Both genetic and environmental factors are important in the pathogenesis of Parkinson’s disease. Asα-synuclein is a major constituent of Lewy bodies, a pathologic hallmark of Parkinson’s dis-ease, genetic aspects ofα-synuclein is widely studied. However, the inlfuence of dietary factors such as quercetin onα-synuclein was rarely studied. Herein we aimed to study the neuropro-tective role of quercetin against various toxins affecting apoptosis, autophagy and aggresome, and the role of quercetin onα-synuclein expression. PC12 cells were pre-treated with quercetin (100, 500, 1,000 μM) and then together with various drugs such as 1-methyl-4-phenylpyridin-ium (MPP+; a free radical generator), 6-hydroxydopamine (6-OHDA; a free radical generator), ammonium chloride (an autophagy inhibitor), and nocodazole (an aggresome inhibitor). Cell viability was determined using a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltertazolium bromide (MTT) assay. Apoptosis was detected by annexin V-lfuorescein isothiocyanate and propidium iodide through the use of lfuorescence activated cell sorter.α-Synuclein expression was detected by western blot assay and immunohistochemistry. The role of α-synuclein was further studied by knocking outα-synuclein using RNA interference. Cell viability increased at lower concen-trations (100 and 500 μM) of quercetin but decreased at higher concentration (1,000 μM). Quercetin exerted neuroprotective effect against MPP+, ammonium chloride and nocodazole at 100 μM. MPP+ induced apoptosis was decreased by 100 μM quercetin. Quercetin treatment in-creasedα-synuclein expression. However, knocking outα-synuclein exerted no signiifcant effect on cell survival. In conclusion, quercetin is neuroprotective against toxic agentsvia affecting var-ious mechanisms such as apoptosis, autophagy and aggresome. Becauseα-synuclein expression is increased by quercetin, the role of quercetin as an environmental factor in Parkinson’s disease pathogenesis needs further investigation.

作者： 刊期： 2015年第07期

Ischemic edema can alter the structure and permeability of the blood-brain barrier. Recent stud-ies have reported that progesterone reduces cerebral edema after cerebral ischemia. However, the underlying mechanism of this effect has not yet been elucidated. In the present study, pro-gesterone effectively reduced Evans blue extravasation in the ischemic penumbra, but not in the ischemic core, 48 hours after cerebral ischemia in rats. Progesterone also inhibited the down-reg-ulation of gene and protein levels of occludin and zonula occludens-1 in the penumbra. These results indicate that progesterone may effectively inhibit the down-regulation of tight junctions, thereby maintaining the integrity of the blood-brain barrier and reducing cerebral edema.

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

Treatment for optic nerve injury by brain-derived neurotrophic factor or the transplantation of human umbilical cord blood stem cells has gained progress, but analysis by biomechanical indicators is rare. Rabbit models of optic nerve injury were established by a clamp. At 7 days after injury, the vitreous body received a one-time injection of 50 μg brain-derived neurotrophic factor or 1 × 106 human umbilical cord blood stem cells. After 30 days, the maximum load, max-imum stress, maximum strain, elastic limit load, elastic limit stress, and elastic limit strain had clearly improved in rabbit models of optical nerve injury after treatment with brain-derived neu-rotrophic factor or human umbilical cord blood stem cells. The damage to the ultrastructure of the optic nerve had also been reduced. These ifndings suggest that human umbilical cord blood stem cells and brain-derived neurotrophic factor effectively repair the injured optical nerve, im-prove biomechanical properties, and contribute to the recovery after injury.

作者： 刊期： 2015年第07期

Deep brain stimulation has become a well-established symptomatic treatment for Parkinson’s disease during the last 25 years. Besides improving motor symptoms and long-term motor com-plications, positive effects on patients’ mobility, activities of daily living, emotional well-being and health-related quality of life have been recognized. Apart from that, numerous clinical trials analyzed effects on non-motor symptoms and side effects of deep brain stimulation. Several technical issues and stimulation paradigms have been and are still being developed to optimize the therapeutic effects, minimize the side effects and facilitate handling. This review summarizes current therapeutic issues,i.e., patient and target selection, surgical procedure and programming paradigms. In addition it focuses on neuropsychological effects and side effects of deep brain stimulation.

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

Both neurons and glia throughout the central nervous system are organized into networks by gap junctions. Among glia, gap junctions facilitate metabolic homeostasis and intercellular communication. Among neurons, gap junctions form electrical synapses that function pri-marily for communication. However, in neurodegenerative states due to disease or injury gap junctions may be detrimental to survival. Electrical synapses may facilitate hyperactivity and bystander killing among neurons, while gap junction hemichannels in glia may facilitate in-lfammatory signaling and scar formation. Advances in understanding mechanisms of plasticity of electrical synapses and development of molecular therapeutics to target glial gap junctions and hemichannels offer new hope to pharmacologically limit neuronal degeneration and en-hance recovery.

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

We previously showed that the repair of bone defects is regulated by neural and vascular signals. In the present study, we examined the effect of topically appliedβ-nerve growth factor (β-NGF) on neurogenesis and angiogenesis in critical-sized bone defects iflled with collagen bone substi-tute. We created two symmetrical defects, 2.5 mm in diameter, on either side of the parietal bone of the skull, and filled them with bone substitute. Subcutaneously implanted osmotic pumps were used to infuse 10 μgβ-NGF in PBS (β-NGF + PBS) into the right-hand side defect, and PBS into the left (control) defect, over the 7 days following surgery. Immunohistochemical staining and hematoxylin-eosin staining were carried out at 3, 7, 14, 21 and 28 days postoperatively. On day 7, expression of β III-tubulin was lower on theβ-NGF + PBS side than on the control side, and that of neuroiflament 160 was greater. On day 14,β III-tubulin and protein gene product 9.5 were greater on theβ-NGF + PBS side than on the control side. Vascular endothelial growth factor expression was greater on the experimental side than the control side at 7 days, and vascular endothelial growth factor receptor 2 expression was elevated on days 14 and 21, but lower than control levels on day 28. However, no difference in the number of blood vessels was observed between sides. Our results indicate that topical application ofβ-NGF promoted neu-rogenesis, and may modulate angiogenesis by promoting nerve regeneration in collagen bone substitute-iflled defects.

作者： 刊期： 2015年第07期

Although ultrasound measurements have been used in previous studies on carpal tunnel syn-drome to visualize injury to the median nerve, whether such ultrasound data can indicate the severity of carpal tunnel syndrome remains controversial. The cross-sectional areas of the median nerve at the tunnel inlet and outlet can show swelling and compression of the nerve at the carpal. We hypothesized that the ratio of the cross-sectional areas of the median nerve at the carpal tunnel inlet to outlet accurately relfects the severity of carpal tunnel syndrome. To test this, high-resolution ultrasound with a linear array transducer at 5–17 MHz was used to assess 77 pa-tients with carpal tunnel syndrome. The results showed that the cut-off point for the inlet-to-outlet ratio was 1.14. Signiifcant differences in the inlet-to-outlet ratio were found among patients with mild, moderate, and severe carpal tunnel syndrome. The cut-off point in the ratio of cross-section-al areas of the median nerve was 1.29 between mild and more severe (moderate and severe) carpal tunnel syndrome patients with 64.7% sensitivity and 72.7% speciifcity. The cut-off point in the ratio of cross-sectional areas of the median nerve was 1.52 between the moderate and severe carpal tunnel syndrome patients with 80.0% sensitivity and 64.7% speciifcity. These results suggest that the inlet-to-outlet ratio relfected the severity of carpal tunnel syndrome.

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

Amentoflavone is a natural biflavone compound with many biological properties, including anti-inlfammatory, antioxidative, and neuroprotective effects. We presumed that amentolfavone exerts a neuroprotective effect in epilepsy models. Prior to model establishment, mice were intragastrically administered 25 mg/kg amentoflavone for 3 consecutive days. Amentoflavone effectively prevented pilocarpine-induced epilepsy in a mouse kindling model, suppressed nu-clear factor-κB activation and expression, inhibited excessive discharge of hippocampal neurons resulting in a reduction in epileptic seizures, shortened attack time, and diminished loss and apoptosis of hippocampal neurons. Results suggested that amentolfavone protected hippocampal neurons in epilepsy micevia anti-inlfammation, antioxidation, and antiapoptosis, and then ef-fectively prevented the occurrence of seizures.

作者： 刊期： 2015年第07期