Schizophrenia is a disease that affects many areas of the brain. The dopamine hypothesis is one of the most widely-accepted ideas in the pathophysiology of schizophrenia. Besides alterations in the dopaminergic system...Schizophrenia is a disease that affects many areas of the brain. The dopamine hypothesis is one of the most widely-accepted ideas in the pathophysiology of schizophrenia. Besides alterations in the dopaminergic system in the central nervous system, there have been several reports of changes in dopaminergic systems in the peripheral blood of schizophrenic patients. Several reports have shown that dopamine receptor expression by lymphocytes is altered in patients with schizophrenia, but the results have been conflicting. We therefore re-assessed D3R and D4R mRNA levels in 11 patients with schizophrenia and 12 healthy subjects and correlated levels with severity of symptoms. D3R and D4R expression in lymphocytes and granulocytes was measured by quantitative RT-PCR and the severity of symptoms and cognitive impairment were assessed using the PANSS and BACS-J. There were no significant differences in mean D3R or D4R mRNA levels in lymphocytes from schizophrenic patients and controls and no significant difference in mean D4R mRNA levels in granulocytes (D3R mRNA undetectable). In patients with schizophrenia, D3R expression was inversely correlated with the total PANSS score (r = 0.768, p = 0.009), while D4R expression was positively correlated with working memory scales (r = 0.895, p = 0.001). In conclusion, these results imply that lymphocyte D3R and D4R are involved in the mechanisms of the disorder and could be used as target markers in the treatment of schizophrenia.展开更多
Because behavior recognition is based on video frame sequences,this paper proposes a behavior recognition algorithm that combines 3D residual convolutional neural network(R3D)and long short-term memory(LSTM).First,the...Because behavior recognition is based on video frame sequences,this paper proposes a behavior recognition algorithm that combines 3D residual convolutional neural network(R3D)and long short-term memory(LSTM).First,the residual module is extended to three dimensions,which can extract features in the time and space domain at the same time.Second,by changing the size of the pooling layer window the integrity of the time domain features is preserved,at the same time,in order to overcome the difficulty of network training and over-fitting problems,the batch normalization(BN)layer and the dropout layer are added.After that,because the global average pooling layer(GAP)is affected by the size of the feature map,the network cannot be further deepened,so the convolution layer and maxpool layer are added to the R3D network.Finally,because LSTM has the ability to memorize information and can extract more abstract timing features,the LSTM network is introduced into the R3D network.Experimental results show that the R3D+LSTM network achieves 91%recognition rate on the UCF-101 dataset.展开更多
Background: fourth generation antipsychotics have been implicated in the blockade of calcium signalling through inhibition of dopamine receptive sites on dopaminergic D2 Receptor (D3R). As a result of the abnormal cal...Background: fourth generation antipsychotics have been implicated in the blockade of calcium signalling through inhibition of dopamine receptive sites on dopaminergic D2 Receptor (D3R). As a result of the abnormal calcium signalling associated with D2R inhibition, changes occur in the motor and memory neural axis leading to the observed behavioural deficits after prolonged haloperidol. Thus, Vitamin D3 receptor (VD3R), a calcium controlling receptor in the striatum can be targeted to relief the neurological symptoms associated with haloperidol (-D2R) induced PD. Aim: This study sets to investigate the role of VD3R activation in vitro and in vivo after haloperidol-induced Dopaminergic (D2R) blockade. In addition, we examined the associated neural activity and behavioural changes in parkinsonian and VDRA intervention mice. Methods: Dopaminergic D2R inhibition was investigated in vitro using Melanocytes isolated from the scale of a Tilapia. In four separate set ups, the cells were cultured in calcium free Ringer’s solution as follows;300 μM haloperidol, 100 μM VD3, 100 mM calcium chloride and a combination of 300 μM haloperidol and 100 μM VD3. Subsequently, dopaminergic vesicle accumulation and calcium signalling were observed in bright field microscopy using blue and green fluorescence probes. In the second phase, PD was induced in adult BALB/c mice (-D2;n = 8) after 14 days of intraperitoneal haloperidol treatment (10 mg/Kg). A set of n = 4 mice were untreated (-D2) while the other group (n = 4) received 100 mg/Kg of VD3 for 7 days (-D2/+VDR). The control groups (n = 4 each) were treated with normal saline (NS) and VD3 (+VDR) for 14 days. At the end of the treatment phase, the animals were assessed in Rotarod, parallel bar-, cylinder-, Y-Maze-, one trial place recognition- and novel object recognition-(NOR) tests. Neural activity was measured using chronic electrode implants placed in the M1 (motor cortex), CPu (striatum), CA1 (hippocampus) and PFC (prefrontal cortex). Neural activity was compared with the outcomes of behavioural tests for memory and motor functions and data was expressed as mean ± SEM (analysed using ANOVA with Tukey post-hoc test, significant level was set at 0.05). Results/Discussion: in vitro outcomes show that VDR increase calcium signalling and reverses the effect of haloperidol;specifically by reducing dopaminergic vesicle accumulation in the cell body. Similarly, in vivo neural recordings suggest an increase in calcium hyperpolarization currents in the CPu and PFC of intervention mice (-D2/+VDR) when compared with the parkinsonian mice (-D2). These animals (-D2/+VDR) also recorded an improvement in spatial working memory and motor function versus the Parkinsonian mice (-D2). These outcomes suggest the role of CPu-PFC corticostriatal outputs in the motor-cognitive decline seen in parkinsonian mice. Similarly, VDRA reduced the neural deficits through restoration of calcium currents (burst activities) in the intervention mice (-D2/+VDR). Conclusion: VDRA treatment reduced the motor-cognitive defects observed in haloperidol induced PD. Our findings suggest the role of VDRA in restoration of calcium currents associated with PFC and CPu corticostriatal outputs seen as burst frequencies in in vivo neural recording.展开更多
Haloperidol-induced dyskinesia has been linked to a reduction in dopamine activity characterized by the inhibition of dopamine receptive sites on D2-receptor (D2R). As a result of D2R inhibition, calcium-linked neural...Haloperidol-induced dyskinesia has been linked to a reduction in dopamine activity characterized by the inhibition of dopamine receptive sites on D2-receptor (D2R). As a result of D2R inhibition, calcium-linked neural activity is affected and seen as a decline in mo-tor-cognitive function after prolonged haloperidol use in the treatment of psychotic disorders. In this study, we have elucidated the relationship between haloperidol-induced tardive dyskinesia and the neural activity in motor cortex (M1), basal nucleus (CPu), prefrontal cortex (PFC) and hippocampus (CA1). Also, we explored the role of Vitamin D3 receptor (VD3R) activation as a therapeutic target in improving motor-cognitive functions in dyskinetic mice. Dyskinesia was induced in adult BALB/c mice after 28 days of haloperidol treatment (10 mg/Kg;intraperitoneal). We established the presence of abnormal involuntary movements (AIMs) in the haloperidol treated mice (-D2) through assessment of the threshold and amplitude of abnormal involuntary movements (AIMs) for the Limbs (Li) and Orolingual (Ol) area (Li and Ol AIMs). As a confirmatory test, the dyskinetic mice (-D2) showed high global AIMs score when compared with the VD3RA intervention group (-D2/+VDR) for Li and Ol AIMs. Furthermore, in the behavioral tests, the dyskinetic mice exhibited a decrease in latency of fall (LOF;Rotarod-P 2/+VDR), 100 mg/Kg for 7 days, CPu-CA1 burst activity was restored leading to a decrease in abnormal movement, and an increase in motor function. Ultimately, we deduced that VD3RA activation reduced the threshold of abnormal movement in haloperidol induced dyskinesia.展开更多
AMD推出基于RV670核心的系列产品获得市场好评。其系列中的顶级型号Radeon HD 3870的3D性能较上一代旗舰R600核心的Radeon HD 2900 XT有较大提升。不过从我们以往的测试来看，Radeon HD 3870的3D性能并不如ONVIDIA的顶级产品GeForce 88...AMD推出基于RV670核心的系列产品获得市场好评。其系列中的顶级型号Radeon HD 3870的3D性能较上一代旗舰R600核心的Radeon HD 2900 XT有较大提升。不过从我们以往的测试来看，Radeon HD 3870的3D性能并不如ONVIDIA的顶级产品GeForce 8800 Ultra。基于R680核心的新旗舰产品——Radeon HD 3870×2，就是在这样背景下诞生，AMD意在靠它重夺显卡旗舰霸主。展开更多
A unit cell geometrical structure was found with the use of symmetry operations corresponding to the point group C3. Based on the symmetry of space group R3, a 3D braided geometrical structure was obtained by transfor...A unit cell geometrical structure was found with the use of symmetry operations corresponding to the point group C3. Based on the symmetry of space group R3, a 3D braided geometrical structure was obtained by transforming the unit-cell. The features corresponding to this braided structure were studied. The fiber volume percentage and variational tendencies of the material were predicted by establishing a geometric model.展开更多
文摘Schizophrenia is a disease that affects many areas of the brain. The dopamine hypothesis is one of the most widely-accepted ideas in the pathophysiology of schizophrenia. Besides alterations in the dopaminergic system in the central nervous system, there have been several reports of changes in dopaminergic systems in the peripheral blood of schizophrenic patients. Several reports have shown that dopamine receptor expression by lymphocytes is altered in patients with schizophrenia, but the results have been conflicting. We therefore re-assessed D3R and D4R mRNA levels in 11 patients with schizophrenia and 12 healthy subjects and correlated levels with severity of symptoms. D3R and D4R expression in lymphocytes and granulocytes was measured by quantitative RT-PCR and the severity of symptoms and cognitive impairment were assessed using the PANSS and BACS-J. There were no significant differences in mean D3R or D4R mRNA levels in lymphocytes from schizophrenic patients and controls and no significant difference in mean D4R mRNA levels in granulocytes (D3R mRNA undetectable). In patients with schizophrenia, D3R expression was inversely correlated with the total PANSS score (r = 0.768, p = 0.009), while D4R expression was positively correlated with working memory scales (r = 0.895, p = 0.001). In conclusion, these results imply that lymphocyte D3R and D4R are involved in the mechanisms of the disorder and could be used as target markers in the treatment of schizophrenia.
基金Supported by the Shaanxi Province Key Research and Development Project (No. 2021GY-280)Shaanxi Province Natural Science Basic Research Program (No. 2021JM-459)the National Natural Science Foundation of China (No. 61772417)
文摘Because behavior recognition is based on video frame sequences,this paper proposes a behavior recognition algorithm that combines 3D residual convolutional neural network(R3D)and long short-term memory(LSTM).First,the residual module is extended to three dimensions,which can extract features in the time and space domain at the same time.Second,by changing the size of the pooling layer window the integrity of the time domain features is preserved,at the same time,in order to overcome the difficulty of network training and over-fitting problems,the batch normalization(BN)layer and the dropout layer are added.After that,because the global average pooling layer(GAP)is affected by the size of the feature map,the network cannot be further deepened,so the convolution layer and maxpool layer are added to the R3D network.Finally,because LSTM has the ability to memorize information and can extract more abstract timing features,the LSTM network is introduced into the R3D network.Experimental results show that the R3D+LSTM network achieves 91%recognition rate on the UCF-101 dataset.
文摘Background: fourth generation antipsychotics have been implicated in the blockade of calcium signalling through inhibition of dopamine receptive sites on dopaminergic D2 Receptor (D3R). As a result of the abnormal calcium signalling associated with D2R inhibition, changes occur in the motor and memory neural axis leading to the observed behavioural deficits after prolonged haloperidol. Thus, Vitamin D3 receptor (VD3R), a calcium controlling receptor in the striatum can be targeted to relief the neurological symptoms associated with haloperidol (-D2R) induced PD. Aim: This study sets to investigate the role of VD3R activation in vitro and in vivo after haloperidol-induced Dopaminergic (D2R) blockade. In addition, we examined the associated neural activity and behavioural changes in parkinsonian and VDRA intervention mice. Methods: Dopaminergic D2R inhibition was investigated in vitro using Melanocytes isolated from the scale of a Tilapia. In four separate set ups, the cells were cultured in calcium free Ringer’s solution as follows;300 μM haloperidol, 100 μM VD3, 100 mM calcium chloride and a combination of 300 μM haloperidol and 100 μM VD3. Subsequently, dopaminergic vesicle accumulation and calcium signalling were observed in bright field microscopy using blue and green fluorescence probes. In the second phase, PD was induced in adult BALB/c mice (-D2;n = 8) after 14 days of intraperitoneal haloperidol treatment (10 mg/Kg). A set of n = 4 mice were untreated (-D2) while the other group (n = 4) received 100 mg/Kg of VD3 for 7 days (-D2/+VDR). The control groups (n = 4 each) were treated with normal saline (NS) and VD3 (+VDR) for 14 days. At the end of the treatment phase, the animals were assessed in Rotarod, parallel bar-, cylinder-, Y-Maze-, one trial place recognition- and novel object recognition-(NOR) tests. Neural activity was measured using chronic electrode implants placed in the M1 (motor cortex), CPu (striatum), CA1 (hippocampus) and PFC (prefrontal cortex). Neural activity was compared with the outcomes of behavioural tests for memory and motor functions and data was expressed as mean ± SEM (analysed using ANOVA with Tukey post-hoc test, significant level was set at 0.05). Results/Discussion: in vitro outcomes show that VDR increase calcium signalling and reverses the effect of haloperidol;specifically by reducing dopaminergic vesicle accumulation in the cell body. Similarly, in vivo neural recordings suggest an increase in calcium hyperpolarization currents in the CPu and PFC of intervention mice (-D2/+VDR) when compared with the parkinsonian mice (-D2). These animals (-D2/+VDR) also recorded an improvement in spatial working memory and motor function versus the Parkinsonian mice (-D2). These outcomes suggest the role of CPu-PFC corticostriatal outputs in the motor-cognitive decline seen in parkinsonian mice. Similarly, VDRA reduced the neural deficits through restoration of calcium currents (burst activities) in the intervention mice (-D2/+VDR). Conclusion: VDRA treatment reduced the motor-cognitive defects observed in haloperidol induced PD. Our findings suggest the role of VDRA in restoration of calcium currents associated with PFC and CPu corticostriatal outputs seen as burst frequencies in in vivo neural recording.
文摘Haloperidol-induced dyskinesia has been linked to a reduction in dopamine activity characterized by the inhibition of dopamine receptive sites on D2-receptor (D2R). As a result of D2R inhibition, calcium-linked neural activity is affected and seen as a decline in mo-tor-cognitive function after prolonged haloperidol use in the treatment of psychotic disorders. In this study, we have elucidated the relationship between haloperidol-induced tardive dyskinesia and the neural activity in motor cortex (M1), basal nucleus (CPu), prefrontal cortex (PFC) and hippocampus (CA1). Also, we explored the role of Vitamin D3 receptor (VD3R) activation as a therapeutic target in improving motor-cognitive functions in dyskinetic mice. Dyskinesia was induced in adult BALB/c mice after 28 days of haloperidol treatment (10 mg/Kg;intraperitoneal). We established the presence of abnormal involuntary movements (AIMs) in the haloperidol treated mice (-D2) through assessment of the threshold and amplitude of abnormal involuntary movements (AIMs) for the Limbs (Li) and Orolingual (Ol) area (Li and Ol AIMs). As a confirmatory test, the dyskinetic mice (-D2) showed high global AIMs score when compared with the VD3RA intervention group (-D2/+VDR) for Li and Ol AIMs. Furthermore, in the behavioral tests, the dyskinetic mice exhibited a decrease in latency of fall (LOF;Rotarod-P 2/+VDR), 100 mg/Kg for 7 days, CPu-CA1 burst activity was restored leading to a decrease in abnormal movement, and an increase in motor function. Ultimately, we deduced that VD3RA activation reduced the threshold of abnormal movement in haloperidol induced dyskinesia.
文摘AMD推出基于RV670核心的系列产品获得市场好评。其系列中的顶级型号Radeon HD 3870的3D性能较上一代旗舰R600核心的Radeon HD 2900 XT有较大提升。不过从我们以往的测试来看，Radeon HD 3870的3D性能并不如ONVIDIA的顶级产品GeForce 8800 Ultra。基于R680核心的新旗舰产品——Radeon HD 3870×2，就是在这样背景下诞生，AMD意在靠它重夺显卡旗舰霸主。
文摘A unit cell geometrical structure was found with the use of symmetry operations corresponding to the point group C3. Based on the symmetry of space group R3, a 3D braided geometrical structure was obtained by transforming the unit-cell. The features corresponding to this braided structure were studied. The fiber volume percentage and variational tendencies of the material were predicted by establishing a geometric model.
