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Li, Shi-Lai,Su, Ming,Peng, Tao,Xiao, Kai-Yin,Shang, Li-Ming,Xu, Bang-Hao,Su, Zhi-Xiong,Ye, Xin-Ping,Peng, Ning,Qin, Quan-Lin,Chen, De-Feng,Chen, Jie,Li, Le-Qun Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.1
Background: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and the outcomes for patients are still poor. It is important to determine the original type of synchronous multinodular HCC for preoperative assessment and the choice of treatment therapy as well as for the prediction of prognosis after treatment. Aims: To analyze clinicopathologic characteristics and prognoses in patients with multicentric occurrence (MO) and intrahepatic metastasis (IM) of synchronous multinodular hepatocellular carcinoma (HCC). Methods: The study group comprised 42 multinodular HCC patients with a total of 112 nodules. The control group comprised 20 HCC patients with 16 single nodular HCC cases and 4 HCC cases with a portal vein tumor emboli. The mitochondrial DNA (mtDNA) D-loop region was sequenced, and the patients of the study group were categorized as MO or IM based on the sequence variations. Univariate and multivariate analyses were used to determine the important clinicopathologic characteristics in the two groups. Results: In the study group, 20 cases were categorized as MO, and 22 as IM, whereas all 20 cases in the control group were characterized as IM. Several factors significantly differed between the IM and MO patients, including hepatitis B e antigen (HBeAg), cumulative tumor size, tumor nodule location, cirrhosis, portal vein and/or microvascular tumor embolus and the histological grade of the primary nodule. Multivariate analysis further demonstrated that cirrhosis and portal vein and/or microvascular tumor thrombus were independent factors differentiating between IM and MO patients. The tumor-free survival time of the MO subjects was significantly longer than that of the IM subjects ($25.7{\pm}4.8$ months vs. $8.9{\pm}3.1$ months, p=0.017). Similarly, the overall survival time of the MO subjects was longer ($31.6{\pm}5.3$ months vs. $15.4{\pm}3.4$ months, p=0.024). The multivariate analysis further demonstrated that the original type (p=0.035) and Child-Pugh grade (p<0.001) were independent predictors of tumor-free survival time. Cirrhosis (p=0.011), original type (p=0.034) and Child-Pugh grade (p<0.001) were independent predictors of overall survival time. Conclusions: HBeAg, cumulative tumor size, tumor nodule location, cirrhosis, portal vein and/or microvascular tumor embolus and histological grade of the primary nodule are important factors for differentiating IM and MO. MO HCC patients might have a favorable outcome compared with IM patients.
Qin, Li-Li,Wang, Qin-Rong,Wang, Qian,Yao, Hong,Wen, Li-Jun,Wu, Li-Li,Ping, Na-Na,Xie, Jun-Dan,Chen, Mei-Yu,Chen, Su-Ning Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.12
The diagnosis of latent Mycobacterium tuberculosis infection (LTBI) is recommended in hematological malignancy patients and before hematopoietic stem cell transplantation (Guidelines for the prevention and management of infectious complications of solid organ transplantation, 2004). Compared to traditional methods such as tuberculin skin test (TST), T-SPOT.TB has been shown to be more specific. In the present study we enrolled 536 patients for whom T-SPOT.TB was performed, among which 295 patients also received the TST test. The agreement (79%) between T-SPOT.TB and TST was poor (x=0.274, P<0.001). The patients with positive T-SPOT.TB results numbered 62 (11.6%), in which only 20 (48.8%) of the 41 receiving the TST test had positive results. A majority of the patients with T-SPOT.TB positive results had some other evidence ofTB, such as TB history, clinical symptoms and an abnormal chest CT scan. Active TB was found in 9 patients, in which 2 had negative TST results. We followed up the patients and no one developed active TB. Our study suggested that the T-SPOT.TB may be more useful for screening LTBI and active TB in hematological malignancy patients and hematopoietic stem cell transplant recipients than the TST test.
Cordblood-Based High-Throughput Screening for Deafness Gene of 646 Newborns in Jinan Area of China
Shou-Xia Li,Ding-Li Chen,Su-Bin Zhao,Li-Li Guo,Hai-Qin Feng,Xiao-Fang Zhang,Li-Li Ping,Zhi-Ming Yang,Cai-Xia Sun,Gen-Dong Yao 대한이비인후과학회 2015 Clinical and Experimental Otorhinolaryngology Vol.8 No.3
Objectives. Infants with slight/mild or late-onset hearing impairment might be missed in universal newborn hearing screening (UNHS). We identified the mutation hot spot of common deaf gene in the newborns in Jinan area population by screening the mutation spot with neonate cord blood, in order to make clear whether the neonate cord blood for screening is feasible. Methods. Six hundred and forty-six newborns were subjected to both UNHS and genetic screening for deafness by using neonate cord blood. The newborn genetic screening targeted four deafness-associated genes, which were commonly found in the Chinese population including gap junction beta-2 protein (GJB2), gap junction beta-3 protein (GJB3), solute carrier family 26 member 4 (SLC26A4), and mtDNA 12S rRNA. The most common 20 spot mutations in 4 deaf genes were detected by MassARRAY iPLEX platform and mitochondrial 12S rRNA A1555G and C1494T mutations were sequenced using Sanger sequencing. Results. Among the 646 newborns, 635 cases passed the UNHS and the other 11 cases (1.7%) did not. Of the 11 failures, two cases were found to carry homozygous GJB2 p.R143W pathogenic mutation, one case was found to have heterozygous GJB2 235delC mutation, and another one case carried heterozygous GJB3 p.R180X pathogenic mutation. Six hundred and thirty-five babies passed the newborn hearing screening, in which 25 babies were identified to carry pathogenic mutations, including 12 heterozygotes (1.9%) for GJB2 235delC, eight heterozygotes (1.3%) for SLC26A4 IVS7-2A>G, one heterozygote (0.2%) for p.R409H, two homozygotes (0.3%) for m.1494C>T, and two homozygotes (0.3%) for m.1555A>G. Conclusion. Newborn genetic screening through the umbilical cord blood for common deafness-associated mutations may identify carriers sensitive to aminoglycoside antibiotic, and can effectively prevent or delay hearing loss occurs.
Zhang, Yan-Li,Li, Qing,Yang, Xiao-Mei,Fang, Fang,Li, Jun,Wang, Ya-Hui,Yang, Qin,Zhu, Lei,Nie, Hui-Zhen,Zhang, Xue-Li,Feng, Ming-Xuan,Jiang, Shu-Heng,Tian, Guang-Ang,Hu, Li-Peng,Lee, Ho-Young,Lee, Su-J American Association for Cancer Research 2018 Cancer research Vol.78 No.9
<P>Matricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signaling events to perform dual functions in HCC microenvironment.</P><P>Tumor-associated macrophages (TAM) represent key regulators of the complex interplay between cancer and the immune microenvironment. Matricellular protein SPON2 is essential for recruiting lymphocytes and initiating immune responses. Recent studies have shown that SPON2 has complicated roles in cell migration and tumor progression. Here we report that, in the tumor microenvironment of hepatocellular carcinoma (HCC), SPON2 not only promotes infiltration of M1-like macrophages but also inhibits tumor metastasis. SPON2-α4β1 integrin signaling activated RhoA and Rac1, increased F-actin reorganization, and promoted M1-like macrophage recruitment. F-Actin accumulation also activated the Hippo pathway by suppressing LATS1 phosphorylation, promoting YAP nuclear translocation, and initiating downstream gene expression. However, SPON2-α5β1 integrin signaling inactivated RhoA and prevented F-actin assembly, thereby inhibiting HCC cell migration; the Hippo pathway was not noticeably involved in SPON2-mediated HCC cell migration. In HCC patients, SPON2 levels correlated positively with prognosis. Overall, our findings provide evidence that SPON2 is a critical factor in mediating the immune response against tumor cell growth and migration in HCC.</P><P><B>Significance:</B> Matricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signaling events to perform dual functions in HCC microenvironment.</P><P><B>Graphical Abstract:</B> http://cancerres.aacrjournals.org/content/canres/78/9/2305/F1.large.jpg. <I>Cancer Res; 78(9); 2305–17. ©2018 AACR</I>.</P><P><B>Graphical Abstract</B></P><P> [Figure]</P>
Association of Urinary Cesium with Breast Cancer Risk
Qin, Ya-Chao,Tang, Lu-Ying,Su, Yi,Chen, Li-Juan,Su, Feng-Xi,Lin, Ying,Zhang, Ai-Hua,Ren, Ze-Fang Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.22
Background: The aim of this study is to examine the association of urinary cesium with breast cancer risk. Materials and Methods: We collected survey data and urine specimens from 240 women with incident invasive breast cancer before their treatment and 246 age-matched female controls between October 2009 and July 2010. Urinary concentrations of cesium were determined by inductively coupled plasma mass spectrometry. Interviews were conducted by face-to-face to obtain information on potential breast cancer risk factors. Logistic regression analysis was used to estimate the associations. Results: Creatinine-adjusted levels [median ($25^{th}$, $75^{th}$) ug/g] of cesium in cases and controls were 17.6 (13.1, 24.0) and 19.3 (15.3, 25.7), respectively. After adjustment for potential risk factors, women in the second and highest tertile of cesium showed a decreased risk of breast cancer in a dose-dependent manner as compared with those in the lowest tertile [ORs and 95% CIs: 0.75 (0.46-1.22) and 0.50 (0.30-0.82), respectively]. This decrease was more evident in women with ER positive or localized clinical stage in an exploratory stratification analysis. Conclusions: These findings suggest that cesium may have anticancer efficacy and urinary cesium has potential as a biomarker for breast cancer risk assessment.
Su, Yuhong,Xiong, Yuanzhu,Zhang, Qin,Liu, Weimin,Jiang, Siwen,Yu, Li,Xia, Xuanyan,Zeng, Rong,Deng, Changyan Asian Australasian Association of Animal Productio 2002 Animal Bioscience Vol.15 No.10
In aiming to identify the genes or genetic regions responsible for quantitative traits, a swine reference population had been constructed using three Large White boars and seven Meishan dams as parents. Five $F_1$ males and 23 $F_1$ females were intercrossed to generate 147 $F_2$ offspring. Thirty-one microsatellite markers covering Sus scrofa chromosomes (SSC) 2, 4, 6 and 7 were genotyped for all members. Construction of genetic microsatellite maps was performed using the CRIMAP software package. The lengths of these chromosomes were longer than MARC maps. They were 158.6cM, 180.3cM, 197.3cM and 171.4cM, respectively. A two modified orders of markers were observed for SSC6 and SSC7. The female map on SSC6 was shorter than male map, and the contrary was on SSC 2, 4 and 7.
Improvement of Resistive Switching Uniformity in TiO_x Film by Nitrogen Annealing
Yingtao Li,Yan Wang,Su Liu,Shibing Long,Hangbing Lv,Qin Wang,Sen Zhang,Ming Liu 한국물리학회 2011 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.58 No.3
The uniformity of resistive switching parameters is important to resistive random access memory (RRAM) device development. This work reports a remarkably improved uniformity of resistive switching parameters in atomic-layer-deposited titanium-oxide films. The broad variations of the resistive switching parameters in the as-deposited TiOx films can be improved by nitrogen annealing. Based on the results of the X-ray photoelectron spectroscopy (XPS) depth profile, the improved uniformity of resistive switching in the nitrogen-annealed TiO_x films may result from the higher density of oxygen vacancies in TiO_x films due to nitrogen annealing.
The Effects of Ginsenoside Rb1 on JNK in Oxidative Injury in Cardiomyocytes
Chun-Su Yuan,Jing Li,Zuo-Hui Shao,Jing-Tian Xie,Chong-Zhi Wang,Srinivasan Ramachandran,Jun-Jie Yin,Han Aung,Chang-Qing Li,Gina Qin,Terry Vanden Hoek 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.7
Reactive oxygen species (ROS) can induce oxidative injury via iron interactions (i.e. Fenton chemistry and hydroxyl radical formation). Our prior work suggested that American ginseng berry extract and ginsenoside Re were highly cardioprotective against oxidant stress. To extend this study, we evaluated the protective effect of protopanaxadiol-type ginsenoside Rb1 (gRb1)on H2O2-induced oxidative injury in cardiomyocytes and explored the ROS-mediated intracellular signaling mechanism. Cultured embryonic chick cardiomyocytes (4-5 day) were used. Cell death was assessed by propidium iodide and lactate dehydrogenase release. Pretreatment with gRb1 (0.01, 0.1, or 1 μM) for 2 h and concurrent treatment with H2O2 (0.5 mM) for 2 h resulted in a dose-dependent reduction of cell death, 36.6 ± 2.9% (n = 12, p < 0.05), 30.5 ± 5.1% (n = 12, p < 0.05) and 28.6 ± 3.1% (n = 12, p < 0.01) respectively, compared to H2O2-exposed cells (48.2 ± 3.3%, n = 12). This cardioprotective effect of gRb1 was associated with attenuated intracellular ROS generation as measured by 6-carboxy-2’, 7’-dichlorodihydrofluorescein diacetate, preserved the mitochondrial membrane potential as determined using JC-1. In the ESR study, gRb1 exhibited the scavenging DPPH and hydroxyl radical activities. Furthermore, our data showed the increased JNK phosphorylation (p-JNK) in H2O2-exposed cells was suppressed by the pretreatment with gRb 1 (1 μM) (p < 0.01). Co-treatment of gRb1 with a specific inhibitor of JNK SP600125 (10 μM) further reduced the p-JNK and enhanced the cell survival after H2O2exposure. Collectively, our results suggest that gRb1 conferred cardioprotection that was mediated via attenuating ROS and suppressing ROS-induced JNK activation.