Ocean tide and waves beneath the ross ice shelf, antarctica.

The ocean tide in the southern Ross Sea is principally diurnal. The tropic tide range (double amplitude) is between 1 and 2 meters, depending on the location, and is closely related to the local water-layer thickness. The range of the tropic tide is more than three times the range of the equatorial tide. Cotidal and coamplitude charts were made for the largest diurnal constituents, K(1) and O(1) and a provisional cotidal map was made for the semidiurnal constituent M(2). The amplitudes of the diurnal tide constituents are larger in the Ross Sea than in the adjacent southern Pacific Ocean, indicating the existence of a diurnal resonance related to the shape and depth of the sea. Waves related to ocean swell propagate into the ice-covered region from the northern Ross Sea. These waves have amplitudes near 1 centimeter, and periods in the range 1 to 15 minutes. The speed at which these waves travel is successfully predicted by flexural wave theory.

A Climatic Freshening of the Deep Atlantic North of 50{degrees}N over the Past 20 Years.

Observations made in summer 1981 show a significant and widespread decrease in salinity, averaging 0.02 per mil, in deep waters of the subpolar North Atlantic over the past two decades. This implies a relatively rapid response of deep water formation to climatic perturbation.

Photoluminescence of self-trapped excitons in boron nitride nanotubes.

The excitation energy dependence and temperature dependence of photoluminescence from boron nitride nanotubes and hexagonal BN powder samples are reported. The results are discussed within a model attributing the broad 3.2 eV luminescence from these samples to self-trapped excitons in the low-dimensional structures of BN nanotubes and of nano-arch surface reconstructions on h-BN sheet edge faces in powder. An empirical model accounting for the unusual combination of excitation and temperature dependence of photoluminescence seen in these measurements is suggested. For the model to be consistent with the hypothesis of self-trapped excitons on BN nanotubes, it may be necessary to show that the cores of multiwall nanotubes are selectively probed by light tuned below the h-BN exciton.

Co-purification of p34cdc2/p58cyclin A proline-directed protein kinase and the retinoblastoma tumor susceptibility gene product: interaction of an oncogenic serine/threonine protein kinase with a tumor-suppressor protein.

Proline-directed protein kinase (PDPK) is characterized as a cytoplasmic oncogenic serine/threonine kinase that is activated by growth factor-mediated mechanisms and is proposed to function in mammalian somatic cells as an S phase promoting factor. The present study was undertaken to assess the hypothesis that p34cdc2/p58cyclinA PDPK is a physiologically relevant form of the p34cdc2 protein kinase that phosphorylates and inactivates the product of the retinoblastoma/osteosarcoma tumor susceptibility gene (Rb protein). In the course of these studies it was determined (fortuitously) that the p34cdc2/p58cyclinA PDPK purified from the cytosol of FM3A mouse mammary carcinoma cells was 'contaminated' by several high molecular weight substrate proteins that essentially co-purified with the protein kinase, one of which was identified as the Rb protein itself (p105Rb). High-resolution fast protein liquid chromatography (FPLC) revealed that the Rb protein co-purified with a particular subset of the PDPK heterodimer, i.e. with a single species of the 58 kDa cyclinA doublet. The subset of PDPK associated with the Rb protein exhibited somewhat lower specific enzyme activity, as judged by in vitro kinase assays and comparative Western blotting. Immunoprecipitation studies confirmed that p105Rb is physically associated with the p34cdc2/p58cyclin A PDPK. Further studies confirmed that the underphosphorylated Rb protein (p105Rb) present in G1 lysates of synchronized human MG63 osteosarcoma cells could be readily phosphorylated by purified PDPK in vitro, resulting in the characteristic shift in the apparent molecular mass (SDS-PAGE) of the Rb protein that is reported to accompany the hyperphosphorylation and functional inactivation of this protein. Moreover, the induction of the cyclin A subunit of PDPK in these synchronized MG63 cells was found to be closely correlated with the cell cycle-dependent phosphorylation of the Rb protein. From these studies it is concluded that the growth factor-sensitive PDPK is a physiological Rb kinase, which may function to inactivate the Rb protein in vivo.

Two potentially oncogenic cyclins, cyclin A and cyclin D1, share common properties of subunit configuration, tyrosine phosphorylation and physical association with the Rb protein.

Originally identified as a 'mitotic cyclin', cyclin A exhibits properties of growth factor sensitivity, susceptibility to viral subversion and association with a tumor-suppressor protein, properties which are indicative of an S-phase-promoting factor (SPF) as well as a candidate proto-oncogene. Other recent studies have identified human cyclin D1 (PRAD1) as a putative G1 cyclin and candidate proto-oncogene. However, the specific enzymatic activities and, hence, the precise biochemical mechanisms through which cyclins function to govern cell cycle progression remain unresolved. In the present study we have investigated the coordinate interactions between these two potentially oncogenic cyclins, cyclin-dependent protein kinase subunits (cdks) and the Rb tumor-suppressor protein. The distribution of cyclin D isoforms was modulated by serum factors in primary fetal rat lung epithelial cells. Moreover, cyclin D1 was found to be phosphorylated on tyrosine residues in vivo and, like cyclin A, was readily phosphorylated by pp60c-src in vitro. In synchronized human osteosarcoma cells, cyclin D1 is induced in early G1 and becomes associated with p9Ckshs1, a Cdk-binding subunit. Immunoprecipitation experiments with human osteosarcoma cells and Ewing's sarcoma cells demonstrated that cyclin D1 is associated with both p34cdc2 and p33cdk2, and that cyclin D1 immune complexes exhibit appreciable histone H1 kinase activity. Immobilized, recombinant cyclins A and D1 were found to associate with cellular proteins in complexes that contain the p105Rb protein. This study identifies several common aspects of cyclin biochemistry, including tyrosine phosphorylation and the potential to interact directly or indirectly with the Rb protein, that may ultimately relate membrane-mediated signaling events to the regulation of gene expression.

STIM1: a novel phosphoprotein located at the cell surface.

STIM1 is a novel candidate growth suppressor gene mapping to the human chromosome region 11p15.5 that is associated with several malignancies. STIM1 overexpression studies in G401 rhabdoid tumour, rhabdomyosarcoma and rodent myoblast cell lines causes growth arrest, consistent with a potential role as a tumour growth suppressor. We used highly specific antibodies to show by immunofluorescence and cell surface biotinylation studies that STIM1 is located at the cell surface of K562 cells. Western blot analysis revealed that the 90-kDa STIM1 protein is ubiquitously expressed in various human primary cells and tumour cell lines. STIM1 is not secreted from cells and does not appear to undergo proteolytic processing. We show evidence of post-translational modification of STIM1, namely phosphorylation and N-linked glycosylation. Phosphorylation of STIM1 in vivo occurs predominantly on serine residues. Thus, STIM1, the putative tumour growth suppressor gene is ubiquitously expressed and has features of a regulatory cell-surface phosphoprotein.

Activation of cyclin A-dependent kinases associated with WAF1 degradation during radiation-induced apoptosis.

We describe here the further characterisation of the radiation response of a pair of isogenic Burkitt's lymphoma cell lines which differ significantly in their susceptibility to radiation-induced apoptosis. In both cases a marked inhibition of cyclin A-dependent kinase activity was observed at 4 h post-irradiation which recovered to normal levels in the susceptible line by 12 h but remained inhibited in the resistant cell line. Under these conditions the cellular abundance of p58cyclinA and p33cdk2 did not significantly change in the two cell types and there was no evidence for phosphorylation changes in p33cdk2 which might account for the activity differences. In parallel with the changes in activity, p21WAF1 increased initially in both cell lines, declined in the sensitive cell line as the activity recovered but remained high in the resistant cell line. This appears to be explained by a more rapid turn-over of p21WAF1 in the sensitive cell line and an increased association of p21WAF1 with cyclin kinase as determined by immunoprecipitation. These results implicate p21WAF1 in the regulation of cyclin-dependent kinases during radiation-induced apoptosis, with persistence of induced p21WAF1 being associated with a more resistant phenotype.

Tumor-derived inducible heat-shock protein 70 (HSP70) is an essential component of anti-tumor immunity.

The anti-apoptotic function and tumor-associated expression of heat-shock protein 70 (HSP70) is consistent with HSP70 functioning as a survival factor to promote tumorigenesis. However, its immunomodulatory activities to induce anti-tumor immunity predict the suppression of tumor growth. Using the Hsp70.1/3(-/-)(Hsp70(-/-)) mouse model, we observed that tumor-derived HSP70 was neither required for cellular transformation nor for in vivo tumor growth. Hsp70(-/-) murine embryonic fibroblasts (MEFs) were transformed by E1A/Ras and generated tumors in immunodeficient hosts as efficiently as wild-type (WT) transformants. Comparison of Bcr-Abl-mediated transformation of WT and Hsp70(-/-) bone marrow and progression of B-cell leukemogenesis in vivo revealed no differences in disease onset or survival rates, and Eµ-Myc-driven lymphoma in Hsp70(-/-) mice was phenotypically indistinguishable from that in WT Eµ-Myc mice. However, Hsp70(-/-) E1A/Ras MEFs generated significantly larger tumors than their WT counterparts in C57BL/6 J immune-competent hosts. Concurrent with this was a reduction in intra-tumoral infiltration of innate and adaptive immune cells, including macrophages and CD8(+) T cells. Evaluation of several potential mechanisms revealed an HSP70-chemokine-like activity to promote cellular migration. These observations support a role for tumor-derived HSP70 in facilitating anti-tumor immunity to limit tumor growth and highlight the potential consequences of anti-HSP70 therapy as an efficacious anti-cancer strategy.

Are you Y2K-ready for low vision assistive technology?

The new Millennium brings a new breed of low vision assistive technology--some of it straight out of science fiction--and a surge in patients who can benefit from it.