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Objective To investigate the effect of FCGR3A polymorphisms on NK cell function. Methods Peripheral blood samples from can?cer patients were collected and FCGR3A polymorphisms were confirmed by PCR. In vitro proliferation rates,ADCC activity,and expression of NK cell activating receptors were compared under trastumab stimulation. Results This study showed that the wild?type FCGR3A exhibited a higher affinity to trastumab along with better NK cell proliferation and ADCC activity than the mutant type. Compared to the patients with wild?type FC?GR3A,the proliferation rates of NK cells in patients with the mutant type were reduced by approximately 8?fold. In addition,the expression of NK cell activating receptors in patients with wild?type FCGR3A was higher than in patients with the mutant type. Conclusion Mutations in FC?GR3Areduce NK cell function,causing a poor reaction to monoclonal antibody.
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Objective To explore the enhancement effects and mechanisms of IL-32β on human cervical carcinoma cells C33A to hypoxic/hypoglycemic condition.Methods After cultured in hypoxia/hypoglycemic circumstance and normal circumstance for 20 hours respectively, the mRNA and protein expression of IL-32β in C33A cells were detected by real time-polymerase chain reaction (RT-PCR) and Western blotting respectively.Trypan blue stain was used to detect C33A cells viability in hypoxia/hypoglycemic circumstance and adding 10, 100,500 ng/ml IL-32β circumstance.The xenografted tumor of nude mice was established by intraperitoneal injection, and their volumes were tested for a given time after injecting 0, 1.0 mg/kg IL-32β.siRNA was used to construct IL-32β knockdown cells and detect the expression of VEGF.Results Under the hypoxia/hypoglycemic circumstance, the expressions of IL-32β mRNA were (6.12 ± 0.03) times of the normal circumstance (F =43.16, P ＜ 0.05), the expressions of IL-32β protein were (2.23 ± 0.04) times of the normal circumstance (F =22.32, P ＜ 0.05).The C33A cells viability in hypoxia/hypoglycemic circumstance was (51.92 ± 3.41) ％, whereas, viability in 10 ng/ml IL-32β group was (55.23 ± 3.92) ％ (F =14.25, P ＜ 0.05), viability in 100 ng/ml IL-32β group was (62.52 ± 4.14) ％ (F =35.53, P ＜ 0.01), viability in 500 ng/ml IL-32β group was (69.14 ± 2.45) ％ (F =56.28, P ＜ 0.01).After 28 days, the volume of xenografted tumor of 0 mg/kg IL-32β group was (578 ± 64)mm3, and 1.0 mg/kg IL-32β group up to (1 402 ± 142) mm3 (F =27.84, P ＜ 0.01).In addition, compared with control group, the expression of VEGF in IL-32β knockdown C33A cells was significantly decreased (F =36.85, P ＜ 0.05).Conclusion IL-32β can enhance the resistance to hypoxic/hypoglycemic condition of C33A cells, which is associated with the increase of VEGF.
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Objective To discuss and analyze clinical pathological characteristics of senile recurrent ovarian cancer and its influences on prognosis.Methods 140 senile ovarian cancer patients who have been admitted in ourhospital were selected as study subjects.103 cases with recurrent ovarian cancer were selected as observation group (group A),and the rest 37 cases who did not suffer from recurrent ovarian cancer were selected as control group(group B).Pathological characteristics of carcinoma tissues after their first admission in our hospital were compared between the two groups.And pathological characteristics of carcinoma tissues of group A after their second admissionin our hospital were analyzed,comprehensively analyzed prognosis situations and clinical pathological characteristics of patients in these two groups.Results In group A,the number of poorly differentiated carcinoma tissues was obviouslymore than group B,and the number of patients whose neoplasm staging was M stage was more than that in group B,the differences between the two groups were significant (x2 =13.48,15.87,all P ＜ 0.05).The incidence rate of adverse reactions between the two groups also had statistical significance(x2 =13.8,11.6,14.5,13.9,14.9,13.4,all P ＜0.05).Conclusion The clinical pathological characteristics of senile recurrent ovarian cancer can reflect patients'prognosis situations in some degree,and has certain clinical value in evaluation of patients' disease recurrence and prognosis.
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Plant programmed cell death (PCD) plays an important role in plant growth and development as well as defensive response against biotic and abiotic stresses. Fumonisin B1 (FB1) is a fungi toxin, which is a competitive inhibitor of ceramide synthase in de novo sphingolipid biosynthesis. FB1 can induce PCD in both animal and plant cells. To dissect this pathway, a genetic screen for fumonisin B1 resistant (fbr) mutants, and identified 11 fbr mutants was carried out. Genetic analysis showed that these 11 mutants belonged to 9 complementary groups or genetic loci. Here a detailed phenotypic analysis of fbr136 was reported. In addition to the resistance to FB1, fbr136 also showed resistance other PCD-inducing compounds, including H2O2 and paraquat. Furthermore, FB1-induced PR1 expression was reduced in fbr136, suggesting that a PCD pathway is likely impaired in the mutant. When stained with nitroblue tetrazolium (NBT), fbr136 showed a reduced accumulation of reactive oxygen species (ROS) induced by FB1. The fbr136 mutation was roughly mapped onto chromosome Ⅲ, where no other fbr mutants have been previously identified. It is proposed that FBR136 may act as an important regulator in a sphingolipid-mediated PCD pathway, involved in the generation of ROS.