The six parameters, root iength、 crown Length、 crown width、 neck width 、 crown thickness and neck thickness,of 508 front teeth from the adult of Liaoning Han nationality were measured with automatic vernier calipers. The measurement values were obtained and compared with that values measured by Wang Huiuyn.

Objective To identify the transcriptional start site and clone a novel transcript variant of MYCT1(Myc target 1)for further study of its structure and function. Methods Transcriptional start site was confirmed using MYCT1 conserved sequence by 5′-RACE method and a novel MYCT1 isoform was cloned by splicing with 3′-RACE PCR product. Then,the cDNA or amino acid sequence between MYCT1 and its isoform was compared using bioinformatics server. Finally,the expression profile of this novel transcript in different cell lines was detected through RT-PCR. Re-sults A 1 106 bp transcript named MYCT1-TV(Myc target 1 transcript variant 1)was successfully cloned,and its transcriptional start site was confirmed which located at 140 bp upstream of the ATG start codon of MYCT1-TV. MYCT1-TV shows no obviously structural difference with MYCT1 and is widely expressed in various cell lines. Conclusion The transcriptional start site analysis and MYCT1-TV cloning provide an experi-mental basis for the further exploration and understanding of the function and the transcriptional regulation mechanism of MYCT1.

Objective To explore the effect of miR-24-2 on the in vitro proliferation of U-2OS cells. Methods U-2OS cells were randomly allocat-ed into 4 groups:miR-24-2 mimic group,miR-24-2 inhibitor group,negative control group,and normal control group. MicroRNAs were transfected into U-2OS cells using Lipofectamine?2000. miR-24-2 expression level and the proliferation of U-2OS cells after transfection were detected by real-time quantitative RT-PCR(RT-qPCR)and MTT proliferation assays,respectively. Results RT-qPCR results showed that miR-24-2 level was sig-nificantly higher in the miR-24-2 mimic group and lower in the miR-24-2 inhibitor group than those in the controls,indicating the successive trans-fection. MTT proliferation assay results proved that the cell viability was significantly lower in the U-2OS cells transfected with miR-24-2 mimic and higher in inhibitor groups compared to the control. Conclusion MiR-24-2 inhibits growth of the U-2OS cells,which could be a potential biomarker in the treatment of osteosarcoma.

Objective:Our aim was to study the relationship between factor v Leiden (FⅤL) mutation and Chinese Budd-Chiari syndrome (BCS). Methods:Twenty-nine BCS patients (25 patients with sporadic BCS,4 with familial BCS ),29 healthy persons were detected for FⅤL mutation with PCR-RFLP.Results: FⅤL mutation was detected in 3 of 4 patients with familial BCS. Two patients in A family and one patient in B family had FⅤL mutation. The mutation was heterozygous. The mutation frequency was 0.0517 in 29 pationts with BCS, 0.3750 in 4 with familial BCS.The frequency of FⅤL mutation in patients and healthy persons showed no statistical difference,but frequency of FⅤL mutation between patients with familial BCS and healthy persons showed significant difference.Conclusion:The FⅤL mutation was related to Chinese familial BCS, but not related to Chinese BCS.

Objective To explore miR-362-3 p expression in laryngeal cancer tissues and its effect on migration of Hep2 cells. Methods miR-362-3 p expression in 50 pairs of tumor and adjacent normal tissues was detected by real-time PCR after sample collection. The relationships between miR-362-3 p expression and clinical pathological characteristics in patients with laryngeal cancer were analyzed.mi R-362-3 p mimic, inhibitor, and control microRNA were transfected into Hep-2 cells. Transfection efficiency was determined by real-time PCR. Wound-healing and transwell assays were used to evaluate Hep-2 migration. Results miR-362-3 p expression was significantly higher in cancer tissues than in adjacent normal tissues (P ＜ 0.05). miR-362-3 p expression was statistically significantly related to node metastasis and clinical stage. Transfection with miR-362-3 p mimic and inhibitor significantly increased and decreased Hep-2 cell migration, respectively (both P ＜ 0.05). Conclusion miR-362-3 p is up-regulated in laryngeal cancer tissues and promotes laryngeal cancer cell migration, suggesting that it acts as a potential oncogene in laryngeal cancer.

OBJECTIVETo investigate the role of transglutaminase 3 (TGM3) gene in laryngeal carcinogenesis.

METHODSThe authors detected the deletion indirectly through loss of heterozygosity (LOH) analysis at DNA level using 4 STR primers within and near TGM3 gene in 72 cases, and detected the differential expression of TGM3 gene in 8 cases of paired normal and cancerous tissue of laryngeal carcinoma by Northern blot.

RESULTSLOH was found existing in all of the microsatellite loci, and the LOH frequencies were 25.76%, 20.00%, 38.10% and 18.75% at D20S17, D20S607, D20S99 and D20S841 respectively; LOH concerning at least one polymorphism locus accounted for 61.11%. No correlation of clinical stage, lymph node metastasis and differentiation with the LOH of TGM3 gene was observed, P>0.05. TGM3 gene expressed significantly higher in normal tissues than in paired cancerous tissues.

CONCLUSIONTGM3 gene might play an important role in laryngeal carcinogenesis and further researches will be needed to clarify the possible mechanisms.

Blotting, Northern ; Calcium-Binding Proteins ; genetics ; DNA, Neoplasm ; genetics ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Humans ; Laryngeal Neoplasms ; enzymology ; genetics ; Loss of Heterozygosity ; Microsatellite Repeats ; RNA, Neoplasm ; genetics ; metabolism ; Transglutaminases ; genetics