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Biomedical subjects

B Ying

Publications and source records attributed to B Ying.

15 recordsLinked to original sources

Reconstruction of mandibular symphyseal defects by trifocal distraction osteogenesis: an experimental study in Rhesus.

Mandibular symphyseal defects caused by tumor surgery, trauma, or congenital misshape can produce maxillofacial deformity and functional handicap. Recently, the technique of distraction osteogenesis has become a valuable reconstructive method for craniofacial bone defects. Four adult rhesus monkeys were used in this study. The anterior mandibulectomy (ranged from canine to canine) was performed, and bilateral transport segments (ranged from first premolar to first molar) were created. Custom-made multiplanar distractors were applied for the reconstruction of the monkeys' artificial mandibular symphyseal defects by trifocal distraction osteogenesis. After a delay period of 7 days, the bilateral transport discs were distracted forward and inward simultaneously. Serial X-ray and three-dimensional CT films were taken within the experimental period. Two monkeys were sacrificed at 8 and 16 weeks, respectively, after the completion of distraction. The distracted calluses and united areas between bilateral transport discs were harvested and processed for histological examination. The mandibular symphyseal defects in all animals were repaired successfully and the anterior mandibular contours were similar to the normal ones. Perfect bone regeneration in the distraction gaps was found, and fibro-bony union between the bilateral transport segments was observed in the midline region at 16 weeks after the end of distraction. The success of distraction osteogenesis for repair of mandibular symphseal defects in monkeys by this distractor may provide an alternative method to reconstruct the anterior part of mandible.

Animals↗

[Evaluation on the effect of synthetic hydroxyapatite for drinking water defluoridation in field study].

In order to evaluate the effect of synthetic hydroxyapatite on drinking water defluoridation, a coagulative precipitation method and a flow column system was tested in the fields. The defluoridation capacity of coagulative precipitation method was 4.19 mg/g, and the method was simple on operation, but more reagents were needed with high cost for operation. The defluoridation capacity of flow column system was 6 mg/g and the saturated hydroxyapatite could be reused after regeneration. The operation of household defluoridator based on flow column system is simple, with low cost and high capacity in defloridation. The system will be applied in the fluorosis areas.

Durapatite↗

[Optimizing the synthesis of hydroxyapatite as a method for the defluoridation of drinking water].

As the cheaper raw materials for the synthesis of hydroxyapatite as a defluoridator, calcium hydroxide and phosphoric acid are used. Hydroxyapatite is made by a hydro-synthesis method, and optimum conditions are determined by batch test for defluoridation with respect to the consumption of phosphoric acid, reaction time and acid-washed product. The results showed that the defluoridation capacity of the synthetic hydroxyapatite for break through (F- 1.0 mg/L is considered as the break through point) was F- 5.6 mg/g in column test, and F- 10.7 mg/g for saturation in column test. After optimization of the synthesis method, the defluoridation capacity of hydroxyapatite is much higher than activated alumina and bone charcoal, which are used currently.

Fluorides↗

[Study on the defluoridation of drinking water with synthetic hydroxyapatite].

Synthetic hydroxyapatite was used as a material for the defluoridation of drinking water. The defluoridation capacity, regeneration the capability of defluoridator and the corresponding parameters of defluoridation and regeneration have been studied with batch and column test. The results showed that the defluoridation capacity of synthetic hydroxyapatite on F- was 3.7-4.3 mg/g in batch test, 5.6 mg/g for break through (1.0 mg/L is considered as the break through point) in column test, and 10.7 mg/g for saturation in column test. The efficiency of regeneration was 46%-64% for saturated hydroxyapatite with surface-coating method.

Durapatite↗

Three novel TBX5 mutations in Chinese patients with Holt-Oram syndrome.

Holt-Oram syndrome (HOS) is an autosomal dominant syndrome that comprises upper limb and cardiac defects. The gene responsible for HOS, TBX5, was isolated and many mutations have been identified in HOS patients. We analyzed 11 Chinese HOS patients (7 from three families and 4 sporadic cases) for TBX5 mutation by single strand conformation polymorphisms (SSCPs). Three SSCP changes were detected in two of the three familial cases and one sporadic case. Sequence analysis identified three novel, heterozygous mutations in TBX5: a frameshift mutation caused by one base deletion [C416del] in one family, a mis-sense mutation (Gln49Lys) induced by a base substitution (C145A) in another family, and the other mis-sense mutation (Ile54Thr) by T161C in one sporadic case. The patients with the frameshift mutations had severer clinical manifestations that involved aplasia/hypoplasia of the arm and thumbs, while those with the mis-sense mutations presented with milder anomalies such as absent or hypoplastic thumbs but without arm abnormalities. These observations may support a genotype-phenotype correlation in HOS patients with TBX5 mutation.

Amino Acid Substitution↗

Molecular cloning and mapping of a novel ADAM gene (ADAM29) to human chromosome 4.

Members of the ADAM family (type I integral membrane protein with a disintegrin and metalloprotease domain) have been implicated in many important biological processes involving cell-cell and cell-matrix interactions, such as fertilization and myoblast fusion. We report here the cDNA sequence of a novel human ADAM gene (ADAM29) that contains a putative fusion peptide. Northern blot analysis revealed that the mRNA of ADAM29 is highly expressed in the testis. By radiation hybrid panel mapping, the ADAM29 gene was assigned to human chromosome 4q34.2-qter.

ADAM Proteins↗

[No arresting aorta undergoing open heart surgery with CPB through a right anterolateral thoracotomy].

We performed operation of CPB without arresting aorta on 57 cardiac patients through a right anterolateral thoracotomy. Results showed: except that one case of ASD required a 2nd time thoracotomy to hemostasis for a lot of drainage, another case of residual shunt postoperation of TOF was not satisfactory in repair, the others are perfect. There were no operative or hospitalized mortality, no incision infection. It has also solve the psychological distress of female patients provoking by midline showy scar of median sternotomy, so it has acquire a good surgical cosmetic effect.

Adolescent↗

Mouse adenovirus type 1 early region 1A is dispensable for growth in cultured fibroblasts.

Mouse adenovirus type 1 (MAV-1) mutants with deletions of conserved regions of early region 1A (E1A) or with point mutations that eliminate translation of E1A were used to determine the role of E1A in MAV-1 replication. MAV-1 E1A mutants expressing no E1A protein grew to titers comparable to wild-type MAV-1 titers on mouse fibroblasts (3T6 fibroblasts and fibroblasts derived from Rb+/+, Rb+/-, and Rb-/- transgenic embryos). To test the hypothesis that E1A could induce a quiescent cell to reenter the cell cycle, fibroblasts were serum starved to stop DNA replication and cellular replication and then infected with the E1A mutant and wild-type viruses. All grew to equivalent titers. Steady-state levels of MAV-1 early mRNAs (E1A, E1B, E2, E3, and E4) from 3T6 cells infected with wild-type or E1A mutant virus were examined by Northern analysis. Steady-state levels of mRNAs from the mutant-infected cells were comparable to or greater than the levels found in wild-type virus infections for most of the early regions and for two late genes. The E2 mRNA levels were slightly reduced in all mutant infections relative to wild-type infections. E1A mRNA was not detected from infections with the MAV-1 E1A null mutant, pmE109, or from infections with similar MAV-1 E1A null mutants, pmE112 and pmE113. The implications for the lack of a requirement of E1A in cell culture are discussed.

Adenovirus E1A Proteins↗

Construction and identification of a recombinant adenovirus which expresses human interferon-gamma.

An E1-deleted adenoviral vector, pAdl2/RSV-IFN-bpA, harboring human IFN-gamma cDNA, and plasmid pJM17 were cotransfected into a human embryo kidney cell line 293 by the calcium-phosphate precipitation method. Six strains of recombinant adenovirus (rAd) were obtained after 11-day incubation. PCR analysis indicated that all six rAds contained human IFN-gamma cDNA. The biological activity of IFN-gamma was detected in the supernatant of the cultured 293 cells following rAd infection, and it could be blocked by the antibody against IFN-gamma. The B16F10 cells infected with the purified rAd (RSV/IFN-01) didn't show cytopathic effect (CPE), and more biological activity of IFN-gamma was detected in the supernatant of the infected B16F10 cells with increased MOI (multiple of infection) values. Therefore, the recombinant adenovirus constructed in this study can express and secrete human IFN-gamma.

Adenoviruses, Human↗

Interaction of mouse adenovirus type 1 early region 1A protein with cellular proteins pRb and p107.

We demonstrated functional associations between mouse adenovirus type 1 (MAV-1) early region 1A (E1A) protein and both the mouse retinoblastoma protein (pRb) and the mouse pRb-related protein, p107. Interactions between MAV-1 E1A and mouse pRb or mouse p107 proteins were examined in infected cell lysates using a mouse embryonic fibroblast cell line infected with wild-type and mutant MAV-1 viruses. Using a polyclonal antibody to MAV-1 E1A, exogenously added mouse pRb or mouse p107 was coimmunoprecipitated from wild-type, dIE105 (CR1 delta)-, and dIE106 (CR3 delta)-infected cell lysates. No coimmunoprecipitation was seen with cell lysates from dIE102 (CR2 delta) or pmE109, a mutant virus that produces no detectable E1A protein due to an ATG to TTG point mutation in the initiator methionine. Introduction of mouse pRb into SAOS-2 cells resulted in a flat and enlarged cell phenotype, whereas cotransfection of mouse pRb and MAV-1 E1A resulted in a significant reduction of flat cells, presumably due to E1A binding pRb. CR1 delta and CR2 delta E1A proteins were less effective at reducing the number of flat, enlarged cells induced by pRb expression than were the CR3 delta or wild-type E1A proteins. The reduced ability of these mutants to inactivate pRb relative to wild-type E1A correlated with their reduced ability to bind pRb in the in vitro coimmunoprecipitation experiments. As a measure of p107/MAV-1 E1A complex formation in MAV-1-infected cells, we used mobility shift assays to examine cell extracts for the presence of p107-containing E2F protein-DNA complexes. Mock-, dIE102-, and pmE109-infected cell extracts formed a p107-containing complex, whereas wild-type-infected cell extracts did not. Thus the formation of a p107-E2F complex in wild-type- or these mutant-infected extracts inversely correlated with the presence of E1A-p107 complexes identified in the vitro coimmunoprecipitation experiments. This is consistent with E1A-p107 complexes forming in wild-type MAV-1-infected cells.

Adenovirus E1A Proteins↗

Different malignant phenotypes induced in a stable, subdiploid, benign epithelial clone by DNA transfection.

Progression to malignancy in carcinomas has been studied in a stable, benign, subdiploid, cloned epithelial cell line (A5P/B10) sensitive to Geneticin at 100 micrograms/ml. A total of 28 cell lines were selected for Geneticin - resistance and inoculated into the footpads of syngeneic animals following co-transfection with pSV2neo and genomic DNA, or transfection with plasmid constructs containing neo and the activated Ha-ras oncogene. The behavior of 12 cell lines cotransfected with normal genomic DNA and inoculated into 146 footpads was the same as the A5P/B10 cells. Low grade primary tumors were produced in 122 footpads by 13 cell lines transfected with Ha-ras, and a proportion (61/122) produced well-differentiated lymph node metastases. One of 3 cell lines cotransfected with genomic DNA from a malignant cell line (BC1) produced 8 anaplastic primary tumors with anaplastic metastases. Cell lines from lymph nodes involved by these anaplastic tumors were sensitive to Geneticin, and genomic DNA from 2 clones of these cells failed to produce a malignant phenotype when co-transfected into the A5P/B10 cells. These results indicated that the progression to a malignant phenotype induced in benign cells from a spontaneous epithelial tumor by co-transfection with genomic DNA from malignant cells was different from that induced by the ras oncogene.

Animals↗