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Biomedical subjects

C Du

Publications and source records attributed to C Du.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Micro-anatomy of the apical lateral foramina of permanent teeth].

OBJECTIVE: To provide data of apical lateral foramina of Chinese people's permanent teeth. METHODS: The shape and diameter of the apical lateral foramina in 1,502 permanent teeth were observed under the XTL-2 stero-microscope. RESULTS: The shape and diameter of 230 apical lateral foramina in the permanent teeth can be divided into four types: round (61.31%, diameter: 0.09-0.26 mm), oval (36.96%, diameter: 0.12-0.28 mm), renal (1.30%), and irregular (0.43%). The occurrence of the apical lateral foramina is 15.31% (230/1,502). CONCLUSIONS: The apical lateral foramina are found in 1/7 of 1,502 permanent teeth.

Dental Pulp Cavity↗
PubMed2000

[Comparative study of three common G6PD gene mutations in Yao and Han People in Guangxi].

OBJECTIVE: To study G6PD gene mutation diversity in Yao and Han people in Guangxi and compare the genotypic frequencies. METHODS: The three common G6PD gene mutations in Chinese were investigated in 34 G6PD deficient individuals from Yao and 37 from Han people by using an amplification refractory mutation system (ARMS). RESULTS: Among 34 cases of G6PD deficiency of Yao people, the genotypic frequencies of G1376T, G1388A and A95G were 41.2%, 26.5% and 14.7%, respectively. A case of C1311T was detected. As compared with that in Han people, the respective frequencies were 16.2%, 40.6% and 5.4%. CONCLUSION: The main G6PD mutations in Yao people were the same with Han people in Guangxi, but G1376T mutation was higher than that in Han people. The C1311T mutation in Yao people in Guangxi was reported for the first time.

Adolescent↗
PubMed1999

Overexpression of wild-type retinoic acid receptor alpha (RARalpha) recapitulates retinoic acid-sensitive transformation of primary myeloid progenitors by acute promyelocytic leukemia RARalpha-fusion genes.

Retinoic acid receptor alpha (RARalpha) is the target of several chromosomal translocations associated with acute promyelocytic leukemias (APLs). These rearrangements fuse RARalpha to different partner genes creating the chimeric proteins: PML-RARalpha, PLZF-RARalpha, and NPM-RARalpha. Although the vast majority of APLs respond to retinoic acid therapy, those associated with PLZF-RARalpha are resistant. We have used retroviruses to express PML-RARalpha, PLZF-RARalpha, NPM-RARalpha, RARalpha403 (a dominant negative mutant of RARalpha), and wild-type RARalpha in murine bone marrow progenitors and found that all of these constructs blocked differentiation and led to the immortalization of myeloid progenitors. This cellular transformation is specific to an alteration of the RARalpha pathway because overexpression of RARbeta, RARgamma, or RXRalpha did not result in similar growth perturbations. Pharmacological doses of RA induced differentiation and inhibited proliferation of cells transformed with either of the APL fusion genes, including PLZF-RARalpha, whereas physiological retinoic acid concentrations were sufficient to reverse the phenotype of cells transformed with wild-type RARalpha. The cellular responses to retinoic acid were accompanied by a sharp decrease in the amount of the RARalpha-fusion proteins expressed in the cells. Our findings suggest that the oncogenicity of RARalpha-fusion proteins results from their nature to behave as unliganded RARalpha in the presence of physiological concentrations of retinoic acid.

Animals↗
PubMed1999

Tyrphostin B42 inhibits IL-12-induced tyrosine phosphorylation and activation of Janus kinase-2 and prevents experimental allergic encephalomyelitis.

IL-12 is a macrophage-derived cytokine that induces proliferation, cytokine production, and cytotoxic activity of T and NK cells. Signaling through its receptor, IL-12 induces these cellular responses by tyrosine phosphorylation and activation of Janus kinase-2 (Jak-2), Tyk-2, Stat3, and Stat4. We have used tyrphostin B42 (AG490), a Jak-2 inhibitor, to determine the role of Jak-2 kinase in IL-12 signaling and IL-12-induced T cell functions. Treatment of activated T cells with tyrphostin B42 inhibited the IL-12-induced tyrosine phosphorylation and activation of Jak-2 without affecting Tyk-2 kinase. In contrast, treatment with tyrphostin A1 inhibited the tyrosine phosphorylation of Tyk-2 but not that of Jak-2 kinase. Inhibition of either Jak-2 or Tyk-2 leads to a decrease in the IL-12-induced tyrosine phosphorylation of Stat3, but not of Stat4, protein. While inhibition of Jak-2 lead to programmed cell death, the inhibition of Jak-2 or Tyk-2 resulted a decrease in IFN-gamma production. We have further tested the in vivo effects of tyrphostin B42 in experimental allergic encephalomyelitis, a Th1 cell-mediated autoimmune disease. In vivo treatment with tyrphostin B42 decreased the proliferation and IFN-gamma production of neural Ag-specific T cells. Treatment of mice with tyrphostin B42 also reduced the incidence and severity of active and passive EAE. These results suggest that tyrphostin B42 prevents EAE by inhibiting IL-12 signaling and IL-12-mediated Th1 differentiation in vivo.

Animals↗
PubMed1999

Three-dimensional nano-HAp/collagen matrix loading with osteogenic cells in organ culture.

Transplantation of osteogenic cells with a suitable matrix is one strategy for engineering bone tissue. Three-dimensional distribution and growth of cells within the porous scaffold are of clinical significance for the repair of large bony defects. A nano-HAp/collagen (nHAC) composite that mimics the natural bone both in composition and microstructure to some extent was employed as a matrix for the tissue engineering of bone. A porous nHAC composite was produced in sheet form and convolved to be a three-dimensional scaffold. Using organ culture techniques and the convolving method, we have developed three-dimensional osteogenic cells/nHAC constructs in vitro. Scanning electron microscopic and histological examination has demonstrated the development of the cells/material complex. Spindle-shaped cells migrating out of bone fragments continuously proliferated and migrated throughout the network of the coil. The porous nHAC scaffold provided a microenvironment resembling that seen in vivo, and cells within the composite eventually acquired a tridimensional polygonal shape. In addition, new bone matrix was synthesized at the interface of bone fragments and the composite.

Animals↗
PubMed1999

Conservation of cys-cys trp structural triads and their geometry in the protein domains of immunoglobulin superfamily members.

In almost all members of the immunoglobulin superfamily (IgSF) for which an experimental structure has been determined, a triad (C-CW) consisting of two cysteine residues that form a disulfide bond and a neighboring tryptophan can be found in the core of the protein fold. We analyzed the geometry of these C-CW triads among a database of 60 Fab crystal structures and found it to be remarkably conserved. We identified C-CW triads of a similar configuration in other members of the IgSF such as T cell receptor (TCR), major histocompatibility complex antigens (MHC), cell surface antigens CD4 and CD8, and cell-adhesion molecules. We used this C-CW pattern to search a database of non-IgSF proteins, and identified several proteins that contain a disulfide bridge associated with a tryptophan in a similar configuration. Examination of the distances and orientations between triads found in adjacent domains in Fab fragments and TCR also reveal a high degree of conservation, which reflects the invariance of the inter-chain domain packing. This high degree of conservation of the geometry of the C-CW triad in IgSF structures suggests that the Trp may contribute significantly to the stability of the disulfide bond. Knowledge of these geometric parameters may prove useful in the construction and validation of theoretical models of Ig, TCR, and other IgSF members.

Animals↗
PubMed1999

[Molecular characterization of glucose-6-phosphate dehydrogenase variants in four ethnic groups in Yunnan province of China].

OBJECTIVE: In order to understand the molecular evolution, race origin and the relationship between the G6PD gene structure and clinical symptoms, the authors identified the molecular characterization of glucose-6-phosphate dehydrogenase and determined the G6PD gene frequency in four ethnic groups in Yunnan province of China. METHODS: The point mutations of G6PD were detected by Mismatch-PCR/RE, SSCP,ARMS,DNA sequence and so on. G6PD gene frequency was determined by Hardy-Weinberg Law. RESULTS: G6PD G1388A, G1376T,A95G mutations were determined in Bai and Dai people for the first time and G1388A also in Harni people by DNA sequence. G6PD C1024T were detected in Dai population by Mismatch-PCR/RE. The gene frequency of G6PD in Bai population in Dali city is 0.0113, and the incidence is 1.19% which are different from those in Dai population. CONCLUSION: G6PD G1388A,G1376T, A95G and C1024T are the mutations in national minorities as well as in the Han people. The results suggest that different national minorities of China may have the same ancestor. The incidence of G6PD deficiency and the G6PD gene frequency in Bai population are different from those in Dai population. The distribution of G6PD deficiency in Yunnan is associated with the distribution of malaria epidemic in that province.

China↗
PubMed1999

[Detection of RB1 mutations by using quantitative fluorescent mutiplex PCR].

OBJECTIVE: To develop a half-automatic, simple, non-radioactive technique for rapid detection of mutation in the RB gene. METHODS: Quantitative fluorescent multiplex PCR (QFM-PCR) involves amplification of the promoter region and all 27 exons of the RB1 gene with fluorescein labeled primers in multiplex sets. Primers were divided into multiplex sets of three to seven pairs of primers, also contained were internal control primers C4. Four external controls were also tested by using nullisomic, monosomic, diploid, and trisomic for RB1. The number of copies of a fragment in a test sample was calculated by comparing fluorescence intensity of the fragment with these standards. Fragment value detection and subsequent calculations were performed automatically by Fragment Manager 2.1 Software. RESULTS: Small deletions, insertions and whole exon deletion in the RB1 gene were detected from genomic DNA. Sequencing analysis and RB tumor homozygous mutation comfirmed the defects detected by QFM-PCR. CONCLUSION: The approach is a rapid, cost-effective initial method for screening patient samples. It has been used to identify approximately 50% positives of tested samples. The mutations shown were not only small deletion and insertion, but also the single copy exons heterozygous mutation in the RB1 gene which the previously used methods were unable to detect. These features make the technique an attractive approach to clinical diagnosis of gene defects.

Fluorescence↗
PubMed1999

[Detection of R277Q mutation of SRD5alpha2 gene by amplification refractory mutation system].

OBJECTIVE: To set up a simple method for identifying the mutation of R227Q of SRD5alpha2 gene which is one of the most common mutations in congenital hypospadias in China. METHODS: The amplification refractory mutation system(ARMS) was employed in detecting the SRD5alpha2 gene R227Q mutation in congenital hypospadias confirmed by PCR-SSCP and DNA sequencing. RESULTS: The ARMS was successfully applied to the detection of the R227Q mutation of SRD5alpha2 gene. Three out of 23 congenital hypospadias were positive for R227Q mutation. The mutations determined by ARMS were in full agreement with those obtained by the DNA sequencing. CONCLUSION: This is a simple, rapid and accurate method. It can be used for detecting the SRD5alpha2 gene R227Q mutation in congenital hypospadias and male pseudohermaphroditism.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1999

[Detection of three common G6PD gene point mutations in Guangdong province by using ARMS].

OBJECTIVE: To detect three common G6PD gene point mutations, G1388A, G1376T and A95G, in Guangdong province and to estimate the approximate frequencies. METHODS: Using the amplification refractory mutation system(ARMS) method to detect G1388A and G1376T and the newly developed ARMS to identify A95G mutation. RESULTS: Ninety cases of G6PD deficient male were examined, and 42 of them were identified to be G1388A(46.7%), 14 G1376T(15.6%), and 12 A95G(13.3%). Totally 68 out of the 90 cases(75.6%) were of the three common mutations. The rest belong to rare or undefined mutations. CONCLUSION: ARMS method can be used in detecting common mutations of G6PD gene with the benefits of simple, fast, economic, and accurate.

Alleles↗
PubMed1999

[Studies on a G6PD polymorphic site, cDNA C1311T].

OBJECTIVE: To use amplification refractory mutation system(ARMS) method to detect the G6PD cDNA C1311T mutation, estimate its frequency in a normal south Chinese population, and investigate whether IVS-11 C93T mutation is the cause of certain G6PD deficient cases. METHODS: DNA sequencing was used to confirm the C1311T and the IVS-11 C93T mutations. ARMS was set up to detect the C1311T and to estimate its frequency. RESULTS: Three cases of C1311T mutation were found in 40 G6PD deficient samples. The optimal condition for ARMS was established. Using this method, 19 cases of C1311T were detected in 103 normal men, and the frequency of this polymorphic mutation was estimated to be 18.4% in southern Chinese population. Four cases with G6PD deficiency were demonstrated to be C at the IVS-11 93 position. At the same time, a case of IVS-11 93 C-->T was found in a normal man. CONCLUSIONS: ARMS is a simple, time-saving, and reliable method for detecting known G6PD gene point mutation. The frequency of C1311T in a normal south Chinese population is 18.4%. IVS-11 C93T might be another polymorphic site of the G6PD gene, and it is not the cause of enzyme deficiency in certain G6PD deficient cases.

Asian People↗
PubMed1999

[Study on G487A mutation of the glucose-6-phosphate dehydrogenase gene].

OBJECTIVE: In order to reveal the molecular evolution and ethnic origin and immigration, on the basis of G6PD G487A mutation, and estimate the incidence of the mutation in Bai, Dai, and Han people in Yunnan and Guangxi. METHOD: G6PD deficient individuals were studied by using PCR-RE, PCR-SSCP and DNA sequencing. RESULTS: The G487A mutation in Bai and Dai people was identified for the first time and its relative incidences were 6/66 and 1/52, respectively. The individuals of G6PD G487A mutation showed the features of G6PD clinic type III. No G487A was found in Han people in Guangxi(0/46). CONCLUSION: The G6PD G487A mutation revealed in some ethnic groups of China implies that different national minorities of Chinese may be origined from a common ancestor.

Asian People↗
PubMed1999

[A study of load stress on an implant and a tooth supported fixed bridge for the first mandibular molar].

OBJECTIVE AND METHODS: A study of load stress on an implant and a tooth supported fixed bridge for the first mandibular molar was performed by means of 3-D FEA in order to reveal the displacement and stress distribution. RESULTS: The results show that the maximum displacement of the second premolar is greater than that of the terminal implant, but there is no difference between the mean (mean) under dispersed load statistically, due to the framework function of the bridge. The stress concentration appears around the neck of the abutments, on the contrary, a little stress is found around the apical portion of the second premolar. When the load concentrates on-to the abutments, the displacement and stress value increase obviously. CONCLUSION: The attention should be paid to the load and occlusion of the terminal implant. This kind of bridge design may be used in clinical practice.

Dental Implantation↗
PubMed1998

Tissue response to nano-hydroxyapatite/collagen composite implants in marrow cavity.

The tissue response to a nano-hydroxyapatite/collagen composite implanted in a marrow cavity was investigated by histology and scanning electron microscopy. A Knoop microhardness test was performed to compare the mechanical behavior of the composite and bone. The ultrastructural features of the composite, especially the carbonate-substituted hydroxyapatite with low crystallinity and nanometer size, made it a bone-resembling material. It was bioactive, as well as biodegradable. At the interface of the implant and marrow tissue, solution-mediated dissolution and giant cell mediated resorption led to the degradation of the composite. Interfacial bone formation by osteoblasts was also evident. The process of implant degradation and bone substitution was reminiscent of bone remodeling. The composite can be incorporated into bone metabolism instead of being a permanent implant. For lack of the hierarchical organization similar to that of bone, the composite exhibited an isotropic mechanical behavior. However, the resistance of the composite to localized pressure could reach the lower limit of that of the femur compacta.

Animals↗
PubMed1998

Prevention of experimental allergic encephalomyelitis via inhibition of IL-12 signaling and IL-12-mediated Th1 differentiation: an effect of the novel anti-inflammatory drug lisofylline.

Experimental allergic encephalomyelitis (EAE) is an inflammatory, CD4+ Th1-mediated autoimmune disease, which serves as a model for multiple sclerosis. We examined the effect of a novel anti-inflammatory drug, lisofylline (LSF), on EAE induced either by injection of mouse spinal cord homogenate or following transfer of myelin basic protein-reactive T cells. Orally administered LSF significantly inhibited EAE in both cases, decreasing peak clinical scores by >70% and >80%, respectively. In addition, analysis of representative spinal cord sections from LSF-treated mice showed complete lack of demyelination and lymphocyte infiltration. The reduction in EAE correlated with the inhibition of Th1 differentiation by LSF in vivo, as indicated by a reduction in T cell IFN-gamma production ex vivo after Ag restimulation. The inhibition of Th1 differentiation in vivo is consistent with a block in IL-12 receptor signaling, because LSF blocked IL-12-driven Th1 differentiation and T cell proliferation in vitro, yet had no effect on IL-12 secretion from APCs ex vivo or in vitro.

Adoptive Transfer↗