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Articles by Lin Mei
Total Records ( 3 ) for Lin Mei
  Bo Ding , Lin Mei and Xuejun Sha
  By discussing the development of 4-WFRFT, a discrete sequence algorithm for 4-WFRFT based on DFT is introduced and this makes it possible to use 4-WFRFT in a discrete time system. On the basis of analyzing the rotating, squeezing effect to the digital signal constellation by 4-WFRFT process also the similarity of 4-WFRFT signal to Gaussian distribution and the anti-scanning competence of 4-WFRFT signal, an alterable-parameter secure communication system is introduced based on 4-WFRFT secure communication system. Moreover, in the light of frequency-hopping patterns, a dynamic alterable-parameter strategy for single parameter 4-WFRFT and three strategies for multi-parameters 4-WFRFT are designed to avoid a non-receiver’s intercepting and decoding. "Tracking coefficient" is defined to judge the anti-scanning capacity. The results of simulation show that the alterable-parameter 4-WFRFT secure communication system has strong practical significance.
  Chang- Hoon Kim , Hannah Neiswender , Eun Joo Baik , Wen C. Xiong and Lin Mei
  Wnt regulation of muscle development is thought to be mediated by the β-catenin-TCF/LEF-dependent canonical pathway. Here we demonstrate that β-catenin, not TCF/LEF, is required for muscle differentiation. We showed that β-catenin interacts directly with MyoD, a basic helix-loop-helix transcription factor essential for muscle differentiation and enhances its binding to E box elements and transcriptional activity. MyoD-mediated transactivation is inhibited in muscle cells when β-catenin is deficient or the interaction between MyoD and β-catenin is disrupted. These results demonstrate that β-catenin is necessary for MyoD function, identifying MyoD as an effector in the Wnt canonical pathway.
  Daria Krivosheya , Lucia Tapia , Joshua N. Levinson , Kun Huang , Yunhee Kang , Rochelle Hines , Annie K. Ting , Ann Marie Craig , Lin Mei , Shernaz X. Bamji and Alaa El-Husseini
  Perturbations in neuregulin-1 (NRG1)/ErbB4 function have been associated with schizophrenia. Affected patients exhibit altered levels of these proteins and display hypofunction of glutamatergic synapses as well as altered neuronal circuitry. However, the role of NRG1/ErbB4 in regulating synapse maturation and neuronal process formation has not been extensively examined. Here we demonstrate that ErbB4 is expressed in inhibitory interneurons at both excitatory and inhibitory postsynaptic sites. Overexpression of ErbB4 postsynaptically enhances size but not number of presynaptic inputs. Conversely, knockdown of ErbB4 using shRNA decreases the size of presynaptic inputs, demonstrating a specific role for endogenous ErbB4 in synapse maturation. Using ErbB4 mutant constructs, we demonstrate that ErbB4-mediated synapse maturation requires its extracellular domain, whereas its tyrosine kinase activity is dispensable for this process. We also demonstrate that depletion of ErbB4 decreases the number of primary neurites and that stimulation of ErbB4 using a soluble form of NRG1 results in exuberant dendritic arborization through activation of the tyrosine kinase domain of ErbB4 and the phosphoinositide 3-kinase pathway. These findings demonstrate that NRG1/ErbB4 signaling differentially regulates synapse maturation and dendritic morphology via two distinct mechanisms involving trans-synaptic signaling and tyrosine kinase activity, respectively.
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