naeije robert (26 Ergebnisse)

Hardcover. Zustand: Wie neu. privately owned book. as new from the publisher. remains wrapped in plastic. language - english.

Zustand: New. This is a Brand-new US Edition. This Item may be shipped from US or any other country as we have multiple locations worldwide.

Zustand: New. This is a Brand-new US Edition. This Item may be shipped from US or any other country as we have multiple locations worldwide.

Zustand: Sehr gut. Zustand: Sehr gut | Seiten: 316 | Sprache: Englisch | Produktart: Bücher | The major characteristic pathological findings of pulmonary vascular remodelling are increased wall thickening of pulmonary vessels and mus- larization of small arteries. In laboratory animals, decreased ambient oxygen concentrations cause similar pathological findings, including pulmonary smooth muscle hypertrophy and proliferation [22,23]. It has been suggested that proliferation of pulmonary arterial smooth muscle cells (PASMC) is a key component of pulmonary vascular remodelling, and several in vitro studies have also addressed that exposure to hypoxia can stimulate prolife- tion of PASMC [13,4,1]. The proliferation of the PASMC begins when the cells enter into the cell cycle. The most important molecular event necessary for the progress of the cell cycle is phosphorylation of retinoblastoma protein by cyclin-dependent kinase (CDK)-cyclin complexes. The CDK activity can be inhibited by CDK inhibitors and the expression of CDK inhibitor is a major regulator of the transition between each phase of the cell cycle [7]. Previous studies have noted that CDK inhibitor p27 plays an important role in the inhibition of the CDK activity and proliferation in vascular smooth muscle cells [2,3]. The G1 phase in severe hypoxia is suggested to involve the CKI p27, because the expression of p27 increased in several cell-lines when they were exposed to extreme hypoxia [20,5]. Previous reports indicate that hypoxia decreases the p27 expression in the murine lung [23,24] and we found that PGI2 suppresses hypox- induced proliferation of PASMC and maintains p27 in PASMC [20].

Zustand: New. pp. 802.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - This heavily revised second edition of this critical book details the structure, function and imaging of the normal right heart both at rest and under the stresses of high altitude and exercise. Extensively revised chapters cover the pathophysiology and pathobiology of right heart dysfunction, both in experimental models and human disease, including congenital heart disease and pulmonary hypertension.The Right Heart provides a concise up-to-date guide on the latest advances in our understanding of role of the right heart in the cardiopulmonary circuit and is an indispensable up-to-date resource for clinicians interested in this topic.

Paperback. Zustand: Brand New. 4th new edition. 802 pages. 10.98x8.50x1.81 inches. In Stock.

Zustand: Used. pp. 316.

Einband - flex.(Paperback). Zustand: New. Edited byAndrew J. Peacock, Golden Jubilee National Hospital, Glasgow, UKRobert Naeije, The Free University of Brussels, BelgiumLewis J. Rubin, University of California, San Diego, La Jolla, U.

Taschenbuch. Zustand: Neu. The Right Heart | Sean P. Gaine (u. a.) | Taschenbuch | xvi | Englisch | 2016 | Springer | EAN 9781447169529 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Zustand: Used. pp. 316 49:B&W 6.14 x 9.21 in or 234 x 156 mm (Royal 8vo) Perfect Bound on White w/Gloss Lam.

Buch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - This heavily revised second edition of this critical book details the structure, function and imaging of the normal right heart both at rest and under the stresses of high altitude and exercise. Extensively revised chapters cover the pathophysiology and pathobiology of right heart dysfunction, both in experimental models and human disease, including congenital heart disease and pulmonary hypertension.The Right Heart provides a concise up-to-date guide on the latest advances in our understanding of role of the right heart in the cardiopulmonary circuit and is an indispensable up-to-date resource for clinicians interested in this topic.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The heart and lung are intricately linked. When the heart is affected by disease, the lungs will often show some related pathological or clinical conditions and vice versa. Pulmonary heart disease is by definition a condition when the lungs cause the heart to fail. The left ventricle in combination with the other structures in the 'left heart' pumps blood throughout the body. The right ventricle (and structures of the 'right heart') pumps blood to the lungs where it is oxygenated and returned to the left heart for distribution. In normal circumstances, the right heart pumps blood into the lungs without any resistance. The lungs usually have minimal pressure and the right heart easily pumps blood through. However when there is lung disease present, like emphysema, chronic obstructive lung disease (COPD) or pulmonary hypertension- the small blood vessels become very stiff and rigid. The right ventricle is no longer able to push blood into the lungs and eventually fails. This is known as pulmonary heart disease. Pulmonary heart disease is also known as right heart failure or cor pulmonale. The chief cause of right heart failure is the increase in blood pressure in the lungs (pulmonary artery).

Zustand: New. In.

Zustand: New. In.

Taschenbuch. Zustand: Neu. Neuware.

Taschenbuch. Zustand: Neu. Problems of High Altitude Medicine and Biology | Almaz Aldashev (u. a.) | Taschenbuch | viii | Englisch | 2007 | Springer | EAN 9781402062995 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Paperback. Zustand: Brand New. reprint edition. 339 pages. 9.25x6.10x0.77 inches. In Stock.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The major characteristic pathological findings of pulmonary vascular remodelling are increased wall thickening of pulmonary vessels and mus- larization of small arteries. In laboratory animals, decreased ambient oxygen concentrations cause similar pathological findings, including pulmonary smooth muscle hypertrophy and proliferation [22,23]. It has been suggested that proliferation of pulmonary arterial smooth muscle cells (PASMC) is a key component of pulmonary vascular remodelling, and several in vitro studies have also addressed that exposure to hypoxia can stimulate prolife- tion of PASMC [13,4,1]. The proliferation of the PASMC begins when the cells enter into the cell cycle. The most important molecular event necessary for the progress of the cell cycle is phosphorylation of retinoblastoma protein by cyclin-dependent kinase (CDK)-cyclin complexes. The CDK activity can be inhibited by CDK inhibitors and the expression of CDK inhibitor is a major regulator of the transition between each phase of the cell cycle [7]. Previous studies have noted that CDK inhibitor p27 plays an important role in the inhibition of the CDK activity and proliferation in vascular smooth muscle cells [2,3]. The G1 phase in severe hypoxia is suggested to involve the CKI p27, because the expression of p27 increased in several cell-lines when they were exposed to extreme hypoxia [20,5]. Previous reports indicate that hypoxia decreases the p27 expression in the murine lung [23,24] and we found that PGI2 suppresses hypox- induced proliferation of PASMC and maintains p27 in PASMC [20].

Buch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The major characteristic pathological findings of pulmonary vascular remodelling are increased wall thickening of pulmonary vessels and mus- larization of small arteries. In laboratory animals, decreased ambient oxygen concentrations cause similar pathological findings, including pulmonary smooth muscle hypertrophy and proliferation [22,23]. It has been suggested that proliferation of pulmonary arterial smooth muscle cells (PASMC) is a key component of pulmonary vascular remodelling, and several in vitro studies have also addressed that exposure to hypoxia can stimulate prolife- tion of PASMC [13,4,1]. The proliferation of the PASMC begins when the cells enter into the cell cycle. The most important molecular event necessary for the progress of the cell cycle is phosphorylation of retinoblastoma protein by cyclin-dependent kinase (CDK)-cyclin complexes. The CDK activity can be inhibited by CDK inhibitors and the expression of CDK inhibitor is a major regulator of the transition between each phase of the cell cycle [7]. Previous studies have noted that CDK inhibitor p27 plays an important role in the inhibition of the CDK activity and proliferation in vascular smooth muscle cells [2,3]. The G1 phase in severe hypoxia is suggested to involve the CKI p27, because the expression of p27 increased in several cell-lines when they were exposed to extreme hypoxia [20,5]. Previous reports indicate that hypoxia decreases the p27 expression in the murine lung [23,24] and we found that PGI2 suppresses hypox- induced proliferation of PASMC and maintains p27 in PASMC [20].

HRD. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

HRD. Zustand: New. New Book. Shipped from UK. Established seller since 2000.

Zustand: New. pp. 802.

Gebunden. Zustand: New. Edited byAndrew J. Peacock, Golden Jubilee National Hospital, Glasgow, UKRobert Naeije, The Free University of Brussels, BelgiumLewis J. Rubin, University of California, San Diego, La Jolla, USA.

Book/CD-ROM. Zustand: Brand New. 4th har/psc edition. 785 pages. 11.26x8.78x1.54 inches. In Stock.

Buch. Zustand: Neu. Neuware.