Multi-Job Intelligent Scheduling with Cross-Device Federated Learning

Recent years have witnessed a large amount of decentralized data in various (edge) devices of end-users, while the decentralized data aggregation remains complicated for machine learning jobs because of regulations and laws. As a practical approach to handling decentralized data, Federated Learning (FL) enables collaborative global machine learning model training without sharing sensitive raw data. The servers schedule devices to jobs within the training process of FL. In contrast, device scheduling with multiple jobs in FL remains a critical and open problem. In this paper, we propose a novel multi-job FL framework, which enables the training process of multiple jobs in parallel. The multi-job FL framework is composed of a system model and a scheduling method. The system model enables a parallel training process of multiple jobs, with a cost model based on the data fairness and the training time of diverse devices during the parallel training process. We propose a novel intelligent scheduling approach based on multiple scheduling methods, including an original reinforcement learning-based scheduling method and an original Bayesian optimization-based scheduling method, which corresponds to a small cost while scheduling devices to multiple jobs. We conduct extensive experimentation with diverse jobs and datasets. The experimental results reveal that our proposed approaches significantly outperform baseline approaches in terms of training time (up to 12.73 times faster) and accuracy (up to 46.4% higher).Comment: To appear in TPDS; 22 pages, 17 figures, 8 tables. arXiv admin note: substantial text overlap with arXiv:2112.0592

Predictors of Hypertension in Mauritians with Normotension and Prehypertension at Baseline : A Cohort Study

Information on the predictors of future hypertension in Mauritians with prehypertension is scant. The aim of this study was to analyze the 5-year and 11-year risk of hypertension and its predictors in people with normotension and prehypertension at baseline in Mauritius in 1987. This was a retrospective cohort study of 883 men and 1194 women of Mauritian Indian and Mauritian Creole ethnicity, aged 25-74 years old, free of hypertension at baseline in 1987 with follow-up examinations in 1992 and 1998 using the same methodology. The main outcome was 5- and 11-year risk of hypertension. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated. The 5-year risk of hypertension was 5.4-times higher in people with prehypertension compared with normotensive individuals at baseline. The corresponding odds for prehypertensive people at baseline regarding 11-year hypertension risk was 3.39 (95% CI 2.67-4.29) in the adjusted logistic regression models. Being of Creole ethnicity (OR 1.42; 95% CI 1.09-1.86) increased the 11-year odds of hypertension compared with the Indian population. It is of importance to screen for people with prehypertension and implement strategies to reduce their systolic blood pressure levels to the recommended levels of 120/80 mmHg. Special attention needs to be given to Mauritians of Creole ethnicity.Peer reviewe

Faktor-Faktor Yang Mempengaruhi Pengungkapan Tanggung Jawab Sosial

Penelitian ini bertujuan untuk menentukan faktor-faktor yang mempengaruhi luasnya tingkat pengungkapan tanggung jawab sosial Perusahaan (Corporate Social Responsibility) dengan menguji pengaruh ukuran Perusahaan, profitabilitas, leverage, kepemilikan insti­tusional, ukuran dewan komisaris, ukuran dewan direksi, dan ukuran komite audit. Sampel yang digunakan adalah Perusahaan sektor pertambangan terdaftar di Bursa Efek Indonesia selama 2010-2012. Data diperoleh dari laporan keuangan auditan dan laporan tahunan serta laporan keberlanjutan (sustainability report) jika ada. Penelitian ini menggunakan pendekatan kuantitatif dengan analisis regresi linear berganda. Penelitian ini menunjukkan bahwa ukuran Perusahaan dan komite audit memiliki pengaruh positif terhadap peng­ungkapan tanggung jawab sosial. Tidak ditemukan bukti pengaruh profitabilitas, leverage, kepemilikan institusional, ukuran dewan komisaris, dan ukuran dewan direksi terhadap terhadap pengungkapan tanggung jawab sosial

Integrated gene-based and pathway analyses using UK Biobank data identify novel genes for chronic respiratory diseases

BackgroundChronic respiratory diseases have become a non-negligible cause of death globally. Although smoking and environmental exposures are primary risk factors for chronic respiratory diseases, genetic factors also play an important role in determining individual’s susceptibility to diseases. Here we performed integrated gene-based and pathway analyses to systematically illuminate the heritable characteristics of chronic respiratory diseases.MethodsUK (United Kingdom) Biobank is a very large, population-based prospective study with over 500,000 participants, established to allow detailed investigations of the genetic and nongenetic determinants of the diseases. Utilizing the GWAS-summarized data downloaded from UK Biobank, we conducted gene-based analysis to obtain associations of susceptibility genes with asthma, chronic obstructive pulmonary disease (COPD) and pneumonia using FUSION and MAGMA software. Across the identified susceptibility regions, functional annotation integrating multiple functional data sources was performed to explore potential regulatory mechanisms with INQUISIT algorithm. To further detect the biological process involved in the development of chronic respiratory diseases, we undertook pathway enrichment analysis with the R package (clusterProfiler).ResultsA total of 195 susceptibility genes were identified significantly associated with chronic respiratory diseases (Pbonferroni < 0.05), and 24/195 located out of known susceptibility regions (e.g. WDPCP in 2p15). Within the identified susceptibility regions, functional annotation revealed an aggregation of credible variants in promoter-like and enhancer-like histone modification regions and such regulatory mechanisms were specific to lung tissues. Furthermore, 110 genes with INQUISIT score ≥1 may influence diseases susceptibility through exerting effects on coding sequences, proximal promoter and distal enhancer regulations. Pathway enrichment results showed that these genes were enriched in immune-related processes and nicotinic acetylcholine receptors pathways.ConclusionsThis study implemented an integrated gene-based and pathway strategy to explore the underlying biological mechanisms and our findings may serve as promising targets for future clinical treatments of chronic respiratory diseases

Family-based whole-exome sequencing identifies novel loss-of-function mutations of FBN1 for Marfan syndrome

Background Marfan syndrome (MFS) is an inherited connective tissue disorder affecting the ocular, skeletal and cardiovascular systems. Previous studies of MFS have demonstrated the association between genetic defects and clinical manifestations. Our purpose was to investigate the role of novel genetic variants in determining MFS clinical phenotypes. Methods We sequenced the whole exome of 19 individuals derived from three Han Chinese families. The sequencing data were analyzed by a standard pipeline. Variants were further filtered against the public database and an in-house database. Then, we performed pedigree analysis under different inheritance patterns according to American College of Medical Genetics guidelines. Results were confirmed by Sanger sequencing. Results Two novel loss-of-function indels (c.5027_5028insTGTCCTCC, p.D1677Vfs*8; c.5856delG, p.S1953Lfs*27) and one nonsense variant (c.8034C>A, p.Y2678*) of FBN1 were identified in Family 1, Family 2 and Family 3, respectively. All affected members carried pathogenic mutations, whereas other unaffected family members or control individuals did not. These different kinds of loss of function (LOF) variants of FBN1 were located in the cbEGF region and a conserved domain across species and were not reported previously. Conclusions Our study extended and strengthened the vital role of FBN1 LOF mutations in the pathogenesis of MFS with an autosomal dominant inheritance pattern. We confirm that genetic testing by next-generation sequencing of blood DNA can be fundamental in helping clinicians conduct mutation-based pre- and postnatal screening, genetic diagnosis and clinical management for MFS

The Last April

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Human spermatogenic failure purges deleterious mutation load from the autosomes and both sex chromosomes, including the gene DMRT1

Gonadal failure, along with early pregnancy loss and perinatal death, may be an important filter that limits the propagation of harmful mutations in the human population. We hypothesized that men with spermatogenic impairment, a disease with unknown genetic architecture and a common cause of male infertility, are enriched for rare deleterious mutations compared to men with normal spermatogenesis. After assaying genomewide SNPs and CNVs in 323 Caucasian men with idiopathic spermatogenic impairment and more than 1,100 controls, we estimate that each rare autosomal deletion detected in our study multiplicatively changes a man’s risk of disease by 10% (OR 1.10 [1.04–1.16], p,261023), rare X-linked CNVs by 29%, (OR 1.29 [1.11–1.50], p,161023), and rare Y-linked duplications by 88% (OR 1.88 [1.13–3.13], p,0.03). By contrasting the properties of our case-specific CNVs with those of CNV callsets from cases of autism, schizophrenia, bipolar disorder, and intellectual disability, we propose that the CNV burden in spermatogenic impairment is distinct from the burden of large, dominant mutations described for neurodevelopmental disorders. We identified two patients with deletions of DMRT1, a gene on chromosome 9p24.3 orthologous to the putative sex determination locus of the avian ZW chromosome system. In an independent sample of Han Chinese men, we identified 3 more DMRT1 deletions in 979 cases of idiopathic azoospermia and none in 1,734 controls, and found none in an additional 4,519 controls from public databases. The combined results indicate that DMRT1 loss-of-function mutations are a risk factor and potential genetic cause of human spermatogenic failure (frequency of 0.38% in 1306 cases and 0% in 7,754 controls, p = 6.261025). Our study identifies other recurrent CNVs as potential causes of idiopathic azoospermia and generates hypotheses for directing future studies on the genetic basis of male infertility and IVF outcomes.This work was partially funded by the Portuguese Foundation for Science and Technology FCT/MCTES (PIDDAC) and co-financed by European funds (FEDER) through the COMPETE program, research grant PTDC/SAU-GMG/101229/2008. IPATIMUP is an Associate Laboratory of the Portuguese Ministry of Science, Technology, and Higher Education and is partially supported by FCT. AML is the recipient of a postdoctoral fellowship from FCT (SFRH/BPD/73366/2010). CO is supported by a grant from the United States National Institutes of Health (R01 HD21244), JDS is supported by Damon Runyon Clinical Investigator Award, Alex's Lemonade Stand Foundation Epidemiology Award, and the Eunice Kennedy Shriver Children's Health Research Career Development Award NICHD 5K12HD001410. Support for humans studies and specimens were provided by the NIH/NIDDK George M. O'Brien Center for Kidney Disease Kidney Translational Research Core (P30DK079333) grant to Washington University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript