رسالة جامعية
Νευροεκφύλιση και κυτταρικός θάνατος σε πειραματικό μοντέλο τραυματικής κάκωσης του εγκεφάλου ; Neurodegeneration and cell death in an experimental model of traumatic brain injury
| العنوان: | Νευροεκφύλιση και κυτταρικός θάνατος σε πειραματικό μοντέλο τραυματικής κάκωσης του εγκεφάλου ; Neurodegeneration and cell death in an experimental model of traumatic brain injury |
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| المؤلفون: | Polyzoidis, Stavros, Πολυζωίδης, Σταύρος |
| بيانات النشر: | Aristotle University Of Thessaloniki (AUTH) Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ) |
| سنة النشر: | 2012 |
| المجموعة: | National Archive of PhD Theses (National Documentation Centre Greece) |
| مصطلحات موضوعية: | Τραυματική κάκωση εγκεφάλου, Νευροεκφύλιση - οξεία αξονική κάκωση, Νευραναγέννηση - αυξητικός παράγοντας, Φλεγμονή - αστροκυττάρωση, Απόπτωση, Νέκρωση, Αυτοφαγία, Πειραματικό μοντέλο κάκωσης διάπτωσης βάρους, Traumatic brain injury, Neurodegeneration - acute axonal injury, Neuroregeneration - neurorepair, Inflammation - astrocytosis, Apoptosis, Autophagy, Necrosis, Experimental model drop weight injury, Ιατρική και Επιστήμες Υγείας, Βασική Ιατρική, Medical and Health Sciences, Basic Medicine |
| الوصف: | The leading cause of death until the age of 45 is traumatic brain injury (TBI) and its complications. This study aimed in the investigation, in several time points within the initial period of 14 days, of the mechanisms activated post TBI induced by use of the experimental model of drop weight injury (DWI) in mice. The experiments were performed on 23 C57/ Black6 mice, 21 (n=21) of which were subjected to moderate or severe injury (NSS ≥ 6). Two mice (n=2), which were not traumatized, consisted the sham group. Animals were humanly euthanized at 4 hours and at 1, 2, 3, 4, 7 and 14 days post-TBI. Each of the seven time-point groups consisted of three randomly chosen mice, while the sham ones, were sacrificed on day 2 and day 14. Histochemistry, immunohistochemistry, immunofluorescence and double immunofluorescence was performed for the identification of dying neurons (NeuN), neurodegeneration (FJB), acute axonal injury (APP), inflammation (Mac-3), reactive astrocytosis (GFAP), neuroregeneration (GAP-43), IGF activation, apoptosis (casp-3), autophagy (beclin-1) and necrosis with use of Hematoxyline-Eosin staining. Τhe microscopic study of sections included the whole hemisphere bilaterally. Neuronal loss started immediately post-TBI and evolved gradually until 14 days. Neurodegeneration and neuroregeneration were identified bilaterally on traumatized and sham mice, evolved in a parallel manner and their impact was greater on the ipsilateral hemisphere. Acute axonal injury and inflammation were activated only ipsilaterally, while astrocytes on the same hemisphere exhibited a temporary decrease in their population at 4hours. Astrocytosis was recorded thereafter bilaterally and its kinetics was synchronized or followed that of neurodegeneration. IGF activation was recorded only ipsilaterally, was delayed and lasted significantly less compared to the general neuroregeneration activity, while its kinetics largely concurred with that of inflammation and astrogliosis. The decline of IGF coincided with the activation of ... |
| نوع الوثيقة: | doctoral or postdoctoral thesis |
| اللغة: | Greek, Modern (1453-) |
| العلاقة: | http://hdl.handle.net/10442/hedi/36446Test |
| DOI: | 10.12681/eadd/36446 |
| الإتاحة: | https://doi.org/10.12681/eadd/36446Test http://hdl.handle.net/10442/hedi/36446Test |
| رقم الانضمام: | edsbas.901B57A7 |
| قاعدة البيانات: | BASE |
| DOI: | 10.12681/eadd/36446 |
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