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We report a case of bispectral index (BIS) falling to zero during absolute alcohol embolization of an intracranial arteriovenous malformation (AVM) under anesthesia. This case highlights the unusual effect of a therapeutic dose of parenteral alcohol on the central nervous system using BIS monitoring.A 29-yr-old male with a left parieto-occipital arteriovenous malformation underwent neuroendovascular embolization under general anesthesia. During injection of absolute alcohol injection into the AVM nidus, the patient developed hypertension and tachycardia coincident with a profound and sustained reduction of BIS values to zero, despite a stable level of anesthesia. Immediate angiography revealed no evidence of hemorrhage or new changes in the patient's cerebral vasculature. Post-procedure, the patient remained drowsy for several hours with signs of alcohol intoxication. He had full neurological recovery.In the presence of normal cerebral angiographic findings, suppression of BIS values may serve as an early indicator of CNS responses to intracranial injection of absolute alcohol for embolization of an arteriovenous malformation.

γ-aminobutyric acid (GABA) is an amino acid used for mitigating the detrimental effects of heat stress in broilers. In addition, a growing body of literature suggests that the in ovo feeding of various nutrients can enhance the post-hatch thermotolerance of broilers. Therefore, we hypothesized that the supplementation of GABA during incubation might have positive effects in heat-stressed broilers. Chicks hatched from eggs were divided into three groups described as follows: chicks hatched from eggs incubated at normal temperature and then raised under thermoneutral temperature (CON); chicks hatched from eggs incubated at normal temperature but raised under cyclic heat stress (HS) (CON+HS); and chicks hatched from eggs injected with 60 mg of GABA dissolved in 0.6 mL of distilled water but raised under cyclic HS (G10+HS). The HS was applied between 28 and 31 days of age with ambient temperatures raised from 22 ± 1 °C to 33 ± 1 °C for 6 h daily. Compared to the CON group, average daily weight gain was significantly lower in the CON+HS but not in the G10+HS group. Feed intake was significantly decreased in both the CON+HS and G10+HS groups. Compared to the CON group, plasma corticosterone levels were significantly increased in the CON+HS group, but not the G10+HS group. Hepatic mRNA levels of the acetyl-CoA carboxylase gene (ACC) were significantly reduced in the G10+HS group compared to the CON group. In addition, positive Pearson correlation coefficients were found in mRNA levels between fatty acid synthase (FAS) and nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1) (r = 0.55, p < 0.05), NOX1 and NOX4 (r = 0.65, p < 0.01), and catalase (CAT) and superoxide dismutase (SOD) (r = 0.62, p < 0.05). Taken together, the results suggest that this study can serve as a basis for future work focusing on the in ovo feeding of GABA as a technique to combat heat stress in broilers.

Male mice of the BALB/c strain were given a solution of 15% ethanol as their only source of fluid for periods varying from 5 weeks to 8 months. For behavioral testing, they were compared with control groups which had received either an isocaloric solution of sucrose or tap water. Memory was tested by using spontaneous alternation behavior in a T maze. Each test consisted of two forced trials (acquisition) followed by a free trial (test) given at different acquisition--test intervals (from 30 s to 24 h). Results from two independent experiments showed that after 25 weeks of ethanol administration there was an accelerated rate of decay of spontaneous alternation as a function of the acquisition--test interval. Such a phenomenon persisted after ethanol was omitted from the diet. A third experiment showed that when tested on two successive sessions separated by a 5 h interval, experimental subjects exhibited a decreased ability to perform normally on the second test. Our data are interpreted as showing that long-term ethanol administration results in accelerated forgetting and increased vulnerability to proactive interference and, as such, they are compared to the memory dysfunctions observed in amnesic patients.

Using two inbred strains of mice which have similar rates of alcohol metabolism, we asked whether prenatal alcohol exposure would cause greater incidence and severity of defects in the development of two forebrain fiber tracts, the corpus callosum and the anterior commissure, in mice prone to these defects (BALB/c) than in mice not prone to these defects (C57BL/6). Pregnant animals were fed 0.6 kcal/g body weight of a Sustacal-based liquid diet containing 0, 15, 17.5, 20, or 25% ethanol-derived calories from day 7 to fetal assessment on day 18 of gestation. Most of alcohol's greatest effects and the greatest strain differences in alcohol's effects on fetal variables were produced by the 17.5% diet. This dose had inhibitory effects on fetal body, brain, and midsagittal corpus callosum and anterior commissure growth. All these effects, except that on brain weight, were significantly greater in C57s than in BALBs. When the results were compared with prenatal growth curves for normal untreated mice, the effect of alcohol on corpus callosum but not anterior commissure growth was largely explained by its effects on overall development. The 17.5% diet had a greater specific effect on size of the anterior commissure in C57s than BALBs but increased the incidence and severity of its permanent dysmorphology in BALBs more than in C57s. Anterior commissure size and morphology may be sensitive indicators of alcohol's effects on prenatal brain development. Hereditary differences in rate of maternal alcohol metabolism no doubt have important consequences for risks arising from prenatal alcohol exposure. However, this study clearly indicates that inherited factors, other than those that influence rate of alcohol metabolism, are important influences on the overall fetal response and the specific responses of the anterior commissure to prenatal alcohol exposure.

The effects of a mega dose of ascorbic acid (AA) on alcohol induced peroxidative damages were investigated in guinea pigs. In the present study, four groups of male guinea pigs were maintained for 30 days as follows. (1) Control group (1 mg AA/100 g body wt); (2) Ethanol group (1 mg AA/100 g body wt. + 9 g ethanol/kg body wt); (3) AA group (25 mg AA/100 g body wt); (4) AA + ethanol group (25 mg AA/100 g body wt. + 9 g ethanol/kg). Results revealed that alcohol induced significant lipid peroxidation, since the lipid peroxidation products malondialdehyde (MDA), hydroperoxides and conjugated dienes were elevated. The activities of scavenging enzymes superoxide dismutase (SOD), catalase were reduced. However, supplementation of AA along with alcohol reduced the lipid peroxidation products in the liver and enhanced the activities of scavenging enzymes. Activities of glutathione peroxidase and reductase were also greater in guinea pigs given alcohol + AA in comparison with those given alcohol alone. Administration of ascorbic acid also reduced the activity of gamma-glutamyl transpeptidase (GGT), the marker enzyme of alcohol induced toxicity. The vitamin E level, which was reduced by alcohol intake, was raised by the co-administration of AA and alcohol. These studies suggest that a mega dose of AA helps in the prevention of alcohol induced oxidative stress by enhancing the antioxidant capacity and also by reducing the lipid peroxidation products.

Brain-Machine Interfaces (BMIs) have shown great potential for generating prosthetic control signals. Translating BMIs into the clinic requires fully implantable, wireless systems; however, current solutions have high power requirements which limit their usability. Lowering this power consumption typically limits the system to a single neural modality, or signal type, and thus to a relatively small clinical market. Here, we address both of these issues by investigating the use of signal power in a single narrow frequency band as a decoding feature for extracting information from electrocorticographic (ECoG), electromyographic (EMG), and intracortical neural data. We have designed and tested the Multi-modal Implantable Neural Interface (MINI), a wireless recording system which extracts and transmits signal power in a single, configurable frequency band. In prerecorded datasets, we used the MINI to explore low frequency signal features and any resulting tradeoff between power savings and decoding performance losses. When processing intracortical data, the MINI achieved a power consumption 89.7% less than a more typical system designed to extract action potential waveforms. When processing ECoG and EMG data, the MINI achieved similar power reductions of 62.7% and 78.8%. At the same time, using the single signal feature extracted by the MINI, we were able to decode all three modalities with less than a 9% drop in accuracy relative to using high-bandwidth, modality-specific signal features. We believe this system architecture can be used to produce a viable, cost-effective, clinical BMI.

AbstractDevelopmental studies in animals often violate the assumption of statistical independence of observations due to the hierarchical nature of the data (i.e., pups cluster by litter, correlation of individual observations over time). Mixed effect modeling (MEM) provides a robust analytical approach for addressing problems associated with hierarchical data. This article compares the application of MEM to traditional ANOVA models within the context of a developmental study of prenatal ethanol exposure in mice. The results of the MEM analyses supported the ANOVA results in showing that a large proportion of the variability in both behavioral score and brain weight could be explained by ethanol. The MEM also identified that there were significant interactions between ethanol and litter size in relation to behavioral scores and brain weight. In addition, the longitudinal modeling approach using linear MEM allowed us to model for flexible weight gain over time, as well as to provide precise estimates of these effects, which would be difficult in repeated measures ANOVA. © 2007 Wiley Periodicals, Inc. Dev Psychobiol 49: 664–674, 2007.