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Blasting is a relatively economical and efficient excavation method compared to other methods such as mechanical excavation. However, when tunnel sites are located near residential areas, the charge weight is often reduced to limit the impacts of vibration and noise. This makes it difficult to maintain the scheduled excavation advance rate. In recent years, however, advanced blasting technologies such as computerized jumbos and high-accuracy electronic detonators have allowed better control over tunnel blasting vibrations. Additionally, new vibration measurement systems have been introduced that enable the simultaneous monitoring and analysis of blast vibration results. Here, we applied these advanced technologies in a restricted blasting zone to reduce the environmental impact and enable the excavation advance rate to be maintained.

Objective: To clarify the genetic, clinicopathologic, and neuroimaging characteristics of patients with hereditary diffuse leukoencephalopathy with spheroids (HDLS) with the colony stimulating factor 1 receptor ( CSF-1R ) mutation. Methods: We performed molecular genetic analysis of CSF-1R in patients with HDLS. Detailed clinical and neuroimaging findings were retrospectively investigated. Five patients were examined neuropathologically. Results: We found 6 different CSF-1R mutations in 7 index patients from unrelated Japanese families. The CSF-1R mutations included 3 novel mutations and 1 known missense mutation at evolutionarily conserved amino acids, and 1 novel splice-site mutation. We identified a novel frameshift mutation. Reverse transcription PCR analysis revealed that the frameshift mutation causes nonsense-mediated mRNA decay by generating a premature stop codon, suggesting that haploinsufficiency of CSF-1R is sufficient to cause HDLS. Western blot analysis revealed that the expression level of CSF-1R in the brain from the patients was lower than from control subjects. The characteristic MRI findings were the involvement of the white matter and thinning of the corpus callosum with signal alteration, and sequential analysis revealed that the white matter lesions and cerebral atrophy relentlessly progressed with disease duration. Spotty calcifications in the white matter were frequently observed by CT. Neuropathologic analysis revealed that microglia in the brains of the patients demonstrated distinct morphology and distribution. Conclusions: These findings suggest that patients with HDLS, irrespective of mutation type in CSF-1R , show characteristic clinical and neuroimaging features, and that perturbation of CSF-1R signaling by haploinsufficiency may play a role in microglial dysfunction leading to the pathogenesis of HDLS.

We have been developing highly radiation-tolerant n + -in-p planar pixel sensors for use in the high-luminosity LHC. Novel n + -in-p structures were made using various combinations of the bias structures (punch-through or polysilicon resistor), isolation structures (p-stop or p-spray), and thicknesses ( 320 μ m or 150 μ m ). The 1-chip pixel modules with thin FE-I4 pixel sensors were evaluated using test beams, before and after 2 × 10 15 n eq / cm 2 irradiation. The full depletion voltages were estimated to be 44±10 V and 380±70 V, in the non-irradiated and the irradiated modules, respectively. A reduction of efficiency was observed in the vicinity of the four pixel corners and underneath the bias rail after the irradiation. The global efficiencies were > 99 % and > 95 % in the non-irradiated and the irradiated modules, respectively. The collected charges were uniform in the depth direction at bias voltages well above the full depletion voltages. The encapsulation of vulnerable edges with adhesive or parylene prevented HV sparking. Bump bonding with the SnAg solder bumps was performed at HPK with 150 μ m - and 320 μ m - thick sensors and chips. No disconnection of bumps was observed after 10 thermal cycles between −40 and +50 °C, with a temperature slew rate of > 70 K / min .

In this paper we present RD small diodes were employed to investigate the width from the active diode to the dicing edge and the guard rings. Tests involving the diodes showed that the strong increase of leakage current was attributed to the edge current when the lateral depletion zone reaches the dicing edge and the lateral depletion along the silicon surface was correlated with the ‘field’ width. The onset was observed at a voltage of 1000 V when the width was equal to ∼400 μm. The pixel sensors that were diced at a width of 450 μm could successfully maintain a bias voltage of 1000 V. Hybrid flip-chip pixel modules with dummy and real chips were also fabricated. Lead (PbSn) solder bump bonding proved to be successful. However, lead-free (SnAg) solder bump bonding requires further optimization.

We investigated the presence of autoantibodies againstglutamate receptor (GluR) Ε2 in serum and cerebrospinal fluid (CSF) samples from 12 consecutive patients with acute encephalitis/encephalopathy by immunoblotting using recombinant GluRΕ2 as antigen. In 4 patients, IgM autoantibodies against GluRΕ2 were detected in CSF in the early phase of the disease but were not detectable after several months. Seizures and psychiatric symptoms were noted during the acute phase of the disease in these 4 patients, who showed various degrees of residual amnesia. Immunotherapy was performed on 3 patients (patients 1, 3 and 4), and they showed marked improvements. Immunohistochemistry using these patients’ sera showed that immunoreactivity is specifically detected in the cytoplasm of rat hippocampal and cortical neurons. The clinical features and neuroimaging findings of patients with IgM autoantibodies against GluRΕ2 in CSF resemble those of patients with reversible autoimmune limbic encephalitis.

Machado-Joseph disease (MJD) is an autosomal dominant, multisystem neurodegenerative disorder involving predominantly cerebellar, pyramidal, extrapyramidal, motor neuron and oculomotor systems. Although it was first reported in families of Portuguese-Azorean descent, MJD has also been described in non-Azorean families from various countries, being one of the most common hereditary spinocerebellar degenerations. With the use of highly polymorphic microsatellite DNA polymorphisms, we have assigned the gene for MJD to the long arm of chromosome 14 (14q24.3-q32) by genetic linkage to microsatellite loci D14S55 and D14S48 (multipoint lod score Zmax = 9.719).

We investigated the presence of autoantibodies against glutamate receptor (GluR) epsilon2 in serum and cerebrospinal fluid (CSF) samples from 12 consecutive patients with acute encephalitis/encephalopathy by immunoblotting using recombinant GluR epsilon2 as antigen. In 4 patients, IgM autoantibodies against GluR epsilon2 were detected in CSF in the early phase of the disease but were not detectable after several months. Seizures and psychiatric symptoms were noted during the acute phase of the disease in these 4 patients, who showed various degrees of residual amnesia. Immunotherapy was performed on 3 patients (patients 1, 3 and 4), and they showed marked improvements. Immunohistochemistry using these patients' sera showed that immunoreactivity is specifically detected in the cytoplasm of rat hippocampal and cortical neurons. The clinical features and neuroimaging findings of patients with IgM autoantibodies against GluR epsilon2 in CSF resemble those of patients with reversible autoimmune limbic encephalitis.

An n-type semiconducting diamond thin film was obtained by microwave enhanced plasma chemical vapor deposition using phosphine (PH3) as a dopant source. A homoepitaxial diamond thin film with a thickness of about 300 nm was grown on the {111} surface of a type Ib diamond with a variety of dopant concentrations. Over a wide range of dopant concentrations (PH3/CH4: 1000–20 000 ppm), the n-type conduction was confirmed by Hall-effect measurements. The activation energy of carriers was 0.43 eV. The Hall mobility of about 23 cm2/V s has been obtained at around 500 K for the 1000 ppm sample. No significant increase of hydrogen has been observed by secondary-ion-mass-spectroscopy analysis for the phosphorous doped layers.

This paper discusses the necessity of supporting the cooperative management of TCP/IP-based networks and describes a platform for this kind of management. The Internet and intra/extranets tend to be managed by organizations that have different management skills and policies. Because these organizations use different network management systems, their cooperation causes many problems. One is an increased load on the managed network devices, and another is the difficulty of sharing management results/status among the organizations. We have designed a platform that enables the different network management systems to cooperate in solving these problems. The feasibility of the platform is discussed in terms of our prototype implementation and its application to an Internet backbone service.

To investigate the molecular mechanism of mutant Cu/Zn superoxide dismutase (SOD) associated with familial amyotrophic lateral sclerosis (FALS), mutant (A1a4Thr, Gly85Arg, Gly93Ala, and two base-pair deletion in the 126th codon), as well as wild-type (wt), Cu/Zn SODs were expressed in COS7 cells. The formation of granular cytoplasmic aggregates accompanied by collapse of the cytoplasm was observed in cells expressing mutant Cu/Zn SODs, but not in cells expressing mutant Cu/Zn SODs. The aggregates contained ribosome-like particles and endoplasmic reticulum. These results suggest the possibility that mutant Cu/Zn SODs promote the formation of aggregates which are toxic to cells.

We have measured Raman spectra of a diamond film prepared on the (111) surface of cubic boron nitride(c‐BN) by the dc plasma chemical vapor deposition method. The polarization property of the Raman line of diamond agrees well with that of LO phonon for the (111) surface of c‐BN. The agreement between the polarization property of Raman lines of diamond and c‐BN indicates a possibility of the heteroepitaxial growth of the diamond film on the (111) surface of c‐BN. It is found that the diamond layers on c‐BN are under tensile stress of 2.2×1011 dyn/cm2. The value of the corresponding tensile strain agrees well with the lattice mismatch calculated from the lattice constants of c‐BN and diamond, supporting the possibility of the heteroepitaxial growth of the diamond film. Raman spectroscopy is a powerful technique not only to estimate the stress in the diamond film but also to determine the crystallographic orientation.

Growth inhibitory factor (GIF) is a small (7 kDa), heat-stable, acidic, hydrophilic metallothionein (MT)-like protein. GIF inhibits the neurotrophic activity in Alzheimer's disease (AD) brain extracts on neonatal rat cortical neurons in culture. GIF has been shown to be drastically reduced and down-regulated in AD brains. In neurodegenerative diseases in humans, GIF expression levels are reduced whereas GFAP expression levels are markedly induced in reactive astrocytes. Both GIF and GIF mRNA are present at high levels in reactive astrocytes following acute experimental brain injury. In chronological observations the level of GIF was found to increase more slowly and remain elevated for longer periods than that of glial fibrillary acidic protein (GFAP). These differential patterns and distribution of GIF and GFAP seem to be important in understanding the mechanism of brain tissue repair. The most important point concerning GIF in AD is not simply the decrease in the level of expression throughout the brain, but the drastic decrease in the level of expression in reactive astrocytes around senile plaques in AD. Although what makes the level of GIF decrease drastically in reactive astrocytes in AD is still unknown, supplements of GIF may be effective for AD, based on a review of current evidence. The processes of tissue repair following acute brain injury are considered to be different from those in AD from the viewpoint of reactive astrocytes.

Neurological symptoms often preceded diagnosis of malignancy. Anti-cancer therapy and immunological treatments are relatively effective for Lambert-Eaton myasthenic syndrome, but often disappointing for subacute cerebellar degeneration or sensory neuropathy. Examination of anti-neuronal antibodies, which are characteristic of some clinical type of this syndrome, is very important for early diagnosis of the malignancy and treatment for neurological symptoms.

We report a 72-year-old man with sporadic amyotrophic lateral sclerosis (ALS) who showed concomitant histopathology of Alzheimer's disease (AD) and incidental Lewy body disease. The patient presented at the age of 70 years with distal upper limb amyotrophy. Thereafter, gait disturbance and respiratory distress progressed. Neuropathological examination showed mild frontal lobe and anterior spinal root atrophy. There was moderate loss of upper and lower motor neurons, and Bunina bodies and skein-like inclusions were present in the spinal anterior horns and facial and hypoglossal nuclei, confirming the pathology of ALS. In addition, however, numerous amyloid plaques were observed throughout the entire cerebral neocortex, nucleus accumbens and amygdaloid body. Many neurofibrillary tangles were also evident in the medial temporal cortex. Moreover, the substantia nigra showed mild degeneration, and Lewy bodies were found in the substantia nigra, locus ceruleus, basal nucleus of Meynert and peripheral autonomic ganglia. Although neither parkinsonism nor dementia was noted during the clinical course, our final neuropathological diagnosis was sporadic ALS, AD and incidental Lewy body disease (or presymptomatic Parkinson's disease). Whether or not the coexistence of these three diseases in the same patient was merely coincidental is of considerable interest.

Recently, several missense mutations in the Cu/Zn superoxide dismutase gene (SOD1) have been reported as a putative cause of chromosome-21q-linked familial amyotrophic lateral sclerosis (FALS). We have discovered a novel missense mutation (substitution of Thr for Ala4) in exon 1 (GCC to ACC) in two FALS patients from one Japanese FALS family. No mutations were found in 17 cases of sporadic ALS. The enzyme activity of recombinant fusion protein containing the Cu/Zn superoxide dismutase (SOD) with the Ala4-to-Thr mutation was significantly reduced in E. coli. On the other hand, in the expression system in insect cells using Baculovirus, the mutant SOD expressed an enzyme activity as high as wild-type SOD. These results suggest that the stability of SOD with the Ala4-to-Thr mutation is disrupted especially in the fusion protein. Autopsy was carried out on one of the two patients, and the pathological findings were typical of FALS with posterior column involvement. These results raise the possibility that mutation of the SOD1 is responsible for FALS with broader pathological involvement.

A 16-year old woman with LGL leukemia developed peripheral neuropathy. She showed virus-associated hemophagocytic syndrome (VAHS)-like signs including high fever, liver dysfunction, huge splenomegaly, hepatomegaly and pancytopenia. The presence of chronic active EB virus infection was proved by marked high titers for IgG and IgA antibodies to the Epstein-Barr viral capsid and early antigens and low titers of antibody to Epstein-Barr nuclear antigens. She showed dysesthesia and paresthesia of bilateral lower extremities with marked swelling and tenderness, and later developed muscular weakness and atrophy with areflexia of lower extremities. Findings of the central nervous system dysfunction were not observed except for the acceleration of jaw jerk. Pleocytosis and increased protein levels in the cerebrospinal fluid were found. Pulse therapy of methyl-prednisolone and high dose intravenous immunoglobulin therapy (20 g/day for 3 days) were effective for neurological findings. The increased neopterin in the cerebrospinal fluid suggested that peripheral neuropathy was caused by activated macrophages.

A patient, 50-year-old female, developed progressive weakness of lower extremities, and gait disturbance for 2 years. Neurological examination revealed hyperreflexia with pathological reflex, fasciculation in the limbs and tongue, muscle weakness and atrophy in distal limbs, but no sensory disturbance. Needle EMG showed neurogenic findings compatible with motor neuron disease (MND). Laboratory data showed polyclonal IgM hyperimmunoglobulinemia, positive several autoimmune antibodies including antisingle strand DNA antibody (Ab), ENAab, SS-A ab and RA. There were no antibodies for gangliosides and Myelin-associated glycoprotein (MAG), but positive antibody for 54KD protein of cerebral gray and white matter. The clinical manifestations including gait disturbance and muscle weakness, and serum IgM level were moderately improved by plasmapheresis which is considered important for consideration of causes of MND.

We describe a family with hereditary dentatorubropallidoluysian atrophy (DRPLA). 4 patients through 3 successive generations showed a wide clinical variety. The female proband with onset in the elderly developed choreiform involuntary movement, dementia, hyperreflexia and, at the progressive stage, mild ataxia. However she had never displayed epilepsy and myoclonus. The 2 sons showed dementia, choreoathetoid movement and ataxia. The grandson developed typical signs and symptoms of progressive myoclonus epilepsy. The brain CT in the proband showed severe cerebellar and brain stem atrophy, moderate cerebral cortical atrophy and diffuse low density lesions in the deep cerebral white matter. Her neuropathological examination revealed the atrophy and gliosis of cerebral and cerebellar white matter concomitant with both dentatorubral and pallidoluysian system degeneration. The present study indicates that hereditary DRPLA can include multiple clinical variants even in the same family and the degeneration of cerebral and cerebellar white matter besides dentatorubral and pallidoluysian system.

A 70-year-old woman was admitted to our hospital because of rapidly progressive cerebellar ataxia. Neurological examinations showed saccadic eye movement, downbeat nystagmus, scanning speech, proximal dominant muscle weakness and severe truncal and limb ataxia. Based on these clinical features, she was suspected to have paraneoplastic cerebellar degeneration (PCD), although the malignant tumor was not detected through clinical intensive surveys. Her serum and CSF revealed to have anti-Purkinje cell antibodies immunohistochemically, and western blot analysis showed that they reacted with 58 kd band. In view of previous reports of PCD, she was strongly suspected to have gynecological cancers. The trial laparotomy found early stage fallopian tubal cancer, which had not been detected by CT scan, ultrasonogram and MRI. It is important to detect and characterize these autoantibodies found in the PCD patients for early diagnosis and treatment of underlying cancer.

Serum IgG in a patient with chronic polyneuropathy after Mycoplasma pneumoniae infection reacted with ganglioside GM1, GD1b and asialo-GM1 on thin-layer chromatograms using an immunostaining technique as well as an enzyme-linked immunosorbent assay, suggesting that the galactosyl (beta 1-3)N-acetylgalactosaminyl moiety could be a target antigen in this patient. Serum IgG reacting with these glycolipids may be involved in the pathogenesis of both motor and sensory neuropathies in this patient.

32-inch AS-IPS LCDs TV with RGB-LED backlight system was developed, which modulates each primary backlight's brightness and converts each primary image data in every frame. Red, green, and blue backlight brightness are modulated respectively depending on inputted image data. The image data are converted according to modulated backlight brightness. As a result, not only the dynamic contrast ratio but also the color gamut of low gray levels is significantly improved.

We have measured Raman spectra of a diamond film prepared on the (100) surface of cubic boron nitride(c‐BN) by the dc plasma chemical vapor deposition method. It is found that the polarization property of the Raman line of diamond coincides well with that of the LO phonon for the (100) surface of c‐BN. The coincidence between the polarization property of Raman lines of diamond and c‐BN evidences heteroepitaxial growth of the diamond film on the (100) surface of c‐BN.

We report a 26-year-old woman with Creutzfeldt-Jakob disease (CJD) who had received cadaveric dural material 33 months before the onset of neurologic symptoms. This is the fourth case in which a dural graft was the putative source of the CJD agent. All four cases had the grafting before changes in the sterilization procedure adopted in 1987 to inactivate the CJD agent.

Mixed analog and digital circuits are realized on a 1.5 mu m silicon-gate CMOS chip with +5 V power supply only. The circuit uses CMOS digital gate arrays of 0.32 K to 19.6 K cells and is created without any additional turnaround time or any restriction on the design. Typical internal digital gate (two-input NAND) speed, with a fanout of 3 and a wire length of 3 mm, is 1.4 ns. A voltage comparator with +or-8 mV maximum input offset voltage and 60 ns response time, digital-to-analog and analog-to-digital converters with 4-, 6-, and 8-bit resolution, respectively, and an analog switch of 25 Omega on-resistance can be realized on the same chip with digital circuits. Using this technology, about one-tenth of the turnaround time can be achieved compared with full-custom LSIs for the same system. The product development flow and computer-aided-design tools for designing mixed analog and digital gate arrays are the same as for digital gate arrays. >

The molecular structures of six Ln(dpm) 3 (Ln = Sm, Eu, Gd, Tb, Dy and Ho; dpm = (CH 3 ) 3 CCOCHCOC(CH 3 ) 3 ) have been determined by gas-phase eletron diffraction. The experimental data are consistent with a trigonal prismatic structure with the slightly pitched OLnO planes. The observed LnO distances show the predicted lanthanide contraction: r a (SmO) = 2.278(7) A to r a (HoO) = 2.226(8) A. The OLnO and the pitch angles also depend on the atomic number. The structural parameters of the dpm ligand are as follows (average values with stranded deviations): r a (CO) = 1.279(8) A, r a (CC r ) = 1.411(12) A, r a (CC t ) = 1.523(19) A, r a (C t C m = 1.548(9) A, r a (O…O) = 2.716(23)A, ∠OCC r = 124.5(6)°, ∠CC r C′ = 122.2(5)° and ∠C r CC t = 117.6(9)°.

It is known that the antibody to human myelin-associated glycoprotein (MAG) reacts with a subset of human mononuclear cells (MNC) mediating a natural killer (NK) activity. The properties of the target molecule of the anti-MAG antibody, however, have not yet been elucidated. Three (GC-J4, MC-P2, and MC-P4) of five murine monoclonal antibodies (mAb) to MAG bound to human MNC. Moreover, MC-P2 and MC-P4 inhibited the binding of 125I-labeled anti-Leu-7 to MNC in a dose-dependent fashion. Conversely, anti-Leu-7 inhibited the binding of MC-P2 and MC-P4 to MNC, but did not inhibit the binding of GC-J4. Therefore, it is possible that MC-P2 and MC-P4 bind directly to or close to the Leu-7 epitope, and that GC-J4 binds to the epitope which is distinct from the Leu-7 epitope. The electrophoretic patterns of immunoprecipitates with GC-J4, MC-P2 and anti-Leu-7 from detergent lysates of surface-labeled human MNC were very similar. The target molecules of anti-Leu-7 and anti-MAG mAb have apparent m.w. of 205, 170, 150, 135, 110, 85, 65, and 55 kDa. All of the molecules precipitated by these mAb are monomeric or noncovalently associated proteins, because the electrophoretic mobilities of the proteins remained unchanged whether the samples were reduced or not. MC-P4 may have a higher affinity for the 65 kDa molecule than the other mAb, and precipitates the 58 kDa molecule as well. Therefore, the fine antigenic specificity of MC-P4 is slightly different from those of anti-Leu-7 or MC-P2. The implication of these results is that mAb, whose specificity is directed to the carbohydrate part of human MAG, reacts with the Leu-7 reactive molecules on human MNC, and that at least two epitopes detected by anti-MAG mAb coexist on the surface molecules with various apparent m.w.

"タイトスカートを製作する場合のダーツの位置およびその分量について,第5報で得たスライディングゲージ法による横切断面図を用いてその設定法を試みた.ダーツの位置の設定は,ウエストおよびヒップ位置に腹部を含む横切断面複合図を作製し,その図に接する長方形を描き,図の中心点と4つの角を結ぶ対角線をダーツの位置設定の基準線とし,その線から前後中心に向かって8度の位置(前後第1ダーツ),脇の方向に12.8度の位置(前後第2ダーツ),幅径の基準線(脇ダーツ)とウエスト廻り線との交点をそれぞれのダーツの位置とした.その各位置問の全被験者寸法の平均値によって前後別の比率を求めた.ダーツ分量の設定は,複合図のウエスト廻り線からヒップ廻り線への出張りの分量により,各ダーツの分量の配分をすることが妥当と考え,各ダーツ位置の出張り分を計り全被験者の平均値を求め,前後別にその比率を算出し各ダーツ分量の設定率とした.そのダーツの位置および分量の設定率を用いて着用実験を行なったところ,腰部の体型は複雑であり適合しにくい者のいることがわかった.そこで各角度からの検討を加え,腹部出張り体型,でん部出張り体型,脇出張り体型,標準体型の4つの体型に分類した.その体型別にダーツの位置および分量の設定率を求め,その比率を用いて試案としてのタイトスカートの作図をし,トワールによって実物製作をして着用実験を行なったところ,一応好ましい結果を得ることができた.しかし更に検討を必要とする問題もあり,試案としてのタイトスカートの作図について,更に研究を進めたいと思う.終わりに本実験に御協力下さった本学服飾コースの学生に深く感謝する."