18 research outputs found

    A 20 W, Less-Than-1-kHz Linewidth Linearly Polarized All-Fiber Laser

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    We report a continuous-wave high-output power and narrow-linewidth all-fiber laser at 1550 nm with the master oscillator power amplifier (MOPA) configuration. An all-fiber distributed feedback seed laser was boosted by three cascaded fiber amplifiers. In the experiment, we adopted a large-mode-area (LMA) Er3+:Yb3+-co-doped polarization-maintaining fiber to increase nonlinear thresholds and avoided the broadening of the laser linewidth. A linear-polarization fiber laser with average output power of 20 W, linewidth of 0.88 kHz, and power jitter less than 2% was finally achieved

    The involvement of PI3K-mediated and L-VGCC-gated transient Ca2+ influx in 17β-estradiol-mediated protection of retinal cells from H2O2-induced apoptosis with Ca2+ overload.

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    Intracellular calcium concentration ([Ca(2+)]i) plays an important role in regulating most cellular processes, including apoptosis and survival, but its alterations are different and complicated under diverse conditions. In this study, we focused on the [Ca(2+)]i and its control mechanisms in process of hydrogen peroxide (H2O2)-induced apoptosis of primary cultured Sprague-Dawley (SD) rat retinal cells and 17β-estradiol (βE2) anti-apoptosis. Fluo-3AM was used as a Ca(2+) indicator to detect [Ca(2+)]i through fluorescence-activated cell sorting (FACS), cell viability was assayed using MTT assay, and apoptosis was marked by Hoechst 33342 and annexin V/Propidium Iodide staining. Besides, PI3K activity was detected by Western blotting. Results showed: a) 100 μM H2O2-induced retinal cell apoptosis occurred at 4 h after H2O2 stress and increased in a time-dependent manner, but [Ca(2+)]i increased earlier at 2 h, sustained to 12 h, and then recovered at 24 h after H2O2 stress; b) 10 μM βE2 treatment for 0.5-24 hrs increased cell viability by transiently increasing [Ca(2+)]i, which appeared only at 0.5 h after βE2 application; c) increased [Ca(2+)]i under 100 µM H2O2 treatment for 2 hrs or 10 µM βE2 treatment for 0.5 hrs was, at least partly, due to extracellular Ca(2+) stores; d) importantly, the transiently increased [Ca(2+)]i induced by 10 µM βE2 treatment for 0.5 hrs was mediated by the phosphatidylinositol-3-kinase (PI3K) and gated by the L-type voltage-gated Ca(2+) channels (L-VGCC), but the increased [Ca(2+)]i induced by 100 µM H2O2 treatment for 2 hrs was not affected; and e) pretreatment with 10 µM βE2 for 0.5 hrs effectively protected retinal cells from apoptosis induced by 100 µM H2O2, which was also associated with its transient [Ca(2+)]i increase through L-VGCC and PI3K pathway. These findings will lead to better understanding of the mechanisms of βE2-mediated retinal protection and to exploration of the novel therapeutic strategies for retina degeneration

    Dual‐Energy CT in Breast Cancer: Current Applications and Future Outlooks

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    Abstract Breast cancer is the most prevalent cancerous tumor in women, characterized by different subtypes and varying responses to treatment. The continued evolution of breast cancer diagnosis and management has resulted in a transition from a one‐size‐fits‐all approach to a new era of personalized treatment plans. Therefore, it is essential to accurately identify the biological characteristics of breast tissue in order to minimize unnecessary biopsies of benign lesions and improve the overall clinical process, leading to reduced expenses and complications associated with invasive biopsy procedures. Challenges for future research include finding ways to predict the response of breast cancer patients to adjuvant systemic treatment. Dual‐energy CT (DECT) is a new imaging technology integrating functional imaging and molecular imaging. Over the past decade, DECT has gained relevancy, especially in oncological radiology. This article proposed a literature review of the application and research status of DECT in breast cancer treatment strategy determination and prognosis prediction

    miR-183-5p Is a Potential Molecular Marker of Systemic Lupus Erythematosus

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    Objective. To investigate microRNA (miRNA) expression profiles in individuals with systemic lupus erythematosus (SLE) and identify the valuable miRNA biomarkers in diagnosing and monitoring SLE. Methods. Next-generation sequencing (NGS) was performed to assess miRNA amounts in peripheral blood mononuclear cells (PBMCs) from four SLE cases and four healthy controls. Quantitative polymerase chain reaction (qPCR) was carried out for validating candidate miRNAs in 32 SLE cases and 32 healthy controls. In addition, receiver operating characteristic (ROC) curve analysis was completed to evaluate diagnostic performance. Finally, the associations of candidate miRNAs with various characteristics of SLE were analyzed. Results. A total of 157 miRNAs were upregulated, and 110 miRNAs were downregulated in PBMCs from SLE cases in comparison to healthy controls, of which the increase of miR-183-5p and decrease of miR-374b-3p were validated by qPCR and both showed good diagnostic performance for SLE diagnosis. Besides, miR-183-5p expression levels displayed a positive association with SLE disease activity index (SLEDAI) and anti-dsDNA antibody amounts. Conclusion. Our data indicated that miR-183-5p is a promising biomarker of SLE

    A tailored series of engineered yeasts for the cell-dependent treatment of inflammatory bowel disease by rational butyrate supplementation

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    ABSTRACTIntestinal microbiota dysbiosis and metabolic disruption are considered essential characteristics in inflammatory bowel disorders (IBD). Reasonable butyrate supplementation can help patients regulate intestinal flora structure and promote mucosal repair. Here, to restore microbiota homeostasis and butyrate levels in the patient’s intestines, we modified the genome of Saccharomyces cerevisiae to produce butyrate. We precisely regulated the relevant metabolic pathways to enable the yeast to produce sufficient butyrate in the intestine with uneven oxygen distribution. A series of engineered strains with different butyrate synthesis abilities was constructed to meet the needs of different patients, and the strongest can reach 1.8 g/L title of butyrate. Next, this series of strains was used to co-cultivate with gut microbiota collected from patients with mild-to-moderate ulcerative colitis. After receiving treatment with engineered strains, the gut microbiota and the butyrate content have been regulated to varying degrees depending on the synthetic ability of the strain. The abundance of probiotics such as Bifidobacterium and Lactobacillus increased, while the abundance of harmful bacteria like Candidatus Bacilloplasma decreased. Meanwhile, the series of butyrate-producing yeast significantly improved trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice by restoring butyrate content. Among the series of engineered yeasts, the strain with the second-highest butyrate synthesis ability showed the most significant regulatory and the best therapeutic effect on the gut microbiota from IBD patients and the colitis mouse model. This study confirmed the existence of a therapeutic window for IBD treatment by supplementing butyrate, and it is necessary to restore butyrate levels according to the actual situation of patients to restore intestinal flora

    Correlation of Serum Soluble Interleukin-7 Receptor and Anti-C1q Antibody in Patients with Systemic Lupus Erythematosus

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    Background. Serum concentrations of soluble interleukin-7 receptor (sIL-7R) and anti-C1q antibody have recently been identified as unique serological markers for lupus nephritis (LN) in patients with systemic lupus erythematosus (SLE). In this study, we evaluated the correlation of serum sIL-7R and anti-C1q in SLE patients. Methods. Sera from 134 patients with SLE and 84 healthy cohorts were tested for levels of sIL-7R and anti-C1q antibodies in terms of ELISA. Correlations of the sIL-7R and anti-C1q autoantibodies were evaluated. Results. The serum concentrations of sIL-7R and anti-C1q antibodies were significantly higher in SLE patients and LN patients in comparison with healthy individuals/controls and SLE patients with non-LN, respectively. In addition, both sIL-7R and anti-C1q concentrations were found to significantly correlate with the SLE disease activity as evaluated by SLEDAI scores. Interestingly, the serum sIL-7R concentration was strongly correlated with the level of anti-C1q antibodies (r=0.2871, p=0.0008) but not statistically correlated with other serological markers, including the anti-dsDNA and complements C3 and C4 concentrations in SLE patients. Conclusion. Both serum sIL-7R and anti-C1q antibodies were strongly associated with disease activity and LN in SLE patients, suggesting that they may be reliable serological markers for identification of SLE patients with active diseases and LN

    The effect of the PI3K inhibitor LY294002 (LY) on the cell viability and the [Ca<sup>2+</sup>]<sub>i</sub> of primary cultured SD rat retinal cells in H<sub>2</sub>O<sub>2</sub> injury and βE2 protection.

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    <p>A: Western blot results of the activation of the PI3K/Akt pathway after βE2 treatment for 0.5 hrs; B: Quantitative data of A; C, E, G, and I: Cell viability quantitative data; D, F, H, and J: [Ca<sup>2+</sup>]<sub>i</sub> quantitative data; C and D: The effects of LY treatments for 24 hrs and 0.5 hrs on the cell viability and the resting [Ca<sup>2+</sup>]<sub>i</sub>; E and F: The inhibitory effect of LY pretreatment for 0.5 hrs on the increased cell viability and [Ca<sup>2+</sup>]<sub>i</sub> induced by 10 μM βE2 treatment for 0.5 hrs (10 μM LY in E, 10 μM and 20 μM LY in F); G and H: The effect of LY pretreatment for 0.5 hrs on the decreased cell viability and increased [Ca<sup>2+</sup>]<sub>i</sub> induced by 100 μM H<sub>2</sub>O<sub>2</sub> treatment for 2 hrs (10 μM LY in G, 10 μM and 20 μM LY in H); I and J: The dose-dependent attenuating impact of 20-50 μM LY pretreatment for 0.5 hrs on the βE2 retinal protective role against H<sub>2</sub>O<sub>2</sub> injury, which is associated with the dose-dependent attenuation of the increased [Ca<sup>2+</sup>]<sub>i</sub> (Protocol of drug application: LY for 0.5 hrs, E2 for 0.5 hrs and H<sub>2</sub>O<sub>2</sub> for 2 hrs). Values shown are the Mean ±SD. *represents P<0.05, **represents P<0.01 and ***represents P<0.001 compared with the control group; # represents P<0.05, ## represents P<0.01 and ### represents P<0.001 compared with the βE2 (E, F) or H<sub>2</sub>O<sub>2</sub> (G, I, J) application groups; $ represents P<0.05, $$ represents P<0.01 and $$$ represents P<0.001 compared with the βE2 and H<sub>2</sub>O<sub>2</sub> co-application group by one-way ANOVA statistical analysis. (B: n indicates 3 independent replicates; C, E, G, I: n indicates 3 independent replicates with 4 samples per condition per experiment; D, F, H, J: n indicates 3 independent replicates with 5 samples per condition per experiment.).</p

    The effect of the L-VGCC blocker nifedipine (N) on the alteration of [Ca<sup>2+</sup>]<sub>i</sub> during H<sub>2</sub>O<sub>2</sub> injury and βE2 retinal protection.

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    <p>A: Cell viability under 10-30 μM nifedipine treatments for 24 hrs; B: [Ca<sup>2+</sup>]<sub>i</sub> at different time points after 20 μM nifedipine application; C, D: The effects of 20 μM nifedipine pretreatment for 2 hrs on the increase in [Ca<sup>2+</sup>]<sub>i</sub> due to 10 μM βE2 treatment for 0.5 hrs or 100 μM H<sub>2</sub>O<sub>2</sub> treatment for 2 hrs; E, F: The attenuated effect of 20 μM nifedipine pretreatment for 2 hrs on the increased cell viability and [Ca<sup>2+</sup>]<sub>i</sub> due to βE2 and H<sub>2</sub>O<sub>2</sub> co-treatment. N is 20 μM nifedipine in B, C, D, E, and F. Values shown are the Mean ±SD. *represents P<0.05, **represents P<0.01 and ***represents P<0.001 compared with the control group; # represents P<0.05, ## represents P<0.01 compared with the H<sub>2</sub>O<sub>2</sub> group (E, F) and ### represents P<0.001 compared with the βE2 group (C); $ represents P<0.05 compared with the βE2 and H<sub>2</sub>O<sub>2</sub> co-application group by one-way ANOVA statistical analysis. (A: n indicates 5 independent replicates with 5 samples per condition per experiment; B, C, D, E, F: n indicates 3 independent replicates with 4 samples per condition per experiment.).</p
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