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Pentacene was vapor-deposited on the NaCl substrate and friction-transferred PTFE layer. Pentacene molecules crystallized in bulk phase and/or thin film phase depending on the deposition condition. The polarized absorption spectra of pentacene/PTFE double layer showed an anisotropic feature. Pentacene oriented uniaxially taking edge-on state on a PTFE layer. The electrical property of pentacene/PTFE double layer also indicated anisotropic feature. The field effect mobility along to the traverse of the friction direction was 4.2 × 10−1 cm2/Vs.

The absorption spectrum of merocyanine (BTET) film deposited on a NaCl substrate showed a broad absorption band in the wavelength region between 450 nm and 550 nm and a narrow peak at 640 nm. The former bands were assigned to the absorption bands of α- and β-form crystal, the latter peak was assigned to J-band. BTET film was composed of square-shaped and rectangular crystals grown epitaxially. The square-shaped crystal was composed of α-form and the rectangular crystal was composed of α-form and J-aggregate. The formation mechanism of J-aggregate in film was discussed.

Since the I/O bandwidth demand for mobile consumer electronics has been growing rapidly, the importance of high-speed low-power I/O links has also been increasing. Among proposed I/O architectures, [1] and [2] are attractive solutions. However, for an application that needs the burst-mode operation, the lock-in time should be within the period of several tens of bits. Therefore, the PLL-based phase rotator with a longer lock-in time, is not suitable for this purpose. In this paper, a 1.296-to-5.184Gb/s transceiver uses an injection-locking-based CDR. The proposed CDR architecture, dual-edge injection-locked oscillator CDR (DILO-CDR), realizes fast lock (≪20 bits), continuous-rate capability (1.296 to 5.184Gb/s) and 2× power efficiency [2.4mW/(Gb/s)] of previous fast-lock continuous-rate CDRs [3, 4].

Mutations in the ELA2 gene encoding neutrophil elastase (NE) in patients with severe congenital neutropenia (SCN) are involved in the pathogenesis of this disorder, possibly due to the abnormal protein trafficking and accelerated apoptosis of myeloid cells. In this study we precisely examined the localization of NE in neutrophils and myeloid precursor cells in bone marrow in patients with SCN using immunofluorescence microscopy equipped with three-dimensional analysis program. Three patients with SCN were enrolled in this study. All patients with SCN showed heterozygous mutation in the ELA2 gene. In normal subjects the pattern of localization of NE in mature neutrophils was almost similar to those of myeloperoxidase (MPO), proteinase 3, lysosomal associated membrane protein 2 (LAMP2). Administration of G-CSF to normal subjects did not affect the pattern of the localization of these proteins in neutrophils. In contrast, mature neutrophils elicited by the administration of G-CSF in patients with SCN NE predominantly localized to the plasma membranes. A small part of NE was detected in the cytoplasmic compartment. The pattern of localization of NE was significantly different from those of MPO, proteinase 3, and LAMP2 in SCN patients, suggesting the abnormal traffic of NE to granules. Adaptor proteins 3 (AP3) specifically shuttles transmembrane cargo proteins from the trans-Golgi to lysosomes. AP3 of myeloid progenitor cells enriched for CD33-positive cells in normal bone marrow was localized in both cytoplasm and plasma membranes. The localization pattern of AP3 was completely consistent with those of NE, MPO, and LAMP2. The localization of AP3 of promyelocytes in patients with SCN was observed in both plasma membranes and cytoplasm. This finding was completely similar to that in normal myeloid precursor cells. However, the localization of NE of promyelocytes in SCN patients was predominantly in plasma membrane. The figures merged apparently presented the different localization of NE and AP3. This result was confirmed by the 3-dimensional analysis with histogram. The localizations of other constituents of primary granules, MPO, poteinase 3, and LAMP2, were consistent with those of AP3. These observations suggest that the mislocalization of NE in myeloid precursor cells in SCN patients does not result from a generalized impairment of protein trafficking but is specific to the mutant NE. The abnormal localization of NE may be involved in the pathogenesis of SCN associated with ELA2 mutation.

Primary granule proteases provide negative feedback on granulopoiesis. Recent study showed that neutrophil elastase potentially inhibits granulopoiesis by enzymatic digestion of G-CSF. We studied the effects of neutrophil elastase on granulopoiesis in the interaction of G-CSF and G-CSF receptor (G-CSFR). Primitive myeloid cells of the bone marrow in normal subjects were purified based on the expression of CD34 and G-CSFR by FACS Vantage. The cells were incubated with or without human neutrophil elastase for 2 hours in serum-deprived media. Cells were washed once and then cultured in various serum-deprived conditions. The proliferation and colony formation of CD34+/G-CSFR+ cells in the presence of G-CSF were significantly reduced by the pretreatment of elastase. Furthermore, those of CD34+/G-CSFR+ cells in response to hematopoietic factors without G-CSF were similarly inhibited by elastase. On the other hand, the responses of CD34+/G-CSFR− cells were not affected by the treatment of elastase in the stimulation of any hematopoietic factors. When CD34+ cells were incubated with or without elastase, further G-CSFR expression was analysed by flow cytometry. The treatment of elastase did not affect the expression of surface expression of G-CSFR on CD34+ cells. Next, the binding of G-CSF to G-CSFR was examined by flow cytometry using antibody to G-CSF. The mean channel of fluorescence of G-CSF binding to G-CSFR-positive cells was reduced by the treatment of elastase, suggesting the loss of the binding of G-CSF to G-CSFR. When CD34+/G-CSFR+ cells were treated with elastase, the observation by confocal immunofluorescence microscopy revealed neither accumulation of elastase on the surface of cell membrane nor in intracellular compartment. No evidences that cells treated with elastase directly cleave the G-CSF leading to inactivation of G-CSF. Collectively, these results suggest that G-CSFR-positive cells are selectively affected by neutrophil elastase, and that neutrophil elastase as negative regulator may play a role in modulating granulopoiesis through G-CSF-G-CSFR interaction.

Researches to predict the ship motions and accelerations to be induced on a nuclear ship in waves were carried out by model tests and theoretical computations.Firstly, the responses of the ship, which advances with various speed in regular waves coming from various directions, were measured and compared with the computed results by so-called strip theory.Secondly, the model tests in irregular waves having a certain energy spectrum were carried out, and the short term distribution of the probability of the responses were estimated through the cumulative energy density of the spectrum of the responses which were derived both by the test results and the computations.Finally, the long term distribution of the responses were also estimated by using the derived short term distribution and the probability of occurrence of sea state at the northern North Atlantic Ocean.