HERMES Models 3036-2 and 3041 Experimentes in the HEG

Experiments on two HERMES models, 3036-2 and 3041, were performed in the HEG facility. The tests were conducted at two diaphragm burst conditions, approximately 50 and 100 MPa, with two respective enthalpies of approcimately 13 and 21 MJ/kg. Model 336-2 had an angle of incidence of 40 o and Model 3041 an angle of incidence of 30 o. Both models had their body flap and elevon deflected, 20 o for Model 3036-2 and 10 o for Model 3041. To complement these surface measurements, LIF was undertaken on Model 3036-2 and Holographic Interferometry on both models. Repeatability experiments were conducted on both models at the four test conditions, with reasonable repeatability found. Pressure and/or enthalpy effects were also investigated

Limited Redundancy in Phosphorylation of Retinoblastoma Tumor Suppressor Protein by Cyclin-Dependent Kinases in Acute Lymphoblastic Leukemia

Cyclin-dependent kinases (CDKs) successively phosphorylate the retinoblastoma protein (RB) at the restriction point in G(1) phase. Hyperphosphorylation results in functional inactivation of RB, activation of the E2F transcriptional program, and entry of cells into S phase. RB unphosphorylated at serine 608 has growth suppressive activity. Phosphorylation of serines 608/612 inhibits binding of E2F-1 to RB. In Nalm-6 acute lymphoblastic leukemia extracts, serine 608 is phosphorylated by CDK4/6 complexes but not by CDK2. We reasoned that phosphorylation of serines 608/612 by redundant CDKs could accelerate phospho group formation and determined which G(1) CDK contributes to serine 612 phosphorylation. Here, we report that CDK4 complexes from Nalm-6 extracts phosphorylated in vitro the CDK2-preferred serine 612, which was inhibited by p16(INK4a), and fascaplysin. In contrast, serine 780 and serine 795 were efficiently phosphorylated by CDK4 but not by CDK2. The data suggest that the redundancy in phosphorylation of RB by CDK2 and CDK4 in Nalm-6 extracts is limited. Serine 612 phosphorylation by CDK4 also occurred in extracts of childhood acute lymphoblastic leukemia cells but not in extracts of mobilized CD34(+) hemopoietic progenitor cells. This phenomenon could contribute to the commitment of childhood acute lymphocytic leukemia cells to proliferate and explain their refractoriness to differentiation-inducing agents