Objective To investigate the correlation between the polymorphism of XRCC2 gene,a DNA double-strand break repair(DDSBR)gene,and the susceptibility to lung cancer in population of North China.Methods By PCR-based restriction fragment length polymorphism(RLFP)technique(PCR-RLFP),a case-control study was performed among 300 patients with lung carcinoma and 300 healthy controls to detect XRCC2(C41657T)polymorphism.Results There was no significant difference in XRCC2(C41657T)allele frequencies between lung cancer patients and healthy controls(P=0.16).The C/C,C/T and T/T genotype frequencies were 72.7%,24.0% and 3.3% in lung cancer patients,and 76.3%,22.0% and 1.7% in healthy controls,respectively.There was no significant difference in C/C and C/T genotype frequencies between cancer patients and healthy controls(?2=0.48,P=0.48).However,the C/T genotype frequency in non-smoke group was significantly higher in lung cancer patients than in healthy controls(?2=6.67,P=0.01).The risk for lung cancer in non-smokers was 2.11 times higher in C/T genotype carriers than that in C/C genotype carriers.There was no significant difference in C/C and C/T genotype frequency between lung cancer patients and healthy controls in the smoke group(P=0.16).Conclusion Overall,there was no significant correlation between genetic polymorphism of XRCC2(C41657T)and the susceptibility to lung cancer.But the C/T genotype might increase the risk of suffering from lung cancer in no-smoking populations of Northern China.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; DNA Methylation ; DNA-Binding Proteins ; genetics ; Female ; Histone-Lysine N-Methyltransferase ; genetics ; Humans ; Male ; Middle Aged ; Myelodysplastic Syndromes ; genetics ; Nuclear Proteins ; genetics ; Transcription Factors ; genetics ; Young Adult

Adult ; Female ; Granuloma, Respiratory Tract ; pathology ; Humans ; Lung, Hyperlucent ; pathology ; Male ; Middle Aged

Objective To establish a stable primary culture of rat cerebellar granule neurons in vitro for further study the toxic effects of chronic arsenic exposure on cerebellar cells.Methods Cerebellar cortices were taken from brain of Wistar rat 5-7 day old after born under stereoscopic microscope.Single cell suspension was acquired after digestion and washing with trypsin (0.25％) and DNase Ⅰ solution,respectively.Granule cells were purified from other cells by differential velocity adherence method for two times.Rat cerebellar granule neurons were seeded in culture plate pre-coated with poly-L-lysine.Neurons growth,development and synaptic connections were observed daily.The neurons were identified by neuron specific enolase (NSE) immunofluorescence technique.Results The neurons were affixed to the culture plate in 24 hours,in reticular arrangement observed under contrast microscope.Granule cells gradually turned round from oval and outlines became clearer in 2-3 days.In 4-6 days,there were a wide range of synaptic connections among the neurons and a mature nerve cell network formed.A large quantity of cerebellar granule neurons was seen by NSE identification.Few bigger cells such as purkinjes cells and glial cell outlines were also seen in the same visual field.Conclusions This is a successful primary culture method for acquirement of rat cerebellar granule neurons.The method can provide experimental basis for future studies the toxic effects of chronic arsenic exposure on cerebellar cells.

OBJECTIVE: To determine the sensitivity of cetuximab induced apoptosis in laryngeal squamous carcinoma cells Hep-2, and to evaluate the synergistic killing effects and regulation mechanism of cetuximab alone or cetuximab in combination with chemotherapeutic agents (cisplatin) or radiation means on Hep-2 cells. METHOD: To investigate the cytotoxicities of cetuximab, cisplatin and radiation, cell counting kit-8 (CCK-8) assay was used for the detection of cell growth inhibition ratio, and fluorescence activated cell sorter FACS for the apoptotic rate and cell cycle distribution. RESULT: Cetuximab had inhibitive effect on Hep-2 cells within a certain range of concentration in a time- and dose-dependence manner. The inhibition concentration 50% (IC50) of cetuximab on Hep-2 cells for 24 h was 1 036.84 microg/ml. For application of cisplatin and radiation, the apoptotic rate of Hep-2 cell was higher by combining with cetuximab than their single or combined administration. Moreover, the cell cycle arrested at G0/G1 phase. CONCLUSION Laryngeal cancer Hep-2 cells was sensitive to the cetuximab induced apoptosis. Cetuximab combined with cisplatin and/or radiation can increase the antiproliferative effects on Hep-2 cells. These findings suggest the synergistic combination of cetuximab and cytotoxic agents was sequence depended.
Antibodies, Monoclonal, Humanized ; pharmacology ; Apoptosis ; drug effects ; radiation effects ; Cell Line, Tumor ; Cetuximab ; Cisplatin ; pharmacology ; Combined Modality Therapy ; Humans

Background and purpose: The previous work of this study has showed that the treatment of liver cancer cells with emodin could induce endoplasmic reticulum (ER) stress and apoptosis. Given the cross-talk between ER stress and autophagy, this study aimed to investigate whether blockage of autophagy, a defense mechanism against environmental stress, could improve the killing effect of emodin on liver cancer cells. Methods: The CYTO-ID auto-phagy detection kit and Western blot were used to determine autophagy in liver cancer cells. After combined treatment with chloroquine (CQ) and emodin, cancer cell survival was analyzed by ATPlite assay and clonogenic assay. Apoptosis was detected by both flow cytometry analysis and Western blot. Results: Autophagy could be induced in liver cancer cells after treatment with emodin. Inhibition of autophagy significantly increased growth-inhibitory effect of emodin on both HepG2 and Huh7 cancer cells. The combination treatment with CQ and emodin promoted remarkable apoptosis in liver cancer cells, evidenced by the increase in the percentage of cells in sub-G1 phase and the higher expression lever of cleaved caspase-3. Conclusion: Therapeutically targeting autophagy is capable of enhancing cytotoxicity of emodin in liver cancer cell lines.

Objective To investigate the mechanism of recurrent laryngeal nerve injury during total thyroidectomy.Methods The clinical data of 36 patients suffering from recurrent laryngeal nerve injury in total thyroidectomy from 2003 to 2014 was analyzed retrospectively.Results 21 cases had temporary recurrent laryngeal nerve injury while 16 cases had permanent injury.The cases of injury included giant thyroid goitre,with variation of recurrent laryngeal nerve,undergoing secondary surgery,with tumor invasion and complicating thyroiditis.During the first surgery,the incidence of temporary recurrent laryngeal nerve injury was 0.43％,and the incidence of permanent damage was 0.27％.The temporary and permanent injury incidence of secondary surgery after initial subtotal thyroidectomy was 4.59％ and 4.59％,respectively.For patients with grade 3 thyroid gland,that was 1.81％ and 0.30％,respectively and 0.51％,0.72％ respectively in malignant cases.In cases complicating thyroiditis temporary recurrent laryngeal nerve injury occurred in 1.01％.Conclusions There is increased risk of recurrent laryngeal nerve injury in giant goiter cases undergoing secondary operations.Hence it is suggested that initial surgical procedure be hemithyroidectomy or total thyroidectomy

RNA interference (RNAi) has been proved as a novel approach for gene therapy. However, RNAi mono-therapy only aims at single gene, it therefore may ultimately fail to cure cancers caused by polygene variation. To overcome the deficiency of RNAi mono-therapy, "combinatorial RNA interference" (coRNAi) was put forward as a new strategy. By co-expressing the inducers of RNAi triggering single or multiple targets directly and other RNA- or protein-based silencers, coRNAi keeps target genes silent, prevents carcinogenic progression and induces apoptosis of tumor cells. This paper mainly reviews the major strategies of coRNAi and their applications in cancer gene therapy.
Animals ; Apoptosis ; Genetic Therapy ; methods ; Humans ; MicroRNAs ; genetics ; Neoplasms ; genetics ; pathology ; therapy ; Oncogenes ; RNA Interference ; RNA, Small Interfering ; genetics ; RNA, Small Nuclear ; genetics

Objective To establish a method of inducing dendritic cells(DC)from rat bone marrow cells in vitro,and identify the phenotype and function characteristics.Methods The rat bone malToW cells were collected and cultured in vitro under the condition of recombinant rat GM-CSF(rrGM-CSF)and recombinant rat IL-4(rrIL-4).After 2 weeks,the morphological character of DCs was observed under light microscope and scanning electron microscope.Expression of MHC-Ⅱ,CD80 and CD86 were detected by flow cytometry.The ability to stimulate allogenic T cells of the cultured DCs was detected by mixed lymphocyte reaction.Results DCs showed typical morphology with elongated dendritic processes under inversion microscope and scanning electron microscope.DCs at day 6 revealed immature phenotype,including MHC-Ⅱ(29.03 ±4.39)%,CD80(21.98±7.08)%and CD86(25.94±6.80)%.DCs at day 12 showed higher expression of MHC-Ⅱ(74.05±5.97)%,CD80(79.85±6.53)%and CD86(81.00±7.47)%,and stimulatory capacity of allogenic T cells,compared with that in DCs at day 6.Conclusion Matured DCs could be generated from rat bone marrow cells and attendance with rrGM-CSF and rrIL-4,which present the feasibility for further research on its application to allograft immunorejection.

Objective To investigate the effect of iodine excess on thyroid follicle epithelial ultrstructure and the relationship between thyroid iniury and autoimmune thyroiditis. Methods NOD.H-2h4 mice and Kunming mice were randomly divided into four groups receiving plain water,5 fold,10 fold,and 100 fold excessive iodine water.4,8 and 24 weeks after receiving iodine water,the mice were killed.After fixation with osmic acid and dual staining with uranyl chloride and citrate lead,thyroid gland ultrstructure was examined with electron microscopy.Resuits Iodine treated NOD.H-2h4 mice exhibited marked accumulation of peroxisome and secondary lysosomes,apoptosis and necrosis of thyroid epithelial cell.damage of thyroid follicles and lymphocvtic infiltration.The observed changes induced by iodine were in a dose dependent way.Conclusion The oxidative iniury on the thyroid epithelial cells induced by iodine excess might be the prerequisite for the creation of autoimmune thyroiditis.