1,112 research outputs found

    Vortex states in iron-based superconductors with collinear antiferromagnetic cores

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    Magnetism in the FeAs stoichiometric compounds and its interplay with superconductivity in vortex states are studied by self-consistently solving the Bogoliubov-de Gennes equations based on a two-orbital model with including the on-site interactions between electrons in the two orbitals. It is revealed that for the parent compound, magnetism is caused by the strong Hund's coupling, and the Fermi-surface topology aids to select the spin-density-wave (SDW) pattern. The superconducting (SC) order parameter with s± = Δ0 cos (kx) cos (ky) symmetry is found to be the most favorable pairing for both the electron- and hole-doped cases while the local density of states exhibits the characteristic of nodal gap for the former and full gap for the latter. In the vortex state, the emergence of the field-induced SDW depends on the strength of the Hund's coupling and the Coulomb repulsions. The field-induced SDW gaps the finite-energy contours on the electron- and hole-pocket sides, leading to the dual structures with one reflecting the SC pairing and the other being related to the SDW order. These features can be discernable in STM measurements for identifying the interplay between the field-induced SDW order and the SC order around the core region. © 2009 The American Physical Society.published_or_final_versio

    Increased DMT1 expression and iron content in MPTP-treated C57BL/6 mice

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    2003-2004 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

    Unique pattern of infections in chronic granulomatous disease – The Asian experience

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    Conference Theme: Inflammatory Basis of Perinatal and Childhood DiseasesSymposium 40: InfectionBackground: Chronic granulomatous disease (CGD) is a phagocytic disorder caused by defective NADPH oxidase activity. Affected individuals are susceptible to bacterial infections, mycosis and hyperinflammatory complications. Variations in the epidemiology of infectious diseases across geographical regions can lead to distinct clinical phenotypes. Objective: To identify the unique clinical characteristics of a large cohort of CGD patients in China and Southeast Asia referred for genetic studies from 2003 to 2012. Methods: 53 patients with genetically-confirmed CGD were included and their clinical features were analyzed. CYBB and CYBA mutations were studied by Sanger sequencing, and NCF1 ‘GT’ deletion hotspot mutation was studied on genomic DNA by GeneScan. Results: 44 patients with X-CGD had CYBB mutations (missense[n=16]; nonsense[n=8]; deletion[n=9]; insertion[n=2]; intron mutation[n=9]). Nine patient had AR-CGD (CYBA[n=5]; NCF1 75_76delGT[n=4]). The median age at presentation and diagnosis was higher in AR-CGD (7m and 66m) compared with X-CGD (3m and 22m). The commonest presentations were pneumonia (58%), skin and perianal abscess (49%), lymphadenitis (42%) and recurrent diarrhea (30%). Aspergillosis and salmonellosis occurred at a frequency similar to published studies (13% and 19% respectively), but the commonest infection was BCG (43%) and 11% had disseminated BCG. 21% of patients had tuberculosis. Fulminant melioidosis and Chromobacterium violaceum infections occurred in 3 patients and two of their male siblings. Hyperinflammatory conditions included polyarthritis (n=3) and pulmonary granuloma (n=2). Death was recorded in 8 patients (15%). Conclusion: Melioidosis and C. violaceum indigenous to Southeast Asia can cause life-threatening infections in CGD patients. The high incidence of mycobacterial infections is associated with universal BCG vaccination and endemicity of tuberculosis. Such observations emphasize the role of respiratory burst as an immune defense mechanism against these pathogens. These infections are seldom reported in Caucasian cohorts, illustrating the importance of regional collaborative studies to facilitate pattern recognition and early diagnosis of primary immunodeficiencies.published_or_final_versio

    GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity

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    RATIONALE: Albuminuria is an early clinical feature in the progression of diabetic nephropathy (DN). Podocyte insulin resistance is a main cause of podocyte injury, playing crucial roles by contributing to albuminuria in early DN. G protein-coupled receptor 43 (GPR43) is a metabolite sensor modulating the cell signalling pathways to maintain metabolic homeostasis. However, the roles of GPR43 in podocyte insulin resistance and its potential mechanisms in the development of DN are unclear. METHODS: The experiments were conducted by using kidney tissues from biopsied DN patients, streptozotocin (STZ) induced diabetic mice with or without global GPR43 gene knockout, diabetic rats treated with broad-spectrum oral antibiotics or fecal microbiota transplantation, and cell culture model of podocytes. Renal pathological injuries were evaluated by periodic acid-schiff staining and transmission electron microscopy. The expression of GPR43 with other podocyte insulin resistance related molecules was checked by immunofluorescent staining, real-time PCR, and Western blotting. Serum acetate level was examined by gas chromatographic analysis. The distribution of gut microbiota was measured by 16S ribosomal DNA sequencing with faeces. RESULTS: Our results demonstrated that GPR43 expression was increased in kidney samples of DN patients, diabetic animal models, and high glucose-stimulated podocytes. Interestingly, deletion of GPR43 alleviated albuminuria and renal injury in diabetic mice. Pharmacological inhibition and knockdown of GPR43 expression in podocytes increased insulin-induced Akt phosphorylation through the restoration of adenosine 5'-monophosphate-activated protein kinase α (AMPKα) activity. This effect was associated with the suppression of AMPKα activity through post-transcriptional phosphorylation via the protein kinase C-phospholipase C (PKC-PLC) pathway. Antibiotic treatment-mediated gut microbiota depletion, and faecal microbiota transplantation from the healthy donor controls substantially improved podocyte insulin sensitivity and attenuated glomerular injury in diabetic rats accompanied by the downregulation of the GPR43 expression and a decrease in the level of serum acetate. CONCLUSION: These findings suggested that dysbiosis of gut microbiota-modulated GPR43 activation contributed to albuminuria in DN, which could be mediated by podocyte insulin resistance through the inhibition of AMPKα activity

    Hierarchical CO2-protective shell for highly efficient oxygen reduction reaction

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    The widespread application of intermediate-temperature solid oxide fuel cells is mainly being hurdled by the cathode's low efficiency on oxygen reduction reaction and poor resistance to carbon dioxide impurity. Here we report the fabrication of a hierarchical shell-covered porous cathode through infiltration followed by microwave plasma treatment. The hierarchical shell consists of a dense thin-film substrate with cones on the top of the substrate, leading to a three-dimensional (3D) heterostructured electrode. The shell allows the cathode working stably in CO2-containing air, and significantly improving the cathode's oxygen reduction reactivity with an area specific resistance of ∼0.13 Ωcm2 at 575°C. The method is also suitable for fabricating functional shell on the irregularly shaped substrate in various applications

    Random Lasing Action from Randomly Assembled ZnS Nanosheets

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    Lasing characteristics of randomly assembled ZnS nanosheets are studied at room temperature. Under 266-nm optical excitation, sharp lasing peaks emitted at around 332 nm with a linewidth less than 0.4 nm are observed in all directions. In addition, the dependence of lasing threshold intensity with the excitation area is shown in good agreement with the random laser theory. Hence, it is verified that the lasing characteristics of randomly assembled ZnS nanosheets are attributed to coherent random lasing action

    Introgression of Chromosome 3Ns from Psathyrostachys huashanica into Wheat Specifying Resistance to Stripe Rust

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    Wheat stripe rust is a destructive disease in the cool and humid wheat-growing areas of the world. Finding diverse sources of stripe rust resistance is critical for increasing genetic diversity of resistance for wheat breeding programs. Stripe rust resistance was identified in the alien species Psathyrostachys huashanica, and a wheat- P. huashanica amphiploid line (PHW-SA) with stripe rust resistance was reported previously. In this study, a P. huashanica 3Ns monosomic addition line (PW11) with superior resistance to stripe rust was developed, which was derived from the cross between PHW-SA and wheat J-11. We evaluated the alien introgressions PW11-2, PW11-5 and PW11-8 which were derived from line PW11 for reaction to new Pst race CYR32, and used molecular and cytogenetic tools to characterize these lines. The introgressions were remarkably resistant to CYR32, suggesting that the resistance to stripe rust of the introgressions thus was controlled by gene(s) located on P. huashanica chromosome 3Ns. All derived lines were cytologically stable in term of meiotic chromosome behavior. Two 3Ns chromosomes of P. huashanica were detected in the disomic addition line PW11-2. Chromosomes 1B of substitution line PW11-5 had been replaced by a pair of P. huashanica 3Ns chromosomes. In PW11-8, a small terminal segment from P. huashanica chromosome arm 3NsS was translocated to the terminal region of wheat chromosomes 3BL. Thus, this translocated chromosome is designated T3BL-3NsS. These conclusions were further confirmed by SSR analyses. Two 3Ns-specific markers Xgwm181 and Xgwm161 will be useful to rapidly identify and trace the translocated fragments. These introgressions, which had significant characteristics of resistance to stripe rust, could be utilized as novel germplasms for wheat breeding
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