bluuebunny/crossref_metadata_2025_split huggingface dataset:
Experimental Investigation of Film Cooling Flow Induced by Shaped Holes on a Turbine Blade
Authors: BARTHET Sylvain , BARIO François 
Published: July 2010

Abstract: The present study is the second half of a piece of work carried out in collaboration with SNECMA. It investigates shaped hole film cooling, numerically and experimentally. The aim of this paper is the experimental analysis of shaped hole film cooling on a large scale turbine blade (1.4 m chord).The test section is a large scale turbine inlet guide vane cascade. The test airfoil is equipped with a row of nine 50° sloped shaped holes. They are located on the suction side at 20% of the curvilinear length of the blade from the stagnation point. The inlet film cooling hole diameter is 12 mm.The test jet flow is heated to 55°C above the crossflow temperature. Velocity and temperature field measurements have been done to obtain mean and fluctuating values. The results are compared to those obtained by Béral1 on the same experimental apparatus and in the same test conditions, for a row of cylindrical holes.
Aging and the Role of Reactive Nitrogen Species
Authors: DREW BARRY , LEEUWENBURGH CHRISTIAAN 
Published: July 2010

AbstractThe role of reactive oxygen species and its effects on aging has received considerable attention in the past 47 years since Dr. Denham Harman first proposed the “free radical theory of aging.” Though not completely understood due to the incalculable number of pathways involved, the number of manuscripts that facilitate the understanding of the underlying effects of reactive radical species on the oxidative stress on lipids, proteins, and DNA and its contribution to the aging process increases nearly exponentially each year. More recently, the role of reactive nitrogen species, such as nitric oxide and its by‐products—nitrate (NO3−), nitrite (NO2−), peroxynitrite (ONOO−), and 3‐nitrotyrosine—have been shown to have a direct role in cellular signaling, vasodilation, and immune response. Nitric oxide is produced within cells by the actions of a group of enzymes called nitric oxide synthases. Presently, there are three distinct isoforms of nitric oxide synthase: neuronal (nNOS or NOS‐1), inducible (iNOS or NOS‐2), and endothelial (eNOS or NOS‐3), and several subtypes. While nitric oxide (NO•) is a relative unreactive radical, it is able to form other reactive intermediates, which could have an effect on protein function and on the function of the entire organism. These reactive intermediates can trigger nitrosative damage on biomolecules, which in turn may lead to age‐related diseases due to structural alteration of proteins, inhibition of enzymatic activity, and interferences of the regulatory function. This paper will critically review the evidence of nitration and the important role it plays with aging. Furthermore, it will summarize the physiological role of nitration as well as the mechanisms leading to proteolytic degradation of nitrated proteins within biological tissues.
The Role of Apoptosis in the Normal Aging Brain, Skeletal Muscle, and Heart
Authors: POLLACK MICHAEL , PHANEUF SHARON , DIRKS AMIE , LEEUWENBURGH CHRISTIAAN 
Published: July 2010

AbstractDuring aging, there is a significant loss of some postmitotic cells, for example, cardiac and skeletal myocytes. Mitochondrial damage and dysfunction with age may trigger increased apoptosis, and this may explain this increase in cell loss. However, it is still unknown if apoptosis plays an important role in normal aging. In vitro it has been shown that several mitochondrial proteins can influence apoptosis, depending on factors such as the mitochondrial membrane potential and cellular redox status. It remains possible that mitochondrial dysfunction due to chronic oxidative stress with age is a cause of apoptosis in vivo. This cell loss may be due to mitochondrial‐triggered apoptosis caused by age‐associated increases in oxidant production or increased activation of mitochondrial permeability transition pores. Results from our laboratory and others are reviewed that relate to apoptosis in the normal aging of the brain cortex, heart, and skeletal muscle. Particular attention is paid to the role of cytochrome c release from mitochondria and alterations in the pro‐ and anti‐apoptotic proteins, Bax and Bcl‐2, respectively. Our results demonstrate that a tissue‐specific adaptation of the Bcl‐2/Bax ratio occurs with age and may directly influence the release of cytochrome c.
Delaying Brain Mitochondrial Decay and Aging with Mitochondrial Antioxidants and Metabolites
Authors: LIU JIANKANG , ATAMNA HANI , KURATSUNE HIROHIKO , AMES BRUCE N. 
Published: July 2010

AbstractMitochondria decay with age due to the oxidation of lipids, proteins, RNA, and DNA. Some of this decay can be reversed in aged animals by feeding them the mitochondrial metabolites acetylcarnitine and lipoic acid. In this review, we summarize our recent studies on the effects of these mitochondrial metabolites and mitochondrial antioxidants (α‐phenyl‐N‐t‐butyl nitrone andN‐t‐butyl hydroxylamine) on the age‐associated mitochondrial decay of the brain of old rats, neuronal cells, and human diploid fibroblast cells. In feeding studies in old rats, these mitochondrial metabolites and antioxidants improve the age‐associated decline of ambulatory activity and memory, partially restore mitochondrial structure and function, inhibit the age‐associated increase of oxidative damage to lipids, proteins, and nucleic acids, elevate the levels of antioxidants, and restore the activity and substrate binding affinity of a key mitochondrial enzyme, carnitine acetyltrasferase. These mitochondrial metabolites and antioxidants protect neuronal cells from neurotoxin‐ and oxidant‐induced toxicity and oxidative damage; delay the normal senescence of human diploid fibroblast cells, and inhibit oxidant‐induced acceleration of senescence. These results suggest a plausible mechanism: with age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a deformation of structure of enzymes, with a consequent decrease of enzyme activity as well as substrate binding affinity for their substrates; an increased level of substrate restores the velocity of the reaction and restores mitochondrial function, thus delaying mitochondrial decay and aging. This loss of activity due to coenzyme or substrate binding appears to be true for a number of other enzymes as well, including mitochondrial complex III and IV.
Melatonin Reduces Oxidant Damage and Promotes Mitochondrial Respiration
Authors: REITER RUSSEL J. , TAN DUN XIAN , MANCHESTER LUCIEN C. , EL‐SAWI MAMDOUH R. 
Published: July 2010

AbstractMelatonin has a number of properties as a consequence of which it could be beneficial to animals as they age. Of particular interest are its ubiquitous actions as a direct and indirect antioxidant and free radical scavenger. Besides directly detoxifying a variety of reactive oxygen and reactive nitrogen species, at least one product that is formed as a result of these interactions is also a potent free radical scavenger. Thus, the product that is formed when melatonin detoxifies hydrogen peroxide, that is, N1‐acetyl‐N2‐formyl‐5‐methoxykynuramine is an efficient scavenger, at least equivalent to melatonin itself. This antioxidant cascade increases the ability of melatonin to resist oxidative damage. Other actions of melatonin, such as stimulation of antioxidative enzymes also improves its status as an antioxidant. Finally, recent observations documenting melatonin's ability to stimulate electron transport and ATP production in the inner‐mitochondrial membrane also has relevance for melatonin as an agent that could alter processes of aging. These findings, coupled with diminished melatonin production in advanced age, has prompted scientists to consider melatonin in the context of aging. As of this writing there is no definitive evidence to prove that melatonin alters the rate of aging, although data relating to melatonin deferring some age‐related degenerative conditions is accumulating rapidly.
Prevention of Mitochondrial Oxidative Damage Using Targeted Antioxidants
Authors: KELSO GEOFFREY F. , PORTEOUS CAROLYN M. , HUGHES GILLIAN , LEDGERWOOD ELIZABETH C. , GANE ALISON M. , SMITH ROBIN A. J. , MURPHY MICHAEL P. 
Published: July 2010

AbstractMitochondrial‐targeted antioxidants that selectively block mitochondrial oxidative damage and prevent some types of cell death have been developed. These antioxidants are ubiquinone and tocopherol derivatives and are targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation. Because of the large mitochondrial membrane potential, these cations accumulated within mitochondria inside cells, where the antioxidant moiety prevents lipid peroxidation and protects mitochondria from oxidative damage. The mitochondrially localized ubiquinone also protected mammalian cells from hydrogen peroxide‐induced apoptosis while an untargeted ubiquinone analogue was ineffective against apoptosis. When fed to mice these compounds accumulated within the brain, heart, and liver; therefore, using these mitochondrial‐targeted antioxidants may help investigations of the role of mitochondrial oxidative damage in animal models of aging.
Reaction of Carnosine with Aged Proteins
Authors: HIPKISS ALAN R. , BROWNSON CAROL , BERTANI MARIANA F. , RUIZ EMILIO , FERRO ALBERT 
Published: July 2010

AbstractCellular aging is often associated with an increase in protein carbonyl groups arising from oxidation‐ and glycation‐related phenomena and suppressed proteasome activity. These “aged” polypeptides may either be degraded by 20S proteasomes or cross‐link to form structures intractable to proteolysis and inhibitory to proteasome activity. Carnosine (β‐alanyl‐l‐histidine) is present at surprisingly high levels (up to 20 mM) in muscle and nervous tissues in many animals, especially long‐lived species. Carnosine can delay senescence in cultured human fibroblasts and reverse the senescent phenotype, restoring a more juvenile appearance. As better antioxidants/free‐radical scavengers than carnosine do not demonstrate these antisenescent effects, additional properties of carnosine must contribute to its antisenescent activity. Having shown that carnosine can react with protein carbonyls, thereby generating “carnosinylated” polypeptides using model systems, we propose that similar adducts are generated in senescent cells exposed to carnosine. Polypeptide‐carnosine adducts have been recently detected in beef products that are relatively rich in carnosine, and carnosine's reaction with carbonyl functions generated during amino acid deamidation has also been described. Growth of cultured human fibroblasts with carnosine stimulated proteolysis of long‐labeled proteins as the cells approached their “Hayflick limit,” consistent with the idea that carnosine ameliorates the senescence‐associated proteolytic decline. We also find that carnosine suppresses induction of heme‐oxygenase‐1 activity following exposure of human endothelial cells to a glycated protein. The antisenescent activity of the spin‐trap agent α‐phenyl‐N‐t‐butylnitrone (PBN) towards cultured human fibroblasts resides in N‐t‐butyl‐hydroxylamine, its hydrolysis product. As hydroxylamines are reactive towards aldehydes and ketones, the antisenescent activity of N‐t‐butyl‐hydroxylamine and other hydroxylamines may be mediated, at least in part, by reactivity towards macromolecular carbonyls, analogous to that proposed for carnosine.
Therapeutics against Mitochondrial Oxidative Stress in Animal Models of Aging
Authors: MELOV SIMON 
Published: July 2010

AbstractDuring the course of normal metabolism, reactive oxygen species (ROS) are produced from within the respiratory chain of the mitochondria. These ROS have the capacity to oxidize and damage a variety of cellular constituents including lipids, DNA, and proteins. We have taken a genetic and pharmacological approach in delineating the range of molecular targets that can be oxidatively damaged by mitochondrial ROS. Specifically, we use mice that are lacking the mitochondrial form of superoxide dismutase (sod 2−/−mice) to better understand the possible phenotypes that can arise from mitochondrial oxidative stress.sod 2−/−mice can be used to test the efficacy of antioxidants, and more generally the efficacy of antioxidants against mitochondrial oxidative stress. We have evaluated superoxide dismutase/catalase mimetics in this mammalian model of mitochondrial oxidative stress, and have shown a high degree of efficacy in protecting against ROS produced within the mitochondria. Similarly, we have employed the nematodeCaenorhabditis elegansto test the hypothesis that effective antioxidant therapy can prolong the life span of an invertebrate.
Membrane Fatty Acid Unsaturation, Protection against Oxidative Stress, and Maximum Life Span
Authors: PAMPLONA REINALD , BARJA GUSTAVO , PORTERO‐OTÍN MANUEL 
Published: July 2010

AbstractAging is a progressive and universal process originating endogenously that manifests during postmaturational life. Available comparative evidence supporting the mitochondrial free radical theory of aging consistently indicates that two basic molecular traits are associated with the rate of aging and thus with the maximum life span: the presence of low rates of mitochondrial oxygen radical production and low degrees of fatty acid unsaturation of cellular membranes in postmitotic tissues of long‐lived homeothermic vertebrates in relation to those of short‐lived ones. Recent research shows that steady‐state levels of free radical‐derived damage to mitochondrial DNA (mtDNA) and, in some cases, to proteins are lower in long‐ than in short‐lived animals. Thus, nonenzymatic oxidative modification of tissue macromolecules is related to the rate of aging. The low degree of fatty acid unsaturation in biomembranes of long‐lived animals may confer advantage by decreasing their sensitivity to lipid peroxidation. Furthermore, this may prevent lipoxidation‐derived damage to other macromolecules. Taking into account the fatty acid distribution pattern, the origin of the low degree of membrane unsaturation in long‐lived species seems to be the presence of species‐specific desaturation pathways that determine membrane composition while an appropriate environment for membrane function is maintained. Mechanisms that prevent or decrease the generation of endogenous damage during the evolution of long‐lived animals seem to be more important than trying to intercept those damaging agents or repairing the damage already inflicted. Here, the physiological meaning of these findings and the effects of experimental manipulations such as dietary stress, caloric restriction, and endocrine control in relation to aging and longevity are discussed.
Electrospinning of Poly(vinyl alcohol) Nanofibers Loaded with Hexadecane Nanodroplets
Authors: Arecchi A. , Mannino S. , Weiss J. 
Published: July 2010

Abstract:  The feasibility of producing poly(vinyl alcohol) (PVA) nanofibers containing fine‐disperse hexadecane droplets by electrospinning a blend of hexadecane‐in‐water emulsions and PVA was investigated. Hexadecane oil‐in‐water nanoemulsions (d10= 181.2 ± 0.1 nm) were mixed with PVA at pH 4.5 to yield polymer‐emulsion blends containing 0.5 to 1.5 wt% oil droplets and 8‐wt% PVA. The solution properties of emulsions and emulsion‐PVA blends (viscosity, conductivity, surface tension) were determined. Solutions were electrospun and the morphology and thermal properties of deposited fiber mats characterized by scanning electron microscopy and differential scanning calorimetry. Fiber mats were dissolved in buffer to liberate incorporated hexadecane droplets and the buffer solutions analyzed by optical microscopy, UV‐spectroscopy, and light scattering. Analysis of dry fiber mats and their solutions showed that emulsion droplets were indeed part of the electrospun fiber structures. Depending on the concentration of hexadecane in the initial emulsion‐polymer blends, droplets were dispersed in the fibers as individual droplets or in form of aggregated flocs of hexadecane droplets. Nanofibers with spindle‐like perturbations or nanofibers containing bead‐like structures with approximately 5 times larger than the size of droplets in the original nanoemulsion were obtained. Remarkably, incorporation of hexadecane droplets in fibers did not alter size of individual droplets, that is, no coalescence occurred. The manufacture of solid matrix containing nanodroplets could be of substantial interest for manufacturers wishing to develop encapsulation system for lipophilic functional compounds such as lipid‐soluble flavors, antimicrobials, antioxidants, and bioactives with tailored release kinetics.Practical Applications:  The paper describes the formation of electrospun nanofibers from hydrophilic polymers that contain fine‐disperse emulsion droplets. By incorporating emulsion droplets, a large variety of lipophilic ingredients can be easily loaded into the fibers’ hydrophilic polymer matrix. This is of practical importance as to date the only way to include a lipophilic ingredient in a nanofibers is by dissolving the lipophilic ingredient and polymer in an organic solvent followed by electrospinning. However, use of an organic solvent is (a) not feasible if one wants to electrospin hydrophilic polymers, and (b) use of organic solvents is generally highly undesirable in the food industry. Our results should be of interest to a number of industries such as the food, pharmaceutical, chemical, and personal care industries that are generally in need of novel matrices that can serve as carrier vehicles and release functional components such as flavors, antimicrobials, antioxidants, drugs, and bioactives.
Design and Characterization of an Aequorin‐based Bacterial Biosensor for Detection of Toluene and Related Compounds
Authors: Zeinoddini Mehdi , Khajeh Khosro , Behzadian Farida , Hosseinkhani Saman , Saeedinia Ali‐Reza , Barjesteh Hesam 
Published: July 2010

ABSTRACTAn aequorin‐based Escherichia coli strain JM109 biosensor was constructed and characterized for its potential to detect toluene and related compounds in aqueous solutions. The biosensor was constructed based on a PGL2 plasmid carrying the lower pathway promoter (Pu) of the xyl operon of Pseudomonas putida mt‐2, which was incorporated with transcriptional activator xylR and fused to aequorin cDNA named pGL2‐aequorin. Binding of xylR protein to a subset of toluene‐like compounds activates transcription at the Pu promoter, thus expression of aequorin is controlled by xylR and Pu. In this work we have compared the effect of Shine‐Dalgarno (SD) and T2 rrnβ terminator sequence in the expression of aequorin. According to the sensitivity of aequorin and increase in the signal‐to‐noise ratio, this reporter enzyme has reasonable sensitivity compared with other reporter systems. The results indicate higher expression of aequorin in the presence of SD and T2 rrnβ. The activity of aequorin in recombinant whole‐cell biosensor was linear from 1 to 500 μm of toluene. The bioluminescence response was specific for toluene‐like molecules, so this biosensor cells would be able to detect toluene derivative contamination in environmental samples, accurately.
Quantum Yields and Kinetics of the Firefly Bioluminescence Reaction of Beetle Luciferases
Authors: Niwa Kazuki , Ichino Yoshiro , Kumata Shiho , Nakajima Yoshihiro , Hiraishi Yoshihiro , Kato Dai‐ichiro , Viviani Vadim R. , Ohmiya Yoshihiro 
Published: July 2010

AbstractQuantum yields of firefly bioluminescence reactions were determined for beetle luciferases from the three main families of luminous beetles emitting different bioluminescence colors. Quantum yield (QY) was significantly correlated with luminescence spectrum. The green light‐emitting luciferase of the Brazilian click beetle, Pyrearinus termitilluminans, whose luminescence spectrum had the shortest peak wavelength of all the luciferases investigated, had the highest QY (0.61). Mutant analyses of active site‐substituted Pyrocoelia miyako luciferases showed that, although kcat was decreased by the mutations, the QY was not significantly affected.
Development of a biomarker for Geobacter activity and strain composition; Proteogenomic analysis of the citrate synthase protein during bioremediation of U(VI)
Authors: Wilkins Michael J. , Callister Stephen J. , Miletto Marzia , Williams Kenneth H. , Nicora Carrie D. , Lovley Derek R. , Long Philip E. , Lipton Mary S. 
Published: July 2010

SummaryMonitoring the activity of target microorganisms during stimulated bioremediation is a key problem for the development of effective remediation strategies. At the US Department of Energy's Integrated Field Research Challenge (IFRC) site in Rifle, CO, the stimulation of Geobacter growth and activity via subsurface acetate addition leads to precipitation of U(VI) from groundwater as U(IV). Citrate synthase (gltA) is a key enzyme in Geobacter central metabolism that controls flux into the TCA cycle. Here, we utilize shotgun proteomic methods to demonstrate that the measurement of gltA peptides can be used to track Geobacter activity and strain evolution during in situ biostimulation. Abundances of conserved gltA peptides tracked Fe(III) reduction and changes in U(VI) concentrations during biostimulation, whereas changing patterns of unique peptide abundances between samples suggested sample‐specific strain shifts within the Geobacter population. Abundances of unique peptides indicated potential differences at the strain level between Fe(III)‐reducing populations stimulated during in situ biostimulation experiments conducted a year apart at the Rifle IFRC. These results offer a novel technique for the rapid screening of large numbers of proteomic samples for Geobacter species and will aid monitoring of subsurface bioremediation efforts that rely on metal reduction for desired outcomes.
Diagnostic value of anti‐modified citrullinated vimentin in rheumatoid arthritis
Authors: MARAINA Che Hussin Che , NURDAYANA Abdul Karim , RUSNI Dollah , AZWANY Yaacob 
Published: July 2010

AbstractBackground:  Rheumatoid factors (RF) are currently used in the diagnosis of rheumatoid arthritis (RA). Several other autoantibodies found in RA are directed to epitopes in citrullinated proteins such as anti‐cyclic citrullinated and recently anti‐modified citrullinated vimentin (MCV).Objective:  In this study we determined the sensitivity and specificity of anti‐MCV in comparison with anti‐cyclic citrullinated peptide (CCP) antibodies and RF in RA patients and in a control group using the American College of Rheumatology (ACR) criteria as the gold standard.Materials and methods:  A cross sectional study was conducted from January to December 2008 on 100 patients with RA and 153 patients with arthritis or arthralgia but not fulfilling ACR criteria for RA. Serum from each subject was tested for anti‐MCV, anti‐CCP antibodies and immunoglobulin G (IgG) RF by enzyme‐linked immunosorbent assay. Sensitivity and specificity of the tests were evaluated using the ACR criteria as the gold standard.Results:  The sensitivity of RF was 85% with 74.5% specificity. For anti‐CCP antibodies the sensitivity was 71% and the specificity was 94.8%. The sensitivity of anti‐MCV antibodies was 80% with 59.5% specificity. The area under the curve for RF was 0.759, for anti‐CCP antibodies was 0.866 and for anti‐MCV antibodies was 0.681, while for at least one positive test it was 0.691.Conclusion:  Anti‐CCP antibodies have higher diagnostic specificity and positive predictive value than RF and anti‐MCV antibodies. RF has the highest sensitivity when compared to anti‐CCP and anti‐MCV antibodies. Thus anti‐MCV antibody is not a better marker when compared to RF or anti‐MCV antibody in the diagnosis of RA patients.