The toxic effect of non-steroidal anti-inflammatory drugs (NSAIDs) during development has been widely investigated. While it has been shown that these drugs impair central nervous development and compromise the neural activity, the effects of these substances on the development of peripheral nerves are still not clarified. In the present study, sciatic nerves withdrawn from three experimental groups of 4-week-old rats, prenatally exposed to either saline solution, or diclofenac sodium, and controls not exposed to any substance, were evaluated in terms of axon number, cross-sectional area of axon and myelin sheet thickness as well as of the ultrastructure of nerve fibers. Comparisons of stereological estimations among these three groups showed that axon number and mean axon cross-sectional area, but not average myelin sheet thickness, were significantly decreased in rats that were exposed to both diclofenac sodium and also to the saline solution, in comparison of the control group. Electron microscope analysis revealed, in both treated groups, deterioration of myelin sheaths that was more pronounced in rats that were exposed to diclofenac sodium. Altogether, these findings show that the prenatal administration of both diclofenac sodium and saline solution impairs peripheral nervous system development, thus suggesting that this potential teratogenic effect should be also taken into consideration in the clinical use of these substances in pregnant patients.

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In this study, volume densities of white and grey matters of cervical segments of spinal cords of quail were investigated stereologically. In both sexes, mature, six quails were used as material of this study. All animals were fixed by perfusing in 10% buffered formalin. Tissue specimens were obtained from cervical spinal cords. These tissue specimens were cut every fiftieth section at 5 μm thickness by a microtome. And mean six or seven sections were examined from every block by this method at microscope. After that, these sections were stained by haematoxylin eosin and photographed. Densities of volumes of all tissues of cervical segments of whole spinal cords and white and grey matters were calculated with principle of Cavalieri. As a result, total volume of spinal cord, volumes of white and grey matters of cervical segment and volume rates of white and grey matters were calculated.

Further studies in this area are needed due to the popular use of mobile telephones and relatively high exposure on developing brain.

Preeclampsia is a disease characterized by hypertension and proteinuria occurred after 20 weeks of gestation. Preeclampsia is a major cause of maternal and fetal morbidity and mortality.  The pathophysiological mechanism of preeclampsia is not known exactly yet. Preeclampsia endothelial cell dysfunction, associated with inadequate trophoblastic invasion is characterized by abnormal placentation. Vascular endothelial growth factor (VEGF) according to is an angiogenic cytokine, Annexin A5 is among endogenous peptides are both expressed from placental trophoblasts and Apelin is a multifunctional peptide and expressed by placental trophoblasts and endothelial cells. It was aimed to investigate roles of these parameters occurring in preeclampsia and to compare immunoreactivity of them in normal and preeclamptic placenta. In this study, placentas were collected from 20 normotensive pregnant women as controls, 16 mild-preeclamptic pregnant women, and 16 severe preeclamptic women. VEGF, Annexin A5 and Apelin were examined in samples of placenta tissues by streptavidin-biotin-peroxidase complex immunohistochemical methods. Immunoreactivity scores (IRS) were obtained for each parameter.  VEGF and Apelin IRS were increased significantly in preeclamptic groups compared with control group (p <0.026, p<0.002 respectively). But Annexin A5 IRS was decreased significantly in preeclamptic groups compared with control group (p<0.04). In correlation with the intensity of disease, increase in VEGF and Apelin, and decrease in Annexin A5 supports roles of hemo-dynamic alterations in fetoplacental circulation and structural alterations in uteroplacental bed occurring in preeclampsia.