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Search Results: 1 - 10 of 127058 matches for " Huihua Li "
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Impact of Three Oral Antidiabetic Drugs on Markers of β-Cell Function in Patients with Type 2 Diabetes: A Meta-Analysis
Jin Lu, Jiajie Zang, Huihua Li
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076713
Abstract: Background The effect of metformin, pioglitazone and sitagliptin on β-cell function in the treatment of type 2 diabetes is controversial. Therefore, we performed a systematic review and meta-analysis to obtain a better understanding in the β-cell effects of metformin, pioglitazone and sitagliptin. Methods We searched Pubmed and the Cochrane Center Register of Controlled Trials to identify relevant studies. Trials investigating effects of sitagliptin, metformin or pioglitazone on β-cell function were identified. The primary outcomes were homeostasis model assessment of β-cells (HOMA-β) and proinsulin/insulin ratio (PI/IR). Secondary outcome was hemoglobin A1c level. We used version 2 of the Comprehensive Meta Analysis software for all statistical analyses. Results Metformin monotherapy was more effective than sitagliptin in improving HOMA-β (18.01% (95% CI 11.09% to 24.94%) vs. 11.29% (95% CI 9.21% to 13.37%), P = 0.040) and more effective (?0.137 (95% CI ?0.082 to ?0.192)) than both sitagliptin (?0.064 (95% CI ?0.036 to ?0.092), P = 0.019) and pioglitazone (?0.068 (95% CI ?0.044 to ?0.093), P = 0.015) in decreasing PI/IR. Metformin and sitagliptin combined (40.23% (95%CI 32.30% to 48.16%)) were more effective than sitagliptin and pioglitazone (11.82% (95% CI 6.61% to 17.04%), P = 0.000) and pioglitazone and metformin(9.81% (95% CI 1.67% to 17.95%), P = 0.022) in improving HOMA-β and decreasing PI/IR (?0.177 (95% CI ?0.118 to ?0.237); ?0.080 (95% CI ?0.045 to ?0.114), P = 0.007; ?0.038 (95% CI, ?0.005 to 0.071), P = 0.023). Limitations The included RCTs were of short duration (12–54 weeks). We could not determine long term effects on β-cells. Conclusions Metformin improves β-cell function more effectively than pioglitazone or sitagliptin in type 2 diabetes patients. Metformin and sitagliptin improved HOMA-β and PI/IR more than other combinations.
Phosphatidylinositol 3-kinase inhibitor(LY294002) induces apoptosis of human nasopharyngeal carcinoma in vitro and in vivo
Hanguo Jiang, Desheng Fan, Gengyin Zhou, Xiaofang Li, Huihua Deng
Journal of Experimental & Clinical Cancer Research , 2010, DOI: 10.1186/1756-9966-29-34
Abstract: The activation of the PI3K/Akt and its effect on CNE-2Z cells in vivo and in vitro was investigated by MTT assay, flow cytometry, western blot, ELISA, terminal deoxyribonucleotide transferase-mediated nick-end labeling assays (TUNEL), and immunohistochemical analyses, using PI3K inhibitor, LY294002.The results showed that LY294002 inhibited the phosphorylating of Akt (S473), cell proliferation, and induced apoptosis in CNE-2Z cells. However, our experiment results also demonstrated that apoptosis-induced LY294002 was directly regulated by caspase-9 activation pathway.These data suggested that PI3K inhibitor, LY294002, induced apoptosis by caspase-9 activation pathway and might be as a potentially useful target for therapeutic intervention in nasopharyngeal carcinoma patients.Nasopharyngeal carcinoma (NPC) has a distinct epidemiology and distribution, southern China and Southeast Asia are the highest risk areas, while rare in most parts of the world. Although many NPC patients may undergo radiation therapy for possibly cure and new strategies have improved survival for patients with metastasis, 30%-40% NPC patients die from local recurrence and metastasis. A better understanding of signaling pathways contributing to NPC survival and apoptosis will provide targets for new therapeutic agents.The phosphatidylinositol-3 OH kinase (PI3K)/Akt signaling pathway has been shown to contribute to cancer survival, apoptosis, and regulating a variety of cellular processes. In particular, Akt serine/threonine kinase is believed to play a critical role in controlling the balance between cell survival and apoptosis [1]. Previous studies had shown that phosphatidylinositol 3,4,5-trisphosphate(PIP3) generated by PI3K acts as a lipid second messenger essential for the translocation of protein kinase B(Akt) to the plasma membrane [2,3]. Akt is phosphorylated at two sites, T308 in kinase domain and S473 in regulatory tail. Phosphorylation at T308 and S473 is essential for maximal Akt act
Four kinds of ENU-induced white spot mice and chromosome locations of the mutant genes
Baojin Wu,Huihua Mao,Yixiang Shao,Zhengfeng Xue,Houda Li
Chinese Science Bulletin , 2003, DOI: 10.1007/BF02901753
Abstract: “Phenotype-driven” is the name for an approach used to study gene functions through mutagenesis, location and cloning of the mutant gene. In this study, 150 male C57BL/6J(B6) mice were treated with ENU and reproduced a total offspring of 3860. Of these descendants, 210 exhibited mutation phenotypes by screening, and more than 10 of them are hereditable. Four kinds of mutant mice, named Wbct, W 1Bao, W 2Bao, and W 2Bao, showed dominant hereditary white spot mutation with partial albinism on their belly, distal limbs and tail terminal. To map these mutant genes, 39 microsatellites, equally distributed on the mouse genome and with difference between B6 and DBA/2J (D2), were selected to scan the genome after discrimination of the white spots in the F2 mice [(B6xD2)xD2]. It is found that, the log odds score (LODS) between W 1Bao and D5Mitl68 is 0.56, and the LODS of W 1Bao and D5Mit352 is 4.47. With the gradual application of microsatellites D5Mit290, D5Mit312, D5Mit308 and D5Mit356 that are close to the mutant gene, and the number of F2 mice going up to 537, the mutant W 1Bao is located between D5Mit356 and D5Mit308 on chromosome 5, about 42.19 cM from the centromere. In the same way, W 2Bao and W 3Bao are mapped nearby W 1Bao, and Wbct is located on chromosome 1, about 41.6 cM from the centromere. After searching for the mouse genome database (MGD) and performing a one-by-one study of all genes located on chromosome subregion, it is believed that thekit gene is an excellent candidate for the white spot mutations of W 1Bao, W 2Bao and W 3Bao.
Preparation of BST nanocrystals embedded in SiO2 film by magnetron sputtering for nonvolatile memory applications
Li Wang,HongFang Sun,HuiHua Zhou,Jing Zhu
Chinese Science Bulletin , 2011, DOI: 10.1007/s11434-010-4159-3
Abstract: We develop a method that uses magnetron sputtering to fabricate barium strontium titanate (BST) nanocrystals embedded in dielectric SiO2 films. Transmission electron microscope images show that the BST nanocrystals have an average diameter of 5 nm and are well distributed in the SiO2 film. In addition, we also analyze the BST nanocrystals composition deviation during the sputtering process by electron dispersive spectroscopy.
Screening E3 Substrates Using a Live Phage Display Library
Zhengguang Guo, Xiaorong Wang, Huihua Li, Youhe Gao
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076622
Abstract: Ubiquitin ligases (E3s) determine specificity of ubiquitination by recognizing target substrates. However, most of their substrates are unknown. Most known substrates have been identified using distinct approaches in different laboratories. We developed a high-throughput strategy using a live phage display library as E3 substrates in in vitro screening. His-ubiquitinated phage, enriched with Ni-beads, could effectively infect E. coli for amplification. Sixteen natural potential substrates and many unnatural potential substrates of E3 MDM2 were identified through 4 independent screenings. Some substrates were identified in different independent experiments. Additionally, 10 of 12 selected candidates were ubiquitinated by MDM2 in vitro, and 3 novel substrates, DDX42, TP53RK and RPL36a were confirmed ex vivo. The whole strategy is rather simple and efficient. Non-degradation substrates can be discovered. This strategy can be extended to any E3s as long as the E3 does not ubiquitinate the empty phage.
Patterns of Linkage Disequilibrium?of LRRK2?across Different Races: Implications for Genetic Association Studies
Huihua Li, Yik Ying Teo, Eng King Tan
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0075041
Abstract: Genome Wide Association Studies (GWASs) have identified trait-associated polymorphisms via a hypothesis-free approach. However, it is challenging when attempting to reproduce GWAS findings in different populations as it fundamentally relies on the similar patterns of linkage disequilibrium (LD) between the unknown causal variants and the genotyped single nucleotide polymorphisms (SNPs). To address this potential limitation, we examined the regional LD pattern of leucine-rich repeat kinase 2 (LRRK2) gene, which is responsible for both autosomal dominant and sporadic Parkinson’s disease (PD), in Caucasians (CEU), Japanese (JPT) and Chinese (CHB) from HapMap and Chinese (CHS), Malays (MAS) and Indians (INS) from the Singapore Genome Variation Project (SGVP) utilizing the traditional heatmaps and targeted analysis of LRRK2 gene via Monte Carlo simulation through varLD scores of these ethnic groups. Both heatmaps and targeted analysis showed that LD pattern of JPT was different from that of INS (P=0.0001); while LD pattern of CEU was different from that in Asian except for INS (all P=0.0001). Our study suggests that there is a higher chance to detect associations between PD and those trait-associated SNPs of LRRK2 gene found in Caucasian studies in INS, while those found in Japanese studies are likely to be better replicated among CHB.
Clinical Application of Primary Suture Following Three-Port Laparoscopic Common Bile Duct Exploration: A Report of 176 Cases  [PDF]
Shengze Li, Huihua Cai, Donglin Sun, Xuemin Chen, Shengyong Liu, Xinquan Wu, Yong An, Jing Chen, Chun Yang, Yaping Sun, Xiaoyan Lu
Surgical Science (SS) , 2015, DOI: 10.4236/ss.2015.61001
Abstract: Objective: To investigate the feasibility, safety and the clinical value of primary suture following 3-port laparoscopic common bile duct exploration (LCBDE). Methods: From January 2012 to September 2014, 176 patients suffered from choledocholithiasis were treated with primary suture following 3-port LCBDE and the clinical data were retrospectively analyzed. Results: All cases were operated successfully and none was converted to open surgery. The duration of operation was 92.2 ± 18.8 min and the length of postoperative hospital stay was 4.4 ± 3.7 d. Postoperative bile leakage occurred in 2 cases and these patients recovered by simple drainage for 3 to 7 days without re-operation. All patients recovered smoothly without any serious complications. Conclusions: Primary suture following 3-port LCBDE is safe, effective and mini-invasive, which is worthy of further clinical application.
Macrophage-Stimulated Cardiac Fibroblast Production of IL-6 Is Essential for TGF β/Smad Activation and Cardiac Fibrosis Induced by Angiotensin II
Feifei Ma, Yulin Li, Lixin Jia, Yalei Han, Jizhong Cheng, Huihua Li, Yongfen Qi, Jie Du
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035144
Abstract: Interleukin-6 (IL-6) is an important cytokine participating in multiple biologic activities in immune regulation and inflammation. IL-6 has been associated with cardiovascular remodeling. However, the mechanism of IL-6 in hypertensive cardiac fibrosis is still unclear. Angiotensin II (Ang II) infusion in mice increased IL-6 expression in the heart. IL-6 knockout (IL-6-/-) reduced Ang II-induced cardiac fibrosis: 1) Masson trichrome staining showed that Ang II infusion significantly increased fibrotic areas of the wild-type mouse heart, which was greatly suppressed in IL-6-/- mice and 2) immunohistochemistry staining showed decreased expression of α-smooth muscle actin (α-SMA), transforming growth factor β1 (TGF-β1) and collagen I in IL-6-/- mouse heart. The baseline mRNA expression of IL-6 in cardiac fibroblasts was low and was absent in cardiomyocytes or macrophages; however, co-culture of cardiac fibroblasts with macrophages significantly increased IL-6 production and expression of α-SMA and collagen I in fibroblasts. Moreover, TGF-β1 expression and phosphorylation of TGF-β downstream signal Smad3 was stimulated by co-culture of macrophages with cardiac fibroblasts, while IL-6 neutralizing antibody decreased TGF-β1 expression and Smad3 phosphorylation in co-culture of macrophage and fibroblast. Taken together, our results indicate that macrophages stimulate cardiac fibroblasts to produce IL-6, which leads to TGF-β1 production and Smad3 phosphorylation in cardiac fibroblasts and thus stimulates cardiac fibrosis.
Effect of MDM2 SNP309 and p53 codon 72 polymorphisms on lung cancer risk and survival among non-smoking Chinese women in Singapore
Hui Chua, Daniel Ng, Serena Choo, San Lum, Huihua Li, Li Soh, Kanaga Sabapathy, Adeline Seow
BMC Cancer , 2010, DOI: 10.1186/1471-2407-10-88
Abstract: We therefore examined the role of the SNPs in the p53 pathway (p53 codon 72 and MDM2 SNP309) on lung cancer risk and prognosis of a life-time non-smoking female Chinese population, in a hospital-based case-control study of 123 cases and 159 age-matched controls, by PCR analysis.Our findings reveal that the risk of lung cancer among individuals with the MDM2 SNP309 TT genotype was 2.1 (95% CI 1.01-4.36) relative to the GG genotype, contrary to initial expectations that the GG genotype with elevated MDM2 levels will increase cancer risk. Those who had this genotype in combination with the p53 Pro allele had a risk of 2.5 (95% CI 1.2-5.0). There was however no effect of either polymorphism on age at diagnosis of lung cancer or on overall survival.The results thus demonstrate that the MDM2 SNP309 TT rather than the GG genotype is associated with increased risk of lung cancer in this population, suggesting that other mechanisms independent of increased MDM2 levels can influence cancer susceptibility.The TP53 tumour suppressor pathway plays a critical role in cell cycle regulation and apoptosis in many cancers, including lung carcinomas [1], and variation in the genes that regulate this pathway may exert an important influence on tumour development, and hence, cancer risk. Recent interest has focused on the murine double minute-2 protein (MDM2), a nuclear phospoprotein that inhibits p53 activity by promoting its degradation [2]. A single nucleotide polymorphism (SNP309) in the MDM2 promoter has been found to influence transcription of this gene via a greater affinity for the SP1 transcription factor, and hence, individuals with the GG genotype have higher MDM2 levels leading to attenuation of the p53 pathway [3,4]. This has been especially so in the case of females, due to the involvement of the MDM2 SNP in the estrogen receptor signaling pathway [3].Several epidemiologic studies have evaluated this association with varying results. No overall association between MDM2 SNP
Glucocorticoid Receptor and Sequential P53 Activation by Dexamethasone Mediates Apoptosis and Cell Cycle Arrest of Osteoblastic MC3T3-E1 Cells
Hui Li, Wenwei Qian, Xisheng Weng, Zhihong Wu, Huihua Li, Qianyu Zhuang, Bin Feng, Yanyan Bian
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037030
Abstract: Glucocorticoids play a pivotal role in the proliferation of osteoblasts, but the underlying mechanism has not been successfully elucidated. In this report, we have investigated the molecular mechanism which elucidates the inhibitory effects of dexamethasone on murine osteoblastic MC3T3-E1 cells. It was found that the inhibitory effects were largely attributed to apoptosis and G1 phase arrest. Both the cell cycle arrest and apoptosis were dependent on glucocorticoid receptor (GR), as they were abolished by GR blocker RU486 pre-treatment and GR interference. G1 phase arrest and apoptosis were accompanied with a p53-dependent up-regulation of p21 and pro-apoptotic genes NOXA and PUMA. We also proved that dexamethasone can’t induce apoptosis and cell cycle arrest when p53 was inhibited by p53 RNA interference. These data demonstrate that proliferation of MC3T3-E1 cell was significantly and directly inhibited by dexamethasone treatment via aberrant GR activation and subsequently P53 activation.
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