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Fusion of atlas with the occipital bone is a rare congenital anomaly known as occipitocervical synostosis, occipitalization of atlas, assimilation of atlas or atlanto-occipital fusion. We describe two cases of occipitocervical synostosis identified amongst one-hundred dry adult human occipital bones from the collection of Ege University, School of Medicine, Department of Anatomy (incidence 0.5%). The synostosis was complete type for both cases. Occipitocervical synostosis is clinically important as it may cause narrowing of foramen magnum which may compress the brainstem, vertebral artery and cranial nerves, and during surgical approaches to the craniovertebral region.

Background: Thrombospondin-4 (TSP4) upregulates in the spinal cord following peripheral nerve injury and contributes to the development of neuropathic pain (NP). We investigated the effects of cyanocobalamin alone or in combination with morphine on pain and the relationship between these effects and spinal TSP4 expression in neuropathic rats. Methods: NP was induced by chronic constriction injury (CCI) of the sciatic nerve. Cyanocobalamin (5 and 10 mg/kg/day) was administered 15 days before CCI and then for 4 and 14 postoperative days. Morphine (2.5 and 5 mg/kg/day) was administered only post-CCI. Combination treatment included cyanocobalamin and morphine, 10 and 5 mg/kg/day, respectively. All drugs were administered intraperitoneally. Nociceptive thresholds were detected by esthesiometer, analgesia meter, and plantar test, and TSP4 expression was assessed by western blotting and fluorescence immunohistochemistry. Results: CCI decreased nociceptive thresholds in all tests and induced TSP4 expression on the 4th postoperative day. The decrease in nociceptive thresholds persisted except for the plantar test, and the increased TSP4 expression reversed on the 14th postoperative day. Cyanocobalamin and low-dose morphine alone did not produce any antinociceptive effects. High-dose morphine improved the decreased nociceptive thresholds in the esthesiometer when administered alone but combined with cyanocobalamin in all tests. Cyanocobalamin and morphine significantly induced TSP4 expression when administered alone in both doses for 4 or 14 days. However, this increase was less when the two drugs are combined. Conclusions: The combination of cyanocobalamin and morphine is more effective in antinociception and partially decreased the induced TSP4 expression compared to the use of either drug alone.

Glutamate is one of the main excitatory neurotransmitters in the central nervous system (CNS), involved in neural transmission, development, differentiation and plasticity. It plays a vital role in neural pathways for cognition, memory and learning, and synapse induction and elimination during development, cell migration, differentiation and death. Glutamate is continuously released from neurons and uptaken from extracellular fluid. AbstractObjectives: Graphene is a quasi-two-dimensional material with unique electrical and chemical properties. In terms of biomedical applications of graphene, nervous system would be an ideal breakthrough model because neural cells are electroactive. Extreme glutamate concentrations cause excitotoxicity. In this study, we aimed to investigate if graphene can increase the resistance to glutamate stress in B35 rat neuroblastoma cells as a cultured cell model for central nervous system neurons.Methods: B35 neuroblastoma cells were grown in DMEM-F12 growth medium containing 10% fetal bovine serum. Graphene oxide (GO) powder was coated onto glass slides with chitosan as a thin film. B35 cells were cultured on GO films. Cells cultivated on glass slides were used as controls. After 24 h of cell culture, L-glutamine induced excitotoxicity was imposed on B35 cells. After 24 h of glutamate-induced stress, cell morphology was examined by scanning electron microscopy. Cell viability was measured with MTT assay. Results:The effects of glutamate stress on cell viability were visible as early as 1 h. The cell viability on GO films was higher than that on glass slides, and cells recovered from stress within 6 h on GO surfaces. After 24 h, viability on glass surfaces was 54% lower than that on GO surfaces; these findings were supported with cell morphology observations. Conclusion:The results of this study showed that GO has a protective role in reducing glutamate-induced excitotoxicity in B35 cell culture, indicating a potential use of GO for treatment of excitotoxicity induced neurodegenerative diseases.