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Biomedical subjects

Y Xie

Publications and source records attributed to Y Xie.

At least 325 records · Page 18Linked to original sources
PubMed1996

Modulation of multidrug resistance gene (mdr-1) with antisense oligodeoxynucleotides.

1. Multidrug resistance is the major obstacle to successful cancer chemotherapy. Circumventing multidrug resistance therefore represents a high priority for clinical anti-cancer treatment. Among many reversal strategies, antisense oligodeoxynucleotides may offer a molecular targeting tool for overcoming cellular multidrug resistance. 2. Two 17-mer phosphorothioate antisense oligomers, complementary to the 5' end of the ATG initiator codon-containing region and loop-forming site (located at nucleotides 991-1007 from the first ATG codon) in mdr-1 cDNA sequence, were synthesized. The purpose was to study their effects on the function and expression of P-glycoprotein and mdr-1 gene. 3. The results showed that 10 mumol/l antisense oligomers could significantly inhibit the growth of multidrug resistant K562/Adm cells cultured in adriamycin-containing medium. No such effect was observed for parental (sensitive) K562/S cells. Intracellular daunorubicin accumulation increased greatly in the K562/Adm cells after they were treated with oligomers for 48 h and P-glycoprotein synthesis was strikingly reduced. 4. Further investigation with [alpha-32P]dCTP incorporation by the reverse transcriptase-polymerase chain reaction method revealed that antisense oligomers could result in a reduction in the level of mdr-1 mRNA, probably through hindering mdr-1 gene transcription. 5. The high reversal efficiency and specificity of antisense oligomers in regulating mdr-1 gene expression suggest a potential clinical application in gene therapy for drug resistant malignancies.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

The influence of Glu44 and Glu56 of cytochrome b5 on the protein structure and interaction with cytochrome c.

The gene encoding trypsin-solubilized bovine liver microsomal cytochrome b5 (82 residues in length) has been mutated, in which the codons of Glu44 and Glu56 were changed to those of Ala. The mutated genes were expressed in Escherichia coli successfully and three mutant proteins (E44A, E56A and E44/56A) were obtained. The UV-visible, CD and 1H NMR spectra of proteins have been studied. The results show that the mutagenesis at surface residues does not alter the secondary and tertiary structures of cytochrome b5 significantly. The interactions between recombinant cytochrome b5 and its mutants with cytochrome c were studied by using optical difference spectra. The results demonstrated that both Glu44 and Glu56 of cytochrome b5 participate in the formation of a complex between cytochrome b5 and cytochrome c.

Animals↗
PubMed1996

Vascular manifestations of small solitary pulmonary masses. Angiographic-pathologic correlations and clinical significance.

RATIONALE AND OBJECTIVES: By performing pulmonary specimen angiographies, the authors attempted to determine the pathologic correlations of the vascular-related radiologic manifestations within, at the edge of, and adjacent to the small solitary pulmonary masses, and to evaluate their usefulness in differentiating small bronchogenic carcinomas from tuberculomas. METHODS: A total of 29 resected lobe specimens with 1.5- to 3.5-cm solitary pulmonary masses, including 24 carcinomas and 5 tuberculomas, were studied prospectively with preoperative radiographs, postoperative specimen arteriographies (in 19 carcinomas and 5 tuberculomas), and venographies (in 5 carcinomas), 10- to 15 micrograms-thick whole-mount sections, and 5-micrograms-thick slices for the examination of angiographic-pathologic correlation. Another series of chest radiographs and conventional tomographs of 100 patients with 1- to 3-cm peripheral pulmonary masses, including 60 carcinomas and 40 tuberculomas, were reviewed retrospectively and analyzed with the chi-square test. RESULTS: Specimen angiographies showed the intralesion avascularity, small arterial speculation, and lobulation or notch at the mass margin with arterial compression, as well as vascular convergence to the mass, in both carcinoma and tuberculoma groups. The irregular arterial wall (79.2%) and venous dilation distal to the mass (100%) were found in the carcinoma group only. Microscopically, arterial or venous fibrous hyperplasia was observed in both carcinomas and tuberculomas, whereas the arterial erosion by tumor tissue and tumor emboli within the vessels were found in carcinomas only. The retrospective review of the 100 patients showed that two radiologic signs of the vascular convergence to the mass and the vascular dilation distal to the mass occurred at similar frequencies (12%-13%) between the carcinoma and tuberculoma groups. CONCLUSIONS: In addition to compression of vessels by tumor and vessel occlusion by tumor embolus, pulmonary vascular fibrotic hyperplasia can cause intramass avascularity. Small vessels running vertically into or from the mass margin can construct the spiculation sign of the tuberculomas. Any evidence of pulmonary vascular irregularity will indicate a bronchogenic carcinoma. The vascular convergence to the mass and the vascular dilation distal to the mass are not specific radiologic signs for small solitary bronchogenic carcinomas.

Adenocarcinoma↗
PubMed1996

Vpr-induced cell cycle arrest is conserved among primate lentiviruses.

We previously reported that expression of human immunodeficiency virus type 1 strain NL4-3 (HIV-1(NL4-3))vpr causes cells to arrest in the G2 phase of the cell cycle. We examined the induction of cell cycle arrest by other HIV-1 isolates and by primary lentiviruses other than HIV-1. We demonstrate that the vpr genes from tissue culture-adapted or primary isolates of HIV-1 are capable of inducing G2 arrest. In addition, we demonstrate that induction of cell cycle arrest is a conserved function of members of two other groups of primate lentiviruses, HIV-2/simian immunodeficiency virus strain sm (SIVsm)/SIVmac and SIVagm. vpr from HIV-1, HIV-2, and SIVmac induced cell cycle arrest when transfected in human (HeLa) and monkey (CV-1) cells. vpx from HIV-2 and SIVmac did not induce detectable cell cycle arrest in either cell type, and SIVagm vpx was capable of inducing arrest in CV-1 but not HeLa cells. These results indicate that induction of cell cycle perturbation is a general property of lentiviruses that infect primates. The conservation of this viral function throughout evolution suggests that it plays a key role in virus-host relationships, and elucidation of its mechanism may reveal important clues about pathology induced by primary lentiviruses.

Alleles↗
PubMed1996

Characterization of the rat Na+/H+ exchanger isoform NHE4 and localization in rat hippocampus.

The kinetics of the Na+/H+ exchanger (NHE) isoform NHE4 were studied by measuring 22Na+ fluxes in stably transfected NHE-deficient fibroblasts. Unlike NHE1, NHE2, and NHE3, activation of this isoform is dependent on hyperosmolarity-induced cell shrinkage. It is virtually inactive at isosmolarity and most active at 490 mosM. When induced by cell shrinkage, NHE4 exhibits a sigmoidal response to increasing extracellular Na+ concentrations, suggesting allosteric or cooperative binding kinetics. In comparison, NHE1 and -3 exhibit hyperbolic velocity vs. extracellular Na+ concentration responses at both iso- and hyperosmolar conditions. Unlike NHE1 and NHE4, hyperosmolarity-induced cell shrinkage inhibits NHE3 activity in transfected fibroblasts, reducing maximum velocity by 40%, with no effect on binding affinity to extracellular Na+.NHE4 is relatively insensitive to inhibition by amiloride analogues in the order 5-(N,N-dimethyl)amiloride > 5-(N,N-hexamethylene)amiloride ride > amiloride > 5-(N-ethyl-N-isopropyl)amiloride. Time-dependent inhibition of activity by cytochalasin D suggests a relationship between the actin cytoskeleton and regulation by cell shrinkage. By in situ hybridization of fixed tissues, NHE4 mRNA was found to be highly expressed in the cavi amnoni fields of rat hippocampus. The kinetics of this exchanger, when considered with its unusual tissue distribution in renal inner medullary collecting tubules and hippocampus, are-consistent with NHE4 having a specialized role in cell functions.

Amiloride↗
PubMed1996

FISH mapping of centromere protein C (CENPC) on human chromosome 4q31-->q21.

Centromere protein C (CENP-C), a human centromere autoantigen, is a component of the inner kinetochore plate. CENP-C is required for maintaining proper kinetochore size and a timely transition to anaphase. In this study using fluorescence in situ hybridization to metaphase chromosomes, the human CENP-C gene (CENPC) was mapped on chromosome 4, region q13-->q21.

Chromosomal Proteins, Non-Histone↗
PubMed1996

Evidence that a nereistoxin metabolite, and not nereistoxin itself, reduces neuronal nicotinic receptors: studies in the whole chick ciliary ganglion, on isolated neurons and immunoprecipitated receptors.

Nereistoxin (100 microM, 2-10 min) blocks nicotinic receptors in the intact chick ciliary ganglion. This effect mimics blockade by the reducing agent dithiothreitol (2 mM, 20 min), which is not reversed until oxidation with dithiobisnitrobenzoic acid (1 mM, 5 min). After treating intact ganglia with either nereistoxin or dithiothreitol, the affinity alkylating agent bromoacetylcholine causes irreversible blockade that cannot be reversed by dithiobisnitrobenzoic acid. These data suggest that nereistoxin, or a metabolite, acts to reduce nicotinic receptors, although nereistoxin differs from dithiothreitol in that agonists only partially protect against nereistoxin reduction. In studies on chick retina, we previously proposed that a metabolite of nereistoxin (such as dihydronereistoxin) is the actual reducing agent for neuronal nicotinic receptors. Current findings in chick ciliary ganglion supporting this hypothesis include: 1) changing pH alters the minimal nereistoxin concentration needed for blockade in intact ganglia, but has little effect on the minimal concentration needed for dithiothreitol, 2) application of a quaternary analog of nereistoxin has little effect on intact ganglion, but a quaternary analog of dihydronereistoxin blocks nicotinic receptors by reduction, 3) nereistoxin weakly oxidizes rather than reduces immunoprecipitated receptors from chick brain and 4) in whole-cell patch-clamp studies, nereistoxin clearly does not reduce receptors on chick ciliary neurons, although dihydronereistoxin mimics receptor blockade by dithiothreitol, and requires oxidation by dithiobisnitrobenzoic acid for reactivation. Together, these data suggest that nereistoxin is not a direct reducing agent for neuronal nicotinic receptors.

Acetylcholine↗
PubMed1996

Antisense RNA inhibition of the putative vacuolar H(+)-ATPase proteolipid of Dictyostelium reduces intracellular Ca2+ transport and cell viability.

Transport of Ca2+ via a P-type pump into the contractile vacuole of Dictyostelium discoideum appears to be facilitated by vacuolar proton (V-H+) ATPase activity. To investigate the involvement of the V-H(+)-ATPase in this process using molecular techniques, we cloned a cDNA (vatP) encoding the putative proteolipid subunit of this enzyme. The deduced protein product of this cDNA is composed of 196 amino acids with a calculated M(r) of 20,148 and the primary structure exhibits high amino acid sequence identity with V-H(+)-ATPase proteolipids from other organisms. vatP is a single-copy gene and it produces one approximately 900 nt transcript at relatively constant levels during growth and development. Attempts to disrupt the endogenous gene using vatP cDNA were unsuccessful. But, expression of vatP antisense RNA reduced the levels of vatP message and V-H(+)-ATPase activity by 50% or more. These antisense strains grew and developed slowly, especially under acidic conditions, and the cells seemed to have difficulty forming acidic vesicles. During prolonged cultivation, all of the antisense strains either reverted to a wild-type phenotype or died. Thus in Dictyostelium, unlike yeast, the V-H(+)-ATPase seems to be indispensable for cell viability. When different antisense strains were analyzed for Ca2+ uptake by the contractile vacuole, they all accumulated less Ca2+ than control transformants. These results are consistent with earlier pharmacological studies which suggested that the V-H(+)-ATPase functions in intracellular Ca2+ transport in this organism.

Amino Acid Sequence↗
PubMed1996

Preliminary evidence for a theory of the fractal city.

"In this paper, we argue that the geometry of urban residential development is fractal. Both the degree to which space is filled and the rate at which it is filled follow scaling laws which imply invariance of function, and self-similarity of urban form across scale. These characteristics are captured in population density functions based on inverse power laws whose parameters are fractal dimensions. First we outline the relevant elements of the theory in terms of scaling relations and then we introduce two methods for estimating fractal dimension based on varying the size of cities and the scale at which their form is detected. Exact and statistical estimation techniques are applied to each method respectively generating dimensions which measure the extent and the rate of space filling. These methods are then applied to residential development patterns in six industrial cities in the northeastern United States...."

Americas↗
PubMed1996

Dynamic changes of mechanically activated channels and K+ channels at injury site of peripheral nerve in rat.

Ectopic ion channels developed locally at the injury site after nerve damage by light ligation around common sciatic nerve of the rats. Different channel types have different processes of formation, accumulation and degeneration. During the first three days after injury, mechanically activated channels that are modulated by CA++ channel activities first appeared. As the nerve fibers begin to be excited by TEA, a blocker of K+ channels, suggesting that the accumulation of K+ channels, the responsibility of mechanically activated channels was declining. Onset of K+ channels was from the 3rd postoperative day and lasted up to the fiftieth day. This time course of K+ channel development was closely related to allodynia and hyperalgesia of neuropathic animal behaviour. The results suggest that chronic contraction injury induces a dynamic change in the ectopic mechanically activated channels and K+ channels at the injury site of nerve and there is an interchange in the development time courses of the mechanically activated channels and K+ channels.

Action Potentials↗
PubMed1996

Neurobiological mechanisms of the meridian and the propagation of needle feeling along the meridian pathway.

The present experiments attempt to find the meridian phenomenon and how the needle feeling propagates along the given meridian channels. The neurobiological mechanisms of the meridian were studied with neuroelectrical recording from the motor neurons and CB-HRP retrograde histochemistry technique in both rats and cats. The results demonstrated that most, but not all, of alpha motor neurons supplying a muscle group of a given meridian were selectively activated by afferent inputs originating not only from homonymous or heterogeneous, but synergistic muscle, but also from the skin nerve overlying the muscle group of the homonymous meridian. However, the afferent inputs from the heterogeneous meridian have very weak or no effect. On the other hand, the labeled motor neurons supplying a given meridian muscles from a discrete longitudinal column with a definite bound in the lateral ventral horn. There are oriented dendro-dendristes projections between the labeled motor neurons. The characteristics of both selective responses of the motor neurons to afferent inputs and their neuro-anatomical arrangements in spinal cord offer neurobiological evidence for the meridian phenomenon.

Acupuncture Therapy↗
PubMed1996

Studies on the transfer techniques of three maize genes.

Maize transformation has been carried out through microprojectile bombardment, ultrasonication in a DNA buffer, and ovary-injection with a self-made microinjector. The plasmid pB48.415, which carries a 3'-truncated Bt-toxin protein gene and a hygromycin phosphotransferase (hpt) gene, was used in the transformation. Transgenic maize plants were obtained from immature embryos and embryogenic calli bombarded with a particle gun, embryogenic calli ultrasonicated under different conditions of ovaries injected 10-20 hours after pollination. The results of Dot blotting and Southern blotting analyses proved the integration of the Bt gene into maize genome.

Bacillus thuringiensis Toxins↗
PubMed1996

Geographic mobility of scientists: sex differences and family constraints.

Women scientists are much more likely than men scientists to be in two-career marriages. This study examines the argument that the higher prevalence of two-career marriages among women scientists presents a significant impediment to their geographic mobility. Three hypotheses are developed and tested. First, scientists in two-career families are less likely to migrate than scientists in one-career families. Second, the effect of two-career marriages on the probability of migration differs with gender; women are affected more negatively. Third, the effect of children on the probability of migration differs with gender; women are affected more negatively. The empirical work uses a data set of doctoral scientists extracted from the 5% Public Use Microdata Sample from the 1990 census. The first two hypotheses are not confirmed by the empirical results, but we find evidence supporting the third. Family constraints on women scientists' careers generally appear to be weak, but become acute when they have children.

Adult↗
PubMed1996

[Cloning and sequence analysis of the gene encoding the second region of MSA1 from three Chinese isolates of Plasmodium falciparum].

Gene encoding the second region of merozoite surface antigen (MSA1-R2) of three Chinese isolates of Plasmodium falciparum from Hainan, Yunnan and Anhui were amplified by PCR, cloned into M13 and sequenced. Comparison among MSA1-R2 sequences from different isolates of P. falciparum shows that there is no difference among the three Chinese isolates. The sequence of MSA1-R2 of the Chinese isolates are highly homologous with that of WELLCOME from West Africa. The sequence flanking the upstream of the tandem repeats is exactly the same as that of MAD-20, but sequence downstream the repeats exhibit the characteristics of K1 allele, indicating that intragenic recombination of the two MSA1 allelic families exists in the Chinese isolates.

Amino Acid Sequence↗
PubMed1995

Dominant-negative mutants of Grb2 induced reversal of the transformed phenotypes caused by the point mutation-activated rat HER-2/Neu.

To clarify the role of the Shc-Grb2-Sos trimer in the oncogenic signaling of the point mutation-activated HER-2/neu receptor tyrosine kinase (named p185), we interfered with the protein-protein interactions in the Shc.Grb2.Sos complex by introducing Grb2 mutants with deletions in either amino- (delta N-Grb2) or carboxyl-(delta C-Grb2) terminal SH3 domains into B104-1-1 cells derived from NIH3T3 cells expressing the point mutation-activated HER-2/neu. We found that the transformed phenotypes of the B104-1-1 cells were largely reversed by the delta N-Grb2. The effect of the delta C-Grb2 was much weaker. Biochemical analysis showed that the delta N-Grb2 was able to associate Shc but not p185 or Sos, while the delta C-Grb2 bound to Shc, p185, and Sos. The p185-mediated Ras activation was severely inhibited by the delta N-Grb2 but not the delta C-Grb2. Taken together, these data demonstrate that interruption of the interaction between Shc and the endogenous Grb2 by the delta N-Grb2 impairs the oncogenic signaling of the activated p185, indicating that (i) the delta N-Grb2 functions as a strong dominant-negative mutant, and (ii) Shc/Grb2/Sos pathway plays a major role in mediating the oncogenic signal of the activated p185. Unlike the delta N-Grb2, delta C-Grb2 appears to be a relatively weak dominant-negative mutant, probably due to its ability to largely fulfill the biological functions of the wild-type Grb2.

3T3 Cells↗
PubMed1995

HNF3 binds and activates the second enhancer, ENII, of hepatitis B virus.

The basic functional unit of hepatitus B virus (HBV) enhancer II (ENII) is located within nt 1687-1774, which is defined as the B fragment in our previous papers. A major trans-acting factor binding site has been identified within the B fragment. The sequence corresponding to this binding site was named B2. In this paper, several point mutations were introduced into the B2 subunit by PCR-mediated site-directed mutagenesis. CAT analysis indicated that the TGTTTGTTT motif within the B2 subunit was critical for the activity of ENII. Mutations of individual nucleotides within this motif could decrease the activity of ENII. Electrophoresis mobility shift assay revealed that the liver-enriched transcription factors hepatocyte nuclear factor (HNF) 3 alpha and HNF3 beta bound to the B2 subunit specifically and the TGTTTGTTT motif was essential for DNA-protein interaction. Anti-HNF3 alpha and anti-HNF3 beta antisera could block such binding ability. Moreover, HNF3 beta could switch on the activity of ENII in HeLa cells and the activity of ENII could be suppressed by antisense HNF3 alpha and antisense HNF3 beta mRNA in HepG2 cells. These results prompted the conclusion that HNF3 was crucial for the liver-specific activity of ENII, which in turn contributed significantly to the liver specificity of HBV.

Base Sequence↗