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Biomedical subjects

X Tao

Publications and source records attributed to X Tao.

At least 73 records · Page 4Linked to original sources

The relation of the location of haptics of posterior chamber intraocular lenses and peripheral anterior synechia.

PURPOSE: To investigate the occurrence, outcome and influencial factors of the peripheral anterior synechia (PAS) following implantation of posterior chamber intraocular lenses for finding a way to reduce the PAS. SUBJECTS: 40 eyes of 38 senile cataract patients with normal chamber angle and intraocular pressure (IOP) preoperatively were examined. METHODS: Extracapsular cataract extraction was performed under microscope with insertion of a posterior chamber lens implant vaulted anteriorly by 10 degrees. Gonioscopy and slit-lamp examination and photography of the operated eyes were performed 3 to 6 months postoperatively. RESULTS: PAS were found in 20 (50%) of the 40 eyes. Among the 20 eyes with PAS the locations of 23 haptics in 17 eyes corresponded with those of the PAS. PAS were seen more frequently with vertically sulcus-fixated haptics than with the horizontally capsular-fixated haptics, showing a significant difference (P < 0.05). 88% of the eyes with PAS had pupillary deformation, but their visual acuities and IOP were not affected. CONCLUSIONS: PAS is more likely to occur with vertically sulcus-fixated IOL. Rotating the capsular-fixated haptics to the horizontal position may reduce the incidence of PAS. Gonioscopy should be a routine follow-up examination.

Adult↗

Changes of plasma dynorphin levels before and after percutaneous balloon mitral commissurotomy in patients with mitral stenosis.

Plasma dynorphin A1-13 levels were measured in 33 patients with mitral stenosis before and after percutaneous balloon mitral commissurotomy (PBMC). The results show that the basal levels of plasma dynorphin in blood from the antecubital vein in the patients were significantly higher than those in 31 healthy control subjects. The increase in circulating dynorphin closely correlated with the functional cardiac status and the presence of atrial fibrillation. Ten to fifteen minutes after PBMC, plasma dynorphin levels in blood from the femoral vein increased significantly. Seventy-two hours after the procedure, the levels of plasma dynorphin in blood from the antecubital vein had decreased significantly, but they did not decrease to the normal range. Plasma dynorphin levels in blood from the femoral vein were positively correlated with the mean left atrial pressure and the mean right atrial pressure before the first balloon inflation. Plasma dynorphin levels in blood from the antecubital vein were positively correlated with the heart rate and the mean transmitral pressure gradient, and negatively with the mitral valve area before and 72 hours after PBMC.

Adolescent↗

Crystallization and preliminary X-ray studies of the diphtheria Tox repressor from Corynebacterium diphtheriae.

Crystals of the diphtheria tox repressor (DtxR) from Corynebacterium diphtheriae suitable for structure determination have been obtained. DtxR activated with transition metal ions represses the expression of the structural gene for the diphtheria toxin, tox, which is encoded on the genome of a family of closely related corynebacteriophages. The space group of the obtained crystals is trigonal P3(1)21 or its enantiomorph P3(2)21 with a = b = 64.2 A, c = 220.5 A, alpha = beta = 90 degrees, gamma = 120 degrees. Two monomers comprise the asymmetric unit. The crystals diffract to a resolution of better than 3 A.

Bacterial Proteins↗

Determination of the minimal essential nucleotide sequence for diphtheria tox repressor binding by in vitro affinity selection.

The expression of diphtheria toxin in lysogenic toxigenic strains of Corynebacterium diphtheriae is controlled by the heavy metal ion-activated regulatory protein DtxR. In the presence of divalent heavy metal ions, DtxR specifically binds to the diphtheria tox operator and protects a 27-bp interrupted palindromic sequence from DNase I digestion. To determine the consensus DNA sequence for DtxR binding, we have used gel electrophoresis mobility-shift assay and polymerase chain reaction (PCR) amplification for in vitro affinity selection of DNA binding sequences from a universe of 6.9 x 10(10) variants. After 10 rounds of in vitro affinity selection, each round coupled with 30 cycles of PCR amplification, we isolated and characterized a family of DNA sequences that function as DtxR-responsive genetic elements both in vitro and in vivo. Moreover, these DNA sequences were found to bind activated DtxR with an affinity similar to that of the wild-type tox operator. The DNA sequence analysis of 21 unique in vitro affinity-selected binding sites has revealed the minimal essential nucleotide sequence for DtxR binding to be a 9-bp palindrome separated by a single base pair.

Bacterial Proteins↗

T cells which do not express membrane tumor necrosis factor-alpha activate macrophage effector function by cell contact-dependent signaling of macrophage tumor necrosis factor-alpha production.

Previous studies have suggested that T cell contact-dependent signaling of macrophages (Mphi) is mediated by membrane tumor necrosis factor-alpha (memTNF-alpha), based on the observation that anti-TNF-alpha could inhibit T cell-mediated Mphi activation. The current report confirms that anti-TNF-alpha does inhibit activation of interferon-gamma (IFN-gamma)-primed Mphi by paraformaldehyde-fixed activated T cells. However, the involvement of membrane molecules other than memTNF-alpha in the contact-dependent signaling is suggested by two lines of evidence. First, the TH2 clone, AK8, displayed neither secreted TNF-alpha/beta nor memTNF-alpha/beta detectable by bioassay or immunofluorescence. Nonetheless, AK8 cells were equally effective, on a per cell basis, in contact-dependent signaling of M phi activation as TH2 and TH1 cells which do express memTNF-alpha. Second, the expression of memTNF-alpha by the TH2 clone, D10.G4, is maximal 24 h after activation, whereas the ability of this clone to activate Mphi is maximal at 6-8 of activation and declines thereafter. Since TNF-alpha is known to play a critical role in activation of Mphi effector function, it was hypothesized that T cell membrane components other than memTNF-alpha might signal Mphi production of TNF-alpha, thus allowing autocrine TNF-alpha stimulation of Mphi effector function. In support of this, it is demonstrated that paraformaldehyde-fixed activated TH2 cells can induce de novo production and release of TNF-alpha by Mphi. This effect was not an artifactual result of paraformaldehyde fixation since paraformaldehyde-fixed resting T cells did not induce TNF-alpha gene expression. Previous studies have demonstrated a role for autocrine TNF-alpha stimulation in LPS induction of effector function in recombinant IFN-gamma-primed Mphi. The current study confirms that TNF-alpha plays a critical role in T cell contact-dependent signaling of Mphi but indicates that memTNF on the T cells may not be a sine qua non factor for contact-dependent signaling. The data suggest that other T cell membrane molecules contribute to activation of Mphi effector function by stimulation of M phi TNF-alpha production.

Animals↗

Iron, DtxR, and the regulation of diphtheria toxin expression.

In recent years considerable advances have been made in the understanding of the molecular basis of iron-mediated regulation of diphtheria toxin expression. The tox gene has been shown to be regulated by the heavy metal ion-activated regulatory element DtxR. In the presence of divalent heavy metal ions, DtxR becomes activated and binds to a 9 bp interrupted palindromic sequence. The consensus-binding site has been determined by both the sequence analysis of DtxR-responsive operators cloned from genomic libraries of Corynebacterium diphtheriae as well as by in vitro genetic methods using cyclic amplification of selected targets (CASTing). It is now clear that DtxR functions as a global iron-sensitive regulatory element in the control of gene expression in C. diphtheriae. In addition, the metal ion-activation domain of DtxR is being characterized by both mutational analysis and determination of the X-ray structure at 3.0 A resolution.

Bacterial Proteins↗

[Auto-analysis of corneal endothelium with photoelectrical scans and computer].

A quantitative analysis of corneal endothelial cells was made with photoelectrical scans and computer in 67 eyes. No difference was found as regards to the mean cell area and density between the endothelial analysis system and routine square counting. On the other hand, we analyzed corneal endothelial cells between 30 eyes wearing hard contact lens and 30 eyes of age- and sex-matched nonwearing control. The parameters, including cell density individual cell area, area, mean cell area, standard deviation, coefficient of variation of cell size (CV), maximum cell, minimum cell, the ratio of the maximum to minimum cell, and percentage of the hexagoal cells, were automatically displayed. The cell density and mean cell area also showed no significant difference (P > 0.05) between the wearers and nonwearing control, but the CV and the frequency of the hexagonal cells showed significant difference (P < 0.01). The ratio of maximum to minimum cell, the polymegethism and pleomorphism were obviously increased in the wearers. It is highly suggested that computer analysis system is of great value in evaluating corneal endothelial cells.

Adolescent↗

Cysteine-102 is positioned in the metal binding activation site of the Corynebacterium diphtheriae regulatory element DtxR.

DNA sequence analysis of dtxR has shown that the M(r) 25,316 regulatory protein contains a single cysteine residue at position 102. DtxR readily forms inactive disulfide-linked dimers. We have used saturation site-directed mutagenesis of the cysteine codon (TGC) at position 102 in order to determine the role of this residue in metal ion binding. We show that the insertion of amino acids other than cysteine or aspartic acid into this position abolishes DtxR function both in vitro and in recombinant Escherichia coli DH5 alpha:lambda RS45toxPO/lacZ. Only those mutant alleles in which the TGC codon for Cys-102 was replaced by either TGT (Cys) or GCA (Asp) were found to direct the expression of active forms of DtxR that regulate the expression of beta-galactosidase from the toxPO/lacZ transcriptional fusion.

2,2'-Dipyridyl↗

Recent changes in the management and outcome of acute closure after percutaneous transluminal coronary angioplasty.

The major cause of morbidity and mortality associated with percutaneous transluminal coronary angioplasty (PTCA) is acute closure. This study compared the clinical outcome of 2 groups of patients who experienced acute closure during PTCA. One group was treated during a period when intracoronary stents, laser balloons and perfusion balloons were available for treatment of acute closure (group II). These results were compared with the clinical outcome a group of similar patients who were treated for acute closure during a period that immediately preceded the availability of these devices (group I). One hundred sixty-six patients had acute closure in group I, whereas 156 patients experienced acute closure in group II. Baseline clinical characteristics were similar for both groups. There was no difference in ejection fraction, number of vessels diseased, degree of stenosis or number of vessels attempted between the 2 groups. Patients in group II had more balloon inflations and longer balloon inflation times when compared with patients in group I. Of the 156 patients in group II, 47% were treated with either an intracoronary stent, laser balloon or perfusion balloon. Group II patients had fewer Q-wave myocardial infarctions (9.1 vs 20.3%, p = 0.005). In addition, peak creatine phosphokinase levels (826 +/- 1,515 vs 517 +/- 1,050, p < 0.01) and mean residual stenosis (40.7 +/- 33.2 vs 58.0 +/- 34.4%, p < 0.0001) were also lower in group II patients. There was also less coronary artery bypass grafting during the same admission (38.6 vs 29.5%, p = 0.02) in group II patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

T cell-mediated cognate signaling of nitric oxide production by macrophages. Requirements for macrophage activation by plasma membranes isolated from T cells.

Macrophage generation of reactive nitrogen intermediates (RNI) represents a major effector mechanism in anti-microbial immunity and non-septic inflammatory reactions. The induction of macrophage RNI production has been demonstrated to require at least two signals which in microbial infections can be provided by interferon (IFN)-gamma and lipopolysaccharide (LPS). The current study demonstrates that, in the absence of LPS, T lymphocytes can provide cognate signal(s) which synergize with IFN-gamma in stimulating macrophage RNI production, as evidenced by the ability of plasma membranes from T cell clones to activate IFN-gamma-primed macrophages. Although viable resting T cells can activate IFN-gamma-primed macrophages by an interaction that is antigen specific, plasma membranes from resting T cells do not active macrophages. Plasma membranes from T cells activated by immobilized anti-CD3 were able to effectively induce RNI production in IFN-gamma-primed macrophages. However, in contrast to the antigen-specific interaction of macrophages with viable resting T cells, the activation of IFN-gamma-primed macrophages by membranes from activated T cells does not display antigen specificity. Plasma membranes from activated T helper TH2 and from activated TH1 cells were equally effective in activating IFN-gamma-primed macrophages, suggesting that the dominance of TH1 over TH2 cells in cell-mediated responses involving macrophage effectors is not a reflection of differences in their ability to interact with macrophages but rather is a reflection of their different pattern of cytokine production. These results suggest that the T cell-macrophage interaction involves reciprocal activation of both cells--an antigen-specific activation of the T cells which results in the acquisition of T cell membrane components involved in antigen-nonspecific stimulation of the macrophages.

Animals↗

Priority among air pollution factors for preventing chronic obstructive pulmonary disease in Shanghai.

The problems that city environmental protection planners face are how important the air pollution exposures are in relation to chronic obstructive pulmonary disease (COPD) in local residents and which factor should be controlled most urgently. The purpose of our study is to determine the control priority among ambient sulphur dioxide (SO2) inhalable particulates (IP) and indoor use of coal to prevent COPD in residents of the city. Ambient air pollution is mainly from SO2 and IP(< 10 nm). Indoor air pollution is mainly from the use of coal for heating and/or cooking. Distribution of ambient SO2, and IP concentrations were described using a quartic trend surface simulation. When stratified by two extreme levels of ambient SO2 and IP and types of fuel used indoors, eight local area populations in four communities with different combinations of exposure levels were selected. In each community a local area population mostly using coal and one mostly burning gas was chosen. Chronic obstructive pulmonary diseases (COPD, ICD 490-493) including chronic bronchitis, asthma and emphysema, are a major cause of death in residents of Shanghai. The relationship between the three air pollution factors and their health effects were analyzed at the level of mortality (1978-1987, 232,459 person-years), prevalence of symptoms (12,037 persons) of COPD, lung function and non-specific immunologic function (514 women). The results show that indoor use of coal has stronger associations with health than estimated exposure to ambient SO2 or IP.

Adult↗

Binding of the metalloregulatory protein DtxR to the diphtheria tox operator requires a divalent heavy metal ion and protects the palindromic sequence from DNase I digestion.

Transcription of the corynebacteriophage diphtheria tox operon has been shown to be regulated through a corynebacterial determined factor DtxR. The dtxR gene has been recently cloned and expressed in Escherichia coli, and shown to regulate the expression of beta-galactosidase expression from a diphtheria tox promoter/operator-lacZ transcriptional fusion. Tao et al. (Tao, X., Boyd, J., and Murphy, J. R. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 5897-5901) have recently shown by gel mobility shift assay that the binding of DtxR to the tox operator requires a divalent heavy metal ion, as well as the 27-base pair interrupted palindromic sequence. We now show the activation of DtxR in the presence of Co2+, Fe2+, or Mn2+ results in the protection of a 33- and 27-nucleotide region on the coding and non-coding strand from DNase I digestion, respectively. DtxR is also activated in the presence of Ni2+; however, this metalloregulatory factor is only weakly activated by Zn2+. The diphtheria tox regulatory region protected from DNase I digestion in the presence of activated DtxR encompasses the 27-base pair interrupted palindromic sequence.

Bacterial Proteins↗

Specific binding of the diphtheria tox regulatory element DtxR to the tox operator requires divalent heavy metal ions and a 9-base-pair interrupted palindromic sequence.

The structural gene for diphtheria toxin, tox, is carried by a family of closely related corynebacteriophages; however, the regulation of tox expression is controlled by a Corynebacterium diphtheriae-encoded regulatory element, dtxR. The molecular cloning and sequence analysis of dtxR was recently described. Previous studies have suggested that DtxR-mediated regulation of the diphtheria tox operator involves the formation of an iron-repressor complex, which specifically binds to the tox operator. We have expressed and purified DtxR from recombinant Escherichia coli. Immunoblot analysis shows DtxR to be a single M(r) 28,000 protein band in both recombinant E. coli and the C7(-) and C7hm723(-) strains of C. diphtheriae. In addition, we demonstrate that the binding of DtxR to a diphtheria tox promoter/operator probe requires the addition of Mn2+ to the reaction mixture; however, binding may be blocked by addition of the chelator 2,2'-dipyridyl, anti-DtxR antiserum, and excess unlabeled probe to the reaction mixture. Deletion of one of the 9-base-pair inverted repeat sequences from the tox operator results in a loss of DtxR binding. The results presented here demonstrate that regulation of diphtheria toxin expression by DtxR requires direct interaction between this regulatory factor and the tox operator in the presence of a divalent heavy metal ion.

Bacterial Proteins↗

Late follow-up after repair of left ventricular aneurysm and (usually) associated coronary bypass grafting.

This study assesses clinical and operative data (LV) aneurysm was repaired to determine factors that might predict in-hospital and long-term outcome. Long-term follow-up study was obtained in 296 of 298 patients undergoing LV aneurysm repair with or without coronary artery bypass grafting between 1974 and 1986. No patient had sustained a myocardial infarction within 2 weeks of surgery or was undergoing other concurrent cardiac surgery. The average age of the study patients was 57 +/- 9 years and the average ejection fraction was 35 +/- 13%. Ninety percent of the patients underwent concurrent bypass grafting, with an average of 2.2 +/- 1.3 grafts placed. Fourteen (5%) patients died in the hospital, with most deaths attributable to LV dysfunction. Advanced age and less extensive revascularization were correlates of in-hospital mortality. The 10-year survival was 57%, myocardial infarction-free survival 43%, and freedom from death, myocardial infarction and reoperative coronary surgery 41%. Advanced age, systemic hypertension, significant left main coronary artery narrowing and emergent operative status were multivariate correlates of long-term mortality. A low-risk population was defined by the absence of these risk factors, and high-risk by the presence of greater than or equal to 1 risk factors. The 10-year survival was 71% in the low-risk and 41% in the high-risk groups (p = .0006). The 10-year myocardial infarction free survival was 55% in the low-risk and 31% in the high-risk groups (p = 0.0017). LV aneurysm repair may be performed with acceptable in-hospital mortality, and the long-term risk may be stratified.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Diphtheria toxin-related alpha-melanocyte-stimulating hormone fusion toxin. Internal in-frame deletion from Thr387 to His485 results in the formation of a highly potent fusion toxin which is resistant to proteolytic degradation.

We have previously reported the genetic construction and properties of a fusion protein which was composed of the enzymatically active and membrane translocation domains of the diphtheria toxin and the receptor-specific ligand alpha-melanocyte-stimulating hormone (alpha-MSH) (Murphy, J.R., Bishai, W., Borowski, M., Miyanohara, A., Boyd, J., and Nagle, S. (1986) Proc. Natl. Acad. Sci. U.S.A. 83, 8258-8262). While this fusion toxin was found to be selectively toxic for MSH receptor-bearing cells in vitro, it was subject to profound proteolytic degradation in recombinant Escherichia coli making purification difficult. We now report that the deletion of diphtheria toxin fragment B sequences between Thr387 and His485 results in a protease-resistant form of the fusion toxin, DAB389-alpha-MSH. We show that DAB389-alpha-MSH is expressed in high yield in recombinant Escherichia coli, that it is readily purified from crude bacterial lysates by immunoaffinity and high performance liquid chromatography, and its cytotoxic activity toward both human and murine malignant melanoma cell lines is mediated through the MSH receptor.

Animals↗

Effect of an extract of the Chinese herbal remedy Tripterygium wilfordii Hook F on human immune responsiveness.

Tripterygium wilfordii Hook F (TWH) is a vine-like plant that grows in a wide area of south China. An alcohol extract of this plant known as T2 has been suggested to be effective in the treatment of rheumatoid arthritis (RA). To examine the mechanism by which this herbal remedy might be effective in RA, the capacity of T2 to alter human immune responsiveness in vitro was investigated. Human peripheral blood mononuclear cells were obtained from normal adults and separated into purified populations of monocytes, T cells, and B cells. T2 at 0.1-1 micrograms/ml inhibited antigen- and mitogen-stimulated proliferation of T cells and B cells, interleukin-2 (IL-2) production by T cells, and immunoglobulin production by B cells. T2 did not affect IL-2 receptor expression by T cells, IL-1 production by monocytes, or the capacity of monocytes to present antigen. Inhibition could not be accounted for by nonspecific toxicity. These results support the conclusion that T2 exerts a powerful suppressive effect on human immune responses. This action might account for its therapeutic effectiveness in RA.

B-Lymphocytes↗

Induction of tumor necrosis factor by macrophage colony-stimulating factor in vivo.

The effect of human urinary colony-stimulating factor (CSF-1) on the production of tumor necrosis factor (TNF) in vivo was assessed. Purified CSF-1 was administered i.v. to rabbits 4 days prior to injection with lipopolysaccharide (LPS). TNF in the serum prepared from rabbits bled 90 min after LPS injection was measured using cytotoxicity assays employing mouse L929 cells and antirabbit TNF monoclonal antibody. The results indicated that CSF-1 was able to induce the production of TNF in vivo and had a synergistic effect with Propionibacterium acnes.

Animals↗