In Nagoya University Hospital, a Radiology Intelligent Information System (RIIS) is under construction which will be linked with the Hospital Intelligent Information System (HIIS). RIIS is composed of the radiation oncology information system and the diagnostic radiology information system which is named Imaging Diagnosis Intelligent Information System (IDIIS). IDIIS consists of three parts: (a) the Imaging Diagnosis Management System (IDMS); (b) the Picture Archiving and Communication System (PACS); (c) the Report Generation Support System for Imaging Diagnosis (RGSS-ID). Artificial intelligence methodology is applied to RGSS-ID and IDMS which includes the ordering and scheduling system of diagnostic imaging. IDIIS has an important role to improve the quality of patient care and medical education as well as image management and is an essential component for the implementation of HIIS.

Computer Systems↗

PubMedDate not supplied

RGSS-ID: an approach to new radiologic reporting system.

RGSS-ID is a developmental computer system that applies artificial intelligence (AI) methods to a reporting system. The representation scheme called Generalized Finding Representation (GFR) is proposed to bridge the gap between natural language expressions in the radiology report and AI methods. The entry process of RGSS-ID is made mainly by selecting items; our system allows a radiologist to compose a sentence which can be completely parsed by the computer. Further RGSS-ID encodes findings into the expression corresponding to GFR, and stores this expression into the knowledge data base. The final printed report is made in the natural language.

Artificial Intelligence↗

PubMedDate not supplied

Immunohistochemical study of calpain-mediated alpha-crystallin proteolysis in the UPL rat hereditary cataract.

The UPL (Upjohn Pharmaceutical Limited) rat is a dominant hereditary cataract model that develops early-onset cataracts (E-type) in rats homozygous for the trait, and late-onset cataracts (L-type) in heterozygous rats. Using antibodies specific to the calpain-proteolyzed forms of alpha-crystallin, we determined their immunohistochemical localization of the L- and E-rat lenses. Immunoreactivity indicating the proteolyzed forms was detected and found restricted to degenerated lens fibers of the mature stage of the L-rat cataract. Lenses from E-rats, which have abnormally elongated lens fibers during the fetal period, had proteolyzed alpha-crystallin forms at 1 week of age. The results of this present study indicate that calpain-mediated proteolysis of alpha-crystallin occurred in the UPL rat lenses during cataract formation and that calpain may be an important factor in the development of complete lens opacification.

Animals↗

PubMedDate not supplied

Distribution of cells labelled by a monoclonal antibody (A3) against a cloned cell line derived from a rat malignant fibrous histiocytoma.

To pursue the histogenesis of malignant fibrous histiocytoma (MFH), of which the cell of origin is still debated, a monoclonal antibody (A3) was produced against a rat MFH-derived cloned cell line (MT-8). Antigen recognized by A3 was around 80 kDa in molecular weight and was seen on the cytoplasmic membrane of MT-8 cells by immunoelectron microscopy. A3 reacted specifically with MT-8 cells, with another rat MFH-derived cell line (MT-9) and with their induced tumours in syngeneic rats, but not with other rat tumours such as fibrosarcoma, histiocytic sarcoma, malignant meningioma, uterine leiomyosarcoma, endometrial stromal sarcoma, mononuclear cell leukaemia and malignant schwannoma. These findings indicate that A3 has a high specificity for rat MFH cells. In fetuses on gestation days 15, 18 and 20 and in postnatal rats aged 1, 4 and 8 days, A3 reacted with primitive mesenchymal cells in visceral organs and around arteries and bronchi, as well as in the lamina propria of intestinal mucosa, renal interstitium, meninges and perineurium. There were no A3-positive connective tissue cells in organs or other sites in adult rats more than 10 weeks old. It is therefore likely that MFH cells share antigens with primitive mesenchymal cells, which may be multipotent for mesenchymal differentiation. The present study suggests that MFH consists of a population of primitive, undifferentiated mesenchymal cells. A3 also immunolabelled endothelial cells of arteries, venules and pulmonary capillaries in fetal, postnatal and adult rats; vascular endothelial cells in chemically induced hepatic and renal lesions also reacted strongly with A3. However, the significance of endothelial immunoreactivity with A3 remains to be elucidated.

Animals↗

PubMedDate not supplied

Macrophage-like cell line (HS-P) from a rat histiocytic sarcoma.

With future exploration of macrophage properties in mind, we established a novel cell line (HS-P) from a transplantable histiocytic sarcoma, derived originally from a tumour in an aged F344 rat. HS-P was subjected to 70 serial passages, in which the mean doubling time was 15.7 h. The cells, which were round, oval or polygonal in shape, were arranged in a compact sheet. They reacted to varying degrees for lysosomal enzymes (acid phosphatase and non-specific esterase) and with the following antibodies: ED1/ED2 (rat macrophage/histiocyte-specific), OX6 (rat MHC class II-specific), lysozyme antibody and alpha1-antichymotrypsin antibody. Electron microscopically, HS-P cells showed lysosomes and prominent cell projections. These findings indicated that the cultured cells were macrophage-like. Syngeneic rats inoculated subcutaneously or intraperitoneally with HS-P cells invariably developed sarcomatous tumours consisting of monomorphic mononuclear cells, which exhibited cytochemical properties similar to those of cultured HS-P cells. Bioassay and reverse transcription-polymerase chain reaction methods revealed that tumour necrosis factor-alpha increased on addition of lipopolysaccharide (LPS), indicating that HS-P cells remained LPS-responsive. HS-P cells may prove to be a useful tool for in-vitro studies of macrophage function.

Acid Phosphatase↗

PubMedDate not supplied

Differential effects of transforming growth factor-beta1, a fibrogenic factor, on macrophage-like cells (HS-P) and myofibroblastic cells (MT-9) in vitro.

Transforming growth factor-beta1 (TGF-beta1) produced by infiltrating macrophages plays a role in fibrotic disorders through the induction of myofibroblasts. To explore possible mechanisms by which TGF-beta1 may act in this context, we investigated effects of TGF-beta1 on macrophage-like (HS-P) and myofibroblastic (MT-9) cells, two novel cell lines developed by us. Immunocytochemically, the addition of TGF-beta1 (0, 0.1, 0.5, and 1.0 ng/ml) dose-dependently suppressed the expressions of antigens recognized by macrophage/histiocyte-specific antibodies (ED1 and ED2) in HS-P cells, whereas the addition concomitantly increased the number of anti-alpha-smooth muscle actin antibody-positive myofibroblastic cells, suggesting a possible phenotypical modulation of macrophages into myofibroblasts in the fibrotic lesions. By contrast, MT-9 cells did not show such immunophenotypical changes following TGF-beta1 addition. DNA synthesis, measured by tritiated thymidine-incorporation, was inhibited in a dose-dependent manner in MT-9 cells by TGF-beta1 addition (0, 0.1, 0.2, 0.5, 1.0, 5, and 10 ng/ml), but that in HS-P cells was unchanged. Northern blot analysis revealed that expressions of cell cycle-related early genes, c-jun and c-myc, were increased in HS-P cells after TGF-beta1 (1 ng/ml) addition, with c-jun showing peak expression prior to c-myc. By contrast, the peak expressions of c-jun and c-myc were delayed in TGF-beta1 (1 ng/ml)-added MT-9 cells, and their levels were less in MT-9 cells than in HS-P cells. Furthermore, TGF-beta1 (1 and 10 ng/ml) induced DNA laddering in MT-9 cells, but did not in HS-P cells. Based on these findings, it was speculated that TGF-beta1 could have induced G1 arrest in cell cycle and apoptosis in MT-9 cells. The present study showed that there were significant differences in the effects of TGF-beta1 between macrophage-like HS-P cells and myofibroblastic MT-9 cells, presumably depending on divergent susceptibilities to TGF-beta1 between both cell types. Because such cell types are key cells in the fibrogenesis, HS-P and MT-9 might be useful models for investigating the pathogenesis of fibrosis in vitro.

Animals↗