Biomedical subjects

Gamze Tanriover

Publications and source records attributed to Gamze Tanriover.

6 recordsLinked to original sources

PubMed2006

Modified experimental mild traumatic brain injury model.

BACKGROUND: Experimental models of traumatic brain injury (TBI), using a variety of techniques and species, have been devised with the aim of producing repeatable lesions resembling those found in head injuries. There are various TBI models mentioned in the literature. In experimental head trauma models, emphasis has been placed on the severe head injuries. There are only a few models developed to study mild traumatic brain injury (MTBI). In fact, MTBI is as important a problem as severe head injuries for neurosurgeons. METHODS: Fifty-six male Sprague-Dawley rats were subjected to MTBI with a weight-drop device, which was described by Marmarou et al. The said model was used in its original form as well as in modified forms by employing different weights dropped from the same height. Animals were divided into four groups of 14 rats as follows: Group I (n=14), head injury was induced using 450 g-1 m weight-height impact; Group II (n=14), head injury was induced using 350 g-l m weight-height impact; Group III (n=14), head injury was induced using 300 g-1 m weight-height impact; Group IV (n=14), control group, no injury was applied. Animals were evaluated neurologically, physiologically, electrophysiologically, and histopathologically. RESULTS: Group I and II animals (450 and 350 g-1m weight-height impact, respectively) showed the symptoms of severe head injury, whereas Group III animals (300 g-l m) showed more MTBI symptoms. CONCLUSION: We recommend the application of the modified MTBI model used for group III (300 g-l m weight-height impact) as the most appropriate and the simplest model for future MTBI studies.

Animals↗

PubMed2005

PTEN-mediated Akt activation in human neocortex during prenatal development.

Akt is a crucial factor for cell survival and migration. Phosphatase and tensin (PTEN) negatively regulates cell growth and survival by inhibiting PI3K-dependent signaling. PTEN also blocks Akt phosphorylation, a main downstream molecule of PI3K cascade. So far, no studies have shown PTEN expression and Akt phosphorylation levels in the developing human neocortex. Our hypothesis is that spatial and temporal expression of PTEN is likely to modulate developing human brain cortical modeling by regulating Akt activation. Therefore, our aim is to analyze the expression pattern of PTEN and phospho-Akt levels using immunohistochemistry, Western blot, and semiquantitative analysis in the developing human neocortex (n=13 fetuses from first, second, and third trimesters). PTEN expression was decreased parallel to development, but some cells revealed strong nuclear immunoreactivity in the developing neocortex while the active Akt level was increased. Double immunohistochemistry was performed for proliferating cell nuclear antigen (PCNA)-Tuj1 (as neuronal marker) and PCNA-GFAP (Glial marker) to the subsequent sections of PTEN and Akt-stained slides. PCNA (+) cells were mostly positive for glial fibrillary acidic protein (GFAP) and correlated with active-Akt immunoreactivity. Our results suggest that Akt-mediated signaling plays an active role in cell migration, survival, and cerebral cortical modeling throughout prenatal life and that PTEN is the most likely protein to regulate this signaling.

Blotting, Western↗

PubMed2005

Effects of excess vitamin B6 intake on cerebral cortex neurons in rat: an ultrastructural study.

The aim of this study was to investigate whether excess of vitamin B6 leads to ultrastructural changes in cerebral cortex of forty-eight healthy albino rats which were included in the study. Saline solution was injected to to the control groups (CG-10, n = 12 for 10 days; CG-15, n = 12 for 15 days; CG-20, n=12 for 20 days). The three experimental groups (EG-10, n = 12; EG-15, n = 12; EG-20, n = 12) were treated with 5 mg/kg vitamin B6 daily for 10 days (EG-10), 15 days (EG-15) and 20 days (EG-20). Brain tissues were prepared by glutaraldehyde-osmium tetroxide double fixation for ultrastructural analysis. No significant changes were observed in the control groups. The ultrastructural analysis revealed that the numbers of damaged mitochondria, lipofuscin granules and vacuoles were significantly higher in all the experimental groups than in the control groups (p < 0.05). However, synaptic density was significantly decreased in the experimental groups as compared to the control groups (p < 0.05). The results suggest that the excess of vitamin B6 intake causes damage to the cerebral cortex due to cellular intoxication and decreased synaptic density. Thus, careful attention should be paid to the time and dose of vitamin B6 recommended for patients who are supplemented with this vitamin.

Animals↗

PubMed2004

Distribution of N-cadherin in human cerebral cortex during prenatal development.

An important subgroup of adhesion molecules is the superfamily of cadherins, which takes part in cell recognition and differentiation during development. To our knowledge only one study describing N-cadherin expression in developing human brain has been performed so far. Our aim is to identify N-cadherin expression to establish a relationship between its expression and function in human cerebral cortex during prenatal development. In the present study, localization and intensity of N-cadherin was investigated in developing cerebral cortex. Fetuses from spontaneous abortions (n=13) were obtained from first, second, and third trimesters. Western blot analysis revealed three bands and the third trimester samples showed the strongest bands for N-cadherin. Cell processes, axon bundles, and some of the developing neurons revealed immunoreactivity for N-cadherin throughout pregnancy. The immunoreactivity increased in the developing neocortex and expanded from the ventricular layer toward the marginal zone as development progressed. Moreover, the immunoreactivity was strong in vascular endothelium during all three trimesters. We conclude that N-cadherin is dynamically related to the organization of cerebral cortex layers during prenatal development. The dynamic expression pattern implicates N-cadherin as a potential regulator of cell migration, axon extension and fasciculation, the establishment of synaptic contacts, and neurovascular angiogenesis in the developing human cerebral cortex.

Abortion, Spontaneous↗

PubMed2004

Ultrastructural and immunohistochemical similarities of two distinct entities; multiple sclerosis and hereditary motor sensory neuropathy.

In the present study, we present the ultrastructural and immunohistochemical properties of the sural nerves of two patients, one of whom was diagnosed as having multiple sclerosis with involvement of the peripheral nervous system (PNS), and the other as having hereditary motor sensory neuropathy type-I with involvement of the central nervous system (CNS). Expression of several extracellular matrix (ECM) proteins (fibronectin, laminin, and collagen type-IV), intermediate filaments (vimentin) and S-100 protein (marker for the axon-Schwann cell interface) was investigated by means of immunohistochemical methods. In addition, the tissue samples were evaluated ultrastructurally. Immunohistochemical staining revealed increased expression of the ECM molecules mentioned above in relation with the sural nerves of the patients. We hypothesize that this enhanced expression is due to Schwann cell-axon interactions. Vimentin expression was different in Schwann cells and S-100 immunostaining was decreased near the Schwann cell-axon interface. Myelin fragmentation, axon vacuolization, onion bulbs, tomoculous formation, axonal degeneration were found to occur. These results suggest that there is active ECM reorganization in the sural nerve of these patients, and some ultrastructural changes are similar in the damaged axonal organization and in Schwann cells although the changes are not completely the same in the two patients. In conclusion, our study demonstrates that there is an association between the demyelinization process in the CNS and the PNS even though they are affected by different mechanisms.

Adult↗

PubMed2002

Effect of cadmium on sciatic nerve in diabetic rats: an ultrastructural study.

The present study demonstrated the ultrastructural effects of diabetes and cadmium on the peripheral nervous system. In this study we used 52 healthy Swiss male albino rats. They were divided into four groups: control (C), diabetic (D), cadmium (Cd), and diabetic and cadmium (D + Cd). The diabetic condition was induced by intravenous injection of 5 mg alloxan/100 g body weight, via the caudal vein. Cd and D + Cd groups were injected with CdCl2 intraperitoneally (2 mg/Kg/week) for two months. At the end of the experimental period, animals were sacrificed and their sciatic nerves were dissected. The tissue samples were investigated by using light and electron microscopic techniques. Upon investigation, it was seen that myelinated axons in sciatic nerve of diabetic and Cd treatment groups had onion-bulb type myelin destruction, melting, and protrusion. Basal lamina of capillary endothelia of D, Cd, and D + Cd groups were thickened and the endothelial apical membrane was rough. In conclusion, Cd toxicity exacerbated the destructive effect of diabetes on the peripheral nervous system.

Animals↗