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J G Liu

Publications and source records attributed to J G Liu.

At least 37 records · Page 2Linked to original sources
PubMed2000

The murine SCP3 gene is required for synaptonemal complex assembly, chromosome synapsis, and male fertility.

During meiosis, the homologous chromosomes pair and recombine. An evolutionarily conserved protein structure, the synaptonemal complex (SC), is located along the paired meiotic chromosomes. We have studied the function of a structural component in the axial/lateral element of the SC, the synaptonemal complex protein 3 (SCP3). A null mutation in the SCP3 gene was generated, and we noted that homozygous mutant males were sterile due to massive apoptotic cell death during meiotic prophase. The SCP3-deficient male mice failed to form axial/lateral elements and SCs, and the chromosomes in the mutant spermatocytes did not synapse. While the absence of SCP3 affected the nuclear distribution of DNA repair and recombination proteins (Rad51 and RPA), as well as synaptonemal complex protein 1 (SCP1), a residual chromatin organization remained in the mutant meiotic cells.

Animals↗
PubMed2000

Fractal research on red blood cell aggregation.

By analyzing the aggregation images, we found that the distribution of RBCs shows fractal characteristics. A CCA (Cluster-Cluster Aggregation) model was chosen trying to simulate the RBC aggregation and to reveal the relationship between the fractal dimension and the binding energy.

Computer Simulation↗
PubMed1999

Synthesis, characterization and the effect of ligand planarity of [Ru(bpy)2L]2+ on DNA binding affinity.

Two structurally related ligands (L) 4,5,9,18-tetraazaphenanthreno[9,10-b] triphenylene (taptp) and 2,3-diphenyl-1,4,8,9-tetraazatriphenylene (dptatp), and their related complexes of [Ru(bpy)2L]2+ have been synthesized and characterized by elemental analyses, 1H NMR and mass spectra. Their electrochemical properties were also examined. Both complexes emit intense luminescence in organic solvent but are quenched in water to different extents. The interactions of the complexes with calf thymus DNA have been investigated by viscosity, absorption, emission and circular dichroism spectra. The intrinsic binding constants of [Ru(bpy)2(taptp)]2+ and [Ru(bpy)2(dptatp)]2+ are 1.7 x 10(5) and 3.8 x 10(4) M-1, respectively. All data indicate that both complexes bind enantioselectively to double-stranded calf thymus DNA via the intercalative mode, with stronger affinity for the fully planar ligand complex of [Ru(bpy)2(taptp)]2+.

2,2'-Dipyridyl↗
PubMed1999

Methadone-induced desensitization of the delta-opioid receptor is mediated by uncoupling of receptor from G protein.

Chronic exposure of neuroblastoma x glioma (NG108-15) hybrid cells and rat mu-receptor-transfected Chinese hamster ovary (CHO) cells to 10 microM morphine resulted in a compensatory and antagonist-precipitated increase in cAMP accumulation. However, incubation of these cells with 10 microM methadone during chronic exposure to morphine substantially prevented the actions of morphine. Chronic methadone treatment caused a pronounced reduction in agonist-stimulated binding of [35S]GTPgammaS to G proteins, but it did not produce significant down-regulation of delta-opioid receptors, whereas chronic morphine treatment failed to induce either uncoupling of delta-opioid receptors from G proteins or down-regulation of delta-opioid receptors. In contrast to chronic treatment with morphine alone, treatment of cells with morphine and methadone simultaneously resulted in a significant decrease in agonist-stimulated binding of [35S]GTPgammaS to G proteins. The action of methadone-mediated uncoupling of the receptor from the G protein was blocked by the nonselective protein kinase inhibitor [1-(5-isoqinolinesulfony)-2-methylpiprazine](H7), but not by the specific protein kinase C inhibitor, chelerythrine. The data demonstrate that methadone desensitizes the delta-opioid receptor by uncoupling the receptor from the G protein. In this way, methadone antagonizes the morphine-mediated adaptive sensitization and overshoot of adenylate cyclase. The functional desensitization of opioid receptors by methadone may explain why methadone is effective in the treatment of morphine dependence.

Animals↗
PubMed1999

The difference between methadone and morphine in regulation of delta-opioid receptors underlies the antagonistic effect of methadone on morphine-mediated cellular actions.

To investigate the cellular and molecular basis for using methadone in substitution therapy for morphine addiction, the difference between methadone and morphine in causing desensitization of delta-opioid receptors was examined, and the effects of methadone pretreatment on opiate-induced inhibition of forskolin-stimulated cAMP accumulation was studied. Methadone substantially attenuated the ability of [D-Ala2,D-Leu5]enkephalin (DADLE), morphine and methadone to inhibit forskolin-stimulated cAMP accumulation. Methadone was able to block the morphine-induced compensatory increase in intracellular cAMP levels and naloxone-precipitated cAMP overshoot after chronic exposure to morphine. The protein kinase inhibitor (1-5-isoquinolinesulfony)-2-methylpiperazine) (H7) could significantly block the chronic methadone treatment-induced loss of the ability of DADLE to inhibit adenylate cyclase. The protein kinase inhibitor chelerythrine was able to block the acute methadone treatment-induced loss of the ability of DADLE to inhibit adenylate cyclase. In contrast, morphine did not cause a substantial desensitization of the delta-opioid receptor. These results indicate that methadone is different from morphine in its regulation of the delta-opioid receptor. In addition, these results also indicate that the mechanisms of delta-opioid receptor desensitization induced by acute and chronic methadone treatment are different.

Adenylyl Cyclases↗
PubMed1999

l-S.R-daurisoline protects cultured hippocampal neurons against glutamate neurotoxicity by reducing nitric oxide production.

AIM: To explore mechanisms of l-S.R-daurisoline (DS)-mediated protection of cultured hippocampal neurons from sodium glutamate (Glu) cytotoxicity. METHODS: Cultured neurons obtained from rat hippocampus were used to examine the protective effect of DS against Glu neurotoxicity. Cell viability was estimated using trypan blue dye exclusion method and [3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) assay. Release of nitric oxide (NO) from the hippocampus was assayed using rat thoracic aorta in vitro. RESULTS: DS 0.01-10 mumol.L-1 concentration-dependently inhibited Glu cytotoxicity and increased cell viability with 50% prevention of cell death 2.8 mumol.L-1 (95% confidence limit 1.2-5.9 mumol.L-1). This protection was mostly attenuated by L-arginine (Arg) 1 mmol.L-1. DS 0.01-10 mumol.L-1 did not prevent sodium nitropusside (SNP) 500 mumol.L-1-induced cytotoxicity. DS 10 mumol.L-1 blocked Glu-elicited relaxation of the endothelium-denued rat aortic rings contracted by norepinephrine (NE) 10 mumol.L-1 in the presence of hippocampal tissue, but did not affect that induced by SNP. This indicated that DS inhibited Glu-triggered NO generation but did not prevent the effects of NO. CONCLUSION: DS prevented neurons from Glu neurotoxicity by inhibiting Glu-triggered NO generation.

Alkaloids↗
PubMed1999

Effects of opioid receptor agonists on cAMP second messenger system.

AIM: To study the mechanism underlying the difference in physical dependence potential of morphine (Mor), methadone (Met), buprenorphine (Bup), etorphine (Eto), and dihydroetorphine (DHE). METHODS: Adenylate cyclase of NG108-15 cells were used for studying the effects of different opiates on cAMP second messenger system. RESULTS: Bup, DHE, and Eto were distinct from Mor in naloxone-precipitated rebound response of cAMP in NG108-15 cells chronically treated with these opiates. Naloxone given to NG108-15 cells treated with Mor for 24 h produced marked rebound response of adenylate cyclase. While no such rebound response was detected when the cells were treated with Bup, DHE, and Eto for 24 h. The naloxone-induced rebound response of cAMP in chronic Met-treated NG108-15 cells was also lower than that in chronic Mor-treated NG108-15 cells. Following a prolonged exposure to Bup, DHE, and Eto for 72 h, the naloxone-induced rebound response of cAMP in these cells was still markedly lower than that in Mor-treated cells. The substitution of Mor with Bup, Met, DHE, and Eto inhibited naloxone-induced rebound response of cAMP in chronic Mor-treated NG108-15 cells. CONCLUSION: There were distinct differences among these opiates in regulating cAMP second messenger system, which was related to their physical dependence potential.

Adenylyl Cyclases↗
PubMed1999

Effects of low-pH treatment on cAMP second messenger system regulated by different opioid agonists.

AIM: To study the mechanism of opioid agonists in regulation of cAMP second messenger system. METHODS: Low-pH treatment was used to deplete the stimulatory G protein (Gs) function. The effects of some opiates on adenylate cyclase were compared between control and low-pH treatment membranes. RESULTS: In contrast to dehydroetorphine (DHE), etorphine (Eto), morphine (Mor) and methadone (Met) substantially increased the inhibitory effects on adenylate cyclase in membranes prepared from naive and chronic Mor- or Met-treated NG108-15 cells by low-pH treatment. In contrast to Mor, DHE and Eto did not result in significant decrease in the inhibitory effects on adenylate cyclase in membranes from the cells treated chronically with DHE or Eto. Marked rebound of adenylate cyclase was also not observed in membranes from chronic DHE or Eto-treated cells when precipitated with naloxone. Low-pH treatment eliminated naloxone-induced rebound of adenylate cyclase in chronic Mor-treated cells. CONCLUSION: The difference in opiate-induced functional adaptive alteration of Gs is at least one biochemical mechanism of developing opiate tolerance and dependence.

Adenylyl Cyclases↗
PubMed1999

[Guided bone regeneration by using biodegradable co-polymer membranes in rabbits].

OBJECTIVE: To repair long bone segmental defects using biodegradable poly epsilon-caprolactone (PCL) and polylactic acid(PLA) co-polymer membranes, and explore its role and mechanism in guided bone regeneration (GBR). METHODS: Rabbit radial segmental defects (1.2 cm in length, retain the periosteum) were created in this study, 24 animals were divided into 2 groups. The membranes were used to enclose the defects in experimental group, and no treatment in control group. After 3, 6, and 12 weeks of operation, X-ray, gross and histological examinations were observed. RESULTS: The bone regeneration of experimental group was better than that of control group. Three weeks after operation, obvious external callus along the membrane were found in experimental group, and bony linking composed of external callus bridge were found in 6 weeks after operation. After 12 weeks of operation, callus bridge outside the membrane and bony reunion inside the membrane were achieved in experimental group. While in control group, typical nonunion was observed after 6 weeks of operation. CONCLUSION: Guided bone regeneration can be achieved by using biodegradable membrane. The defects are repaired by the means of outside membrane callus and relatively late inside membrane callus. The membrane can prevent the ingrowth of fibrous tissue into defect area, thus nonunion are avoid, and keep a high concentration of nutritive elements, also serve as a frame for osteocyte growth to enhance bone healing.

Absorbable Implants↗
PubMed1998

The synaptonemal complex protein SCP3 can form multistranded, cross-striated fibers in vivo.

The synaptonemal complex protein SCP3 is part of the lateral element of the synaptonemal complex, a meiosis-specific protein structure essential for synapsis of homologous chromosomes. We have investigated the fiber-forming properties of SCP3 to elucidate its role in the synaptonemal complex. By synthesis of SCP3 in cultured somatic cells, it has been shown that SCP3 can self-assemble into thick fibers and that this process requires the COOH-terminal coiled coil domain of SCP3, as well as the NH2-terminal nonhelical domain. We have further analyzed the thick SCP3 fibers by transmission electron microscopy and immunoelectron microscopy. We found that the fibers display a transversal striation with a periodicity of approximately 20 nm and consist of a large number of closely associated, thin fibers, 5-10 nm in diameter. These features suggest that the SCP3 fibers are structurally related to intermediate filaments. It is known that in some species the lateral elements of the synaptonemal complex show a highly ordered striated structure resembling that of the SCP3 fibers. We propose that SCP3 fibers constitute the core of the lateral elements of the synaptonemal complex and function as a molecular framework to which other proteins attach, regulating DNA binding to the chromatid axis, sister chromatid cohesion, synapsis, and recombination.

3T3 Cells↗
PubMed1998

Developmental role of PTHrP in murine molars.

Although PTHrP is produced in multiple fetal tissues, its precise physiological functions have yet to be clearly elucidated. The present study was undertaken to elucidate the biological role of PTHrP in the development of tooth. In rat tooth germs, the PTHrP and its receptor genes were expressed in the enamel organ and dental mesenchyme, respectively. When mouse tooth explants were cultured with antisense oligodeoxyribonucleotides (ODN) against mouse PTHrP mRNA in serum-free medium, an invasion of bone tissue was observed in the tooth germs. On the other hand, the explants cultured without ODN or with sense ODN showed normal histological structures similar to those observed in vivo. These results suggest that PTHrP is essential for tooth development and for the protection of tooth germs from the invasion of bone tissue.

Animals↗
PubMed1997

The Sycp1 loci of the mouse genome: successive retropositions of a meiotic gene during the recent evolution of the genus.

The murine Sycp1 gene is expressed at the early stages of meiosis. We show that it is composed of a number of small exons and localized on mouse chromosome 3. In the laboratory strains, two retrogenes were also identified. The first one (Sycp1-ps1), on chromosome 7, has accumulated point mutations and deletions and is not transcribed. A second retrogene (Sycp1-ps2), on chromosome 8, is inserted within the continuity of a moderately repeated element, in an intron of another gene (Cad11). The two retroposition events can be dated to distinct periods in the evolution of the Muridae. Sycp1-ps2 has kept features indicative of a relatively recent origin, namely a nearly intact coding region, a poly(A) tail, and 14-bp terminal repeats. Its recent origin was confirmed by the fact that it is found in all the laboratory strains of mice, but neither in a recent isolate from Mus musculus domesticus wild stocks nor in the closely related subspecies M. musculus musculus, M. m. molossinus, M. m. castaneus, and M. m. bactrianus. Appearance of the more ancient Sycp1-ps1 retrogene is concomitant with the radiation of the genus. It is present in various Mus species (M. spretus, M. spicilegus, M. macedonicus, and M. cookii), but neither in the rat nor in the more closely related Pyromis genus. Transposition of retrotranscripts during meiosis and their hereditary establishment thus appear to occur relatively frequently. They may, therefore, play a significant role in the evolutionary process.

Animals↗
PubMed1996

Localization of the N-terminus of SCP1 to the central element of the synaptonemal complex and evidence for direct interactions between the N-termini of SCP1 molecules organized head-to-head.

The synaptonemal complex (SC) is a meiosis-specific, tripartite structure essential for synapsis of homologous chromosomes; it contains a central element positioned between two lateral elements and transversal filaments connecting the lateral elements. In mammals, a major constituent of the transversal filament is known: the SCP1 protein. It contains a long central coiled-coil motif and the molecules are probably organized as dimers, each forming a coiled-coil fiber. We have now developed a new sensitive procedure for immunoelectron microscopy of synaptonemal complex proteins and determined the exact localization of the two nonhelical ends of the SCP1 protein within the mouse synaptonemal complex. We found that the N-terminal end of the SCP1 protein is located within the central element of the synaptonemal complex, whereas the C-terminal end is close to or within the lateral element of the synaptonemal complex. This result supports the notion that SCP1 is an extended filamentous protein and that the two molecules of the putative SCP1 dimer are likely to have the same polarity. The observation that the N-termini are confined to the central element indicated that SCP1 dimers, anchored in opposite lateral elements, could establish contact with each other in the central element via their N-termini. To test this possibility we used the yeast two-hybrid system and found that the N-terminal end of the SCP1 protein indeed strongly interacted with itself, but not with other protein domains tested. We therefore suggest that a transversal filament consists of one or more pairs of SCP1 dimers, each pair being organized in a head-to-head arrangement with the C-termini anchored in the lateral elements and the two N-termini being joined in the central element.

Animals↗
PubMed1996

Expression of cytokeratin 14 in ameloblast-lineage cells of the developing tooth of rat, both in vivo and in vitro.

In the search for a cell marker useful for studying tooth development, immunohistochemical studies using antibodies against cytokeratin 14 (K14), c-Met/hepatocyte growth factor receptor and amelogenin were carried out in the developing tooth of the newborn rat and in primary cultured cells of the ameloblast lineage, including inner enamel epithelium cells, preameloblasts and ameloblasts, prepared from the mandibular incisors of postnatal 7-day-old rats. The appearance of K14 was cell- and differentiation-stage specific, i.e. there was a weak expression signal within inner enamel epithelial cells that were in the proliferating stage, and there were strong signals within preameloblasts and ameloblasts that were in the post-proliferating and amelogenesis stages, respectively. In the culture system, c-Met appeared in all cells, whereas K14 and amelogenin appeared mainly in clustered cells that were considered to be in the post-proliferating stage. K14 was detected earlier than amelogenin, and it was also confirmed by immunofluorostaining that c-Met, K14 and amelogenin were coexpressed in ameloblasts. These findings indicate that K14 is a good new marker for ameloblast-lineage cells during rat tooth development both in vivo and in vitro.

Ameloblasts↗
PubMed1996

Hepatocyte growth factor is involved in the morphogenesis of tooth germ in murine molars.

The patterns of gene expression for hepatocyte growth factor (HGF) and its receptor, c-Met, were revealed in the tooth germ of rat mandibular molars using RT-PCR. In situ hybridization demonstrated that the HGF gene was expressed only in the cells of the dental papilla of the tooth germ in vivo. The characteristic temporospatial distribution of HGF and c-Met during germ development was revealed using immunohistochemical studies in vivo. In order to demonstrate the functional role played by HGF in tooth development, HGF translation arrest by antisense phosphorothioate oligodeoxynucleotide (ODN) was carried out in vitro. In the control experiment, explants of tooth germs from embryonic 14 day mice were cultured in a modification of Trowell's system under serum-free and chemically defined conditions for two weeks. Other explants were cultured with 15mer antisense or sense ODN targeted to the HGF mRNA. Both the control and the sense-treated explants showed normal histological structure, as observed in vivo. On the other hand, antisense-treated explants exhibited an abnormal structure in which the enamel organs were surrounded by a thin layer of dentin and dental papilla, appearing 'inside-out' compared to the control and sense-treated explants, although the cytodifferentiation of ameloblasts and odontoblasts was not inhibited. The explants treated with recombinant human HGF combined with antisense ODN showed normal development, indicating that exogenous HGF rescued the explants from the abnormal structure caused by antisense ODN. The findings of a BrdU incorporation experiment suggested that the imbalance between the proliferation activity of the inner enamel epithelium and that of the dental papilla caused by HGF translation arrest results in the abnormal structure of the tooth germ. These results indicate that HGF is involved in the morphogenesis of the murine molar.

Animals↗
PubMed1996

Visual evoked potential enhancement by an artificial neural network filter.

The application of an artificial neural network filter (ANNF) to estimate the visual evoked potential (VEP) is presented. VEP is the gross electrical response of the brain to visual stimuli. Due to the low SNR, it is difficult to extract response from individual stimulus trials. The ANNF we used estimates the deterministic component of the signal and removes the noise uncorrelated with the stimulus, even when the noise is colored. The ANNF is trained through back-error propagation with a data set consisting of a training signal and a target signal. The training signal is the raw VEP from a single trial having a SNR of about -5 dB, while the target signal has a higher SNR which is achieved by ensemble averaging 100 stimulus trials. Simulated signals were generated to test the performance of the ANNF. Results show that the ANNF could greatly enhance the SNR of the VEP to single visual stimulus. Thus the total number of ensembles is reduced. In clinical applications, the traditional ensemble averaging method requires a hundred ensembles to determine the VEP. When ANNF is used, about 20 ensembles are sufficient for the same purpose.

Adolescent↗