Ontogeny, distributions and relative frequencies of somatostatin-immunoreactive cells were investigated in the proventriculus of the chicken embryos with incubation periods. Samples were taken from 10 groups(10 days of incubation to hatching) and studied by immunogistochemical methods. The findings were as follows. Somatostatin-immunoreactive cells were observed from 12 days of incubation in the proventricular glands and after that increased with incubation periods. The first observation time of these cells in the epithelium were at 15 days of incubation in the basal portion but in 16 and 17 days of incubation, no immunoreactive cells were observed in the epithelium but after that a few immunoreactive cells were observed in the basal portion and gastric gland regions. The shpaes of these cells were spherical to spindle in the proventricular glands and spherical to round in the epithlium and gastric gland.

Field infectious bursal disease viruses 9IBDVs) were isolated from IBDV-suspected commercial chickens. The variable region in VP2 gene of six Korean IBDV isolates (K-IBDVs) and IBD vaccines was examined using the reverse transcriptase/polymerase chain reaction-restriction fragment length polymorphism (RT/PCR-RFLP) assay. With all K-IBDVs and vaccine IBDVs, a 474-bp fragment of the VP2 gene was amplified and tested with various restriction enzymes. Resseriction enzymes BstNI and StyI differentiated K-IBDV isolates and IBD vaccines into four groups. Reseriction enzyme profiles of K-IBDV isolates were different from them of IBD vaccines. K-IBDV isolates except for 310 isolate had specific SspI and TaqI recognition sites, which were recognized in highly virulent IBDVs, but IBD vaccines had no those sites. This study showed that RT/PCR-RFLP assay was thought to be valuable tool for differentiation of IBDVs and identification of highly virulent IBDV.

To elucidate the involvement of interleukin-1beta converting enzyme (ICE) in the courseof experimental autoimmune encephalomyelitis (EAE), we induced EAE by immunizing rats with an emulsion of rat spinal cord homogenate with complete Freund's adjuvant supplemented with Mycobacterium tuberculosis(H37Ra, 5mg/ml) and then examined the expression of ICE in the spinal cord of rats with EAE. In normal rate spinal cords, ICE is constitutively, but weakly, expressed in ependmal cells, neurons, and some neuroglial cells. In EAE, many inflammatory cells are positive for ICE, and the majority of ICE+ cells were identified as ED1+ macrophages. During this stage of EAE, the number of ICE+ cells in brain cells, including neurons and astrocytes, increased and these cells also had incresed ICE immunoreactivity. These findings suggest that the upregulation of ICE in both brain cells and invading hematogenous cells is stimulated by a secretory product from inflammatory cells, and that this enzyme is involved in the pathogenesis of EAE via the production of IL-1 beta.