Objective:To establish three-dimensional(3D)finite element model of the mandible first molar,and to study the stress distribution.Methods:3D finite element model of the mandible first molar was constructed by CT image reconstruction technique.Then MIMICS software was used to separate the areas and finish 3D calculation.GEOMAGIC software was applied to modify and generate a NURBS surface in each patch.All components of the model were assembled under the ANSYS preprocessor.Specific material parame-ters were selected to simulate the various restoration and dentin status.The 3D finite element model was applied to analyze the stress distribution of the molar under 1 4 different pressure loading conditions.Results:The 3D finite element model of the mandible first molar was established,which was consistent to the situation observed in the clinical environment.The pressure loading n2,n8,n9,n1 0,n1 1 , n1 2,n1 3,n1 4 can be used to represent the bite pressure.Conclusion:It is a practical and accurate way to establish 3D finite element model by CT image reconstruction technique and reverse engineering software MIMICS and GEOMAGIC.

Objective:To establish three-dimensional(3D) finite element models of the first mandibular molar restored with three post and core systems.Methods:Three 3D finite element models of the restored first mandibular molars were constructed by using CT image reconstruction technique.Then MIMICS software was used to separate the areas and to finish 3D calculation.GEOMAGIC software was applied to modify and generate a NURBS surface in each patch.All components of the models were assembled under the ANSYS preprocessor.Specific materials parameters were selected to simulate the various restoration and dentin status.Results:The 3D finite element models of restored first mandible molars were successfully established,which were consistent to the situation observed in the clinical environment.Conclusion:It is a practical and accurate method to establish three-dimensional finite element models by CT image reconstruction technique and reverse engineering software MIMICS and GEOMAGIC.

Objective To investigate the clinical efficacy of lengthening osteotomy for leg bone defect. Methods The clinical data of 22 patients who received lengthening osteotomy for leg bone defect from February 2005 to March 2011 were retrospectively analyzed. Operative methods were designed according to the patients' general condition, condition of fracture nonunion and bone defect accompanied by osteomyelitis. They included Z-shaped, oblique, and cortical bone osteotomy. The modified Ilizarov external fixator was used after osteotomy. Bone lengthening was performed 1 week after the operation, and the lengthening rate was 0.5-1mm/d. Results The bone defects achieved bone union in the 22 patients by fixation and lengthening for 3-10 months (8 months on average), followed by external fixation for 6 months to achieve clinical union. The follow-up period for all the patients ranged from 12 to 15 months, and remediable complication was found in 2 patients (1 mild, 1 moderate), and no irredeemable complication was observed. Conclusions Lengthening osteotomy is safe, reliable, and easy to operate. Furthermore postoperative nursing care is simple and complications are less, thus it is an ideal surgical method for leg bone defect.

Objective To investigate the changes of iodide uptake and the expression of thyroidspecific genes in poorly differentiated follicular thyroid carcinoma (FTC) cells after transfection of human TSH receptor (hTSHR) gene in vitro. Methods The recombinant eukaryotic expression plasmid PcDNA3. 1/hTSHR-cDNA was transformed into DH5a bacterial for amplification and then the recombinant plasmid was extracted. The recombinant was identified with PCR amplifying, restriction enzyme digestion analysis and DNA sequencing. The recombinant plasmid pcDNA3.1/hTSHR was transfected into FTC-133 cell line by lipofectin methodin vitro. Immunofluorescence, iodide uptake studies and real time-PCR were applied to detect target protein expression. Statistical analysis was performed with t-test using SPSS 13. 0 software. Results Kpn Ⅰ and Xba Ⅰ restriction enzyme digestion, PCR amplifying and DNA sequencing confirmed that pcDNA3. 1/hTSHR was successfully constructed. After transfection of the recombinant plasmid pcDNA3. 1/hTSHR-cDNA and the stimulation of hTSH, the tumor cells displayed the expression of hTSHR protein at cell surface and cytoplasm. The iodine uptake in pcDNA3. 1/hTSHR transfected cells was 2. 9 times higher than that of control(pcDNA3.1(+) transfected cells) group(t = 28.63, P ＜0. 01). The expression of TSHR,NIS, TPO and Tg (mRNA levels) in pcDNA3. 1/hTSHR transfected cells were also significantly elevated by 1.74 (t =5.959, P＜0.01), 7.2 (t =3.807,P＜0.05), 2.88 (t=4.769,P＜0. 01) and 2.67 times (t=6.388,P ＜0.01) respectively compared to those of the control group. Conclusion The study demonstrates that iodide uptake may be reactivated by hTSHR receptor gene transfection in poorly differentiated FTC cell.

Adult ; Cartilage ; pathology ; surgery ; Female ; Humans ; Metatarsophalangeal Joint ; pathology ; Sesamoid Bones ; pathology ; surgery

OBJECTIVETo identify the mutations of iduronate-2-sulfatase (IDS) gene, and to establish a basis of prenatal gene diagnosis of Hunter syndrome.

METHODSUrine glycosaminoglycan (GAG) assay was used to preliminary diagnosis of mucopolysaccharidosis. PCR-denaturing high-performance liquidchromatograptly (PCR-DHPLC) analysis was performed to detect the mutation in exons 9, 3, 8 of the IDS gene. DNA sequencing was applied to analyze the mutation detected by PCR-DHPLC.

RESULTSAbnormal peaks were found by PCR-DHPLC. A new frame-mutation (1569+TT) in exon 9 of IDS gene was identified by DNA sequencing. Two "T"q inserted in position 1569 base pair (1569+TT) caused a substitution of codon 482 (TTA, leucine) to 482 (TTT, phenylalanine). The "TT" insertion results in the decrease of amino acids from 550 to 482. The patient is a hemizygote and his mother is a heterozygote.

CONCLUSIONA new frame-shift mutation of IDS gene is found to report. The mutation (1569+TT) results in 68 amino acids lost. Probably it causes the enzyme activity seriously dropped down and being pathologically the basis of disease.

Child, Preschool ; Chromatography, High Pressure Liquid ; DNA Mutational Analysis ; Humans ; Iduronate Sulfatase ; genetics ; Male ; Molecular Sequence Data ; Mucopolysaccharidoses ; genetics ; Mucopolysaccharidosis II ; enzymology ; genetics ; Mutation

The paper introduces a helical tomotherapy (HT) adaptive system in assessment of parotid gland dose variation in head and neck cancer. The system, which helical therapy unit is equipped with, is based on megavoltage computed tomography (MVCT) images to calculate the actual volume and dose of region of interest (ROI). Whether to change plan is judged on the fact for the realization of adaptive radiotherapy. One case of nasopharyngeal carcinoma was as a sample to evaluate parotid gland dose variation during the treatment. On every week and last time, patient was scanned by MVCT before treatment, a total of eight MVCT images. As the treatment progressed, the parotid gland volume was shrinking and the dose was increasing. The parotids volume variation was negatively related with D50 and V1 (both P < 0.05).
Adult ; Head and Neck Neoplasms ; diagnostic imaging ; Humans ; Male ; Parotid Gland ; diagnostic imaging ; Radiotherapy Dosage ; Radiotherapy Planning, Computer-Assisted ; instrumentation ; methods ; Software ; Tomography, Spiral Computed ; instrumentation ; methods

OBJECTIVEStudying on G6PD polymorphism from Hakka population in Guangdong province.

METHODSIdentifying the variants of G6PD gene and determining the frequencies respectively with the use of amplified refractory mutation system(ARMS), polymerase chain reaction-single strand conformation polymorphism(PCR-SSCP) and ABI 3100 DNA sequencing technologies.

RESULTSMutations of G6PD gene in cDNA 1388 (G-->A), 1376 (G-->T), 95 (A-->G), 392 (G-->T), 1024 (C-->T), 1311 (C-->T) have been found.

CONCLUSIONG6PD cDNA 1388 (G-->A), 1376 (G-->T), 95(A--> G), 392 (G-->T), 1024 (C-->T) and 1311 (C-->T) accompanied with intron 11 (93 T-->C) are the common mutations in Chinese population. cDNA 1388 (G-->A), cDNA 1376 (G-->T) are the most popular G6PD gene variants in Hakka population. In this study, no new type of G6PD gene mutation was found in the Hakkas of Guangdong.

Asian Continental Ancestry Group ; genetics ; China ; DNA Mutational Analysis ; Glucosephosphate Dehydrogenase ; genetics ; Glucosephosphate Dehydrogenase Deficiency ; ethnology ; genetics ; Humans ; Introns ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA

OBJECTIVETo study the effects of benzo(a)pyrene (BaP) on the cell cycle distribution and activities of mitogen-activated protein kinase (MAPK) signal molecules (ERK1/2, JNK1/2 and p38) in human embryo lung cells (HELF), and to investigate the relationship between alterations of MAPK protein phosphorylation and the cell cycle distributions.

METHODSThe phosphorylation of MAPK were induced by exposing HELF cells to BaP at 0.1, 0.5, 2.5 and 12.5 micromol/L. The phosphorylation and protein expression levels of ERK1/2, JNK1/2 and p38 were determined through western-blotting assay. And the flow cytometry assay was used to measure the cell cycle effects in HELF cells after treatment with 2.5 micromol/L BaP for 24 h.

RESULTSThe phosphorylation levels of ERK1/2, JNK1/2 and p38 were significantly increased through BaP exposure. In addition, the phosphorylation of these three MAPKs has similar alteration pattern. We found that exposure of cells to 2.5 microM of BaP for 24 h resulted in a decrease of G(0) and G(1) population by 11.9% (F = 41.38, P < 0.01) and an increase of S population by 17.2% (F = 68.13, P < 0.01). Three chemical inhibitors of MAPK (AG126, SP600125 and SB203580) could significantly inhibit the cell cycle alteration because of BaP treatment.

CONCLUSIONERK1/2, JNK1/2 and p38 could positively regulate the BaP independently induced cell cycle alterations.

Benzo(a)pyrene ; toxicity ; Cell Cycle ; drug effects ; Cells, Cultured ; Fibroblasts ; drug effects ; metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Lung ; cytology ; embryology ; MAP Kinase Kinase 4 ; metabolism ; MAP Kinase Signaling System ; drug effects ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mitogen-Activated Protein Kinase 8 ; metabolism ; Mitogen-Activated Protein Kinase 9 ; metabolism ; Signal Transduction ; drug effects ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo study the molecular mechanism of the inhibitory effects of vitamin C on benzo[a]pyrene (B[a]P)-induced changes of cell cycle in human embryo lung fibroblast (HELF) cells.

METHODSThe stable transfectants, HELF transfected with antisense cyclin D1 and antisense CDK4, were established. Cells were cultured and pretreated with vitamin C before stimulation with B[a]P for 24 h. The expression levels of cyclin D1, CDK4, E2F1, and E2F4 were determined by Western blot. Flow cytometric analysis was employed to detect the distributions of cell cycle.

RESULTSB[a]P significantly elevated the expression levels of cyclin D1, E2F1, and E2F4 in HELF cells. Vitamin C decreased the expression levels of cyclin D1, E2F1, and E2F4 in B[a]P-stimulated HELF cells. Dose-dependent relationships were not found between the different concentrations of vitamin C (10, 100, 500, 1000, and 5000 micromol/L) and the expression levels of cyclin D1, E2F1, and E2F4 in HELF cells. The expression levels of cyclin D1, E2F1, and E2F4 in B[a]P-treated transfectants were lower than those in B[a]P-treated HELF cells. The expression levels of cyclin D1 and E2F4 treated with vitamin C and antisense cyclin D1 were decreased compared with those treated with antisense cyclin D1 alone. The effects of vitamin C combined with antisense CDK4 on the expression levels of cyclin D1 and E2F1/E2F4 were similar to those of antisense CDK4 alone. B[a]P progressed HELF cells from G1 to S phase. Both vitamin C and antisense cyclin D1 suppressed the changes of cell cycle progressed by B[a]P. However, antisense CDK4 did not attenuate the above changes. Vitamin C combined with antisense CDK4 markedly suppressed B[a]P-induced changes of cell cycle as compared with antisense CDK4. But the inhibitory effects of vitamin C combined with antisense cyclin D1 on B[a]P-induced changes of cell cycle were similar to those of vitamin C alone or antisense cyclin D1 alone.

CONCLUSIONSB[a]P progressed HELF cells from G1 to S phase via intracellular signaling pathway of cyclin D1/E2F. Vitamin C may modulate this signaling pathway to protect cells from injury caused by B[a]P.

Ascorbic Acid ; pharmacology ; Benzo(a)pyrene ; Blotting, Western ; methods ; Cell Cycle ; drug effects ; physiology ; Cells, Cultured ; Cyclin D1 ; metabolism ; Cyclin-Dependent Kinase 4 ; metabolism ; Dose-Response Relationship, Drug ; E2F1 Transcription Factor ; metabolism ; Fibroblasts ; cytology ; drug effects ; metabolism ; G1 Phase ; drug effects ; physiology ; Humans ; Lung ; cytology ; embryology ; RNA, Antisense ; genetics ; S Phase ; drug effects ; physiology ; Transfection ; methods