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Articles by C Feng
Total Records ( 6 ) for C Feng
  A Martinez Alcantara , E Ballesteros , C Feng , M Rojas , H Koshinsky , V. Y Fofanov , P Havlak and Y. Fofanov

Summary: PIQA is a quality analysis pipeline designed to examine genomic reads produced by Next Generation Sequencing technology (Illumina G1 Genome Analyzer). A short statistical summary, as well as tile-by-tile and cycle-by-cycle graphical representation of clusters density, quality scores and nucleotide frequencies allow easy identification of various technical problems including defective tiles, mistakes in sample/library preparations and abnormalities in the frequencies of appearance of sequenced genomic reads. PIQA is written in the R statistical programming language and is compatible with bustard, fastq and scarf Illumina G1 Genome Analyzer data formats.

  E. W Jackson , C Feng , P Fenn and P. Chen

Resistance to Phomopsis seed decay (PSD) in soybean (Glycine max [L.] Merr.) could provide dependable control of this important disease that affects seed quality. Studies have shown that single dominant genes that are allelomorphically different confer low levels of PSD in MO/PSD-0259 and PI 80837. The objectives of this research were to identify simple sequence repeat (SSR) markers linked to genes for PSD resistance in PI 80837 and MO/PSD-0259 and to associate the resistance genes to known linkage groups. Crosses were made between the PSD-susceptible cultivar Agripro 350 and each of the resistant lines MO/PSD-0259 and PI 80837. F2 populations from each cross were grown and inoculated in the field. Individual plant reactions were characterized by determining the levels of seed infection, and DNA of F2 plants was extracted for SSR analysis and mapping. F2 segregation data showed that different single dominant genes condition PSD resistance in MO/PSD-0259 and PI 80837. Resistance in PI 80837 was linked to Sat_177 (4.3 cM) and Sat_342 (15.8 cM) on molecular linkage group (MLG) B2. In MO/PSD-0259, resistance was linked to Sat_317 (5.9 cM) and Sat_120 (12.7 cM) on MLG F. These data support work by Berger and Minor (Berger RD, Minor HC. 1999. An restriction fragment length polymorphism (RFLP) marker associated with resistance to Phomopsis seed decay in soybean PI 417479. Crop Sci 39:800–805.) in which PSD resistance in PI 417479, the resistant parent used to develop MO/PSD-0259, was associated with RFLP marker A708 on MLG F. These SSR markers should be useful in selection for resistant genotypes in breeding programs.

  L Xiao , C Feng and Y. Chen

Glucocorticoid (GC) has been shown to affect the neuronal survival/death through a genomic mechanism, but whether or not it does through a nongenomic mechanism is unknown. Using a previously identified GR-deficient primary hippocampal neuron culture, we show here that a 15-min coexposure of N-methyl-d-aspartate (NMDA) with corticosterone at a stress-induced level significantly enhances neuronal death compared to NMDA alone. This enhancing effect of GC can be mimicked by the BSA-conjugated corticosterone, which is plasma membrane impermeable and cannot be blocked by RU38486 spironolactone. Furthermore, using a calcium-imaging technique, we found that B could increase both the percentage of neurons showing a significant increment of intracellular free calcium ([Ca2+]i) due to NMDA stimulation and the amplitude of [Ca2+]i increment in the individual responsive cells. Interestingly, this boosting effect of GC on [Ca2+]i increment could be blocked by the NMDA receptor subunit 2A (NR2A)-specific antagonist [(R)-[(S)-1-(4-bromo-phenyl)-ethylamino]-(2,3-dioxo-1,2,3,4-tetrahydro-quinoxalin-5-yl)-methyl]-phosphonic acid (NVP-AAM077) but not by the NMDA receptor subunit 2B (NR2B)-specific antagonist Ro25-6981. Moreover, we also found that GC can dramatically attenuate the NMDA-induced activation of ERK1/2 without affecting that of p38; and that the NMDA-induced ERK1/2 activation and its attenuation by GC both can be occluded by the NVP-AAM077 but not by Ro25-6981. Consistently, the enhancing effect of GC on NMDA neurotoxicity can also be blocked by NVP-AAM077 and the ERK1/2 inhibitor PD98059 but not by Ro25-6981 and p38 inhibitor SB203580. Indeed, the NMDA neurotoxicity itself can be blocked by Ro25-6981 or SB203580, whereas it is increased by NVP-AAM077 and PD98059. Therefore, it is probable that NMDA triggers a prodeath signaling through the NR2B-p38 MAPK pathway, and a prosurvival signaling through the NR2A-ERK1/2 MAPK pathway, whereas the latter was negatively regulated by rapid GC action. Taken together, the present data suggest a nongenomic action by GC that enhances NMDA neurotoxicity through facilitating [Ca2+]i increment and attenuating the NR2A-ERK1/2-mediated neuroprotective signaling, implicating a novel pathway underlying the regulatory effect of GC on neuronal survival/death.

  G Fan , C Feng , Y Li , C Wang , J Yan , W Li , J Feng , X Shi and Y. Bi

Background: We carried out animal experiments based on the orthogonal design L8(27) setting seven factors with two different levels of each and 10 groups of rats. The nutrients tested were tyrosine, glycine, methionine, taurine, ascorbic acid, thiamine and zinc.

Objectives: The objective of this study was to explore the optimal combinations of nutrients for prevention or amelioration of lead-induced learning and memory impairment.

Methods: Rats were supplemented with nutrients by gavage once a day in two experiments: one was simultaneous nutrient supplementation with lead acetate administration (800 mg l–1) for 8 weeks (prophylactic supplementation) and the other was nutrient supplementation for 4 weeks after the cessation of 4 weeks of lead administration (remedial supplementation). Morris water maze was initiated at ninth week. Rats were terminated for assays of levels of Pb in blood, activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS) in hippocampus, levels of nitric oxide (NO) in hippocampus and expressions of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine monophosphate (cAMP) response element-binding protein messenger RNA in hippocampus.

Results: Results showed that in prophylactic supplementation, methionine, taurine, zinc, ascorbic acid and glycine were the effective preventive factors for decreasing prolonged escape latency, increasing SOD and NOS activities and NO levels in the hippocampus, respectively. On the other hand, in remedial supplementation, taurine was the effective factor for reversing Pb-induced decrease in activities of SOD, NOS and levels of NO.

Conclusions: In conclusion, the optimum combinations of nutrients appear to be methionine, taurine, zinc, ascorbic acid and glycine for the prevention of learning and memory impairment, while taurine and thiamine appear to be the effective factors for reversing Pb neurotoxicity.

  S Paruchuri , H Tashimo , C Feng , A Maekawa , W Xing , Y Jiang , Y Kanaoka , P Conley and J. A. Boyce

Of the potent lipid inflammatory mediators comprising the cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only LTE4 is stable and abundant in vivo. Although LTE4 shows negligible activity at the type 1 and 2 receptors for cys-LTs (CysLT1R and CysLT2R), it is a powerful inducer of mucosal eosinophilia and airway hyperresponsiveness in humans with asthma. We show that the adenosine diphosphate (ADP)–reactive purinergic (P2Y12) receptor is required for LTE4-mediated pulmonary inflammation. P2Y12 receptor expression permits LTE4 -induced activation of extracellular signal-regulated kinase in Chinese hamster ovary cells and permits chemokine and prostaglandin D2 production by LAD2 cells, a human mast cell line. P2Y12 receptor expression by LAD2 cells is required for competition between radiolabeled ADP and unlabeled LTE4 but not for direct binding of LTE4, suggesting that P2Y12 complexes with another receptor to recognize LTE4. Administration of LTE4 to the airways of sensitized mice potentiates eosinophilia, goblet cell metaplasia, and expression of interleukin-13 in response to low-dose aerosolized allergen. These responses persist in mice lacking both CysLT1R and CysLT2R but not in mice lacking P2Y12 receptors. The effects of LTE4 on P2Y12 in the airway were abrogated by platelet depletion. Thus, the P2Y12 receptor is required for proinflammatory actions of the stable abundant mediator LTE4 and is a novel potential therapeutic target for asthma.

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