Certifying the restricted isometry property is hard

This paper is concerned with an important matrix condition in compressed sensing known as the restricted isometry property (RIP). We demonstrate that testing whether a matrix satisfies RIP is NP-hard. As a consequence of our result, it is impossible to efficiently test for RIP provided P \neq NP

Effects of Dietary Leucine Supplementation on Muscle Mass and Markers of Protein Degradation in Overloaded Skeletal Muscles of Young Adult and Aged Rats

The hypertrophic response to overload in fast-twitch skeletal muscle is impaired in aged humans and rats, and upregulation of protein degradation pathways are hypothesized to be a contributing factor. Muscle growth occurs when protein synthesis is greater than protein degradation. Dietary supplementation of the essential amino acid leucine has been shown to reduce protein degradation in both young and aged skeletal muscle. Specifically, leucine acts in part by attenuating 5'-AMP-activated protein kinase (AMPK) activation as well as the translocation of the forkhead box transcription factor 3A (FoxO3, known to promote transcription of mRNAs encoding degradation pathway proteins) to the nucleus. Akt (a promoter of muscle growth) prevents translocation of FoxO3 into the nucleus by phosphorylating FoxO3 phosphorylation at Ser[superscript]318/321. However, AMPK, inhibits Akt's phosphorylation of FoxO3, allowing it to enter the nucleus and increase transcription of protein degradation pathway genes encoding ubiquitin ligase proteins such as muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx, or Atrogin-1). During the aging process, AMPK Thr[superscript]172 phosphorylation (and thus its activation) is increased, purportedly inhibiting gains in muscle mass and strength. Although dietary leucine supplementation has been shown to enhance muscle hypertrophy in response to resistance training in young humans, the potential for leucine supplementation to enhance overload-induced muscle hypertrophy in aged humans or animal models has not been examined. Thus, the aim of this study was to determine whether dietary leucine supplementation can attenuate markers of protein degradation and rescue hypertrophy during overload in the fast-twitch skeletal muscles of aged rats to levels comparable to their younger counterparts. It was hypothesized that dietary leucine supplementation during 7 days of fast-twitch plantaris muscle overload would enhance plantaris muscle hypertrophy in aged rats to levels observed in young adult rats not receiving leucine. It was also hypothesized that dietary leucine supplementation during the overload period would alter markers of protein degradation (enhance FoxO3 phosphorylation and reduce the levels of AMPK phosphorylation, Atrogin-1 protein content, and MuRF1 protein content) in the overloaded fast-twitch plantaris muscles of the aged rats to levels observed in young adult rats not receiving leucine. Young adult (8 mo.) and old (33 mo.) male Fisher 344 x Brown Norway F1 Hybrid (FBN) rats underwent a 1-week unilateral overload of the fast-twitch plantaris muscles via tenotomy of the synergistic gastrocnemius muscle. Within each age group, animals were matched for body weight and separated into either a dietary leucine supplementation group (normal rat chow supplemented by an additional 5% leucine content in place of 5% of the carbohydrate content; n = 7/age group) or placebo group (normal rat chow; n = 6/age group). The leucine groups started the leucine-enriched diet 2 days prior to, and throughout, the overload intervention. All animals had ad libitum access to water and chow during the entire experiment; no differences in daily calorie consumption were observed between the placebo vs. leucine groups within each age group. At the end of the overload period, sham-operated and overloaded plantaris muscles were harvested and analyzed via western blotting for the phosphorylations of AMPK and FoxO3 as well as total levels of Atrogin-1 and MuRF1. Dietary leucine enrichment significantly (p [equal to or less than] 0.05) enhanced overload-induced plantaris muscle hypertrophy in old, but not in young adult, animals. Sham and overloaded plantaris muscle AMPK phosphorylation was significantly higher in aged animals receiving normal chow compared to young adult animals; however, leucine supplementation in old animals reduced this AMPK phosphorylation to levels similar to young adult animals. Compared to placebo, leucine also non-significantly (p = 0.07) enhanced FoxO3 phosphorylation in the overloaded muscles of both young adult and old animals (thus theoretically reducing FoxO3 translocation to the nucleus). Accordingly, leucine also non-significantly (p = 0.07) reversed the overload-induced increase (from a 22.8% increase to a 17.0% decrease) in Atrogin-1 content in aged muscles and non-significantly (p = 0.14) enhanced the overload-induced decrease in MuRF1 content in the muscles of both age groups. These findings indicate that a leucine-enriched diet may potentially enhance overload-induced growth of aged fast-twitch muscle, in part by suppressing pathways known to stimulate protein degradation.  M.S

A Leucine-enriched Diet Enhances Overload-induced Growth and Suppresses Markers of Protein Degradation in Aged Rat Skeletal Muscle

Introduction: The hypertrophic response to overload in fast-twitch skeletal muscle is impaired in aged humans and rats, and upregulation of protein degradation pathways are hypothesized to be a contributing factor. Muscle growth occurs when protein synthesis is greater than protein degradation. Dietary supplementation of the essential amino acid leucine has been shown to reduce protein degradation in both young and aged skeletal muscle. Specifically, leucine acts in part by attenuating 5\u27-AMP-activated protein kinase (AMPK) activation as well as the translocation of the forkhead box transcription factor 3A (FoxO3, known to promote transcription of mRNAs encoding degradation pathway proteins) to the nucleus. Akt (a promoter of muscle growth) prevents translocation of FoxO3 into the nucleus by phosphorylating FoxO3 phosphorylation at Ser318/321. However, AMPK, inhibits Akt\u27s phosphorylation of FoxO3, allowing it to enter the nucleus and increase transcription of protein degradation pathway genes encoding ubiquitin ligase proteins such as muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx, or Atrogin-1). During the aging process, AMPK Thr172 phosphorylation (and thus its activation) is increased, purportedly inhibiting gains in muscle mass and strength. Although dietary leucine supplementation has been shown to enhance strength gians in response to resistance training in young humans, the potential for leucine supplementation to enhance overload-induced muscle hypertrophy in aged humans or animal models has not been examined. Thus, the aim of this study was to determine whether dietary leucine supplementation can attenuate markers of protein degradation and rescue hypertrophy during overload in the fast-twitch skeletal muscles of aged rats to levels comparable to their younger counterparts. It was hypothesized that dietary leucine supplementation during 7 days of fast-twitch plantaris muscle overload would enhance plantaris muscle hypertrophy in aged rats to levels observed in young adult rats not receiving leucine. It was also hypothesized that dietary leucine supplementation during the overload period would alter markers of protein degradation (enhance FoxO3 phosphorylation and reduce the levels of AMPK phosphorylation, Atrogin-1 protein content, and MuRF1 protein content) in the overloaded fast-twitch plantaris muscles of the aged rats to levels observed in young adult rats not receiving leucine. Methods: Young adult (8 mo.) and old (33 mo.) male Fisher 344 x Brown Norway F1 Hybrid (FBN) rats underwent a 1-week unilateral overload of the fast-twitch plantaris muscles via tenotomy of the synergistic gastrocnemius muscle. Within each age group, animals were matched for body weight and separated into either a dietary leucine supplementation group (normal rat chow supplemented by an additional 5% leucine content in place of 5% of the carbohydrate content; n = 7/age group) or placebo group (normal rat chow; n = 6/age group). The leucine groups started the leucine-enriched diet 2 days prior to, and throughout, the overload intervention. All animals had ad libitum access to water and chow during the entire experiment; no differences in daily calorie consumption were observed between the placebo vs. leucine groups within each age group. At the end of the overload period, sham-operated and overloaded plantaris muscles were harvested and analyzed via western blotting for the phosphorylations of AMPK and FoxO3 as well as total levels of Atrogin-1 and MuRF1. A 2x2x2 ANOVA with repeated measures was used for analyses of the effects of age, dietary intervention, and overload (the repeated measure) on muscle hypertrophy. A 2x2 ANOVA was used to measure the percent changes in hypertrophy and western blot analyses. Post-hoc comparisons were accomplished via a Fisher\u27s Least Significant Difference test, with statistical significance being set at p ≤ 0.05. Results: Dietary leucine enrichment significantly (p ≤ 0.05) enhanced overload-induced fast-twitch plantaris muscle hypertrophy in old, but not in young adult, animals. A similar effect was also observed in the slow-twitch soleus muscles, but western blotting analyses are only presented for the fast-twitch plantaris muscles. Sham and overloaded plantaris muscle AMPK phosphorylation was significantly higher in aged animals receiving normal chow compared to young adult animals; however, leucine supplementation in old animals reduced this AMPK phosphorylation to levels similar to young adult animals. Compared to placebo, leucine also non-significantly (p = 0.07) enhanced FoxO3 phosphorylation in the overloaded muscles of both young adult and old animals (thus theoretically reducing FoxO3 translocation to the nucleus). Accordingly, leucine also non-significantly (p = 0.07) reversed the overload-induced increase (from a 22.8% increase to a 17.0% decrease) in Atrogin-1 content in aged muscles and non-significantly (p = 0.14) enhanced the overload-induced decrease in MuRF1 content in the muscles of both age groups. Discussion: These novel findings indicate that a leucine-enriched diet may potentially enhance overload-induced growth of aged fast-twitch muscle, in part by suppressing pathways known to stimulate protein degradation. This is in accord with previous findings of leucine’s suppressive effect on protein degradation in both young adult and aged skeletal muscle under resting conditions. The fact that leucine supplementation enhanced overload-induced hypertrophy only in the old (and not the young) animals may reflect the high growth stimulus of the chronic overload model. That is, the balance of protein synthesis/degradation rates under such a large chronic growth stimulus may not be the limiting factor in young animals, in which muscle growth is not impaired (i.e., synthesis/degradation rates may reach futile levels, and another factor such as sarcomere assembly may be limiting). However, the impaired balance of protein synthesis/degradation rates may be the limiting factor to growth in aged muscle, and leucine may correct this imbalance to restore muscle growth to levels observed in young animals

A Leucine-enriched Diet Enhances Overload-induced Growth and Markers of Protein Synthesis in Aged Rat Skeletal Muscle

Introduction: The hypertrophic response to overload in fast-twitch skeletal muscle is impaired in aged humans and rats, and impaired protein synthesis pathway activation is hypothesized to be a contributing factor. Muscle growth occurs when protein synthesis exceeds protein degradation. Dietary supplementation of the essential amino acid leucine has been shown to enhance protein synthesis in both young and aged skeletal muscle. Leucine acts in part by activating mammalian target of rapamycin (mTOR; a key upstream regulator of protein synthesis pathways) as well as by attenuating the activation of 5\u27-AMP-activated protein kinase (AMPK; a negative regulator of mTOR and protein synthesis). During the aging process, AMPK Thr172 phosphorylation (and thus its activation) is increased, purportedly inhibiting gains in muscle mass and strength. Although dietary leucine supplementation has been shown to enhance strength gains in response to resistance training in young humans, the potential for leucine supplementation to enhance overload-induced muscle hypertrophy in aged humans or animal models has not been examined. Thus, the aim of this study was to determine whether dietary leucine supplementation can enhance markers of protein synthesis and rescue hypertrophy in overloaded fast-twitch skeletal muscles of aged rats to levels comparable to their younger counterparts. It was hypothesized that dietary leucine supplementation during 7 days of fast-twitch plantaris muscle overload would enhance plantaris muscle hypertrophy in aged rats to levels observed in young adult rats not receiving leucine. It was also hypothesized that dietary leucine supplementation during the overload period would suppress AMPK phosphorylation and enhance markers of protein synthesis [70 kDa ribosomal protein S6 kinase (p70S6k), ribosomal protein S6 (rpS6), and eukaryotic elongation factor 2 (eEF2)] in the overloaded fast-twitch plantaris muscles of the aged rats to levels observed in young adult rats not receiving leucine. Methods: Young adult (8 mo.) and old (33 mo.) male Fisher 344 x Brown Norway F1 Hybrid (FBN) rats underwent a 1-week unilateral overload of the fast-twitch plantaris muscles via tenotomy of the synergistic gastrocnemius muscle. Within each age group, animals were matched for body weight and separated into either a dietary leucine supplementation group (normal rat chow supplemented by an additional 5% leucine content in place of 5% of the carbohydrate content; n = 7/age group) or placebo group (normal rat chow; n = 6/age group). The leucine groups started the leucine-enriched diet 2 days prior to, and throughout, the overload intervention. All animals had ad libitum access to water and chow during the entire experiment; no differences in daily calorie consumption were observed between the placebo vs. leucine groups within each age group. At the end of the overload period, sham-operated and overloaded plantaris muscles were harvested and analyzed via western blotting for the phosphorylations of AMPK, p70S6k, rpS6, and eEF2. A 2x2x2 ANOVA with repeated measures was used for analyses of the effects of age, dietary intervention, and overload (the repeated measure) on muscle hypertrophy. A 2x2 ANOVA was used to measure the percent changes in hypertrophy and western blot analyses. Post-hoc comparisons were accomplished via a Fisher\u27s Least Significant Difference test, with statistical significance being set at p ≤ 0.05. Results: Dietary leucine enrichment significantly (p ≤ 0.05) enhanced overload-induced fast-twitch plantaris muscle hypertrophy in old, but not in young adult, animals. A similar effect was also observed in the slow-twitch soleus muscles, but western blotting analyses are only presented for the fast-twitch plantaris muscles. Sham and overloaded plantaris muscle AMPK phosphorylation (Thr172) was significantly higher in aged animals receiving normal chow compared to young adult animals; however, leucine supplementation in old animals reduced this AMPK phosphorylation to levels similar to young adult animals. Phospho-p70S6k (Thr389) and phospho-rpS6 (Ser235/Ser236) were significantly lower in old vs. young overloaded muscles under placebo conditions, but leucine partially restored both p70S6k and rpS6 phosphorylations in old overloaded muscles to that of young adult overloaded muscles. Overload significantly increased total eEF2 content and decreased inhibitory eEF2 phosphorylation (Thr56; normalized to total eEF2) in young adult muscles regardless of leucine supplementation. Total eEF2 content was unaffected by overload in old placebo muscles, but leucine supplementation in old animals non-significantly (p = 0.09) restored the overload-induced increase in total eEF2 content. Muscle eEF2 phosphorylation was unaffected by overload or leucine supplementation in old animals. Discussion: These novel findings indicate that a leucine-enriched diet may potentially enhance overload-induced growth of aged fast-twitch muscle, in part by enhancing pathways known to stimulate protein synthesis. This is in accord with previous findings of leucine’s stimulating effect on protein synthesis in both young adult and aged skeletal muscle under resting conditions. The fact that leucine supplementation enhanced overload-induced hypertrophy only in the old (and not the young) animals may reflect the high growth stimulus of the chronic overload model. That is, the balance of protein synthesis/degradation rates under such a large chronic growth stimulus may not be the limiting factor in young animals, in which muscle growth is not impaired (i.e., synthesis/degradation rates may reach futile levels, and another factor such as sarcomere assembly may be limiting). However, the impaired balance of protein synthesis/degradation rates may be the limiting factor to growth in aged muscle, and leucine may correct this imbalance to restore muscle growth to levels observed in young animals

An Annotated Bibliography of Objective Pilot Performance Measures

FINAL REPORT - February-September 1981Author William F. Moroney taught at NPS in Operations Research and Naval Aviation Safety. Author Ted R. Mixon was a student in Operations Research.[Robert] Buckout's review in 1962 was the last comprehensive examination of the pilot performance measurement PPM literature. This annotated bibliography attempts to 1 gather the PPM literature written subsequent to 1962 into one source 2 describe the scenarios and measures used in collecting PPM data and 3 summarize the major premises and findings of each article. A variety of sources including computer aided literature search were used to identify candidate articles. Ultimately all referenced material was divided into three categories 1 objective pilot performance measurement 2 subjective pilot performance measures and 3 general analysis and review articles. The objective performance measure category was arranged as follows Field Conditions, Simulator Conditions, Laboratory Conditions, and Combination of Field Conditions, Simulator andor Laboratory Conditions. For each of the objective measure articles reviewed, the following parameters were reported subjects, equipment, scenario, measures and summary. For the subjective measures and general analysis and review articles the authors abstract was generally duplicated. In addition to the 189 articles addressing objective performance measurement, 30 articles dealing with subjective measures and 143 related analyses and review articles are contained in the bibliography.Approved for public release; distribution is unlimited

Gene Expression Profiling and Identification of Resistance Genes to Aspergillus flavus Infection in Peanut through EST and Microarray Strategies

Aspergillus flavus and A. parasiticus infect peanut seeds and produce aflatoxins, which are associated with various diseases in domestic animals and humans throughout the world. The most cost-effective strategy to minimize aflatoxin contamination involves the development of peanut cultivars that are resistant to fungal infection and/or aflatoxin production. To identify peanut Aspergillus-interactive and peanut Aspergillus-resistance genes, we carried out a large scale peanut Expressed Sequence Tag (EST) project which we used to construct a peanut glass slide oligonucleotide microarray. The fabricated microarray represents over 40% of the protein coding genes in the peanut genome. For expression profiling, resistant and susceptible peanut cultivars were infected with a mixture of Aspergillus flavus and parasiticus spores. The subsequent microarray analysis identified 62 genes in resistant cultivars that were up-expressed in response to Aspergillus infection. In addition, we identified 22 putative Aspergillus-resistance genes that were constitutively up-expressed in the resistant cultivar in comparison to the susceptible cultivar. Some of these genes were homologous to peanut, corn, and soybean genes that were previously shown to confer resistance to fungal infection. This study is a first step towards a comprehensive genome-scale platform for developing Aspergillus-resistant peanut cultivars through targeted marker-assisted breeding and genetic engineering

Effects of Dietary Leucine Supplementation on Muscle Mass and Markers of Protein Degradation in Overloaded Skeletal Muscles of Young Adult and Aged Rats

The hypertrophic response to overload in fast-twitch skeletal muscle is impaired in aged humans and rats and upregulation of protein degradation pathways are hypothesized to be a contributing factor. Muscle growth occurs when protein synthesis is greater than protein degradation. Dietary supplementation of the essential amino acid leucine has been shown to reduce protein degradation in both young and aged skeletal muscle. Specifically leucine acts in part by attenuating 5'-AMP-activated protein kinase (AMPK) activation as well as the translocation of the forkhead box transcription factor 3A (FoxO3 known to promote transcription of mRNAs encoding degradation pathway proteins) to the nucleus. Akt (a promoter of muscle growth) prevents translocation of FoxO3 into the nucleus by phosphorylating FoxO3 phosphorylation at Ser[superscript]318/321. However AMPK inhibits Akt's phosphorylation of FoxO3 allowing it to enter the nucleus and increase transcription of protein degradation pathway genes encoding ubiquitin ligase proteins such as muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx or Atrogin-1). During the aging process AMPK Thr[superscript]172 phosphorylation (and thus its activation) is increased purportedly inhibiting gains in muscle mass and strength. Although dietary leucine supplementation has been shown to enhance muscle hypertrophy in response to resistance training in young humans the potential for leucine supplementation to enhance overload-induced muscle hypertrophy in aged humans or animal models has not been examined. Thus the aim of this study was to determine whether dietary leucine supplementation can attenuate markers of protein degradation and rescue hypertrophy during overload in the fast-twitch skeletal muscles of aged rats to levels comparable to their younger counterparts. It was hypothesized that dietary leucine supplementation during 7 days of fast-twitch plantaris muscle overload would enhance plantaris muscle hypertrophy in aged rats to levels observed in young adult rats not receiving leucine. It was also hypothesized that dietary leucine supplementation during the overload period would alter markers of protein degradation (enhance FoxO3 phosphorylation and reduce the levels of AMPK phosphorylation Atrogin-1 protein content and MuRF1 protein content) in the overloaded fast-twitch plantaris muscles of the aged rats to levels observed in young adult rats not receiving leucine. Young adult (8 mo.) and old (33 mo.) male Fisher 344 x Brown Norway F1 Hybrid (FBN) rats underwent a 1-week unilateral overload of the fast-twitch plantaris muscles via tenotomy of the synergistic gastrocnemius muscle. Within each age group animals were matched for body weight and separated into either a dietary leucine supplementation group (normal rat chow supplemented by an additional 5% leucine content in place of 5% of the carbohydrate content; n = 7/age group) or placebo group (normal rat chow; n = 6/age group). The leucine groups started the leucine-enriched diet 2 days prior to and throughout the overload intervention. All animals had ad libitum access to water and chow during the entire experiment; no differences in daily calorie consumption were observed between the placebo vs. leucine groups within each age group. At the end of the overload period sham-operated and overloaded plantaris muscles were harvested and analyzed via western blotting for the phosphorylations of AMPK and FoxO3 as well as total levels of Atrogin-1 and MuRF1. Dietary leucine enrichment significantly (p [equal to or less than] 0.05) enhanced overload-induced plantaris muscle hypertrophy in old but not in young adult animals. Sham and overloaded plantaris muscle AMPK phosphorylation was significantly higher in aged animals receiving normal chow compared to young adult animals; however leucine supplementation in old animals reduced this AMPK phosphorylation to levels similar to young adult animals. Compared to placebo leucine also non-significantly (p = 0.07) enhanced FoxO3 phosphorylation in the overloaded muscles of both young adult and old animals (thus theoretically reducing FoxO3 translocation to the nucleus). Accordingly leucine also non-significantly (p = 0.07) reversed the overload-induced increase (from a 22.8% increase to a 17.0% decrease) in Atrogin-1 content in aged muscles and non-significantly (p = 0.14) enhanced the overload-induced decrease in MuRF1 content in the muscles of both age groups. These findings indicate that a leucine-enriched diet may potentially enhance overload-induced growth of aged fast-twitch muscle in part by suppressing pathways known to stimulate protein degradation.

Human Capital, Networks and Segmentation in the Market for Academic Economists

Academic labor markets often exhibit steep hierarchies, with institutions at the top attempting to attract newly minted doctorates from similarly situated institutions in an effort to maintain or improve their reputations. Yet, despite recent research on labor market segmentation in academe, the literature has heretofore been under-theorized. This paper provides a straightforward formal model that generates a three-tiered hierarchy of academic institutions, wherein academic departments affiliated with top-tier universities endeavor to hire only from within the group, while those in the bottom tier are unable to employ faculty with degrees from top departments. The results from statistical tests applied to data from economics departments in the U.S. indicate that top-tier departments employ 3.5 to 3.8 (2.5 to 2.9) more assistant professors from top-tier institutions, ceteris paribus, than bottom (middle) tier departments