42 research outputs found

    Production of bio resin from palm oil

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    Nowadays, the demand for fossil fuels is quite high. But, the extensive use of fossil fuels is causing the gradual decrease of fossil fuels. Therefore, a way to get rid of widespread of using fossil fuels is by developing a new renewable source that can benefit our environment. Resin is one of the important polymeric in the chemical industry. Resins such as alkyd resins are widely used in coatings and paint industry. There are many researches about producing a resin from renewable sources such as vegetable oils. The naturally used vegetable oils in producing resin are soyabean, rapeseed, coconut, castor or linseed oils. Other than that, there are many potential vegetable oils such as karawila, nahar, rubber or safflower oil. Scientist and engineers are dedicated to find another alternative to replace using fossil fuels as the main components in resin making. This study was inspired to do a research by using palm oil as the main components in making renewable resin or bio resin. In this study, waste cooking oil was used as the main component in making bio resin. The synthesis of resin begins with alcoholysis of waste cooking oil with glycerol followed by esterification process. Then, the monoglyceride was reacted with anhydride to obtain bio resin. The resulting product which is bio resin was characterized for physiochemical properties, thermogravimetric analysis (TGA), the infrared spectrum using Fourier Transform Infrared Spectroscopy (FTIR), melting point using Differential Scanning Calorimeter (DSC). The result was compared with previous literature about producing resin from renewable material such as karawila seed oil. The expected resin is feasible in replacing synthetic resin. Thus, improvements and more research need to be made as to market the resin

    Intrinsic motivation as a double-edged sword: Investigating effects on well-being and the role of flex place practices as moderator to buffer adverse effects

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    Ensuring employee well-being is a crucial task for organizations. While previous research has mainly focused on positive effects of intrinsic motivation, in this study, we took a more comprehensive view on intrinsic motivation and work-related well-being. More specifically, building on conservation of resources theory, we focused on two facets of work-related well-being (job satisfaction and emotional exhaustion) and examined direct (beneficial) and indirect (adverse) effects on well-being via detachment as an inconsistent mediation model. Furthermore, we took a closer look at how the use of flex place practices (FPPs), giving employees the opportunity to choose from where to work, can attenuate potential adverse effects of high intrinsic motivation. We collected data from 408 employees of a European manufacturer at two points of measurement, the first one before and the second one after the introduction of FPPs. Results showed that intrinsic motivation had a positive direct effect on changes in well-being, and an adverse indirect effect on changes in well-being via reduced detachment. For employees using FPPs, this adverse indirect effect was dissolved. This research is among the first to explore potential downsides of intrinsic motivation and the role of FPPs in the functioning of intrinsic motivation

    Unlimited Paid Time Off Policies:Unlocking the Best and Unleashing the Beast

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    Unlimited paid time off policies are currently fashionable and widely discussed by HR professionals around the globe. While on the one hand, paid time off is considered a key benefit by employees and unlimited paid time off policies (UPTO) are seen as a major perk which may help in recruiting and retaining talented employees, on the other hand, early adopters reported that employees took less time off than previously, presumably leading to higher burnout rates. In this conceptual review, we discuss the theoretical and empirical evidence regarding the potential effects of UPTO on leave utilization, well-being and performance outcomes. We start out by defining UPTO and placing it in a historical and international perspective. Next, we discuss the key role of leave utilization in translating UPTO into concrete actions. The core of our article constitutes the description of the effects of UPTO and the two pathways through which these effects are assumed to unfold: autonomy need satisfaction and detrimental social processes. We moreover discuss the boundary conditions which facilitate or inhibit the successful utilization of UPTO on individual, team, and organizational level. In reviewing the literature from different fields and integrating existing theories, we arrive at a conceptual model and five propositions, which can guide future research on UPTO. We conclude with a discussion of the theoretical and societal implications of UPTO

    Staying in touch while at work : Relationships between personal social media use at work and work-nonwork balance and creativity

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    Personal social media use at work is usually deemed counterproductive work behaviour reducing employee productivity. However, we hypothesized that it may actually help employees to coordinate work and nonwork demands, which should in turn increase work-related creativity. We used ecological momentary assessment across one working day with up to ten hourly measurements on 337 white-collar workers to measure personal social media use, work-nonwork balance and creativity, resulting in a total of 2244 hourly measurements. Multilevel modelling revealed that personal social media use was associated with better work-nonwork balance, but with lower levels of creativity between- and within-persons. Work-nonwork balance did not mediate the relationship between personal social media use and creativity. More research is needed to understand why employees use social media at work for personal purposes and how this affects their well-being and job performance

    Epigenome-wide association study of serum urate reveals insights into urate co-regulation and the SLC2A9 locus

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    Elevated serum urate levels, a complex trait and major risk factor for incident gout, are correlated with cardiometabolic traits via incompletely understood mechanisms. DNA methylation in whole blood captures genetic and environmental influences and is assessed in transethnic meta-analysis of epigenome-wide association studies (EWAS) of serum urate (discovery, n = 12,474, replication, n = 5522). The 100 replicated, epigenome-wide significant (p < 1.1E–7) CpGs explain 11.6% of the serum urate variance. At SLC2A9, the serum urate locus with the largest effect in genome-wide association studies (GWAS), five CpGs are associated with SLC2A9 gene expression. Four CpGs at SLC2A9 have significant causal effects on serum urate levels and/or gout, and two of these partly mediate the effects of urate-associated GWAS variants. In other genes, including SLC7A11 and PHGDH, 17 urate-associated CpGs are associated with conditions defining metabolic syndrome, suggesting that these CpGs may represent a blood DNA methylation signature of cardiometabolic risk factors. This study demonstrates that EWAS can provide new insights into GWAS loci and the correlation of serum urate with other complex traits

    Meta-analyses identify DNA methylation associated with kidney function and damage

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    Chronic kidney disease is a major public health burden. Elevated urinary albumin-to-creatinine ratio is a measure of kidney damage, and used to diagnose and stage chronic kidney disease. To extend the knowledge on regulatory mechanisms related to kidney function and disease, we conducted a blood-based epigenome-wide association study for estimated glomerular filtration rate (n = 33,605) and urinary albumin-to-creatinine ratio (n = 15,068) and detected 69 and seven CpG sites where DNA methylation was associated with the respective trait. The majority of these findings showed directionally consistent associations with the respective clinical outcomes chronic kidney disease and moderately increased albuminuria. Associations of DNA methylation with kidney function, such as CpGs at JAZF1, PELI1 and CHD2 were validated in kidney tissue. Methylation at PHRF1, LDB2, CSRNP1 and IRF5 indicated causal effects on kidney function. Enrichment analyses revealed pathways related to hemostasis and blood cell migration for estimated glomerular filtration rate, and immune cell activation and response for urinary albumin-to-creatinineratio-associated CpGs

    Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity.

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    Many genetic loci affect circulating lipid levels, but it remains unknown whether lifestyle factors, such as physical activity, modify these genetic effects. To identify lipid loci interacting with physical activity, we performed genome-wide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,979 individuals of European, African, Asian, Hispanic, and Brazilian ancestry, with follow-up of suggestive associations in an additional 131,012 individuals. We find four loci, in/near CLASP1, LHX1, SNTA1, and CNTNAP2, that are associated with circulating lipid levels through interaction with physical activity; higher levels of physical activity enhance the HDL cholesterol-increasing effects of the CLASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol-increasing effect of the CNTNAP2 locus. The CLASP1, LHX1, and SNTA1 regions harbor genes linked to muscle function and lipid metabolism. Our results elucidate the role of physical activity interactions in the genetic contribution to blood lipid levels

    Epigenome-wide association study of serum urate reveals insights into urate co-regulation and the SLC2A9 locus

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    Serum urate concentration can be studied in large datasets to find genetic and epigenetic loci that may be related to cardiometabolic traits. Here the authors identify and replicate 100 urate-associated CpGs, which provide insights into urate GWAS loci and shared CpGs of urate and cardiometabolic traits.Elevated serum urate levels, a complex trait and major risk factor for incident gout, are correlated with cardiometabolic traits via incompletely understood mechanisms. DNA methylation in whole blood captures genetic and environmental influences and is assessed in transethnic meta-analysis of epigenome-wide association studies (EWAS) of serum urate (discovery, n = 12,474, replication, n = 5522). The 100 replicated, epigenome-wide significant (p < 1.1E-7) CpGs explain 11.6% of the serum urate variance. At SLC2A9, the serum urate locus with the largest effect in genome-wide association studies (GWAS), five CpGs are associated with SLC2A9 gene expression. Four CpGs at SLC2A9 have significant causal effects on serum urate levels and/or gout, and two of these partly mediate the effects of urate-associated GWAS variants. In other genes, including SLC7A11 and PHGDH, 17 urate-associated CpGs are associated with conditions defining metabolic syndrome, suggesting that these CpGs may represent a blood DNA methylation signature of cardiometabolic risk factors. This study demonstrates that EWAS can provide new insights into GWAS loci and the correlation of serum urate with other complex traits.</p

    Meta-analyses identify DNA methylation associated with kidney function and damage

    Get PDF
    Chronic kidney disease is a major public health burden. Elevated urinary albumin-to-creatinine ratio is a measure of kidney damage, and used to diagnose and stage chronic kidney disease. To extend the knowledge on regulatory mechanisms related to kidney function and disease, we conducted a blood-based epigenome-wide association study for estimated glomerular filtration rate (n = 33,605) and urinary albumin-to-creatinine ratio (n = 15,068) and detected 69 and seven CpG sites where DNA methylation was associated with the respective trait. The majority of these findings showed directionally consistent associations with the respective clinical outcomes chronic kidney disease and moderately increased albuminuria. Associations of DNA methylation with kidney function, such as CpGs at JAZF1, PELI1 and CHD2 were validated in kidney tissue. Methylation at PHRF1, LDB2, CSRNP1 and IRF5 indicated causal effects on kidney function. Enrichment analyses revealed pathways related to hemostasis and blood cell migration for estimated glomerular filtration rate, and immune cell activation and response for urinary albumin-to-creatinineratio-associated CpGs.Many genetic loci have been identified to be associated with kidney disease, but the molecular mechanisms are not well understood. Here, the authors perform epigenome-wide association studies on kidney function measures to identify epigenetic marks and pathways involved in kidney function.</p
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