Human Hendra virus infection causes acute and relapsing encephalitis.

Aim: To study the pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis.

Methods: Autopsy tissues were investigated by light microscopy, immunohistochemistry and in situ hybridization.

Results: In the patient with acute pulmonary syndrome but not clinical acute encephalitis, vasculitis was found in the brain, lung, heart and kidney.

53-year-old man with rapid cognitive decline.

Kufs' disease (adult neuronal ceroid lipofuscinosis) is a rare form of neurodegenerative lysosomal storage disease, the genetic basis of which remains obscure. We present a case of a 53-year-old man with a long history of adult onset epilepsy who presented with confusion and amnesia, and subsequently underwent rapidly progressive cognitive decline associated with myoclonic jerks. The clinical diagnosis was Creutzfeldt Jakob disease.

Intrapartum stillbirths in hospital unrelated to uteroplacental vascular insufficiency.

The aim of this study was to investigate the causes of intrapartum asphyxia and its relationship to placental abnormalities. Twenty intrapartum fetal death autopsies carried out over a 10-year period in one hospital pathology department associated with a large obstetric unit were reviewed. All the intrapartum fetal deaths occurred in the hospital, while the mothers were being monitored during and after labor.

Selective loss of synaptic proteins in Alzheimer's disease: evidence for an increased severity with APOE varepsilon4.

A pathological feature of Alzheimer's disease (AD) is an area-specific neuronal loss that may be caused by excitotoxicity-related synaptic dysfunction. Relative expression levels of synaptophysin, dynamin I, complexins I and II, N-cadherin, and alphaCaMKII were analysed in human brain tissue from AD cases and controls in hippocampus, and inferior temporal and occipital cortices. Synaptophysin and dynamin I are presynaptic terminal proteins not specific to any neurotransmitter system whereas complexin II, N-cadherin, and alphaCaMKII are specific for excitatory synapses.

GABA(A) receptor beta isoform protein expression in human alcoholic brain: interaction with genotype.

Chronic alcohol misuse by human subjects leads to neuronal loss in regions such as the superior frontal cortex. Reduced GABA transmission may mediate this. The expression of GABA(A) receptor beta(1), beta(2), and beta(3) isoform proteins was analyzed by western blotting in vulnerable (superior frontal cortex) and spared (primary motor cortex) cortical tissue obtained at autopsy from Caucasian subjects, and the effect of genotypes of candidate genes for alcoholism assessed.