pulmonary and RV hypertrophies in a model of non-vasoreactive PH. Greater ability to distribute into the tissue could contribute to the greater structural improvement by macitentan compared with bosentan.
- Published
- 2015
- Full Text
- View/download PDF
8. Fiberoptic intubation and laryngeal morbidity: a randomized controlled trial.
- Author
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Heidegger T, Starzyk L, Villiger CR, Schumacher S, Studer R, Peter B, Nuebling M, Gerig HJ, and Schnider TW
- Subjects
- Anesthesia, Inhalation, Erythema pathology, Female, Hoarseness epidemiology, Hoarseness etiology, Humans, Male, Prospective Studies, Vocal Cords injuries, Fiber Optic Technology, Intubation, Intratracheal adverse effects, Intubation, Intratracheal instrumentation, Larynx injuries, Postoperative Complications epidemiology
- Abstract
Background: Tracheal intubation with neuromuscular blocking agents is associated with a low incidence of minor vocal cord sequelae (8%). The aim of this noninferiority trial was to demonstrate that the frequency of vocal cord sequelae after fiberoptic intubation with a flexible silicone tube without neuromuscular blocking agents was less than 25% (maximum tolerable inferiority)., Methods: Two-hundred seventy patients were prospectively randomized to two groups. All intubations were performed by anesthesiologists with extensive experience in fiberoptic and conventional techniques. Fiberoptic nasotracheal intubation consisted of a bolus dose of 2 microg/kg fentanyl; 0.25 ml cocaine instillation, 10%, into nasal canals; cricothyroid injection of 2 ml lidocaine, 1%; bronchoscopy; administration of 0.3 mg/kg etomidate; and advancing a flexible silicone tube after loss of consciousness. Orotracheal intubation was performed with a polyvinyl chloride tube after induction with 2 microg/kg fentanyl, 2 mg/kg propofol, and 0.6 mg/kg rocuronium. Patients were examined by laryngoscopy before surgery, 24 h after surgery, and daily until complete restitution. Postoperative hoarseness was assessed by a standardized interview., Results: The incidence of vocal cord sequelae was 11 out of 130 (8.5%) in the fiberoptic group versus 12 out of 129 (9.3%) in the control group (chi-square = 0.057, df = 1, P = 0.81; upper limit of the one-sided 95% confidence interval for the difference: +5.1%). There were no persistent injuries. The incidence of postoperative hoarseness was 4% in both groups., Conclusions: Because fiberoptic intubation without neuromuscular blocking agents is safe regarding vocal cord sequelae, routine use is justified for anesthesiologists experienced in this technique.
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- 2007
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9. Differential effects of kinins on cardiomyocyte hypertrophy and interstitial collagen matrix in the surviving myocardium after myocardial infarction in the rat.
- Author
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Wollert KC, Studer R, Doerfer K, Schieffer E, Holubarsch C, Just H, and Drexler H
- Subjects
- Animals, Atrial Natriuretic Factor biosynthesis, Atrial Natriuretic Factor genetics, Bradykinin drug effects, Bradykinin pharmacology, Enzyme Induction drug effects, Extracellular Matrix pathology, Gene Expression Regulation drug effects, Heart Ventricles drug effects, Heart Ventricles pathology, Hemodynamics drug effects, Hypertrophy, Male, Myocardial Contraction drug effects, Myocardium metabolism, Nitric Oxide Synthase biosynthesis, Nitric Oxide Synthase genetics, Peptidyl-Dipeptidase A analysis, Polymerase Chain Reaction, Rats, Rats, Sprague-Dawley, Receptor, Bradykinin B2, Single-Blind Method, Adrenergic beta-Antagonists pharmacology, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors pharmacology, Bradykinin analogs & derivatives, Bradykinin Receptor Antagonists, Collagen analysis, Extracellular Matrix drug effects, Kinins physiology, Myocardial Infarction pathology, Myocardium pathology, Naphthyridines pharmacology
- Abstract
Background: Left ventricular remodeling after myocardial infarction (MI) involves the hypertrophic growth of cardiomyocytes and the accumulation of fibrillar collagen in the interstitial space. We evaluated the role of kinins in postinfarction ventricular remodeling and their potential contribution to the antiremodeling effects of ACE inhibition and angiotensin II type 1 (AT1) receptor blockade., Methods and Results: Rats underwent coronary artery ligation followed by chronic B2 kinin receptor blockade with icatibant. Additional groups of infarcted rats were treated with the ACE inhibitor lisinopril or the AT1 receptor antagonist ZD7155, each separately and in combination with icatibant. B2 kinin receptor blockade enhanced the interstitial deposition of collagen after MI, whereas morphological and molecular markers of cardiomyocyte hypertrophy (cardiac weight, myocyte cross-sectional area, prepro-atrial natriuretic factor mRNA expression) were not affected. Chronic ACE inhibition and AT1 receptor blockade reduced collagen deposition and cardiomyocyte hypertrophy after MI. The inhibitory action of ACE inhibition and AT1 receptor blockade on interstitial collagen was partially reversed by B2 kinin receptor blockade. However, B2 kinin receptor blockade did not attenuate the effects of ACE inhibition and AT1 receptor blockade on cardiomyocyte hypertrophy., Conclusions: (1) Kinins inhibit the interstitial accumulation of collagen but do not modulate cardiomyocyte hypertrophy after MI. (2) Kinins contribute to the reduction of myocardial collagen accumulation by ACE inhibition and AT1 receptor blockade. (3) The effects of ACE inhibition and AT1 receptor blockade on cardiomyocyte hypertrophy are related to a reduced generation/receptor blockade of angiotensin II.
- Published
- 1997
- Full Text
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10. Survival after myocardial infarction in the rat. Role of tissue angiotensin-converting enzyme inhibition.
- Author
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Wollert KC, Studer R, von Bülow B, and Drexler H
- Subjects
- Animals, Atrial Natriuretic Factor genetics, Base Sequence, Dose-Response Relationship, Drug, Heart drug effects, Hemodynamics drug effects, Lisinopril pharmacology, Male, Molecular Sequence Data, Myocardial Infarction mortality, Myocardial Infarction physiopathology, Organ Size drug effects, Peptidyl-Dipeptidase A genetics, Peptidyl-Dipeptidase A metabolism, RNA, Messenger analysis, Rats, Rats, Sprague-Dawley, Lisinopril therapeutic use, Myocardial Infarction drug therapy
- Abstract
Background: Chronic treatment with high doses of angiotensin-converting enzyme (ACE) inhibitors prolongs survival after myocardial infarction. Since the plasma renin-angiotensin system (RAS) is not consistently activated in the chronic phase after myocardial infarction, the beneficial effects of ACE inhibition have been attributed, in part, to inhibition of an activated tissue RAS. However, a relation between tissue ACE inhibition and long-term efficacy (ie, concerning left ventricular [LV] hypertrophy and survival) has not been established. The present study was designed to evaluate the impact of low-dose ACE inhibition (predominant inhibition of plasma ACE) and high-dose ACE inhibition associated with substantial tissue ACE inhibition) on reversal of LV hypertrophy and 1-year mortality after myocardial infarction in the rat., Methods and Results: Infarcted rats were randomized to placebo, low-dose lisinopril, or high-dose lisinopril (each, n = 80) and compared with sham-operated animals (n = 40). In a separate group of animals, tissue ACE activity was determined after 6 weeks of therapy, demonstrating that both regimens were effective with regard to both plasma and pulmonary ACE inhibition; however, only high-dose lisinopril inhibited renal ACE. Neither dose affected LV ACE activity and ACE mRNA levels as determined by competitive polymerase chain reaction, whereas LV ANF mRNA levels were significantly reduced by high-dose lisinopril. High-dose lisinopril reduced arterial blood pressure and normalized right ventricular and LV weight and resulted in a substantial reduction of 1-year mortality, whereas the low dose did not (1 year mortality: placebo, 56.3%; low dose, 53.3%; high dose, 22.9%, P < .0001 versus low dose and versus placebo)., Conclusions: Hemodynamically effective ACE inhibition is required for reduction of LV hypertrophy and long-term mortality after myocardial infarction in the rat. Sustained inhibition of renal ACE during long-term therapy may contribute to the beneficial effect of high-dose lisinopril. Low-dose lisinopril, although exerting sustained inhibition of the plasma ACE, does not improve survival after myocardial infarction.
- Published
- 1994
- Full Text
- View/download PDF
11. Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium.
- Author
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Hasenfuss G, Reinecke H, Studer R, Meyer M, Pieske B, Holtz J, Holubarsch C, Posival H, Just H, and Drexler H
- Subjects
- Adolescent, Adult, Analysis of Variance, Blotting, Western, Calcium metabolism, Calcium-Transporting ATPases isolation & purification, Cardiomyopathy, Dilated enzymology, Female, Humans, In Vitro Techniques, Kinetics, Male, Middle Aged, Myocardial Ischemia enzymology, Myosins analysis, Reference Values, Calcium-Transporting ATPases metabolism, Cardiomyopathy, Dilated physiopathology, Heart physiopathology, Myocardial Contraction, Myocardial Ischemia physiopathology, Myocardium enzymology, Sarcoplasmic Reticulum enzymology
- Abstract
Expression of sarcoplasmic reticulum (SR) Ca(2+)-ATPase was shown to be reduced in failing human myocardium. The functional relevance of this finding, however, is not known. We investigated the relation between myocardial function and protein levels of SR Ca(2+)-ATPase in nonfailing human myocardium (8 muscle strips from 4 hearts) and in myocardium from end-stage failing hearts with dilated (10 muscle strips from 9 hearts) or ischemic (7 muscle strips from 5 hearts) cardiomyopathy. Myocardial function was evaluated by the force-frequency relation in isometrically contracting muscle strip preparations (37 degrees C, 30 to 180 min-1). In nonfailing myocardium, twitch tension rose with increasing rates of stimulation and was 76% higher at 120 min-1 compared with 30 min-1 (P < .02). In failing myocardium, there was no significant increase in average tension at stimulation rates above 30 min-1. At 120 min-1, twitch tension was decreased by 59% (P < .05) in dilated cardiomyopathy and 76% (P < .05) in ischemic cardiomyopathy compared with nonfailing myocardium. Protein levels of SR Ca(2+)-ATPase, normalized per total protein or per myosin, were reduced by 36% (P < .02) or 32% (P < .05), respectively, in failing compared with nonfailing myocardium. SR Ca(2+)-ATPase protein levels were closely related to SR Ca2+ uptake, measured in homogenates from the same hearts (r = .70, n = 16, and P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
- Full Text
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12. Gene expression of the cardiac Na(+)-Ca2+ exchanger in end-stage human heart failure.
- Author
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Studer R, Reinecke H, Bilger J, Eschenhagen T, Böhm M, Hasenfuss G, Just H, Holtz J, and Drexler H
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- Adult, Animals, Base Sequence, Blotting, Western, Calcium metabolism, Calcium-Transporting ATPases biosynthesis, Female, Gene Library, Guinea Pigs, Humans, Male, Middle Aged, Molecular Sequence Data, Myosins biosynthesis, Oligodeoxyribonucleotides, RNA, Messenger analysis, RNA, Messenger biosynthesis, Rats, Reference Values, Restriction Mapping, Sarcoplasmic Reticulum metabolism, Sodium metabolism, Sodium-Calcium Exchanger, Atrial Natriuretic Factor biosynthesis, Cardiomyopathy, Dilated metabolism, Carrier Proteins biosynthesis, Coronary Disease metabolism, Gene Expression, Myocardium metabolism
- Abstract
The regulation of cytosolic Ca2+ concentration during excitation-contraction coupling is altered in the failing human heart. Previous studies have focused on disturbances in Ca2+ release and reuptake from the sarcoplasmic reticulum (SR), whereas functional studies of the cardiac Na(+)-Ca2+ exchanger, another important determinant of myocyte homeostasis, are lacking for the failing human heart. Using a cardiac Na(+)-Ca2+ exchanger cDNA recently cloned from a guinea pig cDNA library, we investigated the gene expression of the cardiac Na(+)-Ca2+ exchanger in relation to the SR Ca(2+)-ATPase. Expression of both genes was quantified in left ventricular myocardium from 24 failing human cardiac explants and 7 control heart samples in relation to beta-myosin heavy chain mRNA by slot blot analysis. Compared with patients with nonfailing hearts, patients with dilated cardiomyopathy (DCM, n = 13) showed a 55% increase in Na(+)-Ca2+ exchanger mRNA levels (P < .05 versus control value) and a 41% increase in patients with coronary artery disease (CAD, n = 11). In the same hearts, SR Ca(2+)-ATPase mRNA levels were decreased by 50% in DCM and by 45% in CAD (P < .05 for both versus control value). There was a positive correlation between Na(+)-Ca2+ exchanger and SR Ca(2+)-ATPase mRNA levels both in normal and failing human hearts, albeit with different slopes and intercepts of the regression line. The Na(+)-Ca2+ exchanger protein levels as assessed by Western blot analysis and normalized to beta-myosin heavy chain protein were increased in DCM and CAD (P < .05 and P < .01 versus control value, respectively), whereas SR Ca(2+)-ATPase protein levels were reduced (P < .05 for both groups versus control values). Thus, the Na(+)-Ca2+ exchanger gene expression is enhanced in failing human hearts and may, in part, compensate for the depressed SR function with regard to diastolic Ca2+ removal.
- Published
- 1994
- Full Text
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13. Attempts to enhance parathyroid selenomethionine accretion. Effect of EDTA in the rat.
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Potchen EJ and Studer R
- Subjects
- Animals, Calcium pharmacology, Injections, Intravenous, Radioisotopes, Radionuclide Imaging, Rats, Edetic Acid pharmacology, Methionine metabolism, Parathyroid Glands metabolism, Selenium metabolism
- Published
- 1968
- Full Text
- View/download PDF
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