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David Pimentel

Publications and source records attributed to David Pimentel.

7 recordsLinked to original sources
PubMed2007

Ethanol production: energy, economic, and environmental losses.

The prime focus of ethanol production from corn is to replace the imported oil used in American vehicles, without expending more fossil energy in ethanol production than is produced as ethanol energy. In a thorough and up-to-date evaluation of all the fossil energy costs of ethanol production from corn, every step in the production and conversion process must be included. In this study, 14 energy inputs in average U.S. corn production are included. Then, in the fermentation/distillation operation, 9 more identified fossil fuel inputs are included. Some energy and economic credits are given for the by-products, including dried distillers grains (DDG). Based on all the fossil energy inputs, a total of 1.43 kcal fossil energy is expended to produced 1 kcal ethanol. When the energy value of the DDG, based on the feed value of the DDG as compared to that of soybean meal, is considered, the energy cost of ethanol production is reduced slightly, to 1.28 kcal fossil energy input per 1 kcal ethanol produced. Several proethanol investigators have overlooked various energy inputs in U.S. corn production, including farm machinery, processing machinery, and the use of hybrid corn. In other studies, unrealistic, low energy costs were attributed to such inputs as nitrogen fertilizer, insecticides, and herbicides. Controversy continues concerning the energy and economic credits that should be assigned to the by-products. The U.S. Department of Energy reports that 17.0 billion L ethanol was produced in 2005. This represents only less than 1% of total oil use in the U.S. These yields are based on using about 18% of total U.S. corn production and 18% of cornland. Because the production of ethanol requires large inputs of both oil and natural gas in production, the U.S. is importing both oil and natural gas to produce ethanol. Furthermore, the U.S. Government is spending about dollar 3 billion annually to subsidize ethanol production, a subsidy of dollar 0.79/L ethanol produced. With the subsidy, plus the cost of production, the cost of ethanol is calculated to be dollar 1.21/L. The subsidy for a liter of ethanol is 45-times greater than the subsidy per liter of gasoline. The environmental costs associated with producing ethanol are significant but have been ignored by most investigators in terms of energy and economics. The negative environmental impacts on cropland, and freshwater, as well as air pollution and public health, have yet to be carefully assessed. These environmental costs in terms of energy and economics should be calculated and included in future ethanol analyses. General concern has been expressed about taking 18% of U.S. corn, and more in the future, to produce ethanol for burning in automobiles instead of using the corn as food for the many malnourished people in the world. The World Health Organization reports that more than 3.7 billion humans are currently malnourished in the world--the largest number ever in history.

Bioelectric Energy Sources↗
PubMed2006

S-glutathiolation of p21ras by peroxynitrite mediates endothelial insulin resistance caused by oxidized low-density lipoprotein.

OBJECTIVE: To understand the mechanism by which oxidants are linked to insulin resistance, bovine aortic endothelial cells were exposed to oxidized low-density lipoproteins (oxLDL) or peroxynitrite. METHODS AND RESULTS: OxLDL transiently increased phosphorylation of Erk and Akt within 5 minutes, but 60 minutes later, resulted in decreased insulin-induced Akt phosphorylation. OxLDL promoted a 2- to 5-fold increase in oxidant generation as measured by dihydrorhodamine or dihydroethidium oxidation that was ascribed to peroxynitrite. Exogenous peroxynitrite (25 to 100 micromol/L) or oxidized glutathione mimicked the effects of oxLDL. OxLDL increased the S-glutathiolation of p21ras, and adenoviral transfection with either a mutant p21ras (C118S) lacking the predominant site of S-glutathiolation or a dominant-negative mutant restored insulin-induced Akt phosphorylation. The requirement for oxidant-mediated S-glutathiolation and activation of p21ras in mediating insulin resistance was further implicated by showing that insulin signaling was restored by Mek inhibitors or by overexpression of glutaredoxin-1. Furthermore, oxLDL increased Erk-dependent phosphorylation of insulin receptor substrate-1 serine-616 that was prevented by inhibiting oxidant generation, Erk activation, or by the p21ras C118S mutant. CONCLUSIONS: This study provides direct evidence for a novel molecular mechanism by which oxidants can induce insulin resistance via S-glutathiolation of p21ras and Erk-dependent inhibition of insulin signaling.

Alprostadil↗
PubMed2006

Adventitial delivery of dominant-negative p67phox attenuates neointimal hyperplasia of the rat carotid artery.

Several essential components of NADPH oxidase, including p22phox, gp91phox (nox2) and its homologs nox1 and nox4, p47phox, p67phox, and rac1, are present in the vasculature. We previously reported that p67phox is essential for adventitial fibroblast NADPH oxidase O2- production. Thus we postulated that inhibition of adventitial p67phox activity would attenuate angioplasty-induced hyperplasia. To test this hypothesis, we treated the adventitia of carotid arteries with a control adenovirus (Ad-control), a virus expressing dominant-negative p67phox (Ad-p67dn), or a virus expressing a competitive peptide (gp91ds) targeting the p47phox-gp91phox interaction (Ad-gp91ds). Common carotid arteries (CCAs) from male Sprague-Dawley rats were transfected with Ad-control, Ad-p67dn, or Ad-gp91ds in pluronic gel. After 2 days, a 2-F (Fogarty) catheter was used to injure CCAs in vivo. After 14 days, CCAs were perfusion-fixed and analyzed. In 13 experiments, digital morphometry suggested a reduction of neointimal hyperplasia with Ad-p67dn compared with Ad-control; however, the reduction did not reach statistical significance (P = 0.058). In contrast, a significant reduction was achieved with Ad-gp91ds (P = 0.006). No changes in medial area or remodeling were observed with either treatment. Moreover, adventitial fibroblast proliferation in vitro was inhibited by Ad-gp91ds but not by Ad-p67dn, despite confirmation that Ad-p67dn inhibits NADPH oxidase in fibroblasts. These data appear to suggest that a multicomponent vascular NADPH oxidase plays a role in neointimal hyperplasia. However, inhibition of p47phox may be more effective than inhibition of p67phox at attenuating neointimal growth.

Animals↗
PubMed2005

The FOXO3a transcription factor regulates cardiac myocyte size downstream of AKT signaling.

Although signaling mechanisms inducing cardiac hypertrophy have been extensively studied, little is known about the mechanisms that reverse cardiac hypertrophy. Here, we describe the existence of a similar Akt/forkhead signaling axis in cardiac myocytes in vitro and in vivo, which is regulated by insulin, insulin-like growth factor (IGF), stretch, pressure overload, and angiotensin II stimulation. FOXO3a gene transfer prevented both IGF and stretch-induced hypertrophy in rat neonatal cardiac myocyte cultures in vitro. Transduction with FOXO3a also caused a significant reduction in cardiomyocyte size in mouse hearts in vivo. Akt/FOXO signaling regulated the expression of multiple atrophy-related genes "atrogenes," including the ubiquitin ligase atrogin-1 (MAFbx). In cardiac myocyte cultures, transduction with constitutively active Akt or treatment with IGF suppressed atrogin-1 mRNA expression, whereas transduction with FOXO3a stimulated its expression. FOXO3a transduction activated the atrogin-1 promoter in both cultured myocytes and mouse heart. Thus, in cardiomyocytes, as in skeletal muscle, FOXO3a activates an atrogene transcriptional program, which retards or prevents hypertrophy and is down-regulated by multiple physiological and pathological stimuli of myocyte growth.

Angiotensin II↗
PubMed2005

Aquatic nuisance species in the New York State Canal and Hudson River systems and the Great Lakes Basin: an economic and environmental assessment.

A total of 154 aquatic alien species have invaded the New York State Canal and Hudson River systems and a total of 162 aquatic species have invaded the Great Lakes Basin. Some of these invasive species are causing significant damage and control costs in both aquatic ecosystems. In the New York State Canal and Hudson River systems, the nonindigenous species are causing an estimated 500 million dollars in economic losses each year. The economic and environmental situation in the Great Lakes Basin is far more serious from nonindigenous species, with losses estimated to be about 5.7 billion dollars per year. Commercial and sport fishing suffer the most from the biological invasions, with about 400 million dollars in losses reported for the New York State Canal and Hudson River systems and 4.5 billion dollars in losses reported for the Great Lakes Basin.

Animals↗
PubMed2003

Sustainability of meat-based and plant-based diets and the environment.

Worldwide, an estimated 2 billion people live primarily on a meat-based diet, while an estimated 4 billion live primarily on a plant-based diet. The US food production system uses about 50% of the total US land area, 80% of the fresh water, and 17% of the fossil energy used in the country. The heavy dependence on fossil energy suggests that the US food system, whether meat-based or plant-based, is not sustainable. The use of land and energy resources devoted to an average meat-based diet compared with a lactoovovegetarian (plant-based) diet is analyzed in this report. In both diets, the daily quantity of calories consumed are kept constant at about 3533 kcal per person. The meat-based food system requires more energy, land, and water resources than the lactoovovegetarian diet. In this limited sense, the lactoovovegetarian diet is more sustainable than the average American meat-based diet.

Animals↗