Distributed intelligent control and status networking

Over the past two years, the Network Control Systems Branch (Code 532) has been investigating control and status networking technologies. These emerging technologies use distributed processing over a network to accomplish a particular custom task. These networks consist of small intelligent 'nodes' that perform simple tasks. Containing simple, inexpensive hardware and software, these nodes can be easily developed and maintained. Once networked, the nodes can perform a complex operation without a central host. This type of system provides an alternative to more complex control and status systems which require a central computer. This paper will provide some background and discuss some applications of this technology. It will also demonstrate the suitability of one particular technology for the Space Network (SN) and discuss the prototyping activities of Code 532 utilizing this technology

Applying a Space-Based Security Recovery Scheme for Critical Homeland Security Cyberinfrastructure Utilizing the NASA Tracking and Data Relay (TDRS) Based Space Network

Protection of the national infrastructure is a high priority for cybersecurity of the homeland. Critical infrastructure such as the national power grid, commercial financial networks, and communications networks have been successfully invaded and re-invaded from foreign and domestic attackers. The ability to re-establish authentication and confidentiality of the network participants via secure channels that have not been compromised would be an important countermeasure to compromise of our critical network infrastructure. This paper describes a concept of operations by which the NASA Tracking and Data Relay (TDRS) constellation of spacecraft in conjunction with the White Sands Complex (WSC) Ground Station host a security recovery system for re-establishing secure network communications in the event of a national or regional cyberattack. Users would perform security and network restoral functions via a Broadcast Satellite Service (BSS) from the TDRS constellation. The BSS enrollment only requires that each network location have a receive antenna and satellite receiver. This would be no more complex than setting up a DIRECTTV-like receiver at each network location with separate network connectivity. A GEO BSS would allow a mass re-enrollment of network nodes (up to nationwide) simultaneously depending upon downlink characteristics. This paper details the spectrum requirements, link budget, notional assets and communications requirements for the scheme. It describes the architecture of such a system and the manner in which it leverages off of the existing secure infrastructure which is already in place and managed by the NASAGSFC Space Network Project

Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death

Caspase-independent death mechanisms have been shown to execute apoptosis in many types of neuronal injury. P53 has been identified as a key regulator of neuronal cell death after acute injury such as DNA damage, ischemia, and excitotoxicity. Here, we demonstrate that p53 can induce neuronal cell death via a caspase-mediated process activated by apoptotic activating factor-1 (Apaf1) and via a delayed onset caspase-independent mechanism. In contrast to wild-type cells, Apaf1-deficient neurons exhibit delayed DNA fragmentation and only peripheral chromatin condensation. More importantly, we demonstrate that apoptosis-inducing factor (AIF) is an important factor involved in the regulation of this caspase-independent neuronal cell death. Immunofluorescence studies demonstrate that AIF is released from the mitochondria by a mechanism distinct from that of cytochrome-c in neurons undergoing p53-mediated cell death. The Bcl-2 family regulates this release of AIF and subsequent caspase-independent cell death. In addition, we show that enforced expression of AIF can induce neuronal cell death in a Bax- and caspase-independent manner. Microinjection of neutralizing antibodies against AIF significantly decreased injury-induced neuronal cell death in Apaf1-deficient neurons, indicating its importance in caspase-independent apoptosis. Taken together, our results suggest that AIF may be an important therapeutic target for the treatment of neuronal injury

APAF1 is a key transcriptional target for p53 in the regulation of neuronal cell death

p53 is a transcriptional activator which has been implicated as a key regulator of neuronal cell death after acute injury. We have shown previously that p53-mediated neuronal cell death involves a Bax-dependent activation of caspase 3; however, the transcriptional targets involved in the regulation of this process have not been identified. In the present study, we demonstrate that p53 directly upregulates Apaf1 transcription as a critical step in the induction of neuronal cell death. Using DNA microarray analysis of total RNA isolated from neurons undergoing p53-induced apoptosis a 5–6-fold upregulation of Apaf1 mRNA was detected. Induction of neuronal cell death by camptothecin, a DNA-damaging agent that functions through a p53-dependent mechanism, resulted in increased Apaf1 mRNA in p53-positive, but not p53-deficient neurons. In both in vitro and in vivo neuronal cell death processes of p53-induced cell death, Apaf1 protein levels were increased. We addressed whether p53 directly regulates Apaf1 transcription via the two p53 consensus binding sites in the Apaf1 promoter. Electrophoretic mobility shift assays demonstrated p53–DNA binding activity at both p53 consensus binding sequences in extracts obtained from neurons undergoing p53-induced cell death, but not in healthy control cultures or when p53 or the p53 binding sites were inactivated by mutation. In transient transfections in a neuronal cell line with p53 and Apaf1 promoter–luciferase constructs, p53 directly activated the Apaf1 promoter via both p53 sites. The importance of Apaf1 as a p53 target gene in neuronal cell death was evaluated by examining p53-induced apoptotic pathways in primary cultures of Apaf1-deficient neurons. Neurons treated with camptothecin were significantly protected in the absence of Apaf1 relative to those derived from wild-type littermates. Together, these results demonstrate that Apaf1 is a key transcriptional target for p53 that plays a pivotal role in the regulation of apoptosis after neuronal injury

Clinical Features of Polyarteritis Nodosa in Korea

Polyarteritis nodosa (PAN) is a systemic vasculitis characterized by multi-organ involvement with protean manifestations. We evaluated the clinical features of PAN in Korea. Twenty-seven patients were diagnosed as PAN at Seoul National University Hospital between January 1990 and July 2003. The male-to-female ratio was 1.7:1 and mean age at onset (±SD) was 47.4±20 yr. Their presenting features at diagnosis were similar to those reported previously, i.e., myalgia, muscle weakness or leg tenderness (70%), fever (52%), weight loss >4 kg (44%), skin rash (44%), peripheral edema (33%), abdominal pain (33%), and arthralgia/arthritis (30%). However, the prevalence of testicular pain or tenderness was higher (24%) than reported previously and only three (11.5%) had HBsAg positivity without liver enzyme elevation. Nine patients (33%) had a five-factor score (FFS) of 2. Fourteen patients (52%) responded to treatment, 2 patients relapsed and 4 died within 1 yr of diagnosis. During a median follow-up of 55.5 months, three of the four PAN-related deaths had an initial FFS of 2. The clinical features of PAN were not significantly different from those reported previously. However, testicular pain or tenderness was more frequent and patients with a high FFS tended to have a poorer prognosis

Wild Bird Influenza Survey, Canada, 2005

Of 4,268 wild ducks sampled in Canada in 2005, real-time reverse transcriptase–PCR detected influenza A matrix protein (M1) gene sequence in 37% and H5 gene sequence in 5%. Mallards accounted for 61% of samples, 73% of M1-positive ducks, and 90% of H5-positive ducks. Ducks hatched in 2005 accounted for 80% of the sample

Great Lakes Runoff Intercomparison Project Phase 3: Lake Erie (GRIP-E)

Hydrologic model intercomparison studies help to evaluate the agility of models to simulate variables such as streamflow, evaporation, and soil moisture. This study is the third in a sequence of the Great Lakes Runoff Intercomparison Projects. The densely populated Lake Erie watershed studied here is an important international lake that has experienced recent flooding and shoreline erosion alongside excessive nutrient loads that have contributed to lake eutrophication. Understanding the sources and pathways of flows is critical to solve the complex issues facing this watershed. Seventeen hydrologic and land-surface models of different complexity are set up over this domain using the same meteorological forcings, and their simulated streamflows at 46 calibration and seven independent validation stations are compared. Results show that: (1) the good performance of Machine Learning models during calibration decreases significantly in validation due to the limited amount of training data; (2) models calibrated at individual stations perform equally well in validation; and (3) most distributed models calibrated over the entire domain have problems in simulating urban areas but outperform the other models in validation

Enhanced Odor Discrimination and Impaired Olfactory Memory by Spatially Controlled Switch of AMPA Receptors

Genetic perturbations of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) are widely used to dissect molecular mechanisms of sensory coding, learning, and memory. In this study, we investigated the role of Ca(2+)-permeable AMPARs in olfactory behavior. AMPAR modification was obtained by depletion of the GluR-B subunit or expression of unedited GluR-B(Q), both leading to increased Ca(2+) permeability of AMPARs. Mice with this functional AMPAR switch, specifically in forebrain, showed enhanced olfactory discrimination and more rapid learning in a go/no-go operant conditioning task. Olfactory memory, however, was dramatically impaired. GluR-B depletion in forebrain was ectopically variable (“mosaic”) among individuals and strongly correlated with decreased olfactory memory in hippocampus and cortex. Accordingly, memory was rescued by transgenic GluR-B expression restricted to piriform cortex and hippocampus, while enhanced odor discrimination was independent of both GluR-B variability and transgenic GluR-B expression. Thus, correlated differences in behavior and levels of GluR-B expression allowed a mechanistic and spatial dissection of olfactory learning, discrimination, and memory capabilities