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An investigation on the mechanism of neurochemical changes in physically or psychologically stressed mice was carried out. Physical stress was induced by electric foot shocks (2 mA for 5 s at 30-s intervals), and psychological stress was induced by emotional stimuli from electric foot-shocked mice using a communication box. The serum and brain calcium levels and immunohistochemical brain dopamine levels increased, and the ethanol-induced sleeping time was prolonged following exposure to these stimuli. The effects of electric foot shocks on these physiological parameters were greater than those of emotional stimuli. In the psychologically stressed mice, serum and brain calcium levels significantly increased 15 and 60 min, respectively, after the start of exposure to stimuli. Also, the immunohistochemical dopamine levels in the neostriatum and nucleus accumbens regions after 60 min of exposure to psychological stress were higher by 23% (P < 0.01) and 27% (P < 0.01), respectively, than those in unstressed control mice. Moreover, the ethanol-induced sleeping time was prolonged by approximately 60-100% (P < 0.01) in mice exposed to psychological stress for 30-120 min. The effect of emotional stimuli to prolong the ethanol-induced sleeping time was inhibited by intracerebroventricular administration of W-7 (a calmodulin antagonist) or alpha-methyltyrosine (an inhibitor of tyrosine hydroxylase). In light of previous reports that calcium activates dopamine synthesis in the brain via a calmodulin-dependent system, it is suggested that physical or psychological stimuli induce an increase in the brain calcium level, and this increased calcium level in turn enhances dopamine synthesis in the brain. Subsequently, an increased dopamine level induces various physiological changes related to stress-dependent phenomena.

We performed compulsory superselective transcatheter arterial embolization on local hypovascular liver metastases under balloon occlusion using a 1-mm (3 F) coaxial microballoon catheter in 2 cases. One case was a metastasis from breast cancer (maximum diameter 5.5 cm) at segment 7. The other case comprised metastases from rectal cancer (maximum diameter 8 cm) at segments 7 and 8. Absolute ethanol (50%) mixed with Lipiodol (50%) was used for embolization. No major treatment-related complications occurred. No local recurrence was observed in either case in follow-up CT and MR studies of up to 16 and 9 months respectively. This technique may thus be applied as an alternative to surgical resection in the treatment of local hypovascular liver tumors.

Introduction Management of congenital vascular malformations (CVM) remains a major challenge because treatment carries a substantial risk of morbidity and recurrence of the fundamental problem. The new classification of CVM allows a multidisciplinary approach to the treatment with full integration of the several treatment modalities. The multidisciplinary approach was introduced at our CVM Clinic in 1995 and this report summarizes our results to date. Patients and methods The CVM Clinic is attended by 15 different specialties. These allow application of advanced diagnosis and treatments. The interdisciplinary consultation allows proper application of the various treatment modalities including embolosclerotherapy and surgical therapy. The embolosclerosants utilized are absolute ethanol and N-butyl cyanoacrylate (NBCA). These are used for venous malformations (VM), arteriovenous shunting malformations (AVM), and hemolymphatic malformations (HLM). These agents are used independently and as preoperative adjuncts. Among the 438 patients treated between September 1995 and September 1999, there were 99 patients treated with combinations of embolosclerotherapy. There were 286 sessions, 252 of which were for ethanol sclerotherapy and 247 of these employed ethanol alone and five were combined with NBCA. Independent embolotherapy with NBCA was instituted more recently and has been used in 28 sessions. Perioperative embolosclerotherapy has been performed in 43 sessions, mostly as preliminary preparation to reduce subsequent surgical morbidity. Followup assessment of immediate and interim results after completion of multisession therapy has been done using combinations of noninvasive diagnostic testing. Results The immediate success rate of embolosclerotherapy has been 94.7% (271/286 sessions). There has been an immediate 5.2% failure (15/286 sessions). Failures have largely been due to forced abandonment of the sclerosing procedure due to risk of deep venous thrombosis. Interim results though short-term success following completion of multisession therapy, average 3.2 sessions per patient, were satisfactory. Complications, mostly skin damage from embolosclerotherapy were experienced in 31 patients during the 286 sessions performed on 99 patients. These skin complications were discussed and accepted by the multidisciplinary team which recognized unavoidable morbidity accompanying the ethanol therapy when applied to superficially located lesions. The overall morbidity included complication rate per session (14.7%, 42/286) and 31.3% per patient (31/99). Recovery from the skin complications has been mostly spontaneous but one case in which peroneal nerve palsy occurred became permanent. There has been no recurrence the lesions treated successfully, and this has been confirmed through a battery of noninvasive testing. The average follow-up period after completion of multisession therapy is relatively short with 10.6 months (6.0–32 months) only to meet the condition as interim results. Fourteen patients have undergone surgical ablation after preoperative embolosclerotherapy and the surgical morbidity has been minimal. Conclusion An accurate diagnosis and multidisciplinary treatment strategy for management of CVMs can improve overall treatment success with a reduced morbidity and recurrence over conventional approaches. This study reviews current trends in contemporary diagnosis and clinical management of congenital vascular malformations (CVM) of the peripheral vascular system emphasizing our new multidisciplinary approach.

Animals digest food to fuel brain neurometabolism via cellular respiration. This study demonstrates the combination of a biofuel cell (BFC) and an animal brain stimulator (ABS) implanted in a pigeon. Glucose oxidation and oxygen reduction in an enzymatic BFC supplied electrical power to the ABS. Power from the BFC reached 0.12 mW in vitro and 0.08 mW in vivo using only the natural glucose and oxygen in the pigeon's body. A power management integrated circuit is used to harvest energy from the in vivo BFC at a rate of 28.4 mJ over 10 min, which is sufficient for intermittent neurostimulation.

Various transcranial sonotherapeutic technologies have risks related to standing waves in the skull. In this study, we present a comparative study on standing waves using four different activation methods: sinusoidal (SIN), frequency modulation by noise (FMN), periodic selection of random frequency (PSRF), and random switching of both inverse carriers (RSBIC). The standing wave was produced and monitored by the schlieren method using a flat plane and a human skull. The minimum ratio RSW, which is defined by the ratio of the mean of the difference between local maximal value and local minimal value of amplitude to the average value of the amplitude, was 36% for SIN, 24% for FMN, 13% for PSRF, and 4%for RSBIC for the flat reflective plate, and it was 25% for SIN, 11% for FMN, 13% for PSRF, and 5% for RSBIC for the inner surface of the human skull. This study is expected to have a role in the development of safer therapeutic equipment.

Ethanol causes diverse neurologic conditions caused by acute and chronic brain damage. This review provides an overview of Wernicke encephalopathy and other ethanol-related brain changes, such as chronic brain atrophy, Marchiafava-Bignami disease, osmotic demyelination syndrome, chronic hepatic encephalopathy, and acute alcohol withdrawal. As clinical symptoms of this spectrum of diseases have nonspecific neurologic alterations, radiologists should have current radiologic information and understand the imaging findings pertaining to the pathophysiology to support diagnosis.

The study by Kim and colleagues (in press) demonstrated that the expression of nuclear isoform of clusterin is induced by ethanol (EtOH) to participate in apoptotic cell death of neurons in developing rodent brain. EtOH‐induced nuclear clusterin interacts with BclXL, thereby liberating proapoptotic Bax. This study indicates the proapoptotic role of nuclear clusterin in EtOH‐exposed neurons, linking specific nuclear events to alcohol neurotoxicity. The study provides novel insights into the molecular mechanisms underlying fetal alcohol spectrum disorders.

Abstract The effect of ethanol administration on the axoplasmic flow of protein in the rat brain was studied by a subcellular fractionation procedure after intraventricular administration of [ 14 C]-leucine. The fast component of axoplasmic transport was facilitated following continuous ingestion of ethanol for 1–3 weeks. Fractionation of the lysed nerve ending into components showed that an increase in the fast axoplasmic transport of protein was associated with synaptic vesicles and mitochondria. Neither slow axoplasmic transport nor the soluble component of fast axoplasmic flow were altered following continuous ethanol administration. The acute administration of ethanol (3 g/kg body weight, intraperitoneally) also increased the fast axoplasmic transport of protein in paniculate fractions without altering slow axoplasmic flow or the soluble component of fast axoplasmic flow. These changes in fast axoplasmic transport were reversed following the withdrawal of ethanol administration and were not affected by the administration of cycloheximide, a protein synthesis inhibitor. These results indicate clearly that ethanol, administered either acutely or chronically, induces an increase in the fast axoplasmic flow of particulates from the nerve cell body to the nerve ending. Because of well-known and important roles of the fast axoplasmic flow in synaptic function, these changes in axoplasmic flow may well be important in the alteration of CNS function due to ethanol.

Dropped head syndrome (DHS) associated with parkinsonism is not frequent, but it markedly reduces the activities of daily living and is refractory. To elucidate the mechanism and treatment of DHS associated with parkinsonism, we assessed 28 parkinsonian patients with DHS (2 men and 26 women) by examining their clinical features and cervical-muscle-needle and surface electromyographic (EMG) recordings. We also evaluated the effects of lidocaine, muscle afferent block (MAB; 1% lidocaine mixed with ethanol), and botulinum toxin injected into the bilateral sternocleidomastoid muscles (SCMs), which were considered to be the affected muscles. In some patients, DHS occurred after the initiation or loading of dopamine agonists (less common after pergolide than cabergoline and pramipexole). Improvement was noted after a reduction in the dopamine agonist dose in some patients, and loading of l-dopa in others. Needle EMG revealed no evidence for weakness of the dorsal neck muscles. Surface EMG showed a gradual increase in SCMs activity upon passive head lifting. Lidocaine injection into SCMs markedly improved DHS, but the effect was temporary. The effect of botulinum toxin and MAB was not satisfactory. Whereas DHS could have a heterogeneous etiology, dopamine receptor sensitivity may play a role in its pathogenesis. For the treatment of DHS in parkinsonian patients, an increase in the dosage of l-dopa and a decrease in that of the dopamine agonist should be considered. Lidocaine injection (lidocaine test) could be useful for determining the most affected muscle before using botulinum toxin or MAB. Further studies are needed to examine the outcome of such treatments that include GPi-DBS.