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With the aim of the applications for smart composite, the influence of cold drawing on the shape memory effect and mechanical properties of Ti-49.5at%Ni and Ti-50at%Ni was investigated systematically. It was found that the reverse transformation temperatures increased significantly, while the martensitic transformation temperatures decreased with increasing amount of cold drawing. Both the temperature range for reverse and martenistic transformations became larger with increasing amount of cold drawing. A recovery strain above 2% and a recovery stress up to 300MPa can be obtained in cold drawn wires. A two-way shape memory effect was observed in as-cold drawn TiNi wires. These results indicate that cold drawn TiNi wires have many unique shape memory properties which can be applicable for smart composites.

Endothelial nitric oxide synthase (NOS3) is one of the enzymes influencing nitric oxide (NO) function in the human brain. NO is a gaseous neurotransmitter that is involved in a variety of mechanisms in the central nervous system, such as N-methyl-D-aspartate receptor activation and oxidative stress. The evidence from animal pharmacological studies and postmortem studies supports an association between NO and psychotic disorders. Methamphetamine (METH) use disorder is a known psychotic disorder, and we therefore conducted a gene-based case-control study between tagging single nucleotide polymorphisms (SNPs) (rs2070744, rs1799983) in NOS3 and METH-induced psychosis in Japanese subjects (183 with METH-induced psychosis and 267 controls). Written informed consent was obtained from each subject. No significant association was found between any tagging SNP in NOS3 and METH-induced psychosis in the allele/genotype-wise or haplotype-wise analyses. In conclusion, we suggest that NOS3 might not contribute to the risk of METH-induced psychosis in the Japanese population.

The bonded area is largely affected by the surface morphology and mechanical properties of materials by surface activated bonding SAB process, because the room temperature bonding process is carried out under a low temperature and low pressure for short time. Accordingly, interfacial defects cause fatally harmful problems in many cases. For an application of this technique, it is important to know the effect of interfacial defects on fracture behavior. The fracture mechanism and its criterion for the growth of interfacial defects were investigated using the Alsapphire joint. It became clear that the growth of interfacial defects is the dominant factor for crack propagation. An estimation of stress intensity factor for the growth of interfacial defects was tried in two ways, stress criterion and energy criterion. A critical stress intensity factor for the growth of interfacial defects was estimated as 0.3–0.5 MPa m12by the analysis of FEM calculation and experimental observation.

Shape memory alloy (SMA) smart hybrid composites have attracted great attention in recent years as one of the promising smart structures. But until now, special fixture jigs or molds had to be used for constraining TiNi wires during the fabrication process. This makes the fabrication process of TiNi hybrid composites very complex, and restricts the shape and size of fabricated hybrid composites. Here the authors demonstrate a new, simple, and effective method to fabricate TiNi hybrid composites. This method allows the fabrication of TiNi hybrid composites in any shape and size just as the fabrication of ordinary advanced composites such as CFRP and GFRP.

Due to the influence of the welding thermal cycle, the toughness of structural steel generally degenerates. Recently, the intercritically reheated coarse-grained heat-affected zone (IC CG HAZ) was found to demonstrate the worst toughness in welded joint, which was associated with its fracture mechanism. In this article, two IC CG HAZs of a structural steel were prepared by welding thermal-cycle simulation techniques. For the two IC CG HAZs, the static and dynamic fracture toughness were evaluated; the fracture mechanism was also studied. Under both static and dynamic loading, cracks in the IC CG HAZ were found to initiate at the intersection of bainitic ferrite αB/0packets with different orientations, followed by propagation in cleavage. In some crack propagation regions, adjacent cleavage facets are connected by shear, thus producing dimple zones. Though the brittle fracture initiation mechanism remains unchanged, the cleavage facet size, the proportion of the dimple zones between facets, and the distance from the cracking initiation site to the crack tip vary with loading speed and welding conditions. These changes were found to be related to the variations caused by strain rate and welding conditions in fracture toughness for the IC CG HAZs.

Neuropsin is a novel serine protease, the expression of which is highly localized in the limbic areas of the mouse brain and which is suggested to be involved in kindling epileptogenesis and hippocampal plasticity. The 2.1-A resolution crystal structure of neuropsin provides the first three-dimensional view of one of the serine proteases highly expressed in the nervous system, and reveals a serine protease fold that exhibits chimeric features between trypsin and nerve growth factor-gamma (NGFgamma), a member of the kallikrein family. Neuropsin possesses an N-glycosylated "kallikrein loop" but forms six disulfide bonds corresponding to those of trypsin. The ordered kallikrein loop projects proline toward the active site to restrict smaller residues or proline at the P2 position of substrates. Loop F, which participates in forming the S3/S4 sites, is similar to trypsin rather than NGFgamma. The unique conformations of loops G and H form an S1 pocket specific for both arginine and lysine. These characteristic loop structures forming the substrate-binding site suggest the novel substrate specificity of neuropsin and give a clue to the design of its specific inhibitors.

A 16-year-old Japanese girl with 5,10-methylenetetrahydrofolate reductase deficiency showed peripheral neuropathy. There were no significant responses to vitamin B6, vitamin B12or folate, given alone or in combination. With the addition of betaine monohydrate, she has been free from gait disturbance and muscle weakness. The concentration ofS-adenosylmethionine in cerebrospinal fluid, which was undetectable before receiving betaine monohydrate, increased to about the normal level 24 months after treatment with betaine monohydrate.

The method to represent a general infinitesimal deformation as a deformation moment tensor is proposed and the physical meaning of deformation moment tensor in the case of microcracking is made clear. Developing the measuring and analysis system for acoustic emission waveform analysis, these moment tensor components due to microcracking can be determined experimentally. The remarkable method in this study is established to evaluate the moment tensor with the dynamic Green's function of finite media by computer simulation due to finite difference method and the iterative deconvolution with multiple Green's function.

The protective effect of coenzyme Q10(CoQ10) on continuous electric field stimulation-induced muscular injury was investigated in cultured cells established from neonatal rat femoral muscles. After cultivation for 9 days, skeletal muscle cells contracted and relaxed rhythmically for 4 hr in response to continuous electric field stimulation (power, 5 V; duration, 5 msec; amplitude, 3 Hz). After the onset of the stimulation, lactate and lactate dehydrogenase (LDH) release and intracellular Ca2+contents ([Ca2+]i) at relaxation increased gradually. In contrast, the intracellular ATP contents decreased. The addition of 5 μM CoQ10, but not alpha-tocopherol and radical scavengers, to the culture medium protected the cells against these biochemical changes after the stimulation. Verapamil, an inhibitor of Ca2+channels, also attenuated the increase in [Ca2+]iat relaxation and LDH. These results suggested that one of the causal mechanisms of muscular injury is an increase in [Ca2+]idue to the excess entry of extracellular Ca2+and that CoQ10can protect skeletal muscle cells against such undesirable biochemical changes.

K-SAM/FGFR2 gene encodes a receptor tyrosine kinase which belongs to the fibroblast growth factor receptor family and is amplified and overexpressed in KATO-III gastric cancer cells. To characterize K-samproteins in cancer cells, anti-K-samrabbit polyclonal antibody PK1-2 was raised and used for the immunoprecipitation analysis. 135, 125, and 110-kDa transmembrane proteins were detected in KATO-III cell lysate, while a soluble truncated 85-kDa K-samprotein was found in the conditioned medium. The molecular size of the soluble K-samprotein does not match with those predicted from the secreted forms of the K-samcDNA which have been cloned so far. The soluble K-samprotein was highly N-glycosylated like the transmembrane versions, and N-glycosylation appeared to be necessary for its release.

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To study the involvement of the p16 tumor suppressor gene in esophageal cancer development, we examined homozygous deletion of the p16 gene in 13 human esophageal cancer cell lines and 9 gastric cancer cell lines, in which some of genetic alterations have already been characterized. By Southern blot analysis, homozygous deletion was observed in 12 out of the 13 esophageal cancer cell lines (92%), in 2 out of a total of 9 gastric cancer cell lines (22%). It was also found that the p16 gene loss, cyclin D1 amplification and p53 gene mutations occurred independently in these cell lines. These findings suggest that loss or mutations of the p16 gene are involved in most esophageal cancers and that mutation of this gene plays a critical role in the development of esophageal cancer.

Recently radioimmunoassay (RIA) methods have been developed for the determination of nanogram levels of methamphetamine in urine [1–3]. These methods are suitable for rapid screening but require expensive instrumentation. This communication describes a rapid and simple hemagglutination-inhibition (HI) test that might be adaptable to the mass screening of urine samples without special equipment.

This paper reports the possibility of the acoustic emission (AE) application from the results of the testing performed at NASDA (National Space Development Agency of Japan) on H-I rocket motor nozzle holders (graphite/epoxy composites), such as the materials tests, the burst test, and the hydroproof test. Amplitude distribution during the tests show three types of fracture mechanism, such as fiber breakage (over 70 dB), delamination (between 60 and 70 dB) and matrix cracking (under 60 dB). After the middle stage of the burst test, the AE event rate shows saturated behavior, and large scale delamination is observed on the fracture surface. The upper limit speed for data acquisition (40 events s-1) of AE equipment (3000/3104: PAC) underestimated the number of middle amplitude events of the delamination. During the hydroproof test, both large amplitude events and a large number of AE events are detected in spite of the higher threshold (+ 20 dB) than that of the burst test. The strain gages on the hydroproof sample indicate higher strain than that of the burst test. Both AE and strain results show that the hydroproof test sample would have more damage than the burst test sample.

An acoustic emission criterion of fracture is developed for CFRP rocket motor cases. This criterion can be applied to detect failure extension in FRP dynamically. Both the criterion of the fracture theories and the nondestructive evaluation methods for FRP are discussed. The developed AE criterion is based on statistics which include the prior distribution, the data distribution and the posterior distribution. The AE criterion shows the equivalent pressure which relates to the damage extension of the master sample. Three types of the equivalent pressure criteria, such as the fiber breakage criterion, the fiber breakage and delamination criterion, and the all fracture criterion are based on AE amplitude distribution. Weight functions are used in this treatment based on the AE source characterization theory. The predicted burst pressure and the safety ratio are calculated by the equivalent pressure and the proof test pressure. The results of the evaluation indicate that the predicted burst pressure is 7.9 MPa and the safety is 1.6. These results are in good agreement with the strain measurement.

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In budding yeast, SCF complexes, composed of Skp1, Cdc53 and one of the F-box proteins, have been implicated in Cdc34-dependent ubiquitination. Grr1, which is required for degradation of G1 cyclins Cln1 and Cln2 as well as for regulation of glucose repression, is an F-box protein and interacts with Skp1 through the F-box motif. Grr1 also interacts in vitro with phosphorylated Cln1 and Cln2. However, ubiquitination of Cln1 has not been successful in an in vitro reconstituted system. In this study, domain analysis was performed to understand the role of Grr1 in the degradation of Cln2. Grr1 has another motif, leucine-rich repeats (LRR), in addition to the F-box. We found that the LRR is a domain for Cln2 binding. A deletion of half of the LRR abolished the interaction of Grr1 with phosphorylated Cln2 but not with Skp1 in vivo, and a deletion of the F-box abolished the interaction of Grr1 with Skp1 but not with phosphorylated Cln2 in vivo. Based on these results, we constructed grr1 mutants that are defective in association with either Skp1 or Cln2. Cln2 was highly stabilized and accumulated in the phosphorylated forms in the mutant cells. Furthermore, Skp1 associated in vivo with phosphorylated Cln2 in a Grr1-dependent manner. These data suggest that Grr1 is required for degradation of Cln2 through linking phosphorylated Cln2 to Skp1 in a SCFGrr1 complex.

Venom from the honey bee Apis melliferainduces cardiovascular dysfunction. We studied which constituent(s) of the venom induces cardiotoxicity and how, using cultured cardiac myocytes from mouse fetuses. Among the venom constituents, only melittin caused contractile and morphological effects; other peptides, such as apamin and mastparan; enzymes, such as phospholipase A2; and low-molecular-weight compounds, such as histamine and dopamine, did not. Treatment with 4.5 μg/ml melittin, which accounts for about half the dry weight of the venom, induced the same cardiotoxic effects as treatment with 9.0 μg/ml whole venom; these effects were a transient increase in the spontaneous beating rate, then a decrease, then cessation of beating, and finally, morphological degeneration. The cardiotoxicity of whole bee venom was completely destroyed by pretreatment of the venom with antimelittin antibody. These results suggest that bee venom cardiotoxicity is attributable to melittin. When spontaneous beating ceased following the addition of melittin or whole venom, an increase in systolic [Ca2+]iwas observed. On further incubation with melittin or bee venom, morphological injury, such as balloon degeneration, occurred concomitant with a further increase in the [Ca2+]i. An extracellular Ca2+concentration of more than 10(−6) M was necessary for morphological injury. Melittin depolarized the maximum diastolic potentials, inhibited the generation of action potentials, and induced an increase in [Na+]i. Cells were protected against the melittin-induced increase in [Ca2+]iby pretreatment with bepridil, an inhibitor of Na+-Ca2+exchange, but not by Ca2+channel blockers such as verapamil. These observations suggest that the melittin-induced increase in [Ca2+]iwas due to entry of extracellular Ca2+via the sarcolemmal Na+-Ca2+exchange system.

p53 tumour suppressor gene mutations were studied in 118 renal cell carcinomas using paraffin-embedded surgical material. Optimal results were obtained with analysis of exon lengths between 150 and 200 base pairs for polymerase chain reaction. Single strand conformation polymorphism and sequencing analysis revealed only two point mutations (2/118, 2%): one involving codon 135; TGC?TTC (cysteine?phenylalanine) and the other codon 175; CGC?CAC (arginine?histidine). Both of these cases were classified as granular cell subtype on microscopic observation. The data suggest that the p53 tumour suppressor gene is not related to tumour initiation, promotion, or progression of renal cell carcinomas. However, there is the possibility that granular cell type carcinomas may have a different genetic background from clear cell type renal neoplasms.