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1. Effect of chronic intermittent hypoxia (CIH) on neuromuscular junctions and mitochondria in slow- and fast-twitch skeletal muscles of mice—the role of iNOS

Author

L. I. Bannow, G. A. Bonaterra, M. Bertoune, S. Maus, R. Schulz, N. Weissmann, S. Kraut, R. Kinscherf, and W. Hildebrandt

Subjects
Denervation, Muscle atrophy, Mitochondria, Fiber type, Oxidative stress, Neuromuscular junction, Diseases of the musculoskeletal system, RC925-935
Abstract

Abstract Background Obstructive sleep apnea (OSA) imposes vascular and metabolic risks through chronic intermittent hypoxia (CIH) and impairs skeletal muscle performance. As studies addressing limb muscles are rare, the reasons for the lower exercise capacity are unknown. We hypothesize that CIH-related morphological alterations in neuromuscular junctions (NMJ) and mitochondrial integrity might be the cause of functional disorders in skeletal muscles. Methods Mice were kept under 6 weeks of CIH (alternating 7% and 21% O2 fractions every 30 s, 8 h/day, 5 days/week) compared to normoxia (NOX). Analyses included neuromuscular junctions (NMJ) postsynaptic morphology and integrity, fiber cross-sectional area (CSA) and composition (ATPase), mitochondrial ultrastructure (transmission-electron-microscopy), and relevant transcripts (RT-qPCR). Besides wildtype (WT), we included inducible nitric oxide synthase knockout mice (iNOS−/−) to evaluate whether iNOS is protective or risk-mediating. Results In WT soleus muscle, CIH vs. NOX reduced NMJ size (− 37.0%, p < 0.001) and length (− 25.0%, p < 0.05) together with fiber CSA of type IIa fibers (− 14%, p < 0.05) and increased centronucleated fiber fraction (p < 0.001). Moreover, CIH vs. NOX increased the fraction of damaged mitochondria (1.8-fold, p < 0.001). Compared to WT, iNOS−/− similarly decreased NMJ area and length with NOX (− 55%, p < 0.001 and − 33%, p < 0.05, respectively) or with CIH (− 37%, p < 0.05 and − 29%, p < 0.05), however, prompted no fiber atrophy. Moreover, increased fractions of damaged (2.1-fold, p < 0.001) or swollen (> 6-fold, p < 0.001) mitochondria were observed with iNOS−/− vs. WT under NOX and similarly under CIH. Both, CIH- and iNOS−/− massively upregulated suppressor-of-cytokine-signaling-3 (SOCS3) > 10-fold without changes in IL6 mRNA expression. Furthermore, inflammatory markers like CD68 (macrophages) and IL1β were significantly lower in CIH vs. NOX. None of these morphological alterations with CIH- or iNOS−/− were detected in the gastrocnemius muscle. Notably, iNOS expression was undetectable in WT muscle, unlike the liver, where it was massively decreased with CIH. Conclusion CIH leads to NMJ and mitochondrial damage associated with fiber atrophy/centronucleation selectively in slow-twitch muscle of WT. This effect is largely mimicked by iNOS−/− at NOX (except for atrophy). Both conditions involve massive SOCS3 upregulation likely through denervation without Il6 upregulation but accompanied by a decrease of macrophage density especially next to denervated endplates. In the absence of muscular iNOS expression in WT, this damage may arise from extramuscular, e.g., motoneuronal iNOS deficiency (through CIH or knockout) awaiting functional evaluation.

Published
2022
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15. Cellular activities of factor XII in lung fibrosis

Author

F Schramm, S Hadzic, E Jablonska, A Birnhuber, K Rubio, L Schulte, M Kreuter, F Bonella, G Barreto, N Weissmann, G Kwapiszewska, T Renne, P Markart, K T Preissner, A Prasse, and M Wygrecka

Subjects
Medizin
Published
2022

16. Protection against pressure overload-induced right heart failure by uncoupling protein 2 silencing

Author

Oleg Pak, Rolf Schreckenberg, Daniela Haag, Annemarie Wolf, Ralph T. Schermuly, Christine Hirschhäuser, Natascha Sommer, Susanne Rohrbach, Matthias Hecker, Rainer Schulz, Martin Weber, Ludger Fink, N. Weißmann, Baktybek Kojonazarov, Ling Li, Azadeh Esfandiary, Werner Seeger, Akylbek Sydykov, Hossein Ardeschir Ghofrani, Hanna Sarah Kutsche, and Klaus-Dieter Schlüter

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, Cardiac output, Physiology, Hypertension, Pulmonary, Spotlight Original Articles, 030204 cardiovascular system & hematology, Collagen Type I, Mitochondria, Heart, Ventricular Function, Left, Pulmonary hypertension, Muscle hypertrophy, Pulmonary artery banding, 03 medical and health sciences, 0302 clinical medicine, Fibrosis, Physiology (medical), Internal medicine, Cardiac remodelling, medicine, Animals, Myocyte, Myocytes, Cardiac, Uncoupling Protein 2, Gene Silencing, Cells, Cultured, Heart Failure, Mice, Knockout, Pressure overload, Hypertrophy, Right Ventricular, Ventricular Remodeling, business.industry, Fibroblasts, medicine.disease, Cardiac protection, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Endocrinology, Ventricular Function, Right, Ventricular pressure, Reactive Oxygen Species, Cardiology and Cardiovascular Medicine, business
Abstract

Aims The role of uncoupling protein 2 (UCP2) in cardiac adaptation to pressure overload remains unclear. In a classical model of left ventricular pressure overload genetic deletion of UCP2 (UCP2−/−) protected against cardiac hypertrophy and failure. However, in UCP2−/− mice increased proliferation of pulmonary arterial smooth muscle cells induces mild pulmonary hypertension, right ventricular (RV) hypertrophy, and reduced cardiac output. This suggests a different role for UCP2 in RV and left ventricular adaptation to pressure overload. To clarify this situation in more detail UCP2−/− and wild-type mice were exposed to pulmonary arterial banding (PAB). Methods and results Mice were analysed (haemodynamics, morphometry, and echocardiography) 3 weeks after PAB or sham surgery. Myocytes and non-myocytes were isolated and analysed separately. Cell shortening of myocytes and fura-2 loading of cardiomyocytes were used to characterize their function. Brd assay was performed to study fibroblast proliferation. Isolated mitochondria were analysed to investigate the role of UCP2 for reactive oxygen species (ROS) production. UCP2 mRNA was 2.7-fold stronger expressed in RV myocytes than in left ventricular myocytes and stronger expressed in non-myocytes compared with myocytes. Three weeks after PAB, cardiac output was reduced in wild type but preserved in UCP2−/− mice. UCP2−/− had increased RV wall thickness, but lower RV internal diameters and displayed a significant stronger fibrosis. Cardiac fibroblasts from UCP2−/− had reduced proliferation rates but higher collagen-1 expression. Myocytes isolated from mice after PAB banding showed preserved function that was further improved by UCP2−/−. Mitochondrial ROS production and respiration was similar between UCP2−/− or wild-type hearts. Conclusion Despite a mild pulmonary hypertension in UCP2−/− mice, hearts from these mice are well preserved against additional pressure overload (severe pulmonary hypertension). This—at least in part—depends on different behaviour of non-myocytes (fibroblasts).

Published
2019
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18. Effect of chronic intermittent hypoxia (CIH) on neuromuscular junctions and mitochondria in slow- and fast-twitch skeletal muscles of mice-the role of iNOS

Author

L I, Bannow, G A, Bonaterra, M, Bertoune, S, Maus, R, Schulz, N, Weissmann, S, Kraut, R, Kinscherf, and W, Hildebrandt

Subjects
Mice, Knockout, Mice, Interleukin-6, Neuromuscular Junction, Animals, Nitric Oxide Synthase Type II, Atrophy, Hypoxia, Muscle, Skeletal, Mitochondria
Abstract

Obstructive sleep apnea (OSA) imposes vascular and metabolic risks through chronic intermittent hypoxia (CIH) and impairs skeletal muscle performance. As studies addressing limb muscles are rare, the reasons for the lower exercise capacity are unknown. We hypothesize that CIH-related morphological alterations in neuromuscular junctions (NMJ) and mitochondrial integrity might be the cause of functional disorders in skeletal muscles.Mice were kept under 6 weeks of CIH (alternating 7% and 21% OIn WT soleus muscle, CIH vs. NOX reduced NMJ size (- 37.0%, p0.001) and length (- 25.0%, p0.05) together with fiber CSA of type IIa fibers (- 14%, p0.05) and increased centronucleated fiber fraction (p0.001). Moreover, CIH vs. NOX increased the fraction of damaged mitochondria (1.8-fold, p0.001). Compared to WT, iNOSCIH leads to NMJ and mitochondrial damage associated with fiber atrophy/centronucleation selectively in slow-twitch muscle of WT. This effect is largely mimicked by iNOS

Published
2020

22. Loss of the classical transient receptor potential 3 partially protects from hypoxia-induced pulmonary hypertension in mouse

Author

Werner Seeger, Alexandra Erb, Alexander Dietrich, Lutz Birnbaumer, Simone Kraut, C Mayser, N Weißmann, and Monika Brosien

Subjects
Transient receptor potential channel, medicine.medical_specialty, Endocrinology, business.industry, Internal medicine, medicine, Hypoxia (medical), medicine.symptom, medicine.disease, business, Pulmonary hypertension
Published
2020
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28. FHL-1 Is Dispensable for Pressure Overload-Induced Maladaptive Right Ventricular Remodeling and Dysfunction

Author

R. T. Schermuly, J.-H. Fischer, Christine Veith, Akylbek Sydykov, N Weissmann, Bhola K. Dahal, Jochen Wilhelm, F. Grimminger, Grazyna Kwapiszewska, Ludger Fink, HA Ghofrani, D. Neghabian, Himal Luitel, C. Muntanjohl, and Bakytbek Egemnazarov

Subjects
Pressure overload, medicine.medical_specialty, business.industry, Internal medicine, medicine, Cardiology, Ventricular remodeling, medicine.disease, business
Published
2019
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32. Knock out of the NADPH oxidase Nox4 has no impact on life span in mice

Author

Eva Herrmann, N. Weißmann, Flávia Rezende, Sabine Harenkamp, Michael Seimetz, Susanne Schutz, Christoph Schürmann, and Katrin Schröder

Subjects
0301 basic medicine, Male, Telomerase, Aging, Clinical Biochemistry, Longevity, Primary Cell Culture, Gene Expression, Biochemistry, 03 medical and health sciences, Mice, Nox4, Gene expression, Animals, ddc:610, lcsh:QH301-705.5, Lung, Free-radical theory of aging, chemistry.chemical_classification, Mice, Knockout, Reactive oxygen species, lcsh:R5-920, NADPH oxidase, biology, urogenital system, Organic Chemistry, Wild type, NOX4, Telomere Homeostasis, Epithelial Cells, Cell biology, Telomere, Mice, Inbred C57BL, 030104 developmental biology, chemistry, lcsh:Biology (General), NADPH Oxidase 4, biology.protein, cardiovascular system, Female, lcsh:Medicine (General), Research Paper
Abstract

The free radical theory of aging suggests reactive oxygen species as a main reason for accumulation of damage events eventually leading to aging. Nox4, a member of the family of NADPH oxidases constitutively produces ROS and therefore has the potential to be a main driver of aging. Herein we analyzed the life span of Nox4 deficient mice and found no difference when compared to their wildtype littermates. Accordingly neither Tert expression nor telomere length was different in cells isolated from those animals. In fact, Nox4 mRNA expression in lungs of wildtype mice dropped with age. We conclude that Nox4 has no influence on lifespan of healthy mice., Graphical abstract fx1, Highlights • Nox4 is downregulated in murine lungs with increasing age. • Nox4 knock out does not influence total life span in mice. • Nox4 neither affects telomere length nor Tert expression.

Published
2017

33. The role of Mitochondrial Superoxide Release in Acute and Chronic Hypoxia Sensing and Signaling of the Pulmonary vasculature

Author

Susan Scheibe, HA Ghofrani, Natascha Sommer, Mareike Gierhardt, Katharina Schäfer, Oleg Pak, Michael P. Murphy, Maik Hüttemann, Akylbek Sydykov, R. T. Schermuly, Lawrence I. Grossman, and N Weissmann

Subjects
business.industry, Mitochondrial superoxide, Biophysics, Medicine, Cell Biology, Pulmonary vasculature, Pharmacology, business, Biochemistry, Chronic hypoxia
Published
2018
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34. Anti–Human Neutrophil Antigen-3a Induced Transfusion-Related Acute Lung Injury in Mice by Direct Disturbance of Lung Endothelial Cells

Author

Akylbek Sydykov, Yudy Tjahjono, Ulrich J. Sachs, Silke Werth, Stefan Hippenstiel, Behnaz Bayat, N Weissmann, and Sentot Santoso

Subjects
Lipopolysaccharides, Isoantigens, Endothelium, Neutrophils, Acute Lung Injury, Respiratory Mucosa, Lung injury, Biology, Antibodies, Capillary Permeability, Mice, Antigen, In vivo, medicine, Animals, Humans, Mice, Knockout, Membrane Glycoproteins, Lung, medicine.diagnostic_test, Albumin, Membrane Transport Proteins, NADPH Oxidases, Transfusion Reaction, medicine.disease, Actins, Disease Models, Animal, Bronchoalveolar lavage, medicine.anatomical_structure, NADPH Oxidase 2, Immunology, Endothelium, Vascular, Cardiology and Cardiovascular Medicine, Bronchoalveolar Lavage Fluid, Transfusion-related acute lung injury
Abstract

Objective— Antibodies against human neutrophil antigen-3a (HNA-3a) located on choline transporter-like protein 2 induce severe transfusion-related acute lung injury (TRALI). This study aims to identify the mechanism implicated in anti–HNA-3a-mediated TRALI. Approach and Results— Our analysis shows that anti–HNA-3a recognizes 2 choline transporter-like protein 2 isoforms (P1 and P2) on human microvascular endothelial cells from lung blood vessels but reacts only with the P1 isoform on neutrophils. Direct treatment of HNA-3a–positive endothelial cells with anti–HNA-3a, but not with anti–HNA-3b, leads to reactive oxygen species production, increased albumin influx, and decreased endothelial resistance associated with the formation of actin stress filaments and loosening of junctional vascular endothelium-cadherin. In a novel in vivo mouse model, TRALI was documented by significant increase in lung water content, albumin concentration, and neutrophil numbers in the bronchoalveolar lavage on injection of human anti–HNA-3a in lipopolysaccharides-treated, as well as nontreated mice. Interestingly, although neutrophil depletion alleviated severity of lung injury, it failed to prevent TRALI in this model. Infusion of anti–HNA-3a F(ab′) 2 fragments caused moderate TRALI. Finally, mice lacking nicotinamide adenine dinucleotide phosphate oxidase (NOX2 y/ - ) were protected from anti–HNA-3a-mediated TRALI. Conclusions— These data demonstrate the initiation of endothelial barrier dysfunction in vitro and in vivo by direct binding of anti–HNA-3a on endothelial cells. It seems, however, that the presence of neutrophils aggravates barrier dysfunction. This novel mechanism of TRALI primarily mediated by endothelial cell dysfunction via choline transporter-like protein 2 may help to define new treatment strategies to decrease TRALI-related mortality.

Published
2013
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35. The NADPH Oxidase Nox2 Mediates Vitamin D-Induced Vascular Regeneration in Male Mice

Author

Ralf P. Brandes, Matthias S. Leisegang, Andrea Babelova, N. Weißmann, Katrin Schröder, Michael Sze Ka Wong, and Valeska Helfinger

Subjects
0301 basic medicine, Male, medicine.medical_specialty, Endothelium, MAP Kinase Signaling System, Drug Evaluation, Preclinical, 030204 cardiovascular system & hematology, Vascular Remodeling, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Myeloid Cell Differentiation, Calcitriol, Internal medicine, medicine, Animals, Humans, Regeneration, chemistry.chemical_classification, Reactive oxygen species, NADPH oxidase, Membrane Glycoproteins, biology, Regeneration (biology), NOX4, NADPH Oxidases, Chemokine CXCL12, Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, chemistry, NOX1, Knockout mouse, NADPH Oxidase 2, cardiovascular system, biology.protein, MCF-7 Cells, Endothelium, Vascular, Carotid Artery Injuries, Reactive Oxygen Species
Abstract

1α,25-dihydroxy-vitamin D3 (1,25D) exerts protective effects in the vascular system and promotes myeloid cell differentiation, which are important sources of reactive oxygen species. Given that myeloid cell reactive oxygen species derives from Nox-family NADPH oxidases, we hypothesized that this enzyme family contributes to the beneficial effects of 1,25D on vascular regeneration. The function of Nox enzymes in this context was studied in the murine carotid artery electric injury regeneration model. Male mice were treated with daily injections of 1,25D (100 ng/kg · d) for 5 days and carotid injury was induced after 3 days. After injury, 1,25D increased the expression of Nox2 in the carotid artery. As determined by Evans blue staining on day 6, 1,25D improved vascular regeneration in a Nox2-dependent manner. Healing was lost in mice knockout for Nox2, but not in Nox1 or Nox4, knockout mice. Tissue specific knockouts demonstrated that the myeloid, but not the endothelial Nox2, was required for this effect. Mechanistically, the combination of injury and 1,25D induced the mobilization of angiogenic myeloid cells (AMCs) and increased the vascular expression of the cytokine stem cell derived factor (SDF)1, which attracts AMCs to the site of injury. Vitamin D in a Nox2-dependent manner activated MAPKs, and these are known to contribute to SDF1 induction. Accordingly, SDF1 induction was lost after deletion of Nox2. By inducing SDF1 and enhancing the number of AMCs, VitD3 is a novel approach to promote vascular repair.

Published
2016

36. COPD-associated pulmonary hypertension: clinical implications and current methods for treatment

Author

Hans Klose, Hossein Ardeschir Ghofrani, Jan Grimminger, N Weissmann, and Friedrich Grimminger

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, COPD, Referral, business.industry, Hypertension, Pulmonary, Public Health, Environmental and Occupational Health, Pulmonary disease, Disease, 030204 cardiovascular system & hematology, medicine.disease, Pulmonary hypertension, 03 medical and health sciences, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, 030228 respiratory system, medicine, Physical therapy, Immunology and Allergy, Humans, Complication, Intensive care medicine, business, Beneficial effects, Cause of death
Abstract

Chronic obstructive pulmonary disease is the fourth leading cause of death worldwide, one serious complication being pulmonary hypertension, which occurs in up to 30% of patients and increases mortality drastically. Difficulties in diagnosis and the unclear beneficial effects of PH-specific therapy have hitherto resulted in the absence of approved therapies. Consequently, PH and right heart failure in COPD are still currently treated according to symptoms and not underlying cause Areas covered: This review focuses on the current knowledge of its pathogenesis, clinical picture, diagnosis as well as methods for treatment Expert commentary: Since PH-COPD is an orphan disease with grievous consequences, and diagnosis as well as the right choice of possible treatment is crucial, referral to an expert center in cases of suspicion is necessary. Hitherto there is no officially approved treatment available even though several studies have shown notable improvement in selected individuals, making diagnostics, prognostic markers, and the search for therapeutic agents key issues of interest in this field.

Published
2016

37. The role of cytochrome c oxidase subunit 4 isoform 2 (Cox4i2) in chronic hypoxia induced pulmonary hypertension

Author

N Weissmann, Mareike Gierhardt, Natascha Sommer, F Jonas, L Grossman, Karin Quanz, W Seeger, Maik Hüttemann, Simone Kraut, and C Veith-Berger

Subjects
Pulmonary and Respiratory Medicine, Gene isoform, medicine.medical_specialty, biology, business.industry, Protein subunit, medicine.disease, Chronic hypoxia, Pulmonary hypertension, Endocrinology, Internal medicine, COX4I2, medicine, biology.protein, Cytochrome c oxidase, business
Published
2016
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38. Poster session 1

Author

J. Schlueter, T. Brand, D. J. Henderson, V. Boczonadi, P. Humbert, B. Chaudhry, D. Sedmera, J. Svatunkova, R. Kockova, B. Sankova, C. Lopez Sanchez, D. Franco, A. Aranega, V. Garcia-Martinez, E. Demina, V. Miroshikova, A. Denisenko, A. Schwarzman, F. Sanchez-Cabo, C. Torroja, A. Benguria, R. Buchan, P. Srivastava, F. Martinez, P. Barton, S. Cook, A. Dopazo, E. Lara-Pezzi, H. Rai, S. Kumar, A. K. Sharma, S. Mastana, A. Kapoor, C. M. Pandey, S. Agrawal, N. Sinha, J. Lipkova, M. Goldbergova, J. Parenica, J. Bienertova Vasku, A. Vasku, P. Kala, J. Spinar, L. Perez-Cabornero, D. Cantalapiedra, A. Forteza, R. Saez-Villaverde, J. Zumalde, V. Fernandez-Pedrosa, S. Zuniga-Trejos, M. Gil-Borja, M. Lazaro, S. Santillan, M. Costa, N. Cortez-Dias, P. Carrilho-Ferreira, D. Silva, C. Jorge, R. Placido, C. Calisto, M. Fiuza, A. Nunes Diogo, F. J. Enguita, H. H. W. Sillje, B. Lu, H. Yu, M. Zwartbol, W. P. Ruifrok, W. H. Van Gilst, R. A. De Boer, D. Zaliaduonyte-Peksiene, S. Simonyte, V. Lesauskaite, J. Vaskelyte, V. Mizariene, R. Zaliunas, W. Tigchelaar, E. Barlaka, A. Lazou, C. Del Giudice, E. Cipolletta, A. Anastasio, G. Santulli, M. Rusciano, A. S. Maione, P. Campiglia, M. Illario, B. Trimarco, G. Iaccarino, G. A. Frentzou, M. J. Drinkhill, N. A. Turner, S. G. Ball, J. F. X. Ainscough, L. Bertrand, F. Mailleux, J. Hammond, A. Ginion, L. Hue, J. L. Balligand, S. Horman, J. L. Vanoverschelde, C. Beauloye, B. Demeulder, S. L. Puhl, A. Mueller, Y. Devaux, D. R. Wagner, K. Roemer, M. Boehm, C. Maack, D. Miranda-Silva, I. Falcao-Pires, N. Goncalves, D. Moreira-Goncalves, A. F. Leite-Moreira, F. Mraiche, L. Fliegel, J. Xue, G. G. Haddad, L. C. Hsiao, C. Carr, Z. F. Cui, K. Clarke, M. A. D'amico, P. Izzicupo, A. Di Fonso, A. Bascelli, S. Gallina, A. Di Baldassarre, C. Silvestre, P. Fernandez, O. M. Pello, C. Indolfi, F. Civeira, R. Hutter, B. Ibanez, J. Chaves, J. Martinez-Gonzalez, V. Andres Garcia, A. Zabirnik, N. Smolina, A. Malashicheva, E. Omelchenko, T. Sejersen, A. Kostareva, C. Noack, M. P. Zafiriou, A. Renger, R. Dietz, H. J. Schaeffer, M. B. Bergmann, C. Zelarayan, S. Van Linthout, K. Miteva, M. P. Becher, M. Haag, J. Ringe, H.-P. schultheiss, M. Sittinger, C. Tschoepe, T. Kakuchaya, L. Bockeria, E. Golukhova, M. Eremeeva, N. Chigogidze, I. Aslanidi, I. Shurupova, A. Svobodov, A. A. Ramkisoensing, D. A. Pijnappels, J. Swildens, M. J. Goumans, M. J. Schalij, A. A. F. De Vries, D. E. Atsma, A. Gomes, G. M. Costa, C. A. Cordeiro, A. Matsuada, L. B. Rosario, A. P. Freire, M. Bousquenaud, M. Rolland-Turner, F. Maskali, L. Zhang, P. Y. Marie, F. Azuaje, A. J. Smith, G. M. Ellison, C. D. Waring, S. Purushothaman, D. Torella, B. Nadal-Ginard, M. H. Van Marion, D. W. J. Van Der Schaft, M.-J. Goumans, F. P. T. Baaijens, C. V. C. Bouten, N. Kraenkel, K. Kuschnerus, M. Mueller, T. Speer, S. Briand, M. Bader, P. Madeddu, T. F. Luescher, U. Landmesser, A. Papalamprou, C. Vicinanza, D. F. Goldspink, M. Noseda, S. J. Mcsweeney, T. Leja, E. Belian, I. Macaulay, F. Al-Beidh, S. Koenemann, M. S. Abreu Pavia, S. E. Jacobsen, M. D. Schneider, G. Foldes, Z. Bagyura, Z. Lendvai, D. Mathe, T. Nemeth, J. Skopal, I. Foldes, B. Merkely, S. E. Harding, A. J. Candasamy, R. S. Haworth, A. Boguslavsky, F. Cuello, M. J. Shattock, M. Mayr, M. Gautel, M. Avkiran, P. Leszek, B. Sochanowicz, M. Szperl, P. Kolsut, K. Brzoska, W. Piotrowski, T. Rywik, B. Danko, J. Rozanski, M. Kruszewski, N. Bouteldja, R. J. Woodman, C. L. Hewitson, E. Domingo, J. A. Barbara, A. A. Mangoni, R. Carnicer Hijazo, A. B. Hale, X. Liu, S. Suffredini, J. K. Bendall, G. B. S. Lim, N. J. Alp, K. M. Channon, B. Casadei, L. R. Moltzau, J. M. Aronsen, S. Meier, I. Sjaastad, T. Skomedal, J.-B. Osnes, F. O. Levy, E. Qvigstad, P. T. Wright, L. M. K. Pannell, A. R. Lyon, J. Gorelik, A. Guellich, S. F. Vatner, R. Fischmeister, B. Manoury, E. Dubois, J. Hamelet, A. Vanderper, P. Herijgers, D. Langin, F. Gartner, J. Gummert, H. Milting, G. Euler, M. Priess, J. Heger, T. Noll, R. Schulz, T. Doi, T. Akagami, T. Naka, T. Masuyama, M. Ohyanagi, M. Massaro, E. Scoditti, M. Pellegrino, M. A. Carluccio, C. Martines, C. Storelli, R. De Caterina, M. Falck-Hansen, M. E. Goddard, J. E. Cole, N. Astola, A. J. Cross, R. Krams, C. Monaco, M. F. Corsten, W. Verhesen, A. P. Papageorgiou, P. Carai, M. Lindow, S. Obad, G. Summer, L. De Rijck, S. Coort, M. Hazebroek, R. Van Leeuwen, M. Gijbels, M. P. J. De Winther, F. R. M. Stassen, S. Kauppinen, B. Schroen, S. Heymans, Z. Husti, V. Juhasz, L. Virag, A. Kristof, I. Koncz, T. Szel, I. Baczko, N. Jost, J. G. Y. Papp, A. Varro, A. Ghigo, A. Perino, F. Damilano, J. Leroy, V. O. Nikolaev, W. Richter, M. Conti, G. Vandecasteele, E. Hirsch, R. Ang, S. Sebastian, A. Ludwig, L. Birnbaumer, A. Tinker, E. A. Ertel, R. Sube, A. Opel, C. L-H Huang, A. Grace, N. Tribulova, J. Radosinska, B. Bacova, T. Benova, V. Knezl, J. Slezak, T. A. Matsuyama, T. Tanaka, T. Adachi, Y. Jiang, H. Ishibashi-Ueda, T. Takamatsu, J. Kornej, C. Reihardt, J. Kosiuk, A. Arya, G. Hindricks, V. Adams, D. Husser, A. Bollmann, S. Severi, M. Fantini, E. Ravagli, L. A. Charawi, D. Difrancesco, C. Poulet, L. Lu, U. R. Ravens, M. Hoch, T. Koenig, A. Gardiwal, B. Stapel, S. Erschow, A. Froese, B. Weinhold, R. Gerardy-Schahn, G. Klein, D. Hilfiker-Kleiner, K. Chinda, S. Palee, S. Surinkaew, M. Phornphutkul, S. Chattipakorn, N. Chattipakorn, B. Tuana, Z. Kohajda, A. A. Kristof, C. Corici, F. Fulop, N. L. Jost, V. Szuts, D. Menesi, G. L. Puskas, A. Zvara, N. Houshmand, J. G. Papp, N. Al-Shanti, M. Hancock, A. Venturini, C. Stewart, R. Ascione, G. Angelini, M.-S. Suleiman, A. Gonzalez-Tendero, I. Torre, F. Crispi, E. Gratacos, T. Tzanavari, E. Varela, A. Economides, S. Theocharis, C. Pantos, D. V. Cokkinos, A. Karalis, P. Hecker, V. Lionetti, W. C. Stanley, C. Ferrara, N. Piroddi, B. Scellini, C. Ferrantini, V. Sequiera, C. Remedios, L. Carrier, C. Tesi, J. Van Der Velden, C. Poggesi, V. Kooij, G. J. M. Stienen, D. Dooijes, s. Marston, C. Redwood, C. Dos Remedios, I. Diakonov, S. Tokar, M. Sikkel, S. Schlossarek, M. Sauer, A. Papageorgiou, S. Velthuis, E. Lutgens, M. Swinnen, N. Van Rooijen, J. Kzhyshkowska, P. Carmeliet, P. Garcia-Canadilla, F. Garcia-Garcia, I. Iruretagoiena, J. Dopazo, I. Amat-Roldan, M. H. Zhang, Y. H. Zhang, C. E. Sears, B. Wojtas, A. Llach, L. Hove-Madsen, V. Spinelli, L. Sartiani, M. Bucciantini, R. Coppini, E. Russo, A. Mugelli, E. Cerbai, M. Stefani, M. Ibrahim, P. Kukadia, M. Navaratnarajah, U. Siedlecka, C. Van Doorn, M. Yacoub, C. Terracciano, W. Song, N. Curtin, R. Woledge, S. Marston, M. Balteau, N. Tajeddine, G. Behets-Wydemans, C. Dessy, P. Gailly, W. J. Van Der Laarse, S. J. P. Bogaards, D. Van Groen, Y. Y. Wong, I. Schalij, A. Vonk Noordegraaf, F. M. Faz, B. Littlejohns, P. Pasdois, A. P. Halestrap, G. D. Angelini, S. Lemoine, V. Jaspard-Vinassa, F. Vigneron, P. Dos Santos, M. Popescu, A. Vlad, G. Isvoranu, L. Suciu, B. Marinescu, D. Dimulescu, L. Zagrean, P. W. M. Kleikers, K. Wingler, K. Radermacher, A. Sydykov, H. A. Ghofrani, N. Weissmann, H. H. W. Schmidt, A. Poddubnaya, K. E. M. Khurs, S. O. G. Smolenskaya, G. Szucs, Z. Murlasits, S. Torok, G. F. Kocsis, T. Csont, C. Csonka, P. Ferdinandy, R. Dongworth, D. M. Yellon, D. J. Hausenloy, Y. Y. Chen, W. S. Lian, C. F. Cheng, K. H. Khoo, T. C. Meng, G. Youcef, E. Belaidi, L. Fazal, M. P. Vinvent, D. De Paulis, G. Zadigue, C. Richer-Giudicelli, F. Alhenc-Gelas, M. Ovize, A. Pizard, R. Cal, J. Castellano, J. Farre, G. Vilahur, L. Badimon, V. Llorente-Cortes, H. Naz, M. Gharanei, C. Mee, H. Maddock, A. Hussain, O. Pisarenko, V. Shulzhenko, L. Serebryakova, I. Studneva, Y. Pelogeykina, D. Khatri, O. Tskitishvili, E. Barnucz, G. Veres, P. Hegedus, T. Radovits, S. Korkmaz, S. Klein, R. Zoller, M. Karck, G. Szabo, S. Morel, M. A. Frias, C. Rosker, R. W. James, S. Rohr, B. R. Kwak, V. Braunersreuther, B. Foglia, F. Mach, E. Shantsila, S. Montoro-Garcia, L. D. Tapp, S. Apostolakis, B. J. Wrigley, G. Y. H. Lip, E. Sokolowska, K. Przyborowski, K. Kramkowski, W. Buczko, A. Mogielnicki, U. Simonsen, E. R. Hedegaard, B. D. Nielsen, A. Kun, A. Hughes, C. Kroigaard, S. Mogensen, O. Frobert, K. Ait Aissa, J. P. Max, D. Wahl, T. Lecompte, P. Lacolley, V. Regnault, A. Novakovic, M. Pavlovic, A. Vranic, P. Milojevic, I. Stojanovic, M. Jovic, D. Nenezic, N. Ugresic, Q. Yang, G. W. He, L. Calvier, P. Reboul, B. Martin-Fernandez, V. Lahera, F. Zannad, V. Cachofeiro, P. Rossignol, N. Lopez-Andres, V. K. Pulakazhi Venu, R. Baetta, A. Bonomo, A. F. Muro, A. Corsini, A. L. Catapano, G. D. Norata, L. E. Viiri, L. E. Full, T. J. Navin, A. Didangelos, I. Seppala, T. Lehtimaki, A. H. Davies, R. Wait, D. Sedding, P. Stieger, C. Thoelen, S. Fischer, J. M. Daniel, R. Widmer-Teske, K. T. Preissner, N. Alenina, L. A. Rabelo, M. Todiras, V. N. Souza, J. M. Penninger, R. A. Santos, I. A. Leonova, S. A. Boldueva, V. S. Feoktistova, O. V. Sirotkina, M. G. Kolesnichenko, Z. Springo, P. Toth, P. Cseplo, G. Szijjarto, A. Koller, S. Puthenkalam, M. K. Frey, I. M. Lang, R. Madonna, H. Shelat, Y. J. Geng, T. Ziegler, V. Pfetsch, J. Horstkotte, C. Schwab, I. Rohwedde, R. Hinkel, Q. Di, S. Dietzel, U. Deutsch, C. Kupatt, I. Ernens, B. Lenoir, O. Fortunato, A. Caporali, E. Sangalli, D. Cordella, M. Marchetti, G. Spinetti, C. Emanueli, G. Arderiu, E. Pena, M. J. Forteza, V. Bodi, S. Novella, C. Alguero, I. Trapero, I. Benet, C. Hermenegildo, J. Sanchis, F. J. Chorro, A. Nemeth, S. Szabados, A. Cziraki, E. Sulyok, I. G. Horvath, M. Rauh, W. Rascher, I. Sikharulidze, I. B. Bakhlishvili, J. T. T. Laitinen, J. P. Hytonen, O. Leppanen, J. Taavitsainen, A. Partanen, P. Korpisalo, S. Yla-Herttuala, J. Lonn, J. Hallstrom, T. Bengtsson, M. C. Guisasola, E. Dulin, S. Stojkovic, C. Kaun, G. Maurer, K. Huber, J. Wojta, S. Demyanets, T. B. Opstad, A. Pettersen, S. Aakra, H. Arnesen, I. Seljeflot, M. Borrell-Pages, C. Romero, A. Toso, M. Leoncini, L. Tanini, T. Pizzetti, F. Tropeano, M. Maioli, P. Casprini, F. Bellandi, R. F. Antunes, J. C. Kaski, I. E. Dumitriu, E. Wu, A. A. L. Tareen, M. Udovychenko, I. Rudyk, K. Riches, L. Franklin, A. Maqbool, J. Bond, M. L. Koschinsky, D. J. O'regan, K. E. Porter, I. R. Parepa, A. I. Suceveanu, A. Suceveanu, L. Mazilu, L. Cojocaru, A. Rusali, L. A. Tuta, E. Craiu, D. Lindner, C. Zietsch, H.-P. Schultheiss, C. Tschope, D. Westermann, M. Miana, E. Martinez, R. Jurado, C. Delgado, N. Gomez-Hurtado, A. Briones, J. Young, T. J. Geng, A. Brodehl, T. Schmidt, O. Smolenskaya, C. Stegemann, D. Byzov, I. Mikhaylova, N. Chizh, E. Pushkova, O. Synchykova, B. Sandomirsky, O. Freylikhman, O. Rotar, N. Chromova, E. Moguchaya, V. Ivanenko, E. Kolesova, A. Erina, M. Boyarinova, A. Konradi, S. D. Preston, D. Baskaran, A. M. Plonczak, K. Norita, S. V. De Noronha, M. N. Sheppard, A. Haghikia, S. F. Hill, M. Hoepfner, B. Nitzsche, M. Schrader, F. Zengerling, B. Hoffmann, A. Pries, S. Gao, J. T. Laitinen, S. Laidinen, H. Markkanen, H. Karvinen, V. Marjomaki, I. Vajanto, T. T. Rissanen, K. Alitalo, P. Mello Ferrao, M. C. Waghabi, L. R. Garzoni, J. Ritterhoff, C. Weidenhammer, M. Voelkers, W. H. Zimmermann, J. Rabinowitz, P. Most, S. C. Gordts, I. Muthuramu, F. Jacobs, E. Van Craeyveld, E. Nefyodova, B. De Geest, D. R. Tribuddharat, D. R. Sathitkarnmanee, M. R. Buddhisa, M. S. Suwannasaen, D. R. Silarat, D. R. Ngamsangsirisup, D. R. Hawrylowicz, D. R. Lertmemongkolchai, S. Rain, M. L. Handoko, N. Westerhof, A. Vonk-Noordegraaf, F. S. De Man, A. S. Iakovleva, O. A. Mirolyubova, A. Berezin, T. A. Samura, Suwannasaen, Tippayawat, Ngamsangsirisup, D. R. Sutra, Hawrylowicz, Lertmemongkolchai, L. M. Lima, M. G. Carvalho, D. R. G. Junqueira, M. O. Sousa, A. Zampetaki, P. Willeit, L. Tilling, I. Drozdov, M. Prokopi, A. Shah, C. Boulanger, P. Chowienczyk, S. Kiechl, S. H. V. Oliveira, V. Kirillova, E. Prosviryakov, C. T. M. Van Der Pouw Kraan, F. J. P. Bernink, J. M. Baggen, L. Timmers, A. M. Beek, M. Diamant, A. C. Van Rossum, N. Van Royen, A. J. G. Horrevoets, J. E. A. Appelman, A. Zyatenkov, L. S. Kokov, Y. U. D. Volynskiy, M. Krestjyaninov, V. I. Ruzov, A. V. Villar, E. Martinez-Laorden, A. Almela, M. A. Hurle, M. L. Laorden, N. Apaijai, M. K. Mcmullen, J. M. Whitehouse, G. Shine, and A. Towell

Subjects
Gerontology, Physiology, business.industry, Physiology (medical), Cancer research, Medicine, SCRIB gene, Cardiology and Cardiovascular Medicine, business
Published
2012
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39. European Contegra Multicentre Study: 7-Year Results after 165 Valved Bovine Jugular Vein Graft Implantations

Author

Ute Blanz, Dietmar Boethig, Giovanni Stellin, N Weissmann, Thomas Breymann, Willem Daenen, R Hetzer, M A Wojtalik, George E. Sarris, C Planche, and V Tsang

Subjects
Heart Defects, Congenital, Male, Reoperation, Pulmonary and Respiratory Medicine, Cardiac Catheterization, medicine.medical_specialty, Time Factors, Adolescent, medicine.medical_treatment, Transplantation, Heterologous, Kaplan-Meier Estimate, Ventricular Outflow Obstruction, Risk Assessment, Risk Factors, Double outlet right ventricle, Internal medicine, medicine, Animals, Humans, Ventricular outflow tract, Prospective Studies, Cardiac Surgical Procedures, Child, Proportional Hazards Models, Ultrasonography, Tetralogy of Fallot, Cardiac catheterization, Endocarditis, business.industry, Graft Occlusion, Vascular, Infant, Newborn, Calcinosis, Infant, medicine.disease, Surgery, Europe, Transplantation, Stenosis, Treatment Outcome, Great arteries, Child, Preschool, Cardiology, Cattle, Female, Jugular Veins, Cardiology and Cardiovascular Medicine, business
Abstract

Objective: The valved bovine conduit “ Contegra” for RVOTreconstruction became availablefor clin- ical use within a 100% source data monitored and echo core lab controlled prospective European Multicentre Study, carried out from 1999 to 2006. We present the results of this study. Methods: A total of 165 Contegras were im- planted in 8 centres. The mean patient age was 3.9 years (2 days – 18 years, median 2.0). Total fol- low-up was 687 patient years. Diagnoses in- cluded: tetralogy of Fallot (64 patients, 39%), truncus arteriosus (50, 30%), double outlet right ventricle (16, 10%), aortic valve disease/Ross pro- cedure (11, 7%), pulmonary valve atresia (10, 6%), transposition of the great arteries (10, 6%), 4 oth- er malformations (2%). Previous procedures were: 82 patients (50%) – none; 37 (22%) – valved conduit implantation; 14 (8%) aortopulmonary shunt; 6 (4%) catheter intervention. Follow-up appointments which included standardised echo- cardiography investigations were scheduled at 1, 3, 6, and 12 months, then annually. We evaluated freedom from death, explantation, intervention, stenosis, insufficiency, and degeneration. Results were stratified by age, diagnosis group and con- duit size. Results: The 5-year freedom-from rates were: ex- plantation – 90% (for patients aged 1 to 10 years) and 68% (for younger patients); endocarditis – over 92%; catheter intervention – 74% (patients with congenital malformations); stenosis – 75% and more (any group); insufficiency – 50% (12 and 14 mm diameter conduits); any event – 13% (patients under 1 year), 58% (1 to 10 years), 82% (> 10 years). Trace or mild insufficiency was a fre- quent, but not progressive finding. Mild calcifica- tion was detected in only 8 examinations. Conclusions: The performance of the Contegra conduit compares well with that of homografts when used to reconstruct paediatric right ventric- ular outflow tracts. " heart valve surgery l " right ventricular outflow tract l" bovine valved conduit l" longterm followup l" homograft

Published
2009
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40. Preserved right ventricular function in mitochondrial uncoupling protein 2 deficient mice in pressure overload induced right ventricular insufficiency

Author

Baktybek Kojonazarov, R Schreckenberg, R. T. Schermuly, Klaus-Dieter Schlüter, W Seeger, Natascha Sommer, A Esfandiary, Daniela Haag, M. Hecker, Akylbek Sydykov, Rainer Schulz, Oleg Pak, HA Ghofrani, and N Weissmann

Subjects
Pulmonary and Respiratory Medicine, Pressure overload, medicine.medical_specialty, Endocrinology, Ventricular function, business.industry, Internal medicine, Uncoupling protein 2, Ventricular insufficiency, Deficient mouse, Cardiology, Medicine, business
Published
2015
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42. Pro-proliferative and inflammatory signaling converge on the FoxO1 transcription factor in pulmonary hypertension – a new therapeutic approach

Author

N Weissmann, F. Grimminger, Rajkumar Savai, S. S. Pullamsetti, Capecchi, R. T. Schermuly, Hamza M. Al-Tamari, Christian Muecke, W Seeger, Daniel Sedding, Baktybek Kojonazarov, and Rebecca Teske

Subjects
Pulmonary and Respiratory Medicine, Therapeutic approach, business.industry, Immunology, medicine, Cancer research, FOXO1, medicine.disease, business, Pulmonary hypertension, Transcription factor
Published
2015
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43. Pulmonale Hypertonie und schlafbezogene Atmungsstörungen

Author

N Weissmann, Werner Seeger, Rainer Schulz, and H. J. Eisele

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, business.industry, Hypoxia (medical), medicine.disease, Pulmonary hypertension, Cheyne–Stokes respiration, respiratory tract diseases, Hypocapnia, medicine.artery, Heart failure, Periodic breathing, Internal medicine, Pulmonary artery, medicine, Cardiology, Pulmonary venous hypertension, medicine.symptom, business
Abstract

Pulmonary hypertension (PH), i. e. an increase of mean pulmonary artery pressure above 20 mm Hg under resting conditions, can be observed in different forms of sleep-disordered breathing (SDB). In obstructive sleep apnea (OSA) the apnea-associated triggers of hypoxia and intrathoracic pressure swings lead to repetitive rises of pulmonary artery pressure during sleep. In 20 - 30 % of these patients daytime PH occurs. PH in the setting of OSA is usually mild and rarely causes clinically evident cor pulmonale. Effective CPAP therapy has a beneficial influence on pulmonary hemodynamics in OSA. Severe congestive heart failure (i. e. with a LVEF < 40 %) might provoke pulmonary venous hypertension and thereby stimulation of pulmonary stretch and irritant receptors. The ensuing hyperventilation leads to a decrease of pCO (2) levels below the apneic threshold and thus contributes to the emergence of Cheyne Stokes respiration (CSR) in up to one half of the affected patients. Patients suffering from advanced idiopathic pulmonary arterial hypertension (IPAH) might show a similar breathing pattern while asleep. Possible pathogenetic factors of the nocturnal periodic breathing occurring in end-stage IPAH are prolonged circulation times and hypocapnia. In conclusion, SDB might cause PH (OSA-associated PH). On the other hand, PH might lead to the development of SDB (CSR in congestive heart failure, periodic breathing in IPAH).

Published
2005
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44. [Pulmonary arterial hypertension--a disease of the immune system?]

Author

G, Riemekasten, W M, Kuebler, R, Schermuly, H-J, Seyfarth, J, Behr, C, Grohe, M M, Hoeper, A, Olschewski, G, Kwapiszewska, S, Ulrich, R, Voswinckel, N, Weissmann, Heinrich, Worth, R R, Viales, S S, Pullamsetti, and G, Grunig

Subjects
Immunity, Cellular, Receptors, Angiotensin, Receptors, Endothelin, Hypertension, Pulmonary, Antibody Formation, Humans, Adaptive Immunity, Immunity, Innate, Autoantibodies
Published
2014

45. Discovery and pharmacological characterization of a novel potent inhibitor of diacylglycerol-sensitive TRPC cation channels

Author

T, Maier, M, Follmann, G, Hessler, H-W, Kleemann, S, Hachtel, B, Fuchs, N, Weissmann, W, Linz, T, Schmidt, M, Löhn, K, Schroeter, L, Wang, H, Rütten, and C, Strübing

Subjects
Diglycerides, Structure-Activity Relationship, Dose-Response Relationship, Drug, Molecular Structure, Drug Discovery, Indans, Molecular Sequence Data, Humans, Research Papers, Cells, Cultured, TRPC Cation Channels
Abstract

The cation channel transient receptor potential canonical (TRPC) 6 has been associated with several pathologies including focal segmental glomerulosclerosis, pulmonary hypertension and ischaemia reperfusion-induced lung oedema. We set out to discover novel inhibitors of TRPC6 channels and investigate the therapeutic potential of these agents.A library of potential TRPC channel inhibitors was designed and synthesized. Activity of the compounds was assessed by measuring intracellular Ca(2+) levels. The lead compound SAR7334 was further characterized by whole-cell patch-clamp techniques. The effects of SAR7334 on acute hypoxic pulmonary vasoconstriction (HPV) and systemic BP were investigated.SAR7334 inhibited TRPC6, TRPC3 and TRPC7-mediated Ca(2+) influx into cells with IC50 s of 9.5, 282 and 226 nM, whereas TRPC4 and TRPC5-mediated Ca(2+) entry was not affected. Patch-clamp experiments confirmed that the compound blocked TRPC6 currents with an IC50 of 7.9 nM. Furthermore, SAR7334 suppressed TRPC6-dependent acute HPV in isolated perfused lungs from mice. Pharmacokinetic studies of SAR7334 demonstrated that the compound was suitable for chronic oral administration. In an initial short-term study, SAR7334 did not change mean arterial pressure in spontaneously hypertensive rats (SHR).Our results confirm the role of TRPC6 channels in hypoxic pulmonary vasoregulation and indicate that these channels are unlikely to play a major role in BP regulation in SHR. SAR7334 is a novel, highly potent and bioavailable inhibitor of TRPC6 channels that opens new opportunities for the investigation of TRPC channel function in vivo.

Published
2014

46. Arachidonic acid/cytochrome p450-derived mediators decrease hypoxic pulmonary vasoconstriction in isolated, ventilated and perfused mouse lungs

Author

J Bier, M. Heipel, F. Grimminger, D Peters, W Seeger, R. T. Schermuly, Karin Quanz, Ladislau Kiss, N. Weißmann, and Alexandra Erb

Subjects
Pulmonary and Respiratory Medicine, chemistry.chemical_compound, chemistry, Biochemistry, biology, Hypoxic pulmonary vasoconstriction, biology.protein, Cytochrome P450, Arachidonic acid, Pharmacology
Published
2014
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47. P66shc deficient mice develope decreased right heart hypertrophy via a Cyclophilin D dependent mechanism in hypoxia-induced pulmonary hypertension

Author

R Schreckenberg, R. T. Schermuly, N Weissmann, Natascha Sommer, A Ghofrani, Rainer Schulz, K Schlueter, and Mareike Gierhardt

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, business.industry, Hypoxia (medical), medicine.disease, Pulmonary hypertension, Cyclophilin D, Muscle hypertrophy, Endocrinology, Internal medicine, Right heart, medicine, Deficient mouse, medicine.symptom, business
Published
2014
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48. A possible role of serotonin for the development of tobacco smoke-induced lung emphysema and pulmonary hypertension

Author

Alexandra Pichl, Nirmal Parajuli, Daniela Haag, F. Grimminger, Mariola Bednorz, Jan Grimminger, HA Ghofrani, Werner Seeger, Athanasios Fysikopoulos, N Weissmann, Rudolf Reiter, R. T. Schermuly, and Michael Seimetz

Subjects
Pulmonary and Respiratory Medicine, medicine.medical_specialty, business.industry, Internal medicine, Cardiology, Medicine, Lung emphysema, Serotonin, business, medicine.disease, Pulmonary hypertension, Tobacco smoke
Published
2014
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