Microsurgical suturing is the gold standard of nerve coaptation. Although literature on the usefulness of ifbrin glue as an alternative is becoming increasingly available, it remains contradic-tory. Furthermore, no data exist on how both repair methods might inlfuence the morphological aspects (arborization; branching) of early peripheral nerve regeneration. We used the sciatic nerve transplantation model in thy-1 yellow lfuorescent protein mice (YFP;n = 10). Pieces of nerve (1cm) were grafted from YFP-negative mice (n = 10) into those expressing YFP. We per-formed microsuture coaptations on one side and used ifbrin glue for repair on the contralateral side. Seven days after grafting, the regeneration distance, the percentage of regenerating and ar-borizing axons, the number of branches per axon, the coaptation failure rate, the gap size at the repair site and the time needed for surgical repair were all investigated. Fibrin glue repair resulted in regenerating axons travelling further into the distal nerve. It also increased the percentage of arborizing axons. No coaptation failure was detected. Gap sizes were comparable in both groups. Fibrin glue signiifcantly reduced surgical repair time. The increase in regeneration distance, even after the short period of time, is in line with the results of others that showed faster axonal regen-eration after ifbrin glue repair. The increase in arborizing axons could be another explanation for better functional and electrophysiological results after ifbrin glue repair. Fibrin glue nerve coap-tation seems to be a promising alternative to microsuture repair.

作者： 刊期： 2015年第07期

In this study, we aimed to determine gastrointestinal problems associated with neurogenic bowel dysfunction in spinal cord injury patients and to assess the efifcacy of bowel program on gas-trointestinal problems and the severity of neurogenic bowel dysfunction. Fifty-ifve spinal cord injury patients were included in this study. A bowel program according to the characteristics of neurogenic bowel dysfunction was performed for each patient. Before and after bowel program, gastrointestinal problems (constipation, dififcult intestinal evacuation, incontinence, abdominal pain, abdominal distension, loss of appetite, hemorrhoids, rectal bleeding and gastrointestinal induced autonomic dysrelfexia) and bowel evacuation methods (digital stimulation, oral med-ication, suppositories, abdominal massage, Valsalva maneuver and manual evacuation) were determined. Neurogenic bowel dysfunction score was used to assess the severity of neurogenic bowel dysfunction. At least one gastrointestinal problem was identiifed in 44 (80%) of the 55 patients before bowel program. Constipation (56%, 31/55) and incontinence (42%, 23/55) were the most common gastrointestinal problems. Digital rectal stimulation was the most common method for bowel evacuation, both before (76%, 42/55) and after (73%, 40/55) bowel program. Oral medication, enema and manual evacuation application rates were signiifcantly decreased and constipation, dififcult intestinal evacuation, abdominal distention, and abdominal pain rates were signiifcantly reduced after bowel program. In addition, mean neurogenic bowel dysfunction score was decreased after bowel program. An effective bowel program decreases the severity of neurogenic bowel dysfunction and reduces associated gastrointestinal problems in patients with spinal cord injury.

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

MicroRNA-124 (miR-124) is abundantly expressed in neurons in the mammalian central ner-vous system, and plays critical roles in the regulation of gene expression during embryonic neurogenesis and postnatal neural differentiation. However, the expression proifle of miR-124 after spinal cord injury and the underlying regulatory mechanisms are not well understood. In the present study, we examined the expression of miR-124 in mouse brain and spinal cord after spinal cord injury usingin situ hybridization. Furthermore, the expression of miR-124 was examined with quantitative RT-PCR at 1, 3 and 7 days after spinal cord injury. The miR-124 expression in neurons at the site of injury was evaluated by in situ hybridization combined with NeuN immunohistochemical staining. The miR-124 was mainly expressed in neurons through-out the brain and spinal cord. The expression of miR-124 in neurons significantly decreased within 7 days after spinal cord injury. Some of the neurons in the peri-lesion area were NeuN+/miR-124?. Moreover, the neurons distal to the peri-lesion site were NeuN+/miR-124+. These ifndings indicate that miR-124 expression in neurons is reduced after spinal cord injury, and may relfect the severity of spinal cord injury.

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

Prenatal alcohol exposure disrupts the development of normal fetal respiratory function, but whether it perturbs respiratory rhythmical discharge activity is unclear. Furthermore, it is un-known whether the 5-hydroxytryptamine 2A receptor (5-HT2AR) is involved in the effects of prenatal alcohol exposure. In the present study, pregnant female rats received drinking water containing alcohol at concentrations of 0%, 1%, 2%, 4%, 8% or 10% (v/v) throughout the gestation period. Slices of the medulla from 2-day-old neonatal rats were obtained to record respiratory rhythmical discharge activity. 5-HT2AR protein and mRNA levels in the pre-B?tzing-er complex of the respiratory center were measured by western blot analysis and quantitative RT-PCR, respectively. Compared with the 0% alcohol group, respiratory rhythmical discharge activity in medullary slices in the 4%, 8% and 10% alcohol groups was decreased, and the reduc-tion was greatest in the 8% alcohol group. Respiratory rhythmical discharge activity in the 10%alcohol group was irregular. Thus, 8% was the most effective alcohol concentration at attenuating respiratory rhythmical discharge activity. These ifndings suggest that prenatal alcohol exposure attenuates respiratory rhythmical discharge activity in neonatal rats by downregulating 5-HT2AR protein and mRNA levels.

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

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

Aquaporin-4 regulates water molecule channels and is important in tissue regulation and water transportation in the brain. Upregulation of aquaporin-4 expression is closely related to cel-lular edema after early cerebral infarction. Cellular edema and aquaporin-4 expression can be determined by measuring cerebral infarct area and apparent diffusion coefficient using diffu-sion-weighted imaging (DWI). We examined the effects of silencing aquaporin-4 on cerebral infarction. Rat models of cerebral infarction were established by occlusion of the right middle cerebral artery and siRNA-aquaporin-4 was immediately injectedvia the right basal ganglia. In control animals, the area of high signal intensity and relative apparent diffusion coefifcient value on T2-weighted imaging (T2WI) and DWI gradually increased within 0.5–6 hours after cerebral infarction. After aquaporin-4 gene silencing, the area of high signal intensity on T2WI and DWI reduced, relative apparent diffusion coefifcient value was increased, and cellular edema was ob-viously alleviated. At 6 hours after cerebral infarction, the apparent diffusion coefifcient value was similar between treatment and model groups, but angioedema was still obvious in the treat-ment group. These results indicate that aquaporin-4 gene silencing can effectively relieve cellular edema after early cerebral infarction; and when conducted accurately and on time, the diffusion coefifcient value and the area of high signal intensity on T2WI and DWI can relfect therapeutic effects of aquaporin-4 gene silencing on cellular edema.

作者： 刊期： 2015年第07期

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

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

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

Necroptosis is characterized by programmed necrotic cell death and autophagic activation and might be involved in the death process of dopaminergic neurons in Parkinson’s disease. We hypothesized that necrostatin-1 could block necroptosis and give protection to dopaminergic neurons. There is likely to be crosstalk between necroptosis and other cell death pathways, such as apoptosis and autophagy. PC12 cells were pretreated with necroststin-1 1 hour before expo-sure to 6-hydroxydopamine. We examined cell viability, mitochondrial membrane potential and expression patterns of apoptotic and necroptotic death signaling proteins. The results showed that the autophagy/lysosomal pathway is involved in the 6-hydroxydopamine-induced death pro-cess of PC12 cells. Mitochondrial disability induced overactive autophagy, increased cathepsin B expression, and diminished Bcl-2 expression. Necrostatin-1 within a certain concentration range (5–30 μM) elevated the viability of PC12 cells, stabilized mitochondrial membrane potential, inhibited excessive autophagy, reduced the expression of LC3-II and cathepsin B, and increased Bcl-2 expression. These findings suggest that necrostatin-1 exerted a protective effect against injury on dopaminergic neurons. Necrostatin-1 interacts with the apoptosis signaling pathway during this process. This pathway could be a new neuroprotective and therapeutic target in Par-kinson’s disease.

作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期