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Search Results: 1 - 10 of 78240 matches for " LINGMEI; CHEN "
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Molecular identification of forensically significant beetles (Coleoptera) in China based on COI gene
ZHUANG,QUAN; CAI,JIFENG; ZHANG,MENGQI; FENG,HUA; GUO,YADONG; LAN,LINGMEI; CHEN,YAOQING;
Revista Colombiana de Entomología , 2011,
Abstract: precise identification of insect species plays an essential role in the accurate estimation of the postmortem interval (pmi), especially when information on the postmortem phenomenon is not available. sarcosaphagous beetles infest and colonize human and animal remains in the late stage of decomposition, and their morphological similarity poses a great challenge for forensic entomologists, as an existing key may be incomplete or difficult for non-specialists to use. a method for easy and accurate species-level identification at any life stage is required. in this study, a 272-base pair region of the mitochondrial cytochrome oxidase i (coi) gene was used to explore its utility in the identification of forensically important beetles. twenty-four specimens were collected from 14 locations in nine provinces of china. phenogram analysis of the sequenced segments by the unweighted pairgroup method analysis (upgma) method showed that all specimens were properly assigned into six species with strong similarity, which indicates the possibility of separating congeneric species with the short coi fragment. these results will be instrumental for implementation of the chinese database of forensically relevant beetles.
Relationship between Interleukin-10 ?1082A/G Polymorphism and Risk of Ischemic Stroke: A Meta-Analysis
Jun Jin, Wuying Li, Lingmei Peng, Jian Chen, Rong Li, Peihua Wu, Sheng Tan
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094631
Abstract: Objective To analyze the association between ?1082A/G polymorphism in interleukin-10 (IL-10) gene and ischemic stroke (IS) risk by meta-analysis. Methods We carried out a systematic electronic search in PubMed, BIOSIS Previews, Science Direct, Chinese National Knowledge Infrastructure, Chinese Biomedical Database, Weipu database and WANGFANG Database. Pooled odds ratios (ORs) with 95% confidence intervals (95%CIs) were calculated to assess the strength of the association. Results 7 studies were included. There was no significant association between IL-10 ?1082A/G polymorphism and IS risk under all genetic models in overall estimates (A vs. G: OR = 1.23,95%CI = 0.85–1.79;AA vs. GG: OR = 1.01,95%CI = 0.47–2.19; AG vs. GG: OR = 0.76, 95%CI = 0.38–1.55; AA+AG vs. GG: OR = 0.89,95%CI = 0.46–1.73; AA vs. AG+GG: OR = 1.39, 95%CI = 0.91–2.13). Similarly, no associations were found in subgroup analysis based on ethnicity and source of controls. However, removing the study deviating from Hardy–Weinberg equilibrium (HWE) produced statistically significant associations for overall estimates under recessive model(AA VS. AG+GG OR 1.58, 95% CI 1.04–2.42) and among Asians in all genetic models (A VS.G OR 1.64, 95% CI 1.07–2.53; AA vs. GG OR1.91, 95% CI 1.31–2.80; AG vs. GG OR1.44, 95% CI 1.09–1.91; AA+AG vs. GG OR 1.54, 95% CI 1.18–2.01;AA VS. AG+GG OR 1.79, 95% CI 1.07–3.00). Even after Bonferroni correction, the associations were observed still significantly in Asians under the two models (AA vs. GG OR1.91, 95% CI 1.31–2.80, P = 0.0008; AA+AG vs. GG OR 1.54, 95% CI 1.18–2.01, P = 0.001). Conclusion This meta-analysis indicates that IL10 ?1082 A/G polymorphism is associated with IS susceptibility in Asians and the ?1082 A allele may increase risk of IS in Asians. Considering the sample size is small and between-study heterogeneity is remarkable, more studies with subtle design are warranted in future.
The Intracellular Virus-Containing Compartments in Primary Human Macrophages Are Largely Inaccessible to Antibodies and Small Molecules
Hin Chu, Jaang-Jiun Wang, Mingli Qi, Jeong-Joong Yoon, Xiaoyun Wen, Xuemin Chen, Lingmei Ding, Paul Spearman
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035297
Abstract: HIV-1 assembly and release occurs at the plasma membrane of human T lymphocytes and model epithelial cell lines, whereas in macrophages intracellular sites of virus assembly or accumulation predominate. The origin of the intracellular virus-containing compartment (VCC) has been controversial. This compartment is enriched in markers of the multivesicular body, and has been described as a modified endosomal compartment. Several studies of this compartment have revealed the presence of small channels connecting to the plasma membrane, suggesting that instead of an endosomal origin the compartment is a modified plasma membrane compartment. If the compartment is accessible to the external environment, this would have important implications for antiviral immune responses and antiviral therapy. We performed a series of experiments designed to determine if the VCC in macrophages was open to the external environment and accessible to antibodies and small molecules. The majority of VCCs were found to be inaccessible to exogenously-applied antibodies to tetraspanins in the absence of membrane permeabilization, while tetraspanin staining was readily observed following membrane permeabilization. Cationized ferritin was utilized to stain the plasma membrane, and revealed that the majority of virus-containing compartments were inaccessible to ferritin. Low molecular weight dextrans could access only a very small percentage of VCCs, and these tended to be more peripheral compartments. We conclude that the VCCs in monocyte-derived human macrophages are heterogeneous, but the majority of VCCs are closed to the external environment.
Association between Transforming Growth Factor-Beta 1 T869C Polymorphism and Ischemic Stroke: A Meta-Analysis
Lingmei Peng, Peng Li, Jian Chen, Ke Yan, Fuyuan Huo, Lina Han, Can Li, Sheng Tan, Xiaodan Jiang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067738
Abstract: Objective To explore the association between transforming growth factor-beta1 (TGF-β1) T869C polymorphism and risk of ischemic stroke (IS) by performing a meta-analysis based on published articles. Methods Systematic electronic searches of PubMed, Science Direct, BIOSIS Previews, Chinese Biomedical Database, Chinese National Knowledge Infrastructure, and WANFANG Database were performed. The strength of the association was calculated by pooled odds ratios (ORs) with 95% confidence intervals (95%CIs). Subgroup analysis was conducted to explore potential sources of heterogeneity. Sensitivity analysis was performed to elucidate the stability of the outcomes. Publication bias was evaluated by Begg’s funnel plot and Egger’s test. Results A total of 6 studies involving 1701 cases were included. The overall estimates did not show any significant association between TGF-β1 T869C polymorphism and risk of IS under all genetic models (C vs. T: OR = 1.08,95%CI = 0.88–1.32; CC vs. TT:OR = 1.17,95%CI = 0.79–1.72; CT vs. TT: OR = 0.91, 95%CI = 0.68–1.22; CC+CT vs. TT: OR = 0.99, 95%CI = 0.73–1.35; CC vs. CT+TT: OR = 1.23, 95%CI = 0.95–1.59). Similar lacking associations were observed in subgroup analysis based on ethnicity and source of controls. When stratified by study design, significant increased association of IS risk was found in cohort studies under genetic models except recessive model(C vs. T: OR = 1.18, 95%CI = 1.05–1.32; CC vs. TT: OR = 1.40, 95%CI = 1.10–1.77; CT vs. TT: OR = 1.23, 95%CI = 1.02–1.49; CC+CT vs. TT: OR = 1.27, 95%CI = 1.03–1.57; CC vs. CT+TT, OR = 1.21, 95%CI = 0.99–1.47), whereas in case-control studies a significant decreased risk was detected under heterozygote comparison(CT vs. CC: OR = 0.72, 95%CI = 0.57–0.92). However, after correction for multiple testing, the associations were observed to be null significant in both cohort and case-control subgroups among all genetic models. Conclusion This meta-analysis suggested that current epidemiological studies of TGF-β1 T869C polymorphism are too inconsistent to draw a conclusion on the association with IS susceptibility. Given the small sample size and remarkable between-study heterogeneity, further well-designed prospective large-scale studies are warranted.
Full Toxicity Assessment of Genkwa Flos and the Underlying Mechanism in Nematode Caenorhabditis elegans
Yan Qiao, Yunli Zhao, Qiuli Wu, Lingmei Sun, Qinli Ruan, Yanyan Chen, Meng Wang, Jinao Duan, Dayong Wang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0091825
Abstract: Genkwa Flos (GF), the dried flower bud from Daphne genkwa Sieb. et Zucc. (Thymelaeaceae), is a well-known and widely used traditional Chinese medicine. However, we know little about the in vivo mechanism of GF toxicity. Nematode Caenorhabditis elegans has been considered as a useful toxicity assay system by offering a system best suited for asking the in vivo questions. In the present study, we employed the prolonged exposure assay system of C. elegans to perform the full in vivo toxicity assessment of raw-processed GF. Our data show that GF exposure could induce the toxicity on lifespan, development, reproduction, and locomotion behavior. GF exposure not only decreased body length but also induced the formation of abnormal vulva. The decrease in brood size in GF exposed nematodes appeared mainly at day-1 during the development of adult nematodes. The decrease of locomotion behavior in GF exposed nematodes might be due to the damage on development of D-type GABAergic motor neurons. Moreover, we observed the induction of intestinal reactive oxygen species (ROS) production and alteration of expression patterns of genes required for development of apical domain, microvilli, and apical junction of intestine in GF exposed nematodes, implying the possible dysfunction of the primary targeted organ. In addition, GF exposure induced increase in defecation cycle length and deficits in development of AVL and DVB neurons controlling the defecation behavior. Therefore, our study implies the usefulness of C. elegans assay system for toxicity assessment from a certain Chinese medicine or plant extract. The observed toxicity of GF might be the combinational effects of oxidative stress, dysfunction of intestine, and altered defecation behavior in nematodes.
Bone Marrow-Derived Mesenchymal Stem Cells Maintain the Resting Phenotype of Microglia and Inhibit Microglial Activation
Ke Yan, Run Zhang, Chengmei Sun, Lei Chen, Peng Li, Yi Liu, Lingmei Peng, Haitao Sun, Kun Qin, Fanfan Chen, Weiyi Huang, Yuxin Chen, Bingke Lv, Mouxuan Du, Yuxi Zou, Yingqian Cai, Lingsha Qin, Yanping Tang, Xiaodan Jiang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0084116
Abstract: Many studies have shown that microglia in the activated state may be neurotoxic. It has been proven that uncontrolled or over-activated microglia play an important role in many neurodegenerative disorders. Bone marrow-derived mesenchymal stem cells (BMSCs) have been shown in many animal models to have a therapeutic effect on neural damage. Such a therapeutic effect is attributed to the fact that BMSCs have the ability to differentiate into neurons and to produce trophic factors, but there is little information available in the literature concerning whether BMSCs play a therapeutic role by affecting microglial activity. In this study, we triggered an inflammatory response situation in vitro by stimulating microglia with the bacterial endotoxin lipopolysaccharide (LPS), and then culturing these microglia with BMSC-conditioned medium (BMSC-CM). We found that BMSC-CM significantly inhibited proliferation and secretion of pro-inflammatory factors by activated microglia. Furthermore, we found that the phagocytic capacity of microglia was also inhibited by BMSC-CM. Finally, we investigated whether the induction of apoptosis and the production of nitric oxide (NO) were involved in the inhibition of microglial activation. We found that BMSC-CM significantly induced apoptosis of microglia, while no apoptosis was apparent in the LPS-stimulated microglia. Our study also provides evidence that NO participates in the inhibitory effect of BMSCs. Our experimental results provide evidence that BMSCs have the ability to maintain the resting phenotype of microglia or to control microglial activation through their production of several factors, indicating that BMSCs could be a promising therapeutic tool for treatment of diseases associated with microglial activation.
Quantitative Estimation of Annual Runoff Variation from the Hotan River, China
Lingmei Huang,Lina Wu,Bing Shen
Journal of Sustainable Development , 2009, DOI: 10.5539/jsd.v2n2p120
Abstract: Starting from the existing analysis of runoff from the Hotan River, the varying cause of runoff in the Hotan River is analyzed using the annual runoff accumulated curves and the orderly cluster method, pointing out that the runoff from the Hotan River coming from the mountains falls into the natural runoff with the fluctuations because of being subject to climate changes. It is worth noticing that the Xiaota annual runoff flowing into Tarim River was reduced by 0.322 billion m3 in comparison of the postior 1989 series with the prior 1989 series and under the join action by both human being activities and climate changes.
Rab11-FIP1C and Rab14 Direct Plasma Membrane Sorting and Particle Incorporation of the HIV-1 Envelope Glycoprotein Complex
Mingli Qi equal contributor,Janice A. Williams equal contributor,Hin Chu,Xuemin Chen,Jaang-Jiun Wang,Lingmei Ding,Ehiole Akhirome,Xiaoyun Wen,Lynne A. Lapierre,James R. Goldenring ,Paul Spearman
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003278
Abstract: The incorporation of the envelope glycoprotein complex (Env) onto the developing particle is a crucial step in the HIV-1 lifecycle. The long cytoplasmic tail (CT) of Env is required for the incorporation of Env onto HIV particles in T cells and macrophages. Here we identify the Rab11a-FIP1C/RCP protein as an essential cofactor for HIV-1 Env incorporation onto particles in relevant human cells. Depletion of FIP1C reduced Env incorporation in a cytoplasmic tail-dependent manner, and was rescued by replenishment of FIP1C. FIP1C was redistributed out of the endosomal recycling complex to the plasma membrane by wild type Env protein but not by CT-truncated Env. Rab14 was required for HIV-1 Env incorporation, and FIP1C mutants incapable of binding Rab14 failed to rescue Env incorporation. Expression of FIP1C and Rab14 led to an enhancement of Env incorporation, indicating that these trafficking factors are normally limiting for CT-dependent Env incorporation onto particles. These findings support a model for HIV-1 Env incorporation in which specific targeting to the particle assembly microdomain on the plasma membrane is mediated by FIP1C and Rab14.
CAML Does Not Modulate Tetherin-Mediated Restriction of HIV-1 Particle Release
Mohammed S. Ali,Jason Hammonds,Lingmei Ding,Paul Spearman
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009005
Abstract: Tetherin/BST-2 is a recently-identified potent restriction factor in human cells that restricts HIV particle release following particle formation and budding at the plasma membrane. Vpu counteracts tetherin's restriction of particle release in a manner that has not yet been fully defined. We recently identified calcium-modulating cyclophilin ligand (CAML) as a Vpu-interacting protein that also restricts particle release. We hypothesized that CAML may act to enhance tetherin-mediated restriction of particle release and thereby explain how two distinct factors could be responsible for Vpu-responsive restriction.
Characterization of poly (safranine T)-modified electrode and application for simultaneous determination of epinephrine and uric acid coexisting with ascorbic acid
Niu, Lingmei;Lian, Kaoqi;Kang, Weijun;Li, Shan;
Journal of the Brazilian Chemical Society , 2011, DOI: 10.1590/S0103-50532011000200003
Abstract: a poly(safranine t) modified glassy carbon electrode was used for the simultaneous determination of epinephrine (ep) and uric acid (ua) in the presence of ascorbic acid (aa). enhanced electrocatalytic currents and well-separated potentials for ep and ua were observed. the anodic peak currents of ep and ua were linear to the corresponding concentrations in the range of 6.0×10-6-1.0×10-4 mol l-1. in addition, the modified electrode showed good sensitivity and stability. satisfactory results were achieved for the determination of ep and ua in injection solutions of ep and in human urine samples.
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