OBJECTIVE:To compare therapeutic efficacy and safety of lobaplatin or cisplatin combined with tegafur,gimeracil and oteracil potassium in the treatment of advanced metastatic breast cancer.METHODS:A total of 160 patients with advanced metastatic breast cancer were randomly divided into observation group and control group,with 80 cases in each group.Control group was given Cisplatin injection 30 mg/m2 intravenously,every 3 weeks Tegafur,Gimeracil and Oteracil Potassium capsules 50 mg orally after meal,twice a day,for consecutive 14 days.Observation group was given Lobaplatin for injection 30 mg/m2 intravenously,every 3 weeks+Tegafur,Gimeracil and Oteracil Potassium capsules (same usage and dosage as control group),every 3 weeks.A treatment course lasted for 3 weeks,and both groups received 2 courses.Short-term efficacies (ORR、DCR),chemotherapy effects of lymph node,lung,bone and liver,ADR and long-term efficacy were compared between 2 groups.RESULTS:After treatment,ORR(67.50％ vs.46.25％),DCR(85.00％ vs.66.25％),ORR of lymph node metastasis (71.43％ vs.47.83％),ORR of lung metastasis (60.71％ vs.40.00％),DCR of lung metastasis (78.57％ vs.56.00％),ORR of bone metastasis (28.57％ vs.16.67％),1-year survival rates (75.00％ vs.52.50％) and 2-years survival rates (42.50％ vs.17.50％) of observation group were significantly higher than control group;the incidence of chemotherapy ADR in observation group was significantly lower than control group (43.75％ vs.70.00％),with statistical significance (P＜0.05).There was no statistical significance in lymph node metastasis DCR,bone tissue metastasis DCR,liver metastasis ORR and DCR,or half year sarvival rate between 2 groups (P＞0.05).CONCLUSIONS:Compared to cisplatin combined with tegafur,gimeracil and oteracil potassium,lobaplatin combined with tegafur,gimeracil and oteracil potassium show better short-term therapeutic efficacy,therapeutic efficacy of lymph node metastasis,bone metastasis and lung metastasis,more than 1-year long-term therapeutic efficacy and safety in the treatment of advanced metastatic breast cancer.

Objective To describe the growth and development of Schistosoma japonicum in goat and the intensity and tem?poral distribution of eggs excreted by goat feces,so as to provide baseline data for the control and elimination of the role of goat in the transmission of schistosomiasis. Methods The goat animal models of schistosomiasis were established,and stool sam?ples were collected for parasitological examinations. The number of adult worms recovered,variation of schistosomes in goat at different time points post?infection,number of eggs in schistosomes,variation in number and temporal profiles of eggs excreted from goat feces were observed. Results Of the 6 schistosome?infected goat,415 adult worms were recovered,with a mean adult worm recovery of 34.58%(range,23.00%to 45.50%). Among the 5 goat infected with 200 cercariae each,47,93,77, 74 and 73 adult worms were recovered 2,5,8,11 and 14 months post?infection,respectively. There were(200.00 ± 42.33), (226.20±45.88),(168.20±25.85),(183.80±55.13)and(190.80±53.53)eggs detected in female schistosomes. The mean pre?patent period of eggs excreted by 10 infected goat was(37.7±3.02)d. From 2 to 14 months post?infection,7 batches of goat fe?ces were hatched,and there were 30,23,14,1 and 2 times for miracidium intensity of“++++”,“+++”,“++”,“+”and“-”, respectively,with 42.86%,32.86%,20.00%,1.43%and 2.86%constituent ratios of miracidium intensity. Conclusions Ap?proximately 1/3 S. japonicum cercariae may develop to adults in goats post?infection,and the prepatent period of eggs is(37.7± 3.02)d. There is no remarkable decrease seen in the number of adult worms,eggs in female schistosomes and eggs in goat feces within 14 months post?infection. Our findings suggest a long duration for infected goat in the transmission of schistosomiasis ,and there is no evidence to prove the“self?cure”phenomenon in goat,indicating that goat is an important source of infection for schistosomiasis japonica.

Objective To investigate the effect of downregulated activating transcription factor 3 ( ATF3) expression on proliferation of adrenocortical carcinoma cells and its mechanisms. Methods Immunohistochemistry and Western blotting were used to detect the expression of ATF3 in human adrenocortical tumor tissues and cells. Adrenocortical carcinoma cells, Sw-13, and NCI-H259R cells, were transfected with siATF3 using lipidosome 2000, and expression of ATF3 mRNA was determined using RT-PCR; expression of ATF3, cleaved caspase 3, caspase 3, cleaved PARP, and PARP proteins were detected using Western blotting; cell growth inhibition rate and apoptosis rate were monitored using MTT and AnnexinV-FITC/PI, respectively. Sw-13 and NCI-H259R cells were treated with NVP-BEZ235, Perifosine, BKM120, IWP-2, PP2, KN93, Everolimus respectively followed by detected expression of ATF3 mRNA by realtime PCR. The effect of ATF3 on cell proliferation after inhibition of related signaling pathways were detected by MTT. Results The ATF3 in human adrenocortical gland tumor tissues and cells showed high expression. The levels of ATF3 mRNA and protein in Sw-13 and NCI-F259R cells transfected with siATF3 were significantly reduced. Compared with the negative control group ( NC siRNA), siATF3 transfection significantly inhibited the proliferation of Sw-13 and NCI-F259R cells ( P＜0. 05 ), and increased the apoptosis rate ( P＜0.05). Western blotting shown that the levels of cleaved caspase 3 and cleaved PARP protein in siATF3 transfected cells increased significantly; and realtime PCR results indicated that the expression of ATF3 mRNA was dramatically inhibited by PP2, KN93, and IWP-2 in NCI-F259R cells compared with control group ( DMSO ); but ATF3 significantly promoted the proliferation activity of NCI-F259R cells which treated by PP2, KN93, and IWP-2 signaling inhibitors. Conclusion High expression of ATF3 is existed in adrenocortical carcinoma cells. Downregulated ATF3 expression may inhibit cell proliferation and activate apoptosis pathway, resulting in apoptosis in Sw-13 and NCI-F259R cells, this mechanism of action is related to activating Wnt/β-catenin, CaMKI, and SRC pathway.

Objective: To investigate the effect of miR-135a on the malignant biological behaviors of human laryngeal carcinoma epithelial Hep-2 cells and its sensitivity to oxaliplatin. Methods: Samples of laryngeal carcinoma tissues and para-cancerous tissues were collected from 10 patients who underwent laryngectomy in Nanyang Hospital Affiliated to Zhengzhou University-Nanyang City Center Hospital from January 2018 to June 2018. The expression of miR-135a in laryngeal carcinoma tissues and Hep-2 cells was detected by qPCR.After being transfected with miR-135 inhibitor, cell proliferation viability of Hep-2 cells was measured by CCK-8 assay, cell colony formation ability was detected by colony formation assay, and cell proliferation invasion and migration abilities were detected by Transwell analysis, and the expression of SOX2 protein in Hep-2 cells was detected by WB. Hep-2 cells transfected with miR-135 inhibitor were further treated with various concentrations (0.5, 1.0, 1.5 and 2.0 μmol/L) of oxaliplatin, and the cell proliferation viability was detected by CCK-8 while cell apoptosis was detected by Annexin-V-FITC/PI double staining flow cytometry. miR-135a inhibitor plasmid, control pcDNA empty vector (SOX2-Con) plasmid, and pcDNA-SOX2 (SOX2-OE) plasmid were transfected into Hep-2 cells to construct the miR-135a inhibitor+SOX2-Con group and miR-135a inhibitor+SOX2-OE group, and the cell viability, cell colony formation ability, cell invasion and migration ability in two groups were detected. Results: Compared with para-cancerous tissues, miR135a expression in laryngeal cancer tissues was significantly increased (P<0.01). Compared with normal NHP cells, miR-135a expression in Hep-2 cells was significantly increased (P<0.01). miR-135a inhibitor significantly reduced the expression level of miR-135a in Hep-2 cells (P<0.01). miR-135a knockdown significantly reduced the cell proliferation viability, cell colony number, migration, invasion and SOX2 expression in Hep-2 cells (all P <0.01), but significantly enhanced the sensitivity of Hep-2 cells to oxaliplatin (P<0.01). Compared with miR-135a inhibitor+SOX2-Con group, the cell proliferation viability, cell colony number, migration and invasion of Hep-2 cells in miR-135a inhibitor+SOX2-OE group were significantly increased (P<0.01); Meanwhile, the cells of the 2 groups were treated with different concentrations of oxaliplatin, and the results of CCK-8 assay showed that, compared with the miR-135a inhibitor+ SOX2-Con group, the cell proliferation viability of Hep-2 cells in miR-135a inhibitor+SOX2-OE group was significantly increased (P< 0.01). Conclusion: miR-135a knockdown inhibits the malignant biological behaviors and promotes oxaliplatin-sensitivity of Hep-2 cells possibly by inhibiting the expression of the transcription factor SOX2.