Use of Chicken Embryos as an Angiogenesis Model for Central Nervous System Malignant Tumor Research.

AIM: To demonstrate the usability of chicken chorioallantoic membrane (CAM) as an angiogenesis model for the development and treatment of malignant tumors of the central nervous system. MATERIAL AND METHODS: A fresh tumor tissue piece taken from Glioblastoma patients, a malignant tumor of the central nervous system, was transferred to the CAM of chicken embryos and left to incubate in the incubator and their development was monitored. After examining the results of the study macroscopically, CAM tissue samples were evaluated both histochemically and immunohistochemically in terms of angiogenic factors VEGF (Vascular Endothelial Growth Factor), bFGF (basic Fibroblast Growth Factor) and PDGF (Platelet Derived Growth Factor). RESULTS: According to histochemical findings obtained from our study when compared with control embryos, blood vessels, fibroblast count and inflammatory infiltration were observed more in the tumor transplanted groups, especially in the tumordeveloping CAM region. There was also intense pleomorphism and marked hypercellularity in the cells. In our immunohistochemical findings, it was determined that bFGF, PDGF, VEGF staining intensities were higher in tumor transplanted groups compared to control groups, and this elevation was more pronounced in the tumor-developing region. CONCLUSION: As a result, it has been shown that the chicken embryo CAM model may be a suitable in vivo model for cancer angiogenesis studies. The protocol we created in this study will be a source for projects related to the use of therapeutic agents in cancer angiogenesis.

An investigation of the effects of chronic zonisamide, sultiam, lacosamide, clobazam, and rufinamide anti-seizure medications on foliculogenesis in ovarian tissue in prepubertal non-epileptic rats.

We aimed to determine the morphological and histological effects of zonisamide, sultiam, lacosamide, clobazam, and rufinamide on ovarian folliculogenesis in rats. Sixty female Wistar rats were divided into six experimental groups as control, zonisamide, sultiam, lacosamide, clobazam, and rufinamide groups; control solution and drugs were administered by gavage for 90 days. The number of healthy follicles in the control group was significantly higher than in the anti-medication groups (p < 0.001), and the number of corpus luteum was significantly lower (p < 0.001). There was a significant difference in the number of TUNEL positive apoptotic follicles between the control and drug groups (p < 0.001). With EGF, IGF-1, and GDF-9 staining, a very strong immunoreaction was observed in the ovarian multilaminar primary follicle granulosa cells and oocytes in the control group compared to the drug group (p < 0.001). Long-term anti-seizure medication with zonisamide, sultiam, lacosamide, clobazam, and rufinamide from prepubertal to adulthood causes apoptosis and disruption of folliculogenesis in the ovarian follicles of nonepileptic rats.

The Effect of Monosodium Glutamate on Neuronal Signaling Molecules in the Hippocampus and the Neuroprotective Effects of Omega-3 Fatty Acids.

Monosodium glutamate (MSG) is a flavoring substance added to many ready-to-eat foods and has known neurotoxic effects. This study was performed in order to examine the potential toxic effect of MSG on neurons in various regions of the hippocampus in prepubertal rats. It also investigated the protective effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on brain-derived neurotropic factor (BDNF), n-methyl-d-aspartate receptor (NMDA-R), and neuropeptide-Y (NPY) expression in the brain, using immunohistochemical and biochemical methods. Six female prepubertal Wistar albino rats were used in each group. Group 1, the control group, received 0.9% saline solution subcutaneously (sc) on days 1, 3, 5, 7, and 9. Group 2 received 4 mg/g MSG sc on days 1, 3, 5, 7, and 9. Group 3 received MSG + EPA (4 mg/g sc on days 1, 3, 5, 7, and 9. Oral 300 mg/kg for 9 d), while Group 4 received MSG + DHA (4 mg/g sc on days 1, 3, 5, 7, and 9 and 300 mg/kg orally for 9 d, respectively). At the end of the ninth day the hippocampal regions of the brain were removed and either fixed for immunohistochemical staining or stored at -80 °C for biochemical parameter investigation. BDNF, NMDA-R, and NPY expression results were evaluated using immunohistochemistry and an enzyme-linked immunosorbent assay. According to our findings, neurons in the control group hippocampal CA1 and DG regions exhibited strong BDNF, NPY, and NMDA-R reactions, while an expression in both regions decreased in the MSG group (p < 0.00). However, in the MSG-EPA and MSG-DHA groups, BDNF, NPY, and NMDA-R immunoreactions in neurons in the same region were similar to those of the control group (p = 0.00). No significant difference was observed in terms of expression in hippocampal neurons between the MSG-EPA and MSG-DHA groups (p > 0.00). In conclusion, since MSG caused a decrease in BDNF, NMDA-R, and NPY neural signaling molecules in the CA1 and DG regions of the hippocampus of prepubertal rats compared to the control group, care is required over the consumption of MSG, since it may affect memory-related neurons in these age groups. In addition, we concluded that the use of omega-3 fatty acids such as EPA and DHA in addition to MSG may protect against the neurotoxic effects of MSG.