Histological and immunohistochemical investigations on infantile pancreas in cases of sudden infant death syndrome (SIDS).

The sudden infant death syndrome (SIDS) is defined as unexpected death of a previously healthy infant with no cause of death being established. Comprehensive histological and immunohistochemical investigations are required subsequent to autopsy. In 18 cases of sudden infant death, histological (H&E, PAS and iron stain) and immunohistochemical investigations (CD68, CD45RO and LCA) were performed regarding a possible role of pancreatitis in SIDS and histomorphological alterations of the pancreatic islets, respectively. In all the investigated cases, no inflammatory changes of the infantile pancreatic tissue and no other significant histomorphological alterations of the pancreatic islets were found.

Moderate loss of cerebellar Purkinje cells after chronic bilateral common carotid artery occlusion in rats.

Pathological effects of moderate ischemia (oligemia, hypoperfusion) are relevant in relation to vascular factors in dementia. Chronic bilateral common carotid artery occlusion (BCCAO) in adult Wistar rats induces oligemia and leads to acute changes in gene expression, subacute changes in cortical astrocytes and prolonged changes in white matter tracts, while largely sparing neurons in the forebrain areas. Dilation and remodeling of the basilar artery ensures blood flow to the forebrain. The present study examined the hypoxia-sensitive Purkinje cells in the cerebellum after 6 months of BCCAO using conventional neuropathological analysis, immunohistochemistry and high-precision design-based stereologic methods. Purkinje cells in the vermis region revealed abnormally shaped nuclei. A stereologic analysis showed that the mean total number of Purkinje cells within the vermis was statistically significantly smaller in the BCCAO animals than in the control animals (d = 11.8%; P < 0.0001). BCCAO had no significant effect on the mean volumes of the molecular layer, granule cell layer and white matter in the vermis or the entire cerebellum. Remodeling of the basilar artery indicated that secondary vascular perturbations might be responsible for the effects of BCCAO on the cerebellar Purkinje cells.