Visible-wavelength Observations of Jupiter-family Comet Nuclei as Part of Seppcon.

We present the latest analysis and results from SEPPCoN (Survey of Ensemble Physical Properties of Cometary Nuclei). This on-going survey involves studying 100 JFCs - about 25% of the known population - at both mid-infrared and visible wave-lengths to constrain the distributions of sizes, shapes, spins, and albedos of this population. Having earlier reported results from measuring thermal emissions of our sample nuclei [1,2,3,4], we report here progress on the visible-wavelength observations that we have obtained at many ground-based facilities in Chile, Spain, and the United States. To date we have attempted observations of 91% of our sample of 100 JFCs, and at least 64 of those were successfully detected. In most cases the comets were at heliocentric distances between 3.0 and 6.5 AU so as to decrease the odds of a comet having a coma. Of the 64 detected comets, 48 were apparently bare, having no extended emission. Our datasets are further augmented by archival data and photometry from the NEAT program [5]. An important goal of SEPPCoN is to accumulate a large comprehensive set of high quality physical data on cometary nuclei in order to make accurate statistical comparisons with other minor-body populations such as Trojans, Centaurs, and Kuiper-belt objects. Information on the size, shape, spin-rate, albedo and color distributions is critical for understanding their origins and evolutionary processes affecting them.

Down-regulation of beta1,4-galactosyltransferase V is a critical part of etoposide-induced apoptotic process and could be mediated by decreasing Sp1 levels in human glioma cells.

beta1,4-Galactosyltransferase V (beta1,4GalT V; EC 2.4.1.38) is considered to be very important in glioma for expressing transformation-related highly branched N-glycans. Recently, we have characterized beta1,4GalT V as a positive growth regulator in several glioma cell lines. However, the role of beta1,4GalT V in glioma therapy has not been clearly reported. In this study, interfering with the expression of beta1,4GalT V by its antisense cDNA in SHG44 human glioma cells markedly promoted apoptosis induced by etoposide and the activation of caspases as well as processing of Bid and expression of Bax and Bak. Conversely, the ectopic expression of beta1,4GalT V attenuated the apoptotic effect of etoposide on SHG44 cells. In addition, both the beta1,4GalT V transcription and the binding of total or membrane glycoprotein with Ricinus communis agglutinin-I (RCA-I) were partially reduced in etoposide-treated SHG44 cells, correlated well with a decreased level of Sp1 that has been identified as an activator of beta1,4GalT V transcription. Collectively, our results suggest that the down-regulation of beta1,4GalT V expression plays an important role in etoposide-induced apoptosis and could be mediated by a decreasing level of Sp1 in SHG44 cells, indicating that inhibitors of beta1,4GalT V may enhance the therapeutic efficiency of etoposide for malignant glioma.