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A metal nanogrid pattern with high aspect ratio was successfully fabricated on a stretchable substrate using silver ink. The master mold was fabricated by electron-beam lithography and dry etching, whereas the replica mold was replicated from the master mold by ultraviolet nanoimprint lithography. The replica mold was coated with silver ink and covered with a polyester film, which was then pressed using a roller to fill the mold trenches with the silver ink. Next, the silver ink remaining in the bottom of the replica mold was sintered at 120 °C for 5 min. Finally, the sintered silver ink at the bottom of the replica mold was transferred onto a polyester film using an ultraviolet-curable resin. The resulting transparent electrode had a transmittance of 81% at a wavelength of 550 nm and resistance of 11.0 Ω. The strain on the electrode was 22.7% under a tensile load of 0.78 N.

Clinical studies have indicated that diabetes is associated with Alzheimer's disease (AD) and neurodegeneration. However, the mechanisms underlying this association have not been fully elucidated. Diabetes causes neurodegeneration by inducing changes in vascular function and structure, glucose metabolism, and insulin signaling, as well as by modifying β-amyloid (Aβ)/tau metabolisms. In turn, AD influences systemic glucose metabolism by inducing behavioral changes, memory disturbances, hypothalamic dysfunction, frailty and possibly plasma/peripheral Aβ level changes. Hypoglycemia, one of the major conditions encountered during the treatment of patients with diabetes, may also contribute to neurodegeneration. Through this vicious circle, diabetes and AD may cooperate to cause neurodegeneration. Various molecular, cellular, inter-organ, physical and clinical factors might contribute to the bidirectional interactions between diabetes and AD. Explorations of a key factor that underlies the bidirectional interactions, "Factor X", could lead to the development of a potential therapeutic target for neurodegeneration. Factor X should fulfill the following equation: neurodegeneration equals Aβ levels multiplied by Factor X.

Local field potentials (LFPs) are thought to integrate neuronal processes within the range of a few millimeters of radius, which corresponds to the scale of multiple columns. In this study, the model of LFP in the visual cortex proposed by Mazzoni et al. (2008) was adapted to organize a network of two cortical areas, in which pyramidal neurons were divided into two sub-population modeling columns with spatially organized connections to neurons in other areas. Using the model enabled the relationship between neural firing and LFP to be evaluated, in addition to the LFP coherence between the two areas. Results showed that: (1) neurons in a particular sub-population generated the LFP in the area; (2) the spatial consistency of neural firing in the two areas was strongly correlated with LFP coherence; and (3) this consistency was capable of regulating LFP coherence in a lower frequency band, which was originally introduced to neurons in a particular sub-population. These results were derived from a winner-take-all operation in the columnar structure; thus, they are expected to be common in the cortex. It is suggested that the spatial consistency of neural firing is essential for regulating long-range LFP synchronization, which would facilitate neuronal integration processes over multiple cortical areas.

Basal cell nevus syndrome, also known as Gorlin–Goltz syndrome, shows five main pathological features: nevoid basal cell carcinomas; keratocystic odontogenic tumours; congenital skeletal anomalies; calcification of the falx cerebri; and point skin depressions on the palms and/or soles. We encountered a 62-year-old man with basal cell nevus syndrome appearing as multiple cystic lesions in the mandible and maxilla, along with bifid ribs. The multiple cystic lesions were identified on panoramic radiography and computed tomography. Bifid rib was apparent at the left eighth rib on postero-anterior radiography and computed tomography. The multiple cystic lesions were removed by an oral surgery team. Histopathological examination diagnosed the specimens as keratocystic odontogenic tumours. Findings were ambiguous regarding the diagnosis of basal cell nevus syndrome, so the patched homologue 1 ( PTCH1 ) gene was sequenced, identifying a novel mutation (1346T → A). These results strongly suggested that the phenotype had been caused by mutations in the PTCH1 gene. The patient was diagnosed with basal cell nevus syndrome based on genetic investigations. In addition, our findings suggest that a novel mutation (1346T → A) may cause osteoplasty of the mandible, maxilla and ribs.

The hippocampus is known to maintain memories of object-place associations that can produce a scene expectation at a novel viewpoint. To implement such capabilities, the memorized distances and directions of an object from the viewer at a fixed location should be integrated with the imaginary displacement to the new viewpoint. However, neural dynamics of such scene expectation at the novel viewpoint have not been discussed. In this study, we propose a method of coding novel places based on visual scene transformation as a component of the object-place memory in the hippocampus. In this coding, a novel place is represented by a transformed version of a viewer's scene with imaginary displacement. When the places of individual objects are stored with the coding in the hippocampus, the object's displacement at the imaginary viewpoint can be evaluated through the comparison of a transformed viewer's scene with the stored scene. Results of computer experiments demonstrated that the coding successfully produced scene expectation of a three object arrangement at a novel viewpoint. Such the scene expectation was retained even without similarities between the imaginary scene and the real scene at the location, where the imaginary scenes only functioned as indices to denote the topographical relationship between object locations. The results suggest that the hippocampus uses the place coding based on scene transformation and implements the spatial imagery of object-place associations from the novel viewpoint.

Surface treatment of insulator materials has growing needs recently. However, accumulation of charges on the insulator surface limits the applicability of plasma methods for the insulator processing. A radio-frequency-bias method is a good choice but it still has a problem coming from the oscillating sheath potential. In the present study, we are proposing the dual-plasma ion process, a new plasma process that enables for insulator samples to be treated by an energy-controlled, dc ion beam without surface charging. The concept and results of the proof-of-principle experiment are given.

Microdialysis is a powerful in vivo technique for the continuous sampling of small molecules within the extracellular fluid space. However, efforts to collect larger molecules have met with little success. To identify biologically active larger molecules in free-moving animals would be of great benefit. For this purpose, we have developed a novel microdialysis method that allows consistent recovery of large molecules from the brain interstitial space in the awake, free-moving mouse. Using a new "vent" probe with a push-pull perfusion system, the present study successfully demonstrated in vivo sampling of pathophysiologically important macromolecules in free-moving mouse brain. This sampling system allowed monitoring of the dynamic changes in their concentrations. Overall, this novel microdialysis system would provide the opportunity to identify the expression patterns of pathophysiologically important proteins in a variety of physiological and pathological processes for a better understanding of various diseases.

Objectives The aim of this study was to investigate the relationship between cerebral infarction (CI) and the human apurinic/apyrimidinic endonuclease 1/redox effector factor-1 (APE1/REF-1) gene using single-nucleotide polymorphisms (SNPs) and a haplotype-based case–control study. Design and methods We selected 5 SNPs in the human APE1/REF1 gene (rs1760944, rs3136814, rs17111967, rs3136817 and rs1130409), and performed case–control studies in 177 CI patients and 309 control subjects. Results rs17111967 was found to have no heterogeneity in Japanese. The overall distribution of the haplotype-based case–control study constructed by rs1760944, rs3136814 and rs1130409 showed a significant difference. The frequency of the G-C-T haplotype was significantly higher in the CI group than in the control group (2.5% vs. 0.0%, p > 0.001). Conclusions Based on the results of the haplotype-based case–control-study, the G-C-T haplotype may be a genetic marker of CI, and the APE1/REF-1 gene may be a CI susceptibility gene.

Angioid streaks (AS) are eye abnormalities caused by breaks in Bruch’s membrane. The condition is often associated with pseudoxanthoma elasticum (PXE). The ATP-binding cassette, sub-family C (CFTR/MRP), member 6 (ABCC6) is reported to be the causal gene for PXE, although there have been no reports on whether the ABCC6 gene is the causal gene for AS. The aims of this study are to isolate the causal mutations for AS using a haplotype-based case-control study. We genotyped 54 Japanese AS patients and 150 controls for 5 single-nucleotide polymorphisms (SNPs). A simple association study using each SNP and a haplotype-based case-control study were performed. Twelve patients with special haplotypes for AS were selected, and were then subjected to gene sequencing. Six variants were successfully identified as causal mutations for AS (p.R419Q, p.E422K, c.2542delG, Del_Exon23, c.3774-3775insC and p.E1427K), and 4 of these were novel. This method can be applied to both identifying susceptibility variants of multifactorial diseases and isolating mutations in single-gene diseases.

Although the pathophysiology of post-angioplasty restenosis has been extensively studied in extracranial arteries using transluminal vascular injury model in rodents, it is still not well known in the intracranial arteries, which have quite different structures from extracranial arteries. Here, we examined whether 1-min placement of modified intraluminal suture could induce an injury in the internal carotid artery (ICA) in rats and observed temporal profile of histological change after the injury. HE staining showed that the injured intracranial ICA was dilated, while the media was markedly thinned at 1 day after injury. The internal elastic lamina was not observed, and the media contained few cells. At 1 week after injury, a thin layer of neointimal hyperplasia was observed on the luminal side of the internal elastic lamina. Neointimal hyperplasia developed until at least 4 weeks after injury. Morphometric analysis demonstrated that the healing process of the injury was related to arterial remodeling. Immunohistochemical staining for alpha-smooth muscle actin and electron microscopic analysis showed that the neointima was composed of smooth muscle cells. Re-endothelialization was observed from 1 to 4 weeks after injury by immunohistochemical staining for von Willebrand's factor and electron microscopic analysis. Vascular endothelial growth factor was expressed in neointima on days 7 and 14. Interestingly, superoxide anion was not increased in injured arteries on day 3, when the infiltration of macrophages was intensive, but increased on day 7, when infiltrating macrophages almost disappeared. These findings might shed new light on pathophysiology of post-angioplasty restenosis in intracranial arteries.

gamma-Secretase cleaves the transmembrane domains of several integral membrane proteins involved in vasculogenesis. Here, we investigated the role of gamma-secretase in the regulation of postnatal angiogenesis using gamma-secretase inhibitors (GSI). In endothelial cell (EC), gamma-secretase activity was up-regulated under hypoxia or the treatment of vascular endothelial growth factor (VEGF). The treatment of GSI significantly attenuated growth factor-induced EC proliferation and migration as well as c-fos promoter activity in a dose-dependent manner. In vascular smooth muscle cell (VSMC), treatment of GSI significantly attenuated growth factor-induced VEGF and fibroblast growth factor-2 (FGF-2) expression. Indeed, GSI attenuated VEGF-induced tube formation and inhibited FGF-2-induced angiogenesis on matrigel in mice as quantified by FITC-lectin staining of EC. Overall, we demonstrated that gamma-secretase may be key molecule in postnatal angiogenesis which may be downstream molecule of growth factor-induced growth and migration in EC, and regulate the expression of angiogenic growth factors in VSMC.

A novel plasma-based ion process characterized by the dual plasma configuration, which we call the dual-plasma immersion ion process and which has been developed for the surface treatment of electrically insulating materials, is reported. In this process, the plasma is divided into two parts by a negatively biased grid: the target plasma and the driver plasma. The workpiece to be treated is set in the target plasma. If a dc or pulsed positive bias is applied to the driver plasma against the target plasma at ground potential, an ion sheath develops on the grid and a potential difference happens across the ion sheath. When we see the dual-plasma process from the workpiece, it gets the impact of ions from the driver plasma while being immersed in the target plasma at ground potential. Thus, this new process enables treatment of insulating materials because the surface charge induced by the ion impact is completely reduced by the inflow of electrons from the target plasma. In the present paper, the basic idea of the dual-plasma immersion ion process and results of the proof-of-principle experiment are presented.

The discovery of theta-rhythm-dependent firing of rodent hippocampal neurons highlighted the functional significance of temporal encoding in hippocampal memory. However, earlier theoretical studies on this topic seem divergent and experimental implications are invariably complicated. To obtain a unified understanding of neural dynamics in the hippocampal memory, we here review recent developments in computational models and experimental discoveries on the 'theta-phase precession' of hippocampal place cells and entorhinal grid cells. We identify a theoretical hypothesis that is well supported by experimental facts; this model reveals a significant contribution of theta-phase coding to the on-line real-time operation of episodic events, through highly parallel representation of spatiotemporal information.

Abeta is one of the primary therapeutic targets for Alzheimer disease (AD). Abeta vaccination induces the disappearance of Abeta deposits. Since few reports have focused on the reverse phase of Abeta aggregation, we established a new screening system, the in vitro Abeta sink assay, to clarify the process of dissociation of soluble forms from fibrils. Abeta42 was more resistant to dissociation from fibrils to monomers and/or low molecular weight (LMW) soluble oligomers than Abeta40. We applied this system to find a potential therapy for AD. Ultrasound irradiation significantly enhanced the dissociation of soluble Abeta from fibrils, while ultrasound experiments also confirmed the difference between Abeta40 and Abeta42. We found that some compounds enhanced the dissociation of Abeta from fibrils. Here, we proposed that Abeta42 was more resistant to dissociation from fibrils to monomers and/or LMW soluble oligomers than Abeta40, and this system might be useful to identify dissociation of soluble Abeta from fibrils.

Although viral vector systems are efficient to transfect foreign genes into a variety of tissues, safety issues remain in relation to human gene therapy. In this study, we examined the feasibility of a novel nonviral vector system by using high-frequency, low-intensity ultrasound irradiation for transfection into vascular cells, kidneys and the central nerve systems of fetal mice. As a result, expression of the reporter gene, Venus, was readily detected in the central nervous system. The transfected cells were mainly detected in meningeal cells with intracisternal injection. Overall, the present study demonstrated the feasibility of efficient plasmid DNA transfer into several organs, especially the central nervous system, providing a new option for treating various diseases.

A missense mutation (N1411) in Presenilin-2 (PS-2) gene is associated with early-onset familial Alzheimer's disease. In this study, SK-N-SH human neuroblastoma cells were transfected with wild-type and mutant PS-2 gene to examine presenilin-2 effects on apoptosis. Serum deprivation resulted in enhanced apoptosis in mutant PS-2 comparing with wild-type PS-2. Similarly, mutant PS-2 induced lactate dehydrogenase release to greater extent than wild-type PS-2. Time course experiment demonstrated that the increase in caspase-3-like activity was more pronounced and accelerated in mutant PS-2, compared to wild-type PS-2. While a significant decrease in bcl-2, an anti-apoptotic molecule, occurred in the cells overexpressing mutant PS-2, no significant change was observed in bax, a pro-apoptotic molecule, as compared with the cells overexpressing wild-type PS-2. Our study demonstrated that mutant PS-2 induces apoptosis accompanied by increased caspase-3-like activity and decreased bcl-2 expression in neuronal cells after serum-deprivation.

Endohedral fullerenes Si@C 74 were produced by direct current and radio-frequency hybrid arc-discharge. Atomic structure analysis and structural optimization of the Si@C 74 were carried out by high-resolution electron microscopy, image simulation, molecular mechanics and ab initio molecular orbital calculations. Total steric energy of the Si@C 74 was the lowest in the present calculation of C 60 –C 76 clusters. The energy gap of the Si@C 74 was calculated to be 0.098 eV, and the heat of formation per carbon atom is almost the same as that of the C 60 cluster.

The wave function of the implanted μ+ in UNi2Al3 is found to be extended over a hexagonal ring of interstitial lattice sites m or k, closely surrounding the highly symmetrical site b. This site assignment, inferred from the angular dependence of high-field relaxation rates, leads to an equally consistent explanation of the medium- and low-field μSR data. By using available NMR data for the inherent ‘crystal’ electric field gradient (EFG), the μ+-induced EFG at the Al nuclei could be determined.

PC12 cells undergo apoptosis when cultured under conditions of serum deprivation. In this situation, the activity of caspase-3-like proteinases was elevated, and the survival rate could be maintained by treatment with acetyl-DEVD-cho, a specific inhibitor of caspase-3. In a culture of PC12 cells treated with acetyl-DEVD-cho, where caspase-3-like proteinases are not activated, CA074, a specific inhibitor of cathepsin B induced active death of the cells. Cathepsin B antisense oligonucleotides showed a similar effect to CA074 on the induction of active cell death. By double staining of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling and activated caspase-3, the dying cells treated with CA074 were positive for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling staining but negative for activated caspase-3. Ultrastructurally, the cells were relatively large and had nuclei with chromatin condensation. The initiation of cell death by CA074 or the cathepsin B antisense were inhibited by the addition of pepstatin A, a lysosomal aspartic proteinase inhibitor, or by cathepsin D antisense. To examine whether this cell death pathway was present in cell types other than PC12 cells, we analysed dorsal root ganglion neurons obtained from rat embryos on the 15th gestational day, a time when they require nerve growth factor for survival and differentiation in culture. When cultured in the absence of nerve growth factor, the neurons survived in the presence of acetyl-DEVD-cho or acetyl-YVAD-cho. Under these conditions, CA074 reduced the survival rate of the neurons, which was subsequently restored by the further addition of pepstain A. These results suggest that a novel pathway for initiating cell death exists which is regulated by lysosomal cathepsins, and in which cathepsin D acts as a death factor. We speculate that this death-inducing activity is normally suppressed by cathepsin B.

Objective. The purpose of this study was to differentiate reactively enlarged cervical nodes from metastatic nodes by means of color Doppler flow imaging in patients with oral squamous cell carcinoma. Study design. Enlarged lymph nodes with long-axis diameters greater than 10 mm in 30 patients were classified into 4 groups according to color Doppler flow imaging findings. After the patients underwent neck dissection, the findings were correlated with the pathologic features. Results. Color Doppler flow imaging detected 58 enlarged nodes with long-axis diameters greater than 10 mm. Thirty-five lymph nodes showed no color flow signals; of these, 32 (91%) were metastatic and 3 were reactive. Of the 12 lymph nodes with central color flow signals, 11 (92%) were reactively enlarged and 1 was metastatic. Conclusions. The presence of central signals on color Doppler flow imaging appeared to be a significant parameter associated with reactively enlarged benign nodes in patients with oral squamous cell carcinoma.

Carbon soot is produced under various conditions of an arc-discharge plasma in a helium atmosphere and its mass analysis is performed in detail by a laser-desorption time-of-flight spectrometer in order to clarify production ratios of higher fullerenes to C 60 , It is found that the helium-gas pressure P He has a strong effect on the production ratio. In a low pressure region (P He 500 Torr) the production quantity of C 74 is the largest in the higher fullerenes, which almost attains that of C 60 . The overall production ratio is estimated to be in the order, C 60 , C 74 , C 70 , etc. This high-yield C 74 production seems to be related to charged-particle dynamics in the arc-discharge plasma.

A new method for ion-species and isotope separations is described, which is expected to yield higher mass resolution and collection rates than the conventional ion-cyclotron-resonance technique. It is based on the principle that travelling waves with cyclotron frequencies generate charged particle drifts perpendicular to both the direction of wave propagation and external magnetic field lines.

The Fermi surface and the cyclotron mass of a semimetallic compound, CeAs, were determined by use of the dHvA effect. We have found that the cyclotron mass of the hole surface decreases with increasing field. CeAs is a dense Kondo system with low carrier concentration of 0.0024/formula unit.

The Fermi surface and the cyclotron mass both above and below the Neel temperature were determined by the dHvA effect. We have found the Fermi surface of three ellipsoidal electron surfaces, and spherical and nearly octahedral hole surfaces. In addition, we have found an anomalous temperature dependence on the oscillatory amplitude.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra. The ultimate treatment of PD is to repair dopaminergic neurons from degenerative process. As neurotrophic factors have been shown to support the survival and enhance the function of dopaminergic neurons, gene therapy using neurotrophic factors such as glial cell line-derived neurotrophic factor becames center of interests. In the present study, we focused on hepatocyte growth factor (HGF) as a novel neurotrophic and angiogenic growth factor that is a well-known potent pleiotrophic cytokine exhibiting mitogenic, motogenic, and morphogenic activities in a variety of cells.

Objective CYP4A11 is an enzyme that converts arachidonic acid to 20-hydroxyeicosatetraenoic acid, which is involved in regulation of vascular tone in the brain. Recent evidence indicates that the polymorphism of the CYP genes is associated with cerebral infarction (CI). The aim of the present study was to assess the association between the human CYP4A11 gene and CI using a haplotype-based case-control study divided by gender. Methods Three SNPs of the human CYP4A11 gene (rs2269231, rs1126742, and rs9333025) were selected and genotyped for 174 CI patients and 293 controls. The data were assessed for three separate groups: total subjects, men and women. Results In men, the genotype distribution of rs9333025 significantly differed between the CI patients and control subjects (P = 0.047). The distribution of the dominant model of rs9333025 (GG vs. GA + AA) significantly differed between both the total and the men groups (P = 0.033, P = 0.028, respectively). Logistic regression analysis adjusted for the history of hypertension and diabetes mellitus also showed that the GG genotype was significantly more frequent in the CI patients than in the controls, both for the total and men groups (P < 0.001, P = 0.008, respectively). The overall distribution of the haplotypes constructed with the 3 SNPs showed significant differences between the CI and the control in total group (P = 0.049). The T-C-G haplotype was significantly more frequent in control subjects than in the CI patients in the total group (P = 0.020). Conclusions The GG genotype of rs9333025 could be a genetic marker for CI in Japanese men. In addition, the T-C-G haplotype might also be a protective marker for CI in Japanese.

Electrical resistivity of the 5f ferromagnet UGa2 was studied with current along the (1, 0, 0) direction. High resistance values point to a narrow 5f band close to EF. Magnetization measurements under pressure show increasing TC (0.3 K/kbar) and weakly decreasing magnetization at low temperatures.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. The ultimate treatment of PD is to protect dopaminergic neurons from degenerative process. As neurotrophic factors have been shown to support the survival and enhance the function of dopaminergic neurons, gene therapy using neurotrophic factors such as glial cell line-derived neurotrophic factor becames center of interests. In the present study, we focused on hepatocyte growth factor (HGF) as a novel neurotrophic and angiogenic growth factor that is a well-known potent pleiotrophic cytokine exhibiting mitogenic, motogenic, and morphogenic activities in a variety of cells.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons (DAN) in the substantia nigra (SNi). The ultimate treatment of PD is to prevent DAN from the cell death. We previously showed that hepatocyte growth factor (HGF) resulted in effective prevention of DAN from cell death and remarkable behavioral recovery in 6-hydroxy-dopamine-lesioned parkinsonian rats. In this study, we have extend the preclinical exploration to primate model of PD. Seven days after stereotaxic transfection of human HGF plasmid or pVAX1 control plasmid into the unilateral striatum, infusion of MPTP into the right internal carotid artery of animals produces toxin-induced injury to the right nigro-striatal pathway with sparing of other dopaminergic neurons on the infused side and with negligible or little injury to the opposite, untreated side. After 2 to 3 weeks period, animals exhibited stable moderate parkinsonian features. But animals transfecterd with human HGF plasmid showed normal states. Interestingly, animals transfected with pVAX1 plasmid demonstrated the apomorphine and amphetamine-induced rotational asymmetry. However, the transfection of human HGF plasmid resulted in a significant inhibition of abnormal rotation over 3 months. In immunohistochemistry, more than 90% doperminergic neurons of PD model animals transfecred with pVAX1 plasmid were lost, while more than 70% those of animals transfected with human HGF plasmid were survived. Microdialysis demonstrated that concentrations of dopamine in striatum and SNi in animals transfected with human HGF plasmid were higher compared with PD model. Overall, the present study demonstrated that over-expression of human HGF prevented neuronal death in primate PD model, providing a potential of novel gene therapy for PD using human HGF plasmid.

Top of pageAbstract Cerebral occlusive disease caused by atherosclerosis of the cerebral arteries or Moyamoya disease often causes global ischemia of the brain. Although such a condition leads to not only cerebral ischemic events, but also neuropathological changes including dementia, an effective treatment to improve brain ischemic injury has not yet been established. It is known that ischemic stroke induces active angiogenesis, particularly in the ischemic penumbra, which correlates with longer survival in humans. However, the natural course of angiogenesis is not sufficient to compensate for the hypoperfusion state. Recently, a novel therapeutic strategy using genes of angiogenic growth factors and neurotrophic factors has been proposed for the treatment of cerebrovascular disease. In the present study, we examined the effects of hepatocyte growth factor (HGF) in a rat middle cerebral artery occlusion model. First, human HGF gene was transferred into the brain via the cisterna magna using HVJ-envelope vector. The concentration of human HGF and rat HGF in CSF were measured by ELISA at 5 and 12 days after gene transfer. On day 5, as expected, human HGF could be detected in the CSF of rats transfected with human HGF vector, while human HGF protein could not be detected in control rats. The increase in human HGF protein in the CSF continued up to 12 days after transfection. Consistently, up-regulation of c-met was observed in the cerebral cortex as well as the brain stem and cerebellum. Next, the middle cerebral artery was occluded 5 days after HGF gene transfer. Over-expression of the HGF gene resulted in a significant decrease in the infarcted brain area after 24 hours of ischemia, whereas control group showed large infarction (48 ± 3.0 % vs 72 ± 5.9 %, P

New results from muon spin rotation measurements in zero external magnetic field on the antiferromagnetic phase of CeB6 confirm that the actual magnetic structure is likely different from that derived from neutron scattering. Transverse field results on the quadrupolar ordered phase exhibit a behaviour that cannot be explained in terms of proposed induced antiferromagnetic spin structures.

The high-energy tail of the ion energy distribution is heated by an instability with broad-band frequency spectrum having a peak a little above the ion-cyclotron frequency. The tail heating of the ions is enhanced under a mirror configuration of the magnetic field.