Biomedical subjects

Guizhong Liu

Publications and source records attributed to Guizhong Liu.

7 recordsLinked to original sources

PubMed2006

A new texture generation method based on pseudo-DCT coefficients.

In this paper, a new method for generating different texture images is presented. This method involves a simple transform from a certain one-dimensional (1-D) signal to an expected two-dimensional (2-D) image. Unlike traditional methods, the input signal is generated by a simple 1-D function in our work instead of a sample texture. We first transform the 1-D input signal into frequency domain using fast Fourier transform. Based on the sufficient analysis in 2-D discrete cosine transform (DCT) domain, where each of the coefficients expresses a texture feature in a certain direction, the 2-D pseudo-DCT coefficients are then constructed by appropriately rearranging the Fourier coefficients in terms of their frequency components. Finally, the corresponding texture image can be produced by 2-D inverse DCT algorithm. We applied the proposed method to generate several stochastic textures (i.e., cloud, illumination, and sand), and several structural texture images. Experimental results indicate the good performance of the proposed method.

Algorithms↗

PubMed2005

Optimization of integer wavelet transforms based on difference correlation structures.

In this paper, a novel lifting integer wavelet transform based on difference correlation structure (DCCS-LIWT) is proposed. First, we establish a relationship between the performance of a linear predictor and the difference correlations of an image. The obtained results provide a theoretical foundation for the following construction of the optimal lifting filters. Then, the optimal prediction lifting coefficients in the sense of least-square prediction error are derived. DCCS-LIWT puts heavy emphasis on image inherent dependence. A distinct feature of this method is the use of the variance-normalized autocorrelation function of the difference image to construct a linear predictor and adapt the predictor to varying image sources. The proposed scheme also allows respective calculations of the lifting filters for the horizontal and vertical orientations. Experimental evaluation shows that the proposed method produces better results than the other well-known integer transforms for the lossless image compression.

Algorithms↗

PubMed2005

The mechanism of endogenous receptor activation functionally distinguishes prototype canonical and noncanonical Wnts.

Wnt glycoproteins are developmentally essential signaling molecules, and lesions afflicting Wnt pathways play important roles in human diseases. Some Wnts signal to the canonical pathway by stabilizing beta-catenin, while others lack this activity. Frizzled serpentine receptors mediate distinct signaling pathways by both classes of Wnts. Here, we tandemly linked noncanonical Wnt5a with the C-terminal half of Dickkopf-2 (Dkk2C), a distinct ligand of the Wnt coreceptor LRP5/6. Whereas Wnt5a, Dkk2C, or both together were incapable of stimulating endogenous canonical signaling, the Wnt5a/Dkk2C chimera efficiently activated this pathway in a manner inhibitable by specific antagonists of either frizzled or LRP receptors. Thus, activation of the canonical pathway requires ligand coupling of an endogenous frizzled/LRP coreceptor complex, rather than Wnt triggering each receptor independently. Moreover, fusion of Wnt5a with Dkk2C unmasked its ability to signal to Dishevelled through multiple frizzleds, indicating that the lack of functional interaction with LRP distinguishes noncanonical Wnt5a from canonical Wnts in mammalian cells. These findings provide a novel mechanism by which the same receptor can be switched between distinct signaling pathways depending on the differential recruitment of a coreceptor by members of the same ligand family.

Animals↗

PubMed2004

The human Frizzled 6 (HFz6) acts as a negative regulator of the canonical Wnt. beta-catenin signaling cascade.

Previously we have cloned the human Frizzled 1 (HFz1) and shown that it transmits the Wnt-3a-induced canonical pathway. We also cloned the human Frizzled 6 (HFz6) and show in the present study that, as opposed to HFz1, HFz6 did not activate the canonical Wnt pathway following exposure to various Wnts, whether belonging to the Wnt-1 or to the Wnt-5a group. Moreover we show that HFz6 repressed Wnt-3a-induced canonical signaling when co-expressed with HFz1. HFz6 repressed the canonical Wnt cascade activated also by various Wnt signaling intracellular mediators such as Dishevelled-1, a stabilized beta-catenin(S33Y) mutant, and LiCl-mediated repression of glycogen synthase kinase-3beta activity. Removal of HFz6 N'- or C'-terminal sequences abolished HFz6 repressive activity. As the HFz6 repressive effect was not associated with a decrease in the level of beta-catenin, it is suggested that HFz6 does not affect beta-catenin stabilization, implying that HFz6 transmits a repressive signaling that cross-talks with and inhibits the canonical Wnt pathway downstream of beta-catenin destruction complex. HFz6 did not affect the level of nuclear T-cell factor 4 (TCF4) nor did it affect beta-catenin.TCF4 complex formation. However, electrophoretic mobility shift assays indicated that HFz6 repressed the binding of TCF/lymphoid enhancer factor transcription factors to target DNA. Moreover we present data suggesting that HFz6 activates the transforming growth factor-beta-activated kinase-NEMO-like kinase pathway that blocks TCF/lymphoid enhancer factor binding to target promoters, thereby inhibiting the ability of beta-catenin to activate transcription of Wnt target genes.

Adaptor Proteins, Signal Transducing↗

PubMed2004

An autocrine mechanism for constitutive Wnt pathway activation in human cancer cells.

Autocrine Wnt signaling in the mouse mammary tumor virus model was the first identified mechanism of canonical pathway activation in cancer. In search of this transformation mechanism in human cancer cells, we identified breast and ovarian tumor lines with upregulation of the uncomplexed transcriptionally active form of beta-catenin without mutations afflicting downstream components. Extracellular Wnt antagonists FRP1 and DKK1 caused a dramatic downregulation of beta-catenin levels in these tumor cells associated with alteration of biological properties and increased expression of epithelial differentiation markers. Colorectal carcinoma cells with knockout of the mutant beta-catenin allele retained upregulated beta-catenin levels, which also could be inhibited by these Wnt antagonists. Together, these findings establish the involvement of autocrine Wnt signaling in human cancer cells.

Ataxia Telangiectasia Mutated Proteins↗

PubMed2003

A novel mechanism for Wnt activation of canonical signaling through the LRP6 receptor.

LDL receptor-related protein 6 (LRP6) is a Wnt coreceptor in the canonical signaling pathway, which plays essential roles in embryonic development. We demonstrate here that wild-type LRP6 forms an inactive dimer through interactions mediated by epidermal growth factor repeat regions within the extracellular domain. A truncated LRP6 comprising its transmembrane and cytoplasmic domains is expressed as a constitutively active monomer whose signaling ability is inhibited by forced dimerization. Conversely, Wnts are shown to activate canonical signaling through LRP6 by inducing an intracellular conformational switch which relieves allosteric inhibition imposed on the intracellular domains. Thus, Wnt canonical signaling through LRP6 establishes a novel mechanism for receptor activation which is opposite to the general paradigm of ligand-induced receptor oligomerization.

Allosteric Site↗

PubMed2003

[Bio-contact oxidation A/O process experiment on Guanting Reservior water].

The results of the experiments showed that biological contact A/O process had evident removal effect of contaminations such as COD, ammonia nitrogen in water entering into Guanting Reservior and could successfully resume the quality. Under the conditions that air supply flux(gas/ammonia nitrogen) was more than 0.1 L/mg and influent ammonia nitrogen loading was lower than 0.08 kg/(m3.d), effluent COD was steadily 30 mg/L around, ammonia nitrogen removal rate was higher than 60%, and TN removal rate was 1.0%-31.3%. The main control parameter was influent ammonia nitrogen loading, which was proposed to be lower than 0.08 kg/(m3.d).

Ammonia↗