M. flint beal (44 résultats)

Paperback. Etat : Good. No Jacket. Pages can have notes/highlighting. Spine may show signs of wear. ~ ThriftBooks: Read More, Spend Less.

Paperback. Etat : Good. No Jacket. Pages can have notes/highlighting. Spine may show signs of wear. ~ ThriftBooks: Read More, Spend Less.

Etat : Good. Pages intact with minimal writing/highlighting. The binding may be loose and creased. Dust jackets/supplements are not included. Stock photo provided. Product includes identifying sticker. Better World Books: Buy Books. Do Good.

Etat : Very Good. Pages intact with possible writing/highlighting. Binding strong with minor wear. Dust jackets/supplements may not be included. Stock photo provided. Product includes identifying sticker. Better World Books: Buy Books. Do Good.

paperback. Etat : Very Good. Connecting readers with great books since 1972! Used books may not include companion materials, and may have some shelf wear or limited writing. We ship orders daily and Customer Service is our top priority.

Etat : acceptable. Used - Acceptable: All pages and the cover are intact, but shrink wrap, dust covers, or boxed set case may be missing. Pages may include limited notes, highlighting, or minor water damage but the text is readable. Pages may include limited notes and highlighting, but the text cannot be obscured or unreadable. Any access codes or passwords originally included with the book may be expired, used or no longer valid. Image is stock photo and cover art edition may be different than pictured.…

Hard Cover. Etat : Very Good. First Edition. a very good hardcover; an ex-library copy with usual markings; internally pages bright and clean; ---------- SATISFACTION GUARANTEED --------- FAST, COURTEOUS SERVICE ------ ALL ORDERS SHIPPED WITH DELIVERY CONFIRMATION; Size: 7 x 10". Ex-Library.

Paperback. Etat : Fine. Book is in excellent condition. Name label inside front cover. 100% Satisfaction Guaranteed. Orders received before 3PM PT typically ship same day.

Paperback. Etat : New. Book is in excellent condition. 100% Satisfaction Guaranteed. Orders received before 3PM PT typically ship same day.

Paperback. Etat : New. In shrink wrap. Looks like an interesting title.

Etat : good. A copy that has been read, remains in good condition. All pages are intact, and the cover is intact. The spine and cover show signs of wear. Pages can include notes and highlighting and show signs of wear, and the copy can include "From the library of" labels or previous owner inscriptions. 100% GUARANTEE! Shipped with delivery confirmation, if you're not satisfied with purchase please return item! Ships via media mail.…

Etat : Brand New. New. US edition. Expediting shipping for all USA and Europe orders excluding PO Box. Excellent Customer Service.

Etat : 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.

Etat : Brand New. New. US edition. Expediting shipping for all USA and Europe orders excluding PO Box. Excellent Customer Service.

Hard Cover. Etat : Good. No Jacket. First Edition. From an academic library with the usual stamps and labels. A little general wear to the covers. Apart from the library evidence binding tight and contents clean. x [2] 273, [3 index]. Binding is pictorial laminated boards. A00015144.

Etat : Used. pp. 380.

Etat : Used. pp. 380 Illus.

Etat : Used. pp. 380.

Etat : New.

Etat : As New. Unread book in perfect condition.

Etat : New.

Etat : New.

Etat : As New. Unread book in perfect condition.

Etat : New. Divided into two parts, this book covers almost all basic mechanisms of excitotoxicity, from glutamate metabolism, release, activity on various pre- and post-synaptic receptors, reuptake and their regulations. It also focuses on each neurologic disorder where this mechanism seems to play a major role. Editor(s): Ferrarese, Carlo (University of Milano-Bicocca, Ospedale San Gerardo, Monza, Italy); Beal, M. Flint (Cornell University, New York). Num Pages: 362 pages, biography. BIC Classification: PSAN. Category: (G) General (US: Trade); (P) Professional & Vocational; (U) Tertiary Education (US: College). Dimension: 234 x 156 x 22. Weight in Grams: 708. . 2003. Hardback. . . . .…

Taschenbuch. Etat : Neu. Druck auf Anfrage Neuware - Printed after ordering - It can be reasonably anticipated that, over the next generations, the proportion of elderly people will remarkably increase and, with this, the number ofpersons suffering from acute (e.g. cerebral ischemia) or chronic neurodegenerative disorders. To date, approved drugs only alleviate the symptoms ofthese diseases (for instance, acetylcholinesterase inhibitors in Alzheimer disease and L-dopa and dopamine-agonists in Parkinson disease), while none seems to stop the progression of the degenerative processes underlying them. The development of effective preventive or protective therapies has been impeded by the limitations of our knowledge of the causes and the mechanisms by which neurons die in neurodegenerative disorders. Evidence accumulated in the past 20 years indicated that the major excitatory neurotransmitter glutamate may play a role as neurotoxin in several conditions. In particular, the glutamatergic system dysfunction seems to be an early event working as a common pathway in the pathogenesis ofa large number ofacute and chronic neurological disorders, in strict conjunction with other important mechanisms, such as oxidative stress and energetic failure, and probably triggered by different mechanisms in various diseases. In consideration of that, drug discovery efforts over the last decade have been focused on the search for drugs that either reduce glutamate synaptic levels or block its postsynaptic effects. Despite numerous reviews on basic mechanisms and clinical aspects ofthe excitotoxic phenomenon, so far no comprehensive book has covered the topic in all its complexity, starting from basic pharmacological mechanisms, to .animal models of diseases and finally to clinical pathogenic and therapeutic implications.…

Buch. Etat : Neu. Druck auf Anfrage Neuware - Printed after ordering - It can be reasonably anticipated that, over the next generations, the proportion of elderly people will remarkably increase and, with this, the number ofpersons suffering from acute (e.g. cerebral ischemia) or chronic neurodegenerative disorders. To date, approved drugs only alleviate the symptoms ofthese diseases (for instance, acetylcholinesterase inhibitors in Alzheimer disease and L-dopa and dopamine-agonists in Parkinson disease), while none seems to stop the progression of the degenerative processes underlying them. The development of effective preventive or protective therapies has been impeded by the limitations of our knowledge of the causes and the mechanisms by which neurons die in neurodegenerative disorders. Evidence accumulated in the past 20 years indicated that the major excitatory neurotransmitter glutamate may play a role as neurotoxin in several conditions. In particular, the glutamatergic system dysfunction seems to be an early event working as a common pathway in the pathogenesis ofa large number ofacute and chronic neurological disorders, in strict conjunction with other important mechanisms, such as oxidative stress and energetic failure, and probably triggered by different mechanisms in various diseases. In consideration of that, drug discovery efforts over the last decade have been focused on the search for drugs that either reduce glutamate synaptic levels or block its postsynaptic effects. Despite numerous reviews on basic mechanisms and clinical aspects ofthe excitotoxic phenomenon, so far no comprehensive book has covered the topic in all its complexity, starting from basic pharmacological mechanisms, to .animal models of diseases and finally to clinical pathogenic and therapeutic implications.…

Etat : New. pp. 380.

Hardcover. Etat : Like New. LIKE NEW. SHIPS FROM MULTIPLE LOCATIONS. book.

hardcover. Etat : Very Good. Very Good. Dust Jacket may NOT BE INCLUDED.CDs may be missing. SHIPS FROM MULTIPLE LOCATIONS. book.

Etat : As New. Unread book in perfect condition.