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Sökning: WFRF:(Zhu Mingzhu)

  • Resultat 1-6 av 6
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1.
  • Wang, Tao, et al. (författare)
  • The benefit of taxane-based therapies over fluoropyrimidine plus platinum (FP) in the treatment of esophageal cancer : a meta-analysis of clinical studies
  • 2019
  • Ingår i: Drug Design, Development and Therapy. - 1177-8881. ; 13, s. 539-553
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: Fluoropyrimidine plus platinum (FP) is currently the standard treatment for esophageal cancer (EC). In recent years, taxane-based chemotherapy has also been used and has shown good efficacy in EC. This study aims to investigate the advantages of taxane-based over FP chemotherapy, as well as discuss its drawbacks, in the treatment of EC. Patients and methods: A literature search was done for studies comparing clinical outcomes between taxane-based and FP chemotherapy in EC. Pooled analyses were performed to compare the efficacy and grade 3/4 adverse events in patients who received neoadjuvant chemotherapy (NACT), neoadjuvant chemoradiotherapy (NACRT), or definitive chemoradiotherapy (dCRT). Subgroup analyses were also conducted in esophageal squamous cell carcinoma (ESCC). Results: Thirty-one studies with a total of 3,912 patients were included in the analysis. Better long-term survival was found in patients who received taxane-based NACT (progression-free survival (PFS): pooled HR=0.58, P=0.0008; and overall survival (OS): pooled HR=0.50, P<0.00001) and dCRT (PFS: pooled HR=0.75, P<0.0001). In NACRT, taxane-based treatment and FP showed similar efficacy. In ESCC patients, taxane-based treatment showed better OS (NACT: pooled HR=0.57, P=0.02; NACRT: pooled HR=0.51, P=0.03; and dCRT: pooled HR=0.73, P<0.0001) than FP chemotherapy. Furthermore, taxane-based therapy also showed a better short-term response (complete response (CR), objective response rate (ORR), disease control rate (DCR), or pathologic complete response (pCR). However, taxane-based therapy was significantly correlated with a higher incidence of grade 3/4 leukopenia, neutropenia, and diarrhea. Conclusion: Compared to FP, taxane-based therapy produced better clinical response and outcomes in EC patients receiving NACT or dCRT, and in all types of therapy in patients with ESCC. Taxane-based treatment is associated with more frequent toxicity.
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2.
  • Yao, Qiuyu, et al. (författare)
  • The vasodilatory effect of sulfur dioxide via SGC/cGMP/PKG pathway in association with sulfhydryl-dependent dimerization
  • 2016
  • Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : AMER PHYSIOLOGICAL SOC. - 0363-6119 .- 1522-1490. ; 310:11, s. R1073-R1080
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study was designed to explore the role of soluble guanylate cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/PKG pathway in sulfur dioxide (SO2)-induced vasodilation. We showed that SO2 induced a concentration-dependent relaxation of phenylephrine (PE)precontracted rat aortic rings in association with an increase in cGMP concentration, whereas L-aspartic acid beta-hydroxamate (HDX), an inhibitor of SO2 synthase, contracted rings in a dose-dependent manner. Pretreatment of aortic rings with the sGC inhibitor ODQ (30 mu M) attenuated the vasodilatory effects of SO2, suggesting the involvement of cGMP pathway in SO2-induced vasodilation. Mechanistically, SO2 upregulated the protein levels of sGC and PKG dimers, while HDX inhibited it, indicating SO2 could promote cGMP synthesis through sGC activation. Furthermore, the dimerization of sGC and PKG and vasodilation induced by SO2 in precontracted rings were significantly prevented by thiol reductants dithiothreitol (DTT). In addition, SO2 reduced the activity of phosphodiesterase type 5 (PDE5), a cGMP-specific hydrolytic enzyme, implying that SO2 elevated cGMP concentration by inhibiting its hydrolysis. Hence, SO2 exerted its vasodilatory effects at least partly by promoting disulfide-dependent dimerization of sGC and PKG, resulting in an activated sGC/cGMP/PKG pathway in blood vessels. These findings revealed a new mode of action and mechanisms by which SO2 regulated the vascular tone.
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3.
  • Zhu, Kai, et al. (författare)
  • Operation characteristics of a new-type loop heat pipe (LHP) with wick separated from heating surface in the evaporator
  • 2017
  • Ingår i: Applied Thermal Engineering. - : Elsevier Ltd. - 1359-4311 .- 1873-5606. ; 123, s. 1034-1041
  • Tidskriftsartikel (refereegranskat)abstract
    • The loop heat pipe (LHP) has been widely used for cooling devices with high heat flux. In addition to the capillary pumping force, the pressure head due to evaporation has been assumed to play an important role in the circulation of working fluid. Based on such a hypothesis, a new LHP is designed, in which the wick is separated from the heating surface in the evaporator. Experiments show that such a LHP can start up successfully and reach steady operation, which indirectly verified the hypothesis. The influences of heating power, height of steam chamber, pore radius and porosity of wick are comprehensively investigated. The results show that the start-up time of the new-designed LHP is shorter and the temperature fluctuation is smaller at higher heating power. The steam chamber height has clear impacts on the start-up time and the thermal resistance. The start-up time with the steam chamber height of 2 mm is shorter than that of 3 mm, but the thermal resistance is relatively higher. Moreover, a larger pore radius and a higher porosity of the wick can lead to a shorter start-up time and a smaller thermal resistance of the new LHP.
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4.
  • Zhu, Mingzhu, et al. (författare)
  • Effect of endogenous sulfur dioxide in regulating cardiovascular oxidative stress
  • 2014
  • Ingår i: Histology and Histopathology. - : F HERNANDEZ. - 0213-3911 .- 1699-5848. ; 29:9, s. 1107-1111
  • Forskningsöversikt (refereegranskat)abstract
    • In the middle of the 1980s, nitric oxide received extensive attention because of its significant effects in life science. Then, carbon monoxide and hydrogen sulfide were discovered to be gasotransmitters playing important roles in regulating cellular homeostasis. As a common air pollutant, sulfur dioxide (SO2) can cause great harm to the human body by producing free radicals, which causes oxidative damage to various organs. Recently, endogenous SO2 was found to be produced in the cardiovascular system and might be a bioactive molecule regulating the physiological activities including cardiovascular oxidative stress.
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5.
  • Zhu, Mingzhu, et al. (författare)
  • L-cystathionine inhibits oxidized low density lipoprotein-induced THP-1-derived macrophage inflammatory cytokine monocyte chemoattractant protein-1 generation via the NF-kappa B pathway
  • 2015
  • Ingår i: Scientific Reports. - : Nature Publishing Group: Open Access Journals - Option C / Nature Publishing Group. - 2045-2322. ; 5:10453
  • Tidskriftsartikel (refereegranskat)abstract
    • This study aimed to explore whether and how L-cystathionine had any regulatory effect on the inflammatory response in THP-1-derived macrophages cultured in vitro under oxidized low-density lipoprotein (ox-LDL) stimulation. The human monocyte line THP-1 cell was cultured in vitro and differentiated into macrophages after 24 hours of PMA induction. Macrophages were pretreated with L-cystathionine and then treated with ox-LDL. The results showed that compared with the controls, ox-LDL stimulation significantly upregulated the expression of THP-1-derived macrophage MCP-1 by enhancing NF-kappa B p65 phosphorylation, nuclear translocation and DNA binding with the MCP-1 promoter. Compared with the ox-LDL group, 0.3 mmol/L and 1.0 mmol/L L-cystathionine significantly inhibited the expression of THP-1-derived macrophage MCP-1. Mechanistically, 0.3 mmol/L and 1.0 mmol/L L-cystathionine suppressed phosphorylation and nuclear translocation of the NF-kappa B p65 protein, as well as the DNA binding activity and DNA binding level of NF-kappa B with the MCP-1 promoter, which resulted in a reduced THP-1-derived macrophage MCP-1 generation. This study suggests that L-cystathionine could inhibit the expression of MCP-1 in THP-1-derived macrophages induced by ox-LDL via inhibition of NF-kappa B p65 phosphorylation, nuclear translocation, and binding of the MCP-1 promoter sequence after entry into the nucleus.
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6.
  • Zhu, Mingzhu, et al. (författare)
  • L-Cystathionine Inhibits the Mitochondria-Mediated Macrophage Apoptosis Induced by Oxidized Low Density Lipoprotein
  • 2014
  • Ingår i: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 15:12, s. 23059-23073
  • Tidskriftsartikel (refereegranskat)abstract
    • This study was designed to investigate the regulatory role of L-cystathionine in human macrophage apoptosis induced by oxidized low density lipoprotein (ox-LDL) and its possible mechanisms. THP-1 cells were induced with phorbol 12-myristate 13-acetate (PMA) and differentiated into macrophages. Macrophages were incubated with ox-LDL after pretreatment with L-cystathionine. Superoxide anion, apoptosis, mitochondrial membrane potential, and mitochondrial permeability transition pore (MPTP) opening were examined. Caspase-9 activities and expression of cleaved caspase-3 were measured. The results showed that compared with control group, ox-LDL treatment significantly promoted superoxide anion generation, release of cytochrome c (cytc) from mitochondrion into cytoplasm, caspase-9 activities, cleavage of caspase-3, and cell apoptosis, in addition to reduced mitochondrial membrane potential as well as increased MPTP opening. However, 0.3 and 1.0 mmol/L L-cystathionine significantly reduced superoxide anion generation, increased mitochondrial membrane potential, and markedly decreased MPTP opening in ox-LDL + L-cystathionine macrophages. Moreover, compared to ox-LDL treated-cells, release of cytc from mitochondrion into cytoplasm, caspase-9 activities, cleavage of caspase-3, and apoptosis levels in L-cystathionine pretreated cells were profoundly attenuated. Taken together, our results suggested that L-cystathionine could antagonize mitochondria-mediated human macrophage apoptosis induced by ox-LDL via inhibition of cytc release and caspase activation.
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