16 research outputs found

    Kairos: Preemptive Data Center Scheduling Without Runtime Estimates

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    The vast majority of data center schedulers use task runtime estimates to improve the quality of their scheduling decisions. Knowledge about runtimes allows the schedulers, among other things, to achieve better load balance and to avoid head-of-line blocking. Obtaining accurate runtime estimates is, however, far from trivial, and erroneous estimates lead to sub-optimal scheduling decisions. Techniques to mitigate the effect of inaccurate estimates have shown some success, but the fundamental problem remains. This paper presents Kairos, a novel data center scheduler that assumes no prior information on task runtimes. Kairos introduces a distributed approximation of the Least Attained Service (LAS) scheduling policy. Kairos consists of a centralized scheduler and per-node schedulers. The per-node schedulers implement LAS for tasks on their node, using preemption as necessary to avoid head-of-line blocking. The centralized scheduler distributes tasks among nodes in a manner that balances the load and imposes on each node a workload in which LAS provides favorable performance. We have implemented Kairos in YARN. We compare its performance against the YARN FIFO scheduler and Big-C, an open-source state-of-the-art YARN-based scheduler that also uses preemption. Compared to YARN FIFO, Kairos reduces the median job completion time by 73% and the 99th percentile by 30%. Compared to Big-C, the improvements are 37% for the median and 57% for the 99th percentile. We evaluate Kairos at scale by implementing it in the Eagle simulator and comparing its performance against Eagle. Kairos improves the 99th percentile of short job completion times by up to 55% for the Google trace and 85% for the Yahoo trace

    A Hazelnut-Enriched Diet Modulates Oxidative Stress and Inflammation Gene Expression without Weight Gain

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    Introduction. Inflammation is associated with obesity condition and plays a pivotal role in the onset and progression of many chronic diseases. Among several nutraceutical foods, hazelnuts (Corylus avellana L.) are considered an excellent anti-inflammatory and hypolipidemic food being the second richest source of monounsaturated fatty acids among nuts and because they are rich in vitamins, minerals, and phenolic compounds.Materials and Methods. A prospective pilot clinical trial on 24 healthy volunteers who consumed daily, as a snack, 40 g of hazelnuts (261.99 kcal/1096.17 kJ) for six weeks was conducted. Anthropometric measurements, body composition analysis, and nutrigenomic analysis on 12 anti-inflammatory and antioxidant genes were evaluated at baseline (T0) and after hazelnut intervention (T1).Results. No significant changes were detected on body composition analysis after hazelnut consumption. Conversely, significant upregulation was detected for SOD1(2−ΔΔCt=242), CAT (2−ΔΔCt=241), MIF (2−ΔΔCt=412), PPARγ(2−ΔΔCt=589), VDR (2−ΔΔCt=361), MTHFR (2−ΔΔCt=240),and ACE (2−ΔΔCt=216) at the end of the study.Conclusions. According to emerging evidences, hazelnut consumption does not lead to weight gain probably due to the improvement of the body’s antioxidant capacity by the upregulation of genes implied in oxidant reactions and inflammation

    MIG1 Glucose Repression in Metabolic Processes of Saccharomyces cerevisiae: Genetics to Metabolic Engineering

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    Background: Although Saccharomyces cerevisiae has several industrial applications, there are still fundamental problems associated with sequential use of carbon sources. As such, glucose repression effect can direct metabolism of yeast to preferably anaerobic conditions. This leads to higher ethanol production and less efficient production of recombinant products. The general glucose repression system is constituted by MIG1, TUP1 and SSN6 factors. The role of MIG1 is known in glucose repression but the evaluation of effects on aerobic/anaerobic metabolism by deletion of MIG1 and constructing an optimal strain brand remains unclear and an objective to be explored. Methods: To find the impact of MIG1 in induction of glucose-repression, the Mig1 disruptant strain (DeltaMIG1) was produced for comparing with its congenic wild-type strain (2805). The analysis approached for changes in the rate of glucose consumption, biomass yield, cell protein contents, ethanol and intermediate metabolites production. The MIG1 disruptant strain exhibited 25 glucose utilization, 12 biomass growth rate and 22 protein content over the wild type. The shift to respiratory pathway has been demonstrated by 122.86 and 40 increase of glycerol and pyruvate production, respectively as oxidative metabolites, while the reduction of fermentative metabolites such as acetate 35.48 and ethanol 24. Results: Results suggest that DeltaMIG1 compared to the wild-type strain can significantly present less effects of glucose repression. Conclusion: The constructed strain has more efficient growth in aerobic cultivations and it can be a potential host for biotechnological recombinant yields and industrial interests

    The key role of Akt protein kinase in metabolic-inflammatory pathways cross-talk: TNF-alpha down-regulation and improving of insulin resistance in HepG2 cell line

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    BACKGROUND: Elevation of plasma free fatty acids as a principal aspect of type 2 diabetes maintains etiologically insulin insensitivity in target cells. TNF-alpha inhibitory effects on key insulin signaling pathway elements remain to be verified in insulin-resistant hepatic cells. Thus, TNF-alpha knockdown effects on the key elements of insulin signaling were investigated in the palmitate-induced insulin-resistant hepatocytes. The Akt serine kinase, a key protein of the insulin signaling pathway, phosphorylation was monitored to understand the TNF-alpha effect on probable enhancing of insulin resistance. METHODS: Insulin-resistant HepG2 cells were produced using 0.5 mM palmitate treatment and shRNA-mediated TNF-alpha gene knockdown and its down-regulation confirmed using ELISA technique. Western blotting analysis used to assess the Akt protein phosphorylation status. RESULTS: Palmitate-induced insulin resistance caused TNF-alpha protein overexpression 1.2-, 2.78, and 2.25- fold as compared to the control cells at post-treatment times of 8 h, 16 h, and 24 h, respectively. In the presence of palmitate, TNF-alpha expression showed around 30 reduction in TNF-alpha knockdown cells as compared to normal cells. In the TNF-alpha down-regulated cell, Akt phosphorylation was approximately 62 more than control cells after treatment with 100 nM insulin in conjugation with 0.5 mM palmitate. CONCLUSIONS: The obtained data demonstrated that TNF-alpha protein expression reduction improved insulin-stimulated Akt phosphorylation in the HepG2 cells and decreased lipid-induced insulin resistance of the diabetic hepatocytes

    Corrigendum to: Association between abcc8 ala1369ser polymorphism (rs757110 t/g) and type 2 diabetes risk in an iranian population: A case-control study (Endocrine, Metabolic and Immune Disorders - Drug Targets, 2021, 21(3), 441-447, 10.2174/1871530320666200713091827. )

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    Due to oversight on the part of the authors, the names of two of the co-authors have been incorrectly published in the article entitled, “Association between ABCC8 Ala1369Ser Polymorphism (rs757110 T/G) and Type 2 Diabetes Risk in an Iranian Population: A Case-Control Study”, 2021, Vol. 21, No. 3, pp. 441-447 1. The original article can be found online at: https://doi.org/10.2174/1871530320666200713091827. Original: Amin Bakhtiyari, Karimeh Haghani, Salar Bakhtiyari*, Mohammad A. Zaimy, Nooriali Zahed, Ali Gheysarzadeh, Shahram Darabi, Seidali Nahalkhani, Mansour Amraei and Iraj Alipourfard Corrected: Amin Bakhtiyari, Karimeh Haghani, Salar Bakhtiyari*, Mohammad A. Zaimy, Ali Noori-Zadeh, Ali Gheysarzadeh, Shahram Darabi, Ali Seidkhani-Nahal, Mansour Amraei and Iraj Alipourfard. © 2021 Bentham Science Publishers

    Corrigendum to: Association between ABCC8 Ala1369Ser Polymorphism (rs757110 T/G) and Type 2 Diabetes Risk in an Iranian Population: A Case-Control Study

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    Due to oversight on the part of the authors, the names of two of the co-authors have been incorrectly published in the article entitled, "Association between ABCC8 Ala1369Ser Polymorphism (rs757110 T/G) and Type 2 Diabetes Risk in an Iranian Population: A Case-Control Study", 2021, Vol. 21, No. 3, pp. 441-447 1. The original article can be found online at: https://doi.org/10.2174/1871530320666200713091827. Original: Amin Bakhtiyari, Karimeh Haghani, Salar Bakhtiyari*, Mohammad A. Zaimy, Nooriali Zahed, Ali Gheysarzadeh, Shahram Darabi, Seidali Nahalkhani, Mansour Amraei and Iraj Alipourfard Corrected: Amin Bakhtiyari, Karimeh Haghani, Salar Bakhtiyari*, Mohammad A. Zaimy, Ali Noori-Zadeh, Ali Gheysarzadeh, Shahram Darabi, Ali Seidkhani-Nahal, Mansour Amraei and Iraj Alipourfard

    SACCHAROMYCES CEREVISIAE, KEY ROLE OF MIG1 GENE IN METABOLIC SWITCHING: PUTATIVE FERMENTATION/OXIDATION

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    Saccharomyces cerevisiae can utilize a wide range of carbon sources; however, in the presence of glucose the use of alternate carbon sources would be repressed. Several genes involved in the metabolic pathways exert these effects. Among them, the zinc finger protein, Mig1 (multicopy inhibitor of GAL gene expression) plays important roles in glucose repression of Saccharomyces cerevisiae. To investigate whether the alleviation of glucose effect would result in a switch to oxidative production pathway, MIG1 were disrupted in a haploid laboratory strain (2805) of S. cerevisiae. The impact of this disruption was studied under fully aerobic conditions when glucose was the sole carbon source. Our results showed that glucose repression was partly alleviated; i.e., ethanol, as a significant fermentation marker, and acetate productions were respectively decreased by 14.13 and 43.71 compared to the wild type. In Delta MIG1 strain, the metabolic shifting on the aerobic pathway and a significant increase in pyruvate and glycerol production suggested it as an optimally productive industrial yeast strain. However, further studies are needed to confirm these findings

    Association between ABCC8 Ala1369Ser Polymorphism (rs757110 T/G) and Type 2 Diabetes risk in an Iranian population: A Case-Control Study

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    OBJECTIVE: Glucose metabolism increases ATP/ADP ratio within the beta-cells and causes ATP-sensitive K+ (KATP) channel closure and consequently insulin secretion. The enhanced activity of the channel may be a mechanism contributing to the reduced first-phase of insulin secretion observed in T2DM. There is no study to date in the Kurdish ethnic group regarding the relationship between SNP Ala1369Ser (rs757110 T/G) of SUR1 gene and T2DM, and additionally, the results of this association in other populations are inconsistent. Therefore, our aim in this study was to explore the possible association between SNP Ala1369Ser and type 2 diabetes in an Iranian Kurdish ethnic group. METHODS: In this study, we checked out the frequency of alleles and genotypes of SNP Ala1369Ser in T2DM individuals (207 patients; men/women: 106/101) and non-T2DM subjects (201 controls; men/women: 97/104), and their effects on anthropometric, clinical, and biochemical parameters. Genomic DNA was extracted from the leukocytes of blood specimens using a standard method. We amplified the ABCC8 rs757110 polymorphic site (T/G) using a polymerase chain reaction (PCR) method and a designed primer pair. To perform the PCR-RFLP method, the amplicons were subjected to restriction enzymes and the resulting fragments separated by gel electrophoresis. RESULTS: The frequency of the G-allele of Ala1369Ser polymorphism was significantly (0.01) higher in the case group than the control group (19 vs. 9, respectively). In the dominant model (TT vs. TG+GG), there was a significant relationship between this SNP and an increased risk of T2DM (P = 0.00). T2DM patients with TG+GG genotypes had significantly higher fasting plasma insulin and HOMA-IR than those who had the TT genotype (P = 0.02 and 0.01, respectively). CONCLUSIONS: Our study is the first study to investigate the association between Ala1369Ser ABCC8 genetic variation and T2DM in the Kurdish population of western Iran. The obtained results clearly show that Ala1369Ser polymorphism of ABCC8 is associated with an increased risk of T2DM in this population
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