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H Iwasaki

Publications and source records attributed to H Iwasaki.

At least 73 records · Page 4Linked to original sources
PubMed2002

Production of prompt charmonia in e(+)e(-) annihilation at square root of s approximately equals 0.6 GeV.

The production of prompt J/psi, psi(2S), chi(c1), and chi(c2) is studied using a 32.4 fb(-1) data sample collected with the Belle detector at Upsilon(4S) and at 60 MeV below the resonance. The yield of prompt J/psi mesons in the Upsilon(4S) sample is compatible with that of continuum production; we set an upper limit B(Upsilon(4S)-->J/psiX) < 1.9 x 10(-4) at the 95% confidence level, and find sigma(e(+)e(-)-->J/psiX) = 1.47 plus/minus 0.10 plus/minus 0.13 pb. The cross sections for prompt psi(2S) and direct J/psi are measured. The J/psi momentum spectrum, production angle distribution, and polarization are studied.

Journal Article↗
PubMed2002

Observation of B+ --> chi(c0)K+.

Using a sample of 31.3x10(6) BB pairs collected with the Belle detector at the Upsilon(4S) resonance, we make the first observation of the charged B meson decay to chi(c0) and a charged kaon. The measured branching fraction is B(B+-->chi(c0)K+) = (6.0(+2.1)(-1.8)+/-1.1)x10(-4), where the first error is statistical, and the second is systematic.

Journal Article↗
PubMed2001

Observation of the decay B --> Kl+l-.

We report a search for the flavor-changing neutral current decay B-->K(*)l+l- using a 29.1 fb(-1) data sample accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB e+e- storage ring. We observe the decay process B-->Kl+l-(l = e, mu), for the first time, with a branching fraction of B(B-->Kl+l-) = (0.75(+0.25)(-0.21)+/-0.09)x10(-6).

Journal Article↗
PubMed2001

Regulation of the PU.1 gene by distal elements.

The transcription factor PU.1 (also known as Spi-1) plays a critical role in the development of the myeloid lineages, and myeloid cells derived from PU.1(-/-) animals are blocked at the earliest stage of myeloid differentiation. Expression of the PU.1 gene is tightly regulated during normal hematopoietic development, and dysregulation of PU.1 expression can lead to erythroleukemia. However, relatively little is known about how the PU.1 gene is regulated in vivo. Here it is shown that myeloid cell type-specific expression of PU.1 in stable cell lines and transgenic animals is conferred by a 91-kilobase (kb) murine genomic DNA fragment that consists of the entire PU.1 gene (20 kb) plus approximately 35 kb of upstream and downstream sequences, respectively. To further map the important transcriptional regulatory elements, deoxyribonuclease I hypersensitive site mapping studies revealed at least 3 clusters in the PU.1 gene. A 3.5-kb fragment containing one of these deoxyribonuclease I hypersensitive sites, located -14 kb 5' of the transcriptional start site, conferred myeloid cell type-specific expression in stably transfected cell lines, suggesting that within this region is an element important for myeloid specific expression of PU.1. Further analysis of this myeloid-specific regulatory element will provide insight into the regulation of this key transcriptional regulator and may be useful as a tool for targeting expression to the myeloid lineage.

Animals↗
PubMed2001

Kinetics of faceting driven by attractive step-step interactions on vicinal Si(113).

We have studied the far-from-equilibrium kinetics of faceting caused by short-ranged attractive step-step interactions on vicinal Si(113), using scanning tunneling microscopy. We show that a network of step bunches coarsens via both zipping up of the neighboring step bunches and irreversible binding events which alter the local topological configuration. A step-network model which incorporates the irreversible step-bunch-binding events yields quantitative understanding of the experimental results.

Journal Article↗
PubMed2001

Observation of B --> J/psi K(1)(1270).

We report the first observation of the exclusive decay process B-->J/psi K(1)(1270) using a sample of 11.2M BB macro meson pairs collected in the Belle detector at the KEKB asymmetric energy e(+)e(-) collider. We measure branching fractions of B[B(0)-->J/psi K(0)(1)(1270)] = (1.30+/-0.34+/-0.32) x 10(-3) and B[B(+)-->J/psi K(+)(1)(1270)] = (1.80+/-0.34+/-0.39) x 10(-3), where the first error is statistical and the second is systematic. These modes constitute approximately 15% of the total number of B-->J/psi X decays. No evidence is seen for B-->J/psi K(1)(1400) and we set an upper limit for this branching fraction.

Journal Article↗
PubMed2001

AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations.

The t(8;21) is one of the most frequent chromosomal abnormalities associated with acute myeloid leukemia (AML). The translocation, which involves the AML1 gene on chromosome 21 and the ETO gene on chromosome 8, generates an AML1-ETO fusion transcription factor. To examine the effect of the AML1-ETO fusion protein on leukemogenesis, we made transgenic mice in which expression of AML1-ETO is under the control of the human MRP8 promoter (hMRP8-AML1-ETO). AML1-ETO is specifically expressed in myeloid cells, including common myeloid progenitors of hMRP8-AML1-ETO transgenic mice. The transgenic mice were healthy during their life spans, suggesting that AML1-ETO alone is not sufficient for leukemogenesis. However, after treatment of newborn hMRP8-AML1-ETO transgenic mice and their wild-type littermates with a strong DNA-alkylating mutagen, N-ethyl-N-nitrosourea, 55% of transgenic mice developed AML and the other 45% of transgenic mice and all of the wild-type littermates developed acute T lymphoblastic leukemia. Our results provide direct evidence that AML1-ETO is critical for causing myeloid leukemia, but one or more additional mutations are required for leukemogenesis. The hMRP8-AML1-ETO-transgenic mice provide an excellent model that can be used to isolate additional genetic events and to further understand the molecular pathogenesis of AML1-ETO-related leukemia.

Animals↗
PubMed2001

Observation of Cabibbo suppressed B --> D(*)K- decays at Belle.

We report observations of the Cabibbo suppressed decays B-->D((*))K- using a 10.4 fb(-1) data sample accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB e(+)e(-) storage ring. We find that the ratios of Cabibbo suppressed to Cabibbo favored branching fractions are B(B--->D0K-)/B(B--->D0pi(-)) = 0.079+/-0.009+/-0.006, B(B(0)-->D+K-)/B(B(0)-->D+pi(-)) = 0.068+/-0.015+/-0.007, B(B--->D(*0)K-)/B(B--->D(*0)pi(-)) = 0.078+/-0.019+/-0.009, and B(B(0)-->D(*+)K-)/B(B(0)-->D(*+)pi(-)) = 0.074+/-0.015+/-0.006. These are the first observations of the B-->D+K-, D(*0)K-, and D(*+)K- decay processes.

Journal Article↗
PubMed2001

Observation of large CP violation in the neutral B meson system.

We present a measurement of the standard model CP violation parameter sin2 phi(1) based on a 29.1 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. One neutral B meson is fully reconstructed as a J/psi K(S), psi(2S)K(S), chi(c1)K(S), eta(c)K(S), J/psi K(L), or J/psi K(*0) decay and the flavor of the accompanying B meson is identified from its decay products. From the asymmetry in the distribution of the time intervals between the two B meson decay points, we determine sin2 phi(1) = 0.99+/-0.14(stat)+/-0.06(syst). We conclude that we have observed CP violation in the neutral B meson system.

Journal Article↗
PubMed2001

A yeast gene, MGS1, encoding a DNA-dependent AAA(+) ATPase is required to maintain genome stability.

Changes in DNA superhelicity during DNA replication are mediated primarily by the activities of DNA helicases and topoisomerases. If these activities are defective, the progression of the replication fork can be hindered or blocked, which can lead to double-strand breaks, elevated recombination in regions of repeated DNA, and genome instability. Hereditary diseases like Werner's and Bloom's Syndromes are caused by defects in DNA helicases, and these diseases are associated with genome instability and carcinogenesis in humans. Here we report a Saccharomyces cerevisiae gene, MGS1 (Maintenance of Genome Stability 1), which encodes a protein belonging to the AAA(+) class of ATPases, and whose central region is similar to Escherichia coli RuvB, a Holliday junction branch migration motor protein. The Mgs1 orthologues are highly conserved in prokaryotes and eukaryotes. The Mgs1 protein possesses DNA-dependent ATPase and single-strand DNA annealing activities. An mgs1 deletion mutant has an elevated rate of mitotic recombination, which causes genome instability. The mgs1 mutation is synergistic with a mutation in top3 (encoding topoisomerase III), and the double mutant exhibits severe growth defects and markedly increased genome instability. In contrast to the mgs1 mutation, a mutation in the sgs1 gene encoding a DNA helicase homologous to the Werner and Bloom helicases suppresses both the growth defect and the increased genome instability of the top3 mutant. Therefore, evolutionarily conserved Mgs1 may play a role together with RecQ family helicases and DNA topoisomerases in maintaining proper DNA topology, which is essential for genome stability.

Adenosine Triphosphatases↗
PubMed2001

Mechanical stretch induces activation of skeletal muscle satellite cells in vitro.

Cultured quiescent satellite cells were subjected to mechanical stretch in a FlexerCell System. In response to stretch, satellite cells entered the cell cycle earlier than if they were under control conditions. Only a brief period of stretch, as short as 2 h, was necessary to stimulate activation. Additionally, conditioned medium from stretched cells could activate unstretched satellite cells. The presence of HGF on c-met-positive myogenic cells was detected by immunofluorescence at 12 h in culture, and immunoblots demonstrated that HGF was released by stretched satellite cells into medium. Also, stretch activation could be abolished by the addition of anti-HGF antibodies to stretched cultures, and activity in conditioned medium from stretched cells could be neutralized by anti-HGF antibodies. In addition, stretch appeared to cause release of preexisting HGF from the extracellular matrix. These experiments suggest that HGF may be involved in linking mechanical perturbation of muscle to satellite cell activation.

Animals↗
PubMed2001

A unique beta-hairpin protruding from AAA+ ATPase domain of RuvB motor protein is involved in the interaction with RuvA DNA recognition protein for branch migration of Holliday junctions.

The Escherichia coli RuvB protein is a motor protein that forms a complex with RuvA and promotes branch migration of Holliday junctions during homologous recombination. This study describes the characteristics of two RuvB mutants, I148T and I150T, that do not promote branch migration in the presence of RuvA. These RuvB mutants hydrolyzed ATP and bound duplex DNA with the same efficiency as wild-type RuvB, but the mutants did not form a complex with RuvA and were defective in loading onto junction DNA in a RuvA-assisted manner. A recent crystallographic study revealed that Ile(148) and Ile(150) are in a unique beta-hairpin that protrudes from the AAA(+) ATPase domain of RuvB. We propose that this beta-hairpin interacts with hydrophobic residues in the mobile third domain of RuvA and that this interaction is vital for the RuvA-assisted loading of RuvB onto Holliday junction DNA.

Adenosine Triphosphatases↗
PubMed2001

Synthesis and biological evaluations of condensed pyridine and condensed pyrimidine-based HMG-CoA reductase inhibitors.

A series of 3,5-dihydroxyheptenoic acid derivatives containing pyrazolopyridine, isoxazolopyridine, thienopyridine, and pyrazolopyrimidine as a key scaffold was synthesized from condensed pyridine and condensed pyrimidine carboxylic acid esters by homologation, aldol condensation with ethyl acetoacetate dianion, and stereoselective reduction of the 5-hydroxyketone. Several compounds in the series were found to have potent HMG-CoA reductase inhibitory activities in vitro and marked cholesterol biosynthesis inhibitory activities in vivo. It has been shown that these scaffolds can be used as a suitable replacement for the hexahydronaphthalene ring present in naturally occurring HMG-CoA reductase inhibitors.

Administration, Oral↗
PubMed2001

Two KaiA-binding domains of cyanobacterial circadian clock protein KaiC.

kaiABC, a gene cluster, encodes KaiA, KaiB and KaiC proteins that are essential to circadian rhythms in the unicellular cyanobacterium Synechococcus sp. strain PCC 7942. Kai proteins can interact with each other in all possible combinations. This study identified two KaiA-binding domains (C(KABD1) and C(KABD2)) in KaiC at corresponding regions of its duplicated structure. Clock mutations on the two domains and kaiA altered the strength of C(KABD)-KaiA interactions assayed by the yeast two-hybrid system. Thus, interaction between KaiA and KaiC through C(KABD1) and C(KABD2) is likely important for circadian timing in the cyanobacterium.

Adenosine Triphosphate↗
PubMed2001

A new ray-tracing program RIGTRACE for X-ray optical systems.

A new ray-tracing simulation program, RIGTRACE, has been developed specifically for the X-ray optics range. It traces consecutively each ray, following its path from the source to the observation plane, and treats diffraction by a monochromator crystal by adopting the Darwin-Prins theory so that it may be seen how rays of slightly different energies and incident angles reach the plane. It is also possible to treat the case of the laboratory system, in which the optical elements are disposed close to each other. Examples of the application are provided.

Journal Article↗
PubMed2001

Phase determination by wavelength-modulated diffraction. I. Centrosymmetric case.

Wavelength-modulated diffraction was developed by Iwasaki, Yurugi & Yoshimura [Acta Cryst. (1999), A55, 864-870] as a method for phase determination, in which the intensity of Bragg reflections is recorded using radiation whose wavelength is changing continually over a range in the vicinity of the absorption edge of an atom in the crystal. Using a ferrocene derivative crystal (chemical formula C36H32O7Fe, space group P2(1)/a) with the Fe atoms chosen as anomalous scatterers, measurements were made of the intensity gradient dI/d lambda of the reflections with an imaging plate as a detector on a synchrotron radiation source at Ritsumeikan University. In the case of a centrosymmetric crystal, the phase of the structure factor could be derived by measuring only the sign of dI/d lambda at one wavelength in the range. Of 104 reflections measured, the correct phase was assigned to 101 reflections. A discussion is given on the errors involved and on the limits of application of the method.

Journal Article↗
PubMed2001

Measurement of B(0)(d)-B_(0)(d) mixing rate from the time evolution of dilepton events at the upsilon(4S).

We report a determination of the B(0)(d)-&B_(0)(d) mixing parameter Deltam(d) based on the time evolution of dilepton yields in Upsilon(4S) decays. The measurement is based on a 5.9 fb(-1) data sample collected by the Belle detector at KEKB. The proper-time difference distributions for same-sign and opposite-sign dilepton events are simultaneously fitted to an expression containing Deltam(d) as a free parameter. Using both muons and electrons, we obtain Deltam(d) = 0.463+/-0.008 (stat)+/-0.016 (syst) ps(-1). This is the first determination of Deltam(d) from time evolution measurements at the Upsilon(4S). We also place limits on possible CPT violations.

Journal Article↗