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Bi, Jian,Kuesten, Carla,Lee, Hye-Seong,O'Mahony, Michael Elsevier 2018 Food quality and preference Vol.63 No.-
<P><B>Abstract</B></P> <P>This paper proposes a new type of sensory discrimination methods, i.e., paired versions of various sensory discrimination forced-choice methods, which can be regarded as modified versions of the same-different method. The new type of methods possesses the advantage of the same-different test for measuring overall sensory difference, but overcomes its weaknesses of large variations of response bias and lower testing power. An important finding is that this type of methods is closely related to the <I>same-different</I> area theorem and its extension. The <I>same-different</I> area theorem establishes an equivalence between the area under the receiver operating characteristic (ROC) curve of the same-different method and the proportion of correct responses (<I>P<SUB>c</SUB> </I>) in the dual-pair method. This paper re-demonstrates and extends the <I>same-different</I> area theorem. An analytical expression of a general psychometric function for the new type of methods is derived. Performances of the new type of methods are evaluated with testing power and sample size in both difference and similarity/equivalence tests. R codes are provided for the new type of methods for <I>P<SUB>c</SUB> </I>, Thurstonian discriminal distance δ, and variance of <I>d′</I>, where <I>d′</I> is an estimator of δ.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Paired versions of various forced-choice sensory discrimination methods are proposed. </LI> <LI> The same-different area theorem is re-demonstrated and extended. </LI> <LI> A general psychometric function for the paired versions is derived. </LI> <LI> Performances of the paired versions are evaluated. </LI> <LI> R codes of Pc, δ, and variance of <I>d'</I> for the paired versions are provided. </LI> </UL> </P>
Metastasis associated genomic aberrations in stage II rectal cancer
Hong Zhao,Zhi-Zhou Shi,Rui Jiang,Dong-Bing Zhao,Hai-Tao Zhou,Jian-Wei Liang,Xin-Yu Bi,Jian-Jun Zhao,Zhi-Yu Li,Jian-Guo Zhou,Zhen Huang,Ye-Fan Zhang,Jian Wang,Xin Xu,Yan Cai,Ming-Rong Wang,Yu Zhang 한국유전학회 2016 Genes & Genomics Vol.38 No.11
Genomic aberrations of rectal carcinoma, especially DNA copy number changes associated with metastasis were largely unclear. We aim to identify the metastasis associated biomarkers in stage II rectal cancer. Formalin-fixed, paraffin-embedded primary tumor tissues of stage II rectal carcinoma were analyzed by array-based comparative genomic hybridization, and genomic aberrations were identified by Genomic Workbench and SAM software. Copy number changes and mRNA expressions were validated by Real-time PCR in an independent rectal cancer samples. The results showed that the most frequent gains in stage II rectal cancer were at 1q21.2-q23.1, 3p21.31, 11q12.2-q23.3, 12q24.11-q24.31, 12q13.11-q14.1 and losses in 18q11.2-q23, 17q21.33-q22, 13q31.1-q31.3, 21q21.1-q21.3, 8p23.3-p23.1 and 4q22.1-q23. Twenty-two amplifications and five homozygous deletions were also identified. We further found that S100A1 (1q21.3-q23.1), MCM7 (7q22.1) and JUND (19p13.11) were amplified and overexpressed in stage II rectal cancer. Interestingly, the genomic aberrations affected 14 signaling pathways including VEGF signaling pathway and fatty acid metabolism. Most importantly, loss of 13q31.1-q34 and gain of 1q44 were associated with distant metastasis. Our results indicated that these metastasis associated genomic changes may be useful to reveal the pathogenesis of rectal cancer metastasis and identify candidate biomarkers.
endothelial progenitor cells via regulation of the AKT signaling pathway
Jian Zhang,Thi Hong Van Le,Vinoth Kumar Rethineswaran,Yeon-Ju Kim,Woong Bi Jang,Seung Taek Ji,Thanh Truong Giang Ly,Jong Seong Ha,Jisoo Yun,Jae Hun Cheong,Jinsup Jung,Sang-Mo Kwon 대한생리학회-대한약리학회 2021 The Korean Journal of Physiology & Pharmacology Vol.25 No.5
Cardiovascular disease (CVD) and its complications are the leading cause of morbidity and mortality in the world. Because of the side effects and incomplete recovery from current therapy, stem cell therapy emerges as a potential therapy for CVD treatment, and endothelial progenitor cell (EPC) is one of the key stem cells used for therapeutic applications. The effect of this therapy required the expansion of EPC function. To enhance the EPC activation, proliferation, and angiogenesis using dronedarone hydrochloride (DH) is the purpose of this study. DH received approval for atrial fibrillation treatment and its cardiovascular protective effects were already reported. In this study, DH significantly increased EPC proliferation, tube formation, migration, and maintained EPCs surface marker expression. In addition, DH treatment up-regulated the phosphorylation of AKT and reduced the reactive oxygen species production. In summary, the cell priming by DH considerably improved the functional activity of EPCs, and the use of which might be a novel strategy for CVD treatment.
Bi-wen Lin,Ze-long Jiao,Jian-feng Fan,Liang Peng,Lei Li,Zi-gang Zhao,Xiang-yu Ding,이형진 대한의학회 2013 Journal of Korean medical science Vol.28 No.6
The acquisition of metastasis potential is a critical point for malignant tumors. Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) is a potential tumor suppress gene and frequently down-regulated in malignant tumors. It has been implicated that overexpression of MDA-7 led to proliferation inhibition in many types of human tumor. Invasion is an important process which is potential to promote tumor metastasis. However, the role and potential molecular mechanism of mda-7/IL-24 to inhibit the invasion of human melanoma cancer is not fully clear. In this report, we identified a solid role for mda-7/IL-24 in invasion inhibition of human melanoma cancer LiBr cells, including decreasing of adhesion and invasion in vitro, blocking cell cycle, down-regulating the expression of ICAM-1, MMP-2/9, CDK1, the phosphorylation of ERK and Akt, NF-κB and AP-1 transcription activity. Meanwhile, there was an increased expression of PTEN in mda-7/IL-24 over-expression LiBr cells. Our results demonstrated that mda-7/IL-24 is a potential invasion suppress gene, which inhibits the invasion of LiBr cells by the down-regulation of ICAM-1, MMP-2/9, PTEN, and CDK1 expression. The molecular pathways involved were the MAPK/ERK, PI3K-Akt, NF-κB, and AP-1. These findings suggest that mda-7/IL-24 may be used as a possible therapeutic strategy for human melanoma cancer.
Impact of Chemotherapy-Related Hyperglycemia on Prognosis of Child Acute Lymphocytic Leukemia
Zhang, Bi-Hong,Wang, Jian,Xue, Hong-Man,Chen, Chun Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.20
Purpose: To investigate the impact of hyperglycemia during inductive treatment on the prognosis of acute lymphocytic leukemia (ALL) in children. Materials and Methods: Clinical data of 159 ALL childhood cases were reviewed. The patients were divided into the hyperglycemia group (fasting $glucose{\geq}126mg/dl$ and/or random blood $glucose{\geq}200mg/dl$) and the euglycemia group according to the blood glucose values. The X2 test was performed to compare the complete remission rates of the two groups, and Kaplan-Meier and log-rank tests were performed to compare the 5-year overall and relapse-free survival. Results: The incidence of hyperglycemia in the $age{\geq}10-year-old$ group was higher than the younger-age group (P=0.009). Values in the interim- and high-risk groups were higher than the standard-risk group (P=0.028), while there was no significant difference between genders (P=0.056). The complete remission rates of the 2 groups demonstrated no significant difference (P=0.134), while the 5-year OS of the hyperglycemia group was lower than in the euglycemia group ($83.8{\pm}6.0%$ vs $94.9{\pm}2.4%$, P=0.014). The 5 -year RFS was significantly lower than the euglycemia group ($62.9{\pm}8.7%$) vs $80.2{\pm}9.1%$, P<0.001). Conclusions: Children with $age{\geq}10year$ old, and in the middle- and high-risk groups appear prone to complicating hyperglycemia during inductive chemotherapy, associated with lower 5-year OS and RFS.
Shang Jian,Liu Xiu,Bi Yanqing,Yan LiXia,Tian Cuiping,Guan Yu 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.1
Background Breast cancer is one of the solid tumors investigated for gene expression. Objective Our research aimed to investigate the roles of transmembrane protein 106C (TMEM106C) on breast cancer and the underlying mechanisms. Results The results from GEPIA website indicated that TMEM106C was up-regulated in breast cancer and the TMEM106C over-expression was concerned with poor outcomes in breast cancer patients. Moreover, western blotting and qRT-PCR assay also showed that TMEM106C level was up-regulated in breast cancer cells. Our results showed that over-expression of TMEM106C accelerated the malignant phenotypes of MCF7 cells, while TMEM106C silencing displayed the opposite outcomes in MDA-MB-231 cells. Furthermore, TMEM106C over-expression activated PI3K/AKT/mTOR signaling, which reversed by Wortmannin. Similarly, TMEM106C silencing inhibited PI3K/AKT/mTOR signaling, which abolished by 740YP. Moreover, we also confirmed that 740Y-P significantly reversed the function of TMEM106C silencing on the malignant phenotypes of MDA-MB-231 cells. Conclusion This study indicated that TMEM106C could promote the malignant phenotypes of breast cancer cells by activating PI3K/AKT/mTOR signaling.
Liu, Qian,Bi, Jian-Jun,Tian, Yan-Tao,Feng, Qiang,Zheng, Zhao-Xu,Wang, Zheng Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.4
Background: The optimal surgical strategy for the treatment of synchronous resectable gastric cancer liver metastases remains controversial. The aims of this study were to analyze the outcome and overall survival of patients presenting with gastric cancer and liver metastases treated by simultaneous resection. Materials and Methods: Between January 1990 and June 2009, 35 patients diagnosed with synchronous hepatic metastases from gastric carcinoma received simultaneous resection of both primary gastric cancer and synchronous hepatic metastases. The clinicopathologic features and the surgical results of the 35 patients were retrospectively analyzed. Results: The 5-year overall survival rate after surgery was 14.3%. Five patients survived for more than 5 years after surgery. No mortality has occurred within 30 days after resection, although two patients (5.7%) developed complications during the peri-operative course. Univariate analysis revealed that patients with the presence of lymphovascular invasion of the primary tumor, bilateral liver metastasis and multiple liver metastases suffered poor survival. Lymphovascular invasion by the primary lesion and multiple liver metastases were significant prognostic factors that influenced survival in the multivariate analysis (p=0.02, p=0.001, respectively). Conclusions: The presence of lymphovascular invasion of the primary tumor and multiple liver metastases are significant prognostic determinants of survival. Gastric cancer patients without lymphovascular invasion and with a solitary synchronous liver metastasis may be good candidates for hepatic resection. Simultaneous resection of both primary gastric cancer and synchronous hepatic metastases may effectively prolong survival in strictly selected patients.