Immunosuppression abrogates resistance of young rabbits to Rabbit Haemorrhagic Disease (RHD).

Rabbit Haemorrhagic Disease (RHD) is caused by a calicivirus (RHDV) that kills 90% of infected adult European rabbits within 3 days. Remarkably, young rabbits are resistant to RHD. We induced immunosuppression in young rabbits by treatment with methylprednisolone acetate (MPA) and challenged the animals with RHDV by intramuscular injection.

Early acute depletion of lymphocytes in calicivirus-infected adult rabbits.

Rabbit Haemorrhagic Disease (RHD) is a lethal infection caused by calicivirus that kills 90% of the infected adult rabbits within 3 days. The calicivirus replicates in the liver and causes a fulminant hepatitis. Most studies on the pathology of RHD have been focused on the fulminant liver disease.

[Respiratory epithelia in Wistar rats born in low frequency noise plus varying amounts of additional exposure].

Earlier studies of Wistar rat respiratory epithelia exposed to low frequency noise (LFN) (< or =500 Hz, including infrasound) showed that LFN effects trauma on the respiratory tract. In rats gestated and born in LFN environments, trauma was still treated in accordance with 86/609/EC. Respiratory epithelial fragments were prepared for light and scanning/transmission electron microscopy.

[Respiratory epithelia in Wistar rats after 48 hours of continuous exposure to low frequency noise].

Previous studies show that exposure to low frequency noise (LFN) (< or =500 Hz, including infrasound) produces irreversible lesions in Wistar rat respiratory epithelia. Recovery periods for LFN-induced lesions have thus become an object of interest. Changes in the respiratory epithelia of Wistar rats after continuous short-term exposure to LFN are described.

Respiratory epithelia in Wistar rats.

Morphofunctional changes of respiratory epithelia became the object of intense study in Wistar rats after previous research showed that occupationally-simulated exposure to low frequency noise (500 Hz, including infrasound) induced irreversible lesions in these tissues. Aspects of normal respiratory epithelia in rats are lacking in the literature, and are the object of this report. Ten Wistar rats were kept in silence, fed standard rat food, and had unrestrained access to water (treated in accordance with 86/609/CE).