80 cm高度障碍马肢体角度与越障步态特征关联性分析

【目的】测定障碍马80 cm高度越障性能,研究其静态肢体角度和4个阶段步态特征之间的相关性,筛选出与越障性能相关的肢体角度指标,为障碍马体型结构研究提供理论依据。【方法】使用高速摄像机拍摄20匹障碍马静态肢体角度和越障时步态特征。并借助Kinovea视频分析软件提取马匹静态肢体角度和四个时期步态特征数据,分析肢体角度和步态特征的关联性。【结果】在起跳阶段时,头俯仰角和后位后蹄支撑相关系数为0.495*,即呈显著正相关(P<0.05),与起跳位置呈显著负相关(P<0.05)。在悬空阶段时,后球关节和前位后蹄摆动相相关系数为0.564**,即呈极显著正相关(P<0.01)。头俯仰角和跳跃距离呈显著负相关(P<0.05)。在着陆阶段时,后飞节和前肢双支撑相呈显著正相关(P<0.05)。后球关节和前肢双支撑相相关系数为0.568*,即呈极显著正相关(P<0.01)。在缓冲阶段,前球关节和步频呈显著正相关(P<0.05)。股骨倾角和后位前蹄摆动相呈显著正相关(P<0.05)。膝关节和腾空期步幅呈显著正相关(P<0.05)。头俯仰角和前位前蹄摆动相相关系数为0.570**,即呈极显著正相关(P<0.01)。【结论】在80 cm越障过程中,障碍马头俯仰角变异系数为14.59%对起跳阶段,悬空阶段、缓冲阶段有显著影响。髋骨倾角变异系数为20.22%对起跳阶段和着陆阶段有显著影响。后球关节角变异系数为3.83%对悬空阶段和着陆阶段有显著影响。头俯仰角、髋骨倾角、后球关节角等关节角度可作为重要的障碍马体型结构指标,用于评估马匹的越障性能。

EFFECT OF AURICULAR ACUPUNCTURE ON THE LEARNING AND MEMORY AND bcl-2 EXPRESSION IN VASCULAR DEMENTIA RATS

Objective: To study the effect of auricular acupuncture on dysmnesia and the relationship between the memory improvement and bcl 2 protein expression in vascular dementia (VD) rats. Methods: Forty Wistar rats were randomized into control group, VD group, acupuncture+VD group and pseudo operation group, with 10 cases in each group. Rat VD model was established by using 4 vessel occlusion method. Otopoint "Nao" point and "Shen"(MA SC) were punctured, once daily continuously for 15 days. The rats’ memory capability was tested with Y maze method and bcl 2 expression of the brain tissues displayed by immunohistochemical method and measured using MIAS 2000 Image Analyzer. Results: Results showed that the scores of control group, VD group and acupuncture+VD group before operation were 5.68±1.29, 6.07±1.67 and 5.86±1.74 respectively, while following auricular acupuncture treatment, the scores of the 3 groups were 5.81±1.51, 18.06±2.68 and 8.31±1.85 separately, suggesting that the VD rat’s learning and memory abilities in acupuncture+VD group were raised apparently in comparison with those of VD group (P<0.01). In control, VD and acupuncture+VD group, bcl 2 immuno reaction positive neurons in CA 1 area of the hippocampus were 14.31±4.87, 28.67±5.63 and 65.74±8.19 respectively, displaying that the improvement of learning and memory abilities caused by auricular acupuncture treatment may be related to the up regulation of bcl 2 expression (an inhibitory gene of apoptosis). In comparison with control group, the loss of neurons in the pyramidal cell layer of the hippocampal CA 1 area of VD group was more severe, while that of acupuncture group was markedly lighter. Conclusion: Auricular acupuncture of otopoint "Nao" point and "Shen"(MA SC) can raise the learning and memory abilities of VD rats, which may be realized by its inhibitory effect on apoptosis and the protection action on ischemic hippocampal neurons.

Mario Paint： An Accessible Environment of Musical Creativity and Sound Exploration

Mario Paint, the 1992 Nintendo game for the Super NES, remains an accessible environment for musical creativity and sound exploration within its music mode. Although developed for a gaming system, the game＇s music mode is a streamlined tool built upon basic music theory and music composition. Through familiar video game sounds and icon and Westem music notation, players are able to compose chipttme works and explore the nature of sound through an inviting interface. Similar music composition software upgrades the process of composition established in Mario Paint, allowing for digital distribution and dissemination. Mario Paint continues to inspire new projects in the areas of video games and scholastic studies. Mario Paint and its successors are very reasonable entry-level programs for chiptune composers and fledgling music students

Hippocampal HMGB1/TLR4 Pathway Mediates Cognitive Dysfunction in Chronic Stress Mice

Objective Chronic stress can induce cognitive dysfunction,but the underlying mechanisms remain unknown.Studies have confirmed that the high mobility group box 1/Toll-like receptor 4(HMGB1/TLR4)pathway is closely associated with cognitive impairment.Therefore,this research aimed to explore whether the HMGB1/TLR4 pathway involves in chronic stress-induced cognitive dysfunction.Methods The chronic unpredictable mild stress(CUMS)mouse model was established by randomly giving different types of stress every day for four consecutive weeks.Cognitive function was detected by novel object recognition test,Y-maze test,and Morris water maze test.The protein expressions of HMGB1,TLR4,B-cell lymphoma 2(BCL2),and BCL2 associated X(BAX)were determined by Western blot.The damage of neurons in the hippocampal CA1 region was observed by hematoxylin-eosin(HE)staining.Results The protein expressions of HMGB1 and TLR4 were significantly increased in the hippocampus of chronic stress mice.Furthermore,inhibition of the HMGB1/TLR4 pathway induced by ethyl pyruvate(EP,a specific inhibitor of HMGB1)and TAK242(a selective inhibitor of TLR4)treatment attenuated cognitive impairment in chronic stress mice,according to the novel object recognition test,Y-maze test,and Morris water maze test.In addition,administration of EP and TAK242 also mitigated the increase of apoptosis in the hippocampus of chronic stress mice.Conclusion These results indicate that the hippocampal HMGB1/TLR4 pathway contributes to chronic stress-induced apoptosis and cognitive dysfunction.

Airborne fine particulate matter induces cognitive and emotional disorders in offspring mice exposed during pregnancy

Gestational exposure to PM_(2.5) is associated with adverse postnatal outcomes.PM_(2.5) can enter alveoli by using intratracheal instillation,even penetrate through lung cells into the blood circulation.Subsequently,they are transferred across the placenta and fetal blood brain barrier,causing the adverse birth outcomes of offspring.This study demonstrated that the gestational exposure resulted in cognitive and emotional disorders in female offspring although the offspring were not exposed to PM_(2.5).Placental metabolic pathways modulated fetal brain development and played a pivotal role for maternal-placentalfetal interactions in the fetal programming of adult behavioral and mental disorders.Samples of fetus,offspring hippocampus and placenta from the mice exposed to PM_(2.5) were investigated using a comprehensive approach including mass spectrometry-based lipidomics and three-dimensional imaging.The exposure induced the neuro-degeneration in hippocampus,impairment of placental cytoarchitecture,and reprogramming of lipidome,which might affect the modulation of maternal-fetal cross-talk and result in the behavior disorders of offspring.The variation of spatial distribution of lipids was profoundly affected in dorsal pallium and hippocampal formation regions of fetal brain,offspring hippocampus,as well as labyrinth and junctional zones of placenta.The abundance alteration of lipid markers associated with neurodegenerative diseases was validated in transgenic mouse model with Alzheimer’s disease and human cerebrospinal fluid from patients with Parkinson’s disease.The finding could help with the selection of more suitable heterogeneous-related substructures targeting PM_(2.5) exposure and the exploration of PM_(2.5)-induced toxicological effects on neurodegenerative diseases.