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An ISOL-based radioactive nuclear beam (RNB) facility, Tokai Radioactive Ion Accelerator Complex (TRIAC), has been jointly developed by High Energy Accelerator Research Organization (KEK) and Japan Atomic Energy Agency (JAEA). The facility started to supply RNBs for experiments in 2005 and RNBs including fission fragments with energies up to 1.1MeV/A are available in the present. Several experimental studies were performed successfully using 8Li beams with various energies.

Four neonicotinoid nitroguanidine insecticides (imidacloprid, thiamethoxam, clothianidin, and dinotefuran) acting as nicotinic agonists account for 10−15% of worldwide insecticide sales. General methods are needed for synthesis of their guanidine and aminoguanidine metabolites so they may be used as analytical standards and for evaluation of nicotinic receptor potency. The guanidines are obtained by treating the parent nitroguanidines with Fe powder in aqueous C2H5OH containing NH4Cl and isolated by silica chromatography. The aminoguanidines are prepared as mixtures with the guanidines on reaction of the parent nitroguanidines and Zn powder in glacial acetic acid. The imidacloprid aminoguanidine is isolated as the acetone imine or trifluoroacetamide and the clothianidin and dinotefuran aminoguanidines as the acetone imines using silica chromatography. Deprotection under acidic conditions then leads to the aminoguanidine·HCl salts. Because of stability considerations, a pH partitioning method is used to separate thiamethoxam aminoguanidine and guanidine. An alternate procedure to the aminoguanidine of imidacloprid (but not thiamethoxam, clothianidin, or dinotefuran) is reaction with hydrazine hydrate and NH4Cl in anhydrous C2H5OH. Ambiguities in further biological reactions are clarified by synthesizing authentic standards of three purported metabolites formed via the imidacloprid aminoguanidine:  the 1,2,4-triazol-3-one derivative with ethyl chloroformate or ethyl pyrocarbonate, the acetaldehyde imine with acetaldehyde, and the 3-methyl-1,2,4-triazin-4-one derivative with ethyl pyruvate in refluxing toluene. The purported triazolone metabolite is reassigned as the aminoguanidine acetaldehyde imine probably formed as an artifact from acetaldehyde present in the ethyl acetate used for metabolite extraction. Potency at the Drosophila nicotinic receptor is greatly decreased on converting a nitroguanidine to a guanidine or aminoguanidine. In sharp contrast, potency at the vertebrate α4β2 nicotinic receptor is generally increased on conversion from the nitroguanidine to aminoguanidine and particularly guanidine derivatives.

The higher toxicity of neonicotinoid insecticides such as N-(6-chloropyridin-3-ylmethyl)-2-nitroiminoimidazolidine (imidacloprid) to insects than mammals is due in large part to target site specificity at the corresponding nicotinic acetylcholine receptors (nAChRs). We propose that neonicotinoids with a protonated N-unsubstituted imine or equivalent substituent recognize the anionic subsite of the mammalian α4β2 nAChR whereas the negatively charged (δ^-) tip of the neonicotinoid insecticides interacts with a putative cationic subsite of the insect nAChR. This hypothesis can be tested by using two photoaffinity probes that differ only in the N-unsubstituted imine vs negatively charged (δ^-) tip. Synthesis methodology was developed for compounds combining three moieties:  pyridin-3-ylmethyl or 6-chloropyridin-3-ylmethyl and their 4- and 5-azido analogues; imidazolidine, 4-imidazoline or 4-thiazoline; and N-unsubstituted imine, nitroimine, cyanoimine, or nitromethylene. Structure−activity studies compared displacement of [³H]nicotine binding in mammalian α4β2 nAChR and [³H]imidacloprid binding in Drosophila nAChR. Preferred compounds are N-(5-azido-6-chloropyridin-3-ylmethyl) with 2-iminothiazoline for α4β2 (Ki = 0.47 nM) and with 2-nitroiminothiazoline or 2-nitromethyleneimidazolidine for Drosophila (Ki = 0.72−3.9 nM).

We review recent progress and the future of 40-Gbit/s electrical time division multiplexed (ETDM) channel technologies for the optical transport network (OTN), where optical technologies, including high-speed ETDM channel transmission and wavelength division multiplexing (WDM), dramatically enhance network flexibility while reducing transport node cost as well as transmission cost. The 40 Gbit/s channel has recently been specified to be one of the optical channels in OTN. A new digital frame for the optical channels [optical channel transport unit (OTU)] was introduced for the network node interface of OTN in International Telecommunication Union-Telecommunication (ITU-T) standard. The specified data bit rates are 2.7 Gbit/s (OTU1), 10.7 Gbit/s (OTU2), and 43.0 Gbit/s (OTU3). These OTU frames have additional overhead bytes that support the network management overhead for OTN and out-of-band forward error correcting (FEC) codes. We discuss the feasibility and impact of the OTU3 frame in terrestrial networks. A newly developed 43-Gbit/s OTN line terminal prototype that confirms the feasibility of 43-Gbit/s ETDM channels and the OTU3 management capability is discussed. As a guide to the evolution of OTN, modulation formats for 43Gbit/s-based DWDM transmission are described for long distance application with the total capacity over one terabit per second.

To evaluate the acute phase damage to liver by carbon ions, BALB/c mice were irradiated with carbon ions or X-rays after two-thirds partial hepatectomy, and their survival was followed. The 50% lethal dose within 60 days (LD50/60) was 42.2 +/- 0.25 Gy (standard error) for X-rays, and 22.7 +/- 0.25 Gy for carbon ions. The relative biological effectiveness (RBE) of carbon ions was 1.86 (95% confident limits: 1.69-2.04) as calculated from the LD50/60. Mice irradiated at much higher doses, 60 Gy of X-rays or 24 Gy of carbon ions, showed significantly higher serum ammonia levels and lower serum albumin levels than normal, suggesting hepatic failure as a cause of death. Hepatocytes showed karyorrhexis and karyolysis in carbon ion irradiated and spotty necrosis in X-ray irradiated mice, suggesting nuclear damage. Mice irradiated with LD50 of X-rays or carbon ions had a remarkably lower bromodeoxyuridine (BrdU) labeling index and mitotic index than control. Treatments with both BrdU and vincristine showed that none of the hepatocytes that synthesized DNA after irradiation completed mitosis, indicating G2 arrest. The liver weight of irradiated mice significantly decreased depending on the dose. Carbon ions as well as X-rays damaged hepatocytes directly and suppressed liver regeneration leading to fatal liver failure.

The forkhead rhabdomyosarcoma transcription factor (FKHR) is a promising candidate to be the transcription factor that binds to the insulin response element of the insulin-like growth factor-binding protein-1 (IGFBP-1) promoter and mediates insulin inhibition of IGFBP-1 promoter activity. Cotransfection of mouse FKHR increased IGFBP-1 promoter activity 2-3-fold in H4IIE rat hepatoma cells; insulin inhibited FKHR-stimulated promoter activity approximately 70%. A C-terminal fragment of mouse FKHR (residues 208-652) that contains the transcription activation domain fused to a Gal4 DNA binding domain potently stimulated Gal4 promoter activity. Insulin inhibited FKHR fragment-stimulated promoter activity by approximately 70%. Inhibition was abolished by coincubation with the phosphatidylinositol-3 kinase inhibitor, LY294002. The FKHR 208-652 fragment contains two consensus sites for phosphorylation by protein kinase B (PKB)/Akt, Ser-253 and Ser-316. Neither site is required for insulin inhibition of promoter activity stimulated by the FKHR fragment, and overexpression of Akt does not inhibit FKHR fragment-stimulated Gal4 promoter activity. These results suggest that insulin- and phosphatidylinositol-3 kinase-dependent phosphorylation of another site in the fragment by a kinase different from PKB/Akt inhibits transcription activation by the fragment. Phosphorylation of this site also may be involved in insulin inhibition of transcription activation by full-length FKHR, but only after phosphorylation of Ser-253 by PKB/Akt.

Background: A new endoscopic classification of gastroesophageal reflux disease (GERD) has been proposed, and the term mucosal break has been introduced to describe mucosal damage. This new classification was evaluated by endoscopists with different levels of experience. Methods: Fifty endoscopic photographs for each of 20 randomly selected patients with GERD were assessed retrospectively by three groups of seven endoscopists classified by experience: group 1 (100 to 500 procedures), group 2 (500 to 3000), and group 3 (more than 3000). The new classification was modified by adding grade 0 to describe healed mucosal breaks, so that there were five grades. All photographs were assessed twice at an interval of more than 1 week, and @k statistics were used to determine observer variation. Results: Interobserver variation within group 3 (@k = 0.39, n = 21) and between groups 3 and 2 (@k = 0.36, n = 49) was significantly different (p < 0.01) from that between groups 3 and 1 (@k = 0.26, n = 49). Intraobserver variation in group 1 (@k = 0.39, n = 7) was significantly different (p < 0.01) from that in group 2 (@k = 0.51, n = 7) and group 3 (@k = 0.54, n = 7). Conclusions: Observer variation depends on level of endoscopic experience. Only experienced endoscopists should use the new classification for grading of GERD. (Gastrointest Endosc 1999;49:700-4.)

Two-dimensionally quantized electron transport in modulation-doped double-heterojunction structures is investigated using a Monte Carlo simulation in which the energy quantization in a well is considered. Enhanced low-field mobility in the quantum well is observed with increased carrier density. This results from the reduction of optical phonon scattering rates, which can be attributed to the spread of two-dimensional electron gas. It is also demonstrated that carrier transport related to this enhancement and carrier confinement effectively contribute to device operation in a double-heterojunction FET.<>

The insect nicotinic acetylcholine receptor (nAChR) is the target for the major insecticide imidacloprid (IMI) and for the first candidate photoaffinity probe described here. Addition to 1-[(6-chloro-3-pyridinyl)methyl]-4,5-dihydro-2-nitromethylene-1H-imidazolidine (the nitromethylene analog of the nitroimine IMI) of formaldehyde and any one of several primary amines is known to give hexahydro-8-nitroimidazo[1,2-c]pyrimidine derivatives. These imidazopyrimidines with a wide range of N-substituents were found to inhibit [³H]IMI binding to the Drosophila or Musca nAChR by 50% (IC50) at 0.7−38 nM. Esterification of the N-(2-hydroxyethyl) derivative with 2-azido-5-(trimethylstannyl)benzoic acid and then iododestannylation using Na¹²⁵I and chloramine-T provide the candidate photoaffinity probe 6-[2-(2-azido-5-[¹²⁵I]iodobenzoyl)ethyl]-1-[(6-chloro-3-pyridinyl)methyl]-1,2,3,5,6,7-hexahydro-8-nitroimidazo[1,2-c]pyrimidine. This compound (unlabeled) has an IC50 of 8 nM for [³H]IMI binding in Drosophila head membranes, and the ¹²⁵I-labeled photoaffinity probe labels only a 66 kDa protein(s) at a specific site inhibited by (−)-nicotine, consistent with the insecticide-binding subunit of the nAChR.

Summary A study is made of the mechanism of hemolysis by anionic surface-active agents. It is supposed that the primary site of the hemolytic attack by anionic agents is the protein moiety of the red cell membrane at physiological pH. The role of phospholipid release in hemolysis increases as the PH of the medium decreases.

The first results of a field trial held in November 2000, of 1 Tbit/s unidirectional WDM transmission based on a 43 Gbit/s/channel optical transport network interface prototype, are presented. Error-free operation of 25 channels with 100 GHz spacing over a 91 km standard singlemode fibre with forward error correction is verified.

STM-64 (10 Gbit/s) nonregenerative transmission experiments using forward error correcting codes have been conducted for the first time. Bit errors caused by dispersion in the transmission line and optical noise of Er-doped fibre amplifiers were successfully corrected by using (18880, 18865) and (2370, 2358) shortened Hamming codes.

100 4;GHz-spaced 40 channel 43 4;Gbit/s DWDM coherent signal transmission is demonstrated in S-band using novel carrier-suppressed-return-to-zero differential-phase-shift-keying format over a 400 4;km dispersion shifted fibre link consisting of gain-shifted Tm-doped fibre amplifier inline repeaters and bi-directionally pumped distributed Raman amplifiers.

1.2 Tbit/s (30 × 42.7 Gbit/s ETDM channel) WDM transmission over three 125 km spans (span loss: 31.5 dB average) has been demonstrated, based on the use of the carrier-suppressed return-to-zero format and forward error correction in a 50 nm tellurite-based EDFA gain band.

Parallel FEC code transmission is proposed, in which check bits are transmitted on a different wavelength. The signal format is perfectly compatible with SDH in terms of signal wavelength. A smooth upgrade to the FEC system is possible by connecting additional modules. High FEC capability is obtained such that the BER of 10–6 can be improved to 10–11 with a decoding delay of several bits. When the parallel processing number is 8, the GVD tolerance is extended by a factor of 2.5, while the number of L-REPs possible in an optical link is doubled.

The authors propose a method for measuring the group velocity dispersion, including the polarity, of optical fibre by using a single wavelength light source. The method is based on the interplay between phase modulation-amplitude modulation (PM-AM) conversion and self-phase modulation (SPM).

A (18880, 18865) shortened Hamming error-correcting code is proposed for synchronous digital hierarchy (SDH) line terminating multiplexers for all multiplexing levels. Parallel processing, reducing the clock rate, is realised on a CMOS LSI using an innovative matrix method, by which an optical experiment is conducted successfully.

A bit-interleaved SEC shortened Hamming code is proposed for all SDH levels. The error caused by ASE noise in a 156 Mbit/s optical preamplifier is successfully corrected.

A route diversity ‘hitless’ protection switching scheme is proposed that is free from bit loss even for unpredictable system failures. Freely switching between the working and protection paths improves the signal quality at the system output because the system automatically selects the no-error frame.

A self-healing algorithm is proposed for a ring network connected as a logical mesh. It offers good performance in terms of protection line capacity, restoration time, and survivability against multiple failures.

We create a 40Gbit/s multi-lane distribution (MLD) interface converter for STM-256 to STL-256.4 and OTU3 to OTL3.4. We successfully demonstrate a cost-effective optical transceiver for STM-256/OC-768/40G-POS by using our 40Gbit/s MLD interface converter prototype.