bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selection of Sequestering Agents Having Affinity for Calcium Ion for Stabilization of the Emulsifiable Concentrate Formulations
Authors: Kozuki Y. , Ohtsubo T. , Sasaki M. 
Published: August 2009

Abstract
Emulsifiable concentrates (ECs) are often used for pesticides, which are highly soluble in a non-polar solvent. When a pesticide is hardly soluble in a normal non-polar solvent, it is difficult to prepare an EC formulation with high pesticide content. In order to overcome this difficulty, polar solvents are used to enhance the solubility of the pesticide. N-methyl-2-pyrrolidone (NMP) is well-known as one of the most preferred polar solvents. However, many agrochemical manufacturers have started research to remove this solvent from EC formulations because of recent regulations by the authorities. However, it is not easy to find alternative solvents that have both good solvency and a good safety profile. The authors selected diethyl oxalate as an alternative candidate for NMP by using the organic conceptual diagram discussed in the previous report. A pesticide in an EC formulation containing diethyl oxalate as a co-solvent was chemically stable and showed good emulsion stability even after accelerated storage. These results suggested that this solvent could be used as an alternative to NMP. However, a decrease in pH and water content were also observed, and the sample became turbid after storage. As this turbidity was confirmed to be derived from the generation of calcium oxalate, the calcium oxalate generation process was studied. As a result, it is speculated that diethyl oxalate was hydrolyzed to oxalic acid under the acidic conditions and calcium ion, derived from an anionic surfactant contained in the EC formulation, reacted with the oxalic acid to form calcium oxalate. In order to inhibit this reaction, several kinds of sequestering agents were tested. Among them, mono-alcohols were the best though they did not completely inhibit the reaction. Though the mechanism is still unclear, mono-alcohols were effective in blocking the binding of calcium ion and oxalic acid. A mono-alcohol is a structured molecule having a hydrophilic head region and a lipophilic tail region like a surfactant. If calcium ions are dissolved in the water in the EC formulations, even though the water content is low, a mono-alcohol may form something like an inverse micelle, which captures the calcium ions inside.
Assessing the Durability of Engineered Cementitious Composites Under Freezing and Thawing Cycles
Authors: Şahmaran Mustafa , Lachemi Mohamed , Li Victor C. 
Published: August 2009

Abstract
This paper reports the durability performance of non-air-entrained engineered cementitious composites (ECC) when subjected to freezing and thawing cycles. ECC is a newly developed, high-performance, fiber-reinforced, cementitious composite with substantial benefits both in terms of high ductility under uniaxial tensile loading and improved durability due to intrinsically tight crack width of less than 100 μm. To evaluate the frost durability of ECC, freezing and thawing testing in accordance with ASTM C666 Procedure A was conducted. The mass loss, pulse velocity change, and flexural parameters (ultimate deflection and flexural strength) of specimens subjected to freezing and thawing cycles were determined in the test. In addition, air-void parameters, in accordance with ASTM C457, modified point count method, and pore size distribution obtained by mercury intrusion porosimetry technique were studied. To analyze the influence of micro-fibers and high tensile strain capacity on the freezing and thawing durability of ECC, all of the above-mentioned properties were also investigated for a control ECC matrix (ECC without fibers). After 210 cycles of freezing and thawing, the control ECC matrix specimens were severely deteriorated, requiring removal from the test, but still exhibited better performance than the conventional non-air-entrained concrete, which would fail at much earlier cycles. On the other hand, ECC with fibers without air-entrainment had excellent resistance to cycles of freezing and thawing with minimal reduction in ultimate tensile strength and ductility. The observed superior frost durability of ECC over control ECC matrix in terms of lower weight loss, pulse velocity change, and higher flexural load and ductility can be attributed to the following reasons: Increase of pore volume larger than approximately 0.30 μm in diameter, intrinsically high tensile ductility and strength due to the presence of micro-poly-vinyl-alcohol fibers.
Effects of Recombination on Complex Regulatory Circuits
Authors: Martin Olivier C , Wagner Andreas 
Published: August 2009

AbstractMutation and recombination are the two main forces generating genetic variation. Most of this variation may be deleterious. Because recombination can reorganize entire genes and genetic circuits, it may have much greater consequences than point mutations. We here explore the effects of recombination on models of transcriptional regulation circuits that play important roles in embryonic development. We show that recombination has weaker deleterious effects on the expression phenotypes of these circuits than mutations. In addition, if a population of such circuits evolves under the influence of mutation and recombination, we find that three key properties emerge: (1) deleterious effects of mutations are reduced dramatically; (2) the diversity of genotypes in the population is greatly increased, a feature that may be important for phenotypic innovation; and (3) cis-regulatory complexes appear. These are combinations of regulatory interactions that influence the expression of one gene and that mitigate deleterious recombination effects.
The Fitness Cost of Streptomycin Resistance Depends on rpsL Mutation, Carbon Source and RpoS (σS)
Authors: Paulander Wilhelm , Maisnier-Patin Sophie , Andersson Dan I 
Published: August 2009

Abstract
Mutations that cause antibiotic resistance often produce associated fitness costs. These costs have a detrimental effect on the fate of resistant organisms in natural populations and could be exploited in designing drugs, therapeutic regimes, and intervention strategies. The streptomycin resistance (StrR) mutations K42N and P90S in ribosomal protein S12 impair growth on rich medium. Surprisingly, in media with poorer carbon sources, the same StrR mutants grow faster than wild type. This improvement reflects a failure of these StrR mutants to induce the stress-inducible sigma factor RpoS (σS), a key regulator of many stationary-phase and stress-inducible genes. On poorer carbon sources, wild-type cells induce σS, which retards growth. By not inducing σS, StrR mutants escape this self-imposed inhibition. Consistent with this interpretation, the StrR mutant loses its advantage over wild type when both strains lack an RpoS (σS) gene. Failure to induce σS produced the following side effects: (1) impaired induction of several stress-inducible genes, (2) reduced tolerance to thermal stress, and (3) reduced translational fidelity. These results suggest that RpoS may contribute to long-term cell survival, while actually limiting short-term growth rate under restrictive growth conditions. Accordingly, the StrR mutant avoids short-term growth limitation but is sensitized to other stresses. These results highlight the importance of measuring fitness costs under multiple experimental conditions not only to acquire a more relevant estimate of fitness, but also to reveal novel physiological weaknesses exploitable for drug development.
The Mother Enrichment Program: A Genetic System for Facile Replicative Life Span Analysis in Saccharomyces cerevisiae
Authors: Lindstrom Derek L , Gottschling Daniel E 
Published: August 2009

Abstract
The replicative life span (RLS) of Saccharomyces cerevisiae has been established as a model for the genetic regulation of longevity despite the inherent difficulty of the RLS assay, which requires separation of mother and daughter cells by micromanipulation after every division. Here we present the mother enrichment program (MEP), an inducible genetic system in which mother cells maintain a normal RLS—a median of 36 generations in the diploid MEP strain—while the proliferative potential of daughter cells is eliminated. Thus, the viability of a population over time becomes a function of RLS, and it displays features of a survival curve such as changes in hazard rate with age. We show that viability of mother cells in liquid culture is regulated by SIR2 and FOB1, two opposing regulators of RLS in yeast. We demonstrate that viability curves of these short- and long-lived strains can be easily distinguished from wild type, using a colony formation assay. This provides a simplified screening method for identifying genetic or environmental factors that regulate RLS. Additionally, the MEP can provide a cohort of cells at any stage of their life span for the analysis of age-associated phenotypes. These capabilities effectively remove the hurdles presented by RLS analysis that have hindered S. cerevisiae aging studies since their inception 50 years ago.
InSaccharomyces cerevisiae, yKu and Subtelomeric Core X Sequences Repress Homologous Recombination Near Telomeres as Part of the Same Pathway
Authors: Marvin Marcus E , Griffin Craig D , Eyre David E , Barton David B H , Louis Edward J 
Published: August 2009

AbstractUnlike in meiosis where recombination near telomeres is repressed, subtelomeric regions appear to recombine with each other frequently in vegetative cells with no detrimental consequences. To test whether or not such recombination is prevented in the core of chromosomes for maintenance of genome stability, we measured allelic homologous recombination (HR) along chromosome arms and between different ectopic locations. We found that there is an increase of recombination at telomeres in wild-type cells compared with sequences at proximal subtelomeric and interstitial regions of the genome. We also screened for mutations that result in an increase in HR between a telomeric sequence and a more internal sequence, which normally exhibit very low rates of HR. YKU80 was hit most frequently in our screen, and we show that the yKu heterodimer specifically represses HR in the vicinity of telomeres. This repression of HR is not explained solely by the role of yKu in maintaining telomere length, silencing, or tethering to the nuclear periphery. Analysis of mutant strains harboring deleted core X sequences revealed a role for this subtelomeric element in preventing telomeric recombination. Furthermore, core X bestowed this protection as part of the same pathway as yKu. Our findings implicate a role for both yKu and core X in stabilizing the genome against recombination events involving telomeric sequences.
The Association of yKu With Subtelomeric Core X Sequences Prevents Recombination Involving Telomeric Sequences
Authors: Marvin Marcus E , Becker Marion M , Noel Pawan , Hardy Sue , Bertuch Alison A , Louis Edward J 
Published: August 2009

Abstract
The yKu protein of Saccharomyces cerevisiae is important for genome stability by repressing recombination involving telomeric sequences. The mechanism of this repression is not known, but silent heterochromatin such as HML, HMR, and telomeres are compartmentalized at the nuclear periphery and yKu is proposed to interact with these regions and to play a role in telomeric silencing and tethering. We have utilized ChIP on chip, quantitative PCR, and quantitative recombination assays to analyze yKu binding and its effect on genome stability in wild-type and mutant backgrounds. Our data suggest that, although yKu binds to the TG1-3 repeats and other parts of the genome when needed, such as during nonhomologous end-joining, it specifically binds to core X sequences in addition to the mating-type loci, HML and HMR. Association with core X occurred in the absence of Sir proteins, and enhanced binding was observed at silenced ends compared to nonsilenced ends. In contrast, binding to HML and HMR was totally dependent on Sir2–4p and partially dependent on Sir1p with a stronger association at HML in both MATa and MATα strains. Using yku80 separation-of-function mutants, we show a direct correlation between core X binding and recombination rate. We believe our findings support our hypothesis that yKu and core X play a pivotal role in maintaining genome stability through nuclear architecture by mediating a defensive fold-back structure at yeast chromosome ends.
Efficient Ensemble-Based Closed-Loop Production Optimization
Authors: Chen Yan , Oliver Dean S. , Zhang Dongxiao 
Published: August 2009

Summary
With the advances in smart well technology, substantially higher oil recovery can be achieved by intelligently managing the operations in a closed-loop optimization framework. The closed-loop optimization consists of two parts: geological model updating and production optimization. Both of these parts require gradient information to minimize or maximize an objective function: squared data mismatch or the net present value (or other quantities depending on financial goals), respectively. Alternatively, an ensemble-based method can acquire the gradient information through the correlations provided by the ensemble. Computation of the optimal controls in this way is nearly independent of the number of control variables, reservoir simulator, and simulation solver. In this paper, we propose an ensemble-based closed-loop optimization method that combines a novel ensemble-based optimization scheme (EnOpt) with the ensemble Kalman filter (EnKF). EnKF has recently been found suitable for sequential data assimilation in large-scale nonlinear dynamics. It adjusts reservoir model variables to honor observations and propagates uncertainty in time. EnOpt optimizes the expectation of the net present value based on the updated reservoir models. The proposed method is fairly robust, completely adjoint-free and can be readily used with any reservoir simulator. The ensemble-based closed-loop optimization method is illustrated with a waterflood example subject to uncertain reservoir description. Results are compared with other possible reservoir operation scenarios, such as wells with no controls, reactive control, and optimization with known geology. The comparison shows that the ensemble-based closed-loop optimization is able to history match the main geological features and increase the net present value to a level comparable with the hypothetical case of optimizing based on known geology.
FoxO1 Links Insulin Resistance to Proinflammatory Cytokine IL-1β Production in Macrophages
Authors: Su Dongming , Coudriet Gina M. , Hyun Kim Dae , Lu Yi , Perdomo German , Qu Shen , Slusher Sandra , Tse Hubert M. , Piganelli Jon , Giannoukakis Nick , Zhang Jian , Henry Dong H. 
Published: August 2009

OBJECTIVE
Macrophages play an important role in the pathogenesis of insulin resistance via the production of proinflammatory cytokines. Our goal is to decipher the molecular linkage between proinflammatory cytokine production and insulin resistance in macrophages.

RESEARCH DESIGN AND METHODS
We determined cytokine profiles in cultured macrophages and identified interleukin (IL)-1β gene as a potential target of FoxO1, a key transcription factor that mediates insulin action on gene expression. We studied the mechanism by which FoxO1 mediates insulin-dependent regulation of IL-1β expression in cultured macrophages and correlated FoxO1 activity in peritoneal macrophages with IL-1β production profiles in mice with low-grade inflammation or insulin resistance.

RESULTS
FoxO1 selectively promoted IL-1β production in cultured macrophages. This effect correlated with the ability of FoxO1 to bind and enhance IL-1β promoter activity. Mutations of the FoxO1 binding site within the IL-1β promoter abolished FoxO1 induction of IL-1β expression. Macrophages from insulin-resistant obese db/db mice or lipopolysaccharide-inflicted mice were associated with increased FoxO1 production, correlating with elevated levels of IL-1β mRNA in macrophages and IL-1β protein in plasma. In nonstimulated macrophages, FoxO1 remained inert with benign effects on IL-1β expression. In response to inflammatory stimuli, FoxO1 activity was augmented because of an impaired ability of insulin to phosphorylate FoxO1 and promote its nuclear exclusion. This effect along with nuclear factor-κB acted to stimulate IL-1β production in activated macrophages.

CONCLUSIONS
FoxO1 signaling through nuclear factor-κB plays an important role in coupling proinflammatory cytokine production to insulin resistance in obesity and diabetes.
Reductive Metabolism of AGE Precursors: A Metabolic Route for Preventing AGE Accumulation in Cardiovascular Tissue
Authors: Baba Shahid P. , Barski Oleg A. , Ahmed Yonis , O'Toole Timothy E. , Conklin Daniel J. , Bhatnagar Aruni , Srivastava Sanjay 
Published: August 2009

OBJECTIVE
To examine the role of aldo-keto reductases (AKRs) in the cardiovascular metabolism of the precursors of advanced glycation end products (AGEs).

RESEARCH DESIGN AND METHODS
Steady-state kinetic parameters of AKRs with AGE precursors were determined using recombinant proteins expressed in bacteria. Metabolism of methylglyoxal and AGE accumulation were studied in human umbilical vein endothelial cells (HUVECs) and C57 wild-type, akr1b3 (aldose reductase)-null, cardiospecific-akr1b4 (rat aldose reductase), and akr1b8 (FR-1)-transgenic mice. AGE accumulation and atherosclerotic lesions were studied 12 weeks after streptozotocin treatment of C57, akr1b3-null, and apoE- and akr1b3-apoE–null mice.

RESULTS
Higher levels of AGEs were generated in the cytosol than at the external surface of HUVECs cultured in high glucose, indicating that intracellular metabolism may be an important regulator of AGE accumulation and toxicity. In vitro, AKR 1A and 1B catalyzed the reduction of AGE precursors, whereas AKR1C, AKR6, and AKR7 were relatively ineffective. Highest catalytic efficiency was observed with AKR1B1. Acetol formation in methylglyoxal-treated HUVECs was prevented by the aldose reductase inhibitor sorbinil. Acetol was generated in hearts perfused with methylglyoxal, and its formation was increased in akr1b4- or akr1b8-transgenic mice. Reduction of AGE precursors was diminished in hearts from akr1b3-null mice. Diabetic akr1b3-null mice accumulated more AGEs in the plasma and the heart than wild-type mice, and deletion of akr1b3 increased AGE accumulation and atherosclerotic lesion formation in apoE-null mice.

CONCLUSIONS
Aldose reductase–catalyzed reduction is an important pathway in the endothelial and cardiac metabolism of AGE precursors, and it prevents AGE accumulation and atherosclerotic lesion formation.
Genetic Variant in HK1 Is Associated With a Proanemic State and A1C but Not Other Glycemic Control–Related Traits
Authors: Bonnefond Amélie , Vaxillaire Martine , Labrune Yann , Lecoeur Cécile , Chèvre Jean-Claude , Bouatia-Naji Nabila , Cauchi Stéphane , Balkau Beverley , Marre Michel , Tichet Jean , Riveline Jean-Pierre , Hadjadj Samy , Gallois Yves , Czernichow Sébastien , Hercberg Serge , Kaakinen Marika , Wiesner Susanne , Charpentier Guillaume , Lévy-Marchal Claire , Elliott Paul , Jarvelin Marjo-Riitta , Horber Fritz , Dina Christian , Pedersen Oluf , Sladek Robert , Meyre David , Froguel Philippe 
Published: August 2009

OBJECTIVE
A1C is widely considered the gold standard for monitoring effective blood glucose levels. Recently, a genome-wide association study reported an association between A1C and rs7072268 within HK1 (encoding hexokinase 1), which catalyzes the first step of glycolysis. HK1 deficiency in erythrocytes (red blood cells [RBCs]) causes severe nonspherocytic hemolytic anemia in both humans and mice.

RESEARCH DESIGN AND METHODS
The contribution of rs7072268 to A1C and the RBC-related traits was assessed in 6,953 nondiabetic European participants. We additionally analyzed the association with hematologic traits in 5,229 nondiabetic European individuals (in whom A1C was not measured) and 1,924 diabetic patients. Glucose control–related markers other than A1C were analyzed in 18,694 nondiabetic European individuals. A type 2 diabetes case-control study included 7,447 French diabetic patients.

RESULTS
Our study confirms a strong association between the rs7072268–T allele and increased A1C (β = 0.029%; P = 2.22 × 10−7). Surprisingly, despite adequate study power, rs7072268 showed no association with any other markers of glucose control (fasting- and 2-h post-OGTT–related parameters, n = 18,694). In contrast, rs7072268–T allele decreases hemoglobin levels (n = 13,416; β = −0.054 g/dl; P = 3.74 × 10−6) and hematocrit (n = 11,492; β = −0.13%; P = 2.26 × 10−4), suggesting a proanemic effect. The T allele also increases risk for anemia (836 cases; odds ratio 1.13; P = 0.018).

CONCLUSIONS
HK1 variation, although strongly associated with A1C, does not seem to be involved in blood glucose control. Since HK1 rs7072268 is associated with reduced hemoglobin levels and favors anemia, we propose that HK1 may influence A1C levels through its anemic effect or its effect on glucose metabolism in RBCs. These findings may have implications for type 2 diabetes diagnosis and clinical management because anemia is a frequent complication of the diabetes state.
Sleep Duration, Lifestyle Intervention, and Incidence of Type 2 Diabetes in Impaired Glucose Tolerance
Authors: Tuomilehto Henri , Peltonen Markku , Partinen Markku , Lavigne Gilles , Eriksson Johan G. , Herder Christian , Aunola Sirkka , Keinänen-Kiukaanniemi Sirkka , Ilanne-Parikka Pirjo , Uusitupa Matti , Tuomilehto Jaakko , Lindström Jaana ,   on behalf of the Finnish Diabetes Prevention Study Group
Published: August 2009

OBJECTIVE
Both short and long sleep duration have frequently been found to be associated with an increased risk for diabetes. The aim of the present exploratory analysis was to examine the association between sleep duration and type 2 diabetes after lifestyle intervention in overweight individuals with impaired glucose tolerance in a 7-year prospective follow-up.

RESEARCH DESIGN AND METHODS
A total of 522 individuals (aged 40–64 years) were randomly allocated either to an intensive diet-exercise counseling group or to a control group. Diabetes incidence during follow-up was calculated according to sleep duration at baseline. Sleep duration was obtained for a 24-h period. Physical activity, dietary intakes, body weight, and immune mediators (C-reactive protein and interleukin-6) were measured.

RESULTS
Interaction between sleep duration and treatment group was statistically significant (P = 0.003). In the control group, the adjusted hazard ratios (HRs) (95% CI) for diabetes were 2.29 (1.38–3.80) and 2.74 (1.67–4.50) in the sleep duration groups 9–9.5 h and ≥10 h, respectively, compared with for that of the 7–8.5 h group. In contrast, sleep duration did not influence the incidence of diabetes in the intervention group; for sleep duration groups 9–9.5 h and ≥10 h, the adjusted HRs (95% CI) were 1.10 (0.60–2.01) and 0.73 (0.34–1.56), respectively, compared with that in the reference group (7–8.5 h sleep). Lifestyle intervention resulted in similar improvement in body weight, insulin sensitivity, and immune mediator levels regardless of sleep duration.

CONCLUSIONS
Long sleep duration is associated with increased type 2 diabetes risk. Lifestyle intervention with the aim of weight reduction, healthy diet, and increased physical activity may ameliorate some of this excess risk.