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zahlreiche Abb., 116 Seiten, Zustand: sehr gutes Exemplar, minimale Gebrauchsspuren; aus der Bibliothek eines namhaften Neurologen! Sprache: Englisch Gewicht in Gramm: 1100 28,5 x 21,0 cm, gebundene Ausgabe, Hardcover/Pappeinband.

zahlreiche Abb., 123 Seiten, Zustand: sehr gutes, fast neuwertiges Exemplar aus der Bibliothek einer der Autoren! Sprache: Englisch Gewicht in Gramm: 1100 28,5 x 21,0 cm, gebundene Ausgabe, Hardcover/Pappeinband.

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Paperback. Zustand: Brand New. 132 pages. 10.98x8.27x0.30 inches. In Stock.

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Kein Einband. Zustand: Sehr gut. Hardcover, leichte Gebrauchsspuren, Springer 2004, Versand weltweit / international shipping.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The publication of the Vth International Symposium 1995 on 'Mechanisms of Secondary Brain Damage' in Mauls/ltaly is a collection of focused reviews reaching from novel molecular- and cell biological findings to aspects of clinical management in head injury and cerebral ischemia. A specific purpose of these series of meetings introduced in 1984 is for an exchange on problems of mutual interest by international high ranking experts from the basic sciences and related clinical disciplines, such as intensive care medicine, neurology, or neurosurgery. The present volume covers three major areas: (a) Molecular and cell biological mechanisms including inflammation (b) Novel findings on mechanisms and treatment in cerebral ischemia (c) Secondary processes in head injury, regeneration and treatment Molecular-and cell biology is currently attracting attention towards activation of genomic processes associated with the demise of cells referred to as 'programmed cell death' and 'apoptosis' which, actually, might be distinguished from each other. Thus, the phenomenon of delayed neuronal death in selectively vulnerable brain areas following brief interruption of blood flow is scrutinized as to the contribution of the activation of suicide genes. The physiological role of such a response, among others, is removal of surplus neurons during ontogenesis of the brain. Yet, evidence is accumulating that similar mechanisms playa role in cerebral ischemia, probably also trauma, where nerve-and other cells demonstrate features of apoptosis. Observations on protection of neurons by administration of protein synthesis inhibitors in cerebral ischemia provide more direct support.

Taschenbuch. Zustand: Neu. Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma | Alexander Baethmann (u. a.) | Taschenbuch | viii | Englisch | 2012 | Springer | EAN 9783709194676 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Hardcover. Zustand: Brand New. 1st edition. 530 pages. 9.25x6.25x1.25 inches. In Stock.

Zustand: New. pp. viii + 123 Illus.

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Zustand: New. pp. viii + 120 28 Illus.

Taschenbuch. Zustand: Neu. Current Progress in the Understanding of Secondary Brain Damage from Trauma and Ischemia | Proceedings of the 6th International Symposium: Mechanisms of Secondary Brain Damage-Novel Developments, Mauls/Sterzing, Italy, February 1998 | A. Baethmann (u. a.) | Taschenbuch | viii | Englisch | 2012 | Springer | EAN 9783709173121 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Mechanisms of Secondary Brain Damage from Trauma and Ischemia | Recent Advances of our Understanding | A. Baethmann (u. a.) | Taschenbuch | Einband - flex.(Paperback) | Englisch | 2012 | Springer | EAN 9783709172063 | Verantwortliche Person für die EU: Springer Nature Customer Service Center GmbH, Europaplatz 3, 69115 Heidelberg, productsafety[at]springernature[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - Information is provided from the basic and clinical sciences on the mechanisms damaging the brain from trauma or ischemia. New aspects involve the endoplasmic reticulum, mitochondrial failure, pathobiology of axonal injury, molecular signals activating glial elements, or the emerging therapeutical role of neurotrophins. Experimental issues involve a better analysis of the ischemic penumbra, the salvagable tissue. Therapeutic contributions reach from the environmental influence to gene expression, including neuroprotection, such as hibernation mother nature s experiment or hypothermia which is reported to induce cell swelling. Treatment issues deal also with thrombolysis and combination therapies, or with the clearance of adverse blood components LDL/fibrinogen by a novel procedure using heparin. Other highlights are discussing the specificities of pediatric vs. adult brain trauma, or the evolving role of the Apolipoprotein-E e4 gene in severe head injury. An update is also provided on an online assessment of the patient management during the pre- and early hospital phase in Southern Bavaria. The empirical observation of neuroworsening is analyzed in further details, whether this is a specificity autonomously driving the posttraumatic course. Finally, the unsolved question why drug trials in severe head injury have failed so far in view of the promising evidence from the laboratory is subjected to an expert analysis.

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Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The international interdisciplinary gathering of top of secondary brain damage in brain trauma, as ac level clinical and laboratory scientists in Mauls, Italy knowledged from the beginning of these workshops in has developed from its beginning in 1984into a fruitful Mauls, the significance of inflammation is all but clear. tradition where worldwide experts active and knowl Although inflammatory phenomena are seen in trauma edgeable in cerebral ischemia and trauma convene for and ischemia ofthe brain, as activation ofwhite blood update and exchanges of their most recent clinical and cells with emigration into the tissue presumably en experimental findings and concepts. These meetings hancing damage, inflammatory cells may have benefi have, of course, experienced shifts in emphasis from cial properties as well. Thechapter on the Janus-faceof the past until now, corresponding to the most actual inflammation isanalyzing this ambiguity. developments, which were fascinating clinicians and The exploration of novel cell-biological mechanisms laboratory scientists alike. The current Supplement of on a molecular or more systemic basis causing apop Acta Neurochirurgica is an example in case. Its virtue totic cell death, inflammation, or regeneration, provide as before is that authors contribute articles in a review useful objectives for therapeutical interventions ex like manner on their own field of research, according pected to be more specific than the present treatment to the platform presentations at the meeting as indis modalities.

Paperback. Zustand: Brand New. reprint edition. 132 pages. 11.00x8.20x0.40 inches. In Stock.

Paperback. Zustand: Brand New. reprint edition. 140 pages. 11.00x8.20x0.33 inches. In Stock.

Zustand: Sehr gut. Zustand: Sehr gut | Sprache: Englisch | Produktart: Bücher | Information is provided from the basic and clinical sciences on the mechanisms damaging the brain from trauma or ischemia. New aspects involve the endoplasmic reticulum, mitochondrial failure, pathobiology of axonal injury, molecular signals activating glial elements, or the emerging therapeutical role of neurotrophins. Experimental issues involve a better analysis of the ischemic penumbra, the salvagable tissue. Therapeutic contributions reach from the environmental influence to gene expression, including neuroprotection, such as hibernation ¿ mother nature¿s experiment ¿ or hypothermia which is reported to induce cell swelling. Treatment issues deal also with thrombolysis and combination therapies, or with the clearance of adverse blood components ¿ LDL/fibrinogen ¿ by a novel procedure using heparin. Other highlights are discussing the specificities of pediatric vs. adult brain trauma, or the evolving role of the Apolipoprotein-E e4 gene in severe head injury. An update is also provided on an online assessment of the patient management during the pre- and early hospital phase in Southern Bavaria. The empirical observation of neuroworsening is analyzed in further details, whether this is a specificity autonomously driving the posttraumatic course. Finally, the unsolved question why drug trials in severe head injury have failed so far in view of the promising evidence from the laboratory is subjected to an expert analysis.

Acta Neurochir., Suppl., 66. - Wien, New York, 1996, 4°, VIII, 121, (2) pp., 52 Abbildungen, orig. Leinenband mit Schutzumschlag. First Edition! "The publication of the Vth International Symposium 1995 on "Mechanisms of Secondary Brain Damage" in Mauls/ltaly is a collection of focused reviews reaching from novel molecular- and cell biological findings to aspects of clinical management in head injury and cerebral ischemia. A specific purpose of these series of meetings introduced in 1984 is for an exchange on problems of mutual interest by international high ranking experts from the basic sciences and related clinical disciplines, such as intensive care medicine, neurology, or neurosurgery. The present volume covers three major areas: (a) Molecular and cell biological mechanisms including inflammation (b) Novel findings on mechanisms and treatment in cerebral ischemia (c) Secondary processes in head injury, regeneration and treatment Molecular-and cell biology is currently attracting attention towards activation of genomic processes associated with the demise of cells referred to as "programmed cell death" and "apoptosis" which, actually, might be distinguished from each other. Thus, the phenomenon of delayed neuronal death in selectively vulnerable brain areas following brief interruption of blood flow is scrutinized as to the contribution of the activation of suicide genes. The physiological role of such a response, among others, is removal of surplus neurons during ontogenesis of the brain. Yet, evidence is accumulating that similar mechanisms play a role in cerebral ischemia, probably also trauma, where nerve-and other cells demonstrate features of apoptosis. Observations on protection of neurons by administration of protein synthesis inhibitors in cerebral ischemia provide more direct support." Springer.