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Saliva Supernatant miR-21: a Novel Potential Biomarker for Esophageal Cancer Detection
Xie, Zi-Jun,Chen, Gang,Zhang, Xu-Chao,Li, Dong-Feng,Huang, Jian,Li, Zi-Jun Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.12
Objective: To identify whether saliva supernatant miR-21 can serve as a novel potential biomarker in patients with esophageal cancer (EC). Methods: 32 patients with EC and 16 healthy controls were recruited in this study. Total RNA was extracted from saliva supernatant samples for measurement of miR-21 levels using RT-qPCR and relationships between miR-21 levels and clinical characteristics of EC patients were analyzed. Results: miR-21 was significantly higher in the EC than control groups. The sensitivity and specificity were 84.4% and 62.5% respectively. Supernatant miR-21 levels showed no significant correlation with cancer stage, differentiation and nodal metastasis. Conclusions: Saliva supernatant miR-21 may be a novel biomarker for EC.
Properties of an AlGaN/AlN Distributed-Bragg-reflector Structure
Li-Li Zhang,Zhan-Hui Liu,Xiao-Gu Huang,Qing-Fang Li,Rong Zhang,Zi-Li Xie,Xiang-Qian Xiu 한국물리학회 2014 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.65 No.7
An AlGaN/AlN distributed-Bragg-reflector (DBR) structure with a high Al content was grown byusing plasma-assisted molecular beam epitaxy (PA-MBE). The properties of the sample were characterizedby using the transmission electron microscopy, high-resolution X-ray diffraction, atomicforce microscopy, and reflectivity spectrum measurements. The reciprocal space mapping analysisindicated that the strain in the AlGaN layers was partially relaxed. The morphology of the DBRexhibited a surface covered by grains (average size of about 130 nm), and the surface roughness wasabout 2 nm. The spectral measurements showed that the DBR structure presented a peak reflectivityof 68.8% at the center wavelength of 247 nm, which indicated that this DBR structure couldwork in the deep solar-blind UV region with acceptable reflectivity. However, the optical propertiesof the DBR structure were deteriorated by the fluctuation of the Al composition, non-uniformity ofthe layer thickness, the blurry, rough interface in the DBR structure, and so on.
Properties of a CdZnO/ZnO Multiple Quantum-Well Light-Emitting Diode
Zhan-Hui Liu,Li-Li Zhang,Qing-Fang Li,Rong Zhang,Zi-Li Xie,Xiang-Qian Xiu,Bin Liu 한국물리학회 2016 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.69 No.7
A CdZnO/ZnO multiple quantum-well light-emitting diode (LED) structure was successfully grown by using plasma-assisted molecular beam epitaxy on a p-GaN template that had been grown by using metal-organic chemical-vapor deposition on a c-sapphire substrate. The properties of the sample were characterized by using high-resolution X-ray diffraction, transmission electron microscopy, and temperature-dependent photoluminescence measurements. The light output performance of the CdZnO/ZnO QW LED device was also investigated in detail by using I-V and electroluminescence spectral measurements. The characterization showed that our CdZnO/ZnO QW LED structure had good crystalline quality and weaker carrier localization. Owing to the heterojunction structure, the I-V curve indicated that the LED device had a higher turn-on voltage and series resistance. The EL measurement demonstrated that for our LED device’s optoelectronic characteristic, the carrier-screening effect played the dominant role in the emission-energy blue-shift mechanism, and the broadening of the emission energy width was mainly ascribed to the band-filling effect. Without a special heat sinking, the L-I curve exhibited slight efficiency droop after 30 mA.
Association between Pax8-PPARγ1 Rearrangement and Follicular Thyroid Cancer: a Meta-Analysis
Li, Hang-Yu,Xie, Zhi-Hao,Xu, Cong-Hui,Pu, Mei-Ling,Chen, Zi-Yan,Yu, Miao,Wang, Heng-Shu,Zhou, Chen-Ming,Pu, Chao-Yu,Liu, Wei Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.9
Background: Pax8 and peroxisome proliferator-activated receptor gamma 1 gene (Pax8-$PPAR{\gamma}1$) are important factors in tumors. Several studies have suggested that follicular thyroid cancer may arise from Pax8- $PPAR{\gamma}1$ rearrangement. In order to have a better understanding of the association between Pax8-$PPAR{\gamma}1$ rearrangement and follicular thyroid cancer, we conducted the presenmt meta-analysis. Materials and Methods: The information was extracted from PubMed, EMBASE and Web of Science. Statistic analysis was performed with Stata12.0 software. Odds ratios (ORs) were calculated using a fixed-effects model. We also performed heterogeneity and publication bias analyses. Results: Nine studies including 198 follicular thyroid cancer patients and 268 controls were considered eligible. The frequency of Pax8-$PPAR{\gamma}1$ rearrangement was significantly higher in the follicular thyroid cancer group than in the control group, with a pooled OR of 6.63 (95%CI=3.50-12.7). In addition, through subgroup analysis, the OR between Pax8-$PPAR{\gamma}1$ rearrangement and follicular thyroid cancer was 6.04 (95%CI = 3.18-11.5) when using benign tumor tissues as controls. The OR for the method subgroup was 9.99 (95% CI =4.86-20.5) in the RT-PCR. Conclusions: The final results demonstrated that Pax8-$PPAR{\gamma}1$ rearrangement has significant association with follicular thyroid cancer.
Li, Jie,Yang, Chun-Xu,Mei, Zi-Jie,Chen, Jing,Zhang, Shi-Min,Sun, Shao-Xing,Zhou, Fu-Xiang,Zhou, Yun-Feng,Xie, Cong-Hua Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10
Cancer patients often suffer from local tumor recurrence after radiation therapy. Cell cycling, an intricate sequence of events which guarantees high genomic fidelity, has been suggested to affect DNA damage responses and eventual radioresistant characteristics of cancer cells. Here, we established a radioresistant lung cancer cell line, A549R, by exposing the parental A549 cells to repeated ${\gamma}$-ray irradiation with a total dose of 60 Gy. The radiosensitivity of A549 and A549R was confirmed using colony formation assays. We then focused on examination of the cell cycle distribution between A549 and A549R and found that the proportion of cells in the radioresistant S phase increased, whereas that in the radiosensitive G1 phase decreased. When A549 and A549R cells were exposed to 4 Gy irradiation the total differences in cell cycle redistribution suggested that G2-M cell cycle arrest plays a predominant role in mediating radioresistance. In order to further explore the possible mechanisms behind the cell cycle related radioresistance, we examined the expression of Cdc25 proteins which orchestrate cell cycle transitions. The results showed that expression of Cdc25c increased accompanied by the decrease of Cdc25a and we proposed that the quantity of Cdc25c, rather than activated Cdc25c or Cdc25a, determines the radioresistance of cells.
Xi-sheng Xie,Fei-yan Li,Heng-chuan Liu,Yao Deng,Zi Li,Jun-ming Fan 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.2
The effects of LSKL, the peptide antagonist of thrombospondin-1 (TSP-1), on renal interstitial fibrosis in rats subjected to unilateral ureteral obstruction (UUO) were investigated. Rats were divided randomly into three groups (n = 20 each): UUO group, sham-operation group and UUO plus LSKL treatment group. Collagen deposition was studied using histopathology and reverse transcription polymerase chain reaction analysis (RT-PCR). TSP-1, transforming growth factor beta 1 (TGF-β1), phosphorylated Smad2 (pSsmad2) and α-smooth muscle actin (α-SMA) in the kidney were measured using immunocytochemistry, western blotting analysis, RT-PCR and enzyme-linked immunosorbent assay. Biochemical analyses in the serum and urine were made. Histopathology showed severe tubular dilatation and atrophy, interstitial inflammation and collagen accumulation after surgery and LSKL significantly inhibited interstitial fibrosis including tubular injury as well as collagen deposition. The protein and mRNA levels of TSP-1 increased notably at different time point and significantly decreased in the presence of LSKL. The expression of TGF-β1 and pSmad2 were upregulated in the obstructed kidney and substantially suppressed by LSKL treatment. Myofibroblast accumulation could be alleviated after administration of LSKL. Biochemical parameters did not show differences among the three groups. As TSP-1 is the major activator of TGF-β1, we demonstrate that LSKL can attenuate renal interstitial fibrosis in vivo by preventing TSP-1-mediated TGF-β1 activation.
Qian Ding,Xiao-Li Xie,Miao-Miao Wang,Jie Yin,Jin-Mei Tian,Xiao-Yu Jiang,Di Zhang,Jing Han,Yun Bai,Zi-Jin Cui,Hui-Qing Jiang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
The clearance of activated hepatic stellate cells (HSCs) by apoptosis is critical for the reversibility of hepatic fibrosis. Mitochondrial homeostasis is regulated by mitophagy, which is an efficient way of clearing injured mitochondria that plays an important role in apoptosis. However, the role of mitophagy in apoptosis in HSCs and hepatic fibrosis is still unclear. Here, we show that mitophagy is enhanced in parallel with increased apoptosis in hepatic stellate cells during the reversal of hepatic fibrosis. The inhibition of mitophagy suppressed apoptosis in HSCs and aggravated hepatic fibrosis in mice. In contrast, the activation of mitophagy induced apoptosis in HSCs. Furthermore, we confirmed that BCL-B, which is a member of the BCL-2 family, is a regulator mediating mitophagy-related apoptosis. The knockdown of BCL-B resulted in increased apoptosis and mitophagy in HSCs, while the overexpression of BCL-B caused the opposite effects. BCL-B inhibited the phosphorylation of Parkin (a key regulator of mitophagy) and directly bound phospho-Parkin. Altogether, enhanced mitophagy promotes apoptosis in HSCs during the reversal of hepatic fibrosis. BCL-B suppresses mitophagy in HSCs by binding and suppressing phospho-Parkin, thereby inhibiting apoptosis. BCLB- dependent mitophagy is a new pathway for the regulation of apoptosis in HSCs during the regression of hepatic fibrosis