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Biomedical subjects

X D Zhang

Publications and source records attributed to X D Zhang.

At least 19 recordsLinked to original sources
PubMed2004

Characterization of titanium surfaces with calcium and phosphate and osteoblast adhesion.

The titanium surfaces containing calcium, phosphate ions and the carbonate apatite were characterized. The effect of surface chemistry on the initial rabbit osteoblast response on these surfaces was investigated. The cell count and alkaline phosphatase (ALP) specific activity assay were used for biochemical analyses. Scanning electron microscopy was used for morphology observation and in particular X-ray photoelectron spectroscopy (XPS) for surface chemistry characterization. The number of cells adhering to the apatite coating surface was the maximum, the number of cells on the surface containing calcium without phosphate ions was higher than that containing phosphate without calcium, and the number on the unmodified titanium surface was the least. The osteoblasts cultured on the apatite surface exhibited the highest ALP specific activity, next were the ones on the surface containing solely calcium, the lowest were on the unmodified titanium surface. On the substrate surfaces removed of adhered cells, the order of nitrogen amounts detected by XPS was consistent with ones of ALP specific activity and cell number, except for the unmodified titanium surface. For the substrate surfaces removed of adhered osteoblasts, XPS analysis showed that calcium and phosphorous amounts decreased during cell adhesion. After cell culture the Ca2p binding energy (BE) values for apatite coating and the surface containing solely calcium were similar to those of the two surfaces adsorbed bovine serum albumin (BSA). The P2p BE values for the surfaces containing phosphate ions, including the apatite coating and the surface containing solely phosphate ions, showed the same change. But after cell culture the decrease of the P2p BE value for the coating surface was larger than the one for the surface containing solely phosphate ions. Considering the bovine serum albumin adsorption on the same samples, these results indicated that calcium ions on titanium surfaces play a more important role than phosphate ions in initial interactions among culture medium, osteoblasts and titanium surfaces. On the apatite coating surface, calcium ions are active sites for osteoblast adhesion, while calcium and phosphate ions co-exist on titanium surfaces, the former promotes the osteoblast adhesion onto the phosphate sites on titanium surfaces. The cell adhesion was a complicated biological and chemical process relating to surface several elements similar to protein adsorption.

Animals↗
PubMed2004

Evaluation of the expression of collagen type I in porous calcium phosphate ceramics implanted in an extra-osseous site.

The aim of the present study is to demonstrate the newly formed tissue in calcium phosphate (Ca/P) ceramics after extra-osseous implantation by histological and immunohistochemistry (IHC) methods. Synthesis porous Ca/P ceramics without adding any growth factor and living cell were implanted in the dorsal muscle of dogs for 1 and 2 months. Undecalcified and decalcified sections were stained by hematoxylin and eosin (H&E), and IHC, respectively. The histological results showed the beginning of osteogenesis and angiogenesis after being implanted for 1 month and the obvious new bone formation after being implanted for 2 months. IHC were conducted via the avidin-biotin peroxidase complex (ABC) method and the primary antibody was collagen type I. IHC results indicated that collagen type I was expressed within osteoblast-like cells and newly formed bone-like tissue in Ca/P ceramics after 1 month, and in the mineralized matrix of newly formed bone and osteoblasts, some osteocytes and some lacunae after 2 months. No cartilage and chondrocytes were observed in the histological and IHC-stained sections. Evidence of intramembranous osteogenesis was confirmed.

Animals↗
PubMed2003

Effect of spinal cord injury on urinary bladder spinal neural pathway: a retrograde transneuronal tracing study with pseudorabies virus.

OBJECTIVES: To determinate the effect of acute and chronic spinal cord injury (SCI) resulting from thoracic cord transection on the urinary bladder spinal neural pathway. METHODS: Seventy-six adult Sprague-Dawley rats were randomly divided into four groups, non-SCI (normal rats undergoing no surgical procedure except pseudorabies virus [PRV] injection), SCI(b) (SCI and PRV injected immediately after SCI), SCI(c) (SCI and PRV injected at 3 weeks after SCI), and SCI(d) (SCI and PRV injected at 3 months after SCI). Transcardiac perfusion fixation was done at appropriate survival periods after PRV injection into the bladder wall tissue. Sections of the dorsal root ganglion, spinal cord, and brain were processed for visualization of the virus by the streptavidin-peroxidase immunohistochemical procedure. RESULTS: The bladder weight of the non-SCI, SCI(b), SCI(c), SCI(d) rats was 144 +/- 9 mg, 142 +/- 8 mg, 486 +/- 51 mg, and 656 +/- 69 mg, respectively. The time-ordered flow charts of PRV tracing were similar in the non-SCI and SCI rats. The cross-sectional area of the labeled dorsal root ganglion cell profiles increased significantly after SCI (P <0.001): 593 +/- 40 microm2, 588 +/- 39 microm2, 815 +/- 53 microm2, and 902 +/- 57 microm2 in the non-SCI, SCI(b), SCI(c), SCI(d) rats, respectively. The number of labeled cells in the dorsal horn in the L6 and S1 segments 3 days after PRV injection markedly increased in chronic SCI rats, as did the number of labeled motor neurons 4 days after injection. CONCLUSIONS: Acute and chronic SCI have no effect on the process of virus transneuronal transport below the level of the lesion. Subsequent to chronic SCI, reorganization of the micturition reflex pathways may occur.

Acute Disease↗
PubMed2003

Characterization of surface oxide films on titanium and adhesion of osteoblast.

The relationship between surface characteristics of titanium and initial interactions of titanium-osteoblasts was investigated. Titanium plates were heat-treated in different oxidation atmospheres. The third passage rabbit osteoblasts were cultured on the titanium plates for 24h. After the heat-treatment, the crystal structure of the surface oxide films on titanium was identified using X-ray diffractometer and X-ray photoelectron spectroscopy (XPS). The surface roughness of titanium was measured with a profilometer. The surface energy was obtained by measurement of contact angles and calculation with Owens-Wendt-Kaeble's equation. The amount of surface hydroxyl (OH)(s) groups was examined using XPS. The change of binding energy of the some elements on the substrate surface suggested that the interactions between the cells and the titanium involved chemical reactions. The greater surface roughness, higher surface energy and more surface hydroxyl groups resulted in greater numbers of adhered osteoblasts and higher cell activity. Compared to the acidic hydroxyl (OH)(a) groups in (OH)(s) groups and the dispersion component of the total surface energy, the basic hydroxyl (OH)(b) groups and the polar component play more important roles in the osteoblast-titanium interaction.

Alkaline Phosphatase↗
PubMed2002

Effect of water vapor treatment on apatite formation on precalcified titanium and bond strength of coatings to substrates.

In previous investigations, a simple method, precalcification, was developed for bioactivating titanium. After a titanium sample was precalcified in a boiling saturated Ca(OH)(2) solution and then immersed in a calcium phosphate supersaturated solution, an apatite coating rapidly precipitated onto its surface. In the present study, heat-treatment in water vapor was carried out prior to precalcification. Heat-treatment in water vapor stimulated the chemical reaction between titanium, calcium, and phosphate. Coating properties were improved, and the bond strength of the coating to substrate was enhanced.

Apatites↗
PubMed2002

Carbonate apatite coating on titanium induced rapidly by precalcification.

Chemical treatments have been thought to be promised methods for improving bioactivity of titanium. In this work, the effect of precalcification with boiling saturated Ca(OH)2 solution on bioactivation of titanium was investigated. After precalcification and soaking in supersaturated Ca-P solution (SCP), calcium phosphate rapidly precipitated onto the surfaces of titanium, and after only three days an uniform apatite layer was found up to thickness of a few micrometers. The observation using scanning electron microscopy (SEM) showed that the coating was composed of a number of small crystal grains. The investigation by X-ray energy dispersion spectroscopy (EDS), Fourier transform infrared spectroscopy (FTIR) and X-ray diffraction (XRD) indicated that the coating was Ca-deficient carbonate apatite. Based on the analyses for the surfaces and SCP, a mechanism of precipitation of apatite was proposed in thermal dynamics and kinetics.

Apatites↗
PubMed2002

Characterization of surface oxide films on titanium and bioactivity.

Biological properties of titanium implant depend on its surface oxide film. In the present study, the surface oxide films on titanium were characterized and the relationship between the characterization and bioactivity of titanium was studied. The surface oxide films on titanium were obtained by heat-treatment in different oxidation atmospheres, such as air, oxygen and water vapor. The bioactivity of heat-treated titanium plates was investigated by immersion test in a supersaturated calcium phosphate solution. The surface roughness, energy morphology, chemical composition and crystal structure were used to characterize the titanium surfaces. The characterization was performed using profilometer, scanning electronic microscopy, ssesile drop method, X-ray photoelectron spectroscopy, common Bragg X-ray diffraction and sample tilting X-ray diffraction. Percentage of surface hydroxyl groups was determined by X-ray photoelectron spectroscopy analysis for titanium plates and density of surface hydroxyl groups was measured by chemical method for titanium powders. The results indicated that heat-treatment uniformly roughened the titanium surface and increased surface energy. After heat-treatment the surface titanium oxide was predominantly rutile TiO(2), and crystal planes in the rutile films preferentially orientated in (1 1 0) plane with the highest density of titanium ions. Heat-treatment increased the amount of surface hydroxyl groups on titanium. The different oxidation atmospheres resulted in different percentages of oxygen species in TiO(2), in physisorbed water and acidic hydroxyl groups, and in basic hydroxyl groups on the titanium surfaces. The immersion test in the supersaturated calcium phosphate solution showed that apatite spontaneously formed on to the rutile films. This revealed that rutile could be bioactivated. The analyses for the apatite coatings confirmed that the surface characterization of titanium has strong effect on bioactivity of titanium. The bioactivity of the rutile films on titanium was related not only to their surface basic hydroxyl groups, but also to acidic hydroxyl groups, and surface energy. Heat-treatment endowed titanium with bioactivity by increasing the amount of surface hydroxyl groups on titanium and its surface energy.

Journal Article↗
PubMed2002

Dose-response and time course of specific IgE and IgG after single and repeated topical skin exposure to dry trimellitic anhydride powder in a Brown Norway rat model.

BACKGROUND: Trimellitic anhydride (TMA)-induced occupational asthma is thought to be associated with its ability to acylate proteins and to induce production of TMA-specific immunoglobulin (Ig)E. Though the respiratory tract is considered to be a major exposure route leading to airway sensitization, the potential role of dermal exposure producing asthmatic sensitization is not known. The present study examines the ability of dry TMA powder to sensitize Brown Norway rats when applied, topically, to the skin. METHODS: A patch of hair was carefully clipped with scissors on the rat's back. Dry TMA powder (0.3, 1.25, 5 and 20 mg) was administered on days 0, 7, 14 and 21, and the area occluded with surgical tape overnight after each application. Residual powder recovered from the occluded skin was analyzed by proton nuclear magnetic resonance and was still predominantly TMA. Circulating anti-TMA IgE and IgG were measured by ELISA. RESULTS: TMA elicited dose-dependent production of specific IgE and IgG. Specific antibodies were detectable 2 weeks after the first TMA exposure and peaked between 3 and 4 weeks. CONCLUSION: The data suggest that topical skin exposure to dry TMA powder can induce allergic/immunological sensitization as demonstrated by the production of specific antibodies.

Administration, Topical↗
PubMed2001

Tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis of human melanoma is regulated by smac/DIABLO release from mitochondria.

In previous studies we have shown that the sensitivity of melanoma cell lines to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis was determined largely by the level of expression of death receptor TRAIL receptor 2 on the cells. However, approximately one-third of melanoma cell lines were resistant to TRAIL, despite expression of high levels of TRAIL receptor 2. The present studies show that these cell lines had similar levels of TRAIL-induced activated caspase-3 as the TRAIL-sensitive lines, but the activated caspase-3 did not degrade substrates downstream of caspase-3 [inhibitor of caspase-activated DNase and poly(ADP-ribose) polymerase]. This appeared to be due to inhibition of caspase-3 by X-linked inhibitor of apoptosis (XIAP) because XIAP was bound to activated caspase-3, and transfection of XIAP into TRAIL-sensitive cell lines resulted in similar inhibition of TRAIL-induced apoptosis. Conversely, reduction of XIAP levels by overexpression of Smac/DIABLO in the TRAIL-resistant melanoma cells was associated with the appearance of catalytic activity by caspase-3 and increased TRAIL-induced apoptosis. TRAIL was shown to cause release of Smac/DIABLO from mitochondria, but this release was greater in TRAIL-sensitive cell lines than in TRAIL-resistant cell lines and was associated with down-regulation of XIAP levels. Furthermore, inhibition of Smac/DIABLO release by overexpression of Bcl-2 inhibited down-regulation of XIAP levels. These results suggest that Smac/DIABLO release from mitochondria and its binding to XIAP are an alternative pathway by which TRAIL induces apoptosis of melanoma, and this pathway is dependent on the release of activated caspase-3 from inhibition by XIAP and possibly other inhibitor of apoptosis family members.

Apoptosis↗
PubMed2001

The role of NF-kappa B in TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis of melanoma cells.

Previous studies have shown that activation of NF-kappaB can inhibit apoptosis induced by a number of stimuli. It is also known that TNF-related apoptosis-inducing ligand (TRAIL) can activate NF-kappaB through the death receptors TRAIL-R1 and TRAIL-R2, and decoy receptor TRAIL-R4. In view of these findings, we have investigated the extent to which activation of NF-kappaB may account for the variable responses of melanoma lines to apoptosis induced by TRAIL and other TNF family members. Pretreatment of the melanoma lines with the proteasome inhibitor N-acetyl-L-leucinyl-L-leucinyl-L-norleucinal (LLnL), which is known to inhibit activation of NF-kappaB, was shown to markedly increase apoptosis in 10 of 12 melanoma lines with death receptors for TRAIL. The specificity of results for inhibition of NF-kappaB activation was supported by an increase of TRAIL-induced apoptosis in melanoma cells transfected with a degradation-resistant IkappaBalpha. Furthermore, studies with NF-kappaB reporter constructs revealed that the resistance of melanoma lines to TRAIL-induced apoptosis was correlated to activation of NF-kappaB in response to TRAIL. TRAIL-resistant sublines that were generated by intermittent exposure to TRAIL were shown to have high levels of activated NF-kappaB, and resistance to TRAIL could be reversed by LLnL and by the superrepressor form of IkappaBalpha. Therefore, these results suggest that activation of NF-kappaB by TRAIL plays an important role in resistance of melanoma cells to TRAIL-induced apoptosis and further suggest that inhibitors of NF-kappaB may be useful adjuncts in clinical use of TRAIL against melanoma.

Apoptosis↗
PubMed2001

How melanoma cells evade trail-induced apoptosis.

At the doses used clinically, chemotherapy is believed to kill melanoma by a final common 'mitochondrial' pathway that leads to apoptosis. Similarly, several natural defence mechanisms kill melanoma by the same pathways. A corollary to the latter is that survival of melanoma in the host is due to the development of anti-apoptotic mechanisms in melanoma cells. What are these mechanisms? And how might we bypass them to improve the treatment of melanoma?

Animals↗
PubMed2001

[Studies of FISH and karyotype of Gossypium barbadense].

Based on the fluorescent in situ hybridization (FISH) of somatic chromosome of Gossypium barbadense with the probe of genomic DNA (gDNA) of Gossypium arboreum, two sets of chromosomes were easily distinguished by signals hybridized or not. The FISH directly proved that G. barbadense originated from two different diploid species, but was not in concordance with the former point that every chromosome of A sub-genome of tetraploid species was bigger than that of other sub-genome (D genome). The karyotype formula of G. barbadense based on its FISH was 2n = 4x = 52 = 38 m + 14sm(6sat). There were three pairs of satellite chromosomes which were all sm types. Their satellites located in short arms but originated differently from their chromosomes of sub-genome. Fragment translocations occured in the long arms of homologous chromosomes of number 5, 6 and 9 of A sub-genome. It was suggested that the translated fragments come from D sub-genome. The fragments are fairly large with the relative lengths of 19.21%, 17.69% and 12.88% of their whole chromosomes, respectively. At least five pairs of chromosomes in D sub-genome show some hybridized signals of gDNA probe of G. arboreum in their centromere regions, which indicated that there would be chromatin introgressions from A sub-genome.

Gossypium↗
PubMed2001

Relative resistance of fresh isolates of melanoma to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.

In previous studies, we have shown that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) could induce varying degrees of apoptosis in approximately two-thirds of human melanoma lines. In the present study, we have examined the sensitivity of fresh isolates and early passages of melanoma cells to TRAIL-induced apoptosis from eight patients. We found that fresh isolates were relatively resistant to TRAIL-induced apoptosis and that this appeared to be associated with low TRAIL death receptor (TRAIL-R) expression. TRAIL-R expression was also undetectable in tissue sections from the same melanoma. We attempted to create a model for these findings by generation of TRAIL-resistant melanoma lines from TRAIL-sensitive lines grown for prolonged periods in TRAIL. The resulting TRAIL-resistant melanoma cell lines had low TRAIL-R expression, and sensitivity to TRAIL was increased rapidly by pretreatment with proteasome inhibitors known to inhibit activation of nuclear factor-kappaB. However, the latter treatment had no significant effect on the sensitivity of fresh isolates to TRAIL. The levels of the inhibitors of apoptosis, Flice-like inhibitory protein and Bcl-2, also did not relate to resistance to TRAIL-induced apoptosis. These results suggest that down-regulation of TRAIL-R on melanoma cells may be the primary determinant of resistance of fresh isolates to TRAIL, and the basis for this requires further investigation.

Antibodies, Monoclonal↗
PubMed2001

Effects of erysimin G on renal tubular function and 70-pS K+ channel activity of thick ascending limb.

AIM: To study the effect of erysimin G (CH35H52O13) on the thick ascending limb (TAL) 70-pS K+ channel of rat kidney and its effect on diuresis. METHODS: The patch-clamp cell-attached recording technique was used to record the single potassium channel current, and the urine volume (UV) was measured by urethral intubation to determine the diuretic effect. RESULTS: Erysimin G can increase the urine volume and decrease the 70-pS potassium channel activity of TAL. CONCLUSION: Erysimin G has a diuretic effect and its inhibition on the activity of apical 70-pS potassium channel may be the mechanism of its diuretic effect.

Animals↗
PubMed2000

TNF-related apoptosis-inducing ligand-induced apoptosis of melanoma is associated with changes in mitochondrial membrane potential and perinuclear clustering of mitochondria.

Past studies have shown that TNF-related apoptosis-inducing ligand (TRAIL) induced apoptosis in a high proportion of cultured melanoma by caspase-dependent mechanisms. In the present studies we have examined whether TRAIL-induced apoptosis of melanoma was mediated by direct activation of effector caspases or whether apoptosis was dependent on changes in mitochondrial membrane potential (MMP) and mitochondrial-dependent pathways of apoptosis. Changes in MMP were measured by fluorescent emission from rhodamine 123 in mitochondria. TRAIL, but not TNF-alpha or Fas ligand, was shown to induce marked changes in MMP in melanoma, which showed a high correlation with TRAIL-induced apoptosis. This was associated with activation of proapoptotic protein Bid and release of cytochrome c into the cytosol. Overexpression of B cell lymphoma gene 2 (Bcl-2) inhibited TRAIL-induced release of cytochrome c, changes in MMP, and apoptosis. The pan caspase inhibitor z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and the inhibitor of caspase-8 (z-Ile-Glu-Thr-Asp-fluoromethylketone; zIETD-fmk) blocked changes in MMP and apoptosis, suggesting that the changes in MMP were dependent on activation of caspase-8. Activation of caspase-9 also appeared necessary for TRAIL-induced apoptosis of melanoma. In addition, TRAIL, but not TNF-alpha or Fas ligand, was shown to induce clustering of mitochondria around the nucleus. This process was not essential for apoptosis but appeared to increase the rate of apoptosis. Taken together, these results suggest that TRAIL induces apoptosis of melanoma cells by recruitment of mitochondrial pathways to apoptosis that are dependent on activation of caspase-8. Therefore, factors that regulate the mitochondrial pathway may be important determinants of TRAIL-induced apoptosis of melanoma.

Amino Acid Chloromethyl Ketones↗
PubMed2000

Mechanisms of resistance of normal cells to TRAIL induced apoptosis vary between different cell types.

Resistance of normal cells to tumour necrosis factor related apoptosis inducing ligand (TRAIL) induced apoptosis is believed to be mediated by expression of two decoy receptors. Here we show that the expression and localisation of TRAIL receptors (TRAIL-Rs) vary between different cells and that resistance to TRAIL is mediated by different mechanisms. The decoy receptor, TRAIL-R3, appeared important in protection of endothelial cells, whereas lack of surface death receptor expression and as yet unknown intracellular inhibitor(s) of apoptosis downstream of caspase-3 may play a major role in protection of melanocytes and fibroblasts from TRAIL induced apoptosis, respectively. Differential subcellular location of decoy receptors may be an important determinant of their effectiveness in different types of normal cells.

Apoptosis↗
PubMed2000

Differential localization and regulation of death and decoy receptors for TNF-related apoptosis-inducing ligand (TRAIL) in human melanoma cells.

Induction of apoptosis in cells by TNF-related apoptosis-inducing ligand (TRAIL), a member of the TNF family, is believed to be regulated by expression of two death-inducing and two inhibitory (decoy) receptors on the cell surface. In previous studies we found no correlation between expression of decoy receptors and susceptibility of human melanoma cells to TRAIL-induced apoptosis. In view of this, we studied the localization of the receptors in melanoma cells by confocal microscopy to better understand their function. We show that the death receptors TRAIL-R1 and R2 are located in the trans-Golgi network, whereas the inhibitory receptors TRAIL-R3 and -R4 are located in the nucleus. After exposure to TRAIL, TRAIL-R1 and -R2 are internalized into endosomes, whereas TRAIL-R3 and -R4 undergo relocation from the nucleus to the cytoplasm and cell membranes. This movement of decoy receptors was dependent on signals from TRAIL-R1 and -R2, as shown by blocking experiments with Abs to TRAIL-R1 and -R2. The location of TRAIL-R1, -R3, and -R4 in melanoma cells transfected with cDNA for these receptors was similar to that in nontransfected cells. Transfection of TRAIL-R3 and -R4 increased resistance of the melanoma lines to TRAIL-induced apoptosis even in melanoma lines that naturally expressed these receptors. These results indicate that abnormalities in "decoy" receptor location or function may contribute to sensitivity of melanoma to TRAIL-induced apoptosis and suggest that further studies are needed on the functional significance of their nuclear location and TRAIL-induced movement within cells.

Amino Acid Chloromethyl Ketones↗