Vinyl polymerization by metal complexes, 20. Initiation by vinylamine/vinyl alcohol copolymer · copper(II) systems

The polymerization of acrylonitrile (AN) and of methyl methacrylate (MMA) initiated by various copper(II) chelates was studied in the presence of carbon tetrachloride. Several vinylamine (VAm)/vinyl alcohol (VA) copolymers with different contents of NH₂ and OH bearing monomeric units were chosen as polymer ligands as well as polyvinylamine (PVAm)/poly(vinyl alcohol) (PVA) mixtures (of equal NH₂ and OH group contents as the corresponding copolymers), PVAm, and PVA. The activity of the used polymer chelates to initiate the AN and the MMA polymerization was compared at various pH values of the reaction systems. For the polymerization of MMA, the VAm/VA copolymer systems showed a higher activity than the PVAm chelate containing the same amount of NH₂ groups, contrary to the case of the polymerization of AN, where the polymerization activity showed a reverse behavior. The initiation mechanism is discussed.     

Malignant peripheral nerve sheath tumor of small round cell type with pleomorphic spindle cell sarcomatous areas

An unusual case of malignant peripheral nerve sheath tumor (MPNST) arising in the posterior mediastinum of a 59-year-old man is reported. Histopathologically, the tumor showed an admixture of a dense proliferation of small round cells resembling a primitive neuroectodermal tumor (PNET) and a pleomorphic spindle cell sarcomatous area. Abortive rosettes, primitive neural tube-like structures, and a few glandular structures were found in the small round cell area. Small round cells were immunoreactive for neural cell adhesion molecule and synaptophysin, but were not immunoreactive for MIC2 and neuron-specific enolase. Pleomorphic spindle cells were occasionally arranged in a storiform pattern and were diffusely immunoreactive for S-100 protein. The MPNST of small round cell type is distinguishable from PNET by its negative immunoreactivity for MIC2, and the present tumor is assumed to be derived from primitive neuroectodermal cells in the peripheral nerve capable of bidirectional (neuron and Schwann cell) differentiation.     

Epitopic heterogeneity of the CD36 antigen expressed by normal and neoplastic endothelial cells. An immunohistochemical study with a novel monoclonal antibody 8C9.

Phenotypic and functional heterogeneity of endothelial cells (ECs) is being recognized with increasing frequency. Here we report a novel murine monoclonal antibody (MoAb), named 8C9, that detects a unique epitope on the leukocyte differentiation antigen CD36 (platelet glycoprotein IV or IIIb) expressed by both normal and neoplastic ECs. In immunohistochemical and flow-cytometric studies, 8C9-immunoreactivity was detected on capillary ECs, adipocytes, monocytes, platelets and a human monocytoid cell line U-937, which are known to express the CD36 antigen. Blocking experiments using U-937 cells and studies on cryostat sections revealed that a murine MoAb OKM5, which detects the CD36 antigen, blocked the binding of 8C9 to its antigen. Immunoblot analysis showed that 8C9 bound to a 97-kDa membrane protein expressed by U-937 cells treated with phorbol ester. These results indicate that 8C9 detects the CD36 antigen. However, the findings that some OKM5-positive normal ECs in the liver, spleen and lymph nodes as well as neoplastic ECs in a cutaneous angiosarcoma did not react with 8C9, together with the fact that the CD36 antigen does not form a complex or associate with other proteins, suggest epitopic heterogeneity of the CD36 antigen expressed by these tissues.     

Effect of a new antirheumatic drug (CGS10787B) on antibody formation and delayed-type hypersensitivity in BALB/c mice

The effect of CGS10787B on antibody formation and cell-mediated (delayed-type) hypersensitivity in BALB/c mice was examined by using the haemolytic plaque-forming cell assay and the delayed-type footpad reaction with the assay of T-cell subsets. CGS10787B at doses of 5, 25 and 100 mg/kg p.o. enhanced spleen haemolytic plaque-formation on day 4, and spleen rosette-formation on day 5 after immunization. In the assay of T-cell subsets, CGS10787B at the dose of 100 mg/kg reduced the Lyt-23 positive cell subset. In type III hypersensitivity, CGS10787B at doses of 5, 25 and 100 mg/kg p.o. for 6 days reduced dose-relatedly the footpad swelling of the immunized mouse. In type IV hypersensitivity, CGS10787B at doses of 5, 25 and 100 mg/kg p.o. for 6 days diminished dose-dependently the footpad swelling augmented by cyclophosphamide pretreatment. In the assay of T-cell subsets, CGS10787B at doses of 25 and 100 mg/kg increased the Thy-1 positive cell subset. These findings suggest that CGS10787B has an influence on the immune systems, acting on the function of T lymphocytes as well as on the inflammatory process in immunized animals.     

Two cases of limited cutaneous nodular amyloidosis with primary Sj?gren's syndrome]

We described two female patients with primary Sj?gren's syndrome associated with localized cutaneous nodular amyloidosis (LCNA), in which amyloid protein was derived from immunoglobulin light chain. Case 1; a 70-year-old female had complained with polyarthralgia, low-grade fever and parotid gland swelling. She was diagnosed as primary Sj?gren's syndrome. Three years later she noticed brown color small tumor on the thigh and yellow to brown nodules on the bilateral calves of legs. Skin biopsy from the left thigh revealed amyloid L protein deposition, which was positive for anti-lambda light chain staining, in almost entire dermis. Infiltration of lymphocytes and plasma cells around the amyloid deposit were prominent. Case 2; a 51-year-old female had noticed increasing eruption on the hip. Skin biopsy revealed amyloid L protein deposition in the dermis, which was negative for anti-lambda nor kappa light chain staining. When she was refereed to our hospital, she complained of xerostomia and xerophthalmia. She was diagnosed as primary Sj?gren's syndrome. In both cases, histological examination of a minor salivary gland biopsy revealed infiltration of lymphocytes and plasma cells but not amyloid deposit. Serum M protein and urine Bence-Jones protein were not detected. These cases represent localized amyloidosis without systemic involvement. It is widely recognized that Sj?gren's syndrome is frequently accompanied by B cell lymphoproliferative disorders. In LCNA, infiltration of plasma cells around the amyloid deposits was frequently prominent. The relation between these two disorders is discussed.     

Stimulatory effect of CD5 antibody on B cells from patients with rheumatoid arthritis

In order to clarify the role of CD5 antigen on B cell in autoimmunity, we examined B cells from patients with rheumatoid arthritis (RA). The percentages of CD5 positive B cells were increased in peripheral blood from RA compared with normal. Normal and RA B cells were stimulated with two kinds of monoclonal antibodies to CD5 (Leu-1, SL-1) which recognize different epitopes. RA B cells proliferated and secreted IgM by CD5 antibody stimulation in combination with IL-1. Our observations imply that CD5 positive B cells in RA are in their differentiation stage and that CD5 antigen might be one of the triggers to activate CD5 positive B cells in vivo to produce autoantibody.     

PULMONARY ADENOMA AND ENDOCRINE CELL HYPERPLASIA IN SYRIAN GOLDEN HAMSTER TREATED WITH 4-NITROQUINOLINE 1-OXIDE

Chronic effects of 4-nitroquinoline 1-oxide (4 NQO) on the lungs of Syrian golden hamsters were studied. 4 NQO was subcutaneously injected weekly for 3 weeks at a dose of 20 mg/kg body weight. The animals were sacrificed at the 65th and 80th experimental weeks. Two cases of pulmonary adenomas were demonstrated in the 10 4 NQO-treated animals at the 80th week, and the tumor cells contained cytoplasmic lamellar inclusion bodies. In a previous study, we reported 4 NQO- induced pulmonary endocrine cell hyperplasias in the 4 NQO-treated hamster after the 20th experimental week (Jpn. J. Cancer Res., 77,1986). In the present study, 12 pulmonary endocrine cell hyperplasias were recognized in serial sections of the 24 treated animals. The hyperplastic lesions showed positive immunoreactivity to calcitonin. The hyperplastic lesion did not develop to pulmonary endocrine cell neoplasm. ACTA PATHOL JPN 38 : 1097∼1104, 1988.     

Serological confirmation in Ia mutant B6.C-H-2bm12 of gene conversion

Recently it has been suggested that a short segment of the DNA sequence of the Ia beta gene in the mutant B6.C-H-2bm12 (bm12) is derived from the Eb beta gene by a gene-conversion-like mechanism, and that the same segment is also seen in the Ek beta gene. To obtain serological evidence for this idea, we produced an antibody against the "new" determinant on the I-Abm12 molecule by immunizing A.BY mice with bm12 cells. After absorption with B6 lymphocytes to remove antibodies against background antigens, the antisera lysed bm12 cells. Typical Ia peaks were obtained by immunoprecipitation. The absorbed antiserum reacted with B10.A (Ek beta), B10.A(5R) (Eb beta) and B10.S(9R) (Es beta), but not B10. The unabsorbed antiserum is specific for Ia when tested on A background mice. The antiserum lysed spleen cells of Ik strains (A/Sn, A.AL, A.TBR1, and A.TFR1) but not Ak strain, A.TBR13 (KsAkEbSbDb), confirming the presence of antibodies against the I-Ek molecule. This anti-serum also lysed the cells from (A.BY X A.TFR5)F1, which expresses the transcomplementing Eb beta Ek alpha molecule and from the (A.SW X A.TFR5)F1 which expresses the transcomplementing Es beta Ek alpha molecule. These data are consistent with DNA sequence analyses, and show the existence of a determinant (Ia.51) generated in the bm12 mutant by a gene-conversion-like event that is also present in the I-Ek, I-Eb, and I-Es beta polypeptide chains.