Objective To understand the effect of the organic extracts of tap water deeply treated with O3-BAC on DNA damage. Methods During June to July 2005, water samples were collected from 6 sites in waterworks A treated with O3-BAC, the raw water, the pre-chlorination water, the filtration water, the post-ozonation water, the BAC water and the tap water respectively and 4 sites in waterworks B treated by general treatment, the raw water, the pre-chlorination water, the filtration water, and the tap water respectively. The test was carried out on extracts of water sample from waterworks A with dosage(7.00, 3.00, 1.50, 1.00, 0.75, 0.38 L/plate)and waterworks B with dosage(7.00, 3.00, 1.00 L/plate)using S.typhimurium strains TA98 and TA100. Cytokinesis-blocked micronucleus (CBMN) test, Comet assay were used on extracts of water sample from waterworks A with dosage(3.00, 1.50, 0.75, 0.38 L/plate). Human embryo lung fibroblast (KMB17 strain) p53 ELISA were used with dosage(3.00, 1.00, 0.3 L/plate). Results Ames test showed that in the waterworks A, at the dose of 7.0 L, the revertants of the raw water, pre-chlorination water, the filtration water on TA98-S9 and 7.0 L, 3.0 L/plate, the revertants of the raw water, pre-ozonation water, filtration water on TA98+S9 were twice more than that of solvent control; in waterworks B, at the dose of 7.0 L/plate, the revertants of the raw water, pre-chlorination water, filtration water on TA98-S9 and 7.0 L, 3.0 L/plate the revertants of the tap water on TA98-S9, and 7.0 L/plate pre-chlorination water on TA98+S9 were twice more than that of solvent control. Cytokinesis-blocked micronucleus (CBMN) test showed that in waterworks A, at the dose of 3.0 L/plate, the micronucleus rates of the raw water, filtration water were significant high than that of solvent control(P

Objective To investigate the mechanism of improvement of gait behavior in PD rat models by low frequency electrical stimulation of pedunculopontine tegmental nucleus (PPTN) by optogenetics method. Methods (1) Twenty-four healthy adult male SD rats were randomly divided into a sham-operated group 1, a lesion group 1 and a photoactivation group (n=8); normal saline was injected into the right medial frontal tract (MFB) of the sham-operated group 1; 6-hydroxydopamine (6-OHDA) was injected into the lesion group 1 and photoactivation group to induce PD models; two weeks after modeling, injection of adeno-associated virus hsynapsin-ChR2-mcherry into the right PPTN of the three groups was performed, and the photoactivation group received blue-ray stimulation by implanting optical fibers into the PPTN at the same time. (2) Twenty-four healthy adult male SD rats were randomly divided into a sham-operated group 2, a lesion group 2 and a photoinhibition group (n=8);normal saline was injected into right MFB of the sham-operated group 2; 6-OHDA was injected into the lesion group 2 and photoinhibition group to induce PD models; two weeks after modeling, injection of adeno-associated virus hsynapsin-NpHR-mcherry into the right PPTN of the three groups was performed, and the photoinhibition group received yellow-ray stimulation by implanting optical fibers into the PPTN at the same time. (3) Three weeks after injection of adeno-associated virus, Catwalk gait analysis was used to assess the behavioral ability of rats in each group. Results (1) As compared with the sham-operated group 1, lesion group 1 had significantly increased front claw spacing and back front claw spacing, and significantly decreased stride length and pressure of damaged lateral and contralateral limbs, and significantly decreased swing speed of contralateral limb (P<0.05); as compared with those in the lesion group 1, the front claw spacing and back claw spacing were significantly shortened, and stride length and pressure of damaged lateral and contralateral limbs were statistically increased in the photoactivation group (P<0.05). (2) As compared with the sham-operated group 2, lesion group 2 had significantly increased front claw spacing and back front claw spacing, significantly decreased stride length of damaged lateral limb, and significantly decreased pressure and swing speed of damaged lateral and contralateral limbs (P<0.05); no significant differences were noted on the front claw spacing and back front claw spacing, pressure and swing speed of damaged lateral and contralateral limbs between lesion group 2 and photoinhibition group (P>0.05). Conclusion The mechanism of low frequency electrical stimulation of PPTN improving gait behavior of PD rat models is related to activation of PPTN neurons.

Objective:To analyze the related risk factors for vertebral artery tortuosity, and explore the mechanism of vertebral artery tortuosity.Methods:Two hundred and eighty-two patients accepted head/neck and MR angiography in our hospital from October 2016 to October 2017 were selected. The tortuosity degrees of vertebral artery were measured and calculated by PACS system. The differences of tortuosity degrees of vertebral arteries in different age groups were compared. Correlation analysis was performed to determine the correlation between vertebral artery tortuosity and both clinical data and and biochemical levels, and multivariate linear regression analysis was performed to determine the independent risk factors for vertebral artery tortuosity.Results:The tortuosity degrees of the left and right vertebral arteries in these patients ranged from 5.1% to 72.6%. The tortuosity degrees of vertebral arteries in patients aged 40-49 years were significantly higher than those in patients aged 20-29 years and 30-39 years ( P<0.05). Correlation analysis showed that the tortuosity degree of the right vertebral artery was positively correlated with age and triglyceride level ( r=0.232, P=0.000; r=0.172, P=0.004); the tortuosity degree of the left vertebral artery was positively correlated with triglyceride level ( r=0.123, P=0.043). Multivariate regression analysis showed that age ( 95%CI: 0.059-0.194, P=0.000) and triglyceride level ( 95%CI: 0.173-1.942, P=0.019) were independent risk factors for right vertebral artery tortuosity. Triglyceride level ( 95%CI: 0.041-2.559, P=0.043) was independent risk factor for left vertebral artery tortuosity. Conclusion:There are congenital developmental factors associated with vertebral artery tortuosity; some nurture factor, as triglyceride level, may promote its development.

Objective:To investigate the changes in interaction proteome of NUS1 mutant R290C and their relations with pathogenicity of Lennox Gastaut syndrome (LGS). Methods:The wild-type and mutant NUS1(R290C) plasmids were constructed and transfected into human embryonic kidney HEK293T cells; 48 h after that, NUS1 protein expression in HEK293T cells was detected by Western blotting. Co-immunoprecipitation, silver nitrate staining, and proteomic analysis were used to analyze the proteins interacted with wild-type or mutant NUS1 and identify the differential interacting proteins. Enrichment analyses of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were performed to annotate the molecular function and signaling pathways involved in the differential proteins. DisGeNet database was used to analyze the association between differential proteins and human diseases. Protein-protein interaction (PPI) was used to analyze the interaction network of NUS1 with protein folding regulatory proteins (RTN4 and DHDDS) and developmental epileptic encephalopathy related proteins.Results:(1) There was no significant difference in NUS1 protein expression between the wild-type and mutant NUS1 transfected HEK293T cells ( t=0.536, P=0.620). (2) Compared with that with wild-type NUS1 plasmid, number of proteins interacting with mutant NUS1 plasmid was significantly reduced in the transfected cells; 310 differential interacting proteins were screened in the mutant NUS1. (3) GO and KEGG enrichment analyses showed that the differential proteins were mainly involved in protein folding reaction and translation regulation. (4) DisGeNet association analysis showed that the two most relevant proteins in the differential interacting proteins were associated with frontotemporal dementia and developmental epileptic encephalopathy. (5) PPI analysis showed that NUS1 may be involved in occurrence of neurological diseases such as LGS by affecting protein folding signaling pathways. Conclusion:NUS1 mutant R290C alters its interacting protein lineage and mediates the development of LGS and other neurological diseases probably by regulating protein folding-related signaling.

Excessive theta (θ) frequency oscillation and synchronization in the basal ganglia (BG) has been reported in elderly parkinsonian patients and animal models of levodopa (L-dopa)-induced dyskinesia (LID), particularly the θ oscillation recorded during periods when L-dopa is withdrawn (the off L-dopa state). To gain insight into processes underlying this activity, we explored the relationship between primary motor cortex (M1) oscillatory activity and BG output in LID. We recorded local field potentials in the substantia nigra pars reticulata (SNr) and M1 of awake, inattentive resting rats before and after L-dopa priming in Sham control, Parkinson disease model, and LID model groups. We found that chronic L-dopa increased θ synchronization and information flow between the SNr and M1 in off L-dopa state LID rats, with a SNr-to-M1 flow directionality. Compared with the on state, θ oscillational activity (θ synchronization and information flow) during the off state were more closely associated with abnormal involuntary movements. Our findings indicate that θ oscillation in M1 may be consequent to abnormal synchronous discharges in the BG and support the notion that M1 θ oscillation may participate in the induction of dyskinesia.