Oxidation of trichloroethylene and dimethyl sulfide by a marine Methylomicrobium strain containing soluble methane monooxygenase

Sixteen marine methanotrophic bacteria were isolated and 14 marine methanotrophic mixed cultures were obtained. They were assayed for soluble methane monooxygenase (sMMO) by naphthalene oxidation and only one isolate (strain NI) was positive. Strain NI degraded trichloroehylene (TCE) more efficiently than other methanotrophic isolates containing no sMMO only under copper limiting conditions. Dimethyl sulfide (DMS), one of the radiatively important trace gases released from the sea, was transformed to dimethyl sulfoxide (DMSO) by methanotrophs and the efficiency for the transformation of DMS to DMSO was not as much affected by the presence of sMMO as that of TCE. The taxonomical properties of strain NI and phylogenetic analysis based on 16S rDNA genes indicated that strain NI was a type I methanotroph belonging to the genus Methylomicrobium, and closely related to Methylomicrobium pelagicum. The partial mmoX gene of strain NI was amplified by the primers common to three other mmoX genes and its 270 bp were sequenced. 77 residues out of the 89 amino acids derived from the sequences were common among the four mmoX genes.     

Common-gate GaAs f.e.t. oscillator

Frequency tuning, power and noise characteristics of a common-gate GaAs f.e.t. oscillator were investigated. By changing the common-gate lead inductance, the frequency was changed by almost two octaves. The f.m. noise of the low-Q factor f.e.t. oscillator was at the same level as that of a medium-Q factor GaAs impatt oscillator.     

Nucleotide sequence of the Serratia marcescens threonine operon and analysis of the threonine operon mutations which alter feedback inhibition of both aspartokinase I and homoserine dehydrogenase I

The nucleotide sequence of the Serratia marcescens threonine operon (thrA1A2BC) was determined. Three long open reading frames were identified; these open reading frames code for aspartokinase I (AKI)-homoserine dehydrogenase I (HDI), homoserine kinase, and threonine synthase, in that order. The predicted amino acid sequences of these enzymes were similar to the amino acid sequences of the corresponding enzymes in Escherichia coli. The AKI-HDI protein is apparently a tetramer composed of monomer polypeptides that are 819 amino acids long. A deletion analysis revealed that the central and C-terminal region was responsible for threonine-resistant HDI activity, a monomeric fragment extending from the N terminus to residue 306 was responsible for threonine-resistant AKI activity, and an N-terminal portion containing 468 residues was responsible for threonine-sensitive AKI activity. The thrA(1)1A(2)1 and thrA(1)5A(2)5 mutations of threonine-excreting strains HNr21 and TLr156, which result in the loss of threonine-mediated feedback inhibition of both AKI activity and HDI activity, cause single amino acid substitutions (Gly to Asp at position 330 and Ser to Phe at position 352, respectively) in the central region of the AKI-HDI protein. The thrA1+A(2)2 mutation of strain HNr59, which results in a threonine-sensitive AKI and a threonine-resistant HDI, also causes a single amino acid substitution (Ala to Thr at position 479).     

Mutations in the hepatocyte nuclear factor-1alpha/MODY3 gene in Japanese subjects with early- and late-onset NIDDM

Recent studies have shown that mutations in the hepatocyte nuclear factor (HNF)-1alpha gene are the cause of maturity-onset diabetes of the young type 3 (MODY3). We have screened 193 unrelated Japanese subjects with NIDDM for mutations in this gene: 83 with early-onset NIDDM (diagnosis at <30 years of age) and 110 with late-onset NIDDM (diagnosis > or = 30 years of age). All of the members of the latter group also had at least one sibling with NIDDM. The 10 exons, flanking introns, and promoter region were amplified using polymerase chain reaction and were sequenced directly. Mutations were found in 7 of the 83 (8%) unrelated subjects with early-onset NIDDM. The mutations were each different and included four missense mutations (L12H, R131Q, K205Q, and R263C) and three frameshift mutations (P379fsdelCT, T392fsdelA, and L584S585fsinsTC). One of the 110 subjects with late-onset NIDDM was heterozygous for the missense mutation G191D. This subject, who was diagnosed with NIDDM at 64 years of age, also had a brother with NIDDM (age at diagnosis, 54 years) who carried the same mutation, suggesting that this mutation contributed to the development of NIDDM in these two siblings. None of these mutations were present in 50 unrelated subjects with normal glucose tolerance (100 normal chromosomes). Mutations in the HNF-1alpha gene occur in Japanese subjects with NIDDM and appear to be an important cause of early-onset NIDDM in this population. In addition, they are present in about 1% of subjects with late-onset NIDDM.     

Distribution of burst error lengths in Rayleigh fading radio channels

A method for measuring burst errors which occur in v.h.f. or u.h.f. digital land mobile radio channels is described. Then it is noted that the cumulative distribution of burst error lengths in a Rayleigh fading channel is approximately governed by the log-normal distribution.     

Pressureless Sintering of SiC

Pressureless sintering of SiC was accomplished at 2100°C with oxide additives. These additives were the products of the reaction of Al(OH)₃ with HCl and of Y(OH)₃ with HCOOH. These reaction products were dissolved in water and mixed with submicrometer β-SiC. A mixture of equal weights of these additives was effective for the sintering of SiC.     

Operation mechanism of double-mode surface acoustic wave filters with pitch-modulated IDTs and reflectors

One of the authors (KH) previously proposed pitch-modulated interdigital transducers (IDTs) and reflectors for developing low-loss and wideband longitudinally coupled double-mode SAW (DMS) filters. This paper discusses how a wide and flat passband is realized by applying the pitch-modulated IDTs and reflectors to DMS filters. It is shown that the pitch-modulated structure enables one to adjust the location of multiple resonance frequencies simultaneously by varying an effective reflective position with frequency. That is, the IDTs are pitch-modulated so that the outer portion has slightly larger pitch than the inside, and the pitch of the outermost reflectors is made largest. Accordingly, higher-order SAW resonances occur between the two pitch-modulated IDTs. The outer portion of each IDT acts as a reflector, and the inner portion is mainly responsible for SAW excitation. Lower-order SAW resonances occur between the two reflectors.     

Phase Equilibria and Phase Transition of the Ni–Fe–Ga Ferromagnetic Shape Memory Alloy System

Phase equilibria and martensitic and magnetic transitions of the β (B2 and L2₁) phase in the Ni–Fe–Ga system were investigated. The b phase was found to be in equilibrium with the γ (A1 structure) or γ′ (L1₂ structure) phase. The Curie temperature, T _c , equilibrium temperature, T _o 5 (Ms + Af)/2, martensitic transition starting temperature, M _s , and reverse transition finishing temperature, Af , of the β single–phase alloys were sensitive to the Fe and Ga compositions. The Fe substitution for Ni decreased and increased the T _o and T _c , respectively. The Ga substitution for Ni or Fe decreased both the T _o and T _c . The entropy change accompanying the reverse martensitic transition showed compositional dependence due to the magnetic contribution. The saturation magnetization I _s of the Ni–Fe–Ga system showed a strong dependence on the magnetic valence Z _M . The Is values of the Ni–Fe–Ga alloys annealed at 1023 K showed the same Z _m dependence as other ferromagnetic shape memory alloy (FSMA) systems. This article is based on a presentation made in the symposium entitled "Phase Transformations in Magnetic Materials," which occurred during the TMS Annual Meeting, March 12-16, 2006, in San Antonio, Texas, under the auspices of the Joint TMS–MPMD and ASMI–MSCTS Phase Transformations Committee.     

Dual roles of proteasome in the metabolism of presenilin 1

Presenilin 1 (PS1) has been identified as a causative gene for most early-onset familial Alzheimer's disease. Biochemical studies revealed that PS1 exists predominantly as two processed fragments in cells and brain tissues. We prepared stably transfected cells expressing the wild-type and familial Alzheimer's disease-associated mutants of PS1 and investigated the enzyme that participates in the metabolism of PS1. After treatment of the cells with proteasome inhibitors, the full-length PS1 was significantly accumulated. The levels of N- and C-terminal fragments were also increased. The accumulation of PS1 with a deletion of exon 10, which is unable to be processed, on treatment of the transfected cells with lactacystin indicated that proteasome can degrade full-length PS1. A synthetic peptide that includes the processing region of PS1 was cleaved by 20S proteasome at the putative processing sites after Met288 and Glu299. Metabolic labeling experiments showed that the appearance of the N-terminal fragment was attenuated by the inhibitor. Finally, 28-kDa N- and 20-kDa C-terminal fragments were generated by purified PS1 in vitro. These data indicated that the proteasome pathway is involved in PS1 processing. These results demonstrate that the proteasome pathway plays dual roles in processing and degradation of PS1.