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

Identification and characterization of a putative homolog of a spliceosome component, precursor RNA processing 3 in Drosophila melanogaster

Nuclear pre-mRNA splicing occurs in a large RNA-protein complex that contains four small nuclear ribonucleoprotein particles (snRNPs) as well as many protein factors. The Precursor RNA processing 3 (Prp3) is a U4/U6-associated splicing factor. A putative homologue of Prp3, which showed a 45% identity to the human Prp3 in an amino acid sequence, was identified in Drosophila melanogaster (dPrp3). A full-length cDNA clone was isolated and sequenced from the embryonic cDNA library. This gene consisted of 2 exons and contained an open-reading frame that encoded 550 amino acid residues. A Northern blot analysis showed that dPrp3 is expressed both maternally and zygotically. Immunostaining revealed that dPrp3 was localized to the nuclei of nurse cells and follicle cells in early embryos, which is consistent with its role as a component of spliceosome.close1

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 similar to 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.open112025sciescopu

Renaming the DSCR1/Adapt78 gene family as RCAN: regulators of calcineurin

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