Neuroprotection of posttreatment with risperidone,an atypical antipsychotic drug,in rat and gerbil models of ischemic stroke and the maintenance of antioxidants in a gerbil model of ischemic stroke

Risperidone, an atypical antipsychotic drug, has been discovered to have some beneficial effects beyond its original effectiveness. The present study examines the neuroprotective effects of risperidone against ischemic damage in the rat and gerbil induced by transient focal and global cerebral ischemia, respectively. The results showed that pre‐ and posttreatment with 4 mg/kg risperidone significantly protected against neuronal death from ischemic injury. Many NeuN‐immunoreactive neurons and a few F‐J B‐positive cells were found in the rat cerebral cortex and gerbil hippocampal CA1 region (CA1) in the risperidone‐treated ischemia groups compared with those in the vehicle‐treated ischemia group. In addition, treatment with risperidone markedly attenuated the activation of microglia in the gerbil CA1. On the other hand, we found that treatment with risperidone significantly maintained the antioxidants levels in the ischemic gerbil CA1. Immunoreactivities of superoxide dismutases 1 and 2, catalase, and glutathione peroxidase were maintained in the stratum pyramidale of the CA1; the antioxidants were very different from those in the vehicle‐treated ischemia groups. In brief, our present findings indicate that posttreatment as well as pretreatment with risperidone can protect neurons in the rat cerebral cortex and gerbils CA1 from transient cerebral ischemic injury and that the neuroprotective effect of risperidone may be related to attenuation of microglial activation as well as maintenance of antioxidants. © 2014 Wiley Periodicals, Inc.     

Stochastic resonance with differential code in feedforward network with intra-layer random connections.

We examined stochastic resonance with a differential coding scheme using a multilayer feedforward neural network which is composed of intra-layer connections. We show that the network, with random synaptic connections in each layer, encodes an input signal into a spike coherence that represents temporal differences among the inputs. We also demonstrate that both internal and external noise enhance the detection of weak signals. Finally, we discuss how the feedforward network with intra-layer random connections is similar to a membrane in its sensitivity to and amplification of a change in stimulus and suggest that the intensity of internal noise may be tuned in a real brain.     

Fate of migrated esophageal and gastroduodenal stents: experience in 70 patients

PURPOSE: To investigate the frequency of esophageal and gastroduodenal stent migration and the fate of such stents. MATERIALS AND METHODS: The authors studied five types of covered metal stents. Type A stents were nonretrievable polyurethane-covered stents with shouldered ends (n = 169), type B stents were retrievable polyurethane-covered stents with shouldered ends (n = 62), type C stents were retrievable polyurethane-covered stents with flared ends (n = 72), type D stents were retrievable polytetrafluoroethylene-covered stents with shouldered ends (n = 369), and type E stents were separated stents (n = 216). Types A-D stents were esophageal stents, and the type E stent was a gastroduodenal stent. Stents were placed in 888 patients with either benign (n = 43) or malignant (n = 845) causes of stricture. The rate of stent migration was analyzed relative to completeness of migration, the cause of obstruction, stent type, and stent placement location. The fate of migrated stents and the treatment of patients were evaluated. RESULTS: Stent migration occurred in 70 of the 888 patients (7.9%). Migration occurred in 11 of the 43 patients (25%) with benign cause of strictures and 591 of the 845 patients (7.0%) with malignant cause. The migration rates for types A, B, C, D, and E stents were 10%, 4.8%, 24%, 7.3% and 2.8%, respectively. Of the 70 migrated stents, 45 had complete migration and 25 had partial migration. The anastomotic sites were the areas most commonly associated with migration (16%), but this was not statistically significant. Forty of the 70 migrated stents were removed with retrieval devices under fluoroscopic guidance because they were not passed with stool and possibility of complications related to migrated stents. The remaining 30 stents exited via the rectum (n = 15), remained in the body without complications (n = 12), or were surgically removed because they caused complicated intestinal obstructions (n = 3). CONCLUSION: The overall migration rate for esophageal and gastroduodenal stents was 7.9%. Most migrated stents were removed nonsurgically, exited the body spontaneously, or remained in the body in an uncomplicated state. Surgical stent removal was necessary in three patients (4.3%) due to complicated intestinal obstructions.     

Traumatic Axillary Artery Dissection with Radial Artery Embolism

This report describes a case of pathologically proven traumatic arterial dissection, presenting as complete occlusion of the axillary artery with radial artery embolism. Occlusion of the axillary artery by traumatic dissection mimicked transection and radial artery embolism mimicked congenital absence of the radial artery on the initial angiogram, but these were correctly diagnosed with the following sonogram.     

The diagnostic value of multiplanar reconstruction on MDCT colonography for the preoperative staging of colorectal cancer

The purpose of this study was to determine whether multiplanar reconstruction (MPR) images can improve the accuracy of MDCT-based colorectal cancer preoperative staging by receiver-operating characteristic (ROC) analysis. Fifty-five patients with colorectal cancer underwent contrast-enhanced CT colonography using an 8- or 16-row scanner. Two separate interval reviews of the axial MDCT datasets with/without MPR images (coronal and sagittal) were performed independently by two radiologists blinded to both the colonoscopic and histopathologic results. At each review session, the radiologists were asked to determine the colorectal cancer TNM stage within the context of differentiating ≤T3 from T4, N0 from ≥N1 and M0 from M1 using a five-point confidence scale. The radiologists’ performance for staging the colorectal cancer using axial CT datasets with/without MPR images was evaluated using ROC analysis. Sensitivities, specificities and interobserver agreement were assessed. When MPR images were added, significant improvement was achieved by both radiologists for differentiating N0 from ≥N1 in terms of both A_Z (0.651 to 0.769; 0.573 to 0.713) and specificity (26.7 to 69.2%; 23.1 to 76.9%) (P<0.05). For T staging, ROC analysis failed to show a significant improvement in terms of differentiating ≤T3 from T4 for either radiologist (P>0.05), but a significant improvement in the specificity (70 to 90%; 80 to 92%) was achieved by one radiologist (P<0.05). In terms of the M staging, a significant improvement in the Az (0.844 to 0.996) was observed for the combined interpretation of the axial and MPR images by one radiologist (P<0.05). Furthermore, substantial or almost perfect interobserver agreement was achieved for all TNM stagings for the combined interpretations (κ=0.641–0.866), whereas only fair to substantial agreement was achieved for the axial images alone (κ=0.337-0.707). In conclusion, the combined interpretation of the axial and MPR MDCT images significantly improved the local staging of colorectal cancer compared with assessments based on axial images alone.     

Increased senile plaques without microglia in Alzheimer's disease

Summary To clarify the association of microglia with senile plaques, the brains from 13 patients with Alzheimer's disease (AD) and 23 nondemented aged controls were investigated immunohistochemically by a double-labeling method using anti--protein antiserum and anti-ferritin antibody, which is a recently reported microglia marker. In addition, a quantitative analysis was performed. The senile plaques which appeared initially in the nondemented aged controls consisted of a diffuse type without any amyloid cores and these were found in the group aged 50–59 years. The great majority of them were found to contain no ferritin-positive microglia. The number and proportion (percentage) of microglia-containing diffuse plaques increased with age. Classical and compact plaques began to appear in the brains of the group aged 70 years and over, and practically all of them contained microglia. These results suggest that microglia are not associated with initial plaque formation, but correlate with amyloid core formation. In AD, the most prominent feature was that the diffuse plaques, which contained either no or only a few ferritin-positive microglia, increased markedly.Supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan     

Muscle-Specific Receptor Tyrosine Kinase Antibody Positive Myasthenia Gravis Current Status

Muscle-specific tyrosine-kinase-antibody-positive myasthenia gravis (MuSK-MG) has emerged as a distinct entity since 2001. This disease has been reported worldwide, but with varying rates among patients with generalized acetylcholine-receptor-antibody-negative MG. MuSK-MG was detected in approximately 37% of generalized acetylcholine receptor antibody-negative MG. MuSK-MG patients were predominantly female with more prominent facial and bulbar involvement and more frequent crises. Disease onset tended to be earlier. Patients tended to have a relatively poor edrophonium response but showed prominent decrement in the repetitive nerve stimulation test in the facial muscles. Patients were more likely to display poor tolerance of, or a lack of improvement with, anticholinesterase agents. Somewhat better response was observed with steroids and plasma exchange. Most were managed successfully with aggressive immunomodulatory therapies, although a higher proportion of MuSK-MG patients had a refractory course when compared with other forms of generalized MG. I present here an up-to-date overview on MuSK-MG based on our experience at the University of Alabama at Birmingham and the existing literature.     

SK2 channels are neuroprotective for ischemia-induced neuronal cell death

In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca²⁺-activated K⁺ channels type 2 (SK2 channels) provides a negative feedback on N-methyl--aspartate receptors (NMDARs), reestablishing Mg²⁺ block that reduces Ca²⁺ influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia.     

Sodium butyrate prevents radiation-induced cognitive impairment by restoring pCREB/BDNF expression

Sodium butyrate is a histone deacetylase inhibitor that affects various types of brain damages. To investigate the effects of sodium butyrate on hippocampal dysfunction that occurs after whole-brain irradiation in animal models and the effect of sodium butyrate on radiation exposure-induced cognitive impairments,adult C57BL/6 mice were intraperitoneally treated with 0.6 g/kg sodium butyrate before exposure to 10 Gy cranial irradiation. Cognitive impairment in adult C57BL/6 mice was evaluated via an object recognition test 30 days after irradiation. We also detected the expression levels of neurogenic cell markers(doublecortin)and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor. Radiation-exposed mice had decreased cognitive function and hippocampal doublecortin and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression. Sodium butyrate pretreatment reversed these changes. These findings suggest that sodium butyrate can improve radiation-induced cognitive dysfunction through inhibiting the decrease in hippocampal phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression. The study procedures were approved by the Institutional Animal Care and Use Committee of Korea Institute of Radiological Medical Sciences(approval No. KIRAMS16-0002) on December 30, 2016.