Brain structural changes in preschool children with MRI-negative epilepsy.

PURPOSE: To investigate abnormalities in cortical and subcortical structures of the brain in preschool children with MRI-negative epilepsy. METHODS: Cortical thickness, cortical mean curvature, cortical surface area, cortical volume, and volumes of subcortical structures were measured using Freesurfer software in preschool children with epilepsy and age-matched controls. RESULTS: Findings showed cortical thickening in the left fusiform gyrus, left middle temporal gyrus, right suborbital sulcus, and right gyrus rectus, and cortical thinning mainly in the parietal lobe of preschool children with epilepsy compared to controls. The difference in cortical thickness in the left superior parietal lobule remained after correction for multiple comparisons and was negatively correlated with duration of epilepsy. Cortical mean curvature, surface area, and volume were mainly altered in the frontal and temporal lobes. Changes in mean curvature in the right pericallosal sulcus were positively correlated with age at seizure onset, and changes in mean curvature in the left intraparietal sulcus and transverse parietal sulcus were positively correlated with frequency of seizures. There were no significant differences in the volumes of the subcortical structures. CONCLUSION: Changes in preschool children with epilepsy occur in the cortical rather than subcortical structures of the brain. These findings further our understanding of the effects of epilepsy in preschool children and will inform management of epilepsy in this patient population.

Normal development of costal element ossification centers of sacral vertebrae in the fetal spine: a postmortem magnetic resonance imaging study.

PURPOSE: This postmortem magnetic resonance imaging (MRI) study of the fetal spine aimed to describe the timing of appearance, shape, volume, and relative positions of the S1-S3 costal element ossification centers (CEOCs). METHODS: We obtained sagittal 3D dual-echo steady-state with water excitation T2 images of the entire spine in 71 fetuses (gestational ages (GAs), 17-42 weeks). Computed tomography and histological examinations were performed on two fetal specimens (GAs, 21 and 30 weeks) to validate the MR images. The presence/absence of each sacral CEOC was recorded according to the GA. CEOC volume was measured. We analyzed the CEOC position relative to the vertebral column and ilium. RESULTS: The S1, S2, and S3 CEOCs first appeared at 23, 22, and 29 weeks, respectively. The S1 and S2 CEOCs could be detected in all fetuses with GAs of ≥ 30 weeks and ≥ 35 weeks, respectively, while the S3 CEOCs were variably present until term. The percentages of detection of the S1 and S2 CEOCs were significantly greater than that of the S3 CEOCs at each GA. At S1 and S2, the CEOC volume increased exponentially with GA. The relative positions of the S1 and S2 CEOCs, but not the S3 CEOCs, significantly correlated with GA (P < 0.001). CONCLUSION: We have described the timeline of appearance as well as the volume and position of the S1-S3 CEOCs in the fetal spine on postmortem MRI according to GA.

Normal development of sacrococcygeal centrum ossification centers in the fetal spine: a postmortem magnetic resonance imaging study.

PURPOSE: To describe the temporal pattern of the appearance of the S1-Co1 centrum ossification centers (COCs) and provide reference data for the S1-S5 COCs and sacral length at various gestational ages (GAs). METHODS: Postmortem magnetic resonance imaging (MRI) was performed on 71 fetuses (GA, 17-42 weeks) using the 3D dual-echo steady-state with water excitation T2 sequence in the sagittal plane. To confirm the reliability of this sequence, the MRI data were compared with the CT and histologic data obtained from two fetuses (GAs, 21 and 30 weeks). The presence or absence of each sacrococcygeal COC was recorded. Sacral length and S1-S5 COC height, sagittal diameter, transverse diameter, cross-sectional area, and volume were measured. RESULTS: All fetuses showed S1-S3 COCs by 17 weeks, S4 COCs by 19 weeks, and S5 COCs by 28 weeks. The S4, S5, and Co-1 COCs were visualized in 70 (98.59%), 51 (71.83%), and 21 (29.58%) fetuses, respectively. Sacral length, height, sagittal, and transverse diameters increased linearly, while cross-sectional area and volume increased exponentially with advancing GA. Mean growth rates of the sagittal and transverse diameters, cross-sectional area, and volume, but not of height, significantly differed among the S1-S5 vertebrae. CONCLUSION: We have presented the timing of appearance of individual sacrococcygeal COCs and the age-specific, normative MRI reference values for sacral length and the morphometric parameters of the sacral COCs, which are of clinical importance in the diagnosis of congenital sacral abnormalities and skeletal dysplasia.

Peroxisome proliferator-activated receptor-gamma activation attenuates diabetic cardiomyopathy via regulation of the TGF-ß/ERK pathway and epithelial-to-mesenchymal transition.

Diabetic cardiomyopathy (DCM) is a kind of disease caused by metabolic disorders and microangiopathy. The main pathophysiological changes of DCM include fibrosis, myocardial cell apoptosis and autonomic neuropathy. Therefore, treatment aimed at these processes may benefit patients with DCM. We designed an experiment with the peroxisome proliferator-activated receptor-gamma (PPARγ) agonist GW 1929 to detect whether the activation of PPARγ could alleviate the degree of DCM. To further detect the mechanism of PPARγ in DCM, we used the PPARγ antagonist GW 9662 and ERK antagonist PD 098059 both in vitro and in vivo and found that PPARγ functioned by inhibiting ERK. We also performed Western blot, PCR, ELISA, immunohistochemistry, TUNEL assay, Sirius red staining and gelatin zymography to investigate inflammation, apoptosis, MMP activity and epithelial-to-mesenchymal transition (EMT). The results showed that the activation of PPARγ inhibited these reactions and inhibiting ERK also simulated this phenomenon. In conclusion, these results demonstrated that PPARγ activation in the diabetic myocardium of mice reduces myocardial fibrosis via regulation of the TGF-ß/ERK pathway and EMT.