Magnetic Properties of Dilute Alloys: Equations for Magnetization and its Structural Fluctuations

The dilute Heisenberg ferromagnet is studied taking into account fluctuations of magnetization caused by disorder. A self-consistent system of equations for magnetization and its mean quadratic fluctuations is derived within the configurationally averaged two-time temperature Green's function method. This system of equations is analised at low concentration of non-magnetic impurities. Mean relative quadratic fluctuations of magnetization are revealed to be proportional to the square of concentration of impurities.Comment: 16 pages, LaTe

Hormad1 mutation disrupts synaptonemal complex formation, recombination, and chromosome segregation in mammalian meiosis

Meiosis is unique to germ cells and essential for reproduction. During the first meiotic division, homologous chromosomes pair, recombine, and form chiasmata. The homologues connect via axial elements and numerous transverse filaments to form the synaptonemal complex. The synaptonemal complex is a critical component for chromosome pairing, segregation, and recombination. We previously identified a novel germ cell-specific HORMA domain encoding gene, Hormad1, a member of the synaptonemal complex and a mammalian counterpart to the yeast meiotic HORMA domain protein Hop1. Hormad1 is essential for mammalian gametogenesis as knockout male and female mice are infertile. Hormad1 deficient (Hormad1-/-) testes exhibit meiotic arrest in the early pachytene stage, and synaptonemal complexes cannot be visualized by electron microscopy. Hormad1 deficiency does not affect localization of other synaptonemal complex proteins, SYCP2 and SYCP3, but disrupts homologous chromosome pairing. Double stranded break formation and early recombination events are disrupted in Hormad1-/- testes and ovaries as shown by the drastic decrease in the γH2AX, DMC1, RAD51, and RPA foci. HORMAD1 co-localizes with cH2AX to the sex body during pachytene. BRCA1, ATR, and γH2AX co-localize to the sex body and participate in meiotic sex chromosome inactivation and transcriptional silencing. Hormad1 deficiency abolishes γH2AX, ATR, and BRCA1 localization to the sex chromosomes and causes transcriptional de-repression on the X chromosome. Unlike testes, Hormad1-/- ovaries have seemingly normal ovarian folliculogenesis after puberty. However, embryos generated from Hormad1-/- oocytes are hyper- and hypodiploid at the 2 cell and 8 cell stage, and they arrest at the blastocyst stage. HORMAD1 is therefore a critical component of the synaptonemal complex that affects synapsis, recombination, and meiotic sex chromosome inactivation and transcriptional silencing. © 2010 Shin et al

iNID: An Analytical Framework for Identifying Network Models for Interplays among Developmental Signaling in Arabidopsis

Integration of internal and external cues into developmental programs is indispensable for growth and development of plants, which involve complex interplays among signaling pathways activated by the internal and external factors (IEFs). However, decoding these complex interplays is still challenging. Here, we present a web-based platform that identifies key regulators and Network models delineating Interplays among Developmental signaling (iNID) in Arabidopsis. iNID provides a comprehensive resource of (1) transcriptomes previously collected under the conditions treated with a broad spectrum of IEFs and (2) protein and genetic interactome data in Arabidopsis. In addition, iNID provides an array of tools for identifying key regulators and network models related to interplays among IEFs using transcriptome and interactome data. To demonstrate the utility of iNID, we investigated the interplays of (1) phytohormones and light and (2) phytohormones and biotic stresses. The results revealed 34 potential regulators of the interplays, some of which have not been reported in association with the interplays, and also network models that delineate the involvement of the 34 regulators in the interplays, providing novel insights into the interplays collectively defined by phytohormones, light, and biotic stresses. We then experimentally verified that BME3 and TEM1, among the selected regulators, are involved in the auxin-brassinosteroid (BR)-blue light interplay. Therefore, iNID serves as a useful tool to provide a basis for understanding interplays among IEFs.X115Ysciescopu

Inhibition of Lipopolysaccharide-Induced iNOS, COX- 2, and TNF-&#945 Expression by Aqueous Extract of Orixa Japonica in RAW 264.7 Cells via Suppression of NF- kB Activity

Purpose: To investigate the anti-inflammatory effects of aqueous extract of Orixa japonica (AEOJ) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.Methods: The expression of mRNA and protein using RT-PCR and Western blot analysis was investigated. The level of nitric oxide (NO) production was analyzed using Griess reaction. Release of prostaglandin E2 (PGE2) and tumor necrosis factor- (TNF-) was determined using sandwich ELISA.Results: AEOJ potently inhibited the production of nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor- (TNF-) in LPS-stimulated RAW 264.7 cells. Consistent with these findings, AEOJ wasalso found to significantly reduce LPS-induced expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF- at the transcriptional level. Additionally, AEOJ attenuated LPSinducedNF-B activity via the inhibition of IB phosphorylation and degradation. It was also found that the NF-B inhibitor N-acetyl cysteine (NAC) attenuated LPS-induced gene expression of iNOS, COX-2,and TNF-. These results indicate that AEOJ attenuates LPS-induced inflammatory mediators such as NO, PGE2, and TNF- via suppression of NF-B activity.Conclusion: These results suggest that AEOJ has a potential activity to alleviate LPS-induced inflammation

Nitrite/nitrate levels in patients after stem cell transplant

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Self-Aligned Top-Gate Metal-Oxide Thin-Film Transistors Using a Solution-Processed Polymer Gate Dielectric.

For high-speed and large-area active-matrix displays, metal-oxide thin-film transistors (TFTs) with high field-effect mobility, stability, and good uniformity are essential. Moreover, reducing the RC delay is also important to achieve high-speed operation, which is induced by the parasitic capacitance formed between the source/drain (S/D) and the gate electrodes. From this perspective, self-aligned top-gate oxide TFTs can provide advantages such as a low parasitic capacitance for high-speed displays due to minimized overlap between the S/D and the gate electrodes. Here, we demonstrate self-aligned top-gate oxide TFTs using a solution-processed indium-gallium-zinc-oxide (IGZO) channel and crosslinked poly(4-vinylphenol) (PVP) gate dielectric layers. By applying a selective Ar plasma treatment on the IGZO channel, low-resistance IGZO regions could be formed, having a sheet resistance value of ~20.6 kΩ/sq., which can act as the homojunction S/D contacts in the top-gate IGZO TFTs. The fabricated self-aligned top-gate IGZO TFTs exhibited a field-effect mobility of 3.93 cm2/Vs and on/off ratio of ~106, which are comparable to those fabricated using a bottom-gate structure. Furthermore, we also demonstrated self-aligned top-gate TFTs using electrospun indium-gallium-oxide (IGO) nanowires (NWs) as a channel layer. The IGO NW TFTs exhibited a field-effect mobility of 0.03 cm2/Vs and an on/off ratio of >105. The results demonstrate that the Ar plasma treatment for S/D contact formation and the solution-processed PVP gate dielectric can be implemented in realizing self-aligned top-gate oxide TFTs

Mathematical modelling long-term effects of replacing Prevnar7 with Prevnar13 on invasive pneumococcal diseases in England and Wales

England and Wales recently replaced the 7-valent pneumococcal conjugate vaccine (PCV7) with its 13-valent equivalent (PCV13), partly based on projections from mathematical models of the long-term impact of such a switch compared to ceasing pneumococcal conjugate vaccination altogether. A compartmental deterministic model was used to estimate parameters governing transmission of infection and competition between different groups of pneumococcal serotypes prior to the introduction of PCV13. The best-fitting parameters were used in an individual based model to describe pneumococcal transmission dynamics and effects of various options for the vaccination programme change in England and Wales. A number of scenarios were conducted using (i) different assumptions about the number of invasive pneumococcal disease cases adjusted for the increasing trend in disease incidence prior to PCV7 introduction in England and Wales, and (ii) a range of values representing serotype replacement induced by vaccination of the additional six serotypes in PCV13. Most of the scenarios considered suggest that ceasing pneumococcal conjugate vaccine use would cause an increase in invasive pneumococcal disease incidence, while replacing PCV7 with PCV13 would cause an overall decrease. However, the size of this reduction largely depends on the level of competition induced by the additional serotypes in PCV13. The model estimates that over 20 years of PCV13 vaccination, around 5000–62000 IPD cases could be prevented compared to stopping pneumococcal conjugate vaccination altogether. Despite inevitable uncertainty around serotype replacement effects following introduction of PCV13, the model suggests a reduction in overall invasive pneumococcal disease incidence in all cases. Our results provide useful evidence on the benefits of PCV13 to countries replacing or considering replacing PCV7 with PCV13, as well as data that can be used to evaluate the cost-effectiveness of such a switch