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Y L Xu

Publications and source records attributed to Y L Xu.

At least 19 recordsLinked to original sources
PubMed1992

Parallel stranded DNA under the scanning tunnelling microscope.

Using scanning tunnelling microscopy, we have directly observed parallel stranded DNA helixes of 43 nucleotides in length. The double helix is right-handed and has an average spacing, 17.43 A (+/- 1 S.D.: 2.30 A), and an average apparent depth, 4.79 A (+/- 1 S.D.: 1.04 A) for each groove. The average pitch of the helical turn is 34 A (+/- 1 S.D.: 3.35 A) and consists of no more than ten base pairs. The diameter of the helix is approx. 17-20 A. Our results provide direct evidence for the existence of a parallel structure of DNA in vitro and some details of its fine structure.

Base Sequence↗
PubMed1992

VCAM-1-, ELAM-1-, and ICAM-1-independent adhesion of melanoma cells to cultured human dermal microvascular endothelial cells.

We have examined the mechanisms by which tumor cells bind to endothelial cells utilizing cultured melanoma cells and microvascular endothelial cells derived from human dermis (HDMEC). The ability of biologic response modifiers (BRM) to modulate the adhesion of melanoma cells to HDMEC was defined and those results were compared with results from human umbilical vein endothelial cells (HUVEC). SK-MEL-2, WM266-4, and Hs 294T melanoma cells all bound to HDMEC and HUVEC monolayers and adherence of melanoma cells was enhanced in a dose- and time-dependent manner by the treatment of HDMEC with interleukin 1 (IL-1) alpha or tumor necrosis factor (TNF) alpha. Similar increases in binding to HDMEC or HUVEC were induced after BRM stimulation, although baseline melanoma cell binding to HUVEC tended to be slightly higher than to HDMEC. In contrast, whereas phorbol 12-myristate 13-acetate (PMA) augmented melanoma cell adherence to HDMEC, PMA failed to increase adherence to HUVEC. The alterations in melanoma cell binding were induced only after pretreatment of endothelial and not melanoma cells with PMA. Studies of the expression of cell adhesion molecules (CAM) on HDMEC and HUVEC using enzyme-linked immunosorbent assay showed that vascular cell adhesion molecule 1 (VCAM-1) is not induced by PMA on HDMEC and intercellular adhesion molecule 1 (ICAM-1) is downregulated on HDMEC by PMA treatment. Endothelial leukocyte adhesion molecule 1 (ELAM-1) is induced by PMA, IL-1 alpha, or TNFalpha, but its expression does not correlate with increased melanoma cell binding MoAb recognizing VCAM-1-inhibited TNFalpha-induced increases in melanoma cell binding to HUVEC. However, anti-VCAM-1 antibody failed to clock melanoma cell binding to PMA or IL-1 alpha-stimulated HDMEC and only partially inhibited melanoma cell binding to TNF alpha-stimulated HDMEC. This study demonstrates that PMA and IL-1 alpha-induced increases in melanoma cell adherence to HDMEC are not mediated via known CAM, including ICAM-1, VCAM-1, or ELAM-1, and may be affected through microvessel-specific novel proteins not previously described on endothelial cells.

Antibodies, Monoclonal↗
PubMed1992

Diminished Clostridium difficile toxin A sensitivity in newborn rabbit ileum is associated with decreased toxin A receptor.

Human infants are relatively resistant to Clostridium difficile-associated diarrhea and colitis compared to adults. In that toxin A is the major cause of intestinal damage with this organism, we compared toxin A receptor binding and biological effects in newborn vs adult rabbit ileum. Purified toxin A (M(r) 308 kD) was labeled with tritium or biotin with full retention of biologic activity. Appearance of specific toxin A brush border (BB) binding was strongly age dependent with minimal [3H]toxin A specific binding at 2 and 5 d of life, followed by gradual increase in binding to reach adult levels at 90 d. Absence of toxin A binding sites in newborn and presence in adult rabbits was confirmed by immunohistochemical studies using biotinylated toxin A. Toxin A (50 ng to 20 micrograms/ml) inhibited protein synthesis in 90-d-old rabbit ileal loops in a dose-dependent fashion. In contrast, inhibition of protein synthesis in 5-d-old rabbit ileum occurred only at the highest toxin A doses (5 and 20 micrograms/ml) and at all doses tested was significantly less than the adult rabbit ileum. In addition, toxin A (5 micrograms/ml) caused severe mucosal damage in adult rabbit ileal explants but had no discernable morphologic effect on 5-d-old rabbit intestine. Our data indicate that newborn rabbit intestine lacks BB receptors for toxin A. The absence of the high-affinity BB receptor for toxin A in the newborn period may explain lack of biologic responsiveness to purified toxin, and the absence of disease in human infants infected with this pathogen.

Age Factors↗
PubMed1991

Determination of eight elements in six human cancer cell lines and two human normal cell lines by PIXE.

Gastric, hepatic, and pulmonary cancer cell lines, and the third passage of normal gastric and pulmonary cell lines were analyzed by proton induced X-ray emission (PIXE) method. The contents of element Sr, Ca, Fe, Zn, P, K, Cu, and As in the cell lines were determined. The Sr, Ca, Fe, Zn, and As contents in cancer cell lines were significantly lower than those in the normal cell lines (p less than 0.05), whereas there were no significant differences for the P, K, and Cu contents (p greater than 0.1). The results suggest that the need of some essential elements has been diminished in cancer cell proliferation.

Cell Line↗
PubMed1991

Conformation of DNA-DNA polymerase I complex observed by scanning tunneling microscopy.

The conformation of a complex of a 41 mer/31 mer DNA fragment and the Klenow fragment of DNA polymerase I of Escherichia coli was studied by scanning tunnelling microscopy (STM). The results shows that near two turns of double helix of this DNA fragment was outside of enzyme while another part containing more than one turn of helix and 10 nucleotides single strand was combined with enzyme. The dimension and shape of DNA polymerase I (KF) in complex were different from that of free enzyme. The conformation of DNA-DNA polymerase I (KF) complex and the application of STM in studying structure of complex of DNA polymerase with DNA were discussed.

Base Sequence↗
PubMed1991

Studies of the modulation of MHC antigen and cell adhesion molecule expression on human dermal microvascular endothelial cells.

Interactions between leukocytes and endothelial cells, particularly in the microvasculature, are important for the initiation and regulation of tissue inflammation. These interactions are regulated by the recognition of specific cell adhesion molecules (CAM) on both leukocytes and endothelial cells. In this study, we examined the modulation of cell surface expression of MHC antigens and the CAM intercellular adhesion molecule 1 (ICAM-1), lymphocyte function antigen 3 (LFA-3), and CD44 on human dermal microvascular endothelial cells (HDMEC) both grown in monolayers and differentiated into capillary-like structures on the basement membrane-like substrate matrigel. HDMEC grown in monolayers or differentiated on matrigel express comparable cell surface MHC class I, LFA-3, CD44, and ICAM-1. ICAM-1, but not LFA-3 or CD44, was increased in expression in a dose- and time-dependent manner by interleukin 1 (IL-1) alpha, tumor necrosis factor (TNF) alpha, lipopolysaccharide (LPS), or interferon (IFN) gamma. Comparable upregulation was observed both in cells grown in monolayers and cells differentiated on matrigel. IL-1 alpha, TNF alpha, and LPS increased ICAM-1 expression on average 100-200% whereas IFN gamma was somewhat less potent. Comparative studies with human umbilical vein endothelial cells (HUVEC) demonstrated consistently lower levels of ICAM-1 expression on HUVEC, but greater increases after cytokine stimulation. Pretreatment with dexamethasone or transforming growth factor (TGF) beta did not affect baseline expression of ICAM-1 or inhibit upregulation of ICAM-1 on HDMEC by IL-1 alpha, TNF alpha, LPS, or IFN gamma. Both IFN gamma and TNF alpha, but not IL-1 alpha increased MHC class I expression, whereas only IFN gamma induced the expression of HLA-DR on HDMEC. The effect of IL-1 alpha, TNF alpha, or IFN gamma was inhibited by antibody to the specific cytokine, but was unaffected by antibody to other cytokines. Additionally, IFN alpha or beta inhibited upregulation of HLA-DR by IFN gamma, but had no effect on the increased MHC class I or ICAM-1 expression mediated by this cytokine. These data demonstrate that the expression of CAM and MHC antigens on small vessel-derived endothelial cells is different from that observed on large-vessel HUVEC, is regulated by the presence of multiple cytokines operating via distinct pathways, and the expression and regulation of these proteins appear to be similar on cells that have been grown in monolayers to those morphologically differentiated into blood vessel-like structures.

Cell Adhesion Molecules↗
PubMed1991

[Unscheduled DNA synthesis (UDS) induced by N-methyl-N'nitro-N-nitrosoguanidine (MNNG) in human gastric mucosal cells].

DNA repair synthesis as estimated by the unscheduled incorporation of tritiated thymidine (3H-TdR) is a useful, economical, and rapidly performed bioassay for detecting DNA-damaging agents. The purpose of this study was to establish the method of MNNG induction and measurement of UDS in human gastric mucosal cells for further study of gastric carcinogenesis and its prevention. Normal gastric mucosal cells isolated from surgical specimens were exposed to various concentrations of MNNG in the presence of 5mM hydroxyurea and 10uCi/ml 3H-TdR in 1% FBS DMEM-F12 medium for 4 hours at 37 degrees C. Immediately following exposure to MNNG the capacity of gastric mucosal cells to undergo DNA synthesis was assayed by autoradiography. The results of the present study indicated that the gastric epithelial cells are capable of repairing MNNG-induced DNA damage. The UDS positive cells were revealed by increased 3H-TdR incorporation into each nucleus, and the UDS level was MNNG dose-dependent.

Cells, Cultured↗
PubMed1990

Cellular factors involved in transcription and Tax-mediated trans-activation directed by the TGACGT motifs in human T-cell leukemia virus type I promoter.

Human T-cell leukemia virus type I (HTLV-I) encodes a 40-kDa nuclear protein, Tax, which stimulates transcription from three 21-base pair (bp) repeats in its U3 region. Tax trans-activation is mediated via cellular factors that interact with the TGACGT motifs in the 21-bp repeats. Gel mobility shift assay and UV cross-linking analysis show that two proteins of 52 and 46 kDa in size bind the 21-bp repeat specifically. Base substitutions in the TGACGT motif which abolished Tax trans-activation abrogated factor binding whereas the repeats containing mutations that did not affect Tax trans-activation supported factor binding as the wild-type repeat. The 52- and 46-kDa factors are present in human T-cell lines Jurkat and MT4 (HTLV-I transformed) and in HeLa cells but are undetectable in a human placental cell line JEG-3, which gave a reduced level of trans-activation. JEG-3 extracts contain a distinct DNA binding activity that shows analogous sequence requirements as the 52- and 46-kDa proteins in interacting with the various 21-bp repeats. c-Jun and CREB (cAMP-responsive element binding factor) can stimulate transcription from HTLV-I long terminal repeats in JEG-3 cells. At least two copies of the 21-bp repeats are required for optimal trans-activation by c-Jun and CREB. Most single point mutations in the TGACGT motif that abolished Tax trans-activation, however, did not affect c-Jun- or CREB-directed transcriptional enhancement. These data indicate that many transcription factors including c-Jun and CREB exert stimulatory effects on HTLV-I transcription although they do not directly respond to Tax. The 52- and 46-kDa cellular proteins most likely are involved directly in Tax-mediated trans-activation, and they are tentatively named Tax activation factors I and II, respectively.

Base Sequence↗
PubMed1990

The selective killing effect of special wavelength light in the treatment of human superficial cancer.

The authors discovered that 0.4-micron to 1.1-microns wavelength light can selectively kill superficial cancer tissue in the human body. Light at a density of integral power 1 to 6 W/cm2 will kill tumor but will affect normal tissues less. The model KS-1 phototherapeutic instrument was made according to these principles and used to treat 34 patients who had a variety of cancers, including carcinomas of the oral cavity, skin, and cervix. The 25 cured patients were then monitored for 1 to 4 years. No side effects were found. Currently there are several hospitals in China that use this instrument for the treatment of some kinds of carcinoma.

Female↗
PubMed1990

The antiatherogenic effects of components isolated from pollen typhae.

Based on the results of previous investigations that pollen Typhae, a Traditional Chinese Medicine, Had antiatherogenic effects, several components were isolated successively from the drug and their effects on porcine aortic endothelial cell (EC) and smooth muscle cell (SMC) cultures as well as on platelet aggregation were examined. 12 components isolated from Pollen Typhae have been identified on their chemical structures and biological effects. 4 of them showed different evident antiatherogenic effects. 1) Isorhamnetin-3-O-rhamnosyl-glucoside could stimulate EC to produce tPA and PGI2; 2) Quercetin-3-O-neohesperidose could protect EC from injury by fibrin, as well as raise tPA activity; 3) beta-Sitosterol palmitate could inhibit SMC proliferation and 4) beta-Sitosterol glucoside showed an inhibitory effect on platelet aggregation. These results would provide some information for the search of new drugs in the treatment and prevention of atherosclerosis.

Animals↗
PubMed1989

Further study of pollen typhae's effects on the production of tPA and PGI, by cultured endothelial cells.

We had reported that Pollen Typhae, a Chinese traditional herbal medicine could reduce atherosclerotic plaque formation in experimental animals. Fraction IV isolated from Pollen Typhae had the ability to raise tPA and PGI2 productions by cultured porcine aortic endothelial cells (EC). In this paper we reported that F.IV was divided chemically into four subfractions named SubF.1-4 among them SubF.2-2 was further separated from SubF.2, and SubF.4-1 from SubF.4. The six subfractions were tested for their effects on the productions of tPA (125I-fibrin plate method) and PGI2(RIA) by porcine endothelial cells. The results showed that SubF.3 could enhance tPA activity and SubF.2-2 could increase PGI2 level. With Chrono-Log 500 Lumi-Aggregometer, SubF.1,2-2 and 3 were found to be able to inhibit platelet aggregation and release reaction. These data indicated that the mechanisms of Pollen Typhae in its antiatherosclerotic effects were multiple which resulted from various biologic effects exerted by various components of this drug. Chemical analyses were performed and their structures were identified, demonstrating that SubF.2-2 was a flavonoid, while SubF.3 was a group of flavonoids, implying there are some antiatherogenic components in flavonoids.

Adult↗
PubMed1989

HTLV-I tax gene product activates transcription via pre-existing cellular factors and cAMP responsive element.

Human T-cell leukemia virus type I (HTLV-I) is the etiological agent of adult T-cell leukemia. The 3' end of HTLV-I proviral DNA encodes the synthesis of two regulatory proteins, tax and rex. The 40-kDa tax protein is a nuclear protein which positively stimulates transcription from the U3 region of the viral long terminal repeat sequence. Three 21-base pair sequences in the U3 region have been found to serve as the cis-element for tax-mediated trans-activation. We now report that the tax protein can trans-activate HTLV-I LTR in the absence of de novo cellular protein synthesis. Saturated mutagenesis of the 21-base pair repeat sequence showed that specific mutations clustered in sequences homologous to the cAMP responsive element (TGACGTCA) abolish trans-activation by tax. Furthermore, although the TGACGTCN element is nearly palindromic, the mutations that abolish trans-activation are localized exclusively in the 5' 6 bases, suggesting the orientation of this element may play a role in transcription. That the purified tax protein does not bind the 21-base pair repeats or nonspecific DNA lends further support to the notion that tax protein does not directly interact with the 21-base pair repeats to activate transcription. Instead, tax most likely acts via cellular transcriptional factor(s) to bring about trans-activation.

Base Sequence↗
PubMed1989

[UV-spectrophotometric analysis of the component of antondin injection by the Monte Carlo method of area fitting].

The Monte Carlo method is a kind of unique calculation method. It can resolve not only the question of define evaluation, but also that of random evaluation. The Monte Carlo area fitting method was applied to UV-spectrophotometry of the multicomponent complex preparations without previous separation. The area of each component of complex preparation within a suitable wavelength range of standard spectrogram was multiplied by certain coefficients, and then the products were obtained to fit the area of the measured multicomponent complex preparations. The method was used to simultaneous determination of barbital, amidopyrine and antipyrine in antondin injection. The experimental data were measured and treated by UV-190 spectrophotometer and microcomputer IBM-PC. The average recoveries of barbital, amidopyrine and antipyrine were 99.1 +/- 1.1% (CV), 99.6 +/- 1.3% (CV), and 99.7 +/- 1.0% (CV), respectively.

Aminopyrine↗
PubMed1988

Genotyping of human alcohol dehydrogenases at the ADH2 and ADH3 loci following DNA sequence amplification.

Humans are polymorphic at two of the alcohol dehydrogenase (ADH) loci important in ethanol metabolism, ADH2 and ADH3. Although the coding regions of these genes are 94% identical, they produce subunits that differ greatly in kinetic properties in vitro. These differences are likely to be reflected in the pharmacokinetics of alcohol metabolism, but studies have been hampered by the need to use liver biopsy specimens to determine the ADH phenotype. This problem has now been overcome by determining the genotype at these loci using DNA that has been amplified in vitro by the polymerase chain reaction. We report here the identification of all three of the ADH2 alleles and both of the ADH3 alleles. Any pair of ADH2 or ADH3 alleles can be distinguished using allele-specific oligonucleotide probes directed at their single base pair difference. In addition, ADH2(2) can be distinguished from ADH2(1) and ADH2(3) by detecting a new MaeIII site created in the third exon by the single base pair alteration in ADH2(2).

Alcohol Dehydrogenase↗
PubMed1987

Effects of uridine diphosphoglucose (UDPG) infusion on 5-phosphoribosyl pyrophosphate (PRPP) levels of mouse tissues.

Uridine diphosphoglucose (UDPG) has been shown to have tissue-specific effects that have proved to be of clinical value in the treatment of some liver ailments. In an effort to determine something about the mechanism of action, we investigated the effect of UDPG on the levels of 5-phosphoribosyl pyrophosphate (PRPP) and PRPP synthetase in mouse liver, spleen and transplanted tumors. Three strains of mice were studied with and without tumors under various experimental conditions. Balb/c mice were infused with UDPG intraperitoneally at levels of 0.16 g/kg/day (0.28 mmole) to 1.6 g/kg/day (2.8 mmoles) for 5 days. At the low dose rate the PRPP level in the liver was found to increase 3-fold. A slight increase was noted in the activity of PRPP synthetase. However, when the UDPG was infused at a level of 2.8 mmoles/kg/day, the increases in both the synthetase and PRPP were inhibited. Both CRF1 and CD8 mice were less sensitive to the effects of UDPG per se. However, the high level of PRPP in the tumors they carried was greatly affected by the UDPG infusion. The tumor-specific inhibition of PRPP suggests that this action might prove to be useful combination therapy with inhibitors of purine and pyrimidine nucleotide synthesis in various rescue regimens. UDPG was found to enter cells intact before it was cleaved into glucose phosphate and UMP. The fact that UDPG was also found in the membrane fraction suggests that either there is a specific transport mechanism or UDPG exerts its action via interaction with the cell membrane.

Adenine↗
PubMed1987

Establishment of a human/Chinese hamster hybrid clone panel.

Combined with the chromosome G-banding, followed by Giemsa-11 techniques and chromosomal marker isozyme analysis, 6 out of 200 subclones have been analyzed in detail. A primary hybrid clone panel has been established, which can be used to map genes on chromosomes 4, 5, 8, 12, 20 and 22. Since the panel contains deleted chromosomes 4, 5, 8 and 12, genes on these chromosomes can be mapped regionally.

Animals↗