Development of multichannel soft tactile sensors having fingerprint structure.

It is possible to accurately recognize the shape of an object or to grip it by setting soft tactile sensors on a robot's hands. We studied a multichannel soft tactile sensor as an artificial hand and evaluated the pressure's response performance from several directions and the slipping and sliding responses. The tactile sensor consisted of multiple pneumatic sensors and a soft cap with a fingerprint structure that was made of silicone gum and was separated from multiple spaces. Evaluation tests showed that the multiple soft tactile sensors estimate both an object's contact force and its contact location. Our tactile sensor also measured the object's roughness by the slide on surface texture.

Robot hand with soft tactile sensors and underactuated control.

We developed a robot hand with three fingers and controlled them using underactuated control to obtain a more flexible grip. With underactuated control, we can flexibly operate an artificial robot hand and reduce the number of actuators. The robot fingers had three joints to imitate human fingers. One finger was driven by one wire and one servo motor for bending and by three torsion springs for extension. We also developed a soft tactile sensor having three pneumatic sensors and mounted it on front of each robot fingers. We obtained the following information from our experimental examinations of the robot hand. It adaptively grasped an object by underactuated control. The soft tactile sensor deftly touched an object, and the data showed the contact position with. By analyzing the data from tactile sensors, we obtained the rough information of the object's shape.

DNA amplification using phi29 DNA polymerase validates gene polymorphism analysis from buccal mucosa samples.

Venous blood is currently the most common source of DNA for gene polymorphism screening; however, blood sampling is invasive and difficult to perform in general dental treatment. Buccal mucosa samples provide an alternative source of DNA, but it is frequently difficult to effectively amplify the DNA owing to the small amounts of sample material obtained. This study was performed to establish a method for performing total genomic DNA amplification from buccal mucosa samples using phi29 DNA polymerase. Total genomic DNA was isolated from buccal mucosa samples obtained from healthy subjects and was amplified using phi29 DNA polymerase. To determine the suitability of the extracted DNA for genotyping, polymerase chain reaction and restriction fragment length polymorphism analyses were performed for the IL-1 gene polymorphism. Genotyping of the IL-1 polymorphism was successful using the amplified DNA from a buccal mucosa, but genotyping was unsuccessful using the unamplified control because of low DNA purity. The method of extracting DNA from a buccal mucosa is painless, simple, minimally invasive, and rapid. Genomic DNA from a buccal mucosa can be amplified by phi29 DNA polymerase in sufficient quantity and quality to conduct gene polymorphism analyses.

Prophylactic effect of lafutidine against the adverse reaction induced in rat stomach by repeated administration of 5-fluorouracil.

We examined the prophylactic effect of lafutidine, a histamine H2 receptor antagonist, on the morphological and functional derangement of the rat stomach after the administration of 5-fluorouracil (5-FU) in the absence or presence of taurocholate Na (TC). Rats were given 5-FU p. o. once daily for 5 days. After 18 hr fasting, the animals were given omeprazole to inhibit acid secretion. Under urethane anesthesia, the stomach was mounted on an ex-vivo chamber, perfused with 100 mM HCl, and both the transmucosal potential difference (PD) and gastric mucosal blood flow (GMBF) were simultaneously measured before and after exposure of the mucosa to 20 mM TC for 30 min. The 5-FU treatment lowered the basal PD with a decrease in the mucosal height and caused few haemorrhagic lesions in the stomach when perfused with 100 mM HCl for 2 hr. The 5-FU treatment had no influence on the reduced PD response caused by TC, but significantly impaired the increase in GMBF after exposure to TC, resulting a marked aggravation of gastric lesions. Lafutidine, given together with 5-FU for 5 days, significantly antagonized the deleterious effect of 5-FU on the basal PD and the GMBF response to TC, and prevented the aggravation of gastric lesions. These effects of lafutidine were not mimicked by cimetidine and disappeared due to the chemical ablation of capsaicin-sensitive afferent neurons. We conclude that 1) 5-FU treatment caused the morphological and functional derangement of the stomach and increased the mucosal vulnerability against acid, and 2) lafutidine prevents such changes caused by 5-FU treatment, probably mediated through capsaicin-sensitive afferent neurons.

Calcium sulphate as a bone substitute for various osseous defects in conjunction with apicectomy.

AIM: The purpose of this study was to investigate the effect of calcium sulphate on various osseous defects when used in conjunction with apicectomy. METHODOLOGY: Mandibular third and fourth premolars of 11 beagle dogs were used. After root-canal treatment and apicectomy, three types of osseous defects were prepared on both sides of the mandible as follows: type 1, osseous defect communicating with the gingival sulcus: type 2, large osseous defect including two roots; type 3, 'through and through' osseous defect. The experimental side was allocated randomly, and the osseous defects were filled with medical grade calcium sulphate. The defects on the opposite side were left unfilled as controls. The dogs were sacrificed at 8 and 16 weeks postoperatively. Undemineralized sections were obtained and examined histomorphometrically. RESULTS: In type 1 defects, bone was not observed on the buccal side of the root on either experimental or control side at 8 and 16 weeks. In both type 2 and 3 defects, bone volume/tissue volume (BV/TV) values on the experimental side were significantly higher than those on the control side (P < 0.01), and mineral apposition rate (MAR) values on the experimental side were significantly higher than those on the control side (P < 0.01). CONCLUSIONS: The use of calcium sulphate was effective in bone regeneration on both large osseous defects and 'through and through' osseous defects. It was less effective in osseous defects communicating with the gingival sulcus.

Guided bone regeneration (GBR) using membranes and calcium sulphate after apicectomy: a comparative histomorphometrical study.

AIM: The purpose of the present study was to evaluate the effects of resorbable and non-resorbable membranes, and calcium sulphate on bone regeneration in osseous defects in conjunction with apicectomy. METHODOLOGY: The mandibular third and fourth premolars of 12 beagle dogs were root treated, and apicectomies were performed. The osseous defects were divided randomly into five groups. In groups A, B and C the osseous defects were covered with e-PTFE membranes, PLGA membranes, and collagen membranes, respectively. In group D, defects were filled with calcium sulphate. Nothing was used in group E, which served as controls. The dogs were sacrificed 4, 8, and 16 weeks after the surgery. Undemineralized sections were obtained and evaluated histomorphometrically. RESULTS: Newly formed cortical bone had closed the defect in the cortical plate in all groups at 16 weeks. The degree of concavity of the new cortical bone at 16 weeks in groups A and D was significantly less than in group B (P < 0.01). The percentage of regenerated bone in group A was significantly greater than in groups B (P < 0.01), C (P < 0.05) and E (P < 0.05). In group D, it was significantly greater than in groups B (P < 0.01) and E (P < 0.05). CONCLUSIONS: The data suggests that e-PTFE membrane is more effective compared to resorbable membranes and controls for bone regeneration after apicectomy, and that calcium sulphate could be substituted for e-PTFE membrane.

Role of nitric oxide in the epileptogenesis of EL mice.

PURPOSE: To understand the role of nitric oxide (NO) in the regulation of seizures, we measured the extracellular levels of the NO metabolites nitrite and nitrate as indices of NO generation in the parietal cortex, hippocampus, and temporal cortex of EL mice. Furthermore, alterations of neuronal, endothelial, and inducible nitric oxide synthetase (nNOS, eNOS, and iNOS, respectively) were observed to correlate them with epileptogenesis. METHODS: EL mice of 20 weeks and 30 weeks of age (before and after the establishment of epileptogenesis, respectively) were used. Nitrite was quantified using the specific absorbancy of diazo dye. NOS isoenzymes (nNOS, iNOS, and eNOS) were also investigated in the hippocampus during development until mice were 30 weeks old. Samples (total protein, 8.33 to 8.43 microg) were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and identified by immunoblotting. RESULTS: EL mice that experienced repetitive seizures showed a remarkable increase in nitrite in the hippocampus at 30 weeks of age compared with EL mice that had no experience of seizures. nNOS and iNOS were major and minor components, respectively, and both increased in parallel with the development of epileptogenesis. eNOS was not detectable. CONCLUSIONS: Excess iNOS (and subsequent increase in harmful NO) and deficient eNOS (and subsequent decrease in NO identified as an endothelium-derived relaxing factor) may work together to form a focus complex.

Cellular mechanism of action of cognitive enhancers: effects of nefiracetam on neuronal Ca2+ channels.

Cellular mechanisms underlying the cognition-enhancing actions of piracetam-like nootropics were studied by recording Ca2+ channel currents from neuroblastoma x glioma hybrid (NG108-15) cells and Xenopus oocytes expressing Ca2+ channels. In NG108-15 cells, nefiracetam (1 microM) produced a twofold increase in L-type Ca2+ channel currents. A similar, but slightly less potent effect was observed with aniracetam, whereas piracetam and oxiracetam exerted no such effects. Cyclic AMP analogs mimicked the nefiracetam action. N-type Ca2+ channel currents inhibited by leucine (Leu)-enkephalin by means of inhibitory G proteins (Go/Gi) were recovered promptly by nefiracetam, whereas those inhibited by prostaglandin E1 via stimulatory G proteins were not affected by nefiracetam. Cells treated with pertussis toxin (500 ng/mL, > 20 hours) were insensitive to nefiracetam. In Xenopus oocytes functionally expressing N-type (alpha1B) Ca2+ channels and delta-opioid receptors, nefiracetam was also effective in facilitating the recovery from Leu-enkephalin-induced inhibition. These results suggest that nefiracetam, and possibly aniracetam, may activate N- and L-type Ca2+ channels in a differential way depending on how they recover from Go/Gi-mediated inhibition.

Two types of aggregate in the cerebral cortex of a seizure-sensitive strain of the Mongolian gerbil.

A 70-kDa protein, P70, found mostly in the pyramidal cells of the cerebral cortex of cobalt-induced epileptogenic rats, has been implicated in epileptogenesis. The presence of a P70-like substance was searched for immunohistochemically in the cerebral cortex of MGS/ldr, a seizure-sensitive strain of the Mongolian gerbil (Meriones unguiculatus) that we previously established. Immunoreactive aggregates were observed in the pyramidal neurons of the motor cortex and the primary somatosensory cortex. Analysis using confocal laser scanning microscopy revealed that the aggregates were often colocalized with a second type of aggregate with red autofluorescence at the marginal zone of the cell somata. Both aggregates appeared and increased before the appearance of generalized tonic-clonic convulsion. These may be involved in some change of physiological function of the cerebral cortex but their presence itself is not enough to determine the occurrence of epileptic seizure because the gerbils that showed no such seizure had both aggregates.

Antiepileptic effects of allopurinol on EL mice are associated with changes in SOD isoenzyme activities.

We have investigated the potential antiepileptic action of superoxide dismutase (SOD) activities in the brain of the epileptic mutant EL mouse. EL mice which experienced frequent seizures (EL[s]) had abnormally low levels of SOD isoenzyme activity in the hippocampal area. Once epileptogenicity was established in these animals, activity of cyanide-sensitive Cu,Zn-SOD was maintained at significantly lower levels than in control mice. However, cyanide-insensitive Mn-SOD activity was not different from non-epileptic controls. In EL mice which had not experienced seizure provoking stimulations and exhibited no seizures (EL[ns]) there was moderately lower levels of SOD isoenzyme activities compared to controls. In spite of the low level of Cu,Zn-SOD activity in EL[s] mice, the Cu,Zn-SOD protein content was high in the hippocampus of these animals, suggesting that inactive Cu,Zn-SOD might be induced during development. After allopurinol (ALP) was given orally to EL[s] mice, Cu,Zn-SOD activities increased dramatically in the hippocampus and seizure activity was decreased. Even after 48 h, when antiepileptic action of ALP was lost, the SOD activity was maintained at the high level associated with initial ALP administration. EL[s] mice also showed DNA fragmentation in the hippocampal CA1 region and the parietal cortex, detected with in situ terminal transferase-mediated dUTP nick labeling with the aid of alkaliphosphatase or peroxidase. The degree of DNA fragmentation was less severe in EL[ns] mice. We propose that abnormalities in region specific Cu,Zn-SOD isoenzyme activity might produce free radicals, leading to DNA fragmentations and cell loss. This might contribute to hippocampal epileptogenesis in EL mice.

Age-related appearance of dystrophic axon terminals in cerebellar and vestibular nuclei of Mongolian gerbils.

In the brains of 360-day-old Mongolian gerbils, numerous swellings immunoreactive to anti-neurofilament antibody were observed in cerebellar and vestibular nuclei. The number of these swellings was the same in two gerbil strains with different susceptibility to spontaneous motor seizures by various stimuli, but much more numerous in gerbils as compared with the 360-day-old Slc:Wistar rats. Such swellings were only occasionally found before 60 days of age in gerbils, but they increased in number about fivefold from 60 to 180 days of age and about quadruple from 180 to 360 days of age. Electron microscopic observation showed that these swellings were dystrophic axon terminals (DATs) whose cytoplasms were occupied with large bundles of neurofilaments, numerous vesicular structures containing membranous and/or granular materials, and many rod-shaped mitochondria. Additionally, other types of DATs displaying degenerative changes of cytoplasmic organelles were observed. ACPase cytochemistry showed that the vesicular structures in the DATs contained ACPase and released it into the cytoplasm.

Developmental and seizure-related regional differences in immediate early gene expression and GABAergic abnormalities in the brain of EL mice.

To examine the hypothesized role of the immediate early gene (IEG) response in synaptic plasticity and in epileptogenesis, we studied the spatial specificity of the expression of IEG in EL mice, a well known mutant model of epilepsy. Also to examine the 'GABA hypothesis' in epilepsy, GABA concentration and GAD activity was determined in micro brain regions (10-300 ng) of EL mice related to the focus in the parietal cortex and the hippocampus. We found that the IEG expression after seizures is not related to the seizure pattern, but to the seizure history, seizure threshold and development of EL[s]. Even in the interictal period, EL mice with long seizure histories and very low seizure thresholds demonstrate IEG expression continuously. This is probably strengthened by repeated seizures. The IEG expression site is however located in the hippocampal CA1, which is the final terminal of various inputs from other areas of the limbic system. It is proposed that the continuous expression of IEGs might play a different role from that of transiently expressed IEGs. Developmentally, the site of IEG expression shifted from one site to another in a very similar manner as in the IEG expression with propagation of paroxysmal discharges in each seizure, and the three-dimensional expression area was gradually expanded, suggesting a change in the regional active site during epileptogenesis. These lines of evidence suggest that during development as well as repetitive seizures, frequent expressions of IEGs and syntheses of Fos and Zif proteins might facilitate synaptic conductivity involved in epileptogenesis. The sites of abnormal GABA concentrations and GAD activities were almost the same in the parietal cortex, around Sidman atlas coronal section No. 300 and in the hippocampal CA1 pyramidal cells as the spatio-temporal specific IEG expression sites. These findings strongly suggest that IEG expression and abnormal GABAergic functions are involved in epileptogenesis in EL mice.

Altered axon terminals containing concentric lamellar bodies of cerebellar Purkinje cells in Mongolian gerbil.

Altered axon terminals containing concentric lamellar bodies were observed in cerebellar and vestibular nuclei of the Mongolian gerbil. The terminals increased in number from 30 days of age onward, and reached about tenfold at 360 days. The numbers were the same in two gerbil strains with different susceptibility to spontaneous motor seizures by various stimuli, but about threefold those in Slc:Wistar rat.

Endoscopic ultrasonographic-guided punctured pancreatic ductography: an initial and successful trial.

A 71-year-old male suffering from an intraductal papillary tumor of the pancreas was admitted to our hospital for further investigation. Diagnostic trials, including endoscopic retrograde pancreatography, did not produce an adequate ductography because of a large amount of mucinous fluid. Therefore, we performed endoscopic ultrasonographic-guided punctured pancreatic ductography (EPPD). This procedure was safely performed without any complications. We report this initial and successful trial of EPPD.

Alcohol consumption and insomnia in a sample of Japanese alcoholics.

The amount of ethanol consumed by chronic alcoholics in a Japanese slum area with persistent insomnia (n = 40) and those without it (n = 40) was compared using a questionnaire. For both groups, the present habitual consumption (PHC) of ethanol per day was most frequently between 60 g and 150 g and no difference was observed between the two groups. In contrast, the maximum habitual consumption (MHC) of ethanol per day throughout the alcoholic history was found to be greater for the insomnia patients than the non-insomniacs (p < 0.001). No difference between the groups was found in the kind of alcoholic drink consumed, with sake (Japanese rice wine) being the most popular in both groups. The results suggest that persistent insomnia in alcoholics is related to excessive alcohol intake and persists even when drinking levels have fallen.