184 research outputs found

    Iron single crystal growth from a lithium-rich melt

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    \alpha-Fe single crystals of rhombic dodecahedral habit were grown from a melt of Li84_{84}N12_{12}Fe∼3_{\sim 3}. Crystals of several millimeter along a side form at temperatures around T≈800∘T \approx 800^\circC. Upon further cooling the growth competes with the formation of Fe-doped Li3_3N. The b.c.c. structure and good sample quality of \alpha-Fe single crystals were confirmed by X-ray and electron diffraction as well as magnetization measurements and chemical analysis. A nitrogen concentration of 90\,ppm was detected by means of carrier gas hot extraction. Scanning electron microscopy did not reveal any sign of iron nitride precipitates.Comment: 13 pages, 4 figure

    Ferromagnetism or slow paramagnetic relaxation in Fe-doped Li3_3N?

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    We report on isothermal magnetization, M\"ossbauer spectroscopy, and magnetostriction as well as temperature-dependent alternating-current (ac) susceptibility, specific heat, and thermal expansion of single crystalline and polycrstalline Li2_2(Li1−x_{1-x}Fex_x)N with x=0x = 0 and x≈0.30x \approx 0.30. Magnetic hysteresis emerges at temperatures below T≈50 T \approx 50\,K with coercivity fields of up to μ0H=11.6 \mu_0H = 11.6\,T at T=2 T = 2\,K and magnetic anisotropy energies of 310 310\,K (27 27\,meV). The ac susceptibility is strongly frequency dependent (f = 10f\,=\,10--10,000 10,000\,Hz) and reveals an effective energy barrier for spin reversal of ΔE≈1100 \Delta E \approx 1100\,K. The relaxation times follow Arrhenius behavior for T>25 T > 25\,K. For T<10 T < 10\,K, however, the relaxation times of τ≈1010 \tau \approx 10^{10}\,s are only weakly temperature-dependent indicating the relevance of a quantum tunneling process instead of thermal excitations. The magnetic entropy amounts to more than 25 25\,J molFe−1 ^{-1}_{\rm Fe}\,K−1^{-1} which significantly exceeds RRln2, the value expected for the entropy of a ground state doublet. Thermal expansion and magnetostriction indicate a weak magneto-elastic coupling in accordance with slow relaxation of the magnetization. The classification of Li2_2(Li1−x_{1-x}Fex_x)N as ferromagnet is stressed and contrasted with highly anisotropic and slowly relaxing paramagnetic behavior.Comment: 12 pages, 10 figure

    Influences on achieving motor milestones: A twin-singleton study

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    In order to determine if twinning impacted achievement of motor milestones the attainment of early motor milestones in twins was examined and compared to published data from singletons of the same age from the same culture and birth years. We examined the influence of twinning, sex, zygosity and birth cohort (1987-2001) on the motor development of twins aged 0 to 24 months. Data on the attainment of motor milestones (turn, sit, crawl, stand and walk) of twins were collected from maternal reports. All data were corrected for gestational age. Data from the twin sample were compared to normative data from singletons, which were available from Child Health Clinics (CHC). Analyses across twin data and the CHC singleton data revealed no differences between twins and singletons in achievement of motor milestones. Girls were able to sit without support slightly earlier than boys, otherwise there were no other sex differences. Birth-order analyses revealed minimal but significant differences in turning over from back to belly and for sitting without support between the first- and second-born. Dizygotic (DZ) twins were faster than monozygotic (MZ) twins in achieving the moment of sit, crawl, stand and walk. Twins born in earlier cohorts were faster in reaching the moment of crawl, sit and walk. It is concluded that there are no differences in time of reaching motor milestones between twins and singletons within the normal range. Sex has minimal to no effect on motor development in early childhood. DZ twins achieve motor milestones sooner than MZ twins. Attainment of gross motor milestones (crawl, stand and walk) is delayed in later birth cohorts

    Life-threatening hypersensitivity pneumonitis induced by docetaxel (taxotere)

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    4 patients with advanced non-small-cell lung cancer (NSCLC) treated with docetaxel developed life-threatening pneumonitis requiring mechanical ventilation. Docetaxel (30–60 mg m−2, according to a different protocol) was infused within one hour with standard premedications. One patient's pneumonitis occurred 5 days after the first dose of docetaxel, and that of the other 3 between the 2nd and 6th cycles. Based on the clinical course, radiological findings of an interstitial pneumonitis, and exclusion of other possible resultant causes, including metastatic cancer, radiation pulmonary injury, infection, or connective tissue disease, hypersensitivity pneumonitis was diagnosed. The patients were treated with hydrocortisone at 1200 mg per day or methylprednisolone at 240 mg per day. Although 3 of the 4 had a partial improvement in lung oxygenation, all patients’ conditions of hypersensitivity pneumonitis persisted and were complicated by other events, such as hospital-acquired infection and tension pneumothorax. The presence of this unusual hypersensitivity pneumonitis, which was so severe as to be life-threatening and refractory to high-dose corticosteroid therapy, should be taken into account during docetaxel treatment. © 2001 Cancer Research Campaig

    Zinc-Regulated DNA Binding of the Yeast Zap1 Zinc-Responsive Activator

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    The Zap1 transcription factor of Saccharomyces cerevisiae plays a central role in zinc homeostasis by controlling the expression of genes involved in zinc metabolism. Zap1 is active in zinc-limited cells and repressed in replete cells. At the transcriptional level, Zap1 controls its own expression via positive autoregulation. In addition, Zap1's two activation domains are regulated independently of each other by zinc binding directly to those regions and repressing activation function. In this report, we show that Zap1 DNA binding is also inhibited by zinc. DMS footprinting showed that Zap1 target gene promoter occupancy is regulated with or without transcriptional autoregulation. These results were confirmed using chromatin immunoprecipitation. Zinc regulation of DNA binding activity mapped to the DNA binding domain indicating other parts of Zap1 are unnecessary for this control. Overexpression of Zap1 overrode DNA binding regulation and resulted in constitutive promoter occupancy. Under these conditions of constitutive binding, both the zinc dose response of Zap1 activity and cellular zinc accumulation were altered suggesting the importance of DNA binding control to zinc homeostasis. Thus, our results indicated that zinc regulates Zap1 activity post-translationally via three independent mechanisms, all of which contribute to the overall zinc responsiveness of Zap1

    Challenges in Whole Exome Sequencing: An Example from Hereditary Deafness

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    Whole exome sequencing provides unprecedented opportunities to identify causative DNA variants in rare Mendelian disorders. Finding the responsible mutation via traditional methods in families with hearing loss is difficult due to a high degree of genetic heterogeneity. In this study we combined autozygosity mapping and whole exome sequencing in a family with 3 affected children having nonsyndromic hearing loss born to consanguineous parents. Two novel missense homozygous variants, c.508C>A (p.H170N) in GIPC3 and c.1328C>T (p.T443M) in ZNF57, were identified in the same ∼6 Mb autozygous region on chromosome 19 in affected members of the family. Both variants co-segregated with the phenotype and were absent in 335 ethnicity-matched controls. Biallelic GIPC3 mutations have recently been reported to cause autosomal recessive nonsyndromic sensorineural hearing loss. Thus we conclude that the hearing loss in the family described in this report is caused by a novel missense mutation in GIPC3. Identified variant in GIPC3 had a low read depth, which was initially filtered out during the analysis leaving ZNF57 as the only potential causative gene. This study highlights some of the challenges in the analyses of whole exome data in the bid to establish the true causative variant in Mendelian disease
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