von Aziza El Harrak
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| [1.] Aeh/Fragment 008 01 - Diskussion Zuletzt bearbeitet: 2014-04-29 23:49:12 Schumann | Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009 |
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| Untersuchte Arbeit: Seite: 8, Zeilen: 1-2 |
Quelle: Sheikh 2009 Seite(n): 8, 9, Zeilen: 8: 1-2; 9: figure |
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| Although interrelation of SD and epilepsy has been considered for a long time, the possible pathophysiological role of SD in epilepsy needs to be elucidated.
Figure 1. Vertical propagation of a negative DC-potential wave after injection of KCl in a neocortical slice. Injection of KCl solution (3 M) via a microelectrode elicited spreading depression-like fluctuation during superfusion with artificial cerebrospinal fluid. Injecting and recording electrodes arranged as shown. Voltage variations were recorded simultaneously by four electrodes (DC1–DC4) which set apart by 1 mm (Adopted from Gorji et al., 2001). |
Although interrelation of SD and epilepsy has been considered for a long time, the possible pathophysiological role of SD in epilepsy needs to be elucidated.
Fig. 1. Propagation of a negative DC-potential wave after injection of KCl in a neocortical slice. Injection of KCl solution (3 M) via a microelectrode elicited spreading depression-like fluctuation during superfusion with artificial cerebrospinal fluid. Injecting and recording electrodes arranged as shown. Voltage variations were recorded simultaneously by four electrodes (DC1–DC4) which set apart by 1 mm. |
The copied text starts on the previous page: Aeh/Fragment_007_19. Note that in Gorji et al., (2001) there is a very similar but slightly different figure with a slightly different figure caption. |
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| [2.] Aeh/Fragment 008 03 - Diskussion Zuletzt bearbeitet: 2014-04-29 17:20:50 Singulus | Aeh, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 8, Zeilen: 3-5 |
Quelle: Gorji 2001 Seite(n): 42, Zeilen: r.col: 46ff |
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| SD is also a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, [e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models.] | SD is a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animals [sic] species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+ , blocking of Na+-K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models [22,149,150,243,337,344,433]. |
The source is not mentioned. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Schumann, Zeitstempel: 20140429231151