BACKGROUND:Implant stability is mainly influenced by peri-implant inflammatory stimulation.
OBJECTIVE:To build a beagle model of peri-implantitis under orthodontic force and to observe the bone remodeling of the Beagle dog model.
METHODS: Micro-implants were randomly implanted into the maxilary interradicular region at the center of the mesial and distal roots of bilateral P2, P3, P4 and M1 of Beagle dogs. One side served as a loaded micro-implant with peri-implantitis under 100 g of orthodontic force at 1, 2, 3, 4 weeks of peri-implantitis, and the force lasted for 1 month. After that, the animals were kiled to prepare specimens with micro-implants. Bone-to-implant contacts were calculated and histological changes of the bone interface under continuous orthodontic force at different stages of peri-implantitis were observed under light microscope.
RESULTS AND CONCLUSION:There were a large number of inflammatory cels after micro-implants were implanted with silk thread ligation to the cervical part. Over time, inflammatory cels were gradualy diffused to the tip of micro-implant, and there were a great quantity of colagenous fibers, osteocytes and active bone remodeling. When the inflammation was diffused to the tip of micro-implant after 2 weeks of peri-implantitis, woven bones composed of newly formed trabeculae appeared, and imflammatory cels dispersed. The medulary cavity was irregular after colagen fibrils absorption, and there were 3-4 layers of osteoblasts in the bone lacunae, with active bone formation. These findings indicate that the Beagle model of pure titanium peri-implantitis under orthodontic force was successfuly built in the experiment, and bone formation became active at 2 weeks after modeling.

Objective To investigate the neuroprotective effect of lateral intracerebroventricular injection of Apelin-13 on the YAP expression and the cerebral ischemia/reperfusion (I/R) injury in Wistar rats.Methods Healthy adult male Wistar rats were randomly divided into the sham group, cerebral I/R group and Apelin-13 treatment group.The middle cerebral artery occlusion model was established with ischemia for 1 hour and reperfusion for 24 hours after restricting food and water intake for 12 hours.Apelin-13 was injected into rats' lateral ventricles of Apelin-13 treatment group after reperfusion.Neural function defects was assessed.The volume of infarction was evaluated by TTC staining.The expression levels of YAP were detected by western blot.Results Compared with the cerebral I/R group,the rats in the Apelin-13 treatment group had abetter neurologic score ((2.67±0.33) vs (1.67±0.33) , P＜0.05), the infarction volume was decreased ((30.60± 1.42) ％ vs (23.70± 2.20) ％,P＜0.05) , and YAP expression level was increased in each part of the cerebral tissue(P＜0.05).Conclusion Apelin-13 has a neuroprotective effect,which plays the therapeutic effect by regulating the expression of YAP on cerebral ischemia/ reperfusion (I/R) injury in Wistar rats.

Objective: To determine the changed expression levels, biological roles and underlying mechanism of LncSox4 in non-small cell lung cancer (NSCLC), providing novel biomarkers for NSCLC diagnosis and therapy. Methods: QRT-PCR was used to detect the expression of LncSox4 in the tumor tissues of NSCLC patients. Colony formation, cell growth curve, Transwell migration and invasion assays were used to determine the effects of LncSox4 knockdown on A549 cell function, respectively. Flow cytometry was used to determine the effects of LncSox4 on the progression of A549 cell cycle. QRT-PCR and western blot were used to explore the expressions of genes and proteins in epithelial-mesenchymal transition (EMT). Results: The expression of LncSox4 was upregulated significantly in carcinoma tissues of NSCLC compared to the para-carcinoma tissues (t=7.109，P＜0.01). The growth rate of A549 cells slowed down in LncSox4 knockdown group and the number of formed cell colonies was less than that in control group(P＜0.01). LncSox4 knockdown reduced the migration and invasion abilities of A549 cells (P＜0.01) and induced cell cycle arrest at G1 phase(P＜0.01). LncSox4 knockdown downregulated the protein expressions of Cyclin D1, c-Myc, N-cadherin, and Vimentin, while upregulated the expression of E-cadherin in A549 cells. LncSox4 knockdown also decreased the expressions of EMT-related transcription factors including snail, slug and twist. Conclusion The high expression of LncSox4 in NSCLC may promote malignant progression of NSCLC by enhancing cell proliferation, migration and invasion, suggesting that it should be a promising target for diagnosis and therapy of NSCLC.

Objective: To investigate the clinicopathologic features of follicular lymphoma (FL) in children. Methods: One female and one male patients with FL diagnosed in the First College of Clinical Medical Science, China Three Gorges University and Beijing Friendship Hospital of the Capital University of Medical Science in February 2016 and June 2015 were studied by HE immunohistochemistry, EBER in situ hybridization, IgH and IgK gene rearrangement analysis and IRF4 fusion gene detection. Results: The two patients′ age were 6.3 and 12 years, respectively. The lesions involved head and neck lymph nodes with duration of more than 2 months. Histopathologically, the lesions consisted of nodular proliferation of lymphoid follicles with diffuse distribution of large cells. Starry sky phenomenon was seen in one of the two cases. Immunohistochemistry showed that one case was positive for bcl-2 and MUM1, but negative for bcl-6 and CD10. Ki-67 index was>50% and oligoclonal IgK rearrangement was observed. The second case showed positivity for bcl-6, and CD10 but negative for bcl-2. Ki-67 index was>50% and clonal IgH FR1-JH and IgH FR2-JH rearrangements were detected. Both cases showed no evidence of IRF4 gene fusion. Conclusions Childhood FL is a rare B-cell lymphoma with characteristic features and high-grade histomorphology. However, its immunophenotype and molecular genetic characteristics are divergent.

Objective: To investigate the expression change, biological role and action mechanism of long non-coding RNA (lncRNA) LINC00978 in non-small cell lung cancer (NSCLC). Methods: The expression levels of LINC00978 in tumor tissues and serum samples of NSCLC patients were detected by the qRT-PCR. The effects of knockdown and overexpression of LINC00978 on the biological function of A549 cells were determined by the CCK-8, colony formation, Transwell migration and invasion assays. The action mechanisms of LINC00978 in NSCLC were investigated by the flow cytometry, qRT-PCR and western blot, respectively. Results: The expression levels of LINC00978 in the tissues ( t =2.465, P ＜0.05) and serum samples ( t =8.781, P ＜0.01) of NSCLC patients increased. The knockdown of LINC00978 inhibited the proliferation, migration and invasion of A549 cells ( P ＜0.01) and induced cell cycle arrest at G1 phase and apoptosis of A549 cells ( P ＜0.01). The knockdown of LINC00978 downregulated the expression of Cyclin D1 and Bcl-2 , and upregulated the expression of Bax ( P ＜0.05). In addition, the knockdown of LINC00978 inhibited the expression of N-cadherin, Vimentin, Snail, Slug and Twist, and promoted the expression of E-cadherin ( P ＜0.05). The overexpression of LINC00978 had the opposite effect. Conclusion LINC00978 is highly expressed in NSCLC and can promote the occurrence and progression of NSCLC, which may serve as a potential target for the diagnosis and therapy of NSCLC.