Objective Neuroinflammation with microglial activation has been implicated to have a strong association with the progressive dopaminergic neuronal loss in Parkinson＇s disease （PD）. The present study was undertaken ...Objective Neuroinflammation with microglial activation has been implicated to have a strong association with the progressive dopaminergic neuronal loss in Parkinson＇s disease （PD）. The present study was undertaken to evaluate the activation profile of microglia in 1-methyl-4-phenyl pyridinium （MPP^＋）-induced hemiparkinsonian rats. Triptolide, a potent immunosuppressant and microglia inhibitor, was then examined for its efficacy in protecting dopaminergic neurons from injury and ameliorating behavioral disabilities induced by MPP^＋. Methods The rat model of PD was established by intranigral microinjection of MPP^＋. At baseline and on day 1, 3, 7, 14, 21 following MPP^＋ injection, the degree of microglial activation was examined by detecting the immunodensity of OX-42 （microglia marker） in the substantia nigra （SN）. The number of viable dopaminergic neurons was determined by measuring tyrosine hydroxylase （TH） positive neurons in the SN. Behavioral performances were evaluated by counting the number of rotations induced by apomorphine, calculating scores of forelimb akinesia and vibrissae-elicited forelimb placing asymmetry. Results Intranigral injection of MPP^＋ resulted in robust activa- tion of microglia, progressive depletion of dopaminergic neurons, and ongoing aggravation of behavioral disabilities in rats. Triptolide significantly inhibited microglial activation, partially prevented dopaminergic cells from death and improved behavioral performances. Conclusion These data demonstrated for the first time a neuroprotective effect of triptolide on dopaminergic neurons in MPP^＋ induced hemiparkinsonian rats. The protective effect of triptolide may, at least partially, be related to the inhibition of MPP^＋-induced microglial activation. Our results lend strong support to the use of immunosuppressive agents in the management of PD.展开更多
Andrej Belyj is the main representative of Russia symbolism. Symbolists pursue the text mystique with massive utilization of myth. But here myth has changed and obtained new myth characteristic, which is manifested in...Andrej Belyj is the main representative of Russia symbolism. Symbolists pursue the text mystique with massive utilization of myth. But here myth has changed and obtained new myth characteristic, which is manifested in Perterburg.展开更多
Traumatic arteriovenous fistula between the axillary artery and vein may present a difficult problem in treatment. There are few reports demonstrating the endovascular repair of this challenge. Herein, we present such...Traumatic arteriovenous fistula between the axillary artery and vein may present a difficult problem in treatment. There are few reports demonstrating the endovascular repair of this challenge. Herein, we present such a case of endovascular repair of traumatic arteriovenous fistula between the axillary artery and vein with false aneurysm formation. The patient was discharged 11 days after successful operation. Oral clopidogrel and aspirin were administerted for 18 months. At one year follow-up, the patient was in good condition and showed no evidence of neurological deficit in the left upper limb.展开更多
文摘Objective Neuroinflammation with microglial activation has been implicated to have a strong association with the progressive dopaminergic neuronal loss in Parkinson＇s disease （PD）. The present study was undertaken to evaluate the activation profile of microglia in 1-methyl-4-phenyl pyridinium （MPP^＋）-induced hemiparkinsonian rats. Triptolide, a potent immunosuppressant and microglia inhibitor, was then examined for its efficacy in protecting dopaminergic neurons from injury and ameliorating behavioral disabilities induced by MPP^＋. Methods The rat model of PD was established by intranigral microinjection of MPP^＋. At baseline and on day 1, 3, 7, 14, 21 following MPP^＋ injection, the degree of microglial activation was examined by detecting the immunodensity of OX-42 （microglia marker） in the substantia nigra （SN）. The number of viable dopaminergic neurons was determined by measuring tyrosine hydroxylase （TH） positive neurons in the SN. Behavioral performances were evaluated by counting the number of rotations induced by apomorphine, calculating scores of forelimb akinesia and vibrissae-elicited forelimb placing asymmetry. Results Intranigral injection of MPP^＋ resulted in robust activa- tion of microglia, progressive depletion of dopaminergic neurons, and ongoing aggravation of behavioral disabilities in rats. Triptolide significantly inhibited microglial activation, partially prevented dopaminergic cells from death and improved behavioral performances. Conclusion These data demonstrated for the first time a neuroprotective effect of triptolide on dopaminergic neurons in MPP^＋ induced hemiparkinsonian rats. The protective effect of triptolide may, at least partially, be related to the inhibition of MPP^＋-induced microglial activation. Our results lend strong support to the use of immunosuppressive agents in the management of PD.
文摘Andrej Belyj is the main representative of Russia symbolism. Symbolists pursue the text mystique with massive utilization of myth. But here myth has changed and obtained new myth characteristic, which is manifested in Perterburg.
文摘Traumatic arteriovenous fistula between the axillary artery and vein may present a difficult problem in treatment. There are few reports demonstrating the endovascular repair of this challenge. Herein, we present such a case of endovascular repair of traumatic arteriovenous fistula between the axillary artery and vein with false aneurysm formation. The patient was discharged 11 days after successful operation. Oral clopidogrel and aspirin were administerted for 18 months. At one year follow-up, the patient was in good condition and showed no evidence of neurological deficit in the left upper limb.
