No abstract

We recently demonstrated that Cellular Nucleic acid Binding Protein (CNBP)(-/-) mouse embryos exhibit forebrain truncation due to a lack of proper morphogenetic movements of the anterior visceral endoderm (AVE) during pre-gastrulation stage (Chen, W., Liang, Y., Deng, W., Shimizu, K., Ashique, A.M., Li, E., Li, Y.P., 2003. The zinc-finger protein CNBP is required for forebrain formation in the mouse, Development 130, 1367-1379). However, CNBP expression pattern in the mouse forebrain suggests that CNBP may have more direct effects during forebrain development. Our data show that CNBP is expressed in tissues of early chick embryo that are the equivalent to the mouse embryo. Using a combination of RNAi-silencing and Retrovirus-misexpression approaches, we investigated the temporal function of CNBP in the specification/development of the chick forebrain during organogenesis. The silencing of CNBP expression resulted in forebrain truncation and the absence of BF-1, Six3 and Hesx1 expression, but not Otx2 in chick embryos. Misexpression of CNBP induced the expression of BF-1, Six3 and Hesx1 in the hindbrain, but not the expression of Otx2. These results offer novel insights into the function of CNBP during organogenesis as the regulator of forebrain formation and a number of rostral head transcription factors. Moreover, CNBP and Otx2 may play roles as regulators of forebrain formation in two parallel pathways. These new insights into CNBP functions underscore the essential role of CNBP in forebrain formation during chick embryo organogenesis.

A case of POEMSsyndrome in a 49-year-old Japanese womanis reported. The patient exhibited prominent edema in her legs at night, but her edema usually improved by the following morning. The plasma concentrations of VEGFin the patient showed diurnal fluctuations; plasma VEGFlevels peaked at night and decreased in the daytime. Immunocytochemical study demonstrated the expression of VEGF in IgA-and^-positive plasma cells in bone marrow. The results indicate that VEGFwas produced at least by plasma cells and that VEGFproduction was regulated by circadian rhythm in synchronization with the developmentof edema.

This present study investigated the effects of the addition of hydroxyapatite (HA) on the flexural strength and microstructure of conventional GIC, and its effect on the cement's initial flexural strength at different storage conditions. Specimens were fabricated by mixing HA in whisker or granule form into commercially prepared GIC, and these were subjected to a threepoint bending test and SEM observations. Some specimens were stored in different conditions from dry to wet for 15 minutes to an hour prior to testing. When compared to the control, specimens with 16-25% HA whiskers added at P/L 1.75 showed a significant increase in the flexural strength (p<0.05), and as well with 19% HA whiskers at P/L 1.75 (p<0.001) and 2.33 (p<0.05). A significant increase was also noted for those with 8-25% HA granules added at P/L's 1.75 (p<0.05), 2.5 (p<0.05) and 3.60 (p<0.01). The addition of HA hastens the development of early (15min, 1 hour) flexural strength of GIC in moist or wet conditions. These results indicate that the addition of HA, regardless of form, improve the flexural and microstructural properties of GIC.

SUMMARYIntraperitoneal administration with anti-CD86 (B7.2) MoAb into the murine model for primary SS in NFS/sld mutant mice resulted in dramatically inhibitory effects on the development of autoimmune lesions, while no signi®cant effects were observed when the mice were administered with anti-CD80 (B7.1) MoAb. We found that spleen cells in the murine SS model treated with anti-CD86 MoAb showed a signi®cant impairment of autoantigen-speci®c T cell proliferation. T cell activation markers (CD44 high , CD45RB low , Mel-14 low ) were signi®cantly down-regulated in the spleen cells gated on CD4 in anti-CD86-treated mice. We detected a higher level of cytokine production of IL-4 from splenic T cells in anti-CD86-treated mice, but not of IL-2, and interferon-gamma (IFN-g), compared with those in the anti-CD80-and PBS-treated SS model. Moreover, serum autoantibody production against a-fodrin autoantigen was almost entirely suppressed in anti-CD86-treated mice. These data provide strong evidence that in autoimmune exocrinopathy resembling SS in NFS/sld mutant mice, the CD86 costimulatory molecule plays a crucial role in the initiation and subsequent progression of Th1-mediated autoimmunity in the salivary and lacrimal glands.