Modelagem e Otimização Termoeconômica de Superestruturas de Ciclos Kalina para Aproveitamento do Calor Rejeitado em Usinas Termelétricas Com Motores de Combustão Interna

Neste trabalho, é realizada a modelagem e otimização utilizando o software EES (Engineering Equation Solver) para aproveitar o calor proveniente de dois rejeitos térmicos: água de resfriamento e gás de exaustão, dos motores de combustão interna (MCI) de uma termelétrica. A modelagem contempla várias alternativas básicas capazes de produzir, individualmente ou em associação, energia elétrica e conta com um ciclo de alta aproveitando os gases da exaustão e outro ciclo de baixa aproveitando a água de resfriamento do motor. A otimização realizada é paramétrica e estrutural, com o objetivo de maximizar o lucro, e selecionar qual ciclo produz potência com menor custo. São realizadas modelagens termodinâmica e econômica para este trabalho, que levam em conta catorze variáveis de decisão para atender os ciclos de alta e de baixa. A principal contribuição é determinar a melhor configuração com base na otimização termoeconômica, visando aumentar a geração de potência da UTE Viana, sem que seja necessário o uso adicional de combustível. Os resultados mostraram que na condição ótima é possível obter um aumento em torno de 7,5% da potência gerada pela termelétrica. Palavras-chave: Ciclo Kalina; Otimização Termoeconômica; Superestrutura; Motor de Combustão Interna; Recuperação de Calor Residual

Protein multi-scale organization through graph partitioning and robustness analysis: Application to the myosin-myosin light chain interaction

Despite the recognized importance of the multi-scale spatio-temporal organization of proteins, most computational tools can only access a limited spectrum of time and spatial scales, thereby ignoring the effects on protein behavior of the intricate coupling between the different scales. Starting from a physico-chemical atomistic network of interactions that encodes the structure of the protein, we introduce a methodology based on multi-scale graph partitioning that can uncover partitions and levels of organization of proteins that span the whole range of scales, revealing biological features occurring at different levels of organization and tracking their effect across scales. Additionally, we introduce a measure of robustness to quantify the relevance of the partitions through the generation of biochemically-motivated surrogate random graph models. We apply the method to four distinct conformations of myosin tail interacting protein, a protein from the molecular motor of the malaria parasite, and study properties that have been experimentally addressed such as the closing mechanism, the presence of conserved clusters, and the identification through computational mutational analysis of key residues for binding.Comment: 13 pages, 7 Postscript figure

Prenatal muscle development in a mouse model for the secondary dystroglycanopathies

The defective glycosylation of α-dystroglycan is associated with a group of muscular dystrophies that are collectively referred to as the secondary dystroglycanopathies. Mutations in the gene encoding fukutin-related protein (FKRP) are one of the most common causes of secondary dystroglycanopathy in the UK and are associated with a wide spectrum of disease. Whilst central nervous system involvement has a prenatal onset, no studies have addressed prenatal muscle development in any of the mouse models for this group of diseases. In view of the pivotal role of α-dystroglycan in early basement membrane formation, we sought to determine if the muscle formation was altered in a mouse model of FKRP-related dystrophy

Developmental regulation of MURF E3 ubiquitin ligases in skeletal muscle

The striated muscle-specific tripartite motif (TRIM) proteins TRIM63/MURF1, TRIM55/MURF2 and TRIM54/MURF3 can function as E3 ubiquitin ligases in ubiquitin-mediated muscle protein turnover. Despite the well-characterised role of MURF1 in skeletal muscle atrophy, the dynamics of MURF isogene expression in the development and early postnatal adaptation of skeletal muscle is unknown. Here, we show that MURF2 is the isogene most highly expressed in embryonic skeletal muscle at E15.5, with the 50 kDa A isoform predominantly expressed. MURF1 and MURF3 are upregulated only postnatally. Knockdown of MURF2 p50A by isoform-specific siRNA results in delayed myogenic differentiation and myotube formation in vitro, with perturbation of the stable, glutamylated microtubule population. This underscores that MURF2 plays an important role in the earliest stages of skeletal muscle differentiation and myofibrillogenesis. During further development, there is a shift towards the 60 kDa A isoform, which dominates postnatally. Analysis of the fibre-type expression shows that MURF2 A isoforms are predominantly slow-fibre associated, whilst MURF1 is largely excluded from these fibres, and MURF3 is ubiquitously distributed in both type I and II fibres

Socioeconomic Inequalities in Mortality Rates in Old Age in the World Health Organization Europe Region

Socioeconomic adversity is among the foremost fundamental causes of human suffering, and this is no less true in old age. Recent reports on socioeconomic inequalities in mortality rate in old age suggest that a low socioeconomic position continues to increase the risk of death even among the oldest old. We aimed to examine the evidence for socioeconomic mortality rate inequalities in old age, including information about associations with various indicators of socioeconomic position and for various geographic locations within the World Health Organization Region for Europe. The articles included in this review leave no doubt that inequalities in mortality rate by socioeconomic position persist into the oldest ages for both men and women in all countries for which information is available, although the relative risk measures observed were rarely higher than 2.00. Still, the available evidence base is heavily biased geographically, inasmuch as it is based largely on national studies from Nordic and Western European countries and local studies from urban areas in Southern Europe. This bias will hamper the design of European-wide policies to reduce inequalities in mortality rate. We call for a continuous update of the empiric evidence on socioeconomic inequalities in mortality rate

Monitoring trends in socioeconomic health inequalities: it matters how you measure

<p>Abstract</p> <p>Background</p> <p>Odds ratio (OR), a relative measure for health inequality, has frequently been used in prior studies for presenting inequality trends in health and health behaviors. Since OR is not a good approximation of prevalence ratio (PR) when the outcome prevalence is quite high, an important problem may arise when OR trends are used in data in which the outcome variable (e.g., smoking or ill-health) is of relatively high prevalence and varies significantly over time. This study is to compare time trends of odds ratio (OR) and prevalence ratio (PR) for examining time trends in socioeconomic inequality in smoking.</p> <p>Methods</p> <p>A total of 147,805 subjects (71,793 men and 76,017 women) aged 25–64 from three Social Statistics Surveys of Korea from 1999 to 2006 were analyzed. Socioeconomic position indicators were occupational class and education.</p> <p>Results</p> <p>While there were no significant p values for trend in ORs of occupational class among men, trends for PRs were significant. In women, p values for OR trends were similar to those for PR trends. In males, RII by log-binomial regression showed a significant increasing tendency while RII by logistic regression was stable between years. In females, trends of RIIs by logistic regression and log-binomial regression produced a similar level of p values.</p> <p>Conclusion</p> <p>Different methods of measuring trends in socioeconomic health inequalities may lead to different conclusions about whether relative inequalities are increasing or decreasing. Trends in ORs may overstate or understate trends in relative inequality in health when the outcome is of relatively high prevalence and that prevalence varies significantly with time.</p

Myogenin Regulates Exercise Capacity and Skeletal Muscle Metabolism in the Adult Mouse

Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogenin's role in adult skeletal muscle is unclear. We sought to determine myogenin's function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we performed indirect calorimetry, monitored blood glucose and lactate levels, and performed histochemical analyses on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low- and high-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle

Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema

BACKGROUND: Several physiological adaptations occur in the respiratory muscles in rodent models of elastase-induced emphysema. Although the contractile properties of the diaphragm are altered in a way that suggests expression of slower isoforms of myosin heavy chain (MHC), it has been difficult to demonstrate a shift in MHCs in an animal model that corresponds to the shift toward slower MHCs seen in human emphysema. METHODS: We sought to identify MHC and corresponding physiological changes in the diaphragms of rats with elastase-induced emphysema. Nine rats with emphysema and 11 control rats were studied 10 months after instillation with elastase. MHC isoform composition was determined by both reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry by using specific probes able to identify all known adult isoforms. Physiological adaptation was studied on diaphragm strips stimulated in vitro. RESULTS: In addition to confirming that emphysematous diaphragm has a decreased fatigability, we identified a significantly longer time-to-peak-tension (63.9 ± 2.7 ms versus 53.9 ± 2.4 ms). At both the RNA (RT-PCR) and protein (immunocytochemistry) levels, we found a significant decrease in the fastest, MHC isoform (IIb) in emphysema. CONCLUSION: This is the first demonstration of MHC shifts and corresponding physiological changes in the diaphragm in an animal model of emphysema. It is established that rodent emphysema, like human emphysema, does result in a physiologically significant shift toward slower diaphragmatic MHC isoforms. In the rat, this occurs at the faster end of the MHC spectrum than in humans

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

Microgenomic Analysis in Skeletal Muscle: Expression Signatures of Individual Fast and Slow Myofibers

BACKGROUND: Skeletal muscle is a complex, versatile tissue composed of a variety of functionally diverse fiber types. Although the biochemical, structural and functional properties of myofibers have been the subject of intense investigation for the last decades, understanding molecular processes regulating fiber type diversity is still complicated by the heterogeneity of cell types present in the whole muscle organ. METHODOLOGY/PRINCIPAL FINDINGS: We have produced a first catalogue of genes expressed in mouse slow-oxidative (type 1) and fast-glycolytic (type 2B) fibers through transcriptome analysis at the single fiber level (microgenomics). Individual fibers were obtained from murine soleus and EDL muscles and initially classified by myosin heavy chain isoform content. Gene expression profiling on high density DNA oligonucleotide microarrays showed that both qualitative and quantitative improvements were achieved, compared to results with standard muscle homogenate. First, myofiber profiles were virtually free from non-muscle transcriptional activity. Second, thousands of muscle-specific genes were identified, leading to a better definition of gene signatures in the two fiber types as well as the detection of metabolic and signaling pathways that are differentially activated in specific fiber types. Several regulatory proteins showed preferential expression in slow myofibers. Discriminant analysis revealed novel genes that could be useful for fiber type functional classification. CONCLUSIONS/SIGNIFICANCE: As gene expression analyses at the single fiber level significantly increased the resolution power, this innovative approach would allow a better understanding of the adaptive transcriptomic transitions occurring in myofibers under physiological and pathological condition