Background and purpose:Previous studies showed activated aryl hydrocarbon receptor (AhR) might be involved in the development of breast cancer induced by polycyclic aromatic hydrocarbons (PHAs) and AhR which was regarded as transcription factors activated by ligand could induced many enzymes expression. Therefore, this study aimed to explore the protein level of AhR and aryl hydrocarbon metabolic enzymes in vivo with a relationship of the breast cancer and pathology indicators. Methods:A case-control study was 1∶1 matched and 65 pairs blood samples were collected, the ELISA was used in testing blood protein levels of the aromatic hydrocarbon receptor and aryl hydrocarbon metabolic enzymes. Meanwhile pathological data was collected. The Rank sum test statistical analysis was used in analyzing measurement data, Spearman test was used in correlation analysis. Results:Statistical analysis revealed that there was no statistical difference in aldehyde dehydrogenase(ALDH), cytochrome P450(CYP450) between the case group and the control group (Z=0.196,P=0.845;Z=0.269,P=0.788);and the AhR, NQO1, GST control group concentrations were lower than that in the case group. There were statistical differences of AhR, quinone oxido-ereductase 1(NQO1), glutatnione-S-transferases(GST) between the control group and the case group(Z=1.956, P=0.041;Z=2.627, P=0.009;Z=3.272, P=0.001). Correlation analysis showed that AhR has a higher correlation in case group with GST, NQO1 (r=0.665, P<0.01;r=0.704, P<0.01). Grouping with the pathology indicators (ER, PR, HER-2)-,+,++,+++, found that the level of grouping by ER, AhR protein levels and GST protein levels have a discrepancies(P<0.05). Conclusion:These results might suggest that the protein levels of AhR and aryl hydrocarbon metabolic enzymes have a signiifcant impact on breast cancer. Detection of enzyme protein levels may be helpful for early detection of breast cancer, prompt treatment options and prognosis are meaningful.

Objective:To investigate the molecular interaction between non-structural protein 3 serine protease of hepatitis C virus(HCV)and wild type P53,and to lay the basis for elucidating the mechanism of oncogenesis of hepatocellular carcinoma(HCC)after infection of HCV.Methods:The recombinant plasmids,pGAD424-NS3,pGAD424-NS315aa- and pGAD424-NS330aa-,were constructed and the interaction between NS3 serine protease and its cofactor NS4A,the interaction between wild type P53 and NS3 serine protease and its N-truncated mutants were dectected qualitatively and quantitatively in yeast two-hybrid system.Results:The results indicated that interaction existed not only between full-length NS3 serine protease and P53,but also between N-truncated mutants of NS3 serine protease and P53.Furthermore,the difference between enzyme activity unit(IU)of β-gal induced by these interactions was not significant(P>0.05).Conclusions:NS3 serine protease of hepatitis C virus and its N-truncated mutants can interact with wild type P53,and the region of NS3 serine protease involved in the interaction may be located in its C-terminal,but not in its N-terminal.

AIMTo investigate the effect of emodin on the voltage dependent potassium (K(V)) currents in rat proximal colon smooth muscle cells.

METHODSWhole cell patch clamp technique was used to record potassium currents including fast transient outward current (I(KA)) and delayed rectifier current (I(Kdr)). Contamination of calcium-dependent potassium currents was minimized with CdCl2 in external solution and EGTA in pipette solution.

RESULTSEmodin (1-30 micromol x L(-1)) reversibly and dose-dependently reduced the amplitude of I(Kdr) with an K(d) value of (1.9 +/- 0.1) micromol x L(-1). I(KA) was also inhibited with 30 micromol x L(-1) emodin to a lesser extent. Although acceleration of the decay rate of the K(V) currents was observed, the block by emodin was not through open block mechanism because a steady state level of inhibition of I(Kdr) was achieved during the first pulse from holding potential -70 mV to + 50 mV after the cells were holding at -70 mV for a three minutes interval in the presence of emodin. Emodin (5 micromol x L(-1)) had no effect on the steady-state activation and inactivation kinetics of K(V) currents, but 30 micromol x L(-1) of emodin produced a positive shift of the voltage dependence of activation, and an increase in the steepness of activation gating as well as shifted the voltage dependence of inactivation to positive direction.

CONCLUSIONEmodin, not through open block mechanism, markedly reduced the amplitude of I(KA) and I(Kdr) and modulated the gating properties of K(V) channels in a reversible and dose-dependent manner.

Animals ; Colon ; cytology ; Delayed Rectifier Potassium Channels ; drug effects ; Emodin ; pharmacology ; Female ; Male ; Myocytes, Smooth Muscle ; drug effects ; Patch-Clamp Techniques ; Potassium Channel Blockers ; pharmacology ; Potassium Channels, Voltage-Gated ; drug effects ; Rats ; Rats, Sprague-Dawley

Objective To investigate the fuction of tumor necrosis factor alpha(TNF-?),interleukin-1 beta(IL-1?) and interleukin-6(IL-6) in children with intracranial infection.Methods TNF-?,IL-1? and IL-6 levels of serum and cerebrospinal fluid(CSF) were determined in the purulent meningitis group(25 cases),tuberculous meningitis group(17 cases),viral meningitis group(30 cases)and control group(20 cases)by enzyme-linked immunosorbent assay(ELISA).Results The levels of TNF-?,IL-1? and IL-6 obviously increased in CSF compared with that in the serum (Pa

Objective To investigate the expression of aquaporin-5(AQP5) in lipo-polysaccharide(LPS)-cigarette smoking inducible SD rats,and the effect of ambroxol chloride(AMB)on its expression. Methods Twenty-one SD rats were randomly divided into three groups: AMB intervention group,model group(LPS-cigarette smoking induction group) and control group.TNF-? was determined from lung homogenate supernatant,bronchial alveolar lavage fluid(BALF) and serum by ELISA.The semi-quantitation of AQP5 transcription and expression were measured by in situ hybridization and immunohistochemistry,respectively. Results TNF-? from lung homogenate supernatant and BALF in model group was more than AMB intervention group and control group(P

OBJECTIVEThe pathogenesis of Tourette syndrome (TS) is associated with the disorders of neurotransmitters, such as dopamine (DA) and excitatory amino acids (EAA). Antiepileptic drugs such as topiramate have shown some effects on TS, but the mechanism has not been clearly identified. The objective of the research was to evaluate the relationship between the pathogenesis of TS and abnormality of neurotransmitters by determining the levels of brain free DA and plasma EAA in iminodipropionitrile (IDPN) induced head twitch response (HTR) rats, and to investigate the effects of topiramate on HTR induced by IDPN.

METHODSForty-eight Sprague-Dawley rats were randomly divided into six groups: blank control, TS model, and haloperidol-(0.5 mg/kg) and topiramate-treated (5, 10 and 20 mg/kg). HTR was induced by 7-day peritoneal injections of IDPN (150 mg/kg daily) and was used as TS model. Brain free DA levels and plasma levels of EAA were measured using ELISA and high performance liquid chromatography respectively 35 days after haloperidol or topiramate administration.

RESULTSBrain free DA levels were significantly lower and plasma EAA levels were significantly higher in the TS model group compared with those in the blank control group (P<0.05). Topiramate of 10 and 20 mg/kg significantly decreased the frequency of IDPN-induced HTR and significantly increased the level of brain free DA when compared with the TS model group (P<0.05). Topiramate of 20 mg/kg treatment as haloperidol treatment significantly decreased plasma EAA levels compared with the TS model group (P<0.05).

CONCLUSIONSThe pathogenesis of TS is related to the super-sensitivity of DA receptor in the center nervous system and the over-effect of plasma EAA. Topiramate can reduce IDPN-induced HTR, probably through the inhibition of DA and DA-receptor combination in the brain and the secretion and release of plasma EEA.

Animals ; Anticonvulsants ; therapeutic use ; Behavior, Animal ; drug effects ; Brain Chemistry ; drug effects ; Dopamine ; analysis ; Excitatory Amino Acids ; blood ; Fructose ; analogs & derivatives ; therapeutic use ; Male ; Rats ; Rats, Sprague-Dawley ; Tourette Syndrome ; drug therapy

Objective To establish a rabbit model of restenosis and analyze the expressions of VEGFmRNA and TGF-?_1mRNA during the intimal proliferation.We also explored the relationship between VEGFmRNA,TGF-?_1mRNA and restenosis.Methods 40 healthy male New Zealand white rabbits were evenly divided into three injury groups and one control group.Right carotid arteries were injured with PCI balloon in the injury groups.10 rabbits of each injury group were sacrificed on weeks 1,2 and 4 after the injury.VEGFmRNA and TGF-?_1mRNA were examined by in situ hybridization.All the samples were analyzed using a computerized imaging analysis system.Results In the injury groups,neointimal areas were significantly larger than those in control group(P

Objective To explore the mediating effects of resilience between family function and geriatric depression. Methods By convenient sampling, 212 elderly people who were from the communities in Yuexiu, Guangxhou city were analyzed by using Geriatric Depression Scale (GDS-30) and Family Concern Index Questionnaire (APGAR) and Connor-Davidson Resilience Scale (CD-RISC) and the self-designed General Condition Questionnaire, and a mediating model was proposed and the impacts of resilience on family function and geriatric depression were tested. Results The incidence rate of depression among the community elderly was 23.6% (50/212), and the average score of APGAR was 7.87 ± 2.83, and the average score of CD-RISC was 83.66 ± 12.88. The scores of GDS-30 showed significantly negative correlation with the scores of APGAR (r=-0.582,P<0.01)and the scores of CD-RISC (r=-0.425, P<0.01), and there was positive correlation between the scores of APGAR and the scores of CD-RISC (r=0.335, P < 0.01). The mediating model had high degree of fitting, and level of path had statistical significance (P < 0.01). Resilience was the mediator between family function and geriatric depression. Family function had direct effects (0.50) on geriatric depression and indirect effects (0.11) through resilience, and the combined effects of family function and resilience determined 45%changing range of geriatric depression. Conclusions Family function was a direct predictor of geriatric depression, and resilience had mediating effects between family function and geriatric depression. Community mental health work should pay enough attention to the effects of family function on the life of the aged, and increased the care to the elderly with family dysfunction, while promote and develop family-centered mental health education, propaganda and psychological guidance, so that improves resilience of the aged and help the aged positively coping and maintain good mental health status.

OBJECTIVETo study the association of blood lipids with the development, clinical stage, allergic condition, and pulmonary function of asthma.

METHODSA total of 56 children with asthma who attended the hospital between October 2016 and March 2017 were enrolled as the asthma group, and 46 children who underwent physical examination as the healthy control group. According to the clinical manifestations, the children with asthma were divided into acute exacerbation group (n=24) and chronic persistent group (n=32). According to the results of skin prick test (SPT) and serum IgE measurement, the children with asthma were divided into non-allergic asthma group (n=16) and allergic asthma group (n=38). Fasting blood lipid levels were measured in both asthma and control groups. Pulmonary function tests were performed for asthmatic children.

RESULTSThere were no significant differences in blood lipid levels between the asthma and control groups (P>0.05). The acute exacerbation group had significantly lower serum levels of high-density lipoprotein (HDL) and total cholesterol compared with the control group and the chronic persistent group (P<0.05). The allergic asthma group had a significantly lower serum HDL level than the non-allergic asthma group (P<0.05). In asthmatic children aged 6-13 years, the ratios of the measured values to the predicted values for forced vital capacity, peak expiratory flow, and maximal expiratory flow at 50% of vital capacity had a linear regression relationship with HDL and were positively correlated with HDL (P<0.05). Forced expiratory volume in one second and maximal mid-expiratory flow had a linear regression relationship with both HDL and LDL and were positively correlated with them (P<0.05).

CONCLUSIONSBlood lipids are associated with the clinical stage, allergic condition, and lung function of childhood asthma. This indicates that blood lipids may be involved in several aspects of the pathogenesis of childhood asthma.

Adolescent ; Asthma ; blood ; physiopathology ; Child ; Child, Preschool ; Female ; Forced Expiratory Volume ; Humans ; Lipids ; blood ; Lung ; physiopathology ; Male ; Vital Capacity