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1.
Langmuir ; 33(44): 12580-12591, 2017 11 07.
Article in English | MEDLINE | ID: mdl-29028355

ABSTRACT

We evaluate the efficiency and capacity of electrochemically reversible insertion electrodes for use in targeted ion removal applications in aqueous solutions. The relative attributes of insertion material chemistry are evaluated by comparing the performance of two different sodium insertion materials, NaTi2(PO4)3 and Na4Mn9O18, in different electrolyte environments. We performed experiments over a range of solution compositions containing both sodium and other non-inserting ions, and we then developed mechanistic insight into the effects of solution concentration and composition on overpotential losses and round trip Coulombic efficiency. In dilute aqueous streams, performance was limited by the rate of ion transport from the bulk electrolyte region to the electrode interface. This leads to slow rates of ion removal, large overpotentials for ion insertion, parasitic charge loss due to water electrolysis, and lower round trip Coulombic efficiencies. This effect is particularly large for insertion electrodes with redox potentials exceeding the water stability window. In solutions with high background concentrations of non-inserting ions, the accumulation of non-inserting ions at the electrode interface limits inserting ion flux and leads to low ion removal capacity and round trip Coulombic efficiency.

2.
Article in English | MEDLINE | ID: mdl-27694206

ABSTRACT

Genomic samples of non-model organisms are becoming increasingly important in a broad range of studies from developmental biology, biodiversity analyses, to conservation. Genomic sample definition, description, quality, voucher information and metadata all need to be digitized and disseminated across scientific communities. This information needs to be concise and consistent in today's ever-increasing bioinformatic era, for complementary data aggregators to easily map databases to one another. In order to facilitate exchange of information on genomic samples and their derived data, the Global Genome Biodiversity Network (GGBN) Data Standard is intended to provide a platform based on a documented agreement to promote the efficient sharing and usage of genomic sample material and associated specimen information in a consistent way. The new data standard presented here build upon existing standards commonly used within the community extending them with the capability to exchange data on tissue, environmental and DNA sample as well as sequences. The GGBN Data Standard will reveal and democratize the hidden contents of biodiversity biobanks, for the convenience of everyone in the wider biobanking community. Technical tools exist for data providers to easily map their databases to the standard.Database URL: http://terms.tdwg.org/wiki/GGBN_Data_Standard.


Subject(s)
Biodiversity , Databases, Nucleic Acid , Genome
3.
Science ; 333(6044): 823, 2011 Aug 12.
Article in English | MEDLINE | ID: mdl-21836000
4.
Environ Sci Technol ; 45(5): 1792-7, 2011 Mar 01.
Article in English | MEDLINE | ID: mdl-21309508

ABSTRACT

Plug-in hybrid electric vehicles (PHEVs) may become part of the transportation fleet on time scales of a decade or two. We calculate the electric grid load increase and emissions due to vehicle battery charging in PJM and NYISO with the current generation mix, the current mix with a $50/tonne CO(2) price, and this case but with existing coal generators retrofitted with 80% CO(2) capture. We also examine all new generation being natural gas or wind+gas. PHEV fleet percentages between 0.4 and 50% are examined. Vehicles with small (4 kWh) and large (16 kWh) batteries are modeled with driving patterns from the National Household Transportation Survey. Three charging strategies and three scenarios for future electric generation are considered. When compared to 2020 CAFE standards, net CO(2) emissions in New York are reduced by switching from gasoline to electricity; coal-heavy PJM shows somewhat smaller benefits unless coal units are fitted with CCS or replaced with lower CO(2) generation. NO(X) is reduced in both RTOs, but there is upward pressure on SO(2) emissions or allowance prices under a cap.


Subject(s)
Air Pollutants/analysis , Air Pollution/statistics & numerical data , Automobiles/statistics & numerical data , Carbon Dioxide/analysis , Vehicle Emissions/analysis , Automobiles/economics , Carbon Dioxide/economics , Carbon Footprint , Conservation of Natural Resources/methods , Nitrogen Oxides/analysis , Sulfur Dioxide/analysis
5.
Clin Genet ; 72(6): 497-505, 2007 Dec.
Article in English | MEDLINE | ID: mdl-17894837

ABSTRACT

We evaluated the contribution of 67 single nucleotide polymorphisms (SNPs) within the beta-globin gene cluster to disease severity in groups of 207 mild- and 305 severe unrelated patients from Thailand with Hemoglobin E (HbE)/beta(0)-thalassemia and normal alpha-globin genes. Our analysis showed that these SNPs comprise two distinct linkage disequilibrium blocks, one containing the beta-globin gene and the other extending from the locus control region (LCR) to the delta gene, which are separated by a recombination hotspot in the narrow region of the beta-globin gene promoter. Forty-five SNPs within the interval including the LCR region and the delta gene showed strong association with disease severity. The strongest association was observed with the XmnI polymorphism located 158-bp upstream to the G gamma gene (p = 4.6E-12). Carriers of the T allele of XmnI were more likely to have a milder disease course and higher level of fetal hemoglobin (HbF) in both the mild (p = 0.005) and severe (p = 8.7E-06) patient groups. Haplotype analysis revealed that the T allele of XmnI was nearly always in cis with the HbE allele. The high frequency of this haplotype may be favored by positive selection against malarial infection. Further studies are needed to validate this hypothesis and determine whether XmnI or another closely linked variant modulates severity and HbF levels in patients with beta(0)-thalassemia/HbE disease.


Subject(s)
Globins/genetics , Hemoglobin E/genetics , Multigene Family , Polymorphism, Single Nucleotide , beta-Thalassemia/genetics , Fetal Hemoglobin/metabolism , Haplotypes , Humans , Linkage Disequilibrium , Locus Control Region , Phenotype , Thailand , beta-Thalassemia/blood
6.
Science ; 293(5531): 860-4, 2001 Aug 03.
Article in English | MEDLINE | ID: mdl-11486087

ABSTRACT

The development of resistance is the main threat to the long-term use of toxins from Bacillus thuringiensis (Bt) in transgenic plants. Here we report the cloning of a Bt toxin resistance gene, Caenorhabditis elegans bre-5, which encodes a putative beta-1,3-galactosyltransferase. Lack of bre-5 in the intestine led to resistance to the Bt toxin Cry5B. Wild-type but not bre-5 mutant animals were found to uptake toxin into their gut cells, consistent with bre-5 mutants lacking toxin-binding sites on their apical gut. bre-5 mutants displayed resistance to Cry14A, a Bt toxin lethal to both nematodes and insects; this indicates that resistance by loss of carbohydrate modification is relevant to multiple Bt toxins.


Subject(s)
Bacterial Proteins/toxicity , Bacterial Toxins , Caenorhabditis elegans Proteins , Caenorhabditis elegans/genetics , Endotoxins/toxicity , Galactosyltransferases/genetics , Galactosyltransferases/metabolism , Insect Proteins , Pest Control, Biological , Amino Acid Sequence , Animals , Bacillus thuringiensis Toxins , Bacterial Proteins/metabolism , Biological Transport , Caenorhabditis elegans/enzymology , Caenorhabditis elegans/metabolism , Cloning, Molecular , Digestive System/enzymology , Digestive System/metabolism , Disorders of Sex Development , Drug Resistance/genetics , Endocytosis , Endotoxins/metabolism , Feeding Behavior , Galactosyltransferases/chemistry , Genes, Helminth , Hemolysin Proteins , Molecular Sequence Data , Mosaicism , Mutation , Receptors, Cell Surface/metabolism , Transformation, Genetic
7.
Genetics ; 157(4): 1425-36, 2001 Apr.
Article in English | MEDLINE | ID: mdl-11290701

ABSTRACT

The translation elongation factor 1 complex (eEF1) plays a central role in protein synthesis, delivering aminoacyl-tRNAs to the elongating ribosome. The eEF1A subunit, a classic G-protein, also performs roles aside from protein synthesis. The overexpression of either eEF1A or eEF1B alpha, the catalytic subunit of the guanine nucleotide exchange factor, in Saccharomyces cerevisiae results in effects on cell growth. Here we demonstrate that overexpression of either factor does not affect the levels of the other subunit or the rate or accuracy of protein synthesis. Instead, the major effects in vivo appear to be at the level of cell morphology and budding. eEF1A overexpression results in dosage-dependent reduced budding and altered actin distribution and cellular morphology. In addition, the effects of excess eEF1A in actin mutant strains show synthetic growth defects, establishing a genetic connection between the two proteins. As the ability of eEF1A to bind and bundle actin is conserved in yeast, these results link the established ability of eEF1A to bind and bundle actin in vitro with nontranslational roles for the protein in vivo.


Subject(s)
Actins/metabolism , Cytoskeleton/metabolism , Fungal Proteins/biosynthesis , Peptide Elongation Factor 1/biosynthesis , Saccharomyces cerevisiae Proteins , Cell Cycle , Cell Division , Fungal Proteins/genetics , Gene Expression , Genes, Fungal , Peptide Elongation Factor 1/genetics , Saccharomyces cerevisiae/genetics , Saccharomyces cerevisiae/growth & development
8.
Genetics ; 157(2): 533-43, 2001 Feb.
Article in English | MEDLINE | ID: mdl-11156976

ABSTRACT

A large collection of yeast actin mutations has been previously isolated and used in numerous studies of actin cytoskeletal function. However, the various mutations have been in congenic, rather than isogenic, backgrounds, making it difficult to compare the subtle phenotypes that are characteristic of these mutants. We have therefore placed 27 mutations in an isogenic background. We used a subset of these mutants to compare the degree to which different actin alleles are defective in sporulation, endocytosis, and growth on NaCl-containing media. We found that the three phenotypes are highly correlated. The correlations are specific and not merely a reflection of general growth defects, because the phenotypes are not correlated with growth rates under normal conditions. Significantly, those actin mutants exhibiting the most severe phenotypes in all three processes have altered residues that cluster to a small region of the actin crystal structure previously defined as the fimbrin (Sac6p)-binding site. We examined the relationship between endocytosis and growth on salt and found that shifting wild-type or actin mutant cells to high salt reduces the rate of alpha-factor internalization. These results suggest that actin mutants may be unable to grow on salt because of additive endocytic defects (due to mutation and salt).


Subject(s)
Actins/genetics , Microfilament Proteins , Mutation , Phenotype , Actins/chemistry , Actins/metabolism , Alleles , Binding Sites , Cell Division/genetics , Cytoskeleton/metabolism , Endocytosis/genetics , Genotype , Mating Factor , Membrane Glycoproteins/metabolism , Models, Molecular , Peptides/genetics , Saccharomyces cerevisiae/genetics , Saccharomyces cerevisiae/physiology , Sodium Chloride/pharmacology , Spores, Fungal/genetics , Temperature , Time Factors
9.
Diabetes ; 46(6): 1081-6, 1997 Jun.
Article in English | MEDLINE | ID: mdl-9166684

ABSTRACT

Maturity-onset diabetes of the young 3 (MODY3) is a type of NIDDM caused by mutations in the transcription factor hepatocyte nuclear factor-1alpha (HNF-1alpha) located on chromosome 12q. We have identified four novel HNF-1alpha missense mutations in MODY3 families. In four additional and unrelated families, we observed an identical insertion mutation that had occurred in a polycytidine tract in exon 4. Among those families, one exhibited a de novo mutation at this location. We propose that instability of this sequence represents a general mutational mechanism in MODY3. We observed no HNF-1alpha mutations among 86 unrelated late-onset diabetic patients with relative insulin deficiency. Hence mutations in this gene appear to be most strongly associated with early-onset diabetes.


Subject(s)
Chromosomes, Human, Pair 12/genetics , DNA-Binding Proteins , Diabetes Mellitus, Type 2/genetics , Mutation/genetics , Nuclear Proteins/genetics , Transcription Factors/genetics , DNA Mutational Analysis , DNA Primers/chemistry , Family , Genetic Linkage , Haplotypes , Hepatocyte Nuclear Factor 1 , Hepatocyte Nuclear Factor 1-alpha , Hepatocyte Nuclear Factor 1-beta , Humans , Pedigree , Polymerase Chain Reaction , Polymorphism, Single-Stranded Conformational
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