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Previously, results of studies from our laboratory have shown that the offspring of ethanol-fed female rats have a significant decrease in serotonin (5-HT) neurons and glia that contain S100B, an essential trophic factor for the development of 5-HT neurons. The deficiency of S100B-immunopositive glia was detected during the vulnerable period in 5-HT neuron development and in brain areas proximal to these neurons. The reductions of both 5-HT neurons and S100B-positive glia were prevented by maternal treatment with a 5-HT(1A) agonist (i.e., ipsapirone or buspirone). In the current study, we investigated whether the offspring of ethanol-fed rats had a general decrease in the density of glial cells in the brain areas that contain 5-HT neurons, and we determined whether these changes were prevented by maternal treatment with ipsapirone between gestational days (GDs) 13 and 20. We estimated the density of vimentin-positive glia of the midline raphe glial structure (MRGS) at GD 20 and postnatal day (PND) 5 and of glial fibrillary acidic protein (GFAP)-positive astrocytes proximal to the dorsal and median raphe at PNDs 5 and 19. The results of this study provide evidence that in utero ethanol exposure is associated with a reduced density of GFAP-immunopositive astrocytes proximal to the dorsal and median raphe. Maternal ipsapirone treatment significantly increased astroglial density in the dorsal raphe at PNDs 5 and 19 and in the median raphe at PND 5, such that it either prevented (dorsal raphe, PNDs 5 and 19) or blunted (median raphe, PND 5) the effects of ethanol.

Abstract Treatment of rats with ethanol for 3 weeks resulted in a significant increase in δ-opiate receptor binding whereas no change in μ-opiate receptor binding was observed. Scatchard analysis showed an increase in δ-receptor affinity without a change in the receptor density. Acute treatment with ethanol did not alter receptor characteristics. The data provide evidence that δ- and μ-opiate receptor sites can be differentially modulated in vivo.

Fetal alcohol syndrome and alcohol‐related birth defects are the result of heavy maternal alcohol consumption during gestation. The magnitude of deficit manifested by the offspring is invariably a consequence of several risk factors that may result in high peak blood alcohol concentrations (BACs), such as the duration, timing, or pattern of alcohol consumption. In addition, the alcohol content of the consumed beverage may play a role in determining offspring developmental consequences. Because higher BACs are positively correlated with risk and severity of brain injury early in postnatal lie, initially it was important to determine how BAC is influenced by alcohol concentration and whether that influence is constant over repeated alcohol treatments. Groups of female Sprague‐Dawley rats received daily intragastric intubations of 5 g/kg alcohol in one of several concentrations: 45% (v/v), 30% (v/v), 22.5% (v/v), or 15% (v/v) for a duration of 18 consecutive days. Blood samples were taken at various times postintubation on days 3,8,13, and 18 of treatment, and analyzed by headspace gas chromatography. Multivariate analyses of peak BAC, average BAC, and time to reach peak BAC revealed some noteworthy results. First, peak BAC and average BAC were significantly lower in the 45% group, compared with the other concentration groups, whereas this group also took a longer time to reach peak BAC than the other three groups. Second, peak BAC and averege BAC were higher on the last day of treatment than any of the other treatment days. These results suggest that alcohol concentration and repeated alcohol exposure can influence BAC and, as such, are important risk factors to be considered in the appraisal of alcohol‐induced fetal brain injuries.

Bei 200 Patienten mit den typischen Zeichen eines organischen Psychosyndroms wurden Hirndurchblutung, cerebraler Verbrauch von Sauerstoff und Glucose sowie der zur Oxydation gelangende Glucoseanteil bestimmt. In 170 Fallen (85%) war eine dieser Grosen fuhrend herabgesetzt, bei 28 Fallen (14%) lagen gesteigerte Werte vor, bei zwei Patienten (1%) waren die Befunde normal. Lediglich in 35 Fallen (17,5%) war eine Minderung der Hirndurchblutung der fuhrende Befund. Bei 68% der von uns untersuchten Patienten waren Storungen des Hirnstoffwechsels mit einem zum Teil erheblichen cerebralen Energiedefizit vorherrschend. Das bedeutet, das beim organischen Psychosyndrom viermal haufiger cerebrale Stoffwechselstorungen im Vordergrund stehen als cerebrale Durchblutungsstorungen. Damit werden auch die aus dem psychopathologischen Bild, dem EEG oder dem Pneumencephalogramm gestellten Diagnosen „cerebrale Durchblutungsstorungen“, „cerebrovasculare Insuffizienz“, „Cerebralsklerose“ oder „Hirnarteriosklerose“ in ihrem Aussagewert zweifelhaft.

In medial tibial stress syndrome (MTSS) bone marrow and periosteal edema of the tibia on the magnetic resonance imaging (MRI) is frequently reported. The relationship between these MRI findings and recovery has not been previously studied. This prospective study describes MRI findings of 52 athletes with MTSS. Baseline characteristics were recorded and recovery was related to these parameters and MRI findings to examine for prognostic factors. Results showed that 43.5% of the symptomatic legs showed bone marrow or periosteal edema. Absence of periosteal and bone marrow edema on MRI was associated with longer recovery (P = 0.033 and P = 0.013). A clinical scoring system for sports activity (SARS score) was significantly higher in the presence of bone marrow edema (P = 0.027). When clinical scoring systems (SARS score and the Lower Extremity Functional Scale) were combined in a model, time to recovery could be predicted substantially (explaining 54% of variance, P = 0.006). In conclusion, in athletes with MTSS, bone marrow or periosteal edema is seen on MRI in 43,5% of the symptomatic legs. Furthermore, periosteal and bone marrow edema on MRI and clinical scoring systems are prognostic factors. Future studies should focus on MRI findings in symptomatic MTSS and compare these with a matched control group.

The level of Met-enkephalin in the brain is inversely correlated with ethanol consumption and is controlled partially through efflux activity of peptide transport system-1 (PTS-1) at the blood-brain barrier (BBB). Prolonged alcohol drinking can perturb aspects of this system, including a loss of control of Met-enkephalin levels at the transcriptional and translational levels, and impaired release of Met-enkephalin from tissue sources. Met-enkephalin levels in whole brain homogenates often first paradoxically increase after a few days of ethanol drinking and then decrease with the development of physical dependence. Which of those various changes drives the others is unclear. To clarify these interactions, we here determined the levels of Met-enkephalin in striatal interstitial fluid (ISF) by microdialysis, striatal tissue homogenates, and serum after chronic ethanol treatment and alcohol withdrawal. Mice received ethanol (5%) in liquid diet for 7 days (ethanol-treated) and others withdrawn for a day following 7-day treatment (withdrawal). There was a significant (P<0.05) difference in the levels of Met-enkephalin in striatal microdialysate between the control (79.1+/-5.9 pg/ml) and ethanol-treated group (94.9+/-4.3 pg/ml), which was lost by withdrawing ethanol (83.9+/-3.8 pg/ml). In contrast, ethanol treatment did not affect Met-enkephalin levels in the striatal tissue. In the ethanol-treated group, there was a significant (P<0.05) reduction of the levels of Met-enkephalin in serum to 70.5% of control levels. This decrease was restored to the level of control by withdrawing ethanol. These reversible changes in ISF and serum are readily explained by the known changes in the efflux activity of PTS-1 at the BBB.

To compare magnetic resonance (MR) imaging and multidetector computed tomography (MDCT) for the assessment of myocardial infarction (MI) after alcohol septal ablation (ASA).Ten patients (mean age, 60 years ± 16) were examined with both MDCT and 1.5-T MR imaging performed 10 minutes after injection, within 3 days after ASA. Half of them had a temporary pacemaker (PM) during MDCT examination. Global image quality (IQ) and localization of MI were noticed on both MDCT and MR images. Volumes of MI, contrast-to-noise ratios (CNR) and signal-to-noise ratios (SNR) were also calculated. ASA effectiveness was evaluated by echocardiography immediately and 3 months after procedure.Global IQ was considered adequate for both procedures. In 8 patients, MI reached the basal part of the septum on both MDCT and MR images. The 2 remaining patients exhibited sparing of the basal septum on MDCT and MR images. Volumes of MI were within the same range with the 2 techniques (MDCT: 22.1 ± 8.8 mL; MR imaging: 23.8 ± 9.4 mL) and correlated well each other (R(2)=0.85, p<0.002). The 2 patients with sparing of the basal interventricular septum had persistent gradient on echocardiography 3 months after ASA, suggesting failure of the procedure. The volumes of MI didn't correlate with the reduction of pressure gradient on echocardiography 3 months after ASA (R(2)=0.02, p<0.05).Evaluation of post ASA MI is feasible with MDCT by comparison with MR imaging. MDCT might serve as an alternative imaging method in case of PM implantation.

Chick embryos given a single dose of ethanol (1.0 g/kg) at the start of incubation (day 0) had widely differing levels of blood alcohol when sacrificed on day 7 and the blood alcohol levels were inversely correlated with whole body and brain weight. Clearance of the alcohol by the embryos was inhibited by simultaneous treatment with 4-methyl pyrazole and this treatment potentiated the brain growth inhibition due to ethanol. Treatment with indomethacin lowered blood alcohol levels on day 7 and protected against the growth inhibition. These data suggest that early chick embryos have varying amounts of alcohol dehydrogenase-like metabolic activity and that higher levels of this activity protect against alcohol-induced brain growth inhibition in this model. If similar variations in the ability to metabolize alcohol exist in human fetuses, it may represent a mechanism by which comparable maternal doses of alcohol produce widely varying fetal effects.

A decline in walking capacity and high energy cost can limit mobility following stroke. Mechanical energy exchange between lower limb and trunk segments can reflect gait inefficiencies, but reveals little about active energy flow between adjacent segments through muscle actions. This study evaluated mechanical energy expenditures (MEEs) during walking in stroke and healthy groups to understand movement control and explore the impact of walking speed on mechanical energy exchanges.Thirteen adults with hemiparesis and six healthy controls walked at self-selected speed. Power curves for each lower limb joint were segmented into concentric and eccentric sources of muscle power and transfer/no-transfer modes to calculate MEEs during stance.MEEs were lower in the stroke group on the affected side compared to the less affected side and compared to controls. Specifically, the affected plantarflexors transferred less energy distally via concentric action in late stance compared to the less affected side. However, the stroke group generated greater energy at the ankle in the absence of transfer compared to controls. Less concentrically transferred energy through midstance and absorbed in late stance was evident by the knee extensors bilaterally in stroke. At the hip, the total energy (no transfer) was reduced on the affected side. Classifying stroke subjects by walking speed (.6m/s) revealed disruptions in harnessing energy through motion and transfer energy across segments in the slower group.The limited ability of those with stroke to exploit intersegmental energy transfer to optimize efficiency may limit endurance and functional independence.