To evaluate species specificity of 20 STRs loci used in our lab. Human DNA and 10 different kinds of common animals' DNA were amplified separately. The PCR products were analysed with PAGE. There are amplified products in DYS388, DYS389, DYS390, D7S809, D13S631 loci of human 'DNA, but not of 10 different kinds of animal DNA tested. There were amplified products in TH01, vWA, AR, CD4, FABP loci for human and animals' DNA, but the lengths of amplified fragment were distinctly different between human and animals. There were products of FES, D12S391, CSF1PO, D19S253, D21S11, FGA, DYS19 loci for human and animals DNA, but the product lengths were not different between human and animals. There were PCR products in SE33 and D11S554 loci for human and animals, their amplified fragment lengths were within the same electrophoretic field. 10 STR loci, such as TH01 etc, were highly specific for human being and the amplified fragments lengths of 8 STR loci, such as FES etc, were different between human and animal tested.

To establish a calculation method of paternity probability in cases of absence of mother. Calculating the accumulated non-father exclusion probability of multiple polymorphic DNA loci was performed. The results showed that in cases of inheritance with Mendelian Law, through testing 8 or more polymorphic DNA loci, the paternity probability may reach 0. 9990 or more. In cases of paternity exclusion, exclusion 3 or more than 3 loci were required. For the purpose of identifying paternity in cases of absence of mother, more than 8 polymorphic DNA loci must be tested. The paternity probability must be more than 0. 9990 in cases of paternity inclusion and in cases of paternity exclusion, 3 or more loci of exclusion is needed.

Since the HLA system is one of the most complex human genetic polym- orphisms,its application in forensic medicine included disputed paternity and criminal identification,have been fairly recognized. The present paper reported the results of our study about the HLA typing in human blood stain,serum and saliva,it was concluded that:(1).The existed strong anti-complementary activity in human blood stain when the amount of complement used in microlym-phocytotoxicity inhibition test(MLIT) was incresed to 10?l,it was found that the results of HLA-All,-B 5 typing in bloodstains were all correct,and the detectable period was at least 90 days; (2).The soluble HLA-A antigens in human serum could reliable detected with MLIT;(3).The soluble HLA-A antigens were also present in the human siliva.

The phenotype distribution of human red cell glyoxalase I of a Han population in Guangzhou area was studied using mixed starch/agarose gel electrophoresis. The phenotype frequencies were: GLOI 1-1 2.57％; GLOI 2-1 29.17％; and GLOI 2-2 68.26％. The gene frequencies were: GLOI~1 0.1716; GLOI~2 0,8284. The phenotyping of GLOI was carried out satisfactorily in 35 bloodstains kept in room temperature for 20 days in 7 bloodstains stored in 4℃ for 105 days exposed in sunshine for 8 hours, as well as kept outdoor overnight, and in 10 putrefactive bloodstains kept in room temperature for 9 days.The GLOI were destroyed in 6 of 7 bloodstains washed by runing water for 2 hours.

Objective To define the correlation between nasopharyngeal carcinoma (NPC) cell radiosensitivity and gene mutation in the ATM/PI3K coding region. Methods The gene mutation in the ATM/PI3K region of nasopharyngeal carcinoma cell lines which vary in radiosensitivity,was monitored by reverse transcription polymerase chain reaction (RT PCR) and fluorescence marked ddNTP cycle sequencing technique.Results No gene mutation was detected in the ATM/PI3K region of either CNE1 or CNE2.Conclusion Disparity in intrinsic radiosensitivity between different NPC cell lines depends on some other factors and mechanism without being related to ATM/PI3K mutations.

Objective To investigate temporal expression of estrogen receptor (ER) in myocardium at non-infarct zone after acute myocardial infarction (AMI) in rats. Methods 120 healthy, male SD rats were randomly divided into three groups: control group, left anterior descending coronary artery (LAD) occlusion group and sham operation group with 8 rats in each group. The murine AMI-model was established by LAD ligation after anesthetization, and the rats in both LAD occlusion group and sham operation group were sacrificed at 2h, 4h, 8h, 12h, 1d, 2d, 4d, and 9d after occlusion. Myocardial samples were collected. H.E and ER immunohistochemical staining were performed. The results were quantitatively evaluated by image analysis system. The data were statistically analyzed with SPSS for Windows. Results ER expression in non-ischemic cardiomyocytes after LAD occlusion became more prominent with extension of LAD occlusion period. There was no significant difference within 12h after AMI, while ER expression was enhanced significantly 24h after ischemia. The enhancement were more evident from 4 to 9 days. Conclusion The results suggested that protective role may be initiated in response to acute ischemia in cardiac cells at non-infarct zone by increased ER expression after LAD occlusion in rats.

Objective To evaluate the cause which leads to the allelic dropouts at D8S1179 locus while performing paternity testing with the AmpFlSTR Profiler Plus kit. Methods A singleplex amplification system for D8S1179 locus (GenBank Accession No. G08710) was used to verify the typing results by using the AmpFlSTR?Profiler plus kit. Dropout alleles were then sequenced. Results G to A transition was identified at the position of the 147th base of the GenBank sequence. The frequency of the G to A transition among the Chinese population was 0.50 X 10"2 (10 out of 2013 unrelated individuals). Conclusion The G to A transition may be located at the binding site of one of the primers of the AmpFlSTR?Profiler Plus kit. It is suggested that the G to A transition might be the cause of the allelic dropout at the D8S1179 locus.

Objective To evaluate the power of the PowerPlex?6 system for paternity testing. Method 633 cases of paternity testing were studied. After the megaplex STR amplification, the PCR products were genotyped by using the ABI377 DNA Sequencer. Results Among the 879 unrelated individuals, 197 alleles and 739 different genotypes were observed. The cumulated discriminating power was 1x 10-30. And the cumulative chance of exclusion was 0.999999999999987. 95 out of 633 cases were excluded. The RCP of all unexcluded cases were ≥0.9990. Gene mutations were found in 19 cases. Conclusion The Po-werPlex?16 system is powerful and reliable for paternity testing.

Objective: To explore the mechanism of orindonin induced apoptosis on NB4 (Human acute promylocytic leukeamia cell line) cells. Methods: The variation of both morphology and inhibitory rate of NB4 cells were observed in culture medium with various concentrations of orindonin at different time in vitro. The activity of Caspase3 was detected before and after apoptosis occurred. Results: orindonin could increase the activity of Caspase3, inhibit the growth and cause apoptosis on NB4 cells significantly. The variations were both in time and dose dependent manner. Conclusion: Orindonin can inhibit the growth of NB4 cells and induce apoptosis. Increasing the activity of Caspase3 may be one of the most important mechanism.

Objective: To investigate the apoptotic effects and its mechanisms on K562 cells caused by Interferon-alpha (INF-?) and Cytarabine (Ara-C). Methods: The variation of both morphology and inhibitory rate of K562 cells was observed in culture medium with IFN-? and various concentrations of Ara-C at different time in vitro. The variation of telomerase activity and P53 protein expression were detected before and after apoptosis occurred. Results: INF-? and Ara-C used concurrently could cause apoptosis and inhibit the growth of K562 cells as well as decrease the telomerase activity and increase P53 protein expression significantly. All these processes showed both in time- and dose-dependent manner. Conclusions: INF-? and Ara-C used concurrently can inhibit the growth of K562 cells and induce apoptosis, inhibiting the telomerase activity and increasing the expression of P53 protein may be one of the most important mechanisms.