作者： 刊期： 2015年第07期

作者： 刊期： 2015年第07期

Electroacupuncture has therapeutic effects on ischemic brain injury, but its mechanism is still poorly understood. In this study, mice were stimulated by electroacupuncture at theBaihui (GV20) acupoint for 30 minutes at 1 mA and 2/15 Hz for 5 consecutive days. A cerebral isch-emia model was established by ligating the bilateral common carotid artery for 15 minutes. At 72 hours after injury, neuronal injury in the mouse hippocampus had lessened, and the number of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling-positive cells reduced after electroacupuncture treatment. Moreover, expression of adenosine monophos-phate-activated protein kinaseα (AMPKα) and phosphorylated AMPKα was up-regulated. Intraperitoneal injection of the AMPK antagonist, compound C, suppressed this phenomenon. Our ifndings suggest that electroacupuncture preconditioning alleviates ischemic brain injury via AMPK activation.

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

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

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

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

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

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

作者： 刊期： 2015年第07期

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

With chromium-hematoxylin staining, we found evidence for the existence of novel age-depen-dent network structures in the dura mater of rat brains. Under stereomicroscopy, we noticed that chromium-hematoxylin-stained threadlike structures, which were barely observable in 1-week-old rats, were networked in specific areas of the brain, for example, the lateral lobes and the cerebella, in 4-week-old rats. In 7-week-old rats, those structures were found to have become larger and better networked. With phase contrast microscopy, we found that in 1-week-old rats, chromium-hematoxylin-stained granules were scattered in the same areas of the brain in which the network structures would later be observed in the 4- and 7-week-old rats. Such age-depen-dent network structures were examined by using optical and transmission electron microscopy, and the following results were obtained. The scattered granules fused into networks with increas-ing age. Cross-sections of the age-dependent network structures demonstrated heavily-stained basophilic substructures. Transmission electron microscopy revealed the basophilic substructures to be clusters with high electron densities consisting of nanosized particles. We report these data as evidence for the existence of age-dependent network structures in the dura mater, we discuss their putative functions of age-dependent network structures beyond the general concept of the dura mater as a supporting matrix.

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

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