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Articles by Liang Kong
Total Records ( 3 ) for Liang Kong
  Tao Li , Kaijin Hu , Libo Cheng , Yin Ding , Yuxiang Ding , Jinling Shao and Liang Kong
  This study aimed to evaluate continuous and simultaneous variations of dental implant diameter and length, and to identify their relatively optimal ranges in the posterior mandible under biomechanical consideration. A 3D finite element model of a posterior mandibular segment with dental implant was created. Implant diameter ranged from 3.0 to 5.0 mm, and implant length ranged from 6.0 to 16.0 mm. The results showed that under axial load, the maximum Von Mises stresses in cortical and cancellous bones decreased by 76.53% and 72.93% respectively, with the increasing of implant diameter and length; and under buccolingual load, by 83.97% and 84.93%, respectively. Under both loads, the maximum displacements of implant-abutment complex decreased by 58.09% and 75.53%, respectively. The results indicate that in the posterior mandible, implant diameter plays more significant roles than length in reducing cortical bone stress and enhancing implant stability under both loads. Meanwhile, implant length is more effective than diameter in reducing cancellous bone stress under both loads. Moreover, biomechanically, implant diameter exceeding 4.0 mm and implant length exceeding 12.0 mm is a relatively optimal combination for a screwed implant in the posterior mandible with poor bone quality.
  Na Li , Jie Song , Liang Kong , Shao-Heng Li , Ya-Nan Jiao , Yu-Hui Yan , Ying-Jia Yao , Ya-Kun Meng , Xiao-Fei Li , Miao-Miao Tong , Nan Zhang , Kai Kang , Ting-Guo Kang and Jing-Xian Yang
  Background and Objective: Mechanical trauma injury is caused by some external force which does harm to the vasculature, tissues and neighboring neuronal cells. This injury is a serious insult to neuronal cells which may release lactate dehydrogenase as the characteristics of cell damage. The release of inflammatory cytokines in injury cells is a normal immune response but the over expression of some pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor-α are detrimental to wound recovery. Suppression of pro-inflammatory cytokines is beneficial to alleviate mechanical trauma injury-induced cell damage. The present study aims to establish the mechanical trauma injury model in vitro and investigate the protective effect of 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside on this model and its mechanism. Materials and Methods: The SH-SY5Y cells were used to establish the mechanical trauma injury model in vitro by scratching out the monolayer and generating an area devoid of cells. Then, the extent of cell damage of the model was measured by lactate dehydrogenase content determination and 12 h was confirmed as the key time point to explore 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside concentration given. The cell viability was measured by cell counting kit-8 to determine the optimal concentration of drug administration. The extent of cell damage was detected by immunofluorescence analysis to observe whether 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside can protect the integrity of the cell structure TUNEL staining was used to detect whether it can decrease cell apoptosis. Finally, Tested the inflammatory cytokine levels (interleukin-6, interleukin-10 and tumor necrosis factor-α) by enzyme-linked immunosorbent assays, reverse transcription-polymerase chain reaction and western blotting to clarify the mechanism of cytoprotection. Data were assessed by the SPSS version 13.0. Results: The 2,3,5, 4’-tetrahydroxystilbene-2-O-glucoside increased viability of SH-SY5Y cells and the migrative ability, protected the integrity of cell structure, reduced apoptosis, decreased pro-inflammatory cytokine levels (interleukin-6 and tumor necrosis factor-α) and increased anti-inflammatory cytokine level (interleukin-10) in mechanical trauma injury-induced SH-SY5Y cell model. Conclusion: These studies demonstrate that 2,3,5, 4’-tetrahydroxystilbene-2-O-glucoside relieves the mechanical trauma injury-induced damage in SH-SY5Y cells by attenuating the levels of inflammatory responses. This might help us to further understand the pharmacological role of 2,3,5,4’-tetrahydroxystilbene-2-O-glucoside in anti-inflammation and neuroprotection in the neural cells.
  Shao- Heng Li , Li-Tong Wang , Xue Deng , Ya- NanJiao , Liang Kong , Martin Fu , Lian-Qun Jia , Jing-Xian Yang and Lu Ren
  Background and Objective: Perimenopausal depression is caused by the impaired function of the ovarium prior to menopause and characterized by a persistent feeling of sadness and loss of interest. Electroacupuncture (EA) therapy has been demonstrated to be effective in patients with depression. The effects of EA in perimenopausal depression as well as the underlying mechanisms remain unclear. This study aimed to elucidate the therapeutic effect of EA on perimenopausal depression and its correlation with the CREB/BNDF signaling pathway to understand the mechanisms underlying the EA effect. Materials and Methods: Chronic Unpredictable Mild Stress (CUMS) combined with bilateral ovariectomy (OVX) were used to establish a rat model of perimenopausal depression. The Open Field Test (OFT) and sucrose preference tests were used to examine the anxiety level and anhedonia effect of OVX+CUMS rat model and the effects of EA. The MTT assay and flow cytometry were used to detect the cell viability and apoptosis of hippocampal neurons. The immunohistochemistry and ELISA assay were utilized for measuring the proteins expressions and RT-PCR for mRNA expressions, respectively. Comparisons among more than two groups were made using one-way analysis of variance (ANOVA) followed by the Least Significant Difference (LSD) test. Results: The EA at the "Shenshu", "Baihui" and "Sanyinjiao" points could reverse the increased and reduced sucrose preference induced by CUMS and OVX. Meanwhile, the reduced cell viability, increased cell apoptosis and impaired function of hippocampal neurons in the perimenopausal depression model rats were prevented by EA treatment. Moreover, EA increased p-CREB and BDNF expression in the hippocampal neurons and this effect was found to be suppressed by the CREB antagonist KG-501. Conclusion: The EA treatment could rescue the impairment induced by OVX+CUMS via CREB/BDNF pathway activation. Taken together, the results suggest that EA could be a potential therapy for perimenopausal depression.
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