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B Sinkovic

Publications and source records attributed to B Sinkovic.

At least 19 recordsLinked to original sources

Field cooling induced changes in the antiferromagnetic structure of NiO films.

The magnetic anisotropy in antiferromagnetic 500 A thick NiO films, before and after the establishment of an exchange bias field with Co84Fe16 ferromagnetic layers, was measured using magnetic linear dichroism in soft x-ray absorption. Both <111> textured NiO and untextured NiO films show exchange-bias induced in-plane magnetic anisotropy of nearly equal magnitude and with the Ni moment axis being nearly parallel to the exchange bias field direction. These results represent the first observation of the key step in the exchange biasing process, namely, repopulation of the antiferromagnetic domains whose magnetization axis is closest to the exchange bias field direction.

Journal Article↗

The pathogenesis of infectious avian encephalomyelitis. 1. The effect of the age of the chicken and the route of administration of the virus.

The age of the chicken at the time of infection with infectious avian encephalomyelitis virus (IAEV) and the route of the administration of the virus had a marked effect on the development of the clinical disease. Chickens given the virus by intramuscular, intraperitoneal and oral routes exhibited a decreased susceptibility to development of clinical disease with increasing age. Irrespective of age, chickens were consistently susceptible to intracerebral inoculation of IAEV. Chickens infected with the virus at 1-, 7- and 14-days of age developed lower neutralising antibody titres to IAEV than chickens infected at 21 and 28 days. A relationship between the ability to produce specific neutralising antibody to IAEV and susceptibility to the development of clinical disease is discussed.

Age Factors↗

The pathogenesis of infectious avian encephalomyelitis. 2. The effect of immunosuppression on the disease.

Normal chickens given infectious avian encephalomyelitis virus (IAEV) orally at 1, 7 or 14 days of age developed infectious avian encephalomyelitis (IAE), whereas those dosed with the virus at 21, 28 and 35 days of age did not. Chickens in all of these age groups that had been treated with cyclophosphamide or testosterone developed clinical IAE. Intraperitoneal inoculation of IAEV immunoglobulin at the time of dosing with the virus, or 48 hours later, protected normal and immunosuppressed chickens against the onset of clinical IAE. The titre of IAEV serum neutralising antibody was found to be lower in normal chickens given the virus at 1, 7 and 14 days of age in older chickens. These results suggest a significant role for the humoral immune system in the pathogenesis of IAE and in the development of immunity to the disease.

Age Factors↗

The pathogenesis of infectious avian encephalomyelitis. 3. The relationship between viraemia, invasion of the brain by the virus, and the development of specific serum neutralising antibody.

An association was demonstrated between the development of clinical infectious avian encephalomyelitis (IAE), the persistence and titre of infectious avian encephalomyelitis virus (IAEV) in the brain of the chicken, the duration of detectable viraemia and the age of the chicken at the time of infection with the virus. The older the chicken at the time of infection the milder the disease, the lower the virus titre in the brain and the shorter the period of viraemia. IAEV serum neutralising antibody was produced earlier after infection in older chickens, and its detection was associated with decreasing virus titres in the brain and the cessation of detectable viraemia. Treatment of chickens with testosterone in ova, to inhibit the development of antibody synthesis, prevented the onset of age-associated resistance and testosterone treated birds were as susceptible to clinical IAE as baby chickens. The results suggested that the ability to produce IAEV serum neutralising antibody was an important component of age-associated resistance to IAE.

Age Factors↗