University Nanosatellite Distributed Satelllite Capabilities to Support TechSat 21

A new way to perform space missions utilizes the concept of clusters of satellites that cooperate to perform the function of a larger, single satellite. Each smaller satellite communicates with the others and shares the processing, communications, and payload or mission functions. The required functionality is thus spread across the satellites in the cluster, the aggregate forming a virtual satellite . The Air Force Research Laboratory (AFRL) initiated the TechSat 21 program to explore the basic technologies required to enable such distributed satellite systems. For this purpose, Space Based Radar (SBR) was selected as a reference mission to help identify technology requirements and to allow an easy comparison to a conventional approach. A summary of the basic mission and the performance requirements is provided. The satellite cluster approach to space missions requires science and technology advances in several key areas. Each of these challenges is described in some detail, with specific stressing requirements driven by the SBR reference mission. These TechSat 21 research and technology areas are being studied in a coordinated effort between several directorates within AFRL and the Air Force Office of Scientific Research. In support of TechSat 21, the Air Force Office of Scientific Research and the Defense Advanced Research Projects Agency are jointly funding 10 universities with grants of $50k/year over two years to design and assemble 10–12 nanosatellites (approx 10kg each) for launch in November 2001. The universities are conducting creative low-cost space experiments to explore the military usefulness of nanosatellites in such areas as formation flying, enhanced communications, miniaturized sensors and thrusters, and attitude control. AFRL is developing a deployment structure and providing advanced microsatellite hardware, and NASA Goddard is providing advanced crosslink communication and navigation hardware and flight algorithms to demonstrate formation flying. Numerous industry partners are also supporting the universities with hardware, design expertise, and test facilities. Areas of particular interest to the TechSat 21 program include autonomous operation and simplified ground control of satellite clusters, intersatellite communications, distributed processing, and formation control. This paper summarizes both hardware and computational challenges that have been identified in both the TechSat 21 and the university nanosatellite programs for implementing operational satellite subsystems to accomplish these tasks

Randomized, Phase II Trial of Pemetrexed and Carboplatin with or without Enzastaurin versus Docetaxel and Carboplatin as First-Line Treatment of Patients with Stage IIIB/IV Non-small Cell Lung Cancer

Enzastaurin is an oral serine/threonine kinase inhibitor that targets protein kinase C-beta (PKC-β) and the phosphatidylinositol-3-kinase/AKT pathway. This trial assessed pemetrexed-carboplatin ± enzastaurin to docetaxel-carboplatin in advanced non-small cell lung cancer.Patients with stage IIIB (with pleural effusion) or IV non-small cell lung cancer and performance status 0 or 1 were randomized to one of the three arms: (A) pemetrexed 500 mg/m and carboplatin area under the curve 6 once every 3 weeks for up to 6 cycles with a loading dose of enzastaurin 1125 or 1200 mg followed by 500 mg daily until disease progression, (B) the same regimen of pemetrexed-carboplatin without enzastaurin, or (C) docetaxel 75 mg/m and carboplatin area under the curve 6 once every 3 weeks for up to six cycles. The primary end point was time to disease progression (TTP).Between March 2006 and May 2008, 218 patients were randomized. Median TTP was 4.6 months for pemetrexed-carboplatin-enzastaurin, 6.0 months for pemetrexed-carboplatin, and 4.1 months for docetaxel-carboplatin (differences not significant). Median survival was 7.2 months for pemetrexed-carboplatin-enzastaurin, 12.7 months for pemetrexed-carboplatin, and 9.2 months for docetaxel-carboplatin (log-rank = 0.05). Compared with the other arms, docetaxel-carboplatin was associated with lower rates of grade 3 thrombocytopenia and anemia but a higher rate of grade 3 or 4 febrile neutropenia.There was no difference in TTP between the three arms, but survival was longer with pemetrexed-carboplatin compared with docetaxel-carboplatin. Enzastaurin did not add to the activity of pemetrexed-carboplatin

CD4(+) T-lymphocytes mediate ischemia/reperfusion-induced inflammatory responses in mouse liver.

The success of orthotopic liver transplantation is dependent on multiple factors including MHC tissue compatibility and ischemic/reperfusion injury. Ischemic/reperfusion (I/R) injury in the liver occurs in a biphasic pattern consisting of both acute phase (oxygen free radical mediated) and subacute phase (neutrophil-mediated) damage. Although numerous studies have given insights into the process of neutrophil recruitment after I/R injury to the liver, the exact mechanism that initiates this subacute response remains undefined. Using a T cell-deficient mouse model, we present data that suggests that T-lymphocytes are key mediators of subacute neutrophil inflammatory responses in the liver after ischemia and reperfusion. To this end, using a partial lobar liver ischemia model, we compared the extent of reperfusion injury between immune competent BALB/c and athymic nu/nu mice. Studies evaluating the extent of liver damage as measured by serum transaminases (GPT) demonstrate similar acute (3-6 h) post-I/R responses in these two mouse models. In contrast, the subacute phase (16-20 h) of liver injury, as measured by both serum GPT levels and percent hepatocellular necrosis, was dramatically reduced in T cell-deficient mice as compared with those with an intact immune system. This reduction in liver injury seen in nu/nu mice was associated with a 10-fold reduction in hepatic neutrophil infiltration. Adoptive transfer of T cell-enriched splenocytes from immune competent mice was capable of reconstituting the neutrophil-mediated subacute inflammatory response within T cell-deficient nu/nu mice. Furthermore, in vivo antibody depletion of CD4+ T-lymphocytes in immune competent mice resulted in a reduction of subacute phase injury and inflammation as measured by serum GPT levels and neutrophil infiltration. In contrast, depletion of CD8+ T-lymphocytes had no effect on these indexes of subacute inflammation. Kinetic analysis of T cell infiltration in the livers of BALB/c mice demonstrated a fivefold increase in the number of hepatic CD4+ T-lymphocytes within the first hour of reperfusion with no significant change in the number of CD8+ T-lymphocytes. In summary, these results implicate CD4+ T- lymphocytes as key regulators in initiating I/R-induced inflammatory responses in the liver. Such findings have implications for therapy directed at the early events in this inflammatory cascade that may prove useful in liver transplantation