Performance, emission, and combustion characteristics of twin-cylinder common rail diesel engine fuelled with butanol-diesel blends

Abstract

Nitrogen oxides and smoke are the substantial emissions for the diesel engines. Fuels comprising high-level oxygen content can have low smoke emission due to better oxidation of soot. The objective of the paper is to assess the potential to employ oxygenated fuel, i.e., n-butanol and its blends with the neat diesel from 0 to 30% by volume. The experimental and computational fluid dynamic (CFD) simulation is carried out to estimate the performance, combustion, and exhaust emission characteristics of n-butanol-diesel blends for various injection timings (9°, 12°, 15°, and 18°) using modern twin-cylinder, four-stroke, common rail direct injection (CRDI) engine. Experimental results reveal the increase in brake thermal efficiency (BTE) by ~ 4.5, 6, and 8% for butanol-diesel blends of 10% (Bu10), 20% (Bu20), and 30% (Bu30), respectively, compared to neat diesel (Bu0). Maximum BTE for Bu0 is 38.4%, which is obtained at 12° BTDC; however, for Bu10, Bu20 and Bu30 are 40.19, 40.9, and 41.7%, which are obtained at 15° BTDC, respectively. Higher flame speed of n-butanol-diesel blends burn a large amount of fuel in the premixed phase, which improves the combustion as well as emission characteristics. CFD and experimental results are compared and validated for all fuel blends for in-cylinder pressure and nitrogen oxides (NO_x), and found to be in good agreement. Both experimental and simulation results witnessed in reduction of smoke opacity, NO_x, and carbon monoxide emissions with the increasing n-butanol percentage in diesel fuel.

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Mortality and its Causes in a German Cohort with Diabetes Mellitus Type 1 after 20 Years of Follow-Up: The JEVIN Trial

Exp Clin Endocrinol Diabetes
DOI: 10.1055/s-0043-113452

Background The JEVIN trial started as a cross-sectional study in 1989/90 in Jena. After a follow-up of more than 20 years, the mortality incidence of JEVIN participants with type 1 diabetes was surveyed. Methods 103 (78.6%) of the 131 JEVIN patients participating at baseline could be examined. 38 persons (36.9%) had deceased. All JEVIN survey data and routine examinations documented in the electronic patient record EMIL® of surviving and deceased participants were used for analyses. We compared the data of the surviving with the deceased participants (follow-up time: 2,166 person-years). Results The incidence rate of death was 1.75/100 person-years. Median observation time for all patients was 23.1 years (range 0.61–26.6 years). Mean age at death was 58.5 years (34.2–78.4 years), and diabetes duration 35 years (3.5–68.5 years). Most frequent causes of death were: cardiovascular diseases (48.2%, n=13) and infections (25.9%, n=7). There were no differences in age (p=0.302), diabetes duration (p=0.371), BMI (p=0.535), blood pressure (p=0.622/0.820), gender (p=0.566), and smoking status (p=0.709) between surviving and deceased persons. The mean HbA1c of the last year before death or last visit was higher in the deceased than surviving persons (7.5% vs. 7.0%; p=0.010). 57.4% of the surviving and 87.0% of the deceased participants had nephropathy (p=0.012), 79.7% vs. 89.7% retinopathy (p=0.241) and 61.4% vs. 63.3% neuropathy (p=0.860), but only nephropathy was significantly associated with increased mortality risk (HR=4.208, CI:1.226-14.440; HR=2.360, CI:0.696-8.004; HR=0.944, CI:0.436-2.043). Conclusions In the JEVIN population with diabetes mellitus type 1 only, diabetic nephropathy was associated with higher mortality risk.
[...]

© Georg Thieme Verlag KG Stuttgart · New York

Article in Thieme eJournals:
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Creatine Fuels the Thermic Effect of Feeding

Publication date: Available online 24 August 2017
Source:Cell Metabolism
Author(s): Alan R. Saltiel
The current obesity epidemic has focused a great deal of attention on cellular pathways of energy expenditure. While a crucial part of this process is diet-induced thermogenesis, the underlying mechanisms have remained unexplained. In this issue of Cell Metabolism, Kazak et al. (2017) describe a new thermogenic pathway in adipocytes that responds to diet overload, involving creatine cycling. These data suggest that this pathway might limit weight gain during overnutrition.

Teaser

The current obesity epidemic has focused a great deal of attention on cellular pathways of energy expenditure. While a crucial part of this process is diet-induced thermogenesis, the underlying mechanisms have remained unexplained. In this issue of Cell Metabolism, Kazak et al. (2017) describe a new thermogenic pathway in adipocytes that responds to diet overload, involving creatine cycling. These data suggest that this pathway might limit weight gain during overnutrition.


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Genetic Depletion of Adipocyte Creatine Metabolism Inhibits Diet-Induced Thermogenesis and Drives Obesity

Publication date: Available online 24 August 2017
Source:Cell Metabolism
Author(s): Lawrence Kazak, Edward T. Chouchani, Gina Z. Lu, Mark P. Jedrychowski, Curtis J. Bare, Amir I. Mina, Manju Kumari, Song Zhang, Ivan Vuckovic, Dina Laznik-Bogoslavski, Petras Dzeja, Alexander S. Banks, Evan D. Rosen, Bruce M. Spiegelman
Diet-induced thermogenesis is an important homeostatic mechanism that limits weight gain in response to caloric excess and contributes to the relative stability of body weight in most individuals. We previously demonstrated that creatine enhances energy expenditure through stimulation of mitochondrial ATP turnover, but the physiological role and importance of creatine energetics in adipose tissue have not been explored. Here, we have inactivated the first and rate-limiting enzyme of creatine biosynthesis, glycine amidinotransferase (GATM), selectively in fat (Adipo-Gatm KO). Adipo-Gatm KO mice are prone to diet-induced obesity due to the suppression of elevated energy expenditure that occurs in response to high-calorie feeding. This is paralleled by a blunted capacity for β3-adrenergic activation of metabolic rate, which is rescued by dietary creatine supplementation. These results provide strong in vivo genetic support for a role of GATM and creatine metabolism in energy expenditure, diet-induced thermogenesis, and defense against diet-induced obesity.

Graphical abstract

Teaser

Kazak et al. investigate the physiological effects of creatine energetics through loss of function of the rate-limiting enzyme glycine amidinotransferase (GATM) in adipose tissue. Adipo-Gatm KO mice cannot counteract increased calories with energy expenditure and gain weight. Their lower metabolic rate can be rescued by dietary creatine supplementation.


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The FGF21-CCL11 Axis Mediates Beiging of White Adipose Tissues by Coupling Sympathetic Nervous System to Type 2 Immunity

Publication date: Available online 24 August 2017
Source:Cell Metabolism
Author(s): Zhe Huang, Ling Zhong, Jimmy Tsz Hang Lee, Jialiang Zhang, Donghai Wu, Leiluo Geng, Yu Wang, Chi-Ming Wong, Aimin Xu
Type 2 cytokines are important signals triggering biogenesis of thermogenic beige adipocytes in white adipose tissue (WAT) during cold acclimation. However, how cold activates type 2 immunity in WAT remains obscure. Here we show that cold-induced type 2 immune responses and beiging in subcutaneous WAT (scWAT) are abrogated in mice with adipose-selective ablation of FGF21 or its co-receptor β-Klotho, whereas such impairments are reversed by replenishment with chemokine CCL11. Mechanistically, FGF21 acts on adipocytes in an autocrine manner to promote the expression and secretion of CCL11 via activation of ERK1/2, which drives recruitment of eosinophils into scWAT, leading to increases in accumulation of M2 macrophages, and proliferation and commitment of adipocyte precursors into beige adipocytes. These FGF21-elicited type 2 immune responses and beiging are blocked by CCL11 neutralization. Thus, the adipose-derived FGF21-CCL11 axis triggers cold-induced beiging and thermogenesis by coupling sympathetic nervous system to activation of type 2 immunity in scWAT.

Graphical abstract

Teaser

Zhe Huang et al. show that cold activates type 2 immune responses and beiging in subcutaneous WAT through an FGF21-CCL11 axis which drives eosinophil recruitment, M2 macrophage accumulation and proliferation and commitment of beige adipocyte precursors. These findings explain how the immune system communicates with sympathetic nerves to control adaptive thermogenesis.


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The Lymphatic Vasculature: Its Role in Adipose Metabolism and Obesity

Publication date: Available online 24 August 2017
Source:Cell Metabolism
Author(s): Noelia Escobedo, Guillermo Oliver
Obesity is a key risk factor for metabolic and cardiovascular diseases, and although we understand the mechanisms regulating weight and energy balance, the causes of some forms of obesity remain enigmatic. Despite the well-established connections between lymphatics and lipids, and the fact that intestinal lacteals play key roles in dietary fat absorption, the function of the lymphatic vasculature in adipose metabolism has only recently been recognized. It is well established that angiogenesis is tightly associated with the outgrowth of adipose tissue, as expanding adipose tissue requires increased nutrient supply from blood vessels. Results supporting a crosstalk between lymphatic vessels and adipose tissue, and linking lymphatic function with metabolic diseases, obesity, and adipose tissue, also started to accumulate in the last years. Here we review our current knowledge of the mechanisms by which defective lymphatics contribute to obesity and fat accumulation in mouse models, as well as our understanding of the lymphatic-adipose tissue relationship.

Teaser

Obesity and cardiovascular diseases are leading causes of death and disability. In this Review, Oliver and Escobedo expose the relationships between lymphatics, metabolism, and obesity and discuss how this knowledge will provide us with better tools to diagnose and treat some of these pathological conditions.


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Pulmonary fluorosis: a review

Abstract

The increased industrialization and improvised human lifestyle lead to a surge in environmental pollution nowadays. Even the chemicals which are known as prophylactic agents were currently liable to be toxic. One among them is inorganic fluoride whose wider application in numerous processes makes it as an inevitable environmental contaminant and industrial pollutant. Although the systemic toxicity of fluoride has been extensively studied, still there is lacuna in the field of pulmonary fluoride toxicity. Hence, we have focused on the molecular mechanism of action of fluoride compounds on pulmonary system. A study of literatures that focused on the potential physiological and toxicological consequences of fluoride on pulmonary system was carried out. The goal of this review is to present an overview of the research carried out till date on the molecular aspects of fluoride exposure with emphasis on pulmonary system and their possible mechanisms.

http://ift.tt/2xh4UP6

Internship Match and Entry Level Exam Performance of Undergraduate versus Graduate Level Didactic Students

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement
Author(s): B. Leonberg




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Teaching Multiculturalism in an Undergraduate Dietetics Course

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement
Author(s): H. Thornton




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Table of Contents

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9





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Registered Dietitians Facilitate Diabetes Training and Care within a Patient Centered Medical Home Care Delivery Model

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement
Author(s): M. McClarney, M. Timmerman, G. Woscyna, C. Hanson




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Disclosure Page

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement





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What's New Online

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9





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Outstanding Dietetics Student Awards, 2017

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9





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Table of Contents

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement





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2017-2018 Officers List and Committee Members

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9





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Sports Dietetics: Impact Beyond Playing Fields

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9
Author(s): Donna S. Martin




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Acknowledgements

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement





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Increased Malnutrition Diagnosis and Reimbursement Indicates Success of Academy of Nutrition and Dietetics Nutrition Focused Physical Exam (NFPE) Hands-on Training Workshop

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement
Author(s): B. Mordarski, R. Hand, J. Wolff, A. Steiber




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Breastfeeding after Gestational Diabetes: GIS Analysis of Maternal-Infant Health Interventions

Publication date: September 2017
Source:Journal of the Academy of Nutrition and Dietetics, Volume 117, Issue 9, Supplement
Author(s): E. MacQuillan, A. Curtis




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