Analysis of genetic diversity among indigenous landraces from sesame (Sesamum indicum L.) core collection in China as revealed by SRAP and SSR markers

Yan‐xin Zhang,Wei Hua,Lin‐han Wang,Zhuo Che,Xiu‐rong Zhang 한국유전학회 2010 Genes & Genomics Vol.32 No.3

The molecular genetic diversity of 404 indigenous landraces from sesame core collection in China were evaluated by 11SRAP and 3 SSR markers, 175 fragments were generated, of which 126 were polymorphic with an average polymorphism rate of 72%. Jaccard’s genetic similarity coefficients (GS=0.7130), Nei's gene diversity (h=0.2418) and Shannon's Information index (I=0.3847) were calculated, a dendrogram of the 404 landraces was made, landraces from various zones were distributed throughout the dendrogram, accessions from different agro‐ecological zones were indistinguishable by cluster analysis, geographical separation did not generally result in greater genetic distance, a similar pattern was obtained using principal coordinates (PCO) analysis. As to seven agro‐ecological zones, the maximum Nei’s gene diversity (h = 0.2613)and Shannon index (I = 0.3980) values in zone VII indicated that they were genetically more diverse than those in other zones, while the least genetically diverse region was zone III (h = 0.1772, I = 0.2858). Nei's genetic identity and genetic distance among landraces from seven agro‐ecological zones were also analyzed, the genetic relationship of seven zones was inferred using the UPGMA method. This study demonstrated that SRAP and SSR markers were appropriate for evaluation of sesame genetic diversities. There existed extensive genetic diverse among indigenous landraces and the abundance of genetic diversity of landraces in different agro‐ecological zones was various. Understanding of these characteristics of indigenous landraces in China can provide theoretical foundation for further collection, effective protection and reasonable utilization of these sesame landraces in breeding.

Implementation of online model updating with ANN method in substructure pseudo-dynamic hybrid simulation

Yan Hua Wang,Jing Lv,Yan Feng,Bo Wen Dai,Cheng Wang,Jing Wu,Zi Yan Chen 국제구조공학회 2021 Smart Structures and Systems, An International Jou Vol.28 No.2

Substructure pseudo-dynamic hybrid simulation (SPDHS) is an advanced structural seismic testing method which combines physical experiment and numerical simulation. Generally, the key components which display nonlinearity first are taken as experimental substructures for actual test, and the remaining parts are modeled in simulation. Model updating techniques can be effectively applied to enhance the model precision of nonlinear numerical elements. Specifically, the constitutive model of the experimental substructure is identified online by the instantaneously-measured data, and the corresponding numerical elements with similar hysteretic behaviors are updated synchronously. Artificial neural network (ANN) can recognize the system which cannot be represented by definite numerical model, and thus avoids the structural response distortion caused by the inherent numerical model defects. In this study, a framework for online model updating in SPDHS with ANN method is expanded to implement actual test validation. Moreover, the effectiveness of ANN method is demonstrated by practical tests of a two-story frame model with bending dampers. Additionally, the unscented Kalman filter technique and offline ANN identification approach are both examined in the test validation. The experimental results show that, under the identical loading history, the online ANN method can significantly reduce the model errors and improve the accuracy of SPDHS.

Associations of Plasma Glucagon Levels with Estimated Glomerular Filtration Rate, Albuminuria and Diabetic Kidney Disease in Patients with Type 2 Diabetes Mellitus

Hua-Xing Huang,Liang-Lan Shen,Hai-Yan Huang,Li-Hua Zhao,Feng Xu,Dong-Mei Zhang,Xiu-Lin Zhang,Tong Chen,Xue-Qin Wang,Yan Xie,Jian-Bin Su 대한당뇨병학회 2021 Diabetes and Metabolism Journal Vol.45 No.6

Background: Type 2 diabetes mellitus (T2DM) is characterized by elevated fasting glucagon and impaired suppression of postprandial glucagon secretion, which may participate in diabetic complications. Therefore, we investigated the associations of plasma glucagon with estimated glomerular filtration rate (eGFR), albuminuria and diabetic kidney disease (DKD) in T2DM patients.Methods: Fasting glucagon and postchallenge glucagon (assessed by area under the glucagon curve [AUCgla]) levels were determined during oral glucose tolerance tests. Patients with an eGFR <60 mL/min/1.73 m2 and/or a urinary albumin-to-creatinine ratio (UACR) ≥30 mg/g who presented with diabetic retinopathy were identified as having DKD.Results: Of the 2,436 recruited patients, fasting glucagon was correlated with eGFR and UACR (r=–0.112 and r=0.157, respectively; P<0.001), and AUCgla was also correlated with eGFR and UACR (r=–0.267 and r=0.234, respectively; P<0.001). Moreover, 31.7% (n=771) presented with DKD; the prevalence of DKD was 27.3%, 27.6%, 32.5%, and 39.2% in the first (Q1), second (Q2), third (Q3), and fourth quartile (Q4) of fasting glucagon, respectively; and the corresponding prevalence for AUCgla was 25.9%, 22.7%, 33.7%, and 44.4%, respectively. Furthermore, after adjusting for other clinical covariates, the adjusted odds ratios (ORs; 95% confidence intervals) for DKD in Q2, Q3, and Q4 versus Q1 of fasting glucagon were 0.946 (0.697 to 1.284), 1.209 (0.895 to 1.634), and 1.521 (1.129 to 2.049), respectively; the corresponding ORs of AUCgla were 0.825 (0.611 to 1.114), 1.323 (0.989 to 1.769), and 2.066 (1.546 to 2.760), respectively. Additionally, when we restricted our analysis in patients with glycosylated hemoglobin <7.0% (n=471), we found fasting glucagon and AUCgla were still independently associated with DKD.Conclusion: Both increased fasting and postchallenge glucagon levels were independently associated with DKD in T2DM patients.

IL-11 promotes the treatment efficacy of hematopoietic stem cell transplant therapy in aplastic anemia model mice through a NF-κB/microRNA-204/thrombopoietin regulatory axis

Yan Wang,Zhi-yun Niu,Yu-jie Guo,Li-hua Wang,Feng-ru Lin,Jing-yu Zhang 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Hematopoietic stem cell (HSC) transplantation could be of therapeutic value for aplastic anemia (AA) patients, and immunosuppressants may facilitate the efficiency of the procedure. As anti-inflammatory cytokine interleukin-11 (IL-11) has a thrombopoietic effect, its use in cases of chronic bone marrow failure, such as AA, has been proposed to induce HSC function. However, the putative mechanisms that may support this process remain poorly defined. We found that decreased miR-204-5p levels were coincident with increased proliferation in mouse HSCs following exposure to IL-11 in vitro. Through inhibiting NF-кB activity, miR-204-5p repression was demonstrated to be a downstream effect of IL-11 signaling. miR-204-5p was shown to directly target thrombopoietin (TPO) via sequence-dependent 3′-UTR repression, indicating that this microRNA-dependent pathway could serve an essential role in supporting IL-11 functions in HSCs. Increased TPO expression in HSCs following IL-11 exposure could be mimicked or blocked by inhibiting or overexpressing miR-204-5p, respectively. Consistent with these in vitro findings, IL-11 promoted HSC engraftment in a mouse model of AA, an effect that was attenuated in cells overexpressing miR-204-5p. The reduction in miR-204-5p levels is an integral component of IL-11 signaling that may play an essential role in treating AA.

CEA, AFP, CA125, CA153 and CA199 in Malignant Pleural Effusions Predict the Cause

Wang, Xin-Feng,Wu, Yan-Hua,Wang, Mao-Shui,Wang, Yun-Shan Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.1

Determination of the cause of malignant pleural effusions is important for treatment and management, especially in cases of unknown primaries. There are limited biomarkers available for prediction of the cause of malignant pleural effusion in clinical practice. Hence, we evaluated pleural levels of five tumor biomarkers (CEA, AFP, CA125, CA153 and CA199) in predicting the cause of malignant pleural effusion in a retrospective study. Kruskal-Wallis or Mann-Whitney U tests were carried out to compare levels of tumor markers in pleural effusion among different forms of neoplasia - lung squamous cell carcinoma, adenocarcinoma, or small cell carcinoma, mesothelioma, breast cancer, lymphoma/leukemia and miscellaneous. Receiver operator characteristic analysis was performed to evaluate sensitivity and specificity of biomarkers. The Kruskal-Wallis test showed significant differences in levels of pleural effusion CEA (P<0.01), AFP (P<0.01), CA153 (P<0.01) and CA199 (P<0.01), but not CA125 (P>0.05), among the seven groups. Receiver operator characteristic analysis showed that, compared with other four tumor markers, CA153 was the best biomarker in diagnosing malignant pleural effusions of lung adenocarcinoma (area under curve (AUC): 0.838 (95%confidence interval: 0.787, 0.888); cut-off value: 10.2U/ml; sensitivity: 73.2% (64.4-80.8)%, specificity: 85.2% (77.8-90.8)%), lung squamous cell carcinoma (AUC: 0.716 (0.652, 0.780); cut-off value: 14.2U/ml; sensitivity: 57.6% (50.7-64.3)%, specificity: 91.2% (76.3-98.0)%), and small-cell lung cancer (AUC: 0.812 (0.740, 0.884); cut-off value: 9.7U/ml; sensitivity: 61.5% (55.0-67.8)%, specificity: 94.1% (71.2-99.0)%); CEA was the best biomarker in diagnosing MPEs of mesothelioma (AUC: 0.726 (0.593, 0.858); cut-off value: 1.43ng/ml; sensitivity: 83.7% (78.3-88.2)%, specificity: 61.1% (35.8-82.6)%) and lymphoma/leukemia (AUC: 0.923 (0.872, 0.974); cut-off value: 1.71ng/ml; sensitivity: 82.8% (77.4-87.3)%, specificity: 92.3% (63.9-98.7)%). Thus CA153 and CEA appear to be good biomarkers in diagnosing different causes of malignant pleural effusion. Our findings implied that the two tumor markers may improve the diagnosis and treatment for effusions of unknown primaries.

Effect of TLR4 and B7-H1 on Immune Escape of Urothelial Bladder Cancer and its Clinical Significance

Wang, Yong-Hua,Cao, Yan-Wei,Yang, Xue-Cheng,Niu, Hai-Tao,Sun, Li-Jiang,Wang, Xin-Sheng,Liu, Jing Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.3

Background/Aim: Toll-like receptor 4 (TLR4) and B7-H1, both normally expressed restricted to immune cells, are found to be aberrantly expressed in a majority of human tumors and may play important roles in regulation of tumor immunity. It has been shown that urothelial bladder cancer (UBC) patients can manifest tumoral immune escape which may be a potential critical factor in tumor pathogenesis and progression. However, so far, the mechanisms of UBC-related immune escape have not been clarified. The aim of this study was to investigate the effect of TLR4 and B7-H1 on immune escape of UBC. Methods: Bladder cancer T24 cells were pre-incubated with LPS and co-cultured with tumor specific CTLs. CTL cytotoxicity and apoptosis rates were measured by MTT assay and flow cytometry, respectively. The effects of an ERK inhibitor on B7-H1 expression and CTL cytotoxicity against T24 cells were also evaluated. In addition, TLR4, B7-H1 and PD-1 protein expression was analyzed by immunohistochemistry in 60 UBC specimens and 10 normal urothelia. Results: TLR4 activation protected T24 cells from CTL killing via B7-H1 overexpression. However PD98059, an inhibitor of ERK, enhanced CTL killing of T24 cells by reducing B7-H1 expression. TLR4 expression was generally decreased in UBC specimens, while B7-H1 and PD-1 were greatly overexpressed. Moreover, expression of both B7-H1 and PD-1 was significantly associated with UICC stage and WHO grade classification. Conclusions: TLR4 and B7-H1 may contribute to immune escape of UBC. Targeting B7-H1 or the ERK pathway may offer new immunotherapy strategies for bladder cancer.

ANN based on forgetting factor for online model updating in substructure pseudo-dynamic hybrid simulation

Yan Hua Wang,Jing Lv,Jing Wu,Cheng Wang 국제구조공학회 2020 Smart Structures and Systems, An International Jou Vol.26 No.1

Substructure pseudo-dynamic hybrid simulation (SPDHS) combining the advantages of physical experiments and numerical simulation has become an important testing method for evaluating the dynamic responses of structures. Various parameter identification methods have been proposed for online model updating. However, if there is large model gap between the assumed numerical models and the real models, the parameter identification methods will cause large prediction errors. This study presents an ANN (artificial neural network) method based on forgetting factor. During the SPDHS of model updating, a dynamic sample window is formed in each loading step with forgetting factor to keep balance between the new samples and historical ones. The effectiveness and anti-noise ability of this method are evaluated by numerical analysis of a six-story frame structure with BRBs (Buckling Restrained Brace). One BRB is simulated in OpenFresco as the experimental substructure, while the rest is modeled in MATLAB. The results show that ANN is able to present more hysteresis behaviors that do not exist in the initial assumed numerical models. It is demonstrated that the proposed method has good adaptability and prediction accuracy of restoring force even under different loading histories.

Hysteretic Behavior of Recycled Aggregate Concrete with Ferronickel Slag-Filled Steel Tubular Columns Subjected to Cyclic Loading

Hua-Yan Chen,Fengxuan Wang,Mianyue Yang,Ai Qi,Guochan Chen,Caisong Luo,Bizhen Wang 한국강구조학회 2023 International Journal of Steel Structures Vol.23 No.1

In order to investigate the hysteretic behavior of recycled aggregate concrete with ferronickel slag-filled steel tubular (RAC-FNSFST) columns, the quasi-static loading was implemented on nine specimens with different replacement ratios (RACs), axial load levels, length–diameter ratios, and diameter–thickness ratios. The hysteretic curves, skeleton curves, deformability, energy dissipation capacity, and stiffness degeneration were studied after loading and failure mechanisms were observed, followed by the construction of FE models for parameter analysis. It is demonstrated that the hysteretic loop curve is full, and the hysteretic performance was not dramatically affected by the replacement ratio of RAC. With axial load level increase, ultimate strength at descending stage degrades quickly, stiffness degeneration accelerates, and hysteretic energy dissipation increases. Stiffness degeneration and hysteresis energy dissipation are enhanced as the length–diameter ratio increases. However, when the diameter–thickness ratio decreases, hysteretic energy dissipation increases, and stiffness degeneration accelerates. In addition, a suitable FE model was established and compared with experimental results. Then a wide range of parameter studies was carried out as a supplement to the experimental study. It is shown that the ultimate strength and ductility of specimens are intimately correlated with the RAC strength, yield strength of steel tube, slenderness ratio, axial load level, and steel ratio.

FNC, a Novel Nucleoside Analogue, Blocks Invasion of Aggressive Non-Hodgkin Lymphoma Cell Lines Via Inhibition of the Wnt/β-Catenin Signaling Pathway

Zhang, Yan,Wang, Chen-Ping,Ding, Xi-Xi,Wang, Ning,Ma, Fang,Jiang, Jin-Hua,Wang, Qing-Duan,Chang, Jun-Biao Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.16

Chemotherapy is the primary therapy for malignant lymphoma (ML). However, the clinical outcome is still far from satisfactory. Consequently, an understanding of the mechanism of modulating cancer cell invasion, migration and metastasis is important for the development of more effective chemotherapeutic agents. FNC, 2'-deoxy-2'-${\beta}$-fluoro-4'-azidocytidine, a novel cytidine analogue, has demonstrated significantly inhibitory effects on proliferation of several non-Hodgkin lymphoma (NHL) cell lines. A previous study indicated that FNC effectively inhibited the growth of Raji and JeKo-1 cells in dose-time dependent effects with $IC_{50}$ values of $0.2{\mu}M$ and $0.097{\mu}M$, respectively. This study was focused on investigating the anti-invasive properties of FNC on NHL cells and its potential mechanisms of action. Cell adhesion and transwell chamber assays were utilized to investigate the anti-invasive effects of FNC on Raji and JeKo-1 cells. Real-time PCR and Western blotting were employed to qualify the expression of ${\beta}$-catenin, the glycogen synthase kinase-3 beta (GSK-$3{\beta}$), E-cadherin vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9). The results revealed that FNC remarkably inhibited the adhesion, migration and invasion of two human aggressive non-Hodgkin lymphoma cell lines in a dose dependent manner. Furthermore, ${\beta}$-catenin, MMP-2, MMP-9, VEGF mRNA and protein levels were decreased after FNC treatment, while GSK-$3{\beta}$ and E-cadherin increased. Our studies thus provide evidence and a rationale that FNC may offer an effective chemotherapeutic agent by regulating the invasion and metastasis of aggressive non-Hodgkin lymphoma via inhibition of the Wnt/${\beta}$-catenin signaling pathway.

Tunicamycin enhances TRAIL-induced apoptosis by inhibition of cyclin D1 and the subsequent downregulation of survivin

Hai-Yan Zhang,Zhen-Xian Du,Bao-Qin Liu,Yan-Yan Gao,Xin Meng,Yifu Guan,Wei-Wei Deng,Hua-Qin Wang 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.5

TNF-related apoptosis-inducing ligand (TRAIL) has been proposed as a promising cancer therapy that preferentially induces apoptosis in cancer cells, but not most normal tissues. However, many cancers are resistant to TRAIL by mechanisms that are poorly understood. In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Of note, tunicamycin did not sensitize the differentiated thyroid epithelial cells to TRAIL-induced apoptosis. Thus, combined treatment with tunicamycin and TRAIL may offer an attractive strategy for safely treating resistant thyroid cancers. TNF-related apoptosis-inducing ligand (TRAIL) has been proposed as a promising cancer therapy that preferentially induces apoptosis in cancer cells, but not most normal tissues. However, many cancers are resistant to TRAIL by mechanisms that are poorly understood. In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Of note, tunicamycin did not sensitize the differentiated thyroid epithelial cells to TRAIL-induced apoptosis. Thus, combined treatment with tunicamycin and TRAIL may offer an attractive strategy for safely treating resistant thyroid cancers.