Message and time efficient multi-broadcast schemes

We consider message and time efficient broadcasting and multi-broadcasting in wireless ad-hoc networks, where a subset of nodes, each with a unique rumor, wish to broadcast their rumors to all destinations while minimizing the total number of transmissions and total time until all rumors arrive to their destination. Under centralized settings, we introduce a novel approximation algorithm that provides almost optimal results with respect to the number of transmissions and total time, separately. Later on, we show how to efficiently implement this algorithm under distributed settings, where the nodes have only local information about their surroundings. In addition, we show multiple approximation techniques based on the network collision detection capabilities and explain how to calibrate the algorithms' parameters to produce optimal results for time and messages.Comment: In Proceedings FOMC 2013, arXiv:1310.459

Liver Adiposity and Metabolic Profile in Individuals with Chronic Spinal Cord Injury

Purpose. To quantify liver adiposity using magnetic resonance imaging (MRI) and to determine its association with metabolic profile in men with spinal cord injury (SCI). Materials and Methods. MRI analysis of liver adiposity by fat signal fraction (FSF) and visceral adipose tissue (VAT) was completed on twenty participants. Intravenous glucose tolerance test was conducted to measure glucose effectiveness (g) and insulin sensitivity (i ). Lipid panel, fasting glucose, glycated hemoglobin (HbA1c), and inflammatory cytokines were also analyzed. Results. Average hepatic FSF was 3.7% ± 2.1. FSF was positively related to TG, non-HDL-C, fasting glucose, HbA1c, VAT, and tumor necrosis factor alpha (TNF-). FSF was negatively related to i and testosterone. FSF was positively related to VAT ( = 0.48, = 0.032) and TNF- ( = 0.51, = 0.016) independent of age, level of injury (LOI), and time since injury (TSI). The associations between FSF and metabolic profile were independent of VAT. Conclusions. MRI noninvasively estimated hepatic adiposity in men with chronic SCI. FSF was associated with dysfunction in metabolic profile, central adiposity, and inflammation. Importantly, liver adiposity influenced metabolic profile independently of VAT. These findings highlight the significance of quantifying liver adiposity after SCI to attenuate the development of metabolic disorders

Impaired Functional Connectivity Underlies Fragile X Syndrome

Fragile X syndrome (FXS), the most common form of inherited intellectual disability, is caused by a developmentally regulated silencing of the FMR1 gene, but its effect on human neuronal network development and function is not fully understood. Here, we isolated isogenic human embryonic stem cell (hESC) subclones-one with a full FX mutation and one that is free of the mutation (control) but shares the same genetic background-differentiated them into induced neurons (iNs) by forced expression of NEUROG-1, and compared the functional properties of the derived neuronal networks. High-throughput image analysis demonstrates that FX-iNs have significantly smaller cell bodies and reduced arborizations than the control. Both FX- and control-neurons can discharge repetitive action potentials, and FX neuronal networks are also able to generate spontaneous excitatory synaptic currents with slight differences from the control, demonstrating that iNs generate more mature neuronal networks than the previously used protocols. MEA analysis demonstrated that FX networks are hyperexcitable with significantly higher spontaneous burst-firing activity compared to the control. Most importantly, cross-correlation analysis enabled quantification of network connectivity to demonstrate that the FX neuronal networks are significantly less synchronous than the control, which can explain the origin of the development of intellectual dysfunction associated with FXS

Liver Adiposity and Metabolic Profile in Individuals with Chronic Spinal Cord Injury

Purpose. To quantify liver adiposity using magnetic resonance imaging (MRI) and to determine its association with metabolic profile in men with spinal cord injury (SCI). Materials and Methods. MRI analysis of liver adiposity by fat signal fraction (FSF) and visceral adipose tissue (VAT) was completed on twenty participants. Intravenous glucose tolerance test was conducted to measure glucose effectiveness (Sg) and insulin sensitivity (Si). Lipid panel, fasting glucose, glycated hemoglobin (HbA1c), and inflammatory cytokines were also analyzed. Results. Average hepatic FSF was 3.7%±2.1. FSF was positively related to TG, non-HDL-C, fasting glucose, HbA1c, VAT, and tumor necrosis factor alpha (TNF-α). FSF was negatively related to Si and testosterone. FSF was positively related to VAT (r=0.48, p=0.032) and TNF-α (r=0.51, p=0.016) independent of age, level of injury (LOI), and time since injury (TSI). The associations between FSF and metabolic profile were independent of VAT. Conclusions. MRI noninvasively estimated hepatic adiposity in men with chronic SCI. FSF was associated with dysfunction in metabolic profile, central adiposity, and inflammation. Importantly, liver adiposity influenced metabolic profile independently of VAT. These findings highlight the significance of quantifying liver adiposity after SCI to attenuate the development of metabolic disorders

Transcriptional Regulation by CHIP/LDB Complexes

It is increasingly clear that transcription factors play versatile roles in turning genes “on” or “off” depending on cellular context via the various transcription complexes they form. This poses a major challenge in unraveling combinatorial transcription complex codes. Here we use the powerful genetics of Drosophila combined with microarray and bioinformatics analyses to tackle this challenge. The nuclear adaptor CHIP/LDB is a major developmental regulator capable of forming tissue-specific transcription complexes with various types of transcription factors and cofactors, making it a valuable model to study the intricacies of gene regulation. To date only few CHIP/LDB complexes target genes have been identified, and possible tissue-dependent crosstalk between these complexes has not been rigorously explored. SSDP proteins protect CHIP/LDB complexes from proteasome dependent degradation and are rate-limiting cofactors for these complexes. By using mutations in SSDP, we identified 189 down-stream targets of CHIP/LDB and show that these genes are enriched for the binding sites of APTEROUS (AP) and PANNIER (PNR), two well studied transcription factors associated with CHIP/LDB complexes. We performed extensive genetic screens and identified target genes that genetically interact with components of CHIP/LDB complexes in directing the development of the wings (28 genes) and thoracic bristles (23 genes). Moreover, by in vivo RNAi silencing we uncovered novel roles for two of the target genes, xbp1 and Gs-alpha, in early development of these structures. Taken together, our results suggest that loss of SSDP disrupts the normal balance between the CHIP-AP and the CHIP-PNR transcription complexes, resulting in down-regulation of CHIP-AP target genes and the concomitant up-regulation of CHIP-PNR target genes. Understanding the combinatorial nature of transcription complexes as presented here is crucial to the study of transcription regulation of gene batteries required for development

Low Blood ALT Activity and High FRAIL Questionnaire Scores Correlate with Increased Mortality and with Each Other. A Prospective Study in the Internal Medicine Department

Background: Low blood ALT, Alanine aminotransferase activity and high FRAIL (Fatigue, Resistance, Ambulation, Illnesses and Loss of Weight) questionnaire scores were previously shown to be associated with frailty and increased risk of mortality. We aimed to correlate these tools with mortality and each other in patients hospitalized in an internal medicine department. Methods: This is a prospective study in a large tertiary hospital. We assessed the predictive value for clinical outcomes of both low ALT blood activity and the pre-frail and frail categories of the “FRAIL„ questionnaire. Results: During a 15 months study, 179 consecutive patients were recruited, of whom 20 died. When all study participants were divided to three groups according to admission ALT levels (below 10 IU/L, 11 to 19 IU/L and above 20 IU/L) we found a statistically significant difference in the rate of mortality: 4 patients died within the group of ALT < 10 IU/L, 14 patients died in the group of 10 IU/L < ALT < 19 IU/L and in the group of patients with ALT > 20 IU/L, only 2 patients died (p = 0.042). A higher score on the FRAIL questionnaire was associated, with statistical significance, with higher risk of mortality (p = 0.029). There was a significant correlation (p = 0.038) between blood ALT activity and the pre-frailty and frailty classifications by the FRAIL Questionnaire. Conclusions: Both the FRAIL questionnaire and blood ALT activity are simple and practical tools for frailty assessment and risk stratification of patients hospitalized in the internal medicine department. Both tool’s results also correlate with each other