Biomedical subjects

F Wang

Publications and source records attributed to F Wang.

At least 307 records · Page 17Linked to original sources

PubMed1999

[Chemical composition of essential oil from leaves of litsea cubeba and its antifungal activities].

The 24 chemical constituents of the essential oil extracted from the leaves of Litsea cubeba have been identified by means of GC-MS technique. Among which, alpha-cis-ocimene(25.11%), 3,7-dimethyl-1,6-octadien-3-ol(16.85%) and n-transnerolidol (13.89%) were the principal components. In vitro this oil had a manifest antifungal activities with MIC between 0.03-0.4 microliter/ml for utilized pathogenic fungi and 1.0-2.0 microliters/ml for moulds.

Acyclic Monoterpenes↗

PubMed1999

[Chemical constituents of the essential oil from the fruits of Lindera glauca and its antifungal activities].

The chemical constituents of the two essential oils extracted from the fruits of Lindera glauca by hydrodistillation and petroleum ether have been studied by means of GC-MS. Among which, 32 kinds of constituents were identified in distilling oil and 22 kinds in solvent oil. The main components in distilling oil were n-carpric acid (25.39%), germacrene A (10.71%), n-dodecanole acid (10.08%), epishyobunol acetate (7.29%) and caryophyllene oxide (5.44%), and in solvent oil were camphene (17.55%), 3,6,6-trimethyl-2-norpinene (16.85%), capric acid, ethyl ester (13.61%), eucalyptol (8.10%), and alpha-cis-ocimene (7.38%), In vitro the distilling oil exhibited more manifest antifungal properties than the solvent oil with MIC between 0.03-0.5 ml/L for pathogenic fungi species and 1.0-1.5 ml/L for moulds. Almost having not contained the sesquiterpenoids and their derivatives in the solvent oil maybe were a reason of poor inhibitory.

Antifungal Agents↗

PubMed1999

[GC-MS analysis and inhibitory activity of the essential oil extracted from the leaves of Lindera communis].

The essential oil isolated from the dried leaves of Lindera communis was analyzed by means of gas chromatography-mass(GC-MS) technique, the structures of 23 chemical components were identified from it in total, among these, (-)-spathulenol(relative content 22.50%), endo-1,3,3-trimethyl-2-norbornanol, acetate (10.06%), caryophyllene oxide (6.74%) and germacrene B(6.71%) were the main constituents. And also the oil in vitro exhibited manifest antifungal and antibacterial activities against 4 fungi pathogen species and 4 bacterial species with MIC between 0.08-0.8 ml/l.

Anti-Bacterial Agents↗

PubMed1999

[Diagnostic value of B-scan in exudative age-related macular degeneration].

PURPOSE: To explore the image features of exudative age-related macular degeneration (AMD) with B-scan. METHODS: Using NIDEK US-3300 model B-scan to observe 31 patients (54 eyes) with AMD. RESULTS: The membranous arc echo was found at the posterior polar and there was a shuttle absence of echo between the echo band and the wall of eyeball in the period of retinal pigment epithelium detachment. During the exudation and hemorrhage absorbed not comletely, mixed echo was seen. A small parenchyma body with protrusion was seen with stronger echo in the late phase when the exudation and hemorrhage were replaced by the scar tissues, it was like a convex lens or a triangle and the top pointed to the globe behind, but it was flat towards the vitreous. CONCLUSION: The B-scan examination is valuable in diagnosis, treatment and follow-up for exudative AMD.

Aged↗

PubMed1998

Ah receptor agonists as endocrine disruptors: antiestrogenic activity and mechanisms.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related compounds induce a broad spectrum of biochemical and toxic responses and disrupt multiple endocrine pathways. Research in this laboratory has focused on characterizing aryl hydrocarbon receptor (AhR)-mediated antiestrogenicity in the rodent uterus and mammary and in human breast cancer cells. TCDD inhibits multiple estrogen (E2)-induced responses in these tissues including development or growth of human mammary and endometrial cancer cells, carcinogen-induced mammary cancer in rats, and mammary cancer in mice bearing breast cancer cell xenografts. The mechanisms of AhR-mediated antiestrogenicity are complex; however, studies on the molecular biology of cross-talk between the AhR and estrogen-receptor (ER) signaling pathways have been initiated using several E2-regulated genes as models. The results indicate that the nuclear AhR complex targets specific genomic core inhibitory dioxin responsive elements (iDREs) in promoter regions of some E2-responsive target genes to inhibit hormone-induced transactivation. The pS2, cathepsin and c-fos genes have functional iDREs, whereas the iDRE in the progesterone receptor gene promoter was not functional. Research has also focused on development of AhR-based antiestrogens which inhibit mammary tumor development and growth but do not exhibit prototypical AhR-induced toxic responses.

Animals↗

PubMed1998

Analysis of the regulatory phosphorylation site in Acanthamoeba myosin IC by using site-directed mutagenesis.

The actin-activated ATPase activity of Acanthamoeba myosin IC is stimulated 15- to 20-fold by phosphorylation of Ser-329 in the heavy chain. In most myosins, either glutamate or aspartate occupies this position, which lies within a surface loop that forms part of the actomyosin interface. To investigate the apparent need for a negative charge at this site, we mutated Ser-329 to alanine, asparagine, aspartate, or glutamate and coexpressed the Flag-tagged wild-type or mutant heavy chain and light chain in baculovirus-infected insect cells. Recombinant wild-type myosin IC was indistinguishable from myosin IC purified from Acanthamoeba as determined by (i) the dependence of its actin-activated ATPase activity on heavy-chain phosphorylation, (ii) the unusual triphasic dependence of its ATPase activity on the concentration of F-actin, (iii) its Km for ATP, and (iv) its ability to translocate actin filaments. The Ala and Asn mutants had the same low actin-activated ATPase activity as unphosphorylated wild-type myosin IC. The Glu mutant, like the phosphorylated wild-type protein, was 16-fold more active than unphosphorylated wild type, and the Asp mutant was 8-fold more active. The wild-type and mutant proteins had the same Km for ATP. Unphosphorylated wild-type protein and the Ala and Asn mutants were unable to translocate actin filaments, whereas the Glu mutant translocated filaments at the same velocity, and the Asp mutant at 50% the velocity, as phosphorylated wild-type proteins. These results demonstrate that an acidic amino acid can supply the negative charge in the surface loop required for the actin-dependent activities of Acanthamoeba myosin IC in vitro and indicate that the length of the side chain that delivers this charge is important.

Acanthamoeba↗

PubMed1998

Reciprocal interactions between beta1-integrin and epidermal growth factor receptor in three-dimensional basement membrane breast cultures: a different perspective in epithelial biology.

Anchorage and growth factor independence are cardinal features of the transformed phenotype. Although it is logical that the two pathways must be coregulated in normal tissues to maintain homeostasis, this has not been demonstrated directly. We showed previously that down-modulation of beta1-integrin signaling reverted the malignant behavior of a human breast tumor cell line (T4-2) derived from phenotypically normal cells (HMT-3522) and led to growth arrest in a three-dimensional (3D) basement membrane assay in which the cells formed tissue-like acini (14). Here, we show that there is a bidirectional cross-modulation of beta1-integrin and epidermal growth factor receptor (EGFR) signaling via the mitogen-activated protein kinase (MAPK) pathway. The reciprocal modulation does not occur in monolayer (2D) cultures. Antibody-mediated inhibition of either of these receptors in the tumor cells, or inhibition of MAPK kinase, induced a concomitant down-regulation of both receptors, followed by growth-arrest and restoration of normal breast tissue morphogenesis. Cross-modulation and tissue morphogenesis were associated with attenuation of EGF-induced transient MAPK activation. To specifically test EGFR and beta1-integrin interdependency, EGFR was overexpressed in nonmalignant cells, leading to disruption of morphogenesis and a compensatory up-regulation of beta1-integrin expression, again only in 3D. Our results indicate that when breast cells are spatially organized as a result of contact with basement membrane, the signaling pathways become coupled and bidirectional. They further explain why breast cells fail to differentiate in monolayer cultures in which these events are mostly uncoupled. Moreover, in a subset of tumor cells in which these pathways are misregulated but functional, the cells could be "normalized" by manipulating either pathway.

Basement Membrane↗

PubMed1998

[Effects of glutamic acid on heat tolerance and 70 kD proteins of Drosophila melanogaster].

From supplement of dietary glutamic acid, the heat tolerance ability of Drosophila and the change of Hsp70(heat shock proteins) were studied. The results showed that the supplement of dietary glutamic acid could increase the survival time and the contents Hsp70 of Drosophila, in the 37 degrees C heat environment; but could not get the Hsp70 rise up when Drosophila were in 25 degrees C. Based on the findings, we could make the conclusion that supplement dietary glutamic acid could benefit the heat tolerance ability of Drosophila, and it might be related to the increase of Hsp70.

Animals↗

PubMed1998

Ion channel modulation as the basis for general anesthesia.

(1) Modulation of the function of the GABA(A) and neuronal nicotinic acetylcholine receptor channels caused by general anesthetics and modulation of the GABA(A) receptor-channel by halothane, enflurane, isoflurane, and n-octanol was channel state-dependent. (3) Halothane modulation of the GABA(A) receptor was independent of subunits, but n-octanol modulation was subunit-dependent. (4) Ethanol at 30-100 microM was very potent in accelerating the desensitization of currents induced by acetylcholine. (5) The ethanol modulation was subunit- and state-dependent, occurring in the alpha3beta4 combination but only weakly in the alpha3beta2 combination. (6) In contrast, halothane at 430 microM (approximately 1 MAC) potently suppressed ACh-induced currents in the alpha3beta2 subunit combination.

Anesthesia, General↗

PubMed1998

Functional implications of the structure of the murine parvovirus, minute virus of mice.

BACKGROUND: Minute virus of mice (MVM) is a single-stranded (ss) DNA-containing, murine parvovirus with a capsid built up of 60 icosahedrally related polypeptide chains, each of which consists of the C-terminal region common to two structural proteins, VP1 and VP2. In infectious virions, most VP2 molecules are cleaved to VP3 by the removal of about 20 amino acids from the N terminus. Of the 587 amino acids in VP2, approximately half are identical to those in the analogous capsid protein of the antigenically distinct canine parvovirus (CPV), the crystal structure of which has previously been determined. The three-dimensional structure determination of MVMi (the immunosuppressive strain of MVM) was previously reported to 3.5 A resolution. RESULTS: We report here an analysis of the MVMi virus structure and provide insights into tissue tropism, antigenicity and DNA packaging. Amino acids determining MVM tissue tropism were found to cluster on, or near, the viral surface. A conserved, glycine-rich, N-terminal peptide was seen to run through a cylindrical channel along each fivefold axis and may have implications for antigenicity. Density within the virion was interpreted as 29 ssDNA nucleotides per icosahedral asymmetric unit, and accounts for over one-third of the viral genome. CONCLUSIONS: The presence of the glycine-rich sequence in the fivefold channels of MVMi provides a possible mechanism to explain how the unique N-terminal region of VP1 becomes externalized in infectious parvovirions. Residues that determine tropism may form an attachment recognition site for a secondary host-cell factor that modulates tissue specificity. The ordering of nucleotides in a similar region of the interior surface in the CPV and MVMi capsids suggests the existence of a genomic DNA-recognition site within the parvoviral capsid.

Amino Acid Sequence↗

PubMed1998

Alterations in TCR-MHC contacts subsequent to cross-recognition of class I MHC and singly substituted peptide variants.

Vesicular stomatitis virus (VSV) elicits H-2Kb-restricted CTLs specific for the immunodominant VSV octapeptide RGYVYQGL. To study the structural features important for interaction between the TCR beta-chain and the peptide/MHC complex, we immunized TCR alpha-chain transgenic mice with the VSV peptide and raised a panel of anti-VSV CTL clones with identical TCR alpha-chains. Consistent with our previous analysis of uncloned populations of primary CTLs, the anti-VSV CTL clones were all Vbeta13+ and expressed TCR beta-chains with highly homologous complementarity-determining region 3 (CDR3) loops. Although the clones expressed similar TCRs, they differed in their ability to cross-react with VSV peptide variants singly substituted at TCR contact positions 4 and 6. These findings allowed us to identify short stretches of amino acids in the C-terminal region of the CDR3beta loop that, when altered, modify the cross-reaction capability of the TCR to position 4 and position 6 variant peptides. To further probe the structural correlates of biologic cross-reactivity, we used cross-reactive CTL clones and cell lines expressing point mutations in H-2Kb to investigate the effect of single amino acid changes in the peptide on the pattern of recognition of the TCR for the peptide/MHC complex. Single conservative substitutions in the peptide were sufficient to alter the recognition contacts between a cross-reactive TCR and the MHC molecule, supporting the idea that the TCR can make overall structural adjustments in MHC contacts to accommodate single amino acid changes in the peptide.

Amino Acid Substitution↗

PubMed1998

Conformational and dynamic changes of Yersinia protein tyrosine phosphatase induced by ligand binding and active site mutation and revealed by H/D exchange and electrospray ionization Fourier transform ion cyclotron resonance mass spectrometry.

Protein tyrosine phosphatases (PTPase) play important roles in the intracellular signal transduction pathways that regulate cell transformation, growth, and proliferation. Here, solvent accessibility is determined for backbone amide protons from various segments of wild-type Yersinia PTPase in the presence or absence of 220 microM vanadate, a competitive inhibitor, as well as an active site mutant in which the essential cysteine 403 has been replaced by serine (C403S). The method consists of solution-phase H/D exchange, followed by pepsin digestion, high-performance liquid chromatography, and electrospray ionization high-field (9.4 T) Fourier transform ion cyclotron resonance mass spectrometry. Proteolytic segments spanning approximately 93.5% of the primary sequence are analyzed. Binding of vanadate reduces the H/D exchange rate throughout the protein, both for the WpD loop and for numerous other residues that are shielded when that loop is pulled down over the active site on binding of the inhibitor. The single active site C403S mutation reduces solvent access to the WpD loop itself, but opens up the structure in several other segments. Although the 3D structure of the ligand-bound C403S mutant is similar to that of the wild-type PTPase, and the C403S mutant and the wild-type enzyme display similar affinities for vanadate, the thermodynamics for binding of vanadate is different for the two proteins. Collectively, these results establish the flexibility of the WpD loop (previously inferred by comparing PTPase X-ray single-cyrstal diffraction structures in the presence and absence of a tungstate inhibitor), as well as several other signficant changes in segment exposure and/or flexibility that are not evident from X-ray structures.

Amino Acid Sequence↗

PubMed1998

Chronic nicotine treatment up-regulates human alpha3 beta2 but not alpha3 beta4 acetylcholine receptors stably transfected in human embryonic kidney cells.

Human nicotinic acetylcholine receptor (AChR) subtypes alpha3 beta2, alpha3 beta2 alpha5, alpha3 beta4, and alpha3 beta4 alpha5 were stably expressed in cells derived from the human embryonic kidney cell line 293. alpha3 beta4 AChRs were found in prominent 2-micrometer patches on the cell surface, whereas most alpha3 beta2 AChRs were more diffusely distributed. The functional properties of the alpha3 AChRs in tsA201 cells were characterized by whole cell patch clamp using both acetylcholine and nicotine as agonists. Nicotine was a partial agonist on alpha3 beta4 AChRs and nearly a full agonist on alpha3 beta2 alpha5 AChRs. Chronic exposure of cells expressing alpha3 beta2 AChRs or alpha3 beta2 alpha5 AChRs to nicotine or carbamylcholine increased their amount up to 24-fold but had no effect on the amount of alpha3beta4 or alpha3 beta4 alpha5 AChRs, i.e. the up-regulation of alpha3 AChRs depended on the presence of beta2 but not beta4 subunits in the AChRs. This was also found to be true of alpha3 AChRs in the human neuroblastoma SH-SY5Y. In the absence of nicotine, alpha3 beta2 AChRs were expressed at much lower levels than alpha3 beta4 AChRs, but in the presence of nicotine, the amount of alpha3 beta2 AChRs exceeded that of alpha3 beta4 AChRs. Up-regulation was seen for both total AChRs and surface AChRs. Up-regulated alpha3beta2 AChRs were functional. The nicotinic antagonists curare and dihydro-beta-erythroidine also up-regulated alpha3 beta2 AChRs, but only by 3-5-fold. The channel blocker mecamylamine did not cause up-regulation of alpha3 beta2 AChRs and inhibited up-regulation by nicotine. Our data suggest that up-regulation of alpha3 beta2 AChRs in these lines by nicotine results from both increased subunit assembly and decreased AChR turnover.

Animals↗

PubMed1998

[Detection of Hep-2 and hepatoma cell line chromosomal aberration by using fluorescence in situ hybridization].

OBJECTIVE: To study the chromosomal aberration of hepatoma cell line (1172) and laryngocarcinoma cell line (Hep-2). METHODS: Fluorescence in situ hybridization (FISH) was used with nine chromosomal special libraries. RESULTS: The abnormal signals indicated that very complicated aberrations existed in the two cell lines. This suggested that the aberrations also existed in other chromosomes not yet studied. In 1172, the major type was structure aberration, but in Hep-2, numerical abnormality was shown in almost all chromosomes studied. CONCLUSION: Compared with traditional cytological methods, this technique has the advantages of being quicker and more accurate and sensitive.

Carcinoma↗

PubMed1998

Rapid deletion of rearranged T cell antigen receptor (TCR) Valpha-Jalpha segment by secondary rearrangement in the thymus: role of continuous rearrangement of TCR alpha chain gene and positive selection in the T cell repertoire formation.

A rearranged T cell receptor (TCR) Valpha and Jalpha gene from a cytochrome c-specific T cell hybridoma was introduced into the genomic Jalpha region. The introduced TCR alpha chain gene is expressed in a majority of CD3 positive and CD4 CD8 double-negative immature thymocytes. However, only a few percent of the double-positive and single-positive thymocytes express this TCR alpha chain. This decrease is caused by a rearrangement of TCR alpha chain locus, which deletes the introduced TCR gene. Analysis of the mice carrying the introduced TCR alpha chain and the transgenic TCR beta chain from the original cytochrome c-specific T cell hybridoma revealed that positive selection efficiently rescues double-positive thymocytes from the loss of the introduced TCR alpha chain gene. In the mice with negatively selecting conditions, T cells expressing the introduced TCR alphabeta chains were deleted at the double-positive stage. However, a large number of thymocytes escape negative selection by using an endogenous TCR alpha chain created by secondary rearrangement maintaining normal thymocyte development. These results suggest that secondary rearrangements of the TCR alpha chain gene play an important role in the formation of the T cell repertoire.

Animals↗

PubMed1998

Structure and expression of the mouse AhR nuclear translocator (mArnt) gene.

Aryl hydrocarbon receptor (AhR) nuclear translocator (Arnt) gene has been isolated and characterized from a mouse genomic DNA library. The gene is about 60 kilobases long and split into 22 exons. An unusual exon/intron junctional sequence was found in the 11th intron of the gene that begins with GC at its 5'-end. The exon/intron arrangement of mArnt gene differs greatly from those of the other members of the same basic-helix-loop-helix/PAS family. The gene is TATA-less and has several transcription start sites. The promoter region of the mArnt gene is GC-rich and contains a number of putative regulatory DNA sequences such as two GC-boxes, a cAMP-responsive element, E-box, AP-1 site, and CAAT-box. Deletion experiments revealed that all these DNA elements made substantial contributions to a high level of expression of the gene, except for the cAMP-responsive element. Of all, two GC-boxes displayed the most dominant enhancing effects. It was demonstrated that there exist specific factors binding to these DNA elements in the nuclear extracts of HeLa cells. Among them, Sp1 and Sp3, and CAAT-box binding factor-A were identified to bind the GC-boxes and CAAT-box, respectively. Expression of MyoD in HeLa cells stimulated the Arnt promoter activity by binding to the E-box.

Amino Acid Sequence↗

PubMed1998

Nonaqueous capillary electrophoresis chiral separations with quaternary ammonium beta-cyclodextrin.

Chiral separation of nonsteroidal anti-inflammatory drugs (profens), 1,1'-binaphthyl-2,2'-diyl-hydrogen phosphate, N-[1-(1-naphthyl)ethyl]phthalamic acid, and derivatized amino acids by a cationic cyclodextrin, quaternary ammonium beta-cyclodextrin (QA-beta-CD), was investigated by capillary electrophoresis (CE) in both aqueous and nonaqueous media. Several profens and amino acids could only be separated by QA-beta-CD in pure formamide system. No chiral separation of the profens was achieved in the following solvents: N-methylformamide, methanol, dimethyl sulfoxide, and water; however, chiral separations of most of the amino acids were obtained in all of these solvents. The effects of other experimental parameters such as the CD concentration and apparent pH (pH*) were also investigated. The first application of nonaqueous CE chiral separation of ketoprofen in a commercially available sample, Actron, was also examined. In addition, the reversal of electroosmotic flow by QA-beta-CD was observed in water, formamide, N-methylformamide, methanol, and dimethyl sulfoxide media.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1998

Sphingosine-1-phosphate in cell growth and cell death.

Recent evidence suggests that branching pathways of sphingolipid metabolism may mediate either apoptotic or mitogenic responses depending on the cell type and the nature of the stimulus. While ceramide has been shown to be an important regulatory component of apoptosis induced by tumor necrosis factor alpha and Fas ligand, sphingosine-1-phosphate (SPP), a further metabolite of ceramide, has been implicated as a second messenger in cellular proliferation and survival induced by platelet-derived growth factor, nerve growth factor, and serum. SPP protects cells from apoptosis resulting from elevations of ceramide. Inflammatory cytokines stimulate sphingomyelinase, but not ceramidase, leading to accumulation of ceramide, whereas growth signals also leading to accumulation of ceramide, whereas growth signals also stimulate ceramidase and sphingosine kinase leading to increased SPP levels. We propose that the dynamic balance between levels of sphingolipid metabolites, ceramide, and SPP, and consequent regulation of different family members of mitogen-activated protein kinases (JNK versus ERK), is an important factor that determines whether a cell survives or dies.

Animals↗