Clinical efficacy and safety of selective trans-cystic intra-operative cholangiography in primary suture following three-port laparoscopic common bile duct exploration / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Intra-operative cholangiography has been shown to be a sensitive and specific method of demonstrating bile duct stones. This study investigated the feasibility, safety, and clinical value of selective trans-cystic intra-operative cholangiography in primary suture following three-port laparoscopic common bile duct exploration, and identified the factors that positively predict the presence of common bile duct stones.</p><p><b>METHODS</b>From January 2008 to January 2011, 252 of 1013 patients undergoing laparoscopic cholecystectomy received selective trans-cystic intra-operative cholangiography and primary suture following three-port laparoscopic common bile duct exploration. Their clinical data were analyzed retrospectively.</p><p><b>RESULTS</b>All operations were successful and none was converted to open surgery. The intra-operative cholangiography time was (8.3 ± 2.5) minutes, and the operative duration was (105.4 ± 23.1) minutes. According to selective intra-operative cholangiography, the positive predictive values of current jaundice, small gallstones (< 0.5 cm) and dilated cystic duct (> 0.3 cm), dilated common bile duct (> 0.8 cm), history of jaundice or gallstone pancreatitis, abnormal liver function test, and preoperative demonstration of suspected common bile duct stones on imaging were 87%, 25%, 42%, 15%, 32%, and 75% for common bile duct stones, respectively. Patients with several factors suggestive of common bile duct stones yielded higher numbers of positive cholangiograms. Unexpected stones were found in 13 patients (5.2%) by intra-operative cholangiography. The post-operative hospital stay was (4.7 ± 2.2) days. Post-operative bile leakage occurred in two cases, and these patients recovered by simple drainage for 3 - 7 days without re-operation. Of the 761 patients who underwent laparoscopic cholecystectomy alone, 5 (0.7%) presented with a retained common bile duct stone requiring intervention. The median follow-up was 12 months, and only one patient who once suffered from bile leakage presented with obstructive jaundice due to bile duct stenosis 6 months postoperatively. The other patients recovered without any serious complications.</p><p><b>CONCLUSIONS</b>Selective intra-operative cholangiography yields acceptably high positive results. It is a safe, effective, and minimally invasive approach in patients with suspected choledocholithiasis and primary suture following three-port laparoscopic common bile duct exploration.</p>

Telomerase activity and telomerase reverse transcriptase expression induced by selenium in rat hepatocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of sodium selenite on telomerase activity, apoptosis and expression of TERT, c-myc and p53 in rat hepatocytes.</p><p><b>METHODS</b>Selenium at doses of 2.5, 5.0, and 10 micromol/kg was given to SD rats by gavage. In rat hepatocytes, telomerase activity was measured by the telomeric repeat amplification protocol (TRAP), apoptosis was detected by flow cytometry, and expressions of telomerase reverse transcriptase (TERT), c-myc and p53 were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). c-Myc and P53 proteins were detected by immunochemistry.</p><p><b>RESULTS</b>Selenium at doses of 2.5, 5.0, and 10 micromol/kg significantly increased hepatocellular telomerase activity and induced apoptosis in a dose-dependent manner. Although selenium at doses of 2.5, 5.0, and 10 micromol/kg displayed no obvious enhancing effect on the TERT mRNA expression in rat hepatocytes (P > 0.05), it significantly increased the c-myc mRNA and p53 mRNA expression at the dose of 10 micromol/kg (P < 0.05). Selenium at doses of 5.0 and 10 micromol/kg obviously increased the content of P53 protein in rat hepatocytes, but only at the dose of 10 micromol/kg, it significantly promoted the value of c-Myc protein in them.</p><p><b>CONCLUSION</b>Selenium can slightly increase telomerase activity and TERT expression, and significantly induce apoptosis and over-expression of c-myc and p53 at relatively high doses. The beneficial effects of selenium on senescence and aging may be mediated by telomerase activation and expression of TERT, c-myc, and p53 in rat hepatocytes.</p>

Construction of cell line of small hairpin RNA-mediated inhibition of HER2/neu gene expression / 中华预防医学杂志

<p><b>OBJECTIVE</b>To establish the stable inhibition of HER2/neu expression by vector-mediated small hairpin RNA in malignant transformed human bronchial epithelial cell line induced by anti-benzo(a)pyrene-trans-7, 8-dihydrodiol-9, 10-epoxide (anti-BPDE).</p><p><b>METHODS</b>The pSIREN-RetroQ-neu recombinant vector targeting HER2/neu was constructed and confirmed by restriction and sequencing analysis, then it was transfected into anti-BPDE malignant transformed 16HBE cells (16HBE-T) through lipofectamine 2000. The control groups included the 16HBE-T cells transfected with negative control vector (negative control) and 16HBE-T. The cells transfected with vectors were screened by puromycin. The HER2/neu mRNA and protein expressions in the vector-transfected 16HBE-T cells were detected by RT-PCR and Western blot method respectively.</p><p><b>RESULTS</b>The pSIREN-RetroQ-neu recombinant vector which inhibited HER2/neu mRNA and protein expressions in the 16HBE-T was constructed. The level of HER2/neu mRNA in the 16HBE-T cells transfected with pSIREN-RetroQ-neu was significantly reduced as compared to the negative control and blank control cells (0.114 +/- 0.003 vs.blank control 0.186 +/- 0.001, t = 39.154, P < 0.05; and negative control 0.182 +/- 0.015, t = 7.564, P < 0.05), while its level did not differ significantly between negative control cells and blank control of 16HBE-T (t = -0.409, P > 0.05). HER2/neu protein level in pSIREN-RetroQ-neu transfected cells was inhibited by 40% and 39% respectively.</p><p><b>CONCLUSION</b>Plasmid-based shRNA expression systems targeted against HER2/neu gene were generated successfully, which resulted in down-regulation of HER2/neu gene expression in the 16HBE-T efficiently.</p>

Cyto-genotoxicity induced by 2, 2', 4, 4'-tetrabromodiphenyl ethers combined with 2, 2', 4, 4', 5-hexachlorobiphenyl treatment in SH-SY5Y cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the cyto-genotoxicity of 2, 2', 4, 4'-tetrabromodiphenyl ethers (PBDE-47) combined with 2, 2', 4, 4', 5-hexachlorobiphenyl (PCB153) treatment in SH-SY5Y cells.</p><p><b>METHODS</b>Exponentially growing SH-SY5Y cells were exposed to different concentrations of PBDE-47 or/and PCB153 for 24 h in vitro. Cell viability, DNA damage, chromosome abnormalities, and DNA-protein crosslinks (DPC) were measured using MTT, comet assay, cytokinesis-block micronucleus (CBMN) test, and SDS-KCl assay respectively.</p><p><b>RESULTS</b>Compared to the each single PBDE-47 groups, the nuclear division index (NDI) was significantly lower (P < 0.05) and the frequencies of micronuclei (MNI), percentage of DNA in the tail, Olive tail moment and DPC were significantly increased (P < 0.05) in the PBDE-47 combined with PCB153 groups. There was a statistical decrease in cell viability in groups of 4 micromol/L PBDE-47 and above combined with PCB153 than that in contrast to the same dose of PBDE-47 group or PCB153 alone (P < 0.05). Significant increase was found in MNI frequency and DPC in 2 micromol/L PBDE-47 and above combined with PCB153 than those in the single PCB153 group (P < 0.05). In the groups of 4 micromol/L PBDE-47 and above combined with PCB153, the cell NDI were significantly lower than that of the single PCB153 group (P < 0.05). Compared to the single PCB153 group, the percentage of DNA in the tail and Olive tail moment was significantly increased in the 8 micromol/L PBDE-47 combined with 5 micromol/L PCB153. Factorial analysis showed that interactions between PBDE-47 and PCB153 existed in inhibiting cell viability, inducing DNA damage, MNI, and DPC formation (P < 0.01), and possessing synergistic effects.</p><p><b>CONCLUSION</b>Some dose of PBDE-47 combined with PCB153 can inhibit cell viability, induce DNA damage, DPC formation, and chromosome abnormalities. The pattern of the combined effect is synergistic in cyto-genotoxicity.</p>

Effects of PBDE-47 on oxidative stress and apoptosis in SH-SY5Y cell / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the oxidative stress and apoptosis induced by 2, 2', 4, 4'-polybrominated diphenyl ethers (PBDE-47) in human neuroblastoma SH-SY5Y cells, and to explore the involved role of reactive oxygen species (ROS) on apoptosis.</p><p><b>METHODS</b>The rate of cellular survivors, intracellular ROS level, malondialdehyde (MDA) content and percentage of apoptosis were measured respectively after the SH-SY5Y cell were exposed to 2, 4, 8 microg/ml PBDE-47 for 24 h in vitro.</p><p><b>RESULTS</b>The rate of cellular survivors in the low dose PBDE-47-treated group was higher than the control group (P < 0.05), but the moderate and high dose PBDE-47-treated groups were significantly lower than the control group (P < 0.05). The MDA contents in the moderate and high dose PBDE-47-treated groups were significantly higher than the control group (P < 0.05) and increased with increase of PBDE-47 exposure concentrations. Compared with the control group, the levels of ROS were significantly increased with increase of PBDE-47 concentrations (P < 0.05). In the moderate and high dose PBDE-47-treated groups, the percentages of apoptosis were significantly higher than that of the control group (P < 0.05).</p><p><b>CONCLUSION</b>PBDE-47 can induce oxidative stress and apoptosis in SH-SY5Y cell. ROS may play an important role in the apoptosis induced by PBDE-47.</p>

HLA-DM polymorphism and risk of trichloroethylene induced medicamentosa-like dermatitis / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To establish the association between genetic polymorphisms of HLA-DMA and HLA-DMB and risk of developing trichloroethylene-induced medicamentosa-like dermatitis (TIMLD).</p><p><b>METHODS</b>Sixty-one cases were medically confirmed to have been affected with TIMLD and 60 controls were selected from exposed workers who were free from TIMLD. The TIMLD cases and controls were similar in terms of age, sex, and duration of exposure. DNA was extracted both from the TIMLD cases and controls, HLA-DMA and HLA-DMB loci were amplified by using Touchdown PCR, and the alleles and genotypes were confirmed by restriction fragment length polymorphism (RFLP) and direct sequencing. Finally, the frequencies of HLA-DMA and HLA-DMB variants were compared between the two groups.</p><p><b>RESULTS</b>The results showed that the frequency of HLA-DMA*0101 and HLA-DMB*0103 alleles was significantly increased in TIMLD patients than in controls (71.3% vs. 55.0% for HLA-DMA*0101; P<0.05) (11.5% vs. 3.3% for HLA-DMB*0103; P<0.05). In addition, the frequency of HLA-DMA*0102-*0102 homozygous genotype was also significantly higher in the controls than in the patients (25.0% vs. 8.2%, P<0.05), whereas the frequency of heterozygous HLA-DMB *0101-*0102 genotype was lower in the patients in comparison with the controls. Conclusion The polymorphisms of HLA-DM may be associated with the susceptibility to TIMLD.</p>

Effects of cadmium on hepatocellular DNA damage, proto-oncogene expression and apoptosis in rats / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the effects of cadmium on hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.</p><p><b>METHODS</b>Cadmium chloride at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by single cell gel electrophoresis (or comet assay), while expression of proto-oncogenes c-myc, c-fos, and c-jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc, c-Fos, and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry.</p><p><b>RESULTS</b>At the doses of 5, 10, and 20 micromol/kg, cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%, 88.40%, and 93.80%, respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the dose of cadmium chloride (r = 0.9172, P < 0.01). Cadmium chloride at the doses of 5, 10, and 20 micromol/kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun. The positive brown-yellow signal for c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rat livers. Apoptotic rates (%) of cadmium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (17.24 +/- 2.98), (20.58 +/- 1.35), and (24.06 +/- 1.77) respectively, being significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride (r = 0.8619, P < 0.05).</p><p><b>CONCLUSION</b>Cadmium at 5-20 micromol/kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.</p>

Inhibitory effects of selenium on telomerase activity and hTERT expression in cadmium-transformed 16HBE cells / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of sodium selenite on telomerase activity and expression of hTERT mRNA in cadmium-transformed 16HBE cells.</p><p><b>METHODS</b>Telomerase activity and expression of genes were measured after cultured cadmium-transformed 16HBE cells were exposed to sodium selenite at different doses (0.625, 1.25, 2.50, 5.00 micromol/L) for 24 hours.</p><p><b>RESULTS</b>Selenium decreased telomerase activity in cadmium-transformed 16HBE cells. There existed an obvious dose-effect relationship between the selenium concentration and these changes. The expression of hTERT and c-myc mRNA also decreased but the expression of mad1 mRNA increased after exposure to selenium for 24 hours. No difference was found in expression of hTRF1 and hTRF2 mRNA after incubated with sodium selenite for 24 hours, compared with control group.</p><p><b>CONCLUSION</b>Selenium inhibits telomerase activity by decreasing hTERT and c-myc mRNA expression and increasing mad1 mRNA expression in cadmium-transformed 16HBE cells and selenium concentration is significantly correlated with these changes.</p>

Effects of selenium on expression of TERT, c-Myc and p53 induced by cadmium in rat liver / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effects of sodium selenite on expression of telomerase reverse transcriptase mRNA, c-Myc and p53 induced by cadmium chloride in rat liver.</p><p><b>METHODS</b>Male SD rats were divided randomly into 6 groups, each group had 5 animals. The groups comprised the control group, Se group (5 micromol/kg sodium selenite), 5 micromol/kg cadmium chloride group, 10 micromol/kg cadmium chloride group, Se (5 micromol/kg sodium selenite) + 5 micromol/kg cadmium chloride group, Se (5 micromol/kg sodium selenite) + 10 micromol/kg cadmium chloride group. After 48 hours of the first injection, the expression of TERT mRNA was measured with RT-PCR and c-Myc, and p53 proteins were measured by immunohistochemistry method.</p><p><b>RESULTS</b>Compared with control group, the expression of TERT was increased in 5 micromol/kg Cd group and 10 micromol/kg Cd group, c-Myc protein was increased in 10 micromol/kg Cd group, and the expression of p53 protein was increased in 5 micromol/kg group and 10 micromol/kg Cd group. TERT expression in Se + 10 micromol/kg Cd group was lower than that of 10 micromol/kg Cd group significantly. c-Myc protein was decreased in Se + 10 micromol/kg Cd group compared with 10 micromol/kg Cd group. p53 protein of Se + 5 micromol/kg Cd group and Se + 10 micromol/kg Cd group were decreased significantly compared with 5 micromol/kg Cd group and 10 micromol/kg Cd group respectively.</p><p><b>CONCLUSION</b>The cadmium at the doses of between 5 and 10 micromol/kg can activate TERT and up-regulate c-Myc and p53 proteins. The selenium at the dose of 5 micromol/kg has the antagonistic effect on expression of TERT, c-Myc and p53 induced by cadmium in rat liver.</p>

Relationship of trichloroethylene-induced medicamentosa like dermatitis to HLA-DMA and HLA-DMB / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the susceptibility of trichloroethylene-induced medicamentosa like dermatitis by comparing the frequency of HLA-DMA and HLA-DMB in patients with trichloroethylene-induced medicamentosa like dermatitis and in normal controls.</p><p><b>METHODS</b>The DNA of lymphocytes in 61 patients with trichloroethylene-induced medicamentosa like dermatitis and in 60 people as the normal control were abstracted by using touchdown PCR amplification of HLA-DMA and HLA-DMB. Then through restriction fragment length polymorphism (RFLP) and sequence base typing, the alleles and genotypes were confirmed. The frequency of HLA-DMA and HLA-DMB in the two groups was compared.</p><p><b>RESULTS</b>The HLA-DMA*0101 allele frequency in patients with trichloroethylene-induced medicamentosa like dermatitis was significantly higher than in the control group (71.3% vs 55.0%, P < 0.05). The allele frequency of HLA-DMA*0103 was significantly higher in the patient group than in the control group (11.5% vs 3.3%, P < 0.05). The ratio of *0102 homozygotes of HLA-DMA*0102 in the patient group was significantly higher than in the control group (25.0% vs 8.2%, P < 0.05). The ratio of *0102 heterozygotes of HLA-DMB*0101 in the patient group was lower than in the control group (P < 0.05).</p><p><b>CONCLUSION</b>The polymorphisms of DMA may be related to the susceptibility of the patients with trichloroethylene-induced medicamentosa like dermatitis.</p>

Effects of selenium and zinc on renal oxidative stress and apoptosis induced by fluoride in rats / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride.</p><p><b>METHODS</b>Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals (four males and four females). Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation (0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4 x 7H2O); and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation (0.2 mg/kg Na2 SeO3 and 29.6 mg/kg ZnSO4 x 7H2O). The activities of serum glutathione peroxidase (GSH-Px), kidney superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and glutathione (GSH) in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry.</p><p><b>RESULTS</b>NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urine gamma-glutamyl transpeptidase (gamma-GT), inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosis, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly.</p><p><b>CONCLUSION</b>Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.</p>

Abnormal expression of eukaryotic translation factors in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the oncogenic potential of mouse translation initiation factor 3 (TIF3) and elongation factor-1delta (TEF-1delta) in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide (NiS).</p><p><b>METHODS</b>Abnormal expressions of human TIF3 and TEF-1delta genes in two kinds of NiS-transformed cells and NiS-tumorigenic cell lines were investigated and analyzed by the reverse transcript polymerase chain reaction (RT-PCR) and fluorescent quantitative polymerase chain reaction (FQ-PCR), respectively.</p><p><b>RESULTS</b>RT-PCR analysis primarily showed that both human TIF3 and TEF-1delta mRNA expressions in two kinds of NiS-transformed cells and NiS-tumorigenic cell lines were increased as compared with controls. FQ-PCR assay showed that the levels of TIF3 expressions in the transformed cells and tumorigenic cells were 3 and 4 times higher respectively, and the elevated expressions of TEF-1delta cDNA copies were 2.7- to 3.5-fold in transformed cells and 4.1- to 5.2-fold in tumorigenic cells when compared with non-transformed cells, indicating that the over-expressions of human TIF3 and TEF-1delta genes were related to malignant degree of the cells induced by nickel.</p><p><b>CONCLUSIONS</b>These findings demonstrate that there are markedly abnormal expressions of TIF3 and TEF-1delta genes during malignant transformation of human bronchial epithelial cell lines induced by crystalline NiS. They seem to be the molecular mechanisms potentially responsible for human carcinogensis due to nickel.</p>

DNA damage, apoptosis and C-myc, C-fos, and C-jun overexpression induced by selenium in rat hepatocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes.</p><p><b>METHODS</b>Sodium selenite at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis (or comet assay). Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP nick end labelling) and flow cytometry. C-myc, c-fos, and c-jun expression in rat hepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method.</p><p><b>RESULTS</b>At the doses of 5, 10, and 20 micromol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite (r=0.9501, P<0.01). Sodium selenite at the doses of 5, 10, and 20 micromol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates (%) of selenium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (3.72 +/- 1.76), (5.82 +/- 1.42), and (11.76 +/- 1.87) respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite (r=0.9897, P<0.01), these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P<0.01.</p><p><b>CONCLUSION</b>Selenium at 5-20 micromol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.</p>

One stage thyroidectomy and bilateral neck dissection for well-differentiated thyroid carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the indications, safety and difficulties of one stage thyroidectomy and bilateral neck lymph node dissection for well-differentiated thyroid carcinoma.</p><p><b>METHODS</b>A retrospective review was carried out in 36 well-differentiated thyroid carcinoma patients so treated from 1990 to 2004. Various incisions including H, L and modified Kocher types were selected according to the location of primary tumor and status of cervical lymph node metastasis. Either total thyroidectomy or sub-total thyroidectomy combined with bilateral neck lymph node dissection according to the principles of modified radical neck lymph node dissection: preserving the internal jugular vein, spinal accessory nerve and sternocleidomastoid muscles.</p><p><b>RESULTS</b>There was no operative death in this group. Postoperative complications included: 2 wound bleeding, 3 recurrent laryngeal nerve resection due to tumor involvement, 1 recurrent laryngeal nerve injury, 2 unilateral internal branch of superior laryngeal nerve injury, 9 unilateral external branch of superior laryngeal nerve injury, 3 unilateral accessory nerve injury, 5 unilateral sympathetic nerve injury, 2 unilateral phrenic nerve injury, 6 chylus fistula, 13 temporary hypoparathyroidism, 2 permanent hypoparathyroidism. The dissected lymph nodes were found to be positive from 0 to 21 in each patient with a mean of 8.3. Of the 36 patients: 31 had bilateral positive lymph nodes; 3 unilateral positive; 2 bilateral negative lymph nodes. The follow up period ranged from 1 to 13 years, Three patients died of distant metastasis, 1 died of cerebral vascular accident. 7 patients lost in follow-up. Totally, 25 patients are still alive, 3 patients had local relapse and were surgically treated again.</p><p><b>CONCLUSION</b>The procedure of one-stage thyroidectomy and bilateral neck lymph node dissection for well-differentiated thyroid carcinoma is safe, as it is mandatory that at least one unilateral internal jugular vein should be preserved; one unilateral recurrent laryngeal nerves and accessory nerves should not be injured. Well-differentiated thyroid carcinoma patients whose bilateral cervical lymph nodes are clinically suspected to be positive (obviously enlarged, hard, purplish grapelike lymph node) or are confirmed pathologically to be positive are indications for one-stage thyroidectomy and bilateral neck lymph node dissection. Total or sub-total thyroidectomy should be undertaken with emphasis that at least one parathyroid with blood supply should be preserved. It is of utmost importance that not only the cancer be completely resected but the function of the organs be preserved.</p>

Over-expressed genes detected by suppression subtractive hybridization in carcinoma derived from transformed 16HBE cells induced by BPDE / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To screen the over differentially expressed genes in carcinoma induced by BPDE-transformed 16HBE cells (16HBE-C cells).</p><p><b>METHODS</b>The suppression subtractive hybridization (SSH) method was performed to profile differentially expressed genes between 16HBE-C cells and 16HBE cells. The cDNA fragments of differentially expressed genes were inserted into TA cloning vector and transformed competent E. coli strain. Positive clones were randomly picked up and identified by the colony PCR method. Dot blot was used to test the same source with the tester. The differentially expressed cDNA fragments were sequenced and compared with known genes and EST database in Genbank.</p><p><b>RESULTS</b>Eight known genes were over-expressed in 16HBE-C cells including eukaryotic translation elongation factor 1 alpha 1, HIF-1 responsive RTP801, ribosomal protein L10 (RPL10), ribosomal protein S29 (RPS29), mitochondrion related genes, and laminin receptor 1. Three differentially expressed cDNA fragments could not be matched to the known genes but to the EST database.</p><p><b>CONCLUSION</b>The SSH method can detect differentially expressed genes between 16HBE-C and 16HBE cells. BPDE-induced carcinogenesis may be related to alteration of at least eight known genes and three unknown genes. These expression data provide a clue to further cloning novel genes and studying functions in BPDE-induced carcinoma.</p>

Effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocyte L-02 cells.</p><p><b>METHODS</b>Lipid peroxide (LPO) level, reduced glutathione (GSH) content, DNA damage, apoptosis, and cell cycle analysis were measured after in vitro cultured L-02 cells were exposed to sodium fluoride at different doses (40 microg/mL, 80 microg/mL, and 160 microg/mL) for 24 hours.</p><p><b>RESULTS</b>Fluoride caused an increase of LPO levels and a decrease of GSH content in L-02 cells. There appeared to be an obvious dose-effect relationship between the fluoride concentration and the observed changes. Fluoride also caused DNA damage and apoptosis and increased the cell number in S phase of cell cycle in the cells tested. There was a statistically significant difference in DNA damage and apoptosis when comparing the high dose of fluoride treated cells with the low dose of fluoride treated cells.</p><p><b>CONCLUSION</b>Fluoride can cause lipid peroxidation, DNA damage, and apoptosis in the L-02 cell experimental model and there is a significant positive correlation between fluoride concentration and these pathological changes.</p>

Impact of low-level lead exposure on neural cell adhesion molecule expression of primarily cultured hippocampal neurons / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the impact of low-level lead exposure on neural cell adhesion molecule (NCAM) expression of primarily cultured hippocampal neurons.</p><p><b>METHODS</b>Wistar rats gestated at 18th day were anaesthetized and paunched to get the pups, the hippocampi of the pups were separated and the hippocampal neurons were primarily cultured. After co-cultivated with different dosage of PbCl(2), the NCAM expression of the neurons were tested with Western blotting at different culture time.</p><p><b>RESULTS</b>Normally, the expression of NCAM at the 1st culture day was very low and its integral obsorbency density was 14; the climax expression time of NCAM of the cultured hippocampal neurons was 3rd to 5th cultured day, and their integral obsorbency density were 2 542 to 2 580; henceforth, the NCAM expression declined. NCAM expression was inhibited significantly by lead during the 2nd to 4th cultured day, and dose-response relationship was observed. The inhibition of lead weakened along with the cultured time prolonged, at 5th cultured day, it disappeared, and the NCAM expression of 10(-2), 10(-3) and 10(-4) mmol/L groups even exceeded the control groups. After that, the expression of NCAM in all groups began to decline, and the dose-response relationship of lead to the NCAM expression was observed again.</p><p><b>CONCLUSION</b>Low-level lead might significantly inhibit the NCAM expression of the primarily cultured Wistar rats' hippocampal neurons, and might delay the climax NCAM expression time.</p>

Effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro / 中华预防医学杂志

<p><b>OBJECTIVES</b>This study was conducted to explore effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro.</p><p><b>METHOD</b>Sodium selenite was added at concentrations of 8.75, 17.50 and 35.00 micromol/L respectively with cadmium chloride at the concentrations of 8.75, 17.50 and 35.00 micromol/L respectively and rat hepatocellular DNA damage was measured with single cell gel electrophoresis (comet assay).</p><p><b>RESULTS</b>Sodium selenite at the concentration of 8.75 micromol/L inhibited DNA damage caused by cadmium chloride at the concentration of 8.75, 17.50 and 35.00 micromol/L in rat liver cells (P < 0.05). Although sodium selenite at 17.50 micromol/L inhibited DNA damage induced by cadmium chloride at 17.50 and 35.00 micromol/L, it did not inhibit DNA damage induced by cadmium chloride at 8.75 micromol/L. Sodium selenite at 35.00 micromol/L did not have antagonistic effects on DNA damage induced by cadmium chloride at 8.75, 17.50 and 35.00 micromol/L. In addition, sodium selenite at 8.75 micromol/L had the best antagonistic effect while cadmium chloride at 8.75 micromol/L, but the antagonistic effect of sodium selenite at 17.50 micromol/L was better than 8.75 micromol/L while cadmium chloride at 17.50 and 35.00 micromol/L.</p><p><b>CONCLUSION</b>The antagonistic effect of selenium on rat hepatocellular DNA damage induced by cadmium related to the concentrations of selenium and also to the concentration ratio between selenium and cadmium.</p>

Studies on the effects of lead on the growth and differentiation of hippocampal neural cells as well as the expression of Oct-2 / 中华预防医学杂志

<p><b>OBJECTIVE</b>In order to explore the effects of lead on the growth and development of cultured hippocampal neural cells and on the expression of Oct-2, the II subtype POU domain protein.</p><p><b>METHODS</b>Experiment cell model was established using primary culture of hippocampal neural cells from SD rat embryos. Target cells were exposed to lead acetate in the different concentrations, i.e. 10(-1), 10(0), 10(1), 10(2), 10(3) micromol/L, while the control group was given the same quantity of the culture medium. The immunohistochemistry method was utilized to detect the expressions of Neurofilament (NF) and Glial Fibrillary Acidic Protein (GFAP), the markers for neuron and astrocyte, respectively, and the expression of Oct-2 as well.</p><p><b>RESULTS</b>The results showed that 10 micromol/L lead acetate treatment caused diminishing of neuronal cell body and the decreases of both axon lengths and inter-cellular connections. In addition, 1 micromol/L lead acetate significantly increased the number of GFAP-positive cells compared with the control group (P < 0.05). By image analysis system, 1 micromol/L lead acetate treatment was found to induce a statistically significant increase of the positive area rate concerning Oct-2 expression in hippocampal neurons and astrocytes, while both positive area rate and integral density of light of Oct-2 expression were found to increase markedly in the groups treated by 10 micromol/L lead acetate (P < 0.01).</p><p><b>CONCLUSIONS</b>Lead acetate treatment may contribute to the inhibitions of both growth and differentiation of hippocampus neurons, and to the stimulation of glial cell hyperplasia simultaneously. In addition, the CNS impairments caused by lead is partly correlated with the enhancement of Oct-2 expression.</p>

Effects of selenium on rat hepatocellular DNA damage, apoptosis and changes of cell cycle induced by cadmium in vivo / 中华预防医学杂志

<p><b>OBJECTIVE</b>This study was conducted to study the effects of sodium selenite on rat hepatocellular DNA damage, apoptosis, changes of cell cycle and DNA relative content induced by cadmium chloride in vivo.</p><p><b>METHODS</b>Both sodium selenite at the dose of 5 micromol/kg and cadmium chloride at the dose of 5 micromol/kg, 10 micromol/kg and 20 micromol/kg were given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by the single cell gel electrophoresis (or comet assay), hepatocellular apoptosis was measured with TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry, DNA relative content (DNA(RC)) and cell cycle were detected with flow cytometry.</p><p><b>RESULTS</b>When sodium selenite at the dose of 5 micromol/kg acted jointly with cadmium chloride at the dose of 5 micromol/kg, 10 micromol/kg and 20 micromol/kg respectively, the results showed that selenium reduced the effect of cadmium on DNA damage and apoptosis and decreased the rates of DNA damage and the rates of apoptosis significantly. Sodium selenite at the dose of 5 micromol/kg increased cell number of G(0)/G(1) period decreased by cadmium chloride at the dose of 5 micromol/kg and increased cell number of G(2)/M period decreased by cadmium chloride at the dose of 10 micromol/kg and 20 micromol/kg. Sodium selenite at the dose of 5 micromol/kg increased DNA relative content reduced by cadmium chloride at the dose of 10 micromol/kg and 20 micromol/kg.</p><p><b>CONCLUSIONS</b>It was suggested that selenium at certain doses could antagonize DNA damage, apoptosis, changes of cell cycle and DNA relative content induced by cadmium in rat hepatocytes in vivo.</p>