Objective:This study aimed to investigate the role of bone morphogenetic protein 2 (BMP2)/Smad8 signaling pathway in T-2 toxin-induced apoptosis of rat articular chondrocytes.Methods:Primary chondrocytes from SD rats were cultured in vitro and exposed to varying concentrations of T-2 toxin (0.00, 0.32, 1.60, 8.00 ng/ml). The changes in chondrocytes survival rate were determined by CCK8, and the apoptosis changes of chondrocytes were determined by TUNEL assay kit. Using a group design, chondrocytes were cultured in complete culture media and culture media containing T-2 toxin (1.60 ng/ml), BMP2 cytokine (500 ng/ml), or T-2 toxin (1.60 ng/ml) + BMP2 cytokine (500 ng/ml), referred to as the control group, T-2 toxin group, BMP2 group, and T-2 toxin + BMP2 group, respectively. The survival rate and apoptosis changes of chondrocytes in each group were determined. The expression levels of Caspase-3, BMP2, BMP receptor Ⅱ (BMP-R Ⅱ), and Smad1/4/5/8 were determined by quantitative real-time PCR. Results:Compared with the 0.00 ng/ml of T-2 toxin group [(100.00 ± 0.00)%, (4.33 ± 0.32)%], the chondrocyte survival rates [(85.77 ± 2.96)%, (72.79 ± 2.31)%, (48.87 ± 1.83)%] of the 0.32, 1.60, and 8.00 ng/ml of T-2 toxin groups were significantly lower ( P < 0.05), and the apoptosis rates [(5.43 ± 0.32)%, (6.17 ± 0.15)%, (5.07 ± 0.13)%] were significantly higher ( P < 0.05). Compared with the control group, the T-2 toxin group had a lower survival rate and a higher apoptosis rate of chondrocytes ( P < 0.05). Compared with the T-2 toxin group, the T-2 toxin + BMP2 group had a higher survival rate and lower apoptosis rate of chondrocytes ( P < 0.05). Compared with the control group, the T-2 toxin group showed higher expression level of Caspase-3 mRNA in chondrocytes, while the expression levels of BMP2, BMP-R Ⅱ, and Smad1/4/8 mRNA were lower ( P < 0.05). Compared with the T-2 toxin group, the expression level of Caspase-3 mRNA was lower in the T-2 toxin + BMP2 group, while the expression levels of BMP2 and Smad8 mRNA were higher ( P < 0.05). Conclusion:BMP2 may partially block the apoptosis of chondrocytes caused by T-2 toxin by regulating the BMP2/Smad8 signaling pathway.

Objective:This study aimed to investigate the role of bone morphogenetic protein 2 (BMP2)/Smad8 signaling pathway in T-2 toxin-induced apoptosis of rat articular chondrocytes.Methods:Primary chondrocytes from SD rats were cultured in vitro and exposed to varying concentrations of T-2 toxin (0.00, 0.32, 1.60, 8.00 ng/ml). The changes in chondrocytes survival rate were determined by CCK8, and the apoptosis changes of chondrocytes were determined by TUNEL assay kit. Using a group design, chondrocytes were cultured in complete culture media and culture media containing T-2 toxin (1.60 ng/ml), BMP2 cytokine (500 ng/ml), or T-2 toxin (1.60 ng/ml) + BMP2 cytokine (500 ng/ml), referred to as the control group, T-2 toxin group, BMP2 group, and T-2 toxin + BMP2 group, respectively. The survival rate and apoptosis changes of chondrocytes in each group were determined. The expression levels of Caspase-3, BMP2, BMP receptor Ⅱ (BMP-R Ⅱ), and Smad1/4/5/8 were determined by quantitative real-time PCR. Results:Compared with the 0.00 ng/ml of T-2 toxin group [(100.00 ± 0.00)%, (4.33 ± 0.32)%], the chondrocyte survival rates [(85.77 ± 2.96)%, (72.79 ± 2.31)%, (48.87 ± 1.83)%] of the 0.32, 1.60, and 8.00 ng/ml of T-2 toxin groups were significantly lower ( P < 0.05), and the apoptosis rates [(5.43 ± 0.32)%, (6.17 ± 0.15)%, (5.07 ± 0.13)%] were significantly higher ( P < 0.05). Compared with the control group, the T-2 toxin group had a lower survival rate and a higher apoptosis rate of chondrocytes ( P < 0.05). Compared with the T-2 toxin group, the T-2 toxin + BMP2 group had a higher survival rate and lower apoptosis rate of chondrocytes ( P < 0.05). Compared with the control group, the T-2 toxin group showed higher expression level of Caspase-3 mRNA in chondrocytes, while the expression levels of BMP2, BMP-R Ⅱ, and Smad1/4/8 mRNA were lower ( P < 0.05). Compared with the T-2 toxin group, the expression level of Caspase-3 mRNA was lower in the T-2 toxin + BMP2 group, while the expression levels of BMP2 and Smad8 mRNA were higher ( P < 0.05). Conclusion:BMP2 may partially block the apoptosis of chondrocytes caused by T-2 toxin by regulating the BMP2/Smad8 signaling pathway.

Osteoarthrosis is a disease characterized by degeneration of articular cartilage,inflammation of the synovial membrane in the joint,and changes of the surrounding joints and subchondral bone.The main pathologic changes of osteoarthrosis are chondrocytes reduction and extracellular matrix degradation,which then affect the synovial membrane and articular cartilage bone plate accompanied by osteophyte formation,lead to a series of joint symptoms and signs.Modern medical research shows that long non-coding RNA (lncRNA) plays a certain role in the pathogenesis and development of osteoarthrosis.In this paper,the advances in the study of lncRNA and osteoarthrosis are reviewed.

BACKGROUND:Proximal humeral internal locking system fixation for complex humeral fractures via deltoid splitting approach provides good clinical results, but certain complications stil existed.
OBJECTIVE:To explore the postoperative complications and the related risk factors for displaced three-part and four-part fractures of proximal humerus treated with proximal humeral internal locking system fixation via deltoid-splitting approach, and to propose the corresponding countermeasures.
METHODS:106 cases with displaced three-part and four-part fractures of proximal humerus were retrospectively analyzed. The relationship between postoperative complications and the related risk factors was analyzed with Logistic regression analysis.
RESULTS AND CONCLUSION:A total of 81 patients were fol owed-up for 12 to 30 months. The mean Constant score at 12 months after operation was (76.57±4.70) points. The postoperative complications occurred in 31 patients (38.3%) of which impingement syndrome involved in 16 cases (19.8%), head-shaft angle loss in six cases (7.4%), head-shaft angle loss combined with screws cut-out in two cases (2.5%), pure screws cut-out in two cases (2.5%), humeral head necrosis in two cases (2.5%), fat liquefaction in five cases (6.2%). Single factor analysis showed that there were significant differences in the superiorly located greater tuberosity, superiorly located plate and Neer classification between impingement group and un-impinged group (P<0.05). There were statistical y significant differences in age, postoperative medial cortical defects and Neer classification between head-shaft angle loss group and un-loss group (P<0.05). By means of logistic regression analysis, the superiorly located greater tuberosity, superiorly located plate and Neer classification were the individual predictors for postoperative impingement syndrome;postoperative medial cortical defect and Neer classification were the individual predictors for postoperative head-shaft angle loss.

Objective To explore the effect of erythropoietin (EPO) on cognition and neuron apoptosis in CA1 region of hippocampus in vascular dementia (VaD) rats.Methods 54 Wistar rats were randomly divided into three groups:sham control group,VaD group,VaD+ EPO group (n=18,each).The bilateral common carotid arteries of Wistar rats were permanently ligated to establish VaD models.Spatial study and memory were observed by Y maze test at 4,8 and 12 weeks after operation.Neuron apoptosis in CA1 area of hippocampus was measured by terminal deoxynucleotidyl-transferase (TdT) mediated dUTP-biotin nick end labeling (TUNEL) method.The protein and mRNA expressions of Bcl 2 and Bax in CA1 region of hippocampus were detected by immunohistochemistry and RT-PCR at 4,8,12 weeks after operation.Results Compared with VaD group,the VaD+ EPO group had better performances including less error reaction times and shorter total reaction time in Y-maze (both P＜0.05) at 4,8,12 weeks after operation.The apoptotic neuronal cells in CA1 region of hippocampus was decreased in VaD+ EPO group than in VaD group at 4,8,12 weeks after operation [(10.50±±2.43) vs.(20.50±± 3.29),(23.92±±3.18) vs.(33.58±3.48) and (36.92±4.10) vs.(54.17±4.26),t=4.23,3.54,5.05,P=0.013,0.024,0.007,respectively].The Bcl-2-positive cells and Bcl-2 mRNA expression were increased,and the Baxpositive cells and Bax mRNA expression were decreased in VaD+ EPO group than in VaD group (all P ＜0.05).Conclusions Erythropoietin can improve cognitive function by inhibiting neuron apoptosis through regulation of Bcl-2 and Bax expression in CA1 region of hippocampus.

Objective:To study the role of adhesion molecules in the pathogenesis of polymyositis. Methods:The abnormal expression of adhesion molecules on T cells in peripheral blood and muscle fibers from patients with myositis was analyzed by two colour immunofluoresence and RT PCR methods respectively. Results:The expression of adhesion molecules including lymphocyte function associated antigen 1(LFA 1 ),very late antigen 4(VLA 4) on T cells in peripheral blood and intercellular adhesion molecule l(ICAM 1) on muscle fibers from patients with myositis was markedly higher than that in the healthy control group. Conclusion: These findings suggested that adhesion molecules may be responsible for the migration of T cells and destraction of muscle fibers.

Objective To study the expression of prepro-orexin mRNA in circadian rhythms and sleep-deprived rats.Methods Sleep was deprived with “rotation cylinder” in rats. RT-PCR was used to determine the change of prepro-orexin mRNA expression in cortex and hypothalamus of circadian rhythms and sleep-deprived rats.Results There was a significant changes of prepro-orexin mRNA expression with circadian rhythms in hypothalamus of rats. But there was no significant change in cortex. More prepro-orexin mRNA expression was found in hypothalamus than in cortex of rats. The expression of prepro-orexin mRNA in hypothalamus and in cortex of rats was not effected by short times of sleep deprivation. However the expression was raised by a 8-hour sleep deprivation.Conclusions There should be a close relationship between orexin and sleep. The control of sleep may be dependent on regulation of orexin in hypothalamus.

AIM: To investigate the effect of antisense oligodeoxynucleotides (AS - ODN) on the intercellsular adhesion molecule- 1 (ICAM- 1 ) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R, the positive percentage of ICAM - 1 expression was measured by flow cytometry before and after giving AS - ODN. RESULTS: The ICAM - 1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group, it increased in 6 hours reoxygenation, and decreased by 40.6 % after giving AS- OND. CONCLUSION: AS - ODN may decrease the expression of ICAM- 1 on endothelial cells in H/R.

Objective: To study caspase-3 activities and the neuroprotective effect of caspase-3 inhibitor Ac-DEVD-CMK in primary cultures of rat hippocampal neurons during hypoxia/reoxygenation (H/R). Methods: After pretreated with Ac-DEVD-CMK or the vector DMSO fo 1 h, primary cultures of rat hippocampal neurons were induced to hypoxia for 3 h, followed by 12 to 48 h of reoxygenation. The neuronal viability was estimated by MTT assay, and caspase-3 cellular activities were measured by a colorimetric method using Ac-DEVD-pNA as a substrate. Results: During H/R, the cultured rat hippocampal neuronal viability gradually decreased, and caspase-3 activities in the primary cultures of rat hippocampal neurons were significantly increased, and peaked at 24 h of reoxygenation. Caspase-3 activities were decreased in the neurons pretreated with Ac-DEVD-CMK in a dose dependent manner. Conclusion: Delayed neuronal death is detected in cultured hippocampal neurons during H/R, and apoptosis mediated by caspase-3 may play an important role in it, and caspase-3 inhibitor has a neuroprotective effect on them.

AIM: To investigate the effect of antisense oligodeoxynucleotides (AS-ODN) on the intercellsular adhesion molecule-1(ICAM-1) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R,the positive percentage of ICAM-1 expression was measured by flow cytometry before and after giving AS-ODN. RESULTS: The ICAM-1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group,it increased in 6 hours reoxygenation, and decreased by 40.6% after giving AS-OND. CONCLUSION: AS-ODN may decrease the expression of ICAM-1 on endothelial cells in H/R.