Objective To investigate occupational exposure among health care workers (HCWs)in a tertiary comprehen-sive hospital,and analyze the causes and preventive measures of occupational exposure.Methods 134 cases of occupational exposure among HCWs in a hospital from January 2010 to December 2013 were analyzed.Results Of HCWs sustained oc-cupational exposure,doctors,nurses,and technicians accounted for 59.70%,19.40%,and 9.70% respectively.The main cause for occupational exposure was non-standardized management of the sharps (46.27%,n=62),followed by unex-pected operation(42.54%,n=57)and inadequate protective measures (11.19%,n=15);The main exposure mode was sharp injury(94.78%,n=127),mucosal exposure accounted for 5.22% (n= 7);42.54% of exposure sources were not clear,57.46% of exposure sources were clear,35.82%,12.69%,3.73%,and 2.24% of which were hepatitis B virus (HBV),hepatitis C virus(HCV),Treponema pallidum(TP),and human immunodeficiency virus(HIV);2.24%(n=3)of exposure sources were co-infection of HBV and HCV;0.74% (n = 1 )was co-infection of HIV,HBV,HCV,and TP. 95.52%of occupational exposures were treated correctly.Conclusion The high-risk population for occupational exposure are nurses,standard occupational precautions and management of the sharps can reduce the occurrence of occupational expo-sure among HCWs.

A Review] The oncogene expression and growth of leukemic cells could be inhibited by antisense oligonucleotide. The selection of target genes is the key step in the research of antisense oligonucleotide on leukemia. The article would review the status and prospect of some target genes of leukemia in the investigation of antisense oligonucleotide.

AIM: To investigate whether antisense oligodeoxynucleotides of hTERT?bcl-2 and c-myc could enhance the sensitivity of leukemia cell K562 to cisplatin. METHODS: The inhibiting effects of cisplatin and cisplatin plus antisense oligodeoxynucleotide on K562 cells were determined by MTT. RESULTS: The inhibiting rate of 20 ?mol/L cisplatin to K562 cell is 17.17%?1.36% and it becomes 25.41%?1.77% ,26.18%?1.43% and 28.29%?1、05%, respectively, as combinated with antisense oligodeoxynucleotide of hTERT?bcl-2 or c-myc. CONCLUSION: These results indicated that antisense oligodeoxynucleotides of hTERT?bcl-2 and c-myc enhanced efficacy of cisplatin in K562 leukemic cells.

AIM: To observe the effect of antisense oligodeoxynucleotide of human telomerase reverse transcriptase(hTERT) on the telomerase activity in Jurkat cells and its mechanism. METHODS: The telomerase activity was detected by TRAP. hTERT protein and mRNA expressions were detected by flowcytometry and RT-PCR. RESULTS: The absorbency of the cells ( A values) was used to represent the telomerase activity. At 48 h and 72 h, the A values of the Jurkat cells treated with antisense oligodeoxynucleotide of hTERT decreased to 0.351?0.051 and 0.238?0.024, respectively, compared to the A value of 0.492?0.051 in the control cells without treatment ( P

AIM: To explore whether human telomerase reverse transcriptase (hTERT) antisense oligodeoxynucleotide (ASODN) could enhance the sensitivity of acute lymphoblastic leukemia cells from relapse patients to cisplatin. METHODS: The expression levels of hTERT protein were detected by immunofluorescence using fluorescence isothiocyanate (FITC), the number of viable cells was determined using the trypan blue dye exclusion assay, and apoptosis was detected by morphological observation and flow cytometric cell cycle analysis. RESULTS: The expression of hTERT protein was inhibited after treatment with hTERT ASODN. Treatment with cisplatin combined with hTERT ASODN had significantly reduced the number of viable acute lymphoblastic leukemic (ALL) cells (P<0.05). In morphological observation of apoptotic cells using Hoechst33258 and PI double staining techniques, cells displayed classic apoptotic changes in the presence of cisplatin or cisplatin combined with hTERT ASODN or ASODN at 48 h. Apoptotic rates of cells treated with cisplatin and ASODN were higher than that of cells treated with cisplatin alone (P<0.05). CONCLUSION: hTERT ASODN could increase sensitivity of cultured primary acute lymphoblastic leukemia cells from relapse patients to cisplatin.

The energy cost of the daily major activities, the basal metabolic rates (BMR), resting metabolic rates (RMR) and total energy expenditure of university students per day under normal conditions were determined respectively by Douglas' method. The average BMR of male and female subjects were 2.80?0.14 and 2.74?0.13 kJ.m-2min-1. (0.669 and 0.656 kcal?m~2?min-1) respectively. The total energy expenditure per day of male students was 11.32 MJ, and of female students 9.92 MJ per day. The energy cost of different activity can be used as the basic data in studies of energy metabolism.

AIM: To explore the effect of human telomerase reverse transcriptase (hTERT) gene antisense phosphorothioate oligodeoxynucleotide (AS PS-ODN) on cisplatin-induced apoptosis in cultured primary acute lymphoblastic leukemia (ALL) cells. METHODS: The expression levels of hTERT protein were detected by immunofluorescence using fluoresce isothiocyanate (FITC) lable. Cell surviving fraction was determined using the trypan blue dye exclusion assay. Apoptosis was detected by morphological observation and flow cytomertric cell cycle analysis. RESULTS: The expression of hTERT protein was inhibited after treated by hTERT AS PS-ODN. Treatment with cisplatin after 24 h of exposure to AS PS-ODN had significantly reduced the number of viable ALL cells. However,there was no difference on ALL cells survival between sense oligodeoxynucleotide (S PS-ODN) /CDDP combination and CDDP-treated cells alone. In morphological observation of apoptotic cells using Hoechst 33258 and PI double staining techniques,cells displayed classic apoptotic changes treated with CDDP or CDDP combined with hTERT AS PS-ODN or S PS-ODN at 48 h. Apoptotic rates of cells added CDDP and AS PS-ODN were higher than that of cells added CDDP only ( P 0.05). CONCLUSION: hTERT AS PS-ODN inhibited the expression of hTERT protein and increased the CDDP-induced apoptosis in primer acute lymphoblastic leukemic cells.

AIM: To explore the effect of hTERT antisense phosphorothioate oligodeoxynucleotide (ASODN) on apoptosis induced by chemotherapeutic drugs in Jurkat cell lines. METHODS: Cell viability was determined using the trypan blue dye exclusion assay. Apoptosis was detected by morphological observation, DNA gel electrophoresis and flow cytometry analysis. RESULTS: The survival rates of Jurkat cells cultured with daunorubicin, vincristin, and etoposide, respectively were similar with that cultured with those chemotherapic drugs plus hTERT ASODN. The survival rates of Jurkat cells cultured with cis-diamminedichicloroplatinum(DDP) added 24 hours later were higher than that cultured with hTERT ASODN and DDP added 24 hours later. The survival rates of Jurkat cells cultured with DDP were similar with that cultured with hTERT SODN and DDP. In morphological observation of apoptotic cells using Giemsa staining, cells displayed classic apoptotic changes treated with DDP or DDP combined with hTERT ASODN or SODN at 48 hours. Agarose gel electrophoresis of genomic DNA from Jurkat cells treated with ASODN and DDP combination for 48 hours showed typical DNA “ladder”. Neither the DNA from Jurkat cells treated with SODN plus DDP nor the DNA from the cells treated with DDP alone showed ladder pattern. Apoptosis rates of Jurkat cells treated with DDP for 48 hours after 24 hours of exposure to ASODN significantly increased. There was significant difference in the percentage of apoptotic Jurkat cells between hTERT ASODN plus DDP and SODN plus DDP or DDP alone, respectively. CONCLUSION: The hTERT ASODN complementary to the translation initiation region of hTERT mRNA enhanced DDP-induced apoptosis in Jurkat cells.

AIM: To explore the effect of hTERT gene antisense phosphorothioate oligodeoxynucleotide (ASODN) on telomerase activity in Raji cells. METHODS: Polymerase chain reaction enzyme-linked immuonassay (PCR-ELISA) was used to determine telomerase activity. The expression levels of hTERT mRNA and protein were assayed by reverse transcriptase polymerase chain reaction (RT-PCR) and immunofluorescence using fluoresce isothiocyanate (FITC) label,respectively. RESULTS: RT-PCR and immunofluorescence assay showed that the expression levels of hTERT mRNA and protein from Raji cells decreased with time after hTERT ASODN treatment. There was no difference in hTERT mRNA and protein levels between control and SODN-treated cells. Telomerase activity decreased when Raji cells were treated with ASODN for 48 h. Telomerase activity of Raji cells was significantly inhibited when treated with ASODN for 72 h. There was no difference in telomerase activity levels between control and hTERT SODN-treated cells. CONCLUSION: hTERT ASODN could inhibit telomerase activity in Raji cells.

AIM: To explore the effect of human telomerase reverse transcriptase (hTERT) gene antisense oligodeoxynucleotide (ASODN) on chemotherapeutic durges-induced apoptosis in CEM cells. METHODS: Cell viability was determined by trypan blue dye exclusion assay. Apoptosis was detected by morphological observation and flow cytomertric cell cycle analysis. RESULTS: The survival rates of CEM cells cultured with daunorubicin, vincristin and (etoposide) respectively were similar with that cultured with those chemotherapic durgs plus hTERT ASODN. The survival rates of CEM cells cultured with cis-diamminedichicloroplatinum (DDP) added 24 h later were higher than that cultured with hTERT ASODN and DDP added 24 h later. The survival rates of CEM cells cultured with DDP were similar with that cultured with hTERT SOND and DDP. In morphological observation of apoptotic cells using Giemsa staining, cells treated with DDP or DDP combined with hTERT ASODN ro SODN at 48 h, displayed classic apoptotic changes. Apoptosis rates of CEM cells treated with DDP for 48 h after 24 h of exposure to ASODN significantly increased. There was significant difference in the percentage of apoptotic cells of CEM cells between hTERT ASODN plus DDP and SODN plus DDP or DDP alone, respectively. CONCLUSION: hTERT ASODN enhances DDP-induced apoptosis of CEM cells.