Inefficient Energy Utilization Research Articles

Entropy generation and pumping power in a turbulent fluid flow through a smooth pipe subjected to constant heat flux

In a heat exchange process, heat transfer and pumping power requirements are the two main considerations. Efforts made to increase heat transfer in a fluid flow usually cause increase in the pumping power requirement. In an effort to avoid inefficient utilization of energy through excessive entropy generation, a thermodynamic analysis of turbulent fluid flow through a smooth duct subjected to constant heat flux has been made in this study. The temperature dependence of the viscosity was taken into consideration in determining the heat transfer coefficient and friction factor. It was shown that the viscosity variation has a considerable effect on both the entropy generation and the pumping power. Pumping power to heat transfer ratio and the entropy generation per unit heat transfer can become very large especially for low heat flux conditions.

Postischemic mechanoenergetic inefficiency is related to contractile dysfunction and not altered metabolism.

Mechanoenergetic inefficiency in postischemic nonnecrotic myocardium may partly be explained by an increased fatty acid (FA) oxidation rate. In the present study, left ventricular (LV) postischemic energy transfer was characterized in 10 intact anesthetized pigs. The LV was stunned by 11 brief left main coronary artery occlusions/reperfusions (20-min accumulated ischemia). Seven pigs served as time controls. The relationship between myocardial oxygen consumption (MVO(2)) and LV pressure-volume area (PVA) was assessed. [(14)C]glucose and [(3)H]oleate markers were used to discriminate between glucose and FA consumption. In stunned hearts, severe postischemic dysfunction was observed, and contractile efficiency was reduced (increased MVO(2)-PVA slope, P = 0.001). Unloaded (nonmechanical) MVO(2) was not affected by ischemia. We observed only a small transient increase in FA preference and conclude that the contribution from increased FA utilization to postischemic mechanoenergetic inefficiency is insignificant. Disrupted postischemic chemical-to-mechanical energy transfer in vivo is, therefore, related to inefficient energy utilization in the contractile apparatus.

Effect of ethanol on energy expenditure.

The thermogenic response induced by ethanol ingestion in humans has not been extensively studied. This study was designed to determine the thermic effect of ethanol added to a normal diet in healthy nonalcoholic subjects, using indirect calorimetry measurements over a 24-h period in a respiration chamber. The thermic effect of ethanol was also measured when ethanol was ingested in the fasting state, using a ventilated hood system during a 5-h period. Six subjects ingested 95.6 +/- 1.8 (SE) g ethanol in 1 day partitioned over three meals; there was a 5.5 +/- 1.2% increase in 24-h energy expenditure compared with a control day in which all conditions were identical except that no ethanol was consumed. The calculated ethanol-induced thermogenesis (EIT) was 22.5 +/- 4.7% of the ethanol energy ingested. Ingestion of 31.9 +/- 0.6 g ethanol in the fasting state led to a 7.4 +/- 0.6% increase in energy expenditure over baseline values, and the calculated EIT was 17.1 +/- 2.2%. It is concluded that in healthy nonalcoholic adults ethanol elicits a thermogenic response equal to approximately 20% of the ethanol energy. Thus the concept of the apparently inefficient utilization of ethanol energy is supported by these results which show that only approximately 80% of the ethanol energy is used as metabolizable energy for biochemical processes in healthy nonalcoholic moderate ethanol consumers.

A general minimum principle for competing populations: Some ecological and evolutionary consequences

The principle introduced by MacArthur (1969. Proc. Natl. Acad. Sci. U.S.A., 64, 1369–1375) that the stable positive equilibrium of an exploitative competition system minimizes the mean squared deviation between available and utilized resources is generalized. It is shown that under less stringent assumptions, the global attractor of a competition system consists of species assortments that minimize a function of consumers' abundances, called inefficient energy utilization. If the minimum is unique (whether or not lying on the boundary of the state space) the global attractor reduces to a globally stable equilibrium. The inefficient energy utilization is the sum of two terms: one, called unutilized productivity, is the squared difference between maximum resource production and consumers' consumption, while the second, called basal energy consumption, is the caloric income to a community necessary for maintaining it at a steady state. The minimum principle is then used to solve some ecological and evolutionary problems. It is demonstrated that if an inverse correlation is assumed between consumers' efficiency and width of the trophic niche, evolution in undisturbed environments leads to assortments of tightly packed specialists.

Metabolism in Human Endomyocardial Biopsies Cardiac Work

The activities of the Krebs cycle (KC), glycolytic pathway (GP), and the hexose monophosphate shunt were studied in endomyocardial biopsies obtained from 25 patients and were related to left ventricular stroke work index (LVSWI). Unexpectedly, KC activity was greater in patients with a reduced LVSWI than in those with a normal or elevated LVSWI. When the cardiac work:KC ratio, defined as LVSWI divided by KC activity, was plotted against LVSWI, the correlation coefficient was 0.86. Cardiac work did not correlate with other metabolic pathways measured. Patients with a reduced LVSWI generated less cardiac work per unit of KC activity than those who had a normal or elevated LVSWI. These data indicate that a reduction in LVSWI below 40 gram-meters/square meter (gm-m/m2) may be associated with either inefficient energy production, inefficient energy utilization, or both.

Effects of dietary level of protein on the maintenance energy requirement and net energetic efficiency for growth of post-weaning rats.

The effects of dietary protein on the maintenance energy requirement (MEm) and net utilization efficiency of metabolizable energy for growth (MEg) were investigated by regression analysis of energy balance with various energy intakes. Weanling rats of the Wistar strain, weighing about 85 g, were given a diet containing 0 to 70% casein freely or in restricted amounts (equivalent to two-thirds or one-third of the intake of the ad libitum group) for 5 days. The MEm was fairly constant in rats given 10 to 50% casein diets, being about 29 kcal/100 g BW/day, but increased at higher or lower dietary protein levels, indicating inefficient energy utilization in protein-malnourished animals. From the slope of the regression line between energy balance and metabolizable energy intake, the net energetic efficiencies for growth were estimated as 68, 71, 74, 77, 82, 83, 80, 78, 77 and 74% with 0, 3, 6, 10, 20, 30, 40, 50, 60 and 70% casein diets, respectively. Weanling rats fed 20 to 30% casein diets utilized the dietary energy for growth most efficiently. At protein levels higher or lower than 20 to 30%, the efficiency was less, showing that MEg utilization depended on dietary protein. The energy necessary for 1 g body weight gain was 2.6 kcal in rats receiving 30% casein diet, but increased with an increase or decrease in the protein level. These data on the food efficiency, MEm, the net efficiency of MEg and the energy necessary for 1 g weight gain show that dietary protein affects energy utilization and that protein-malnourished animals use energy inefficiently.

Evidence for an inefficient energy utilization in cardiac hypertrophy. Studies on the isolated human ventricular myocardium.

Cardiac muscle mechanics and myocardial oxygen consumption were determined in both normal left ventricular wall strips and hypertrophied left ventricular papillary muscle obtained from patients in the process of cardiac surgery (mitral valve replacements, corrections of ventricular septal defects). Isotonic preloaded, isotonic after-loaded and isometric contractions were employed. The oxygen consumption was assessed by gas chromatography. Compared with the normal muscles, cardiac muscle mechanics (shortening, velocity of shortening, cardiac work, cardiac power) were reduced about 40–50 per cent in the hypertrophied muscles. Force-velocity relations were depressed with decreases of both the preload velocity (normal: 0.79±0.08, hypertrophied: 0.38±0.05 muscle lengths/sec,p<0.01) and the maximum isometric tension development (normal: 3.8±0.6, hypertrophied: 2.1±0.48 g/mm2,p<0.01). However, the oxygen consumption per gram/mm2 of developed tension was not depressed, averaging 0.52±0.08 (normal) and 0.92±0.13 µl/mg/beat-10−3 (hypertrophied),p<0.01. At isometric conditions, oxygen consumption was nearly the same in both groups, however, despite a maximum oxygen availability maximum isometric tension development was reduced in the hypertrophied myocardium at about 40–50 per cent. These results demonstrate an inefficient energy utilization in the isolated hypertrophied human ventricular myocardium.

Inefficient energy utilization in chronic cardiac failure. Studies on the isolated, normal and chronically failing human ventricular myocardium.

Myocardial mechanics and oxygen consumption were measured on the isolated human left ventricular myocardium of patients with and without chronic failure of the left side of the heart. Cardiac mechanics were depressed in the chronically failing myocardium whereas the oxygen consumption was not. When related to equal fractions of tension development, the oxygen consumption was markedly increased in the failing group in comparison with the normal one. The oxygen consumption of the minimally loaded failing myoardium was approximately twice that of the minimally loaded normal heart muscle. Maximum oxygen consumption remained approximately the same in both groups. The results show the presence of an inefficient energy utilization in the chronically failing human ventricular myocardium.

Determination of portions of the bismuth III–V and IV–V equilibrium boundaries in single-stage piston-cylinder apparatus

Organic pollutants’ treatment in wastewater has attracted extensive attention due to its degradation-resistance and potentially hazardous to human health. Some organic matters such as persistent organic pollutants (POPs) could exist in environment and resist to decomposition, which may cause chronic intoxication or even cancers. Because photocatalytic technique is efficient, nontoxic, and cost-effective to degrade organic pollutants, some semiconductors including TiO2 and ZnO as photocatalysts have aroused wide public concern. CeO2 has been reported as an efficient photocatalyst in contrast to TiO2 owing to its high oxygen storage, eco-friendly properties and photostability. But inefficient utilization of solar energy due to its intrinsic wide bandgap restrains its further application in real environmental pollutant treatment. In order to improve photocatalytic performances of CeO2, some modifications have been developed such as doping ions, coupling with semiconductor and construction of CeO2-based solid-solution. The purpose of this review is to introduce these techniques, reveals its fundamental mechanisms and the recent researches about photodegradation of organic pollutants in wastewater over CeO2-based photocatalysts. Besides, this review will evaluate the photocatalytic performance for organic pollutants and outlook the challenges and prospects in the future.

The oxygen supply of the human heart ∗

The factors involved in oxygenation of the human heart have been discussed and illustrated in normal subjects and in common forms of heart disease. Within all groups at rest, significant variability in ventricular performance, myocardial oxygen requirements and oxygen supply patterns exists, suggesting that individual resting observations are of little value in detecting abnormalities of the coronary circulation. An exception appears to exist in low cardiac output congestive heart failure where functional coronary insufficiency is postulated due to coronary participation in peripheral vasoconstriction. During exercise, increased myocardial oxygen requirements are met by elevated coronary blood flow in normal coronary subjects, allowing maintenance of resting myocardial oxygen tension. Coronary vascular reserve is inadequate in coronary arterial disease, and a compensatory elevation of myocardial oxygen extraction lowers exercise coronary venous oxygen saturation and, presumably, myocardial oxygen tension. In congestive heart failure, markedly elevated exercise myocardial oxygen requirements place extraordinary demands on the coronary circulation, and in some instances may precipitate insufficiency of the anatomically normal or mildly diseased coronary circulation. An important consequence of coronary insufficiency appears to be compensatory elevation of myocardial oxygen extraction and reduction of myocardial oxygen tension during exercise. These studies demonstrate no relationship between absolute coronary venous oxygen values and angina pectoris, although the precipitation of this symptom may be related to the degree of reduction in coronary venous oxygenation during exercise. Analysis of myocardial lactate, pyruvate and catecholamine metabolism reveals no causal relationship to angina pectoris or coronary vasodilatation. Of the study subjects having angina pectoris, 82 per cent have detectable oxygen supply abnormalities, an incidence in close agreement with that of diffuse versus localized coronary arterial disease. The role of inefficient energy utilization has been suggested in the precipitation of coronary insufficiency in congestive heart failure and obliterative coronary arterial disease. Conversely, reduced myocardial oxygen tension secondary to coronary insufficiency may impair ventricular performance and result in myocardial damage. These problems require further evaluation of the biochemical events associated with coronary insufficiency, and an examination of myocardial energy production and utilization in coronary arterial disease.