Biomedical subjects

G Hu

Publications and source records attributed to G Hu.

At least 91 records · Page 5Linked to original sources

PubMed2000

Synchronization of chaos in coupled systems

The stability of synchronous chaos of coupled oscillators with diffusive and gradient couplings is investigated. The stability boundaries of all transverse modes can be simultaneously drawn by justifying the boundary of a single mode, according to a scaling relation. Therefore, the distribution of stable and unstable regions can be explicitly shown in control parameter space. Bifurcations through different unstable modes, leading to different spatial orders, are analyzed.

Journal Article↗

PubMed2000

Nonlocal chaotic phase synchronization

A novel synchronization behavior, nonlocal chaotic phase synchronization, is investigated. For two coupled Rossler oscillators with only one forced by an injected periodic signal, the phase of the unforced oscillator can be locked to the phase of the periodic signal while the forced one is well unlocked by the signal; in a chain of coupled chaotic oscillators with nearest coupling, the phase of an oscillator (or a cluster) can be locked to another nonneighbor one. Moreover, the mechanism underlying the transition to nonlocal synchronization is discussed in detail.

Journal Article↗

PubMed2000

Intermingled basins and on-off intermittency in a multistate system

We consider a dynamical system containing infinite low-dimensional symmetric invariant subspaces, each of which has a chaotic state. Intermingled basins are found between these multiple chaotic states when they are stable in the subspaces. As a parameter of the system varies, the largest Lyapunov exponent transverse to the invariant subspace can change from negative to positive; then, the system dynamics changes from an intermingled basin state to a multistate on-off intermittency. The statistical behavior and physical transportation property for different dynamic states are investigated in detail.

Journal Article↗

PubMed2000

Collective phase slips and phase synchronizations in coupled oscillator systems

Phase synchronization dynamics in coupled limit cycles with distributed natural frequencies are explored. A synchronization tree from free oscillations to local clustering and global phase locking is found. A desynchronization-induced transition to chaos is shown. Near the onset of various phase synchronization points, a simultaneous quantized stick-slip feature of the phases of oscillators is observed on the desynchronization side and heuristically interpreted in terms of a heteroclinic path instability.

Journal Article↗

PubMed2000

Enhancement of phase synchronization through asymmetric couplings

Phase synchronization in lattices of coupled chaotic oscillators is studied. It is found that phase synchronization can be greatly improved by asymmetric biased coupling. The mechanism responsible for this effect is the transition from a localized wave to synchronized flow and nonlocal phase synchronization.

Journal Article↗

PubMed2000

Generalized synchronization versus phase synchronization

The relation between generalized synchronization and phase synchronization is investigated. It was claimed that generalized synchronization always leads to phase synchronization, and phase synchronization is a weaker form than generalized synchronization. We propose examples that generalized synchronization can be weaker than phase synchronization, depending on parameter misfits. Moreover, generalized synchronization does not always lead to phase synchronization.

Journal Article↗

PubMed2000

p12(DOC-1) is a novel cyclin-dependent kinase 2-associated protein.

Regulated cyclin-dependent kinase (CDK) levels and activities are critical for the proper progression of the cell division cycle. p12(DOC-1) is a growth suppressor isolated from normal keratinocytes. We report that p12(DOC-1) associates with CDK2. More specifically, p12(DOC-1) associates with the monomeric nonphosphorylated form of CDK2 (p33CDK2). Ectopic expression of p12(DOC-1) resulted in decreased cellular CDK2 and reduced CDK2-associated kinase activities and was accompanied by a shift in the cell cycle positions of p12(DOC-1) transfectants ( upward arrow G(1) and downward arrow S). The p12(DOC-1)-mediated decrease of CDK2 was prevented if the p12(DOC-1) transfectants were grown in the presence of the proteosome inhibitor clasto-lactacystin beta-lactone, suggesting that p12(DOC-1) may target CDK2 for proteolysis. A CDK2 binding mutant was created and was found to revert p12(DOC-1)-mediated, CDK2-associated cell cycle phenotypes. These data support p12(DOC-1) as a specific CDK2-associated protein that negatively regulates CDK2 activities by sequestering the monomeric pool of CDK2 and/or targets CDK2 for proteolysis, reducing the active pool of CDK2.

Blotting, Western↗

PubMed2000

Indoor coal combustion emissions, GSTM1 and GSTT1 genotypes, and lung cancer risk: a case-control study in Xuan Wei, China.

The lung cancer mortality rate in Xuan Wei County, China is among the highest in the country and has been associated with exposure to indoor smoky coal emissions that contain high levels of polycyclic aromatic hydrocarbons. This risk may be modified by variation in metabolism genes, including GSTM1, which encodes an enzyme known to detoxify polycyclic aromatic hydrocarbons. To investigate the relationship between GST genotypes and lung cancer risk in Xuan Wei County, we analyzed GSTM1 and GSTT1 genotypes in a population-based case-control study. A total of 122 lung cancer patients and 122 controls, individually matched by age, sex, and home fuel type, were studied. Compared to subjects who used less than 130 tons of smoky coal during their lifetime, heavier users (> or =130 tons) had a 2.4-fold (95% confidence interval, 1.3-4.4) increased risk of lung cancer. The GSTM1-null genotype was associated with a 2.3-fold (95% confidence interval, 1.3-4.2) increased risk of lung cancer. Furthermore, there was some evidence that smoky coal use was more strongly associated with lung cancer risk among GSTM1-null versus GSTM1-positive individuals. In contrast, the GSTT1 genotype was not significantly associated with lung cancer risk. Our data suggest that the GSTM1-null genotype may enhance susceptibility to air pollution from indoor coal combustion emissions.

Air Pollution, Indoor↗

PubMed2000

Visually-induced reorientation illusions as a function of age.

We reported previously that supine subjects inside a furnished room who are tilted 90 degrees may experience themselves and the room as upright to gravity. We call this the levitation illusion because it creates sensations similar to those experienced in weightlessness. It is an example of a larger class of novel static reorientation illusions that we have explored. Stationary subjects inside a furnished room rotating about a horizontal axis experience complete self rotation about the roll or pitch axis. We call this a dynamic reorientation illusion. We have determined the incidence of static and dynamic reorientation illusions in subjects ranging in age from 9 to 78 yr. Some 90% of subjects of all ages experienced the dynamic reorientation illusion but the percentage of subjects experiencing static reorientation illusions increased with age. We propose that the dynamic illusion depends on a primitive mechanism of visual-vestibular interaction but that static reorientation illusions depend on learned visual cues to the vertical arising from the perceived tops and bottoms of familiar objects and spatial relationships between objects. Older people become more dependent on visual polarity to compensate for loss in vestibular sensitivity. Of 9 astronauts, 4 experienced the levitation illusion. The relationship between susceptibility to reorientation illusions on Earth and in space has still to be determined. We propose that the Space Station will be less disorienting if pictures of familiar objects line the walls.

Adolescent↗

PubMed2000

Alterations of amino acid levels from striatum, hippocampus, and cerebral cortex induced by global cerebral ischemia in gerbil.

AIM: To investigate global cerebral ischemia-induced alterations in the levels of glutamate, aspartate, gamma-aminobutyric acid (GABA), glutamine, glycine, and taurine from hippocampus, striatum, and cerebral cortex in gerbils. METHODS: The gerbil global cerebral ischemia model was prepared by bilateral carotid artery occlusion; the contents of amino acids were assayed using high performance liquid chromatography (HPLC) combined with fluorescent detection after precolumn derivatization. RESULTS: After the ligation of bilateral carotid artery for 5 min and reperfusion for 60 min, the contents of glutamate from hippocampus, striatum, and cortex in gerbils were increased by 40%, 49%, and 67%, respectively. Similarly, the global cerebral ischemia resulted in increase by 80%, 69%, and 83% of aspartate contents in hippocampus, striatum, and cortex, respectively. Moreover, the same treatment also induced significant increases in the contents of GABA, glutamine, glycine, and taurine from various brain regions in gerbils. Furthermore, pretreatment with ketamine (120 mg/kg, i.p.) reversed ischemia-evoked increases of glutamate, aspartate, glycine, and glutamine in hippocampus, striatum, and cortex of gerbils. However, administration of ketamine (120 mg/kg, i.p.) markedly suppressed but not abolished the ischemia-induced increases of taurine and GABA from hippocampus, striatum, and cortex in gerbils. CONCLUSION: The increases of glutamate, aspartate, glycine, and glutamine induced by acute global cerebral ischemia may constitute the biochemical basis of ischemic brain damage. Correspondingly, the release of GABA and taurine may be an important self-protective mechanism. Ketamine may protect neurons against ischemic insult by inhibiting global cerebral ischemia-evoked increase of glutamate, glycine, and aspartate.

Animals↗

PubMed2000

[The analysis of linseed oil by FTIR and FT-Raman].

Linseed oil is an important natural sanitarian oil. To qualitative analyses the linseed oil, FTIR and FT-Raman were used to identify the contents of it. It is indicated that each component has characteristic frequency, and can be discriminated from others by IR and Raman spectroscopy. This is useful for the further on-line quantitative analysis and quality control of linseed oil.

Fourier Analysis↗

PubMed1999

mRNA cap recognition: dominant role of enhanced stacking interactions between methylated bases and protein aromatic side chains.

We have determined, by high resolution x-ray analysis, 10 structures comprising the mRNA cap-specific methyltransferase VP39 or specific mutants thereof in the presence of methylated nucleobase analogs (N1-methyladenine, N3-methyladenine, N1-methylcytosine, N3-methylcytosine) and their unmethylated counterparts, or nucleoside N7-methylguanosine. Together with solution affinity studies and previous crystallographic data for N7-methylguanosine and its phosphorylated derivatives, these data demonstrate that only methylated, positively charged bases are bound, indicating that their enhanced stacking with two aromatic side chains of VP39 (Tyr 22 and Phe 180) plays a dominant role in cap recognition. Four key features characterize this stacking interaction: (i) near perfect parallel alignment between the sandwiched methylated bases and aromatic side chains, (ii) substantial areas of overlap in the two-stacked rings, (iii) a 3.4-A interplanar spacing within the overlapping region, and (iv) positive charge in the heterocyclic nucleobase.

Binding Sites↗

PubMed1999

Segmental embolization by ethanol iodized oil emulsion for hepatocellular carcinoma.

The hemodynamic changes of portal vein before and after intra-arterial infusion of ethanol iodized oil emulsion (EIOE) were studied in 4 healthy dogs. Segmental transcatheter arterial embolization (TAE) using EIOE was performed in 55 patients with hepatocellular carcinoma (HCC). Twenty patients subsequently underwent surgery. It was concluded that segmental TAE might lead to double embolization of both hepatic arteries and portal veins. It is a more effective therapeutic method for HCC localized in one or a few segments, as compared with conventional TAE.

Adult↗

PubMed1999

Frequent nuclear/cytoplasmic localization of beta-catenin without exon 3 mutations in malignant melanoma.

Beta-Catenin has a critical role in E-cadherin-mediated cell-cell adhesion, and it also functions as a downstream signaling molecule in the wnt pathway. Mutations in the putative glycogen synthase kinase 3beta phosphorylation sites near the beta-catenin amino terminus have been found in some cancers and cancer cell lines. The mutations render beta-catenin resistant to regulation by a complex containing the glycogen synthase kinase 3beta, adenomatous polyposis coli, and axin proteins. As a result, beta-catenin accumulates in the cytosol and nucleus and activates T-cell factor/ lymphoid enhancing factor transcription factors. Previously, 6 of 27 melanoma cell lines were found to have beta-catenin exon 3 mutations affecting the N-terminal phosphorylation sites (Rubinfeld B, Robbins P, Elgamil M, Albert I, Porfiri E, Polakis P: Stabilization of beta-catenin by genetic defects in melanoma cell lines. Science 1997, 275:1790-1792). To assess the role of beta-catenin defects in primary melanomas, we undertook immunohistochemical and DNA sequencing studies in 65 melanoma specimens. Nuclear and/or cytoplasmic localization of beta-catenin, a potential indicator of wnt pathway activation, was seen focally within roughly one third of the tumors, though a clonal somatic mutation in beta-catenin was found in only one case (codon 45 Ser-->Pro). Our findings demonstrate that beta-catenin mutations are rare in primary melanoma, in contrast to the situation in melanoma cell lines. Nonetheless, activation of beta-catenin, as indicated by its nuclear and/or cytoplasmic localization, appears to be frequent in melanoma, and in some cases, it may reflect focal and transient activation of the wnt pathway within the tumor.

Cell Nucleus↗

PubMed1999

Design and implementation of a novel compression method in a tele-ultrasound system.

This paper represents a novel compression method for ultrasound images in a tele-ultrasound system. The encoder chooses the ultrasound scan line signals as the object to be compressed and transmitted other than the standard video images in conventional methods. Furthermore, nonuniform discrete wavelet transform is proposed considering the different resolutions in axial and lateral directions of ultrasound images. Experimental results show that the new method provides better compression performance than conventional methods in terms of a peak signal-to-noise ratio and processing time.

Algorithms↗

PubMed1999

Regulation of cell adhesion by PAI-1.

Type I plasminogen activator inhibitor (PAI-1) is the primary inhibitor of tissue- and urokinase-type plasminogen activators. It circulates in plasma complexed with vitronectin (VN), the primary PAI-1 binding protein. The somatomedin B (SMB) domain of VN contains both the high affinity PAI-1 binding site and the specific site for urokinase plasminogen activator receptor (uPAR). PAI-1 is able to regulate uPAR-mediated cell adhesion by competing with uPAR for VN binding. Binding of PAI-1 to SMD may also affect integrin-mediated cell adhesion to VN by hindering integrin binding to the RGD sequence adjacent to the uPAR binding site.

Animals↗

PubMed1999

Siah-1 N-terminal RING domain is required for proteolysis function, and C-terminal sequences regulate oligomerization and binding to target proteins.

The Drosophila seven in absentia (sina) gene was initially discovered because its inactivation leads to R7 photoreceptor defects. Recent data indicate that Sina binds to the Sevenless pathway protein Phyllopod, and together they mediate degradation of Tramtrack, a transcriptional repressor of R7 cell fate. Independent studies have shown that Sina and its highly related mammalian homologues Siah-1 and Siah-2 bind to the DCC (deleted in colorectal cancer) protein and promote its proteolysis via the ubiquitin-proteasome pathway. To determine the roles of mammalian Siahs in proteolysis and their interactions with target proteins, we sought to define Siah-1 domains critical for regulation of DCC. Mutant Siah-1 proteins, harboring missense mutations in the carboxy (C)-terminal domain analogous to those present in Drosophila sina loss-of-function alleles, failed to promote DCC degradation. Point mutations and deletion of the amino (N)-terminal RING finger domain of Siah-1 abrogated its ability to promote DCC proteolysis. In the course of defining Siah-1 sequences required for DCC degradation, we found that Siah-1 is itself rapidly degraded via the proteasome pathway, and RING domain mutations stabilized the Siah-1 protein. Siah-1 was found to oligomerize with itself and other Sina and Siah proteins via C-terminal sequences. Finally, evidence that endogenous Siah-1 regulates DCC proteolysis in cells was obtained through studies of an apparent dominant negative mutant of Siah-1, as well as via an antisense approach. The data indicate that the Siah-1 N-terminal RING domain is required for its proteolysis function, while the C-terminal sequences regulate oligomerization and binding to target proteins, such as DCC.

Animals↗

PubMed1999

Neoplastic transformation of RK3E by mutant beta-catenin requires deregulation of Tcf/Lef transcription but not activation of c-myc expression.

Current models predict that beta-catenin (beta-cat) functions in Wnt signaling via activation of Tcf/Lef target genes and that its abundance is regulated by the adenomatous polyposis coli (APC) and glycogen synthase kinase 3beta (GSK3beta) proteins. In colon and other cancers, mutations in APC or presumptive GSK3beta phosphorylation sites of beta-cat are associated with constitutive activation of Tcf/Lef transcription. In spite of assumptions about its oncogenic potential, prior efforts to demonstrate that mutated beta-cat will induce neoplastic transformation have yielded equivocal results. We report here that mutated, but not wild-type, beta-cat proteins induced neoplastic transformation of RK3E, an adenovirus E1A-immortalized epithelial cell line. Analysis of the properties of mutant beta-cat proteins and studies with a dominant negative Tcf-4 mutant indicated that the ability of beta-cat to bind and activate Tcf/Lef factors is crucial for transformation. c-myc has recently been implicated as a critical Tcf-regulated target gene. However, c-myc was not consistently activated in beta-cat-transformed RK3E cells, and a dominant negative c-Myc mutant protein failed to inhibit beta-cat transformation. Our findings underscore the role of beta-cat mutations and Tcf/Lef activation in cancer and illustrate a useful system for defining critical factors in beta-cat transformation.

Adenoviridae↗