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  • 1
    Electronic Resource
    Electronic Resource
    Multichannel interferometer system for the helically symmetric experiment : Papers from the thirteenth topical conference on high temperature plasma diagnostics (2001)
    [S.l.] : American Institute of Physics (AIP)
    Review of Scientific Instruments 72 (2001), S. 1081-1084 
    Details
    ISSN: 1089-7623
    Source: AIP Digital Archive
    Topics: Physics , Electrical Engineering, Measurement and Control Technology
    Notes: A multichannel millimeter-wave interferometer system has been designed, fabricated and installed on the helically symmetric experiment (HSX), located at the University of Wisconsin, Madison. The interferometer system will view the plasma cross section along nine adjacent chords with 1.5 cm spacing. With this arrangement, coverage will span from the low-field side plasma scrape-off layer to well past the magnetic axis. For the plasma densities anticipated on HSX, a solid-state source operating at 288 GHz will be utilized. At this frequency refraction will be manageable, being less than the channel spacing. The source will be bias-tuned and modulated with a sawtooth wave form at 750 kHz in order to generate the intermediate frequency necessary for the heterodyne detection scheme. The signals will be measured using Schottky-diode corner-cube mixers. The interferometer will have sensitivity nedl(approximate)8×1011 cm−2, being able to measure density changes 〈1%. Initially, the phase will be evaluated using analog electronics with bandwidth 〈10 kHz providing real-time line-integrated output. A digital phase comparator scheme will also be implemented whereby the measured wave forms are directly digitized and the phase evaluated using a software-based algorithm. This will increase the time response up to the modulation frequency of 750 kHz. Improved time response will permit measurement of high-frequency density fluctuations along with "fast changes in" the equilibrium profile. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1319366
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The gettering of copper by keV implantation of germanium into silicon (1995)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 78 (1995), S. 3012-3014 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: The gettering of copper by keV implantation of germanium into silicon is investigated. Germanium is implanted at a fixed energy with varying doses into the front side of silicon samples. Copper is thermally evaporated on the backside of the samples and then annealed at 900 °C for 1 h and 10 h, respectively, to allow in-diffusion of the transition metal. Rutherford backscattering spectroscopy, secondary-ion-mass spectroscopy, and cross-section transmission electron microscopy are used to demonstrate that gettering of copper is achieved through stacking faults created by heavy dose germanium implantation and solid-phase epitaxy. © 1995 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.360050
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  • 3
    Electronic Resource
    Electronic Resource
    Formation and characterization of ultrasmall dimension GeSi wire structure by using pulsed laser-induced epitaxy (1996)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 68 (1996), S. 3734-3736 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: (100)Si substrates are patterned with arrays of Ge wires ∼60 nm in width and ∼6 nm in thickness. Ultrasmall dimension GeSi surface wire structures are then formed in Si in a pulsed laser-induced epitaxy process. The wire structures are analyzed by secondary electron microscopy, atomic force microscopy, Auger electron spectroscopy, and cross-sectional transmission electron microscopy. No defects are observed in the wires structures. However, significant side diffusion of Ge, much more than the vertical diffusion occurred during the ∼40 ns pulsed laser-induced epitaxy process, is observed in the Si substrate. Surface evolution is also observed. Possible explanations for the abnormal Ge side diffusion are discussed. © 1996 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.115989
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  • 4
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    Setd1a and NURF mediate chromatin dynamics and gene regulation during erythroid lineage commitment and differentiation (2016)
    Oxford University Press
    Details
    Publication Date: 2016-09-03
    Description: The modulation of chromatin structure is a key step in transcription regulation in mammalian cells and eventually determines lineage commitment and differentiation. USF1/2, Setd1a and NURF complexes interact to regulate chromatin architecture in erythropoiesis, but the mechanistic basis for this regulation is hitherto unknown. Here we showed that Setd1a and NURF complexes bind to promoters to control chromatin structural alterations and gene activation in a cell context dependent manner. In human primary erythroid cells USF1/2, H3K4me3 and the NURF complex were significantly co-enriched at transcription start sites of erythroid genes, and their binding was associated with promoter/enhancer accessibility that resulted from nucleosome repositioning. Mice deficient for Setd1a , an H3K4 trimethylase, in the erythroid compartment exhibited reduced Ter119/CD71 positive erythroblasts, peripheral blood RBCs and hemoglobin levels. Loss of Setd1a led to a reduction of promoter-associated H3K4 methylation, inhibition of gene transcription and blockade of erythroid differentiation. This was associated with alterations in NURF complex occupancy at erythroid gene promoters and reduced chromatin accessibility. Setd1a deficiency caused decreased associations between enhancer and promoter looped interactions as well as reduced expression of erythroid genes such as the adult β-globin gene. These data indicate that Setd1a and NURF complexes are specifically targeted to and coordinately regulate erythroid promoter chromatin dynamics during erythroid lineage differentiation.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 5
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    Methylated Cytosines Mutate to Transcription Factor Binding Sites that Drive Tetrapod Evolution (2015)
    Oxford University Press
    Details
    Publication Date: 2015-11-30
    Description: In mammals, the cytosine in CG dinucleotides is typically methylated producing 5-methylcytosine (5mC), a chemically less stable form of cytosine that can spontaneously deaminate to thymidine resulting in a T•G mismatched base pair. Unlike other eukaryotes that efficiently repair this mismatched base pair back to C•G, in mammals, 5mCG deamination is mutagenic, sometimes producing TG dinucleotides, explaining the depletion of CG dinucleotides in mammalian genomes. It was suggested that new TG dinucleotides generate genetic diversity that may be critical for evolutionary change. We tested this conjecture by examining the DNA sequence properties of regulatory sequences identified by DNase I hypersensitive sites (DHSs) in human and mouse genomes. We hypothesized that the new TG dinucleotides generate transcription factor binding sites (TFBS) that become tissue-specific DHSs (TS-DHSs). We find that 8-mers containing the CG dinucleotide are enriched in DHSs in both species. However, 8-mers containing a TG and no CG dinucleotide are preferentially enriched in TS-DHSs when compared with 8-mers with neither a TG nor a CG dinucleotide. The most enriched 8-mer with a TG and no CG dinucleotide in tissue-specific regulatory regions in both genomes is the AP-1 motif ( TG A C / G T CA N), and we find evidence that TG dinucleotides in the AP-1 motif arose from CG dinucleotides. Additional TS-DHS-enriched TFBS containing the TG/CA dinucleotide are the E-Box motif (G CA GC TG C), the NF-1 motif (GG CA—TG CC), and the GR (glucocorticoid receptor) motif (G-A CA—TG T-C). Our results support the suggestion that cytosine methylation is mutagenic in tetrapods producing TG dinucleotides that create TFBS that drive evolution.
    Electronic ISSN: 1759-6653
    Topics: Biology
    Published by Oxford University Press
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  • 6
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    Intermittent PTH (1-34) injection rescues the retarded skeletal development and postnatal lethality of mice mimicking human achondroplasia and thanatophoric dysplasia (2012)
    Oxford University Press
    Details
    Publication Date: 2012-08-28
    Description: Achondroplasia (ACH) and thanatophoric dysplasia (TD) are caused by gain-of-function mutations of fibroblast growth factor receptor 3 ( FGFR3 ) and they are the most common forms of dwarfism and lethal dwarfism, respectively. Currently, there are few effective treatments for ACH. For the neonatal lethality of TD patients, no practical effective therapies are available. We here showed that systemic intermittent PTH (1-34) injection can rescue the lethal phenotype of TD type II (TDII) mice and significantly alleviate the retarded skeleton development of ACH mice. PTH-treated ACH mice had longer naso-anal length than ACH control mice, and the bone lengths of humeri and tibiae were rescued to be comparable with those of wild-type control mice. Our study also found that the premature fusion of cranial synchondroses in ACH mice was partially corrected after the PTH (1-34) treatment, suggesting that the PTH treatment may rescue the progressive narrowing of neurocentral synchondroses that cannot be readily corrected by surgery. In addition, we found that the PTH treatment can improve the osteopenia and bone structure of ACH mice. The increased expression of PTHrP and down-regulated FGFR3 level may be responsible for the positive effects of PTH on bone phenotype of ACH and TDII mice.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 7
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    Mutant activated FGFR3 impairs endochondral bone growth by preventing SOX9 downregulation in differentiating chondrocytes (2015)
    Oxford University Press
    Details
    Publication Date: 2015-02-26
    Description: Fibroblast growth factor receptor 3 (FGFR3) plays a critical role in the control of endochondral ossification, and bone growth and mutations that cause hyperactivation of FGFR3 are responsible for a collection of developmental disorders that feature poor endochondral bone growth. FGFR3 is expressed in proliferating chondrocytes of the cartilaginous growth plate but also in chondrocytes that have exited the cell cycle and entered the prehypertrophic phase of chondrocyte differentiation. Achondroplasia disorders feature defects in chondrocyte proliferation and differentiation, and the defects in differentiation have generally been considered to be a secondary manifestation of altered proliferation. By initiating a mutant activated knockin allele of FGFR3 (FGFR3K650E) that causes Thanatophoric Dysplasia Type II (TDII) specifically in prehypertrophic chondrocytes, we show that mutant FGFR3 induces a differentiation block at this stage independent of any changes in proliferation. The differentiation block coincided with persistent expression of SOX9, the master regulator of chondrogenesis, and reducing SOX9 dosage allowed chondrocyte differentiation to proceed and significantly improved endochondral bone growth in TDII. These findings suggest that a proliferation-independent and SOX9-dependent differentiation block is a key driving mechanism responsible for poor endochondral bone growth in achondroplasia disorders caused by mutations in FGFR3.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 8
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    A combined estimating function approach for fitting stationary point process models (2014)
    Oxford University Press
    Details
    Publication Date: 2014-05-24
    Description: A composite likelihood technique based on pairwise contributions provides a computationally simple but potentially inefficient approach for fitting spatial point process models. We propose a new estimation procedure that improves the efficiency. Our approach combines estimating functions derived from pairwise composite likelihood estimation and estimating functions that account for correlations among the pairwise contributions. Our method can be used to fit a variety of parametric spatial point process models and can yield more efficient estimators for the clustering parameters than pairwise composite likelihood estimation. We demonstrate the efficacy of our proposed method through a simulation study and an application to the longleaf pine data.
    Print ISSN: 0006-3444
    Electronic ISSN: 1464-3510
    Topics: Biology , Mathematics , Medicine
    Published by Oxford University Press
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  • 9
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    EXPONENTIAL CONVERGENCE RATES OF SECOND QUANTIZATION SEMIGROUPS AND APPLICATIONS (2014)
    Oxford University Press
    Details
    Publication Date: 2014-06-27
    Description: Exponential convergence rates in the L 2 -tail norm and entropy are characterized for the second quantization semigroups by using the corresponding base Dirichlet form. This supplements the well-known result on the L 2 -exponential convergence rate of second quantization semigroups. As applications, birth–death-type processes on Poisson spaces and the path space of Lévy processes are investigated.
    Print ISSN: 0033-5606
    Electronic ISSN: 1464-3847
    Topics: Mathematics
    Published by Oxford University Press
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  • 10
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    A novel FGFR3-binding peptide inhibits FGFR3 signaling and reverses the lethal phenotype of mice mimicking human thanatophoric dysplasia (2012)
    Oxford University Press
    Details
    Publication Date: 2012-12-07
    Description: Gain-of-function mutations in fibroblast growth factor receptor-3 (FGFR3) lead to several types of human skeletal dysplasia syndromes including achondroplasia, hypochondroplasia and thanatophoric dysplasia (TD). Currently, there are no effective treatments for these skeletal dysplasia diseases. In this study, we screened, using FGFR3 as a bait, a random 12-peptide phage library and obtained 23 positive clones that share identical amino acid sequences (VSPPLTLGQLLS), named as peptide P3. This peptide had high binding specificity to the extracellular domain of FGFR3. P3 inhibited tyrosine kinase activity of FGFR3 and its typical downstream molecules, extracellular signal-regulated kinase/mitogen-activated protein kinase. P3 also promoted proliferation and chondrogenic differentiation of cultured ATDC5 chondrogenic cells. In addition, P3 alleviated the bone growth retardation in bone rudiments from mice mimicking human thanatophoric dysplasia type II (TDII). Finally, P3 reversed the neonatal lethality of TDII mice. Thus, this study identifies a novel inhibitory peptide for FGFR3 signaling, which may serve as a potential therapeutic agent for the treatment of FGFR3-related skeletal dysplasia.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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