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F Liu

Publications and source records attributed to F Liu.

At least 109 records · Page 6Linked to original sources
PubMed2002

Measurement of B(D+-->K(*0)l(+)nu(l)).

Using 13.53 fb(-1) of CLEO data, we have measured the ratios of the branching fractions R(+)(e),R(+)(mu) and the combined branching fraction ratio R(+)(l), defined by R(+)(l)=[B(D+-->K(*0)l(+)nu(l))]/[B(D+-->K-pi(+)pi(+))]. We find R(+)(e)=0.74+/-0.04+/-0.05, R(+)(mu)=0.72+/-0.10+/-0.05, and R(+)(l)=0.74+/-0.04+/-0.05, where the first and second errors are statistical and systematic, respectively. The known branching fraction B(D+-->K-pi(+)pi(+)) leads to B(D+-->K(*0)e(+)nu(e))=(6.7+/-0.4+/-0.5+/-0.4)%, B(D+-->K(*0)mu(+)nu(mu))=(6.5+/-0.9+/-0.5+/-0.4)%, and B(D+-->K(*0)l(+)nu(l))=(6.7+/-0.4+/-0.5+/-0.4)%, where the third error is due to the uncertainty in B(D+-->K-pi(+)pi(+)).

Journal Article↗
PubMed2002

Observation of the decay Omega(0)(c)-->Omega(-)e(+)nu(e).

Using the CLEO detector at the Cornell Electron Storage Ring we have observed the Omega(0)(c) (css ground state) in the decay Omega(0)(c)-->Omega(-)e(+)nu(e). We find a signal of 11.4+/-3.8(stat) events. The probability that we have observed a background fluctuation is 7.6x10(-5). We measure B(Omega(0)(c)-->Omega(-)e(+)nu(e)).sigma(e(+)e(-)-->Omega(0)(c)X)=(42.2+/-14.1(stat)+/-5.7(syst)) fb and R=[Gamma(Omega(0)(c)-->Omega(-)pi(+))]/[Gamma(Omega(0)(c)-->Omega(-)enu(e))]=00.41+/-0.19(stat)+/-0.04(syst). This is the first statistically significant observation of an individual decay mode of the Omega(0)(c) in e(+)e(-) annihilation and the first example of a baryon decaying via beta emission, where no quarks from the first generation participate in the reaction.

Journal Article↗
PubMed2002

The roles of terminal sugar residues of surface glycans in the metastatic potential of human hepatocarcinoma.

PURPOSE: The roles of terminal sialyl and fucosyl residues in cell surface glycans in the metastatic potential of H7721 cells, a human hepatocarcinoma cell line, were studied. METHODS: Neuraminidase and alpha-L-fucosidase were used to remove the sialyl and fucosyl residues, respectively. Cell adhesion to fibronectin (Fn), laminin (Ln), and human umbilical vein epithelial cell (HUVEC), as well as chemotactic cell migration and invasion, were selected as the parameters of metastatic potential ex vivo. RESULTS: Sialyl residue is not essential for cell adhesion to Fn, but is important in cell adhesion to Ln and invasion, and is crucial in cell adhesion to HUVEC and migration. In contrast, fucosyl residue contributes more than sialyl residue to cell adhesion to Fn and Ln, but less to adhesion to HUVEC, and is not essential in chemotactic cell migration and invasion. Cell adhesion to HUVEC, migration, and invasion were inhibited by the monoclonal antibody of sialyl Lewis X, but not by the antibody of non-sialyl Lewis X. CONCLUSION: Terminal sialyl residues on cell surface glycans are more important than fucosyl residues in mediating cell adhesion to HUVEC and cell migration/invasion, but the reverse is true in cell adhesion to Fn and Ln.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed2002

Transfection of the nm23-H1 gene into human hepatocarcinoma cell line inhibits the expression of sialyl Lewis X, alpha1,3 fucosyltransferase VII, and metastatic potential.

PURPOSE: The expressions of Lewis antigens, alpha1,3 fucosyltransferase (alpha1,3 FucT)-VII, and the metastatic potential of the 7721 human hepatocarcinoma cell line after the transfection of the cDNA of nm23-H1, a known metastasis-suppressive gene, were studied using mock cells as the control, which were transfected with the pcDNA3 vectors. METHODS: Cell adhesion to human umbilical vein epithelial cells (HUVEC), chemotaxic cell migration through transwells, and invasion through matrigel were selected as the metastasis-related phenotypes to assess the metastatic potential at the cell level. RESULTS: The results showed that the expression of SLe(x) was high, while the expression of Le(x), SDLe(x), and SLe(a) were very low on the surface of the mock cells. After transfection of nm23-H1, the expressions of SLe(x), alpha1,3 FucT-VII, and the cell adhesion to HUVEC, as well as cell migration and invasion were simultaneously decreased in all three clones of nm23-H1-transfected cells. Among different clones, the decreased expressions of SLe(x) and alpha1,3 FucT-VII were roughly correlated to each other, and also, in general, proportional to the ability of cell adhesion to HUVEC, cell migration, and invasion. The expressions of these metastasis-related phenotypes were lowest in clone 3 and highest in clone 4. Only the specific monoclonal antibody to SLe(x) (KM93) significantly abolished the cell adhesion, migration, and invasion, while other monoclonal antibodies against SDLe(x) or Le(x) and SLe(a) only slightly inhibited or entirely failed to inhibit the above-mentioned phenotypes. However, the rate of cell growth was not changed after the transfection of nm23-H1, and the ability of colony formation on the soft agar was only decreased in one clone. CONCLUSIONS: These findings reveal that the down-regulation of alpha1,3 FucT-VII and its product, SLe(x), is one of the mechanisms to explain the metastasis-suppressive effect of the nm23-H1 gene.

Blotting, Northern↗
PubMed2002

Observation of B(0) --> D0pi(0) and B(0) -->D(*0)pi(0).

We have studied the color-suppressed hadronic decays of neutral B mesons into the final states D*0pi(0). Using 9.67 x 10(6) BB pairs collected with the CLEO detector, we observe the decays B( 0) --> D0pi(0) and B( 0) -->D(*0)pi(0) with the branching fractions BB( 0) -->D0pi(0)) = (2.74(+0.36)(-0.32) +/- 0.55)x10(-4) and BB( 0) -->D(*0)pi(0)) = (2.20(+0.59)(-0.52) +/- 0.79)x10(-4). The first error is statistical and the second systematic. The statistical significance of the D0pi(0) signal is 12.1sigma ( 5.9sigma for D(*0)pi(0)). Utilizing the B( 0) -->D*0)pi(0) branching fractions we determine the strong phases delta(I,D(*)) between isospin 1/2 and 3/2 amplitudes in the Dpi and D*pi final states to be cosdelta(I,D) = 0.89 +/-0.08 and cosdelta(I,D*) = 0.89 +/- 0.08, respectively.

Journal Article↗
PubMed2002

Aberrant glycosylation modulates phosphorylation of tau by protein kinase A and dephosphorylation of tau by protein phosphatase 2A and 5.

Microtubule-associated protein tau is abnormally hyperphosphorylated, glycosylated, and aggregated in affected neurons in Alzheimer's disease (AD). We recently found that the aberrant tau glycosylation precedes tau hyperphosphorylation in AD brain. In the present study, we developed assays to determine phosphorylation and dephosphorylation of tau at specific phosphorylation sites by using glycosylated tau purified from AD brain as a substrate. We then studied the effects of the aberrant glycosylation on phosphorylation and dephosphorylation of tau at each specific phosphorylation site. We found that deglycosylation of the aberrantly glycosylated tau decreased the subsequent phosphorylation of tau at Ser214, Ser262, and Ser356 in vitro by protein kinase A. On the other hand, deglycosylation of tau positively modulated the subsequent dephosphorylation by protein phosphatase 2A and protein phosphatase 5 in vitro at the phosphorylation sites Ser198, Ser199, and Ser202. Our results suggest that the aberrant glycosylation may modulate tau protein at a substrate level so that it is easier to be phosphorylated and more difficult to be dephosphorylated at some phosphorylation sites in AD brain. The combined impact of this modulation may be to make tau more susceptible to becoming abnormally hyperphosphorylated.

Adenosine Triphosphate↗
PubMed2002

Signaling by mechanical strain involves transcriptional regulation of proinflammatory genes in human periodontal ligament cells in vitro.

Intracellular signals generated by mechanical strain profoundly affect the metabolic function of osteoblast-like periodontal ligament (PDL) cells, which reside between the tooth and alveolar bone. In response to applied mechanical forces, PDL cells synthesize bone-resorptive cytokines to induce bone resorption at sites exposed to compressive forces and deposit bone at sites exposed to tensile forces in an environment primed for catabolic processes. The intracellular mechanisms that regulate this bone remodeling remain unclear. Here, in an in vitro model system, we show that tensile strain is a critical determinant of PDL-cell metabolic functions. Equibiaxial tensile strain (TENS), when applied at low magnitudes, acts as a potent antagonist of interleukin (IL)-1beta actions and suppresses transcriptional regulation of multiple proinflammatory genes. This is evidenced by the fact that TENS at low magnitude: (i) inhibits recombinant human (rh)IL-1beta-dependent induction of cyclooxygenase-2 (COX-2) mRNA expression and production of prostaglandin estradiol (PGE2); (ii) inhibits rhIL-1beta-dependent induction matrix metalloproteinase-1 (MMP-1) and MMP-3 synthesis by suppressing their mRNA expression; (iii) abrogates rhIL-1beta-induced suppression of tissue inhibitor of metalloprotease-II (TIMP-II) expression; and (iv) reverses IL-1beta-dependent suppression of osteocalcin and alkaline phosphatase synthesis. Nevertheless, these actions of TENS were observed only in the presence of IL-1beta, as TENS alone failed to affect any of the aforementioned responses. The present findings are the first to show that intracellular signals generated by low-magnitude mechanical strain interfere with one or more critical step(s) in the signal transduction cascade of rhIL-1beta upstream of mRNA expression, while concurrently promoting the expression of osteogenic proteins in PDL cells.

Dental Stress Analysis↗
PubMed2002

Expression of leukemia inhibitory factor (LIF)/interleukin-6 family cytokines and receptors during in vitro osteogenesis: differential regulation by dexamethasone and LIF.

The leukemia inhibitory factor/interleukin-6 (LIF/IL-6) family of cytokines is known to play a major role in bone physiology. Although much work has focused on the regulation of bone resorption by IL-6 and related cytokines, their effects on osteoblast development and bone formation have not been as well studied. Previously, we reported that LIF inhibits, in a non-IL-6-dependent manner, osteoblast differentiation and bone nodule formation in the rat calvaria (RC) model, an effect that is antagonized by dexamethasone (Dex). The culture time-sensitive window suggested that LIF targets late preosteoblasts or early osteoblasts, and that this stage-specific effect coincided with a period of low endogenous production of LIF and IL-6. To detect potential crosstalk between members of this family, we have extended these observations by assessing the expression levels of other LIF/IL-6 cytokines (CNTF, OSM, IL-11, CT-1) and their receptors in the same RC cell model treated with or without LIF or Dex. Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that IL-11 and its receptor, CNTF and its receptor, LIFR, and gp130 were constitutively expressed throughout the culture period. Expression of CT-1 and OSM increased with culture time - that is, with osteoblast differentiation - whereas the specific receptor for OSM (OSMR) was highly expressed at early timepoints and either plateaued or decreased thereafter. Continuous treatment with Dex (10(-8) mol/L) inhibited the endogenous production of IL-6, LIF, OSM, IL-11R, and OSMR, but had no detectable effect on the expression of IL-11, CT-1, CNTF, CNTFR, LIFR, or gp130. Finally, treatment with exogenously added LIF stimulated IL-6, LIF, LIFR, and OSMR, but had no other detectable effects. These data indicate that multiple members of the LIF/IL-6 family and their receptors are expressed in RC cell cultures, and are differentially regulated by Dex and LIF, suggesting that these cytokines play a complex and interdependent role, further modulated by glucocorticoid levels, in osteoprogenitor differentiation and bone nodule formation.

Animals↗
PubMed2002

Electric gene transfer to the liver following systemic administration of plasmid DNA.

Recently, there has been an increasing level of interest in electroporation for gene delivery due to the site-specific nature of the delivery, as well as the high efficiency of the method. Electroporation involves the application of a pulsed electric field to cells to enhance cell permeability, resulting in the transit of exogenous polynucleotide across the cytoplasmic membrane. Electroporation is traditionally performed by locally injecting DNA to the site of interest followed by the application of electric field. Compared with the local injection of plasmid DNA to the liver, systemic injection has the advantage of delivering genes to more hepatocytes. We describe here a method for efficient gene transfer to the liver by electroporation following tail vein administration of the naked DNA. The cells expressing the reporter gene are more broadly distributed with this systemic injection, as compared with direct injection.

Animals↗
PubMed2002

A gene therapy for cancer based on the angiogenesis inhibitor, vasostatin.

The growth and persistence of solid tumors and their metastasis are angiogenesis-dependent. Vasostatin, the N-terminal domain of calreticulin inclusive of amino acids 1-180, is a potent angiogenesis inhibitor. To investigate whether intramuscular administration of vasostatin gene has the antitumor activity in mouse tumor models, we constructed a plasmid DNA encoding vasostatin and a control vector. Production and secretion of vasostatin protein by COS cells transfected with the plasmid DNA encoding vasostatin (pSecTag2B-vaso) were confirmed by Western blot analysis and ELISA. Conditioned medium from vasostatin-transfected COS cells apparently inhibited human umbilical vein endothelial cell (HUVEC) and mouse endothelial cell (SVEC4-10) proliferation, compared with conditioned medium from the COS cells transfected with control vector or non-transfected cells. Treatment with pSecTag2B-vaso twice weekly for 4 weeks resulted in the inhibition of tumor growth and the prolongation of the survival of tumor-bearing mice. The sustained high level of vasostatin protein in serum could be identified in ELISA. Angiogenesis was apparently inhibited in tumor by immunohistochemical analysis. Angiogenesis was also inhibited in the chicken embryo CAM assay and mouse corneal micropocket assay. The increased apoptotic cells were found within the tumor tissues from the mice treated with plasmid DNA encoding vasostatin. Taken together, the data in the present study indicate that the cancer gene therapy by the intramuscular delivery of plasmid DNA encoding vasostatin, is effective in the inhibition of the systemic angiogenesis and tumor growth in murine models. The present findings also provide further evidence of the anti-tumor effects of the vasostatin, and may be of importance for the further exploration of the application of this molecule in the treatment of cancer.

Angiogenesis Inhibitors↗
PubMed2002

Porphyrins as early biomarkers for arsenic exposure in animals and humans.

We studied the effect of arsenic exposure on the haem biosynthetic pathway in the rat and humans. Significant increases in protoporphyrin IX, coproporphyrin III, coproporphyrin I were observed in the blood, liver and kidney, and in the urine of rats after a single dose of arsenic. The level of increase was dependent on the arsenic species present. Most of porphyrin concentrations in the tissues increased within 24 hr and urinary excretion elevated within 48 hr. In the human study, we collected urine samples from 113 people who live in Xing Ren of Guizhou Province, a coal-borne arsenicosis endemic area in southwest of PR China and from 30 people who live in Xing Yi (about 80 km southwest of Xing Ren) where arsenicosis is not prevalent. We analyzed the urinary porphyrins using HPLC. Results indicate that all urinary porphyrins were higher in the arsenic exposed group than those in the control group. Women, children and older age people spend much of their time indoors, they had greater increases of urinary arsenic and porphyrins. They were the higher risk groups among the study subjects. A positive correlation between the urinary arsenic levels and porphyrin concentrations demonstrated the effect of arsenic on haem biosynthesis. Significant alteration in the porphyrin excretion profiles of the younger age (<20 y) arsenic exposed group suggested that porphyrins could be used as early warning biomarkers for chronic exposure to arsenic.

Age Factors↗
PubMed2001

Construction of a square-planar molecular box: self-assembly of palladium(II) complexes of 3,6,9,16,19,22-hexaazatricyclo[22.2.2.2(11,14)]triacon-11,13,24,26(1),27,29-hexaene through hydrogen-bonding interactions.

Binuclear palladium(II) complexes of the macrocyclic polyamine 3,6,9,16,19,22-hexaazatricyclo[22.2.2.2(11,14)]triacon-11,13,24,26(1),2 7,29-hexaene (L) are used to construct molecules having special shapes. In this study two binuclear palladium(II) complexes [Pd(2)LI(2)]I(2)and [Pd(2)LCl(2)](NO(3))(2).H(2)O are synthesized and structurally characterized. X-ray crystallography shows that both complexes exist as one-dimensional chains formed via intermolecular hydrogen-bonding N(3)-H(3C)---X in which X is I and Cl. Moreover, the ligands in both complexes adopt a boatlike conformation that may facilitate the formation of the tetranuclear complex. The cationic aqua complex [Pd(2)L(H(2)O)(m)(NO(3))(n)]((4-n)+, obtained by the treatment of [Pd(2)LI(2)]I(2)and [Pd(2)LCl(2)]Cl(2) with AgNO(3), is used as a building block for the construction of a tetranuclear palladium(II) complex [Pd(4)L(2)(C(2)O(4))(2)](NO(3))(4).6H(2)O. X-ray crystallography shows that the tetranuclear complex forms an open, hydrophobic box. These molecular boxes are connected via the hydrogen bond N(3)-H(3C)---O(4B) (symmetry code B: x, 1 + y, z) into a one-dimensional chain. A two-dimensional structure is formed via pi-pi stacking of the plane defined by C6 to C11 in the one chain and its symmetry-related plane (symmetry code C: -x, -1 - y, 2 - z) in another chain. This study exemplifies a new method for the assembly of molecular boxes using a macrocyclic ligand.

Journal Article↗
PubMed2001

Design, synthesis, and biological characterization of bivalent 1-methyl-1,2,5,6-tetrahydropyridyl-1,2,5-thiadiazole derivatives as selective muscarinic agonists.

Selective muscarinic agonists could be useful in the treatment of neurological disorders such as Alzheimer's disease, schizophrenia, and chronic pain. Many muscarinic agonists have been developed, yet most exhibit at best limited functional selectivity for a given receptor subtype perhaps because of the high degree of sequence homology within the putative binding site, which appears to be buried within the transmembrane domains. Bivalent compounds containing essentially two agonist pharmacophores within the same molecule were synthesized and tested for receptor binding affinity and muscarinic agonist activity. A series of bis-1,2,5-thiadiazole derivatives of 1,2,5,6-tetrahydropyridine linked by an alkyloxy moiety exhibited very high affinity (K(i) < 1 nM) and strong agonist activity. The degree of activity depended on the length of the linking alkyl group, which could be replaced by a poly(ethylene glycol) moiety, resulting in improved water solubility, binding affinity, and agonist potency.

Binding, Competitive↗
PubMed2001

Insight into hepatocellular carcinogenesis at transcriptome level by comparing gene expression profiles of hepatocellular carcinoma with those of corresponding noncancerous liver.

Human hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. In this work, we report on a comprehensive characterization of gene expression profiles of hepatitis B virus-positive HCC through the generation of a large set of 5'-read expressed sequence tag (EST) clusters (11,065 in total) from HCC and noncancerous liver samples, which then were applied to a cDNA microarray system containing 12,393 genes/ESTs and to comparison with a public database. The commercial cDNA microarray, which contains 1,176 known genes related to oncogenesis, was used also for profiling gene expression. Integrated data from the above approaches identified 2,253 genes/ESTs as candidates with differential expression. A number of genes related to oncogenesis and hepatic function/differentiation were selected for further semiquantitative reverse transcriptase-PCR analysis in 29 paired HCC/noncancerous liver samples. Many genes involved in cell cycle regulation such as cyclins, cyclin-dependent kinases, and cell cycle negative regulators were deregulated in most patients with HCC. Aberrant expression of the Wnt-beta-catenin pathway and enzymes for DNA replication also could contribute to the pathogenesis of HCC. The alteration of transcription levels was noted in a large number of genes implicated in metabolism, whereas a profile change of others might represent a status of dedifferentiation of the malignant hepatocytes, both considered as potential markers of diagnostic value. Notably, the altered transcriptome profiles in HCC could be correlated to a number of chromosome regions with amplification or loss of heterozygosity, providing one of the underlying causes of the transcription anomaly of HCC.

Carcinoma, Hepatocellular↗
PubMed2001

Effective inhibition of herpes simplex virus 1 gene expression and growth by engineered RNase P ribozyme.

Using an in vitro selection procedure, we have previously isolated ribonuclease P (RNase P) ribozyme variants that efficiently cleave an mRNA sequence in vitro. In this study, an M1GS RNA variant was used to target the mRNA encoding human herpes simplex virus 1 (HSV-1) major transcription activator ICP4. The variant is about 15 times more efficient in cleaving the ICP4 mRNA sequence in vitro than the ribozyme derived from the wild type RNase P ribozyme. Moreover, the variant is also more effective in inhibiting viral ICP4 expression and growth in HSV-1-infected cells than the wild type ribozyme. A reduction of approximately 90% in the expression level of ICP4 and a reduction of 4000-fold in viral growth were observed in cells that expressed the variant. In contrast, a reduction of <10% in the ICP4 expression and viral growth was observed in cells that either did not express the ribozyme or produced a catalytically inactive ribozyme mutant. These results provide direct evidence that RNase P ribozyme variants can be highly effective in inhibiting HSV-1 gene expression and growth and furthermore, demonstrate the feasibility of developing highly effective RNase P ribozyme variants for anti-HSV applications by using in vitro selection procedures.

Animals↗