Objective To establish a database for models of teeth, which could provide a new technology for personal identification based upon teeth and bite mark for forensic medical practice. Method The (X, Y) digital coordinates were established based up on materials concerning shape and arrangement of the teeth by analyzing samples of 400 models of teeth. The position of every tooth's key point corresponding to the origin was obtained, thus, the characters of tooth and dental arch could be calculated rapidly according to Borland C ++ 5.0 computer language under DOS system. Results The models of teeth could be identified automatically. Among the correlative precision indexes, the length was 1.3mm, the angle was 3?. It seems reasonable to select 12-14 teeth points for studying, which needed about 5-7 complete tooth marks. Conclusion This method is one of the bases in studying personal identification relating to tooth and bite mark.

Objective To discuss the condition in which ricochet bullet wound is formed, study its ballistic characters and ability to damage in the body, and establish features for the diagnosis of ricochet bullet wound. Method We shot four Yorkshire pigs by selecting No.54 pistol (made in China) and No.56 semiautomatic rifle with No.51 pistol bullet and No.56 rifle bullet, using quern stone as ricocheting target, copied 12 cases of ricochet bullet wound models and observed the characters of entrance wound, wound cavity and cartridge point. Results The formation of ricochet bullet lies with the properties of the target, the shape and velocity of the bullet, angle of incidence and angle of ricochet; the angle of ricochet formed by sharp bullet with high velocity is smaller than the angle by the round bullet with low velocity under the same circumstance; the wound does not produce an evident temporary cavity; six features for the diagnosis were established according to experimented results. Conclusion The correct diagnosis of ricochet bullet wound is of practical value to judging direction and distance of shot, trajectory reconstruction, analysing purpose of shot and evaluation of injury degree.

Objective To probe the mechanism of Warlker-256 cell apoptosis resulted from permanent and strong magnetic field. Method The amplification, rearrangement, deletion, transcription and expression of P53 were detected in 320 rats treated by magnetic field and 80 controls, using Dot Blot of DNA and RNA, Southern and Northern blot, and immunohistochemical technologies. Results P53 is wild type in Warlker-256 cells, no amplification, rearrangement and deletion were found in either magnetic treated group or control group. The transcription and expression of P53 is significantly enhanced in the treated group versus the control(P

Objective: To further explore TCE-induced hepatotoxicity and its mechanisms by identification of trichloroethylene (TCE) induced abnormal histone methylation in human liver cells. Methods: L-02 cells were treated with 0 and 8 mmol/L TCE for 24 h. Histones were extracted by acid. Liquid chromatography electrospray ionization tandem mass spectrometry (ESI-LC-MS/MS) were used to identify and quantify TCE related histone methylations. TCE induced abnormal methylation of H3K79 me2 and H3K79 me3 were validated by Western blot analysis. The further analysis of the function of histone abnormal methylation modifications were done by single cell gel electrophoresis (SCGE) and Western blot analysis of p53 and ɤH2AX. Results: After treatment with TCE for 24 h in L-02 cells, the 36 TCE related histone methylation sites in 28 peptide segments were identified by MS. After treatment with TCE in concentrations of 0 and 8.0 mmol/L in L-02 cells for 24 h, the relative expression level of histone H3K79 me3 were 1.00±0.06, 0.70±0.09 (t=15.01, P=0.015); the relative expression level of histone H3K79 me2 were 1.00±0.05, 0.74±0.07 (t=16.69, P=0.018); the Olive Tail Moment about DNA damage were 1.46±0.28, 3.12± 0.68 (t=15.22, P=0.018); the relative expression levels of p53 were 1.00±0.04, 1.24±0.04 (t=18.71, P= 0.012); and the relative expression levels of ɤH2AX were 1.00 ± 0.03, 1.56 ± 0.11 (t=8.32, P=0 045). Conclusion TCE can induce changes in the relative expression level of H3K79 me2 and H3K79 me3 in L-02 cell, and induce DNA damage, suggesting that TCE may induce changes in the relative expression level of H3K79 me2 and H3K79 me3 by DNA damage.