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Sökning: WFRF:(Ning Guang)

  • Resultat 11-20 av 20
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11.
  • Lim, Lee Ling, et al. (författare)
  • Aspects of Multicomponent Integrated Care Promote Sustained Improvement in Surrogate Clinical Outcomes: A Systematic Review and Meta-analysis.
  • 2018
  • Ingår i: Diabetes care. - 1935-5548. ; 41:6, s. 1312-1320
  • Tidskriftsartikel (refereegranskat)abstract
    • The implementation of the Chronic Care Model (CCM) improves health care quality. We examined the sustained effectiveness of multicomponent integrated care in type 2 diabetes.We searched PubMed and Ovid MEDLINE (January 2000-August 2016) and identified randomized controlled trials comprising two or more quality improvement strategies from two or more domains (health system, health care providers, or patients) lasting ≥12 months with one or more clinical outcomes. Two reviewers extracted data and appraised the reporting quality.In a meta-analysis of 181 trials (N = 135,112), random-effects modeling revealed pooled mean differences in HbA1c of -0.28% (95% CI -0.35 to -0.21) (-3.1 mmol/mol [-3.9 to -2.3]), in systolic blood pressure (SBP) of -2.3 mmHg (-3.1 to -1.4), in diastolic blood pressure (DBP) of -1.1 mmHg (-1.5 to -0.6), and in LDL cholesterol (LDL-C) of -0.14 mmol/L (-0.21 to -0.07), with greater effects in patients with LDL-C ≥3.4 mmol/L (-0.31 vs. -0.10 mmol/L for <3.4 mmol/L; Pdifference = 0.013), studies from Asia (HbA1c -0.51% vs. -0.23% for North America [-5.5 vs. -2.5 mmol/mol]; Pdifference = 0.046), and studies lasting >12 months (SBP -3.4 vs. -1.4 mmHg, Pdifference = 0.034; DBP -1.7 vs. -0.7 mmHg, Pdifference = 0.047; LDL-C -0.21 vs. -0.07 mmol/L for 12-month studies, Pdifference = 0.049). Patients with median age <60 years had greater HbA1c reduction (-0.35% vs. -0.18% for ≥60 years [-3.8 vs. -2.0 mmol/mol]; Pdifference = 0.029). Team change, patient education/self-management, and improved patient-provider communication had the largest effect sizes (0.28-0.36% [3.0-3.9 mmol/mol]).Despite the small effect size of multicomponent integrated care (in part attenuated by good background care), team-based care with better information flow may improve patient-provider communication and self-management in patients who are young, with suboptimal control, and in low-resource settings.
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13.
  • Shen, Qiuwan, et al. (författare)
  • Effect of A/B-site substitution on oxygen production performance of strontium cobalt based perovskites for CO2 capture application
  • 2015
  • Ingår i: RSC Advances. - : Royal Society of Chemistry. - 2046-2069. ; 5:50, s. 39785-39790
  • Tidskriftsartikel (refereegranskat)abstract
    • Oxy-fuel combustion is one of the proposed technologies which have the potential to achieve zero CO2 emission. Strontium cobalt based perovskite oxygen carriers are promising materials for air separation with a high selectively for oxygen. And these perovskites can produce an oxygen enriched carbon dioxide stream for an oxy-fuel combustion process. The relatively low oxygen production yield may be a drawback of this type of material for this technology. This paper presents an effective approach by A/B-site substitution to improve the oxygen production performance of the perovskites. In this study, a series of different A/B-site substituted SrCo0.8Fe0.2O3-delta were prepared by an EDTA-citrate sol-gel combustion synthesis method. Fixed-bed experiments and TGA measurements were performed to study the effects of A/B-site substitution on cyclic oxygen adsorption/desorption performance of the synthesized samples. The experimental results indicate that the oxygen desorption amounts of different A-site substituted perovskites decrease in the order of BaCo0.8Fe0.2O3-delta > Ba0.5Sr0.5Co0.8Fe0.2O3-delta > SrCo0.8Fe0.2O3-delta > Sr0.5Ca0.5Co0.8Fe0.2O3-delta > MgCo0.8Fe0.2O3-delta. Moreover, B-site substitution by different transition metal ions can significantly modify oxygen adsorption capacity and oxygen desorption performance of SrCo0.8Fe0.2O3-delta. Furthermore, oxygen desorption performance can be improved when Fe ions of the perovskite SrCo0.8Fe0.2O3-delta are substituted by Zr, Cr, Zn, and Ni ions.
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14.
  • Wang, Min, et al. (författare)
  • Apolipoprotein M induces inhibition of inflammatory responses via the S1PR1 and DHCR24 pathways
  • 2019
  • Ingår i: Molecular Medicine Reports. - : Spandidos Publications Ltd. - 1791-2997. ; 19:2, s. 1272-1283
  • Tidskriftsartikel (refereegranskat)abstract
    • © 2019 Spandidos Publications. All rights reserved. Apolipoprotein M (ApoM) is a type of apolipoprotein. It is well known that high-density lipoprotein (HDL) decreases inflammatory responses via the apoM-sphingosine-1-phosphate (S1P) pathway. The present study further investigated the importance of ApoM in the inhibitory effects of HDL on inflammation. Mice with an apoM gene deficiency (apoM-/-) were employed to investigate the effects of ApoM on the expression of interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), S1P receptor-1 (S1PR1) and 3β-hydroxysterol Δ-24-reductase (DHCR24), as compared with in wild-type mice (apoM+/+). Furthermore, cell culture experiments were performed using a permanent human hybrid endothelial cell line (EA.hy926). Cells were cultured in the presence of recombinant human apoM (rec-apoM) or were induced to overexpress apoM (apoMTg); subsequently, cells were treated with tumor necrosis factor-α (TNF-α), in order to investigate the effects of ApoM on IL-1β and MCP-1. The results demonstrated that the mRNA expression levels of IL-1β and MCP-1 were significantly higher in the liver following administration of lipopolysaccharide in apoM-/- mice compared with in apoM+/+ mice. In cell culture experiments, when cells were pre-cultured with rec-apoM or were engineered to overexpress apoM (apoMTg), they exhibited decreased expression levels of IL-1β and MCP-1 following TNF-α treatment compared with in normal apoM-expressing cells (apoMTgN). Furthermore, the mRNA expression levels of IL-1β and MCP-1 were significantly elevated following addition of the S1PR1 inhibitor W146, but not by the scavenger receptor class B type I inhibitor, block lipid transport-1 (BLT-1), in apoMTg cells prior to TNF-α treatment. Conversely, there were no differences in these inflammatory biomarkers under the same conditions in apoMTgN cells. The mRNA expression levels of DHCR24 were significantly reduced by the addition of BLT-1 prior to TNF-α treatment in apoMTg cells; however, there was no difference in the expression of this inflammatory biomarker in apoMTgN cells. In conclusion, ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.
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15.
  • Wei, Jiang, et al. (författare)
  • 17β-estradiol regulates the expression of apolipoprotein M through estrogen receptor α-specific binding motif in its promoter
  • 2017
  • Ingår i: Lipids in Health and Disease. - : BioMed Central (BMC). - 1476-511X. ; 16:1, s. 1-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression. Results: Our results demonstrated either free 17β-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells. Moreover, experiments with the luciferase activity analysis of truncated apoM promoters could demonstrate that a regulatory region (from-1580 to −1575 bp (−GGTCA-)) upstream of the transcriptional start site of apoM gene was essential for the basal transcriptional activity that regulated by the ER-α. With the applications of an electrophoresis mobility shift assay and a chromatin immunoprecipitation assay, we could successfully identify a specific ER-α binding element in the apoM promoter region. Conculsion: In summary, the present study indicates that 17β-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-α-dependent pathway involving ER-α binding element in the promoter of the apoM gene.
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16.
  • Xie, Xu-Qin, et al. (författare)
  • miR-124 Intensified Oxaliplatin-Based Chemotherapy by Targeting CAPN2 in Colorectal Cancer
  • 2020
  • Ingår i: MOLECULAR THERAPY-ONCOLYTICS. - : CELL PRESS. - 2372-7705. ; 17, s. 320-331
  • Tidskriftsartikel (refereegranskat)abstract
    • Our previous study demonstrated that miR-124 was downregulated in colorectal cancer (CRC) compared with normal mucosa, and the downregulated expression of miR-124 was an independent prognostic factor in CRC patients. However, the function of miR-124 in CRC patients treated with chemotherapy is currently unclear. The aim of this study was to determine the miR-124 expression and its regulative role in oxaliplatin (L-OHP)-based chemotherapy of CRC patients. We observed that low miR-124 expression was correlated with worse overall survival (OS) in the 220 patients who received postoperative chemotherapy of 5-fluorouracil [5-FU] +leucovorin+L-OHP (FOLFOX) or capecitabine+L-OHP (XELOX). miR-124 overexpression promoted L-OHP-induced, but not 5-FU-induced, cytotoxicity and apoptosis in HT29 and SW480 cells. CAPN2 was a direct target of miR124, and its protein expression was reduced by forced expression of miR-124. miR-124 inhibited tumorigenesis and promoted OS of mice bearing xenograft tumors, especially upon L-OHP treatment. miR-124 also promoted L-OHP-induced apoptosis and restrained CAPN2 protein expression in xenograft tumors. Our results suggest that miR-124 could be considered as both a predictor of L-OHP-based chemotherapy for personalized treatment and a therapeutic target for CRC.
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17.
  • Yu, Miao mei, et al. (författare)
  • Apolipoprotein M increases the expression of Vitamin D receptor mRNA in colorectal cancer cells detected with duplex fluorescence reverse transcription-quantitative polymerase chain reaction
  • 2017
  • Ingår i: Molecular Medicine Reports. - : Spandidos Publications Ltd. - 1791-2997. ; 16:2, s. 1167-1172
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein M (ApoM) and the Vitamin D receptor (VDR) are apolipoproteins predominantly presenting in high-density lipoprotein (HDL) and a karyophilic protein belonging to the steroid-thyroid receptor superfamily, respectively. Previous studies have demonstrated that ApoM and VDR are associated with cholesterol metabolism, immune and colorectal cancer regulation. In order to investigate whether ApoM affected the expression of VDR in colorectal cancer cells, a single-tube duplex fluorescence reverse transcription-quantitative polymerase chain reaction (RT-qPCR) system was developed to simultaneously detect the mRNA levels of VDR and GAPDH in HT-29 cells overexpressing ApoM. The results demonstrated that the amplification products were confirmed as the specific fragment of VDR/GAPDH using the DNA sequencing instrument. The sensitivity, linear range, correlation coefficient, amplification efficiency, intra-assay and inter-assay coefficients of variation were 40 copies/μl, 4.00×101-4.00×105 copies/μl, 0.999, 92.42%, 0.09-0.34% and 0.32-0.65% for VDR, and 40 copies/μl, 400×101-4.00×105 copies/μl, 0.999, 98.07%, 0.19-0.43% and 0.40-0.75% for GAPDH, respectively. The results indicated that the expression of VDR mRNA was significantly higher in HT-29 cells overexpressing ApoM, compared with the negative control group (P<0.05). In conclusion, the current study successfully developed the single-tube duplex RT-qPCR to simultaneously detect VDR and GAPDH expression in colorectal cancer cells. The methodology results demonstrated that the duplex RT-qPCR system with high sensitivity and specificity could ensure the objectivity and credibility of the detection. The present study confirmed that ApoM significantly increased the expression of VDR in HT-29 cells. In addition, it was hypothesized that ApoM may be involved in antineoplastic activity via the upregulation of VDR expression, which may provide novel directions for the investigation of ApoM in cancer.
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18.
  • Yu, Yang, et al. (författare)
  • Increased mRNA levels of apolipoprotein M and apolipoprotein AI in the placental tissues with fetal macrosomia
  • 2015
  • Ingår i: Archives of Gynecology and Obstetrics. - : Springer. - 1432-0711. ; 291:2, s. 299-303
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study examined mRNA levels of apolipoprotein M (apoM) and apolipoprotein AI (apoAI) in the term placental tissues obtained from 37 women with normal birth weight neonates and from 37 women with macrosomic neonates (birth body weight a parts per thousand yen4,000 g), and further discussed possible clinical significance of these observations. The mRNA levels of apoM and apoAI in the placental tissues were determined by the real time RT-PCR, which demonstrated that both apoM and apoAI mRNA levels were significantly higher in the placentas from macrosomia than those from normal birth. Moreover, we analyzed the overexpressions of apoM and apoAI with the clinical data. Meanwhile we examined several known risk factors of macrosomia including the mRNA levels of insulin-like growth factor I (IGF-I), IGF-II, insulin-like growth factor I receptor (IGF-IR) and IGF-IIR. It demonstrated that apoM expression was significantly positively correlated to the placental weight, fetal birth weight, pregestational body mass index (BMI), weight gain during pregnancy, maternal weight, maternal BMI and the mRNA levels of IGF-IR as well as IGF-IIR. The apoAI mRNA level was statistically significantly correlated to the placental weight, fetal birth weight, IGF-I and IGF-IR mRNA levels. Binary logistic regression analysis suggested that both apoM and apoAI mRNA may considered as independent risk factors for macrosomia. The clinical significance needs further investigation.
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20.
  • Zhu, Bin, et al. (författare)
  • Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling
  • 2018
  • Ingår i: Inflammation. - : Springer. - 0360-3997. ; 41:2, s. 643-653
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract: It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM+/+) group (n = 24) and apoM gene-deficient (apoM−/−) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta (IL-1β) and mRNA levels of IL-1β, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), lung histology, wet/dry weight ratio, and immunohistochemistry were measured at 3 h after the baseline and compared in each group. Our results clearly demonstrated that IL-1β mRNA levels and other inflammatory biomarkers were significantly increased in the lungs of LPS-induced ALI apoM−/− mice compared to those of the apoM+/+ mice. Moreover, when apoM+/+ mice were treated with W146, a S1P receptor (S1PR1) antagonist, these inflammatory biomarkers could be significantly upregulated by LPS-induced ALI. Therefore, it suggests that apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.
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  • Resultat 11-20 av 20
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