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Sequence patterns observed in 5' flanking regions of primate Alu elements.

Retrotransposons have generally been known to integrate randomly into host genomes. Jurka, however, showed some consensus sequence patterns at insertion sites of some mammalian retrotransposons and proposed enzymatic involvement that mediates integration. Jurka used about 400 complete human Alu and rodent ID sequences which retain full length with identical flanking sequences at both ends. In our study, more than 25,000 Alu sequences longer than 250 bp were used for comprehensive analysis to identify any consensus sequence(s) preceding the 5' end of Alu elements. "Entropy" at each nucleotide position within 500 bases of the 5' Alu end was computed. Significant drop of entropy was observed between position -20 and -10 of the 5' end of Alu, suggesting the existence of certain consensus sequence(s) in the region. Frequencies of all possible triplets (total of 64) were measured in the same region. Observation that frequencies of triplets "aaa," "taa," and "tta" in the 5' flanking sequences were high is consistent with Jurka. However, frequencies of triplets "att" and "aca" were also significantly high, which are not the primary candidates for nick site in Jurka.

Alu Elements↗

Genomic organization of nematode 4TM K+ channels.

As many as 50 genes in the C. elegans genome may encode K+ channels belonging to the novel structural class of two-pore (4TM) channels. Many 4TM channels can be grouped into channel subfamilies. We analyzed 4TM channels in C. elegans using methods made possible by having complete genomic sequence. Two genes were chosen for comprehensive analysis, n2P16 and n2P17. By comparing the pattern of conservation in genomic DNA sequences between C. elegans and a closely related species, C. briggsae, we were able to identify all coding regions and predict the gene structure for these two genes. Given the extent of the 4TM channel family, we were surprised to discover that n2P17 produced at least six alternative transcripts encoding a constant central region and variable amino- and carboxyl-termini. Blocks of highly conserved DNA sequences in noncoding regions were also apparent and most likely confer important regulatory functions. The interspecies comparison of the deduced channel proteins revealed that the extracellular loop between M1 and P1 is an apparent hot spot for evolutionary change in both channels. This contrasts with the membrane-spanning domains that are highly conserved. Analysis of intron positions for 36 channels revealed that introns are frequently present at an identical position within the pore region, but very few are located in membrane-spanning domains.

Alternative Splicing↗

Subcellular Ca(2+) dynamics measured with targeted aequorin in chromaffin cells.

In the last years, intracellular organella have emerged as key components in the generation and transduction of Ca(2+) signals in adrenal chromaffin cells. Therefore, accurate measurements of Ca(2+) inside cytoplasmic organella are essential for a comprehensive analysis of the Ca(2+) redistribution that follows cell stimulation. We have engineered the Ca(2+)-sensitive photoprotein aequorin to monitor selectively Ca(2+) within the endoplasmic reticulum and the mitochondria. The targeted aequorins were delivered to the appropriate organelles of bovine chromaffin cells by using a herpes simplex virus-based amplicon vector, which permits efficient gene transfer and high levels of expression in infected cells. We have investigated the relationship between the caffeine and InsP(3)-sensitive Ca(2+) pools and the presence of the Ca(2+)-induced Ca(2+) release (CICR) mechanism in chromaffin cells. We find that ER Ca(2+) pools responding to caffeine and to InsP(3) mostly overlap and that CICR can be induced by Ca(2+) entry elicited by high K(+) depolarization. Moreover, the activation of Ca(2+) channels, either the voltage-gated Ca(2+) channels on the plasma membrane or the channels on the endoplasmic reticulum (ER), generates subplasmalemmal high [Ca(2+)](c) domains that induce Ca(2+) uptake by mitochondria. Interestingly, only a subpopulation of mitochondria, the one contained in the pool located close to the plasma membrane and the ryanodine receptors, take up Ca(2+) efficiently, and the [Ca(2+)](M) reaches values of 300-500 micro M.

Aequorin↗

GhDMT7-mediated DNA methylation dynamics enhance starch and sucrose metabolism pathways to confer salt tolerance in cotton.

This study provides a comprehensive analysis of the impact of DNA methylation in cotton under salt stress conditions, elucidating its effects on gene expression and biological processes. Here, we determined the structures of the DNA methylation landscape across the cotton genome subjected to salt stress using whole-genome bisulfite sequencing (WGBS) and RNA-seq methodologies. We identified 4938 differentially methylated regions (DMRs) correlated with alterations in gene expression. Salt stress induced significant shifts in DNA methylation patterns, particularly in CHH contexts, suggesting context-dependent epigenetic regulation. DMRs were found to be implicated in diverse biological processes and pathways, encompassing protein metabolism, cellular homeostasis, starch and sucrose metabolism, and plant hormone signaling, all pivotal for cotton's adaptation to salt stress. Furthermore, RNA-seq analysis confirmed the impact of DNA methylation on gene expression, uncovering 9642 salt stress-responsive differentially expressed genes (DEGs). These DEGs exhibited enrichment in pathways such as carbohydrate metabolism, cell wall synthesis, and defense response, underscoring the intricate interplay between methylation and gene regulation in stress response. Moreover, the study investigated the role of the key DNA methyltransferase gene GhDMT7 in modulating cotton's response to salt stress, revealing that its downregulation enhanced cotton's salt tolerance, potentially attributed to decreased DNA methylation levels, reduced membrane damage, and enhanced antioxidant capacity. These findings elucidate the role of DNA methylation in abiotic stress resilience and provide insights for crop improvement.

Gossypium↗

Characterization of phosphorylation variants for identifying adaptive alleles in Zea.

Large-scale genome sequencing of maize wild species (teosinte) has uncovered thousands of genetic mutations, but distinguishing causal alleles from neutral variations remains a significant challenge. In this study, we conducted a comprehensive analysis of phosphorylation-associated single-nucleotide variations (pSNVs) to enhance our understanding of adaptive variations in the Zea genus. We collected 234 teosinte genomes from seven different taxa and 507 cultivated maize genomes to identify single-nucleotide variants that target phosphorylation machinery, which is crucial for plant development and environmental adaptation. Our analysis identified 33 687 pSNVs within the Zea genus and revealed a reduction in genetic conservation along with an increase in protein abundance and expression for genes harboring pSNVs. Additionally, pSNVs present stronger purifying selection pressures compared with other missense mutations. We found that maize possesses fewer pSNVs than teosinte, likely due to the effects of selection and hitchhiking. By examining the role of pSNVs related to kinase-substrate rewriting events and exhibiting evolutionary divergence jointly, our results suggest that pSNVs impact multiple traits, particularly flowering time variation between teosinte and maize. Furthermore, we documented the widespread presence of pSNVs in Arabidopsis thaliana, rice, and wheat, identifying 46 pSNVs that have convergently evolved between maize and other species. Our study provides another insight into uncovering adaptive alleles in wild species by incorporating protein signaling sites and emphasizes the potential of utilizing wild species for future crop improvement.

Zea mays↗

Computational evaluation of intraventricular pressure gradients based on a fluid-structure approach.

The dynamics of intraventricular blood flow, i.e. its rapid evolution, implies the rise of intraventricular pressure gradients (IPGs) characteristic of the inertia-driven events as experimentally observed by Pasipoularides (1987, 1990) and by Falsetti et al. (1986). The IPG time course is determined by the wall contraction which, in turn, depends on the load applied, namely the intraventricular pressure which is the sum of the aortic pressure (i.e., the systemic net response) and the IPG. Hence the IPGs account, at least in part, for the wall movement. These considerations suggest the necessity of a comprehensive analysis of the ventricular mechanics involving both ventricular wall mechanics and intraventricular fluid dynamics as each domain determines the boundary conditions of the other. This paper presents a computational approach to ventricular ejection mechanics based on a fluid-structure interaction calculation for the evaluation of the IPG time course. An axisymmetric model of the left ventricle is utilized. The intraventricular fluid is assumed to be Newtonian. The ventricle wall is thin and is composed of two sets of counter-rotating fibres which behave according to the modified version of Wong's sarcomere model proposed by Montevecchi and Pietrabissa and Pietrabissa et al. (1987, 1991). The full Navier-Stokes equations describing the fluid domain are solved using Galerkin's weighted residual approach in conjunction with finite element approximation (FIDAP). The wall displacement is solved using the multiplane quasi-Newton method proposed by Buzzi Ferraris and Tronconi (1985). The interaction procedure is performed by means of an external macro which compares the flow fields and the wall displacement and appropriately modifies the boundary conditions to reach the simultaneous and congruous convergence of the two problems. The results refer to a simulation of the ventricular ejection with a heart rate of 72 bpm. In this phase the ventricle ejects 61 cm3 (ejection fraction equal to 54 percent) and the ventricular pressure varies from 78 mmHg to 140 mmHg. The IPG show an oscillating behaviour with two major peaks at the beginning (11.09 mmHg) and at the end (4.32 mmHg) of the ejection phase, when the flow rate hardly changes, according to the experimental data. Furthermore the wall displacement, the wall stress and strain, the pressure and velocity fields are calculated and reported.

Blood Flow Velocity↗

Intracranial stereotactic positioning systems: Report of the American Association of Physicists in Medicine Radiation Therapy Committee Task Group no. 68.

Intracranial stereotactic positioning systems (ISPSs) are used to position patients prior to precise radiation treatment of localized lesions of the brain. Often, the lesion is located in close proximity to critical anatomic features whose functions should be maintained. Many types of ISPSs have been described in the literature and are commercially available. These are briefly reviewed. ISPS systems provide two critical functions. The first is to establish a coordinate system upon which a guided therapy can be applied. The second is to provide a method to reapply the coordinate system to the patient such that the coordinates assigned to the patient's anatomy are identical from application to application. Without limiting this study to any particular approach to ISPSs, this report introduces nomenclature and suggests performance tests to quantify both the stability of the ISPS to map diagnostic data to a coordinate system, as well as the ISPS's ability to be realigned to the patient's anatomy. For users who desire to develop a new ISPS system, it may be necessary for the clinical team to establish the accuracy and precision of each of these functions. For commercially available systems that have demonstrated an acceptable level of accuracy and precision, the clinical team may need to demonstrate local ability to apply the system in a manner consistent with that employed during the published testing. The level of accuracy and precision required of an individual ISPS system is dependent upon the clinical protocol (e.g., fractionation, margin, pathology, etc.). Each clinical team should provide routine quality assurance procedures that are sufficient to support the assumptions of accuracy and precision used during the planning process. The testing of ISPS systems can be grouped into two broad categories, type testing, which occurs prior to general commercialization, and site testing, performed when a commercial system is installed at a clinic. Guidelines to help select the appropriate tests as well as recommendations to help establish the required frequency of testing are provided. Because of the broad scope of different systems, it is important that both the manufacturer and user rigorously critique the system and set QA tests appropriate to the particular device and its possible weaknesses. Major recommendations of the Task Group include: introduction of a new nomenclature for reporting repositioning accuracy; comprehensive analysis of patient characteristics that might adversely affect positioning accuracy; performance of testing immediately before each treatment to establish that there are no gross positioning errors; a general request to the Medical Physics community for improved QA tools; implementation of weekly portal imaging (perhaps cone beam CT in the future) as a method of tracking fractionated patients (as per TG 40); and periodic routine reviews of positioning accuracy.

Equipment Failure Analysis↗

A dosimetric comparison of 169Yb versus 192Ir for HDR prostate brachytherapy.

For the purpose of evaluating the use of 169Yb for prostate High Dose Rate brachytherapy (HDR), a hypothetical 169Yb source is assumed with the exact same design of the new microSelectron source replacing the 192Ir active core by pure 169Yb metal. Monte Carlo simulation is employed for the full dosimetric characterization of both sources and results are compared following the AAPM TG-43 dosimetric formalism. Monte Carlo calculated dosimetry results are incorporated in a commercially available treatment planning system (SWIFT), which features an inverse treatment planning option based on a multiobjective dose optimization engine. The quality of prostate HDR brachytherapy using the real 192Ir and hypothetical 169Yb source is compared in a comprehensive analysis of different prostate implants in terms of the multiobjective dose optimization solutions as well as treatment quality indices such as Dose Volume Histograms (DVH) and the Conformal Index (COIN). Given that scattering overcompensates for absorption in intermediate photon energies and distances in the range of interest to prostate HDR brachytherapy, 169Yb proves at least equivalent to 192Ir irrespective of prostate volume. This has to be evaluated in view of the shielding requirements for the 169Yb energies that are minimal relative to that for 192Ir.

Biophysical Phenomena↗

Application of Gafchromic film in the dosimetry of an intravascular brachytherapy source.

The methodology of brachytherapy source dosimetry with Gafchromic MD 55-2 film (ISP Technologies, Inc.) is examined with an emphasis on the nonlinearity of the optical density-dose relation within the dynamic dose range, the radial distance-dependent measurement uncertainty, and the format of data presentation. The specific source chosen for this study was a Checkmate (Cordis Corporation) intravascular brachytherapy system. The two-dimensional dose distribution around the source was characterized by a comprehensive analysis of measurement uncertainties. A comparative analysis of the dosimetric data from the vendor and from the scientific literature showed a substantial consistency of the information available for the Checkmate source. Our two-dimensional dosimetric data for the Checkmate source trains is presented in the form of measured along and away dose tables.

Blood Vessels↗

Modeling global and focal hyperarticulation during human-computer error resolution.

When resolving errors with interactive systems, people sometimes hyperarticulate--or adopt a clarified style of speech that has been associated with increased recognition errors. The primary goals of the present study were: (1) to provide a comprehensive analysis of acoustic, prosodic, and phonological adaptations to speech during human-computer error resolution after different types of recognition error; and (2) to examine changes in speech during both global and focal utterance repairs. A semi-automatic simulation method with a novel error-generation capability was used to compare speech immediately before and after system recognition errors. Matched original-repeat utterance pairs then were analyzed for type and magnitude of linguistic adaption during global and focal repairs. Results indicated that the primary hyperarticulate changes in speech following all error types were durational, with increases in number and length of pauses most noteworthy. Speech also was adapted toward a more deliberate and hyperclear articulatory style. During focal error repairs, large durational effects functioned together with pitch and amplitude to provide selective prominence marking of the repair region. These results corroborate and generalize the computer-elicited hyperarticulate adaptation model (CHAM). Implications are discussed for improved error handling in next-generation spoken language and multimodal systems.

Computers↗

Comparative study of ortho- and meta-nitrated inhibitors of catechol-O-methyltransferase: interactions with the active site and regioselectivity of O-methylation.

In this work, we present a comparative case study of "ortho-" and "meta-nitrated" catecholic inhibitors of catechol-O-methyltransferase (COMT), with regard to their interaction with the catalytic site of the enzyme and the in vitro regioselective formation of their mono-O-methyl ether metabolites. In particular, the effects of altering the attachment position of the inhibitors' side-chain substituent, within the classic nitrocatechol pharmacophore, were investigated. For this purpose, we compared two simple regioisomeric nitrocatechol-type inhibitors of COMT, BIA 3-228 and BIA 8-176, which contain the benzoyl substituent attached at the meta and ortho positions, respectively, relative to the nitro group. The two compounds were slowly O-methylated by COMT in vitro, but the particular substitution pattern of each compound was shown to have a profound impact on the regioselectivity of their O-methylation. To provide a plausible interpretation of these results, a comprehensive analysis of the protein-inhibitor interactions and of the relative chemical susceptibility to O-methylation of the catechol hydroxyl groups was performed by means of docking simulations and ab initio molecular orbital calculations. The major structural and chemical factors that determine the enzyme regioselectivity of O-methylation were identified, and the X-ray structure of the complex of COMT with S-adenosyl-l-methionine and BIA 8-176 is herein disclosed. This is the first reported structure of the soluble form of COMT complexed with a nitrocatecholic inhibitor having a bulky substituent group in adjacent position (ortho) to the nitro group. Structural and dynamic aspects of this complex are analyzed and discussed, in the context of the present study.

Animals↗

Structural determinants of adenophostin A activity at inositol trisphosphate receptors.

Adenophostin A is the most potent known agonist of inositol 1,4,5-trisphosphate (InsP(3)) receptors. Ca(2+) release from permeabilized hepatocytes was 9.9 +/- 1.6-fold more sensitive to adenophostin A (EC(50), 14.7 +/- 2.4 nM) than to InsP(3) (145 +/- 10 nM), consistent with the greater affinity of adenophostin A for hepatic InsP(3) receptors (K(d) = 0.48 +/- 0.06 and 3.09 +/- 0.33 nM, respectively). Here, we systematically modify the structures of the glucose, ribose, and adenine moieties of adenophostin A and use Ca(2+) release and binding assays to define their contributions to high-affinity binding. Progressive trimming of the adenine of adenophostin A reduced potency, but it fell below that of InsP(3) only after complete removal of the adenine. Even after substantial modifications of the adenine (to uracil or even unrelated aromatic rings, retaining the beta-orientation), the analogs were more potent than InsP(3). The only analog with an alpha-ribosyl linkage had massively decreased potency. The 2'-phosphate on the ribose ring of adenophostin A was essential and optimally active when present on a five-membered ring in a position stereochemically equivalent to its location in adenophostin A. Xylo-adenophostin, where xylose replaces the glucose ring of adenophostin A, was only slightly less potent than adenophostin A, whereas manno-adenophostin (mannose replacing glucose) had similar potency to InsP(3). These results are consistent with the relatively minor role of the 3-hydroxyl of InsP(3) (the equivalent is absent from xylo-adenophostin) and greater role of the equatorial 6-hydroxyl (the equivalent is axial in manno-adenophostin). This is the first comprehensive analysis of all the key structural elements of adenophostin A, and it provides a working model for the design of related high-affinity ligands of InsP(3) receptors.

Adenosine↗

Inverse agonist up-regulates the constitutively active D3.49(164)Q mutant of the rat mu-opioid receptor by stabilizing the structure and blocking constitutive internalization and down-regulation.

We demonstrated previously that D3.49(164) mutations resulted in constitutive activation of the rat mu-opioid receptor and abolished receptor expression unless cells were pretreated with naloxone, an inverse agonist. In this study, we investigated the properties of the D3.49(164)Q mutant and the mechanisms underlying the effect of naloxone. Naloxone pretreatment up-regulated [(3)H]diprenorphine binding and protein expression of the D3.49(164)Q mutant in a time- and dose-dependent manner without affecting its mRNA level. After naloxone removal, binding and protein expression of the mutant declined with time with no effect on its mRNA level. Naloxone methiodide (a quaternary ammonium analog) caused a maximal up-regulation about 50% of the naloxone effect, indicating that naloxone acts extracellularly and intracellularly. Expression of the mutant was enhanced by inverse agonists, a neutral antagonist, and agonists, with inverse agonists being most effective. In membranes, the mutant was structurally less stable than the wild type upon incubation at 37 degrees C, and naloxone and [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin stabilized the mutant. Coexpression of the dominant-negative mutants GRK2-K220R, arrestin-2(319-418), dynamin I-K44A, rab5A-N133I or rab7-N125I partially prevented the decline in binding of the mutant after naloxone removal. Chloroquine or proteasome inhibitor I reduced the down-regulation of the mutant. These results indicate that the D3.49(164)Q mutant is constitutively internalized via G protein coupled-receptor kinase-, arrestin-2-, dynamin-, rab5-, and rab7-dependent pathways and probably trafficked through early and late endosomes into lysosomes and degraded by lysosomes and proteasomes. Naloxone up-regulates the D3.49(164)Q mutant by stabilizing the mutant protein and blocking its constitutive internalization and down-regulation. To the best of our knowledge, this represents the first comprehensive analysis of the mechanisms involved in up-regulation of constitutively active mutants by an inverse agonist.

Animals↗

The protein kinase complement of the human genome.

We have catalogued the protein kinase complement of the human genome (the "kinome") using public and proprietary genomic, complementary DNA, and expressed sequence tag (EST) sequences. This provides a starting point for comprehensive analysis of protein phosphorylation in normal and disease states, as well as a detailed view of the current state of human genome analysis through a focus on one large gene family. We identify 518 putative protein kinase genes, of which 71 have not previously been reported or described as kinases, and we extend or correct the protein sequences of 56 more kinases. New genes include members of well-studied families as well as previously unidentified families, some of which are conserved in model organisms. Classification and comparison with model organism kinomes identified orthologous groups and highlighted expansions specific to human and other lineages. We also identified 106 protein kinase pseudogenes. Chromosomal mapping revealed several small clusters of kinase genes and revealed that 244 kinases map to disease loci or cancer amplicons.

Animals↗

Climate-driven increases in global terrestrial net primary production from 1982 to 1999.

Recent climatic changes have enhanced plant growth in northern mid-latitudes and high latitudes. However, a comprehensive analysis of the impact of global climatic changes on vegetation productivity has not before been expressed in the context of variable limiting factors to plant growth. We present a global investigation of vegetation responses to climatic changes by analyzing 18 years (1982 to 1999) of both climatic data and satellite observations of vegetation activity. Our results indicate that global changes in climate have eased several critical climatic constraints to plant growth, such that net primary production increased 6% (3.4 petagrams of carbon over 18 years) globally. The largest increase was in tropical ecosystems. Amazon rain forests accounted for 42% of the global increase in net primary production, owing mainly to decreased cloud cover and the resulting increase in solar radiation.

Atmosphere↗

Blood pressure and nutrient intake in the United States.

A data base of the National Center for Health Statistics, Health and Nutrition Examination Survey I (HANES I), was used to perform a computer-assisted, comprehensive analysis of the relation of 17 nutrients to the blood pressure profile of adult Americans. Subjects were 10,372 individuals, 18 to 74 years of age, who denied a history of hypertension and intentional modification of their diet. Significant decreases in the consumption of calcium, potassium, vitamin A, and vitamin C were identified as the nutritional factors that distinguished hypertensive from normotensive subjects. Lower calcium intake was the most consistent factor in hypertensive individuals. Across the population, higher intakes of calcium, potassium, and sodium were associated with lower mean systolic blood pressure and lower absolute risk of hypertension. Increments of dietary calcium were also negatively correlated with body mass. Even though these correlations cannot be accepted as proof of causation, they have implications for future studies of the association of nutritional factors and dietary patterns with hypertension in America.

Adolescent↗

Emergence of resistance to protease inhibitor amprenavir in human immunodeficiency virus type 1-infected patients: selection of four alternative viral protease genotypes and influence of viral susceptibility to coadministered reverse transcriptase nucleoside inhibitors.

Previous data have indicated that the development of resistance to amprenavir, an inhibitor of the human immunodeficiency virus type 1 protease, is associated with the substitution of valine for isoleucine at residue 50 (I50V) in the viral protease. We present further findings from retrospective genotypic and phenotypic analyses of plasma samples from protease inhibitor-naïve and nucleoside reverse transcriptase inhibitor (NRTI)-experienced patients who experienced virological failure while participating in a clinical trial where they had been randomized to receive either amprenavir or indinavir in combination with NRTIs. Paired baseline and on-therapy isolates from 31 of 48 (65%) amprenavir-treated patients analyzed demonstrated the selection of protease mutations. These mutations fell into four distinct categories, characterized by the presence of either I50V, I54L/I54M, I84V, or V32I+I47V and often included accessory mutations, commonly M46I/L. The I50V and I84V genotypes displayed the greatest reductions in susceptibility to amprenavir, although each of the amprenavir-selected genotypes conferred little or no cross-resistance to other protease inhibitors. There was a significant association, for both amprenavir and indinavir, between preexisting baseline resistance to NRTIs subsequently received during the study and development of protease mutations (P = 0.014 and P = 0.031, respectively). Our data provide a comprehensive analysis of the mechanisms by which amprenavir resistance develops during clinical use and present evidence that resistance to concomitant agents in the treatment regimen predisposes to the development of mutations associated with protease inhibitor resistance and treatment failure.

Carbamates↗

Engineering a Saccharomyces cerevisiae wine yeast that exhibits reduced ethanol production during fermentation under controlled microoxygenation conditions.

We recently showed that expressing an H(2)O-NADH oxidase in Saccharomyces cerevisiae drastically reduces the intracellular NADH concentration and substantially alters the distribution of metabolic fluxes in the cell. Although the engineered strain produces a reduced amount of ethanol, a high level of acetaldehyde accumulates early in the process (1 g/liter), impairing growth and fermentation performance. To overcome these undesirable effects, we carried out a comprehensive analysis of the impact of oxygen on the metabolic network of the same NADH oxidase-expressing strain. While reducing the oxygen transfer rate led to a gradual recovery of the growth and fermentation performance, its impact on the ethanol yield was negligible. In contrast, supplying oxygen only during the stationary phase resulted in a 7% reduction in the ethanol yield, but without affecting growth and fermentation. This approach thus represents an effective strategy for producing wine with reduced levels of alcohol. Importantly, our data also point to a significant role for NAD(+) reoxidation in controlling the glycolytic flux, indicating that engineered yeast strains expressing an NADH oxidase can be used as a powerful tool for gaining insight into redox metabolism in yeast.

Ethanol↗