Quantitative data of fetal cortical folding and its developmental changes supply important information in the estimation of fetal age and assessment of brain maturation, so the increasing tendencies of cortical growth and its folding conditions at the beginning of the second and third trimesters with post-mortem Magnetic Resonance Imaging (MRI) were analyzed. 131 fetal specimens of 14-40 weeks gestational age (GA) were selected and scanned with 3.0 T MR. Then the length of folded cortical margin (LFCM) and length of unfolded cortical margin (LUCM) were measured by Photoshop and ZoomMagic software. Degrees of cortical folding (DCF) were calculated by means of (LFCM-LUCM)/LFCM. Growth curves were obtained between the 3 above values and GA, and significant differences in age stages, hemispheres and genders were analyzed. The relationship between LFCM in centimeters, DCF and GA in weeks was described by two exponential growth curves [LFCM=5.325 exp(0.079GA); DCF=11.890 exp(0.043GA)]. The curves increased rapidly after 26 weeks GA, which could be recognized as a cut-off point of fetal cortical and sulcal development. LUCM and GA were described by a logarithmic growth curve which slowed down after 26 weeks GA [LUCM=30.580 Ln(GA)-72.490]. Significant differences of the 3 values before and after 26 weeks GA (p<0.01), but not any in hemispheres and genders were noticed. These results, which may be valuable in assessing normal brain development and can serve as a model in clinical settings, indicate that the cerebral volume first increases and is then followed by increases of the surface area.

Development of the subcortical brain structures during 12-22 weeks GA could be displayed with 7.0-T MRI. The measurement provides significant reference beneficial to the clinical evaluation of fetal brain development.

ABSTRACT. We sought to investigate the relationship between abnormal expression of nitric oxide synthase (NOS) and pathogenesis of cerebral aneurysm. Brain tissues were collected from 36 patients with cerebral aneurysm confirmed by computer tomography with angiography or neurosurgical therapy. The control group consisted of 25 patients of similar age who had no vascular diseases, as confirmed by magnetic resonance imaging. Samples of cortical arterioles were collected. The structure of the aneurysms was detected by hematoxylin and eosin staining, and the expression of inducible NOS was detected by immunohistochemistry. NOS expression was significantly higher in the patient group than in the control group (patients: 30/36 strongly positive; control: 0/25 strongly positive; P < 0.05). In conclusion, the pathogenesis underlying cerebral aneurysm may be due to abnormal expression of NOS, degradation of the extracellular matrix, aggravation of a pro-inflammatory reaction, or a deficiency in arterial elasticity 4277 NOS and pathogenesis of cerebral aneurysm ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 4276-4281 (2015) layer synthesis. These changes may result in a deficiency in vascular remodeling.