BACKGROUND:The development of spinal non-fusion technology promoted movement function protection of adjacent segment and operating segment. In the treatment of cervical spondylosis surgery, non-fusion technology has been widely carried out. For middle-aged patients with cervical spondylosis, the demand for spinal joint movement function is high. Non-fusion technology can improve the postoperative quality of life and slow down the risk of adjacent segment degeneration. OBJECTIVE:To evaluate the clinical efficacy of anterior cervical different implant materials (fusion or non-fusion) in the treatment of single segment of the intervertebral disc degeneration of cervical spondylosis in middle-aged patients. METHODS:This study enrol ed 10 cases of single segmental radiculopathy and cervical myelopathy after cervical intervertebral disc replacement from June 2011 to June 2013. Simultaneously, 10 cases were randomly selected from patients with anterior interbody fusion as the control group. Before treatment, at 1 and 3 months, and 1 year after treatment, changes in range of motion of cervical vertebra were observed using imaging results. Therapeutic effects were assessed using Japanese Orthopaedic Association Scores, Visual Analog Scale and The Neek Disability Index in both groups. RESULTS AND CONCLUSION:Al patients did not suffer from incision fat liquefaction, infection and delayed healing, and had finished fol ow-up for more than 1 year. Results revealed that Japanese Orthopaedic Association Scores and Visual Analog Scale scores were improved at 1 and 3 months, and 1 year after treatment (P<0.05), and no significant difference was detected between the two groups (P>0.05). In the analysis of range of motion of cervical vertebra and The Neek Disability Index, there were significant advantages in non-fusion treatment group (P<0.05). For middle-aged patients with cervical spondylosis, due to its life demand for neck mobility, the repair program of non-fusion cervical intervertebral disc replacement has a clear advantage.

【Objective】 To investigate the effects and potential mechanisms of neurodegenerative lesions in male mice caused by ozone exposure. 【Methods】 We divided 23 C57BL/6N male mice aged 8 to 9 months into control group （clean air group， 11） and ozone group （1 mg/m ³， 4h/d， 12）. After 8 weeks of continuous ozone exposure， the Morris water maze experiment was used to detect the mice’s learning and memory ability， HE dyeing to observe pathological changes in hippocampal tissue cells， and immunoprinting tests to detect the expression levels of Tau， p-Tau and α-synuclein proteins in the cerebral cortex tissue. 【Results】 After 8 weeks of ozone exposure， the mice’s spatial learning and memory ability were impaired to a certain extent， the incubation period decreased with time， and the two lines were separated， but the difference was not statistically significant. Ozone exposure caused changes in the morphology of the mice’s hippocampal tissue cells， disorders in the arrangement of hippocampal neuron， and nuclear wrinkles， and significantly increased levels of p-Tau and α-synuclein protein expressions in cerebral cortex tissues （P<0.01）， but there was no statistical significance in the total Tau expression level. 【Conclusion】 Ozone exposure leads to the loss of learning and memory in mice， changes in hippocampal neurocellular pathology， and increased expression levels of neurodegenerative variable-related proteins.

Objective : To investigate the role of lncSIL in transforming growth factor-β1(TGF-β1)-induced alveo- lar epithelial interstitial transformation (EMT) and its related signaling pathways . Methods : Western blot was used to detect the effect of lncSIL silencing on the expression of E-cadherin ( E-cad) , alpha-smooth muscle actin ( α- SMA) and Collagen I (Col I) in the process of EMT induced by TGF-β1 . LncSIL interacting proteins were ana- lyzed by RNA pulldown . Western blot was used to detect the effect of overexpression or silencing of lncSIL on the expression of its target gene enhancer of zeste homolog 2 (EZH2) and its downstream factors P21 and cyclin-de- pendent kinase 6 (CDK6) . Flow cytometry was used to analyze the effect of lncSIL on cell cycle progression . Results: After lncSIL silencing , the expression of α-SMA and Col I increased , the expression of E-cad decreased . RNA pulldown assay showed that EZH2 was the target protein that interacted with lncSIL , and the expression of EZH2 increased after silencing lncSIL , the expression of EZH2 downstream gene P21 decreased , CDK6 increased . Flow cytometry showed that the number of cells in S phase significantly increased . When lncSIL was overexpressed , the expression of EZH2 and CDK6 was down-regulated , the expression of P21 was up-regulated , and the number of S phase cells significantly decreased . Conclusion LncSIL inhibits TGF-β1-induced alveolar epithelial cell mesen- chymal transition by negatively regulating EZH2/P21 /CDK6 signaling pathway to inhibit cell cycle progression .

Objective: To investigate the effect of LncRNA OIP5-AS1 on radiosensitivity of non-small cell lung cancer (NSCLC) cells and its mechanism. Methods: The radiation-resistant cell A549R was established by using A549 cells irradiated by X-ray 6Gy in 5 fractions. The expression levels of OIP5-AS1 and miR-34c-5p in A549 and A549R cells were detected by qRT-PCR. OIP5-AS1 inhibitor or miR-34c-5p mimetic was transfected into A549R cells, or OIP5-AS1 overexpression plasmid was transfected into A549 cells. Cell apoptosis was detected by flow cytometry. Cell radiosensitivity was analyzed by colony formation assay. The expression levels of p-Chk2 and p-ATM proteins were measured by Western blot. Dual luciferase assay was adopted to verify the relationship between OIP5-AS1 and miR-34c-5p. Results: Compared with A549 cells, the expression of OIP5-AS1 was significantly up-regulated in A549R cells (1.97±0.11 vs.1.01±0.05, P<0.05), whereas the expression of miR-34c-5p was remarkably down-regulated (0.43±0.02 vs.1.02±0.06, P<0.05). The expression levels of p-Chk2 and p-ATM proteins in A549R cells in the silencing OIP5-AS1+ 6Gy group were significantly lower (0.43±0.03 vs.1.39±0.15, 0.51±0.0 5 vs.1.21± 0.11, both P<0.05), whereas the apoptotic rate was significantly higher than those in the silencing control+ 6Gy group [(13.29±1.25)% vs. (28.47±2.31)%, P<0.05)]. The expression levels of p-Chk2 and p-ATM proteins in A549 cells in overexpressing OIP5-AS1+ 6Gy group were significantly higher than those in overexpression control+ 6Gy group (1.23±0.13 vs.0.75±0.06, 1.08±0.11 vs.0.59±0.04, both P<0.05). Inhibiting miR-34c-5p expression reversed the effect of silencing OIP5-AS1 on survival fraction of A549R cells (SER=1.42). OIP5-AS1 negatively regulated the expression of miR-34c-5p. Conclusion Silencing OIP5-AS1 enhances the radiosensitivity of radiation-resistant A549 cells by up-regulating the expression of miR-34c-5p, providing a potential target for radiotherapy of NSCLC cells.

Objective: To observe the platinum drugs resistance effect of N-acetyltransferase 10 (NAT10) overexpression in breast cancer cell line and elucidate the underlining mechanisms. Methods: The experiment was divided into wild-type (MCF-7 wild-type cells without any treatment) group, NAT10 overexpression group (H-NAT10 plasmid transfected into MCF-7 cells) and NAT10 knockdown group (SH-NAT10 plasmid transfected into MCF-7 cells). The invasion was detected by Transwell array, the interaction between NAT10 and PARP1 was detected by co-immunoprecipitation. The impact of NAT10 overexpression or knockdown on the acetylation level of PARP1 and its half-life was also determined. Immunostaining and IP array were used to detect the recruitment of DNA damage repair protein by acetylated PARP1. Flow cytometry was used to detect the cell apoptosis. Results: Transwell invasion assay showed that the number of cell invasion was 483.00±46.90 in the NAT10 overexpression group, 469.00±40.50 in the NAT10 knockdown group, and 445.00±35.50 in the MCF-7 wild-type cells, and the differences were not statistically significant (P>0.05). In the presence of 10 μmol/L oxaliplatin, the number of cell invasion was 502.00±45.60 in the NAT10 overexpression group and 105.00±20.50 in the NAT10 knockdown group, both statistically significant (P<0.05) compared with 219.00±31.50 in wild-type cells. In the presence of 10 μmol/L oxaliplatin, NAT10 overexpression enhanced the binding of PARP1 to NAT10 compared with wild-type cells, whereas the use of the NAT10 inhibitor Remodelin inhibited the mutual binding of the two. Overexpression of NAT10 induced PARP1 acetylation followed by increased PARP1 binding to XRCC1, and knockdown of NAT10 expression reduced PARP1 binding to XRCC1. Overexpression of NAT10 enhanced PARP1 binding to LIG3, while knockdown of NAT10 expression decreased PARP1 binding to LIG3. In 10 μmol/L oxaliplatin-treated cells, the γH2AX expression level was 0.38±0.02 in NAT10 overexpressing cells and 1.36±0.15 in NAT10 knockdown cells, both statistically significant (P<0.05) compared with 1.00±0.00 in wild-type cells. In 10 μmol/L oxaliplatin treated cells, the apoptosis rate was (6.54±0.68)% in the NAT10 overexpression group and (12.98±2.54)% in the NAT10 knockdown group, both of which were statistically significant (P<0.05) compared with (9.67±0.37)% in wild-type cells. Conclusion: NAT10 overexpression enhances the binding of NAT10 to PARP1 and promotes the acetylation of PARP1, which in turn prolongs the half-life of PARP1, thus enhancing PARP1 recruitment of DNA damage repair related proteins to the damage sites, promoting DNA damage repair and ultimately the survival of breast cancer cells.
Breast Neoplasms/enzymology* ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Female ; Humans ; MCF-7 Cells ; N-Terminal Acetyltransferases/metabolism* ; Organoplatinum Compounds/pharmacology* ; Oxaliplatin/pharmacology* ; X-ray Repair Cross Complementing Protein 1

OBJECTIVE: To measure the implicit attitude of nurses towards doctors and analyze its influencing factors. METHODS: A total of 356 nurses were selected as study subjects by convenient sampling method. Their implicit attitude towards doctors was measured by Single Category Implicit Association Test. The related influencing factors were analyzed. RESULTS: The response time of nurses on incompatible tasks was higher than that on compatible tasks [(0.87±0.19) vs(0.76±0.15) s,P<0.01]. The median(M) of D value was 0.34. D value of junior college group was higher than that of undergraduate and above group(M: 0.40 vs 0.27, P<0.01). D value in the nurse group was higher than that in the nurse practitioner group and nurse-in-charge and above group(M: 0.43 vs 0.33, 0.43 vs 0.23, P<0.05). D value of the informal staff group was higher than that of the formal staff group(M: 0.35 vs 0.19, P<0.05). The results of ordered multiple Logistic regression analysis showed that establishment was an independent influencing factor of the implicit attitude of nurses towards doctors(P<0.05), after excluding the influence of confounding factors. CONCLUSION: The implicit attitude of nurses towards doctors is positive and mainly affected by the establishment.

Objective: To understand the relationships between college students’ aggression and self-acceptance, family intimacy and adaptability, and to provide reference for college students’ aggression preventing and intervening. Methods: Using general information questionnaire, Aggression Questionnaire, Self-acceptance Questionnaire and FACES II-CV, 984 college students from 3 colleges in Xinxiang, Henan province were surveyed by questionnaire. Results: The total score of physical aggression, verbal aggression, indirect aggression and aggression in male students was higher than that of female students (t=7.17,4.21,2.05,3.63,P<0.05).The score of physical aggression of only children was higher than that of nononly children (t=2.39,P<0.05).The score of indirect attack of disciplined college students was higher than that of undisciplined college students (t=2.60,P<0.01).There were statistically significant differences in the total scores of indirect attack, hostility and attack among college students with different left-behind experiences (F=3.39,4.61, 3.37, P<0.01).There were statistically significant differences in the total scores of physical aggression, anger and aggression among college students by family income(F=5.70,3.94,3.37,P<0.01).Correlation analysis showed that the total score of college students’ aggression was positively correlated with self-acceptance, negatively correlated with actual family intimacy and actual family adaptability (r=0.37，-0.09，-0.07,P<0.01). Regression analysis showed that self-acceptance, gender, disciplinary action, left-behind experience and expected family adaptability showed significant associations with total score of college students’ aggression (P<0.05). Conclusion Self-acceptance and family closeness and adaptability are associated with aggressive behavior in college students. Schools should carry out targeted psychological health education on self-acceptance to ensure that college students maintain a reasonable level of self-acceptance, and family members should develop certain level of intimacy and adaptability, in order to reduce the occurrence of aggressive behavior of college students.

Virtue ethics and normative ethics are corresponding ethical concepts, and their collision and integration promote the development of ethical system. On the issue of doctor-patient relationship, from virtue to norm is the objective requirement of social transformation and development, and is also the inevitable choice to resolve doctor-patient conflicts and reshape doctor-patient relationships. In the new era, the construction of doctor-patient relationship faces ethical dilemma such as one-sided emphasis on doctors’ virtue cultivation, unclear ethical responsibilities between doctors and patients, and lack of trust and tolerance between doctors and patients. Therefore, it is necessary to strengthen the institutionalization of doctor ethics, clarify the ethical responsibilities of both doctors and patients, optimize the social ethical ecological environment, so as to realize the ethical reconstruction of doctor-patient relationship from virtue to norm.

To study the role of oleanolic acid on interleukin (IL)-1β-stimulated expression of inflammatory cytokines, and to explore its anti-inflammatory mechanism in SW982 cells, the toxicity of oleanolic acid on SW982 cells was detected by MTT; effects of different concentrations of oleanolic acid (5, 10, 20 μmol·L^-1) on the expression of inflammatory factors IL-6, IL-8 and matrix metalloproteinase-1 (MMP-1) was tested at protein and mRNA levels. The study was performed in IL-1β-stimulated SW982 cells together with enzyme-linked immunosorbent assay (ELISA) and real-time fluorescence quantitative PCR (real-time PCR) methods; the influence of oleanolic acid on the phosphorylation of mitogen-activated protein kinase (MAPK), phosphatidyl inositol-3-kinase/Akt (PI3K/Akt) and nuclear transcription factor-κB (NF-κB) signaling pathways related protein was analyzed by Western blot. Results showed that different concentrations of oleanolic acid (≤ 40 μmol·L^-1) were almost non-toxicity to SW982 cells; oleanolic acid significantly inhibited the expression of inflammatory factors in a dose-dependent manner; oleanolic acid restrained extracellular signal-related kinase (ERK), p38, c-jun N-terminal kinase (JNK) and Akt protein phosphorylation and IκB-α protein degradation obviously. The inhibition effect of oleanolic acid on inflammatory factors stimulated by IL-1β may be worked through MAPK, PI3K/Akt and NF-κB signaling pathways.

Objective To establish transgenic mouse models expressing human HSP22 protein.Methods pCAGGS-HA-Wt HSP22 transgenic expressing vector carrying human HSP22 gene was constructed by gene recombination technology.The linearized DNA was got by SalI、Hind Ⅲ and BsaⅪ digestion of PCAGGS-HA-Wt HSP22,purified and microinjected into fertilized eggs from C57BL mice.The tail DNA of pups was tested by PCR and DNA sequencing.Expression of human HSP22 protein was detected by western blot with anti-HA tag monoclonal antibody.Results 4 transgenic founder mice (Tg646,Tg648,Tg649,Tg661) carrying human HSP22 gene were identified by PCR and DNA sequencing.The human HSP22 protein was expressed in the lines Tg646,Tg648 and Tg649 founder mice,but was not expressed in the line Tg661 founder mouse.Conclusions The mouse models expressing human HSP22 protein are established successfully and provide the foundation for HSP22 gene research in vivo.