16 results on '"Zhijie Lei"'
Search Results
2. miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Di Chen, Bing Xu, Rui Wang, Yi Chu, Weijie Wang, Lin Zhou, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Jie Liang
- Subjects
Rho GTPase ,GEFs ,Dock6 ,Gastric cancer ,Metastasis ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Our previous work showed that some Rho GTPases, including Rho, Rac1 and Cdc42, play critical roles in gastric cancer (GC); however, how they are regulated in GC remains largely unknown. In this study, we aimed to investigate the roles and molecular mechanisms of Dock6, an atypical Rho guanine nucleotide exchange factor (GEF), in GC metastasis. Methods The expression levels of Dock6 and miR-148b-3p in GC tissues and paired nontumor tissues were determined by immunohistochemistry (IHC) and in situ hybridization (ISH), respectively. The correlation between Dock6/miR-148b-3p expression and the overall survival of GC patients was calculated by the Kaplan-Meier method and log-rank test. The roles of Dock6 and miR-148b-3p in GC were investigated by in vitro and in vivo functional studies. Rac1 and Cdc42 activation was investigated by GST pull-down assays. The inhibition of Dock6 transcription by miR-148b-3p was determined by luciferase reporter assays. Results A significant increase in Dock6 expression was found in GC tissues compared with nontumor tissues, and its positive expression was associated with lymph node metastasis and a higher TNM stage. Patients with positive Dock6 expression exhibited shorter overall survival periods than patients with negative Dock6 expression. Dock6 promoted GC migration and invasion by increasing the activation of Rac1 and Cdc42. miR-148b-3p expression was negatively correlated with Dock6 expression in GC, and it decreased the motility of GC cells by inhibiting the Dock6/Rac1/Cdc42 axis. Conclusions Dock6 was over-expressed in GC tissues, and its positive expression was associated with GC metastasis and indicated poor prognosis of GC patients. Targeting of Dock6 by miR-148b-3p could activate Rac1 and Cdc42, directly affecting the motility of GC cells. Targeting the Dock6-Rac1/Cdc42 axis could serve as a new therapeutic strategy for GC treatment.
- Published
- 2018
- Full Text
- View/download PDF
3. Highly band-selective meta-surfaces exhibiting perfect near infrared absorption and concurrent visible band sensing: A numerical study
- Author
-
ZhiJie Lei, XiaoShi Qian, Kun Jiang, and Guang Meng
- Subjects
General Engineering ,General Materials Science - Published
- 2022
4. The tumour neovasculature-homing dimeric peptide GX1 demonstrates antiangiogenic activity in the retinal neovasculature
- Author
-
Kaichun Wu, Lu Wang, Jingtao Liu, Jipeng Yin, Haiping Zhang, Xiaoli Hui, Zhijie Lei, Zhiyong Zhang, Ming Zhang, Rutang Fang, Shuhui Liang, Wei Cui, and Yingying Luo
- Subjects
Angiogenesis ,Angiogenesis Inhibitors ,Apoptosis ,Retinal Neovascularization ,Immunofluorescence ,chemistry.chemical_compound ,In vivo ,Cell Movement ,medicine ,Animals ,Receptor ,Cells, Cultured ,Cell Proliferation ,Pharmacology ,medicine.diagnostic_test ,Neovascularization, Pathologic ,Chemistry ,Cell growth ,Endothelial Cells ,Retinal ,In vitro ,Rats ,Mice, Inbred C57BL ,Disease Models, Animal ,Cancer research ,Immunohistochemistry ,Peptides ,Dimerization - Abstract
Identification of molecules specific to the retinal neovasculature will promote antiangiogenic therapy with enhanced targeting ability. The specificity of phage-displayed peptide GX1 (a cyclic 7-mer peptide motif CGNSNPKSC) to gastric cancer neovasculature has been extensively confirmed both in vitro and in vivo. To investigate the potential application of GX1 in antiangiogenic therapy targeting retinal angiogenesis-related diseases, we performed immunohistochemistry and immunofluorescence analyses. GX1 demonstrated positive staining in the retinal neovasculature in an oxygen-induced mouse model of retinopathy (OIR) as well as in rat retinal microvasculature endothelial cells (RMECs), confirming the major role of the GX1 receptor during retinal angiogenesis. Dimeric GX1 was synthesized to increase the binding affinity to the GX1 receptor, and the antiangiogenic effects were examined in RMECs in vitro and the retinal neovasculature in the OIR in vivo. Cell proliferation was evaluated using a Cell Counting Kit-8 (CCK-8) assay, revealing that compared with the GX1 monomer, dimeric GX1 significantly inhibited RMEC proliferation (P 0.05). This finding may be attributed to the enhanced (P 0.05) apoptosis induced by dimeric GX1 in RMECs based on results obtained from TUNEL, flow cytometric and cell cycle analyses. In RMECs, in vitro cell migration and tube formation were significantly inhibited following exposure to dimeric GX1. Intravitreal administration of dimeric GX1 resulted in a greater reduction in the retinal neovascularization in vivo than administration of the GX1 monomer (P 0.05). In conclusion, dimeric GX1 showed greater inhibition of angiogenesis than monomeric GX1 and could be a promising agent for antiangiogenic therapy in retinal angiogenesis-related diseases.
- Published
- 2020
5. Pterostilbene Attenuates Cocultured BV-2 Microglial Inflammation-Mediated SH-SY5Y Neuronal Oxidative Injury via SIRT-1 Signalling
- Author
-
Yinxue Sun, Tao Tang, Zhao Huang, Chen Zhao, Haixiao Liu, Mingyang Song, Qiang Liu, Xiaogang Wang, Qiang Lei, Zhijie Lei, Qiang Zhu, Long Yang, and Bodong Wang
- Subjects
Aging ,Pterostilbene ,SH-SY5Y ,Article Subject ,Cell Culture Techniques ,Inflammation ,medicine.disease_cause ,Biochemistry ,chemistry.chemical_compound ,Downregulation and upregulation ,Sirtuin 1 ,Stilbenes ,medicine ,Humans ,TUNEL assay ,Microglia ,QH573-671 ,Cell Biology ,General Medicine ,medicine.anatomical_structure ,chemistry ,Apoptosis ,Cancer research ,medicine.symptom ,Cytology ,Oxidative stress ,Research Article ,Signal Transduction - Abstract
Microglial inflammation plays an important part in the progression of multiple neurological diseases, including neurodegenerative diseases, stroke, depression, and traumatic encephalopathy. Here, we aimed to explore the role of pterostilbene (PTE) in the microglial inflammatory response and subsequent damage of cocultured neural cells and partially explain the underlying mechanisms. In the coculture system of lipopolysaccharide-activated BV-2 microglia and SH-SY5Y neuroblastoma, PTE (only given to BV-2) exhibited protection on SH-SY5Y cells, evidenced by improved SH-SY5Y morphology and viability and LDH release. It also attenuated SH-SY5Y apoptosis and oxidative stress, evidenced by TUNEL and DCFH-DA staining, as well as MDA, SOD, and GSH levels. Moreover, PTE upregulated SIRT-1 expression and suppressed acetylation of NF-κB p65 subunit in BV-2 microglia, thus decreasing the inflammatory factors, including TNF-α and IL-6. Furthermore, the effects above were reversed by SIRT-1 inhibitor EX527. These results suggest that PTE reduces the microglia-mediated inflammatory response and alleviates subsequent neuronal apoptosis and oxidative injury via increasing SIRT-1 expression and inhibiting the NF-κB signalling pathway.
- Published
- 2020
6. Awakening p53 in vivo by D-peptides-functionalized ultra-small nanoparticles: Overcoming biological barriers to D-peptide drug delivery
- Author
-
Zhenyuan Bian, Yi Guo, Zhijie Lei, Wangxiao He, Min Liu, Yi Zhou, Hao Guo, Jin Yan, Chun Yin, Kaishan Tao, Peng Hou, Simeng Wang, Bohan Ma, and Yijie Li
- Subjects
p53 ,Drug-Related Side Effects and Adverse Reactions ,Medicine (miscellaneous) ,Metal Nanoparticles ,Mice, Nude ,Peptide ,Antineoplastic Agents ,02 engineering and technology ,010402 general chemistry ,01 natural sciences ,chemistry.chemical_compound ,In vivo ,Animals ,Humans ,Molecular Targeted Therapy ,Pharmacology, Toxicology and Pharmaceutics (miscellaneous) ,chemistry.chemical_classification ,Biological Products ,Drug Carriers ,Mice, Inbred BALB C ,Chemistry ,Activator (genetics) ,fungi ,ultra-small nanoparticle ,biosafety ,021001 nanoscience & nanotechnology ,HCT116 Cells ,Small molecule ,0104 chemical sciences ,Cell biology ,Disease Models, Animal ,Nanomedicine ,Treatment Outcome ,Polylysine ,Cancer cell ,Heterografts ,dextrorotary peptide ,Nanocarriers ,Tumor Suppressor Protein p53 ,0210 nano-technology ,Colorectal Neoplasms ,Peptides ,Intracellular ,gold nanoparticle ,Neoplasm Transplantation ,Research Paper - Abstract
Peptides are a rapidly growing class of therapeutics with many advantages over conventional small molecule drugs. Dextrorotary (D)-peptides, with increased enzymatic stability and prolonged plasma half-life in comparison with natural L-peptides, are considered to have great potential as recognition molecules and therapeutic agents. However, the in vivo efficacy of current therapeutic D-peptides is hindered by their inefficient cellular uptake in diseased tissues. Methods: To overcome physiological and cellular barriers to D-peptides, we designed a gold-based ultra-small nanocarrier coupled with polylysine (PLL) and a receptor-targeted peptide to deliver therapeutic D-peptides. Using a D-peptide p53 activator (DPA) as a proof of concept, we synthesized, functionalized and characterized gold- and DPA-based nanoparticles termed AuNP-DPA. Results: AuNP-DPA were effectively enriched in tumor sites and subsequently internalized by cancer cells, thereby suppressing tumor growth via reactivating p53 signaling. More importantly, through a series of in vivo experiments, AuNP-DPA showed excellent biosafety without the common side effects that hinder p53 therapies in clinic trials. Conclusion: The present study not only sheds light on the development of AuNP-DPA as a novel class of antitumor agents for drugging the p53 pathway in vivo, but also supplies a new strategy to use D-peptides as intracellular PPI inhibitors for cancer-targeted therapy.
- Published
- 2018
7. Novel peptide GX1 inhibits angiogenesis by specifically binding to transglutaminase-2 in the tumorous endothelial cells of gastric cancer
- Author
-
Jinpeng Wang, Chao Jian, Kaichun Wu, Na Chai, Miaomiao Tian, Xiaofang Yi, Zhenyuan Bian, Di Chen, Zhijie Lei, Zuhong Tian, Hao Hu, Shiming Peng, Sijun Hu, Guodong Wang, Hao Guo, Pengfei Yu, Ying Zhang, Xiaowei Li, Jian Liu, Yongzhan Nie, Bing Xu, and Niu Huang
- Subjects
Male ,0301 basic medicine ,Cancer Research ,Tissue transglutaminase ,Angiogenesis ,Receptor expression ,Immunology ,Down-Regulation ,Apoptosis ,Peptides, Cyclic ,Article ,Neovascularization ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,Downregulation and upregulation ,Cell Movement ,GTP-Binding Proteins ,Stomach Neoplasms ,Cell Line, Tumor ,Human Umbilical Vein Endothelial Cells ,medicine ,Humans ,Protein Glutamine gamma Glutamyltransferase 2 ,lcsh:QH573-671 ,Receptor ,Cell Proliferation ,Transglutaminases ,Neovascularization, Pathologic ,biology ,Chemistry ,lcsh:Cytology ,Endothelial Cells ,Cell Biology ,Middle Aged ,Prognosis ,Up-Regulation ,030104 developmental biology ,Cell culture ,biology.protein ,Cancer research ,Female ,medicine.symptom ,Oligopeptides - Abstract
The clinical application of GX1, an optimal gastric cancer (GC) targeting peptide, is greatly limited because its receptor in the GC vasculature is unknown. In this study, we screened the candidate receptor of GX1, transglutaminase-2(TGM2), by co-immunoprecipitation (co-IP) combined with mass spectrometry. We found that TGM2 was up-regulated in GC vascular endothelial cells and that GX1 receptor expression was suppressed correspondingly after TGM2 downregulation. A highly consistent co-localization of GX1 receptor and TGM2 was detected at both the cellular and tissue levels. High TGM2 expression was evident in GC tissues from patients with poor prognosis. After TGM2 downregulation, the GX1-mediated inhibition of proliferation and migration and the induction of the apoptosis of GC vascular endothelial cells were weakened or even reversed. Finally, we observed that GX1 could inhibit the GTP-binding activity of TGM2 by reducing its intracellular distribution and downregulating its downstream molecular targets (nuclear factor-kappa B, NF-κB; hypoxia-inducible factor 1-α, HIF1α) in GC vascular endothelial cells. Our study confirms that peptide GX1 can inhibit angiogenesis by directly binding to TGM2, subsequently reducing the GTP-binding activity of TGM2 and thereby suppressing its downstream pathway(NF-κB/HIF1α). Our conclusions suggest that GX1/TGM2 may provide a new target for the diagnosis and treatment of GC.
- Published
- 2018
8. Loss of Barx1 promotes hepatocellular carcinoma metastasis through up-regulating MGAT5 and MMP9 expression and indicates poor prognosis
- Author
-
Yi Cai, Yongzhan Nie, Guodong Wang, Wenbing Xie, Limin Xia, Fan Yu, Yuanyuan Lu, Hao Hu, Chao Lei, Jipeng Yin, Hai-jia Zhang, Xiaowei Li, Kaichun Wu, Jian Liu, Hao Guo, Lu Niu, Wenjie Huang, Xiaodi Zhao, Jie Chen, Zhijie Lei, and Xiangqian Kong
- Subjects
0301 basic medicine ,Poor prognosis ,medicine.medical_specialty ,Matrix (biology) ,MMP9 ,Metastasis ,03 medical and health sciences ,Medicine ,metastasis ,barx homeobox 1 ,Stage (cooking) ,Gene ,mannosyl (alpha-1,6-)-glycoprotein beta-1,6-N-acetyl-glucosaminyltransferase 5 ,Gene knockdown ,business.industry ,hepatocellular carcinoma ,medicine.disease ,digestive system diseases ,Surgery ,030104 developmental biology ,Oncology ,Hepatocellular carcinoma ,matrix metallopeptidase 9 ,Cancer research ,business ,Research Paper - Abstract
Metastasis is the major dominant reason for poor prognosis of hepatocellular carcinoma (HCC) after surgical treatment. However, the molecular mechanism of metastasis has not been well characterzied. Here, we report a novel function of Barx homeobox1 (Barx1) in inhibiting HCC invasion and metastasis. Barx1 expression is significantly decreased in human HCC tissues than in adjacent non-tumorous tissues and normal liver tissues. Low Barx1 expression is correlated with higher tumor-nodule-metastasis stage and indicates poor prognosis. Down-regulation of Barx1 promotes HCC migration, invasion and metastasis, whereas up-regulation of Barx1 inhibits HCC migration, invasion and metastasis. Mannosyl (alpha-1,6-)-glycoprotein beta-1,6-N-acetyl-glucosaminyltransferase 5 (MGAT5) and matrix metallopeptidase 9 (MMP9) are direct target genes of Barx1. Knockdown of Barx1 up-regulates MGAT5 and MMP9 expression in HCC cells with low metastatic capability, whereas over-expression of Barx1 suppresses their expression in HCC cells with high metastatic capability. Knockdown of both MGAT5 and MMP9 significantly decreases the invasion and metastasis abilities induced by Barx1 knockdown. Barx1 expression is negatively correlated with MGAT5 and MMP9 expression in human HCC tissues. Patients with low expression of Barx1 and high expression of MGAT5 or MMP9 are associated with poorer prognosis. Thus, loss of Barx1 represents a prognostic biomarker in human HCC patients.
- Published
- 2017
9. miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Kaichun Wu, Yi Chu, Mingzuo Jiang, Di Chen, Zhijie Lei, Yulong Shang, Rui Wang, Bing Xu, Xiaowei Li, Weijie Wang, Lin Zhou, Jie Liang, Daiming Fan, and Yongzhan Nie
- Subjects
rac1 GTP-Binding Protein ,0301 basic medicine ,Cancer Research ,Motility ,RAC1 ,In situ hybridization ,lcsh:RC254-282 ,Metastasis ,Mice ,03 medical and health sciences ,Cell Movement ,Genes, Reporter ,Stomach Neoplasms ,In vivo ,Cell Line, Tumor ,Biomarkers, Tumor ,medicine ,Animals ,Guanine Nucleotide Exchange Factors ,Humans ,Neoplasm Metastasis ,cdc42 GTP-Binding Protein ,3' Untranslated Regions ,Cell Proliferation ,Chemistry ,Research ,Rho GTPase ,GEFs ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,medicine.disease ,Immunohistochemistry ,In vitro ,Gene Expression Regulation, Neoplastic ,Disease Models, Animal ,MicroRNAs ,030104 developmental biology ,Oncology ,Cancer research ,Heterografts ,RNA Interference ,Dock6 ,Guanine nucleotide exchange factor ,Gastric cancer ,Signal Transduction - Abstract
Background Our previous work showed that some Rho GTPases, including Rho, Rac1 and Cdc42, play critical roles in gastric cancer (GC); however, how they are regulated in GC remains largely unknown. In this study, we aimed to investigate the roles and molecular mechanisms of Dock6, an atypical Rho guanine nucleotide exchange factor (GEF), in GC metastasis. Methods The expression levels of Dock6 and miR-148b-3p in GC tissues and paired nontumor tissues were determined by immunohistochemistry (IHC) and in situ hybridization (ISH), respectively. The correlation between Dock6/miR-148b-3p expression and the overall survival of GC patients was calculated by the Kaplan-Meier method and log-rank test. The roles of Dock6 and miR-148b-3p in GC were investigated by in vitro and in vivo functional studies. Rac1 and Cdc42 activation was investigated by GST pull-down assays. The inhibition of Dock6 transcription by miR-148b-3p was determined by luciferase reporter assays. Results A significant increase in Dock6 expression was found in GC tissues compared with nontumor tissues, and its positive expression was associated with lymph node metastasis and a higher TNM stage. Patients with positive Dock6 expression exhibited shorter overall survival periods than patients with negative Dock6 expression. Dock6 promoted GC migration and invasion by increasing the activation of Rac1 and Cdc42. miR-148b-3p expression was negatively correlated with Dock6 expression in GC, and it decreased the motility of GC cells by inhibiting the Dock6/Rac1/Cdc42 axis. Conclusions Dock6 was over-expressed in GC tissues, and its positive expression was associated with GC metastasis and indicated poor prognosis of GC patients. Targeting of Dock6 by miR-148b-3p could activate Rac1 and Cdc42, directly affecting the motility of GC cells. Targeting the Dock6-Rac1/Cdc42 axis could serve as a new therapeutic strategy for GC treatment. Electronic supplementary material The online version of this article (10.1186/s13046-018-0729-z) contains supplementary material, which is available to authorized users.
- Published
- 2018
10. Additional file 1: of miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Chen, Di, Xu, Bing, Wang, Rui, Chu, Yi, Weijie Wang, Zhou, Lin, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Liang, Jie
- Abstract
Table S6. The sequences of siRNAs and primers. (DOCX 17 kb)
- Published
- 2018
- Full Text
- View/download PDF
11. Additional file 3: of miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Chen, Di, Xu, Bing, Wang, Rui, Chu, Yi, Weijie Wang, Zhou, Lin, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Liang, Jie
- Abstract
Figure S1. The correlation between Dock6, Dock7, or Dock8 expression and the survival of GC patients. Three probes for Dock6 (a), Dock7 (b) and Dock8 (c), respectively, were used to predict the correlation between Dock6, Dock7, or Dock8 expression and the overall or recurrence-free survival of GC patients. The survival data were extracted from Kaplan-Meier plotter database ( www.kmplot.com ). (PDF 3758 kb)
- Published
- 2018
- Full Text
- View/download PDF
12. Additional file 5: of miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Chen, Di, Xu, Bing, Wang, Rui, Chu, Yi, Weijie Wang, Zhou, Lin, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Liang, Jie
- Abstract
Table S3. Univariate and multivariate analyses of factors associated with survival of 90 GC patients. (DOCX 19 kb)
- Published
- 2018
- Full Text
- View/download PDF
13. Additional file 2: of miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Chen, Di, Xu, Bing, Wang, Rui, Chu, Yi, Weijie Wang, Zhou, Lin, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Liang, Jie
- Abstract
Table S1. The expression analysis of Dock6, Dock7 and Dock8 in the Oncomine database (nâ >â 10). (DOCX 18 kb)
- Published
- 2018
- Full Text
- View/download PDF
14. Additional file 6: of miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Chen, Di, Xu, Bing, Wang, Rui, Chu, Yi, Weijie Wang, Zhou, Lin, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Liang, Jie
- Abstract
Figure S2. Dock6 promotes the proliferation of GC cells. (a-b) The construction of SGC-7901 cells with Dock6 over-expression and BGC-823 cells with Dock6 knock-down. Real-time PCR and western blot analyses of Dock6 mRNA or protein expression in the indicated cells. **P
- Published
- 2018
- Full Text
- View/download PDF
15. Additional file 4: of miR-148b-3p inhibits gastric cancer metastasis by inhibiting the Dock6/Rac1/Cdc42 axis
- Author
-
Xiaowei Li, Mingzuo Jiang, Chen, Di, Xu, Bing, Wang, Rui, Chu, Yi, Weijie Wang, Zhou, Lin, Zhijie Lei, Yongzhan Nie, Daiming Fan, Yulong Shang, Kaichun Wu, and Liang, Jie
- Abstract
Table S2. Correlation between Dock6 expression and pathological characteristics of GC patients. (DOCX 19 kb)
- Published
- 2018
- Full Text
- View/download PDF
16. Sparse Circular Array Optimization Using Genetic Algorithm
- Author
-
Ling Zhang, Kesong Chen, Zhijie Lei, and Weiqin Li
- Subjects
Circular buffer ,Distribution (mathematics) ,Chromosome (genetic algorithm) ,Robustness (computer science) ,Computer science ,Position (vector) ,Genetic algorithm ,Sparse approximation ,Element (category theory) ,Algorithm - Abstract
An Improved Genetic Algorithm is presented in this paper to solve the problem of optimum element position design of sparse circular arrays with multiple constraints. The initial feasible solutions for genetic algorithm (GA) which meet multiple design constraints are produced from the framework concerning element position of uniform concentric circular arrays. And let these solutions act as the thinning chromosome, which is used to describe the element distribution of the sparse circular arrays. By utilizing the IGA, a smaller searching space can be achieved, and the freedom of the element can be exploited. Finally, the simulation is done and the numerical results confirm the great efficiency and the robustness of the new algorithm.
- Published
- 2011
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.