Abstract Objective:To explore antitumor effect of NDV HN. Methods: pIRHN nucleic acid vaccin was constructed and was transfectedto Hela cells. Westem blot was used to analyssize the expression of pIRHN nucleic acid vaccine in eukarytic cell. The mode of cell death was de-tected by fluorescence microscope, gel electrophoresis and TUNEL assay. The effect of pIRHN nucleic acid vaccine on the contents of siaha acidin the Hela cell was examined. Results: pIRHN nucleic acid vaccine could be expressed in the eukarytic cell. pIRHN could induced apoptosisafter HeLa cells were transfected. The effect of antitumor responses of pIRHN was correlated with the contents of sialic acid in tumor cells. Con-clusion: The reults of our experiment will provide the theory evidence for the anti tumor mechamism of NDV.

Objective To investigate whether apoptosis is invovled in the immune response of inner ear,and relation between the signal transduction of Caspase-3 and apoptosis. Methods Sixteen healthy,female guinea pigs were employed in this study. The animals in the experiment group were sensitized systematically with keyhole limpet hemocyanin(KLH),then were inoculated in inner ear with the same antigen, and the animals in the control group were injected with the same volume of PBS. The animals were sacrificed at the 5th day after inner ear vaccination. Paraffin sections of cochleas from animals were prepared, TUNEL assay was used to detect apoptotic cells in inner ears, and immunohistochemical method was applied to detect the expression of Caspase-3 in inner ears. Results TUNEL-positive cells are found in the inner ears of the experiment group, but did not in the inner ears of the control group except for a few TUNEL-positive cells in the supporting cells, the stria vascular cells and the spiral ganglion cells. The high expression of Caspase-3 could be detected in the inner ears of the experiment group, but no positive cells of Caspase-3 were found in the inner ears of the control group. Conclusion Apoptosis could be induced by the immune response of inner ear, and Caspase-3 cascade may be involved in the course of apoptosis.

Background The mitochondrial Na+/Ca2+exchanger, NCLX, plays an important role in the balance between Ca2+influx and efflux across the mitochondrial inner membrane in endothelial cells. Mitochondrial metabolism is likely to be affected by the activity of NCLX because Ca2+activates several enzymes of the Krebs cycle. It is currently believed that mitochondria are not only centers of energy produc-tion but are also important sites of reactive oxygen species (ROS) generation and nucleotide-binding oligomerization domain receptor 3 (NLRP3) inflammasome activation. Methods&Results This study focused on NCLX function, in rat aortic endothelial cells (RAECs), induced by glucose. First, we detected an increase in NCLX expression in the endothelia of rats with diabetes mellitus, which was induced by an injection of streptozotocin. Next, colocalization of NCLX expression and mitochondria was detected using confocal analysis. Suppression of NCLX expression, using an siRNA construct (siNCLX), enhanced mitochondrial Ca2+influx and blocked efflux induced by glucose. Un-expectedly, silencing of NCLX expression induced increased ROS generation and NLRP3 inflammasome activation. Conclusions These findings suggest that NCLX affects glucose-dependent mitochondrial Ca2+signaling, thereby regulating ROS generation and NLRP3 in-flammasome activation in high glucose conditions. In the early stages of high glucose stimulation, NCLX expression increases to compensate in order to self-protect mitochondrial maintenance, stability, and function in endothelial cells.

Objective To examine the effects of oxidative stress induced damage to the Prestin expression in HEI-OC1 cells,and to study the mechanism of sensory deafness.Methods We used different concentrations (50μM,100μM,200μM)of hydrogen peroxide canister to cultivate HEI-OC1 cells,and to detect the activity of su-peroxide dismutase(SOD).The quantitative real-time PCR and immunofluorescence were used to detect the prestin expression of mRNA.Results The SOD activity decreased in the HEI-OC1 cells damaged by oxidative stress.The high concentration of the infected group decreased more significantly(F= 9926.293,P<0.01).The expressions of Prestin mRNA and Prestin protein were decreased obviously in the HEI-OC1 cells.The high concentration of in-fected group decreased more significantly (F= 4065.046and7657.217,P<0.01).Conclusion Oxidative stress in-ducing damage inhibits the expression of prestin.Prestin protein may be used as a molecular marker of sensory deafness.

for the detection of their virulent abilities simultaneously.

Objective:To evaluate the reliability of flexural strength and subcritical crack growth(SCG)of WL and HT zirconia ce-ramics under cyclic loading.Methods:Bar-shaped speciments of WL(n =30)and HT(n =30)were fabricated and loaded in three-point bending and cyclically fatigued.The flexural strength and the number of cycles to fracture were obtained from three-point flexural test and cyclic fatigue test respectively.Data were examined using Weibull statistics.Pairs law was used to analysize the subcritical crack growth(SCG),the behavior of which was described in terms of crack velocity as a function of maximum stress intensity factor (KImax ).Results:The Weibull module(m)of WL and HT was 10.64 and 12.04,the stress corrosion cracking susceptive indexes(n) 23.71 and 32.87,the SCG 90% and 76.7%,the KImax 49.6% and 50.9% of its maximum stress intensity factor(KIC ),respectively. Conclusion:WL and HT produce pronounced SCG.The minimum fatigue crack growth rate of HT is lower than that of WL(νHT <νWL ).

Hormones and epigenetic characteristics in a patient with clinically diagnosed adrenal hypoplasia congenita (AHC) were analyzed. Results indicated that plasma ACTH increased, while cortisol, testosterone, LH and FSH decreased. LH, FSH and testosterone did not sufficiently respond to GnRH or hCG stimulation. Gene analysis indicated that C368F mutation was located in exon 1 of DAX-1 gene.

The powder X-ray diffraction Fourier fingerprint pattern technique was used to develop a new quantitation method for the analysis of andrographolide and dehydroandrographolide. And the high performance liquid chromatography method was used to evaluate the quantity of andrographolide and dehydroandrographolide. The relationship of diffraction peak intensity and content of andrographolide and dehydroandrographolide was investigated. The powder X-ray diffraction Fourier fingerprint pattern analysis technique can be used to evaluate the quantity of andrographolide and dehydroandrographolide in the herb simultaneously.

Objective To investigate the efficacy and safety of enriched-calorie formula in post-operative infants with congenital heart disease and malnutrition.Methods All malnourished infants less than 6 months diagnosed congenital heart disease: ventricular septal defect and had undergone surgery in Guangzhou Women and Children`s Medical Center from December 1,2014 to May 30,2015 were included in this study.All cases were randomly divided into intervention group(energy-enriched formula,intervention group)and control group(standard formula,control group)for enteral nutrition intervention and observed for 3 months.Body mass,body length,upper arm circumference,blood prealbumin(PA),retinol binding protein(RBP),and B-terminal pro-brain natriuretic peptide(NT-proBNP)were measured before and after ICU,after discharge,and 1 month and 3 months after operation.Results Fifty-one cases were in intervention group and 50 cases in control group,respectively.There were no significant differences in body mass,body length,arm circumference,PA,RBP,mean enteral nutrition starting time,mechanical ventilation time,length of ICU stay,hospitalization time,and average fluid intake between the two groups(all P>0.05).The average caloric intake in intervention group was significantly higher than in control group [(437.24±6.68)kJ vs.(312.43±86.22)kJ,P=0.001].There was no significant difference in NT-proBNP,PA,and RBP at different time points between the two groups(all P>0.05).The improvement of nutrition in intervention group was significantly higher than that in control group at 1 month(25.0％vs.4.9％,P=0.011)and 3 months(64.1％vs.15.7％,P<0.001)after operation.Body mass increased in intervention group [(0.067±0.348)kg] compared with that in control group,and decreased [(0.125±0.425)kg] in control group(P=0.015).Body weight[(5.46±1.36)kg vs.(4.80±1.01)kg,P=0.008],weight for age Z score(WAZ)(-2.79±1.28 vs.-3.75±1.27,P<0.001),and height for weight Z score(WHZ)(-2.47±1.43 vs.-3.62±1.77,P=0.001)one month after surgery were significantly higher than those before operation.Body weight [(6.78±1.42)kg vs.(5.72±1.01)kg,P<0.001] arm circumference [(12.80±1.17)cm vs.(12.00±0.90)cm,P<0.001],WAZ(-1.60±1.17 vs.-3.10±1.40,P<0.001),height for age Z score(HAZ)(-1.41±1.63 vs.-2.10±1.41,P=0.034),and WHZ(-0.86±1.31 vs.-2.59±2.13,P<0.001)of the two groups at 3 months postoperative were significantly higher than those before operation,and the growth rate of intervention group was faster than control group.There were no significant adverse reactions in both groups.Conclusion Calorie-enriched formula powder can help malnourished infants to catch up after congenital heart disease surgery.

Emerging evidence has indicated that BRCC 36-mediated K63-linked ubiquitination modification was involved in diverse cellular functions , including endocytosis , apoptosis and DNA damage repair .We previously showed that activation of cGMP/PKG pathway con-tributed to the binding of BRCC36 and the pro-fibrotic factor Smad3.The current study tested the hypothesis that BRCC 36 functions as a negative regulator of transforming growth factor-beta ( TGF-β)/Smad3 pathway and participates in cardiac remodeling .In isolated adult mouse cardiac fibroblasts , we have demonstrated that TGF-β1 treatment significantly increased the expression of BRCC 36.Over-expression BRCC36 suppressed TGF-β1-induced Smad3 phosphorylation, nuclear translocation, extracellular matrix molecular expres-sion and cell proliferation .On the contrary, silencing BRCC36 by transfection of adenovirus-carrying BRCC36 shRNA potentiated to
enhance the pro-fibrotic effect of TGF-β.In vivo, under chronic pressure overload condition-induced by transverse aortic constriction , myocardial pro-survival protein Bcl-2 and Mcl-1 expression were significantly decreased and the pro-apoptosis protein Puma was in-creased.However, the cardiac-specific over-expression of BRCC36 significantly increased myocardial Bcl-2 and Mcl-1 and inhibited Puma expression .Interestingly , we also found that sustained pressure overload resulted in a significant myocardial DNA injury in wild type mice, which was characterized by the increase of γH2AX level.However, cardiac-specific BRCC36 over-expression significantly decreased the level of γH2AX in the pressure overloaded heart in the transgenic mice , while effectively enhanced myocardial RAD 51 expression, a marker of DNA damage repair.Furthermore, BRCC36 over-expression effectively attenuated TAC-induced cardiac fibro-sis and remodeling in the transgenic mice , compared with the wild type mice .Collectively , the results have suggested that BRCC 36 ef-fectively protected heart against chronic pressure overload-induced cardiac remodeling though antagonizing TGF-β/Smad3 pathway and enhancing myocardial DNA injury repair response .