How many cerebellar granule cells are generated pre- or postnatally in human is unknown. Using a rigorous design-based stereologic approach we investigated postmortem cerebella from 14 children who died between the first postnatal day (P1) and 11 months of age (M11). We found a statistically significant (p < 0.05) age-related increase in the total number of granule cells from 5.9 × 10(9) at M1 to 37.6 × 10(9) at M10/11 per cerebellar half but not in the total number of Purkinje cells (12.1 × 10(6) at M1 vs. 13.9 × 10(6) at M10/11 per cerebellar half). Accordingly, approximately 85 % of the cerebellar granule cells are generated postnatally in human, and the number of granule cells per Purkinje cell in the human cerebellum increases from 485 at M1 to 2,700 at M10/11, approximately. These data indicate that the human cerebellum has a much higher functional plasticity during the first year of life than previously thought, and may respond very sensitively to internal and external influences during this time. This has important implications for several neuropsychiatric conditions in which cerebellar involvement has been demonstrated.

The image quality of coronary CT angiograms obtained with a DSCT is satisfactory in most patients with AF. In the majority of patients with high and irregular heart rate, the absolute forward approach with end-systolic reconstruction 300 milliseconds after the R-peak yield a higher image quality than diastolic reconstructions. As a result of a significant improvement in temporal resolution, DSCT coronary angiography is feasible in patients with AF and can be used to exclude coronary artery disease in this patient cohort.

Despite much research during recent decades, the etiology and pathogenesis of sudden infant death syndrome (SIDS) remain unknown. Because of the role of the cerebellum in respiratory and cardiovascular control, it has been proposed that it plays an important role in the pathogenesis of SIDS. To date, 5 postmortem studies on the cerebellum of SIDS cases have yielded conflicting results. Using a rigorous design-based stereologic approach, we investigated postmortem cerebella from 9 SIDS patients who died between 2 and 10 months of age and from 9 age- and sex-matched control children. Neither the volumes of the cerebellar external granule cell layer, molecular layer, internal granule cell layer (including the Purkinje cell layer), and white matter nor the total numbers of Purkinje cells, granule cells in the internal granule cell layer, and the number of granule cells per Purkinje cell showed statistically significant differences between the SIDS cases and the controls. Based on these observations, we conclude that structural alterations in cerebellar development are not involved in the etiology and pathogenesis of SIDS.

Inter rater variability was high and indicates substantial observer influence on the outcome of histologic assessments. Cross-match of villous types with the predetermined positions of villous branches of villous trees revealed substantial mismatch between the outcome of stromal classification and 3D-position of the sectioned villi in the placental villous trees.

Sudden infant death syndrome (SIDS) is the leading cause of mortality in infants younger than 1 year in developed countries, but its primary cause remains unknown. Some studies suggest that there may be hypoxia in the cerebellum in SIDS subjects, but mean total Purkinje cell numbers in SIDS versus controls was recently found not to be different. Probably the best marker for chronic hypoxia in a brain region is the microvessel length per unit volume of tissue, that is, the microvessel length density (MLD). Here, we investigated MLDs using a rigorous design-based stereologic approach in all cell layers and white matter in postmortem cerebella from 9 SIDS cases who died between ages 2 and 10 months and from 14 control children, 9 of which were age- and sex- matched to the SIDS cases. We found no differences either in mean MLDs in the cerebellar layers between the SIDS cases and the controls or between controls with a low likelihood of hypoxia and those with a higher likelihood of hypoxia. Immunohistochemical detection of the astrocytosis marker glial fibrillary acidic protein showed no differences between the SIDS and the matched control cases. These data indicate that there is no association of chronic hypoxia in the cerebellum with SIDS.