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Biomedical subjects

H Yasuda

Publications and source records attributed to H Yasuda.

At least 91 records · Page 5Linked to original sources

Glow-peak stability in 6LiF:Mg,Ti (TLD-600) exposed to a Fe-ion beam.

The stability of glow peaks in 6LiF:Mg,Ti (TLD-600) exposed to a high-energy Fe-ion beam was examined in comparison to 137Cs gamma-ray irradiation under changing annealing conditions. The peak areas induced by the Fe ions were much smaller than those by gamma-rays. The sizes and positions of peaks 3-5 in Fe-ion irradiated samples were hardly changed after post-annealing at 100 degrees C x 30 min, regardless of the pre-annealing conditions (fast quenching or subsequent pre-annealing at 100 degrees C x 2 h). Whereas, the peaks in gamma-ray irradiated samples were notably affected by post-annealing; the peak positions and peak-area sizes changed in different ways depending on the pre-annealing conditions. The effects of post-annealing on peak 6 were identical for Fe ions and gamma-rays. These facts suggest that peaks 3-5 in TLD-600 comprised both stable and unstable luminescent centers, and that the latter part would be easily depleted in highly dense ionization.

Cesium↗

Transforming growth factor beta affects osteoclast differentiation via direct and indirect actions.

Transforming growth factor beta (TGF-beta) is abundant in bone and has complex effects on osteolysis, with both positive and negative effects on osteoclast differentiation, suggesting that it acts via more than one mechanism. Osteoclastogenesis is determined primarily by osteoblast (OB) expression of the tumor necrosis factor (TNF)-related molecule receptor activator of NF-kappaB ligand (RANKL) and its decoy receptor osteoprotegerin (OPG), which are increased and decreased, respectively, by osteolytic factors. A RANKL-independent osteoclastogenic mechanism mediated by TNF-alpha has also been shown. Therefore, we investigated TGF-beta effects on osteoclast formation in culture systems in which osteoclastogenic stimulus is dependent on OBs and culture systems where it was provided by exogenously added RANKL or TNF-alpha. Both OPG and TGF-beta inhibited osteoclast formation in hemopoietic cell/OB cocultures, but the kinetics of their action differed. TGF-beta also inhibited osteoclastogenesis in cocultures of cells derived from OPG null (opg-/-) mice. TGF-beta strongly decreased RANKL messenger RNA (mRNA) expression in cultured osteoblasts, and addition of exogenous RANKL to TGFbeta-inhibited cocultures of opg-/- cells partially restored osteoclastogenesis. Combined, these data indicate that the inhibitory actions of TGF-beta were mediated mainly by decreased OB production of RANKL. In contrast, in the absence of OBs, TGF-beta greatly increased osteoclast formation in recombinant RANKL- or TNF-alpha-stimulated cultures of hemopoietic cells or RAW 264.7 macrophage-like cells to levels several-fold greater than attainable by maximal stimulation by RANKL or TNF-alpha. These data suggest that TGF-beta may increase osteoclast formation via action on osteoclast precursors. Therefore, although RANKL (or TNF-alpha) is essential for osteoclast formation, factors such as TGF-beta may powerfully modify these osteoclastogenic stimuli. Such actions may be critical to the control of physiological and pathophysiological osteolysis.

Animals↗

Responses of a direct ion storage dosimeter (DIS-1) to heavy charged particles.

The responses of a direct ion storage dosimeter (DIS-1) to energetic heavy charged particles were examined using (4)He, (12)C, (40)Ar and (56)Fe ion beams at the HIMAC at the National Institute of Radiological Sciences. The efficiency of the DIS-1 on the basis of absorbed dose was almost unity for the helium and carbon ions and was slightly decreased for the argon and iron ions. The linearity in the dose response and the angular independence for these heavy ions were fairly good. Although further studies are necessary, these results suggest that the DIS-1 would be a suitable passive dosimeter for measurements of absorbed dose in a field dominated by heavy charged particles such as the space environment.

Radiation Dosage↗

Increased arterial wall stiffness limits flow volume in the lower extremities in type 2 diabetic patients.

OBJECTIVE: To document an association between arterial wall stiffness and reduced flow volume in the lower-extremity arteries of diabetic patients. RESEARCH DESIGN AND METHODS: We recruited 60 consecutive type 2 diabetic patients who had no history or symptoms of peripheral arterial disease (PAD) in the lower extremities and normal ankle/brachial systolic blood pressure index at the time of the study (non-PAD group) and 20 age-matched nondiabetic subjects (control group). We used an automatic device to measure pulse wave velocity (PWV) in the lower extremities as an index of arterial wall stiffness. At the popliteal artery, we evaluated flow volume and the resistive index as an index of arterial resistance to blood flow using gated two-dimensional cine-mode phase-contrast magnetic resonance imaging. RESULTS: Consistent with previous reports, we confirmed that the non-PAD group had an abnormally higher PWV compared with that of the control group (P < 0.001). To further demonstrate decreased flow volume and abnormal flow pattern at the popliteal artery in patients with a higher degree of arterial wall stiffness, we assigned the 60 non-PAD patients to tertiles based on their levels of PWV. In the highest group, magnetic resonance angiograms of the calf and foot arteries showed decreased intravascular signal intensity, indicating the decreased arterial inflow in those arteries. The highest group was also characterized by the lowest late diastolic and total flow volumes as well as the highest resistive index among the groups. From stepwise multiple regression analysis, PWV and autonomic function were identified as independent determinants for late diastolic flow volume (r(2) = 0.300; P < 0.001). CONCLUSIONS: Arterial wall stiffness was associated with reduced arterial flow volume in the lower extremities of diabetic patients.

Aged↗

Inhibition by the essential oils of peppermint and spearmint of the growth of pathogenic bacteria.

The effects of the, essential oils of peppermint (Mentha piperita L.), spearmint Mentha spicata L.) and Japanese mint (Mentha, arvensis L.), of four major constituents of the esssential oil of peppermint, and of three major constituents of the essential oil of spearmint, on the proliferation of Helicobacter pylori, Salmonella enteritidis, Escherichia coli O157:H7, methicillin-resistant Staphylococcus aureus (MRSA) and methicillin sensitive Staphylococccus aureus (MSSA) were examined. The essential oils and the various constituents inhibited the proliferation of each strain in liquid culture in a dose-dependent manner. In addition, they exhibited bactericidal activity in phosphate-buffered saline. The antibacterial activities varied among the bacterial species tested but were almost the same against antibiotic-resistant and antibiotic-sensitive strains of Helicobacter pylori and S. aureus. Thus, the essential oils and their constituents may be useful as potential antibacterial agents for inhibition of the growth of pathogens.

Culture Media↗

Simulation of the low-Earth-orbit dose rates using secondary radiations from the HZE particles at NIRS-HIMAC.

In order to study biological effects from cyclic dose rates encountered at the low-Earth orbit (LEO), an experimental facility was designed in the Biology room of the Heavy Ion Medical Accelerator in Chiba (NIRS-HIMAC). An incubator placed in this facility is irradiated repeatedly by secondary radiations from HZE-particle beams supplied for independent users. The daily-average dose rate (1.4 mGy d-1) measured for 223 days and short-term dose rates measured for selected beam conditions were comparable to the dose rates observed in past LEO missions. Severe solar particle events can be simulated with hourly maximum dose rate of 2.8 mGy h-1. Preliminary measurements using CR-39 and TLD indicated that the dominant LET range is less than 5 keV micrometers-1. These results demonstrate the possibility of this facility for radiobiology studies of the effects of low dose rates comparable to the LEO environment.

Cesium Radioisotopes↗

Probability of hippocampus cell hits by high-LET space radiation in a low-Earth-orbit mission (STS-91).

High-LET particles (HLP) of space radiation in the brain were measured with plastic nuclear track detectors (PNTD) using a life-size human phantom in the 9th Shuttle-Mir Mission (STS-91). Relationship between PNTD track-formation sensitivity (S) and LET infinity H2O was examined using heavy-ion beams at NIRS-HIMAC. Average fluence of the HLP (HLP10) with LET infinity H2O greater than 10 keV micrometers-1 was evaluated as 1.3 x 10(4) n cm-2 for the 9.8-day low-Earth-orbit mission (400 km x 51.65 degrees). Based on a simple extrapolation of these data, probability of HLP10 hits to hippocampus cells and cell-nuclei were estimated to be 45% and 7.0%, respectively, in a 90-day ISS mission. For 1 year, 91% of cells and 25% of cell-nuclei will be hit by HLP10.

Cell Nucleus↗

[A simple dosimetry method for biological experiments on the International Space Station].

For interpretation of results from future biological experiments in the International Space Station (ISS), radiation doses received by the biological samples must be accurately determined. This paper demonstrates that small integrating detectors, such as thermoluminescent dosemeters (TLDs) and glasses, can be used in a simple way for evaluation of biological doses from space radiation. Statistical errors (type-A uncertainty) of this method would be satisfactorily small relative to those generally observed in biological responses. Permissible levels of systematic errors (type-B uncertainty) should depend on both dosimetry purpose (most-probable or conventional evaluation) and reproducibility of the biological responses. It is expected that this method will be suitably applied to future experiments in the ISS where any instruments have to be small-scale, light-weight, physico-chemically stable and simple in handling.

Animals↗

[Osteoprotegerin (OPG/OCIF) inhibits bone destruction in rheumatoid arthritis models].

Recent discovery of factors involved in bone destruction in Rheumatoid Arthritis (RA) identified its molecular mechanism. Osteoclast differentiation factor (ODF, also called receptor activator of NF-kappaB ligand (RANKL) ) that controls osteoclast differentiation and function has a major role in the bone destruction among them. Osteoclastogenesis inhibitory factor (OCIF, also called osteoprotegerin (OPG) ) that is a decoy receptor for ODF/RANKL is a specific inhibitor of bone destruction. OPG/OCIF may be useful for and applicable to the treatment of bone destruction in RA.

English Abstract↗

New asymmetric reactions of 2-formyl- and 2-acyl-1-[(2,4, 6-triisopropylphenyl)sulfinyl]naphthalenes via diastereomeric rotamers.

Nucleophilic reactions with Grignard reagents and the Mukaiyama aldol reactions of the naphthaldehydes having the (2,4, 6-triisopropylphenyl)sulfinyl group produced products with high stereoselectivity. In these reactions, the stereochemistry of the major products changes depending on the Lewis acids used. Reduction of the 2-acyl-1-[(2,4,6-triisopropylphenyl)sulfinyl]naphthalenes also proceeds with high stereoselectivity but with a different stereochemistry depending on the reducing agents. We have demonstrated, by the mechanistic consideration based on the X-ray crystal structures as well as the (1)H and (13)C NMR spectral data, that the extremely high and specific stereoselectivities of these reactions are due to the predominant rotamer around the C(naph)-S axis. Synthesis of enantiomerically pure 2-naphthylmethanol is provided as an example.

Journal Article↗

A nonproteolytic function of the proteasome is required for the dissociation of Cdc2 and cyclin B at the end of M phase.

Inactivation of cyclin B-Cdc2 kinase at the exit from M phase depends on the specific proteolysis of the cyclin B subunit, whereas the Cdc2 subunit remains present at nearly constant levels throughout the cell cycle. It is unknown how Cdc2 escapes degradation when cyclin B is destroyed. In Xenopus egg extracts that reproduce the exit from M phase in vitro, we have found that dissociation of the cyclin B-Cdc2 complex occurred under conditions where cyclin B was tethered to the 26S proteasome but not yet degraded. The dephosphorylation of Thr 161 on Cdc2 was unlikely to be necessary for the dissociation of the two subunits. However, the dissociation was dependent on the presence of a functional destruction box in cyclin B. Cyclin B ubiquitination was also, by itself, not sufficient for separation of Cdc2 and cyclin B. The 26S proteasome, but not the 20S proteasome, was capable of dissociating the two subunits. These results indicate that the cyclin B and Cdc2 subunits are separated by the proteasome through a mechanism that precedes proteolysis of cyclin B and is independent of proteolysis. As a result, cyclin B levels decrease on exit from M phase but Cdc2 levels remain constant.

Animals↗

Increases in K+ conductance and Ca2+ influx under high glucose with suppressed Na+/K+-pump activity in rat myelinated nerve fibers.

To test the combined effect of high glucose and decreased Na+/K+-pump activity, a condition which closely mimics the diabetic state, on nerve ionic currents, changes in action potential and membrane current induced by high glucose in the presence of ouabain were investigated using voltage clamp analysis in rat single myelinated nerve fibers. In the presence of 0.1 mM ouabain, 30 mM glucose caused a progressive increase in the delayed K+ current as well as persistent decreases in action potential and Na+ current, suggesting that Na+/K+ pump plays an important role in preventing the increase in the K+ current. The latter increase was suppressed by a blocker of Ca2+-activated K+ channels. Two types of voltage-dependent Ca2+ channel blockers (L and N-type) as well as a Na+/Ca2+-exchange blocker diminished the ouabain-induced increase in K+ conductance. These results suggest that high glucose with suppressed Na+/K+ pump activity might induce an increase of Ca2+ influx through either Ca2+ channels or reverse Na+/Ca2+-exchange, possibly leading to the elevation of Ca2+-activated voltage-dependent K+ channels. Both a decrease in inward Na+ current and an increase in K+ conductance may result in decreased nerve conduction. In addition, a possible increase of axoplasmic Ca2+ concentration may lead to axonal degeneration. These results provide a clue for understanding the pathophysiologic mechanism of diabetic neuropathy.

Action Potentials↗

Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation.

We report the p35 and p60 forms of XRCC4 protein, appearing in human leukemia MOLT-4 or U937 cells following X-irradiation or hyperthermia. p35 appeared in conjunction with the cleavage of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and the fragmentation of internucleosomal DNA, and was suppressed by Ac-DEVD-CHO. p35 was also produced in vitro by treating MOLT-4 cell lysate with recombinant caspases, suggesting that p35 was a caspase-cleaved fragment of XRCC4 in apoptotic cell death. p60 was sensitive to treatment with phosphatase or wortmannin and was undetectable in M059J cells deficient in DNA-PKcs. However, p60 was found in ataxia-telangiectasia cells after irradiation. These results indicated p60 as a phosphorylated form of XRCC4, requiring DNA-PKcs but not ataxia-telangiectasia mutated (ATM).

Androstadienes↗

Blocking the glycine-binding site of NMDA receptors prevents the progression of ischemic pathology induced by bilateral carotid artery occlusion in spontaneously hypertensive rats.

This study was designed to investigate the participation of N-methyl-D-aspartate (NMDA) receptors in the progression of the pathology induced by bilateral carotid artery occlusion (BCAo) in spontaneously hypertensive rats (SHRs). We examined the effects of the selective NMDA receptor glycine-binding site antagonist SM-18400 on the mortality rate, deterioration of neurological signs, and formation of brain edema in the SHR-BCAo model. SM-18400 (15 or 30 mg/kg) was administered via the tail vein immediately and 2 h after BCAo. Neurological signs were monitored continuously for 8 h after BCAo, and the mortality rates were followed for 5 days. All SM-18400-treated animals were still alive 5 h after BCAo, whereas 38% of the animals died in the vehicle-treated group. The mortality rates of the SM-18400-treated groups were still lower than those of the vehicle-treated group 5 days after BCAo. In addition, SM-18400 markedly prevented the deterioration of neurological signs. The water content of the telencephalon and diencephalon/mesencephalon in the vehicle-treated group, measured 3 h after BCAo, was significantly higher than in the sham-operated group. SM-18400 significantly inhibited the increase in water content in both regions in a dose-dependent manner. These findings suggest that NMDA receptors participate in the increase in the mortality rate, deterioration of neurological signs, and formation of brain edema following ischemic brain damage in the SHR-BCAo model, and that SM-18400 can prevent ischemic insults.

Animals↗