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Biomedical subjects

N Zhang

Publications and source records attributed to N Zhang.

At least 145 records · Page 8Linked to original sources
PubMed1998

Corrosion resistance and ion dissolution of titanium with different surface microroughness.

In vitro corrosion resistance and ion dissolution of commercial pure titanium with different surface microroughness are studied adopting constant potential meter and atomic absorption spectroscopy. In terms of the surface roughness, titanium samples are divided into 5 groups: smooth surface, machining surface, 2 different microroughness surfaces and macrorough surface. Each group contains three category samples under different treatments: natural oxidation (24 h exposure to air), oxidation under 400 degrees C (400 degrees C, 45 min thermal oxidation), oxidation under 700 degrees C (700 degrees C, 45 min thermal oxidation). In Hanks corrosion media, comparative studies through constant potential anode polarization curves and titanium release rates of the 5 groups of Ti samples demonstrates that oxidation under 400 degrees C best increase corrosion resistance and decrease ion release sharply, oxidation under 700 degrees C is better than natural oxidation. Ti samples with a different surface roughness all have good corrosion resistance and their corrosion resistance drop with the raising of surface roughness. Comparing with macrorough surface and machining surface, microrough surfaces have better corrosion resistance and a lower ion release rate which are similar to those of smooth surfaces. Moreover, the corrosion resistance of machining surface Ti is the lowest. It is hypothesized that surface treatment methods such as surface thermal oxidation, surface aging and so on will improve the corrosion resistance and decrease the ion release rate of rough surface effectively by increasing the thickness of surface protection film, improving its structural uniformity and facilitating the formation of ordered, compact surface protection film.

Biocompatible Materials↗
PubMed1997

Dynamic distribution of chemoattractant receptors in living cells during chemotaxis and persistent stimulation.

While the localization of chemoattractant receptors on randomly oriented cells has been previously studied by immunohistochemistry, the instantaneous distribution of receptors on living cells undergoing directed migration has not been determined. To do this, we replaced cAR1, the primary cAMP receptor of Dictyostelium, with a cAR1-green fluorescence protein fusion construct. We found that this chimeric protein is functionally indistinguishable from wild-type cAR1. By time-lapse imaging of single cells, we observed that the receptors remained evenly distributed on the cell surface and all of its projections during chemotaxis involving turns and reversals of polarity directed by repositioning of a chemoattractant-filled micropipet. Thus, cell polarization cannot result from a gradient-induced asymmetric distribution of chemoattractant receptors. Some newly extended pseudopods at migration fronts showed a transient drop in fluorescence signals, suggesting that the flow of receptors into these zones may slightly lag behind the protrusion process. Challenge with a uniform increase in chemoattractant, sufficient to cause a dramatic decrease in the affinity of surface binding sites and cell desensitization, also did not significantly alter the distribution profile. Hence, the induced reduction in binding activity and cellular sensitivity cannot be due to receptor relocalization. The chimeric receptors were able to "cap" rapidly during treatment with Con A, suggesting that they are mobile in the plane of the cell membrane. This capping was not influenced by pretreatment with chemoattractant.

Animals↗
PubMed1997

Mouse TCOF1 is expressed widely, has motifs conserved in nucleolar phosphoproteins, and maps to chromosome 18.

Mutations in the human TCOF1 gene have been identified in patients with Treacher Collins Syndrome (Mandibulofacial Dysostosis), an autosomal dominant condition affecting the craniofacial region. We report the isolation of the entire mouse Tcof1 coding sequence (3960 bp) by performing a computer-based search for mouse cDNA clones homologous to TCOF1 and generating overlapping RT-PCR products from mouse RNA. Tcof1 is a 1320 amino acid protein of 135 kd with 61.4% identity to TCOF1 and displays repeating motifs enriched for serine- and acidic amino acid-rich regions with potential phosphorylation sites and putative nuclear localization signals. Tcof1 maps to the mouse chromosome 18 region syntenic with human chromosome 5q32-->q33 which contains the TCOF1 locus. Northern blot hybridization indicates Tcof1 expression is ubiquitous in adult tissues and in the embryonic stage, is elevated at 11 dpc when the branchial arches and facial swellings are present in mouse. Our results are consistent with TCOF1 mutations leading to the Treacher Collins syndrome phenotype.

Amino Acid Sequence↗
PubMed1997

Isolation of full-length ATM cDNA and correction of the ataxia-telangiectasia cellular phenotype.

A gene mutated in the human genetic disorder ataxia-telangiectasia (A-T), ATM, was recently identified by positional cloning. ATM is a member of the phosphatidylinositol-3-kinase superfamily, some of which are protein kinases and appear to have important roles in cell cycle control and radiation signal transduction. We describe herein, to our knowledge, for the first time, the cloning of a full-length cDNA for ATM and correction of multiple aspects of the radio-sensitive phenotype of A-T cells by transfection with this cDNA. Overexpression of ATM cDNA in A-T cells enhanced the survival of these cells in response to radiation exposure, decreased radiation-induced chromosome aberrations, reduced radio-resistant DNA synthesis, and partially corrected defective cell cycle checkpoints and induction of stress-activated protein kinase. This correction of the defects in A-T cells provides further evidence of the multiplicity of effector functions of the ATM protein and suggests possible approaches to gene therapy.

Ataxia Telangiectasia↗
PubMed1997

Human breast cancer growth inhibited in vivo by a dominant negative pleiotrophin mutant.

Pleiotrophin (PTN) is a recently described 18- kDa heparin binding growth/differentiation factor. It also is a proto-oncogene; cells transformed by the Ptn gene form highly angiogenic tumors when implanted into the nude mouse. PTN may be an important regulator of transformation in other tumors, because constitutively high levels of expression of the pleiotrophin (Ptn) gene are found in human breast cancer and other malignant cell lines, and its levels of expression are high in many human tumor specimens. To determine whether PTN is an important regulator of the malignant phenotype of human breast cancer cells, we constructed a mutant cDNA to encode a truncated PTN designed to heterodimerize with the product of the endogenous Ptn gene during processing. The mutant gene product blocked transformation of NIH 3T3 cells by the wild type (wt) Ptn gene product. The mutant Ptn cDNA was then introduced into human breast cancer MDA-MB-231 cells, and clonal lines that stably express the mutant Ptn cDNA were selected. The truncated PTN was shown to form heterodimers with the endogenous Ptn gene product in these cells. Furthermore, the MDA-MB-231 cells that express the mutant Ptn gene were no longer transformed; they failed to form plaques or colonies in soft agar and were unable to form tumors in the athymic nude mouse. The results establish an important role of PTN in the dysregulated growth of human breast cancer cells and suggest that constitutive expression of PTN may be essential to the malignant phenotype of human breast cancers in vivo.

3T3 Cells↗
PubMed1997

Interaction between ATM protein and c-Abl in response to DNA damage.

The gene mutated in the autosomal recessive disorder ataxia telangiectasia (AT), designated ATM (for 'AT mutated'), is a member of a family of phosphatidylinositol-3-kinase-like enzymes that are involved in cell-cycle control, meiotic recombination, telomere length monitoring and DNA-damage response. Previous results have demonstrated that AT cells are hypersensitive to ionizing radiation and are defective at the G1/S checkpoint after radiation damage. Because cells lacking the protein tyrosine kinase c-Abl are also defective in radiation-induced G1 arrest, we investigated the possibility that ATM might interact with c-Abl in response to radiation damage. Here we show that ATM binds c-Abl constitutively in control cells but not in AT cells. Our results demonstrate that the SH3 domain of c-Abl interacts with a DPAPNPPHFP motif (residues 1,373-1,382) of ATM. The results also reveal that radiation-induction of c-Abl tyrosine kinase activity is diminished in AT cells. These findings indicate that ATM is involved in the activation of c-Abl by DNA damage and this interaction may in part mediate radiation-induced G1 arrest.

Ataxia Telangiectasia↗
PubMed1997

Cellular localisation of the ataxia-telangiectasia (ATM) gene product and discrimination between mutated and normal forms.

The recently cloned gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) is involved in DNA damage response at different cell cycle checkpoints and also appears to have a wider role in signal transduction. Antibodies prepared against peptides from the predicted protein sequence detected a approximately 350 kDa protein corresponding to the open reading frame, which was absent in 13/23 A-T homozygotes. Subcellular fractionation, immunoelectronmicroscopy and immunofluorescence showed that the ATM protein is present in the nucleus and cytoplasmic vesicles. This distribution did not change after irradiation. We also provide evidence that ATM protein binds to p53 and this association is defective in A-T cells compatible with the defective p53 response in these cells. These results provide further support for a role for the ATM protein as a sensor of DNA damage and in a more general role in cell signalling, compatible with the broader phenotype of the syndrome.

Antibodies↗
PubMed1997

Specific cleavage of the large subunit of replication factor C in apoptosis is mediated by CPP32-like protease.

Recent evidence suggests that the growing family of cysteine proteases related to the interleukin-1beta-converting enzyme (ICE) is of central importance in mediating apoptosis. Proteolytic cleavage of a small group of cellular substrates by these enzymes in association with the onset of apoptosis has been reported. In the present study, we searched a protein data base for potential death substrates possessing the CPP32 cleavage site, DEVD, and identified several candidates including RFC140, the large subunit of replication factor C, which we subsequently demonstrated to be specifically cleaved in a variety of cell types undergoing apoptosis in response to different cytotoxic agents, whereas no degradation is observed in a cell line resistant to etoposide-induced apoptosis. The abrogation of RFC140 cleavage in apoptotic extracts by Ac-DEVD-CHO, a potent inhibitor of CPP32, together with the finding that a CPP32 consensus cleavage sequence, DEVD, exists in RFC140, suggests that CPP32 or a close relative is responsible for RFC140 degradation in apoptosis.

Animals↗
PubMed1997

Circular dichroic spectroscopy of N-acetylglucosaminyltransferase V and its substrate interactions.

beta-1,6-N-Acetylglucosaminyltransferase V (EC 2.4.1.155) catalyzes the transfer of N-acetylglucosamine (GlcNAc) from UDP-GlcNAc in beta(1,6)-linkage to the alpha(1,6)-linked mannose of N-linked oligosaccharides. Circular dichroism (CD) was used to investigate the secondary structure of a recombinant, soluble form of the enzyme and its interaction with UDP-GlcNAc and an inhibitory substrate analog. The CD spectrum of the apoenzyme indicated the presence of small amounts of beta-structure and substantial amounts (>50%) of alpha-helicity. The CD spectra of solutions containing UDP-GlcNAc and different ratios of UDP-GlcNAc:enzyme were measured. Interestingly, the spectrum of each mixture could not be accounted for by simple additivity of the two individual spectra, indicating a change in environment of the chromophores and/or a conformational change of the substrate or protein concomitant with binding. Similar results were obtained with mixtures of UDP and the enzyme. Analysis of the CD difference spectra at three wavelengths yielded an estimated average Kd of 4.4 mM for UDP-GlcNAc and 3.8 mM for UDP. By contrast, addition of the CD spectrum of an inhibitory substrate analog of its oligosaccharide acceptor substrate and the CD spectrum of the enzyme could account for that observed of an inhibitor-enzyme mixture; moreover, addition of the inhibitor to a mixture of UDP-GlcNAc and enzyme did not alter the Kd associated with UDP-GlcNAc binding to the enzyme. These results and kinetic studies reported herein suggest an ordered reaction in which UDP-GlcNAc binds first to the enzyme, followed by the sequential binding of the trisaccharide substrate.

Carbohydrate Sequence↗
PubMed1997

Transforming function of the HOX11/TCL3 homeobox gene.

The HOX11/TCL3 homeobox gene was identified at the breakpoint region in pediatric T-cell acute lymphoblastic leukemia harboring 10q24 chromosomal translocations. We previously reported that primary murine bone marrow cells transduced ex vivo with a recombinant HOX11-containing retrovirus, MSCV-HOX11, gave rise to cell lines at high frequency having characteristics of early myeloid cells. Cell lines were also established from the bone marrow and spleen of transplant recipients sacrificed 5 months after engraftment with MSCV-HOX11-transduced bone marrow cells. These latter lines, which exhibited a more differentiated myelomonocytic phenotype, harbored proviruses encoding a smaller HOX11 protein. None of the mice that received HOX11-expressing bone marrow cells or myeloid cell lines developed leukemia during 6-month observation periods. Here, we report that two bone marrow transplant recipients eventually developed T-cell acute lymphoblastic leukemia-like malignancies at 7 and 12 months posttransplant, indicating that progression to a fully malignant state required additional mutations. One tumor synthesized full-length HOX11 whereas the other expressed the smaller version of the protein. The smaller HOX11 protein suffered a carboxyl-terminal truncation. We subsequently constructed MSCV-based retroviral vectors expressing deleted forms of HOX11 and identified an amino-terminal region that was dispensible for generation of myeloid cell lines having a similar phenotype as those induced by full-length HOX11. We thus conclude that regions near the amino and carboxyl termini of HOX11 are not essential for transforming function, nor do they appear to determine the lineage or stage of differentiation of the target cell for transformation.

Animals↗
PubMed1997

The Drosophila protein Wunen repels migrating germ cells.

In Drosophila, germ cells migrate in embryonic development from the lumen of the developing gut towards the overlying mesoderm, where they enter the gonads. The gene wunen is responsible for guiding the germ cells early in this process. Here we report that the protein Wunen has two properties that allow it to use repulsion to guide the germ cells. Wunen can transform a permissive cellular environment into a repulsive one, and is expressed in the gut in a pattern that guides germ cells towards the mesoderm. Wunen shows strong similarity to the enzyme type 2 phosphatidic acid phophatase (PAP2)4, suggesting that it is involved in lipid metabolism.

Amino Acid Sequence↗
PubMed1997

The role of insulin-like growth factor II in the malignant transformation of rat liver oval cells.

Oval cells are small nonparenchymal epithelial cells that first appear in the periportal areas of the liver and thereafter invade the whole parenchyma when mice or rats are exposed to a variety of chemical carcinogens. In the present study we have analyzed the expression of insulin-like growth factor II (IGF II) in the recently established oval cell line OC/CDE 22 and its malignantly transformed counterpart (the M22 cells) and the biological consequences of the constitutive expression of IGF II in oval cells. OC/CDE 22 cells do not express the above-mentioned growth factor, whereas the M22 cells do and addition of a neutralizing anti-IGF II antibody to M22 cells resulted in an almost complete proliferation stop. The presence of type 1 as well as type 2 insulin-like growth factor receptors in OC/CDE 22 and M22 cells was revealed by Northern blotting; however, only neutralizing antibodies directed against the type 1 IGF receptor were able to inhibit the proliferation of the cultured oval cells. Finally, transfection of an IGF II complementary DNA (cDNA) into OC/CDE 22 cells resulted in the release of active IGF II into the extracellular medium but not in the concomitant malignant transformation of the cells. Taken together these results show that: 1) upon transformation oval cells start producing IGF II and 2) IGF II acts on oval cells as a pure mitogen (without being per se oncogenic) via an autocrine loop involving the activation of the type 1 IGF receptor.

Animals↗
PubMed1997

[Apoptosis and expression of its regulating genes in adenoma and adenocarcinoma of large intestine].

OBJECTIVE: To investigate the effects of apoptosis and its regulating genes in different stages of malignant transformation of large intestine epithelium in colorectal adenoma and adenocarcinoma. METHODS: The density and distribution of the apoptotic cells and the positive expression of p53 and bcl-2 oncoprotein were observed in situ in 32 villous adenomas and 33 papillary adenocarcinomas of the large intestine, using DNA nick end labelling technique and immunohistochemical staining for p53 and bcl-2 oncoprotein. 15 nontumor mucosa were used as controls. RESULTS: The density of apoptotic cells in adenoma and adenocarcinoma was significantly higher than that in nontumor mucosa (P < 0.01), and their density in adenoma was higher than in adenocarcinoma (P < 0.01). The positive rate and staining intensity of p53 and bcl-2 oncoprotein in adenoma and adenocarcinoma were significantly higher than in non tumor mucosa (P < 0.01), their staining intensity in adenocarcinoma was higher than that in adenoma (P < 0.01). In adenoma, the density of apoptotic cells in the bcl-2 oncoprotein positive group was higher than that in the bcl-2 oncoprotein negative group (P < 0.01). CONCLUSION: The abnormal regulation of apoptosis may play an important role in the pathogenesis of large intestine carcinoma. The bcl-2 oncoprotein can inhibit apoptosis in adenoma and adenocarcinoma. However, mutational p53 oncoprotein may likely block apoptosis in adenocarcinoma.

Adenocarcinoma, Papillary↗
PubMed1997

[The healing process of the temporalis myofascial flap in oral reconstruction].

From a prospective study of 36 patients having had temporalis myofascial flap (mean follow-up 32 months), the clinical oral healing process and the histological characteristics of the repaired mucosa were investigated. Among this group, 24 patients were assessed of the clinical scarring over the reconstructed area and 11 patients for histological evaluation of the repaired mucosa. Result showed that the uncovered temporalis myofascial flap in the mouth underwent a consistent healing commencing with an acute inflammatory phase, through chronic inflammatory and proliferative phases to eventual epithelialization by oral mucosa. No major complications affecting the healing flap were noted. The healed mucosa exhibited scarring in 70% of cases and the repaired mucosa demonstrated histological features distinct from the normal mucosa.

Adolescent↗
PubMed1997

[Biocompatibility evaluation of Ti50Ni50-xCux shape memory alloys (I)--corrosion resistance].

By means of electrochemical methods, the corrosion resistance of Ti50Ni50 and Ti50Ni50-xCux (x = 1,2, 4,6,8) was investigated. It is discovered that repassivation potential of Ti50Ni50-xCux (x = 2,4,6,8) alloys is about 200 mV higher than that of Ti50Ni50 alloy. This means that the added Cu raises the repassivation of TiNi shape memory alloys and improves corrosion resistance. Pitting potentials of Ti50Ni50 and Ti50Ni50-xCux (x = 1,2,4,6,8) alloys increase with the rising solution pH value, but the repassivation potentials keep constant. The added Cu has no obvious influence on pitting potential (Epit) of TiNi alloys, meanwhile, the corrosion potential and corrosion rate of Ti50Ni50-xCux (x = 1,2,4,6,8) alloys are irrelevant to its Cu content and the values are almost the same as that of TiNi alloys.

Alloys↗
PubMed1997

[The effect of deture relining on the electromyogram of masticatory muscles in complete denture wearers].

The aim of present study is to assess the effect of complete denture relining on the electromyogram of masticatory muscles. The electromyography and the computer-EMG system were used for collecting and processing bilateral masseter and anterior temporal muscles activities before and after denture relining. The results showed that the mean myoelectric potentials of the masticatory muscles was increased during chewing and maximal biting when the dentures were relined. The conclusion was that the level of the masticatory muscle activity was increased when a clinically acceptable occlusal vertical dimension was obtained by using relining method.

Adult↗
PubMed1997

[The inhibitory effect of Chinese herb Phyllanthus on hepatitis B virus in vitro].

Seven preparations of different species of Chinese herb Phyllarthus with different formulations and additives were studied for their ability to inhibit hepatitis B virus DNA replication, that is the HBsAg and HBeAg expression in a HBV DNA-transfected cell line (2.2.15 cell). The results showed that all the drugs were effectively against HBV replication in vitro. Capsule 1 and tuo cha zhen zhu cao were found to be the most potent anti-HBV extracts of those examined. Both extracts decreased HBaAg expression by nearly 100% at the concentration of 500 mg/L without toxicity on cell growth. Southern blot showed that Capsule 1 inhibited HBV DNA replication in a dose-dependent manner. We observed further, that under similar dosage the drug inhibition to HBsAg and HBeAg expression was lower than that to HBV DNA replication, suggesting that the production of progeny virus particles not only were inhibited at the level of HBV DNA synthesis, but also was affected probably at the level of translation of viral mRNA.

Cell Line↗