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| 008 | 160111s2014 ne | s |||| 0|eng d | ||
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_a9789401789141 _9978-94-017-8914-1 |
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_y201601111135 _zstaff |
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| 050 | 4 | _aRC346-429.2 | |
| 245 | 1 | 0 |
_aIssues in clinical epileptology: a view from the bench / _cedited by Helen E. Scharfman, Paul S. Buckmaster. |
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_aDordrecht : _bSpringer Netherlands : _bSpringer, _c2014. |
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_axxi, 339 páginas : _b50 ilustraciones, 29 ilustraciones en color. |
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_atexto _btxt _2rdacontent |
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_acomputadora _bc _2rdamedia |
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_arecurso en línea _bcr _2rdacarrier |
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_aarchivo de texto _bPDF _2rda |
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_aAdvances in Experimental Medicine and Biology, _x0065-2598 ; _v813 |
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| 500 | _aSpringer eBooks | ||
| 505 | 0 | _aPreface -- Foreword -- Part I Seizures, epileptiform activities and regional localization -- How can we identify ictal and interictal abnormal activity?- How can we translate “epileptiform” activity in vitro into something that is clinically relevant?- What is the importance of abnormal “background” activity in seizure generation?- What is a seizure focus?- What is a seizure network? Very fast oscillations at the interface between normal and epileptic brain -- What is a seizure network? Long-range network consequences of focal seizures -- Is there any such thing as “generalized” epilepsy?- Part II Synaptic plasticity -- Are there really “epileptogenic” mechanisms or only corruptions of “normal” plasticity?- When and how do seizures kill neurons - and is cell death relevant to epileptogenesis?- How is homeostatic plasticity important in epilepsy?- Is plasticity of GABA ergic mechanisms relevant to epileptogenesis?- Do structural changes in GABA neurons give rise to the epileptic state?- Does mossy fiber sprouting give rise to the epileptic state?- Does brain inflammation mediate pathological outcomes in epilepsy?- Are changes in synaptic function that underlie hyperexcitability responsible for seizure activity?- Does epilepsy cause a reversion to immature function?- Are alterations in transmitter receptor and ion channel expression responsible for the epilepsies?- Part III Models and methods -- How do we assess the clinical relevance of models of mesial temporal lobe epilepsy?- How do we make models that are useful in understanding partial epilepsies?- What non-neuronal mechanisms should be studied to understand epileptic seizures?- What epilepsy comorbidities are important to model in the laboratory? Clinical perspectives -- Understanding epilepsy comorbidities: how can animal models help?- What new modeling approaches will help us identify promising drug treatments?- What are the arguments for and against rational therapy for epilepsy?- How can advances in epilepsy genetics lead to better treatments and cures?- How might novel technologies such as optogenetics lead to better treatments in epilepsy?. | |
| 590 | _aPara consulta fuera de la UANL se requiere clave de acceso remoto. | ||
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_aScharfman, Helen E, _eeditor. _982504 |
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_aBuckmaster, Paul S, _eeditor. _9371465 |
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_aSpringerLink (Servicio en línea) _9299170 |
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_iEdición impresa: _z9789401789134 |
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_uhttp://remoto.dgb.uanl.mx/login?url=http://dx.doi.org/10.1007/978-94-017-8914-1 _zConectar a Springer E-Books (Para consulta externa se requiere previa autentificación en Biblioteca Digital UANL) |
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