ORIGINAL PAPER mHealthMon: Toward Energy-Efficient and Distributed Mobile Health Monitoring Using Parallel Offloading

Abstract Although mobile health monitoring where mobile sensors continuously gather, process, and update sensor readings (e.g. vital signals) from patient’s sensors is emerging, little effort has been investigated in an energyefficient management of sensor information gathering and processing. Mobile health monitoring with the focus of energy consumption may instead be holistically analyzed and systematically designed as a global solution to optimization subproblems. This paper presents an attempt to decompose the very complex mobile health monitoring system whose layer in the system corresponds to decomposed subproblems, and interfaces between them are quantified as functions of the optimization variables in order to orchestrate the subproblems. We propose a distributed and energy-saving mobile health platform, called mHealthMon where mobile users publish/access sensor data via a cloud computing-based distributed P2P overlay network. The key objective is to satisfy the mobile health monitoring application’s quality of service requirements by modeling each subsystem: mobile clients with medical sensors, wireless network medium, and distributed cloud services. By simulations based on experimental data, we present the proposed system can achieve up to 10.1 times more energy-efficient and 20.2 times faster compared to a standalone mobil

A genetic screen for modifiers of Drosophila caspase Dcp-1 reveals caspase involvement in autophagy and novel caspase-related genes

BACKGROUND: Caspases are cysteine proteases with essential functions in the apoptotic pathway; their proteolytic activity toward various substrates is associated with the morphological changes of cells. Recent reports have described non-apoptotic functions of caspases, including autophagy. In this report, we searched for novel modifiers of the phenotype of Dcp-1 gain-of-function (GF) animals by screening promoter element- inserted Drosophila melanogaster lines (EP lines). RESULTS: We screened ~15,000 EP lines and identified 72 Dcp-1-interacting genes that were classified into 10 groups based on their functions and pathways: 4 apoptosis signaling genes, 10 autophagy genes, 5 insulin/IGF and TOR signaling pathway genes, 6 MAP kinase and JNK signaling pathway genes, 4 ecdysone signaling genes, 6 ubiquitination genes, 11 various developmental signaling genes, 12 transcription factors, 3 translation factors, and 11 other unclassified genes including 5 functionally undefined genes. Among them, insulin/IGF and TOR signaling pathway, MAP kinase and JNK signaling pathway, and ecdysone signaling are known to be involved in autophagy. Together with the identification of autophagy genes, the results of our screen suggest that autophagy counteracts Dcp-1-induced apoptosis. Consistent with this idea, we show that expression of eGFP-Atg5 rescued the eye phenotype caused by Dcp-1 GF. Paradoxically, we found that over-expression of full-length Dcp-1 induced autophagy, as Atg8b-GFP, an indicator of autophagy, was increased in the eye imaginal discs and in the S2 cell line. Taken together, these data suggest that autophagy suppresses Dcp-1-mediated apoptotic cell death, whereas Dcp-1 positively regulates autophagy, possibly through feedback regulation. CONCLUSIONS: We identified a number of Dcp-1 modifiers that genetically interact with Dcp-1-induced cell death. Our results showing that Dcp-1 and autophagy-related genes influence each other will aid future investigations of the complicated relationships between apoptosis and autophagy

Thermodynamic stability and contributions to the Gibbs free energy of nanocrystalline Ni₃Fe

The heat capacities of nanocrystalline Ni₃Fe and control materials with larger crystallites were measured from 0.4–300 K. The heat capacities were integrated to obtain the enthalpy, entropy, and Gibbs free energy and to quantify how these thermodynamic functions are altered by nanocrystallinity. From the phonon density of states (DOS) measured by inelastic neutron scattering, we find that the Gibbs free energy is dominated by phonons and that the larger heat capacity of the nanomaterial below 100 K is attributable to its enhanced phonon DOS at low energies. Besides electronic and magnetic contributions, the nanocrystalline material has an additional contribution at higher temperatures, consistent with phonon anharmonicity. The nanocrystalline material shows a stronger increase with temperature of both the enthalpy and entropy compared to the bulk sample. Its entropy exceeds that of the bulk material by 0.4 k_B/atom at 300 K. This is insufficient to overcome the enthalpy of grain boundaries and defects in the nanocrystalline material, making it thermodynamically unstable with respect to the bulk control material

Human ERAL1 is a mitochondrial RNA chaperone involved in the assembly of the 28S small mitochondrial ribosomal subunit

The bacterial Ras-like protein Era has been reported previously to bind 16S rRNA within the 30S ribosomal subunit and to play a crucial role in ribosome assembly. An orthologue of this essential GTPase ERAL1 (Era G-protein-like 1) exists in higher eukaryotes and although its exact molecular function and cellular localization is unknown, its absence has been linked to apoptosis. In the present study we show that human ERAL1 is a mitochondrial protein important for the formation of the 28S small mitoribosomal subunit. We also show that ERAL1 binds in vivo to the rRNA component of the small subunit [12S mt (mitochondrial)-rRNA]. Bacterial Era associates with a 3′ unstructured nonanucleotide immediately downstream of the terminal stem–loop (helix 45) of 16S rRNA. This site contains an AUCA sequence highly conserved across all domains of life, immediately upstream of the anti-Shine–Dalgarno sequence, which is conserved in bacteria. Strikingly, this entire region is absent from 12S mt-rRNA. We have mapped the ERAL1-binding site to a 33 nucleotide section delineating the 3′ terminal stem–loop region of 12S mt-rRNA. This loop contains two adenine residues that are reported to be dimethylated on mitoribosome maturation. Furthermore, and also in contrast with the bacterial orthologue, loss of ERAL1 leads to rapid decay of nascent 12S mt-rRNA, consistent with a role as a mitochondrial RNA chaperone. Finally, whereas depletion of ERAL1 leads to apoptosis, cell death occurs prior to any appreciable loss of mitochondrial protein synthesis or reduction in the stability of mitochondrial mRNA

Structural analysis of the Ras-like G protein MglA and its cognate GAP MglB and implications for bacterial polarity

The small G protein MglA and its cognate GAP MglB exemplify a new type of GTPase activation mechanism. In contrast to other Ras-like proteins, the key 'arginine finger' is provided not by the GAP, but by MglA itself

Impact papers on aging in 2009

The editorial board of Aging reviews research papers published in 2009, which they believe have or will have a significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacologic interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically

Foreword

[No abstract