210 research outputs found

    Symmetry-dependent antiferromagnetic proximity effects on valley splitting

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    Various physical phenomena have been discovered by tuning degrees of freedom, among which there is the degree of freedom (DOF) -- "valley". The typical valley materials are characterized by two degenerate valley states protected by time-reversal symmetry (TS). These states indexed by valley DOF have been measured and manipulated for emergent valley-contrasting physics with the broken valley degeneracy. To achieve the valley splitting resulted from TS breaking, previous studies mainly focused on magnetic proximity effect provided by ferromagnetic (FM) layer. Nevertheless, the anti-ferromagnetic (AFM) proximity effect on the valley degeneracy has never been investigated systematically. In this work, we construct the composites consisting of a transitionmetal dichalcogenide (TMD) monolayer and a proximity layer with specific intra-plane AFM configurations. We extend the three-band model to describe the valley states of such systems. It is shown that either "time-reversal + fractional translation" or "mirror" symmetry has been proved to protect valley degeneracy. Additionally, first-principles calculations based on density functional theory (DFT) have been performed to verify the results obtained from the extended tight-binding (TB) model. The TB method introduced in the present work can properly describe the low-energy physics of valley materials that couple to the proximity with complex magnetic configurations. The results expand the range of qualified proximity layers for valley splitting, enabling more flexible manipulation of valley degree

    Compact hollow waveguide mid-infrared gas sensor for simultaneous measurements of ambient CO2 and water vapor

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    A compact, sensitive and stable hollow waveguide (HWG) mid-infrared gas sensor, based on gas absorption lines using wavelength modulation spectroscopy with a second harmonic (WMS-2f) detection scheme, was developed for simultaneous measurements of ambient CO 2 and water vapor. Optimization of the laser modulation parameters and pressure parameter in the HWG are performed to improve the strength of the WMS-2f signal and hence the detection limit, where 14.5-time for CO 2 and 8.5-time for water vapor improvement in system detection limit is achieved compared to those working at 1 atm. The stability of the sensor has been improved significantly by optimizing environmental disturbances, incoupling alignment of the HWG and laser scanning frequency. An Allan variance analysis shows detection limit of the developed sensor of ~3 ppmv for CO 2 and 0.018% for water vapor, which correspond to an absorbance of 2.4 × 10 -5 and 2.7 × 10 -5 , with a stability time of 160 s, respectively. Ambient CO 2 and water vapor measurement have been performed in two days in winter and spring separately. The measurement precision is further improved by applying a Kalman adaptive filter. The HWG gas sensor demonstrates the ability in environmental monitoring and the potential to be used in other areas, such as industrial production and biomedical diagnosis

    Gut dysbiosis in cystic fibrosis

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    In people with CF, intestinal exocrine malfunction, antibiotic usage [1] and swallowing of infected respiratory mucus [2] likely perturb the normal community of commensal bacteria in the gut. People with CF report various intestinal problems which may be alleviated by probiotic administration [3]. There is also evidence that probiotic bacteria can help people with CF fight respiratory infection [4,5]. However, CF-related gut dysbiosis has only recently been subjected to detailed investigation. Using DGGE and culture-based methods, Duytschaever and colleagues [6] showed that children with CF have a quantitatively and qualitatively different faecal microbiota from their healthy siblings

    Respiratory syncytial virus infection in Fischer 344 rats is attenuated by short interfering RNA against the RSV-NS1 gene

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    BACKGROUND: Respiratory syncytial virus (RSV) causes severe bronchiolitis and is a risk factor for asthma. Since there is no commercially available vaccine against RSV, a short interfering RNA against the RSV-NS1gene (siNS1) was developed and its potential for decreasing RSV infection and infection-associated inflammation in rats was tested. METHODS: Plasmids encoding siNS1 or an unrelated siRNA were complexed with a chitosan nanoparticle delivery agent and administered intranasally. Control animals received a plasmid for a non-specific siRNA. After expression of the plasmid in lung cells for 24 hours, the rats were intranasally infected with RSV. RESULTS: Prophylaxis with siNS1 significantly reduced lung RSV titers and airway hyperreactivity to methacholine challenge compared to the control group. Lung sections from siNS1-treated rats showed a sizable reduction in goblet cell hyperplasia and in lung infiltration by inflammatory cells, both characteristics of asthma. Also, bronchoalveolar lavage samples from siNS1-treated animals had fewer eosinophils. Treatment of rats with siNS1 prior to RSV exposure was effective in reducing virus titers in the lung and in preventing the inflammation and airway hyperresponsiveness associated with the infection that has been linked to development of asthma. CONCLUSION: The use of siNS1 prophylaxis may be an effective method for preventing RSV bronchiolitis and potentially reducing the later development of asthma associated with severe respiratory infections

    Epidermal growth factor receptor in breast carcinoma: association between gene copy number and mutations

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    <p>Abstract</p> <p>Background</p> <p>The epidermal growth factor receptor (EGFR) is an available target of effective anti-EGFR therapy for human breast cancer. The aim of this study was to assess the presence of EGFR gene amplification and mutations in breast cancer and to analyze the association between the statuses of these two gene alterations.</p> <p>Materials and methods</p> <p>EGFR gene amplification and mutations were investigated in formalin-fixed, paraffin-embedded tissues from 139 Chinese female patients with breast cancer by means of fluorescence in-situ hybridization (FISH) and fluorescently labeled real-time quantitative polymerase chain reaction (RT-PCR), respectively.</p> <p>Results</p> <p>EGFR gene amplification was observed in 46/139 (33.1%) of cases by FISH. Based on RT-PCR, 2/139 (1.4%) samples had EGFR gene mutations. Overall, only 1 (0.7%) of the cases was identified with both whole gene amplification and mutation, and 92 (66.2%) of cases were negative for both. High gene copy numbers of EGFR had significant correlation with the occurrence of EGFR protein expressions (P = 0.002).</p> <p>Conclusion</p> <p>In this study, EGFR mutations were presented in only two samples, indicating that EGFR mutations should not be employed in future trials with anti-EGFR therapies for breast cancer. However, EGFR whole gene amplification is frequently observed in patients with breast cancer. It will be of significant interest to investigate whether EGFR gene copy number is a suitable screening test for EGFR-targeted therapy for breast cancer.</p

    In silico analyses for potential key genes associated with gastric cancer

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    Background Understanding hub genes involved in gastric cancer (GC) metastasis could lead to effective approaches to diagnose and treat cancer. In this study, we aim to identify the hub genes and investigate the underlying molecular mechanisms of GC. Methods To explore potential therapeutic targets for GC,three expression profiles (GSE54129, GSE33651, GSE81948) of the genes were extracted from the Gene Expression Omnibus (GEO) database. The GEO2R online tool was applied to screen out differentially expressed genes (DEGs) between GC and normal gastric samples. Database for Annotation, Visualization and Integrated Discovery was applied to perform Gene Ontology (GO) and KEGG pathway enrichment analysis. The protein-protein interaction (PPI) network of these DEGs was constructed using a STRING online software. The hub genes were identified by the CytoHubba plugin of Cytoscape software. Then, the prognostic value of these identified genes was verified by gastric cancer database derived from Kaplan-Meier plotter platform. Results A total of 85 overlapped upregulated genes and 44 downregulated genes were identified. The majority of the DEGs were enriched in extracellular matrix organization, endodermal cell differentiation, and endoderm formation. Moreover, five KEGG pathways were significantly enriched, including ECM-receptor interaction, amoebiasis, AGE-RAGE signaling pathway in diabetic complications, focal adhesion, protein digestion and absorption. By combining the results of PPI network and CytoHubba, a total of nine hub genes including COL1A1, THBS1, MMP2, CXCL8, FN1, TIMP1, SPARC, COL4A1, and ITGA5 were selected. The Kaplan-Meier plotter database confirmed that overexpression levels of these genes were associated with reduced overall survival, except for THBS1 and CXCL8. Conclusions Our study suggests that COL1A1, MMP2, FN1, TIMP1, SPARC, COL4A1, and ITGA5 may be potential biomarkers and therapeutic targets for GC. Further study is needed to assess the effect of THBS1 and CXCL8 on GC

    Autophagy and regulation of aquaporins in the kidneys

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    Aquaporins (AQPs) are water channel proteins that facilitate the transport of water molecules across cell membranes. To date, seven AQPs have been found to be expressed in mammal kidneys. The cellular localization and regulation of the transport properties of AQPs in the kidney have been widely investigated. Autophagy is known as a highly conserved lysosomal pathway, which degrades cytoplasmic components. Through basal autophagy, kidney cells maintain their functions and structure. As a part of the adaptive responses of the kidney, autophagy may be altered in response to stress conditions. Recent studies revealed that autophagic degradation of AQP2 in the kidney collecting ducts leads to impaired urine concentration in animal models with polyuria. Therefore, the modulation of autophagy could be a therapeutic approach to treat water balance disorders. However, as autophagy is either protective or deleterious, it is crucial to establish an optimal condition and therapeutic window where autophagy induction or inhibition could yield beneficial effects. Further studies are needed to understand both the regulation of autophagy and the interaction between AQPs and autophagy in the kidneys in renal diseases, including nephrogenic diabetes insipidus

    Chitosan Interferon-γ Nanogene Therapy for Lung Disease: Modulation of T-Cell and Dendritic Cell Immune Responses

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    <p/> <p>The use of chitosan nanoparticles as carriers for expression plasmids represents a major improvement in gene expression technology. We demonstrated previously that treatment with chitosan interferon-γ (IFN-γ) plasmid deoxyribonucleic acid (DNA) nanoparticles (chitosan interferon-γ nanogene [CIN]) led to in situ production of IFN-γ and a reduction in inflammation and airway reactivity in mice, but the mechanism underlying the immunomodulatory effects of CIN remains unclear. In this report, the effect of CIN treatment on the immune responses of CD8<sup>+ </sup>T cells and dendritic cells was examined in a BALB/c mouse model of ovalbumin (OVA)-induced allergic asthma. OT1 mice (OVA-T cell receptor [TCR] transgenic) were also used to test the effects of CIN on OVA-specific CD8<sup>+ </sup>T cells. CIN treatment caused a reduction in IFN-γ production in a subpopulation of OVA-specific CD8<sup>+ </sup>T cells cultured in vitro in the presence of OVA. CIN also reduced apoptosis of the CD8<sup>+ </sup>T cells. Examination of dendritic cells from lung and lymph nodes indicated that CIN treatment decreased their antigen-presenting activity, as evident from the reduction in CD80 and CD86 expression. Furthermore, CIN treatment significantly decreased the number of CD11c<sup>+</sup>b<sup>+ </sup>dendritic cells in lymph nodes, suggesting that endogenous IFN-γ expression may immunomodulate dendritic cell migration and activation. CIN therapy results in a reduction in proinflammatory CD8<sup>+ </sup>T cells and decreases the number and antigen-presenting activity of dendritic cells.</p
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