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Biomedical subjects

W Chao

Publications and source records attributed to W Chao.

At least 19 recordsLinked to original sources
PubMed2006

Nanometer-scale ablation with a table-top soft x-ray laser.

Ablation of holes with diameters as small as 82 nm and very clean walls was obtained in poly(methyl methacrylate) focusing pulses from a Ne-like Ar 46.9 nm compact capillary-discharge laser with a freestanding Fresnel zone plate diffracting into third order. These results demonstrate the feasibility of using focused soft x-ray laser beams for the direct nanoscale patterning of materials and the development of new nanoprobes.

Journal Article↗
PubMed2006

Sub-38 nm resolution tabletop microscopy with 13 nm wavelength laser light.

We have acquired images with a spatial resolution better than 38 nm by using a tabletop microscope that combines 13 nm wavelength light from a high-brightness tabletop laser and Fresnel zone plate optics. These results open a gateway to the development of compact and widely available extreme-ultraviolet imaging tools capable of inspecting samples in a variety of environments with a 15-20 nm spatial resolution and a picosecond time resolution.

Journal Article↗
PubMed2005

Magnetic microstructures and their dynamics studied by X-ray microscopy.

Full-field soft X-ray microscopy in combination with X-ray magnetic circular dichroism as contrast mechanism is a powerful technique to image with elemental specificity magnetic nanostructures and multilayered thin films at high lateral resolution down to 15nm by using Fresnel zone plates as X-ray optical elements. Magnetization reversal phenomena on a microscopic level are studied by recording the images in varying external magnetic fields. Local spin dynamics at a time resolution below 100ps can be addressed by engaging a stroboscopic pump-and-probe scheme taking into account the time pattern of synchrotron storage rings. Characteristic features of magnetic soft X-ray microscopy are reviewed and an outlook into future perspectives with regard to increased lateral and temporal resolution is given.

Journal Article↗
PubMed2005

Nanoimaging with a compact extreme-ultraviolet laser.

Images with a spatial resolution of 120-150 nm were obtained with 46.9 nm light from a compact capillary-discharge laser by use of the combination of a Sc-Si multilayer-coated Schwarzschild condenser and a free-standing imaging zone plate. The results are relevant to the development of compact extreme-ultraviolet laser-based imaging tools for nanoscience and nanotechnology.

Equipment Design↗
PubMed2003

Detection of HIV-1 DNA in microglia/macrophages, astrocytes and neurons isolated from brain tissue with HIV-1 encephalitis by laser capture microdissection.

In HIV-1 encephalitis, HIV-1 replicates predominantly in macrophages and microglia. Astrocytes also carry HIV-1, but the infection of oligodendrocytes and neurons is debated. In this study we examined the presence of HIV-1 DNA in different brain cell types in 6 paraffin embedded, archival post-mortem pediatric and adult brain tissues with HIV-1 encephalitis by Laser Capture Microdissection (LCM). Sections from frontal cortex and basal ganglia were stained by immunohistochemistry for CD68 (microglia), GFAP (astrocytes), MAP2 (neurons), and p24 (HIV-1 positive cells) and different cell types were microdissected by LCM. Individual cells or pools of same type of cells were lysed, the cell lysates were subjected to PCR using HIV-1 gag SK38/SK39 primers, and presence of HIV-1 DNA was confirmed by Southern blotting. HIV-1 gag DNA was consistently detected by this procedure in the frontal cortex and basal ganglia in 1 to 20 p24 HIV-1 capsid positive cells, and in pools of 50 to 100 microglia/macrophage cells, 100 to 200 astrocytes, and 100 to 200 neurons in HIV-1 positive cases but not in HIV-1 negative controls. These findings suggest that in addition to microglia, the infection of astrocytes and neurons by HIV-1 may contribute to the development of HIV-1 disease in the brain.

Adolescent↗
PubMed2001

Retinoic acid (RA) receptor transcriptional activation correlates with inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced ornithine decarboxylase (ODC) activity by retinoids: a potential role for trans-RA-induced ZBP-89 in ODC inhibition.

Evaluation of retinoic acid receptor (RAR) subtype-selective alpha and gamma agonists and antagonists and a retinoid X receptor (RXR) class-selective agonist for efficacy at inhibiting both induction of ornithine decarboxylase (ODC) by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse epidermis and rat tracheal epithelial cells and the appearance of papillomas in mouse epidermis treated in the 2-stage tumor initiation-promotion model indicated that (i) RXR class-selective transcriptional agonists, such as MM11246, were not involved in ODC inhibition; (ii) RAR-selective agonists that induce gene transcription from RA-responsive elements (RAREs) were active at low concentrations; (iii) RAR-selective antagonists that bind RARs and inhibit AP-1 activation on the collagenase promoter but do not activate RAREs to induce gene transcription were less effective inhibitors; and (iv) RARgamma-selective retinoid agonists were more effective inhibitors of TPA-induced ODC activity than RARalpha-selective agonists. These results suggest that RARE activation has a more important role in inhibition of ODC activity than RXR activation or AP-1 inhibition and that RARgamma-selective agonists would be the most useful inhibitors of epithelial cell proliferation induced by tumor promoters. The natural retinoid all-trans-RA induced expression of transcription factor ZBP-89, which represses activation of the GC box in the ODC promoter by the transcription factor Sp1.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2001

Vif is largely absent from human immunodeficiency virus type 1 mature virions and associates mainly with viral particles containing unprocessed gag.

Vif is a human immunodeficiency virus type 1 (HIV-1) protein that is essential for the production of infectious virus. Most of Vif synthesized during HIV infection localizes within cells, and the extent of Vif packaging into virions and its function there remain controversial. Here we show that a small but detectable amount of Vif remains associated with purified virions even after their treatment with the protease subtilisin. However, treatment of these virions with 1% Triton X-100 revealed that most of the virion-associated Vif segregated with detergent-resistant virus particles consisting of unprocessed Gag, indicating that detergent-soluble, mature virions contain very little Vif. To investigate the control of Vif packaging in immature virus particles, we tested its association with Gag-containing virus-like particles (VLPs) in a Vif and Gag coexpression system in human cells. Only a small proportion of Vif molecules synthesized in this system became packaged into VLPs, and the VLP-associated Vif was protected from exogenous protease and detergent treatment, indicating that it is stably incorporated into immature virion-like cores. About 10-fold more Vpr than Vif was packaged into VLPs but most of the VLP-associated Vpr was removed by treatment with detergent. Mutagenesis of the C-terminal sequences in Gag previously shown to be responsible for interaction with Vif did not reduce the extent of Vif packaging into Gag VLPs. Surprisingly, short deletions in the capsid domain (CA) of Gag (amino acid residues 284 to 304 and 350 to 362) increased Vif packaging over 10-fold. The 350 to 363 deletion introduced into CA in HIV provirus also increased Vif incorporation into purified virions. Our results show that Vif can be packaged at low levels into aberrant virus particles or immature virions and that Vif is not present significantly in mature virions. Overall, these results indicate that the Vif content in virions is tightly regulated and also argue against a function of virion-associated Vif.

Animals↗
PubMed2001

Highly productive infection with pseudotyped human immunodeficiency virus type 1 (HIV-1) indicates no intracellular restrictions to HIV-1 replication in primary human astrocytes.

Human astrocytes can be infected with human immunodeficiency virus type 1 (HIV-1) in vitro and in vivo, but, in contrast to T lymphocytes and macrophages, virus expression is inefficient. To investigate the HIV-1 life cycle in human fetal astrocytes, we infected cells with HIV-1 pseudotyped with envelope glycoproteins of either amphotropic murine leukemia virus or vesicular stomatitis virus. Infection by both pseudotypes was productive and long lasting and reached a peak of 68% infected cells and 1.7 microg of viral p24 per ml of culture supernatant 7 days after virus inoculation and then continued with gradually declining levels of virus expression through 7 weeks of follow-up. This contrasted with less than 0.1% HIV-1 antigen-positive cells and 400 pg of extracellular p24 per ml at the peak of astrocyte infection with native HIV-1. Cell viability and growth kinetics were similar in infected and control cells. Northern blot analysis revealed the presence of major HIV-1 RNA species of 9, 4, and 2 kb in astrocytes exposed to pseudotyped (but not wild-type) HIV-1 at 2, 14, and 28 days after infection. Consistent with productive infection, the 9- and 4-kb viral transcripts in astrocytes infected by pseudotyped HIV-1 were as abundant as the 2-kb mRNA during 4 weeks of follow-up, and both structural and regulatory viral proteins were detected in infected cells by immunoblotting or cell staining. The progeny virus released by these cells was infectious. These results indicate that the major barrier to HIV-1 infection of primary astrocytes is at virus entry and that astrocytes have no intrinsic intracellular restriction to efficient HIV-1 replication.

Astrocytes↗
PubMed2000

Human immunodeficiency virus type 1 can infect human retinal pigment epithelial cells in culture and alter the ability of the cells to phagocytose rod outer segment membranes.

Human immunodeficiency virus type 1 (HIV-1) has been found in the vitreous of persons with AIDS. Here we investigated the susceptibility of human retinal pigment epithelial (RPE) cells to HIV-1 infection in culture and the effects of HIV-1 on the phagocytic function of the RPE. We found that 10 of 11 populations of RPE cells isolated from different fetal or adult eyes were susceptible to low-level replication of HIV-1/NL4-3 as determined by the detection of viral DNA and spliced viral RNA encoding envelope. HIV-1 infection was not inhibited by recombinant soluble CD4, suggesting that CD4 is not required for virus entry into RPE cells. RPE cells fused with target cells constitutively expressing HIV-1 envelope glycoproteins, indicating that HIV-1 enters cells by receptor-mediated fusion. Exposure to HIV-1 or recombinant gp120 caused a two- to four-fold increase in the binding and uptake of isolated rod outer segments by RPE cells. These findings introduce a new cell target of HIV-1 replication in the eye and indicate that RPE cells function aberrantly when exposed to HIV-1 or its envelope glycoprotein.

Adult↗
PubMed2000

Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study.

BACKGROUND & AIMS: Helicobacter pylori-infected gastric mucosa evolves through stages of chronic gastritis, intestinal metaplasia (IM), glandular atrophy (GA), and dysplasia before carcinoma develops. We studied if H. pylori eradication would alter the course of premalignant histologic changes in the stomach. METHODS: Volunteers from the Yantai County in China underwent upper endoscopy with biopsy specimens obtained from the antrum and corpus. H. pylori-infected subjects were randomized to receive either a 1-week course of omeprazole, amoxicillin, and clarithromycin (OAC) or placebo. At 1 year, endoscopies with biopsies were repeated. RESULTS: A total of 587 H. pylori-infected subjects were randomized to OAC (n = 295) and placebo (n = 292). At 1 year, H. pylori was eradicated in 226 subjects assigned to OAC. In the placebo group, 245 patients remained H. pylori infected. Analysis of paired samples obtained from the same patients showed that acute and chronic gastritis decreased in both the antrum and corpus after H. pylori eradication (P<0.001) and activity of IM decreased in antrum (P = 0.014). In the H. pylori-infected group, antral biopsy specimens had more pronounced acute gastritis (P = 0.01), whereas corpus specimens showed increased acute and chronic gastritis (P<0.001) and a marginal increase in GA (P = 0.052). When histologic changes were compared between the 2 groups, decrease in acute and chronic gastritis was more frequent after H. pylori eradication (P<0.001) but changes in IM were similar. In the H. pylori-infected group, increase in GA was seen in the corpus (P = 0.01). CONCLUSIONS: At 1 year, H. pylori eradication is beneficial in preventing progression of pathologic changes of the gastric mucosa.

Adult↗
PubMed2000

Synthesis and analgesic activity of N-(N-acetyl-L-amino-acyl)-5-methoxytryptamines.

5-Methoxytryptamine was acylated with N-acetyl-L-amino acids to give rise the corresponding N-(N-acetyl-L-amino acyl)-5-methoxytryptamines. The analgesic activity was evaluated by the tail flick test. Among the 6 compounds, the analgesic potency of N-(N-acetyl-tryptophanyl)-5-methoxytryptamine (5e) and N-(N-acetyl-glycyl)-5-methoxytryptamine (5a) are much more potent than that of melatonin.

Analgesics↗
PubMed2000

Synthesis and analgesic activity of N,N'-dicarbonyltryptamines.

5-Methoxytryptamine and L-tryptophan methyl ester were acylated with malonic acid, dimethyl malonate, or succinic anhydride to produce the corresponding N,N'-dicarbonyltryptamine derivatives. The analgesic activity was evaluated by the tail flick test. All of the compounds exhibited desirable analgesic potency. This result is consistent with that of N-(N-acetyl-L-tryptophanyl)-5-methoxytryptamine and confirmed that introducing substituted tryptamine into the amide chain of melatonin does enhance analgesic potency.

5-Methoxytryptamine↗
PubMed2000

Synthesis of RGD containing peptides and their vasodilation effect.

APLRV, SLRR, RGDS, and RGDF were synthesized by use of the solution method via the corresponding protective intermediates. After fragment condensation and deprotection, APLRVRGDS, APLRVRGDF, SLRRRGDS, and SLRRRGDF were obtained. The effect of these RGD containing peptides on rat aortic strips pretreated with noradrenaline (NE) were observed. The relaxing extents of contracted strips for them at three doses (10(-5) mol/L, 10(-6) mol/L and 10(-7) mol/L) indicated that, in a few cases, this kind of combination of these fragments may enhance the desirable activity.

Amino Acid Sequence↗
PubMed2000

The effect of systematic variation in retrospective conduct disorder reports on antisocial personality disorder diagnoses.

A diagnosis of antisocial personality disorder (ASPD) requires a conduct disorder (CD) diagnosis. A CD diagnosis is often obtained retrospectively. This study tested the influence of current behavior on CD recall and the association between recent behavior change and inconsistencies in contemporaneous and retrospective CD reports. Five hundred young adults reported ASPD; retrospective CD; current problem behavior; and, at ages 12 to 15 years, contemporaneous CD. True-positive, true-negative, false-positive, and false-negative CD and ASPD groups were identified. The results supported the hypotheses. Participants whose current behavior agreed with past behavior provided reliable retrospective CD reports. Inaccurate diagnoses occurred among participants whose current behavior was inconsistent with past behavior, either becoming more problematic (CD and ASPD false positives) or less problematic (CD and ASPD false negatives) over time.

Adolescent↗
PubMed1999

Nonoperative treatment of posterior tibial tendon dysfunction.

One of the most common causes of acquired flatfoot deformity in adults is dysfunction of the posterior tibial tendon. The main function of the posterior tibial tendon is to invert the midfoot and lock the transverse tarsal joints (talonavicular and calcaneocuboid joints). When the tendon fails to function properly, a progressive flatfoot deformity develops. Because the disease process is a continuum, a staging system has been devised to offer guidelines for nonoperative and operative treatment of this problem. The rationale for nonoperative treatment of this disorder is to support the longitudinal arch and to decrease the valgus angulation of the calcaneus for flexible flatfoot deformity, and to immobilize and support the hindfoot and midfoot for rigid flatfoot deformities. The success of nonoperative treatment first requires the assessment of the flexibility of the flatfoot deformity. For a flexible deformity, the custom orthosis should be fitted with the foot and ankle in a corrected position as close to the neutral position as possible. Whereas, for a rigid deformity, it is imperative for the custom orthosis to be fitted with the affected foot and ankle in an in situ position.

Adult↗
PubMed1997

The redox state of cysteines in human immunodeficiency virus type 1 Vif in infected cells and in virions.

HIV-1 Vif has two conserved cysteine residues in positions 114 and 133, both of which were found to be essential for HIV-1 infection and for Vif function in transcomplementation assays (X-Y. Ma, P. Sova, W. Chao, and D. J. Volsky, 1994, J. Virol. 68: 1714-1720). We evaluated here the redox status and disulfide bond formation of Vif cysteines inside cells or in virions and tested the role of Vif cysteines in Vif distribution in cells and in virions. Immunoblot analysis of Vif in wild type virus-infected cells and virions under different redox conditions revealed that the cysteine residues are readily accessible to chemical interaction but they do not form intramolecular disulfide bonds either inside cells or in virions, nor do they form covalent bonds with other proteins in either compartment. Cysteine mutants of Vif resembled wildtype Vif in their intracellular and virion distribution, indicating that Vif cysteines do not affect intracellular Vif transport and packaging into virions. We conclude that the cysteines in Vif do not form sulfhydryl bonds either intracellularly or in virions and may contribute to Vif activity rather than structure.

Cell Line↗