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Ningbo, China

Pei R.Z.,Yinzhou Peoples Hospital
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi | Year: 2013

To study the clinical outcome, adverse effect and treatment cost of homoharringtonine (HHT) in combination with all-trans retinoic acid (ATRA) and arsenic trioxide (AS2O3) for newly diagnosed with patients acute promyelocytic leukemia (APL). Clinical data of treatment of newly diagnosed patients with APL in experimental group (HHT + ATRA + AS2O3, n = 14) and control group \[Idarubicin (IDA) + ATRA + AS2O3, n = 21\] were analyzed retrospectively. The therapeutic effects, side effects and costs during induction therapy were compared between the two groups. (1) The complete remission (CR) rate were 92.9% (13/14) and 95.2% (20/21) in experimental group and control group, respectively. The time to achieve CR were (28.1 ± 3.8) and (31.7 ± 4.2) days, respectively (P > 0.05). The negative rate of PML-RARα fusion gene at the time of CR were 76.9% (10/13) and 75.0% (15/20), respectively, and that in CR patient at the end of the first cycle treatment were 100.0% (13/13) and 95.0% (19/20), respectively (P > 0.05). (2) 5-year overall survival (OS) rate were (92.6 ± 0.6)% and (89.9 ± 0.5)%, respectively (P > 0.05), 5-year disease free survival (DFS) rate were 100.0% and (86.8 ± 0.6)%, respectively (P > 0.05). (3) During induction therapy, the incidence of infection in experimental and control group were 23.1% (3/13), 60.0% (12/20), respectively (P < 0.05). The amount of platelet transfusion were (54.7 ± 29.6) and (76.5 ± 25.6) units, respectively (P > 0.05), and that of fresh frozen plasma were (1157.1 ± 238.4) and (1423.5 ± 324.6) ml, respectively (P > 0.05). The total medical costs (excluding HHT and IDA) in experimental and control group were (36074.9 ± 1245.6) and (50564.5 ± 3658.4)CNY, respectively (P < 0.05). HHT in combination with ATRA and AS2O3 regimen for newly diagnosed APL has a better efficacy, a higher long-term survival rate, and a lower costs, which is one of the reasonable choice. Source

Song Y.,Yinzhou Peoples Hospital | Fu Z.,Peoples Care | Yu W.,Peoples Care
Molecular Cancer | Year: 2015

Background: MicroRNAs (miRNAs) have been identified as important posttranscriptional regulators involved in various biological and pathological processes of cells, but their association with tumor chemoresistance has not been fully understood. Methods: We detected miR-27a expression in two lung adenocarcinoma cell lines, A549 and A549/CDDP, and then investigated the effects of miR-27a on the metastasis and the chemosensitivity of cancer cells, using both gain- and loss-of-function studies. The correlation between miR-27a level and chemoresistance was further investigated in clinical lung adenocarcinoma specimens. Results: miR-27a was significantly up-regulated in cisplatin-resistant lung adenocarcinoma A549/CDDP cells compared with parental A549 cells. miR-27a regulates epithelial-mesenchymal transition (EMT) and cisplatin resistance in vitro and modulates response of lung adenocarcinoma cells to cisplatin in vivo. Further studies identified Raf Kinase Inhibitory Protein (RKIP) as a direct and functional target of miR-27a. Small interfering RNA-mediated RKIP knockdown revealed similar effects as that of ectopic miR-27a expression, while overexpression of RKIP attenuated the function of miR-27a in lung adenocarcinoma cells. Increased miR-27a expression was also detected in tumor tissues sampled from lung adenocarcinoma patients treated with cisplatin-based chemotherapy and was proved to be correlated with low expression of RKIP, decreased sensitivity to cisplatin, and poor prognosis. Conclusion: Our results suggest that up-regulation of miR-27a could suppress RKIP expression and in turn contribute to chemoresistance of lung adenocarcinoma cells to cisplatin. © 2014 Li et al.; licensee BioMed Central Ltd. Source

Hu J.,Yinzhou Peoples Hospital
Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery | Year: 2011

To explore a simple and accurate method for localization of upper airway obstruction in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and provide instructions for surgical treatment. Fifty OSAHS patients confirmed by PSG underwent acoustic rhinometric and pharyngometric assessment by Eccovision. The parameters were recorded, including nasal minimal cross-sectional area (NMCA), distance of MCA from the nostril (DCAN), minimum cross-sectional area at the nasal valve(MCA), nasal resistance (NR) and nasal volume from 0 to 6 cm from the nostril (NCV), as well as pharyngeal cross-sectional area (CSA) and volume from 4.8 to 15.0 cm. The sensitivity and specificity of acoustic rhinometry and pharyngometry on localization of airway obstruction was determined by a comprehensive imaging and endoscopic study. In 50 cases with severe OSAHS, NMCA, DCAN, MCA, NCV, NR were (0.61 +/- 0.35) cm2, (2.06 +/- 0.12) cm, (0.87 +/- 0.12) cm2, (9.24 +/- 2.31)cm3 and (0.51 +/- 0.32)kPa/(L x min), respectively. Pharyngeal CSA and volume were statistically significantly lower than that in control group (P < 0.01). The value of DCAN was (2.06 +/- 0.12) cm, (9.50 +/- 4.08) cm, (13.10 +/- 2.52) cm in type I II, III patient, respectively. Compared with the control group, the difference was statistically significant. Acoustic rhinometry and pharyngometry is a simple and safe method in localization of airway obstruction in patients with OSAHS. Source

Xu X.,Zhejiang University | Wang L.,Zhejiang University | Xu C.,Zhejiang Chinese Medical University | Zhang P.,Shaoxing University | And 4 more authors.
Coronary Artery Disease | Year: 2013

OBJECTIVES: Matrix metalloproteinases (MMPs) are a group of endopeptidases involved in the pathogenesis of atherosclerosis, and MMP gene polymorphisms may contribute toward the risk of coronary heart disease. Within this context, our aim was to examine whether MMP1, MMP3, and MMP9 gene polymorphisms are associated with susceptibility to acute coronary syndrome (ACS) or angiographic coronary artery disease (CAD). METHODS: The MMP1 -519 A/G, MMP3 -1171 5A/6A, and MMP9 -1562 C/T polymorphisms were evaluated in 1574 individuals. Genotypes of patients with ACS (n=660) and angiographically defined CAD (n=382) were compared with ACS-free (n=914) and non-CAD controls (n=466). RESULTS: The MMP3 5A allele occurred at a higher frequency in patients with ACS than in ACS-free individuals (P=0.001). Logistic regression analysis showed that the 5A/5A genotype of MMP3 was associated with a significantly increased risk of ACS [adjusted odds ratio (OR)=2.297, 95% confidence interval (CI)=1.105-4.775, P=0.026, 5A/5A vs. 6A/6A]. The CT and TT variant genotypes of MMP9 were associated with the occurrence of CAD (adjusted OR=1.425, 95% CI=1.045-1.943, P=0.025, CT+TT vs. CC). None of the MMP1 -519 A/G polymorphisms was associated with ACS or CAD. Because of linkage disequilibrium, MMP1 and MMP3 polymorphisms were combined on chromosome 11q22.3, and the 5A-1171-G-519 haplotype had a genetic risk factor for ACS (OR=1.505, 95% CI=1.219-1.857, P=0.00013), whereas the 6A-1171-G-519 haplotype had a decreased risk of ACS (OR=0.815, 95% CI=0.677-0.981, P=0.03). CONCLUSION: Taken together, the present findings indicate that genetic variations in MMP3 and MMP9 genes may be useful genetic markers for determining susceptibility to CAD in the Chinese Han population. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source

Recent studies have implied that miRNAs act as crucial modulators for epithelial-to-mesenchymal transition (EMT). We found that miR-134 expression correlated with invasive potential and EMT phenotype of NSCLC cells. Functional assays demonstrated that miR-134 inhibited EMT in NSCLC cells. In addition, we showed that Forkhead Box M1 (FOXM1) is a direct target of miR-134. Knockdown of FOXM1 reversed EMT resembling that of miR-134 overexpression. We further found that FOXM1 was involved in TGF-β1-induced EMT in A549 cells. These findings suggest that miR-134 acts as a novel EMT suppressor in NSCLC cells. © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. Source

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