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Biomedical subjects

X G Wang

Publications and source records attributed to X G Wang.

At least 19 recordsLinked to original sources

A note on chaotic unimodal maps and applications.

Based on the word-lift technique of symbolic dynamics of one-dimensional unimodal maps, we investigate the relation between chaotic kneading sequences and linear maximum-length shift-register sequences. Theoretical and numerical evidence that the set of the maximum-length shift-register sequences is a subset of the set of the universal sequence of one-dimensional chaotic unimodal maps is given. By stabilizing unstable periodic orbits on superstable periodic orbits, we also develop techniques to control the generation of long binary sequences.

Algorithms↗

Adhesiveness of dental resin-based restorative materials investigated with atomic force microscopy.

This study aimed to show that the polymerization contraction of dental methacrylate-based materials, when used as adhesives on hard substrate, produces voids at the material-substrate interface. This phenomenology is closely related with the nanoleakage and the sealing ability of these materials. One prime/bond system, three restorative composite resins, and one orthodontic bonding system were cured by using mirror-like glass slides as a compliance-free reference substrate. The adhesive surface was analyzed by atomic force microscopy, and the polymerization contraction of bulk material was tested by laser beam-scanning method. Nanoperiodic structure of three-dimensional (3D) images, section analysis, and roughness characteristics (R(a) and R(z)) indicated that polymerization contraction produced voids at the interface. When the adhesive surface was exposed to oral simulating fluids (water, ethanol, and lactic acid solutions), hydrolytic degradation involved some hundreds of nanometers in depth. In visible light-cured (VLC) materials, the interface porosity decreased when an irradiation pause ( approximately 2 min) was carried out during gelation.

Adhesiveness↗

Two different life-history strategies determine the competitive outcome between Dirhinus giffardii (Chalcididae) and Pachycrepoideus vindemmiae (Pteromalidae), ectoparasitoids of cyclorrhaphous Diptera.

Dirhinus giffardii Silvestri and Pachycrepoideus vindemmiae Rondani are solitary parasitoids attacking puparia of many cyclorrhaphous flies. They are not typical ectoparasitoids, as they feed on host pupae within puparia that develop from the exoskeleton of host larvae. Dirhinus giffardii did not kill its host until the parasitoid egg developed into a larva, while P. vindemmiae permanently paralysed its host at the time of oviposition. As a result, ovipositing into a young host puparium (< 1 day old) in which the host pupa has not yet fully formed resulted in complete death of offspring in P. vindemmiae, but D. giffardii, although suffering higher mortality than in older host puparia, still showed a level of successful development. In a choice experiment, both parasitoids preferred to attack 2- to 3-day-old puparia in which the host pupae had fully formed, rather than 1-day-old host puparia. Pachycrepoideus vindemmiae always prevailed in competition because it injected venom that not only paralysed the host, but also caused the death of D. giffardii larvae in multi-parasitized hosts. Dirhinus giffardii preferred to attack unparasitized hosts rather than hosts previously parasitized by P. vindemmiae, while P. vindemmiae did not show a preference between unparasitized hosts and hosts previously parasitized by D. giffardii.

Animals↗

Is the voltage gate of connexins CO2-sensitive? Cx45 channels and inhibition of calmodulin expression.

The sensitivity of Cx45 channels to CO2, transjunctional voltage ( V(j)) and inhibition of calmodulin (CaM) expression was tested in oocytes by dual voltage clamp. Cx45 channels are very sensitive to V(j) and close with V(j) preferentially by the slow gate, likely to be the same as the chemical gate. With a CO2-induced drop in junctional conductance ( G(j)), both the speed of V(j)-dependent inactivation of junctional current ( I(j)) and V(j) sensitivity increased. With 40-mV V(j)-pulses, the tau of single exponential I(j) decay reversibly decreased by;40% during CO2 application, and G(j steady state)/G(j peak) decreased multiphasically, indicating that both kinetics and V(j) sensitivity of chemical/slow V(j) gating are altered by changes in [H(+)](i) and/or [Ca(2+)](i). CaM expression was inhibited with oligonucleotides antisense to CaM mRNA. With 15 min CO2, relative junctional conductance ( G(jt)/ G(jt0)) dropped to 0% in controls, but only by;17% in CaM-antisense oocytes. Similarly, V(j) sensitivity was significantly lessened in CaM-antisense oocytes. The data indicate that both the speed and sensitivity of V(j)-dependent inactivation of the junctional current of Cx45 channels are affected by CO2 application, and that CaM plays a key role in channel gating.

Animals↗

Newly imported larval parasitoids pose minimal competitive risk to extant egg-larval parasitoid of tephritid fruit flies in Hawaii.

Competitive displacement of fruit fly parasitoids has been a serious issue in the history of fruit fly biological control in Hawaii. This concern regarding competitive risk of new parasitoids has led to an overall tightening of regulations against the use of classical biological control to manage fruit flies. Fopius arisanus (Sonan), an egg-larval parasitoid, is the most effective natural enemy of tephritid fruit flies in Hawaii. This study evaluated the competitive risk of two recently introduced larval parasitoids, Diachasmimorpha kraussii Fullaway and Psyttalia concolor (Szépligeti), to F. arisanus attacking the Mediterranean fruit fly, Ceratitis capitata (Wiedemann). Fopius arisanus won almost all intrinsic competitions against both larval parasitoids through physiological suppression of egg development. 83.3% of D. kraussii eggs and 80.2% of P. concolor eggs were killed within three days in the presence of F. arisanus larvae within the bodies of multi-parasitized hosts. The mechanism that F. arisanusemploys to eliminate both larval parasitoids is similar to that it uses against three other early established larval fruit fly parasitoids: F. vandenboschi (Fullaway), D. longicaudata (Ashmead) and D. tryoni (Cameron). It suggests that introduction of these larval parasitoids poses minimal competitive risk to F. arisanus in Hawaii.

Animals↗

Allosteric behaviour of 1:5 hybrids of mutant subunits of Clostridium symbiosum glutamate dehydrogenase differing in their amino acid specificity.

Hybrid hexamers were made by refolding mixtures of two mutant forms of clostridial glutamate dehydrogenase. Mutant Cys320Ser (C320S) has a similar activity to the wild-type enzyme, but is unreactive with Ellman's reagent, 5,5'-dithiobis(2-nitrobenzoate) (DTNB). The triple mutant Lys89Leu/Ala163Gly/Ser380Ala (K89L/A163G/S380A), active with norleucine but not glutamate, is inactivated by DTNB, since the amino acid residue at position 320 is a cysteine residue. The chosen ratio favoured 1:5 hybrids of the triple mutant and C320S. The renatured mixture was treated with DTNB and separated on an NAD(+)-agarose column to which only C320S subunits bind tightly. Fractions were monitored for glutamate and norleucine activity and for releasable thionitrobenzoate to establish subunit stoichiometry. A fraction highly enriched in the 1:5 hybrid was identified. Homohexamers (C320S with 40 mM glutamate and 1 mM NAD(+) at pH 8.8, or K89L/A163G/S380A with 70 mM norleucine and 1 mM NAD(+) at pH 8.5) showed allosteric activation; succinate activated C320S approx. 50-fold (EC(50)=70 mM, h=2.4), and glutarate gave approx. 30-fold activation (EC(50)=35 mM, h=2.3). For the triple mutant, corresponding values were 80 mM and 2.2 for succinate, and 75 mM and 1.7 for glutarate, but maximal activation was only about 2-fold. In the 1:5 hybrid, with only one norleucine-active subunit per hexamer, responses to glutarate and succinate were still co-operative, and activation was more extensive than in the triple mutant homohexamer. A single norleucine-active subunit can thus respond co-operatively to a substrate analogue at the other five inactive sites. On the other hand, similar hyperbolic dependence on the norleucine concentration for the hybrid and the triple mutant homohexamer reflected the inability of C320S subunits to bind norleucine. With glutamate at pH 8.8, an h value of 3.6 was obtained for the 1:5 hybrid, in contrast with an h value of 5.2 for the C320S homohexamer. The "foreign" subunit evidently impedes inter-subunit communication to some extent.

Chromatography, Affinity↗

Purified cholera toxin B subunit from transgenic tobacco plants possesses authentic antigenicity.

Cholera toxin B subunit (CTB) mature protein was stably expressed in transgenic tobacco plants under the control of the CaMV 35S promoter and TMV Omega fragment. Fusion of the PR1b signal peptide coding sequence to the CTB mature protein gene increased the expression level by 24-fold. The tobacco-synthesized CTB (tCTB) was purified to homogeneity by a single step of immunoaffinity chromatography. The purified tCTB is predominantly in the form of pentamers with molecular weight identical to the native pentameric CTB, indicating that the PR1b-CTB fusion protein has been properly processed in tobacco cells. Furthermore, by immunodiffusion and immunoelectrophoresis, we have shown that the antigenicity of the purified tCTB is indistinguishable from that of the native CTB protein.

Animals↗

Contribution of an aspartate residue, D114, in the active site of clostridial glutamate dehydrogenase to the enzyme's unusual pH dependence.

Glutamate dehydrogenase from Clostridium symbiosum displays unusual kinetic behaviour at high pH when compared with other members of this enzyme family. Structural and sequence comparisons with GDHs from other organisms have indicated that the Asp residue at position 114 in the clostridial enzyme may account for these differences. By replacing this residue by Asn, a mutant protein has been created with altered functional properties at high pH. This mutant protein can be efficiently overexpressed in Escherichia coli, and several criteria, including mobility in non-denaturing electrophoresis, circular dichroism (CD) spectra and initial crystallisation studies, suggest a folding and an assembly comparable to those of the wild-type protein. The D114N mutant enzyme shows a higher optimum pH for activity than the wild-type enzyme, and both CD data and activity measurements show that the distinctive time-dependent reversible conformational inactivation seen at high pH in the wild-type enzyme is abolished in the mutant.

Aspartic Acid↗

Conversion of a glutamate dehydrogenase into methionine/norleucine dehydrogenase by site-directed mutagenesis.

In earlier attempts to shift the substrate specificity of glutamate dehydrogenase (GDH) in favour of monocarboxylic amino-acid substrates, the active-site residues K89 and S380 were replaced by leucine and valine, respectively, which occupy corresponding positions in leucine dehydrogenase. In the GDH framework, however, the mutation S380V caused a steric clash. To avoid this, S380 has been replaced with alanine instead. The single mutant S380A and the combined double mutant K89L/S380A were satisfactorily overexpressed in soluble form and folded correctly as hexameric enzymes. Both were purified successfully by Remazol Red dye chromatography as routinely used for wild-type GDH. The S380A mutant shows much lower activity than wild-type GDH with glutamate. Activities towards monocarboxylic substrates were only marginally altered, and the pH profile of substrate specificity was not markedly altered. In the double mutant K89L/S380A, activity towards glutamate was undetectable. Activity towards L-methionine, L-norleucine and L-norvaline, however, was measurable at pH 7.0, 8.0 and 9.0, as for wild-type GDH. Ala163 is one of the residues that lines the binding pocket for the side chain of the amino-acid substrate. To explore its importance, the three mutants A163G, K89L/A163G and K89L/S380A/A163G were constructed. All three were abundantly overexpressed and showed chromatographic behaviour identical with that of wild-type GDH. With A163G, glutamate activity was lower at pH 7.0 and 8.0, but by contrast higher at pH 9.0 than with wild-type GDH. Activities towards five aliphatic amino acids were remarkably higher than those for the wild-type enzyme at pH 8.0 and 9.0. In addition, the mutant A163G used L-aspartate and L-leucine as substrates, neither of which gave any detectable activity with wild-type GDH. Compared with wild-type GDH, the A163 mutant showed lower catalytic efficiencies and higher K(m ) values for glutamate/2-oxoglutarate at pH 7.0, but a similar k(cat)/K(m) value and lower K(m) at pH 8.0, and a nearly 22-fold lower S(0.5) (substrate concentration giving half-saturation under conditions where Michaelis-Menten kinetics does not apply) at pH 9.0. Coupling the A163G mutation with the K89L mutation markedly enhanced activity (100-1000-fold) over that of the single mutant K89L towards monocarboxylic amino acids, especially L-norleucine and L-methionine. The triple mutant K89L/S380A/A163G retained a level of activity towards monocarboxylic amino acids similar to that of the double mutant K89L/A163G, but could no longer use glutamate as substrate. In terms of natural amino-acid substrates, the triple mutant represents effective conversion of a glutamate dehydrogenase into a methionine dehydrogenase. Kinetic parameters for the reductive amination reaction are also reported. At pH 7 the triple mutant and K89L/A163G show 5 to 10-fold increased catalytic efficiency, compared with K89L, towards the novel substrates. In the oxidative deamination reaction, it is not possible to estimate k(cat) and K(m) separately, but for reductive amination the additional mutations have no significant effect on k(cat) at pH 7, and the increase in catalytic efficiency is entirely attributable to the measured decrease in K(m). At pH 8 the enhancement of catalytic efficiency with the novel substrates was much more striking (e.g. for norleucine approximately 2000-fold compared with wild-type or the K89L mutant), but it was not established whether this is also exclusively due to more favourable Michaelis constants.

Amino Acid Oxidoreductases↗

Calmodulin colocalizes with connexins and plays a direct role in gap junction channel gating.

The direct calmodulin (CaM) role in chemical gating was tested with CaM mutants, expressed in oocytes, and CaM-connexin labeling methods. CaMCC, a CaM mutant with greater Ca-sensitivity obtained by replacing the N-terminal EF hand pair with a duplication of the C-terminal pair, drastically increased the chemical gating sensitivity of Cx32 channels and decreased their Vj sensitivity. This only occurred when CaMCC was expressed before Cx32, suggesting that CaMCC, and by extension CaM, interacts with Cx32 before junction formation. Direct CaM-Cx interaction at junctional and cytoplasmic spots was demonstrated by confocal immunofluorescence microscopy in HeLa cells transfected with Cx32 and in cryosectioned mouse liver. This was confirmed in HeLa cells coexpressing Cx32-GFP (green) and CaM-RFP (red) or Cx32-CFP (cyan) and CaM-YFP (yellow) fusion proteins. Significantly, these cells did not form gap junctions. In contrast, HeLa cells expressing only one of the two fusion proteins (Cx32-GFP, Cx32-CFP, CaM-RFP or CaM-YFP) revealed both junctional and non-junctional fluorescent spots. In these cells, CaM-Cx32 colocalization was demonstrated by secondary immunofluorescent labeling of Cx32 in cells expressing CaM-YFP or CaM in cells expressing Cx32-GFP. CaM-Cx colocalization was further demonstrated at rat liver gap junctions by Freeze-fracture Replica Immunogold Labeling (FRIL).

Animals↗

[Synthesis and spectroscopic properties of rare earth complexes with o-phthalate and 1,10-phenanthroline].

The complexes of rare earth ions (Nd3+, Sm3+) with o-phthalate and 1,10-phenanthroline have been synthesized and characterized by elemental analysis, 1H NMR, IR, and DTA-TG. The compositions of complexes have been confirmed to be RE2L3.2H2O and RE2L3 phen.2H2O (RE: rare earth ions, L: o-phthalic, phen: 1,10-phenanthroline), their far-IR and FT-Raman spectra have been discussed and studied.

Chelating Agents↗

Expression of a recombinant human RGR opsin in Lentivirus-transduced cultured cells.

PURPOSE: Our goals were to produce a functional recombinant RPE retinal G protein-coupled receptor (RGR) opsin for biochemical studies and to test the efficiency of a lentiviral vector for transgene expression of human RGR. METHODS: A human RGR cDNA was cloned into a replication-defective lentiviral vector, and recombinant hRGR-Lentivirus was prepared for transduction of the ARPE-19, a human retinal pigment epithelium (RPE) cell line, and COS-7 cells. Recombinant RGR expression was detected by Western blot analysis, and functionality of the protein was tested by a [3H]all-trans-retinal binding assay. RESULTS: RGR protein was detected in each cell type after transduction with recombinant virus and was not observed in untreated cells. RGR expression in ARPE-19 cells increased steadily for up to 10 days after transduction and was stable for at least 6 months. The transduced ARPE-19 cells produced approximately 100-fold higher amounts of RGR protein than the transduced COS-7 cells. When cell membranes from the ARPE-19 cells were incubated with [3H]all-trans-retinal, the chromophore bound specifically to the expressed protein. Uptake of [3H]all-trans-retinol into the ARPE-19 cells was followed by specific binding of radiolabeled retinoid to RGR. CONCLUSIONS: Using a Lentivirus-derived gene delivery system, we were able to express high amounts of human RGR protein in the ARPE-19 human RPE cell line. The transduced ARPE-19 cells remain able to process all-trans-retinol, and the expressed protein is capable of binding to the all-trans-retinal chromophore. The Lentivirus-based expression of functional RGR can be used to study RGR in cultured cells and to test in vivo transduction of quiescent RPE cells.

Animals↗

Slow gating of gap junction channels and calmodulin.

Certain COOH-terminus mutants of connexin32 (Cx32) were previously shown to form channels with unusual transjuctional voltage (V(j)) sensitivity when tested heterotypically in oocytes against Cx32 wild type. Junctional conductance (G(j)) slowly increased by severalfold or decreases to nearly zero with V(j) positive or negative, respectively, at mutant side, and V(j) positive at mutant side reversed CO(2)-induced uncoupling. This suggested that the CO(2)-sensitive gate might be a V(j)-sensitive slow gate. Based on previous data for calmodulin (CaM) involvement in gap junction function, we have hypothesized that the slow gate could be a CaM-like pore plugging molecule (cork gating model). This study describes a similar behavior in heterotypic channels between Cx32 and each of four new Cx32 mutants modified in cytoplasmic-loop and/or COOH-terminus residues. The mutants are: ML/NN+3R/N, 3R/N, ML/NN and ML/EE; in these mutants, N or E replace M105 and L106, and N replace R215, R219 and R220. This study also reports that inhibition of CaM expression strongly reduces V(j) and CO(2) sensitivities of two of the most effective mutants, suggesting a CaM role in slow and chemical gating.

Animals↗

Calmodulin directly gates gap junction channels.

Cytosolic changes control gap junction channel gating via poorly understood mechanisms. In the past two decades calmodulin participation in gating has been suggested, but compelling evidence for it has been lacking. Here we show that calmodulin indeed is associated with gap junctions and plays a direct role in chemical gating. Expression of a calmodulin mutant with the N-terminal EF hand pair replaced by a copy of the C-terminal pair dramatically increases the chemical gating sensitivity of gap junction channels composed of connexin 32 and decreases their sensitivity to transjunctional voltage. The increased chemical gating sensitivity, most likely because of the higher overall Ca(2+) binding affinity of this mutant as compared with native calmodulin, and the decreased voltage sensitivity are only observed when the mutant is expressed before connexin 32. This indicates that the mutant, and by extension native calmodulin, must interact with connexin 32 before gap junctions are formed. Immunofluorescence data suggest further that this interaction leads to incorporation of native or mutant calmodulin into the connexon as an integral regulatory subunit.

Animals↗

Chemical gating of gap junction channels.

Chemical gating of gap junction channels is a complex phenomenon that may involve intra- and intermolecular interactions among connexin domains and a cytosolic molecule (calmodulin?) that may function as channel plug. This article focuses on the methodology we have employed for studying the molecular basis of chemical gating by lowered cytosolic pH. Our approach has combined molecular genetics and biophysics, using exposure to 100% CO(2) for assaying chemical gating efficiency. Chimeras of connexin 32 (Cx32) and connexin 38 (Cx38) and Cx32 mutants modified at residues of the cytoplasmic loop, the initial C-terminus domain, or both have been expressed in Xenopus oocytes, and channel expression and gating have been tested electrophysiologically by double voltage clamp. In addition, various channel forms, including homotypic, heterotypic, and heteromeric channel combinations, have been evaluated for chemical gating sensitivity.

Animals↗

Insights into the mechanism of domain closure and substrate specificity of glutamate dehydrogenase from Clostridium symbiosum.

Comparisons of the structures of glutamate dehydrogenase (GluDH) and leucine dehydrogenase (LeuDH) have suggested that two substitutions, deep within the amino acid binding pockets of these homologous enzymes, from hydrophilic residues to hydrophobic ones are critical components of their differential substrate specificity. When one of these residues, K89, which hydrogen-bonds to the gamma-carboxyl group of the substrate l-glutamate in GluDH, was altered by site-directed mutagenesis to a leucine residue, the mutant enzyme showed increased substrate activity for methionine and norleucine but negligible activity with either glutamate or leucine. In order to understand the molecular basis of this shift in specificity we have determined the crystal structure of the K89L mutant of GluDH from Clostridium symbiosum. Analysis of the structure suggests that further subtle differences in the binding pocket prevent the mutant from using a branched hydrophobic substrate but permit the straight-chain amino acids to be used as substrates. The three-dimensional crystal structure of the GluDH from C. symbiosum has been previously determined in two distinct forms in the presence and absence of its substrate glutamate. A comparison of these two structures has revealed that the enzyme can adopt different conformations by flexing about the cleft between its two domains, providing a motion which is critical for orienting the partners involved in the hydride transfer reaction. It has previously been proposed that this conformational change is triggered by substrate binding. However, analysis of the K89L mutant shows that it adopts an almost identical conformation with that of the wild-type enzyme in the presence of substrate. Comparison of the mutant structure with both the wild-type open and closed forms has enabled us to separate conformational changes associated with substrate binding and domain motion and suggests that the domain closure may well be a property of the wild-type enzyme even in the absence of substrate.

Amino Acid Oxidoreductases↗

Tropomyosin is localized in the nuclear matrix and chromosome scaffold of Physarum polycephalum.

The nuclei and chromosomes were isolated from plasmodia of Physarum polycephalum. The nuclear matrix and chromosome scaffold were obtained after the DNA and most of the proteins were extracted with DNase I and 2 M NaCl. SDS-PAGE analyses revealed that the nuclear matrix and chromosome scaffold contained a 37 kD polypeptide which is equivalent to tropomyosin in molecular weight. Immunofluorescence observations upon slide preparations labeled with anti-tropomyosin antibody showed that the nuclear matrix and chromosome scaffold emanated bright fluorescence, suggesting the presence of the antigen in them. Immunodotting results confirmed the presence of tropomyosin in the nuclear matrix and chromosome scaffold. Immunoelectron microscopic observations further demonstrated that tropomyosin was dispersively distributed in the interphase nuclei and metaphase chromosomes.

Animals↗