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Biomedical subjects

Hiroaki Katsuragi

Publications and source records attributed to Hiroaki Katsuragi.

8 recordsLinked to original sources

Toll-like receptor 9 acts at an early stage in host defence against pneumococcal infection.

Toll-like receptor 9 (TLR9) induces an inflammatory response by recognition of unmethylated CpG dinucleotides, mainly present in prokaryotic DNA. So far, TLR9-deficient mice have been shown to be more sensitive than wild-type mice to viral, but not to bacterial infections. Here, we show that mice deficient in TLR9 but not in TLR1, TLR2, TLR4 and TLR6 or IL-1R/IL-18R are more susceptible to a respiratory tract bacterial infection caused by Streptococcus pneumoniae. Intranasal challenge studies revealed that TLR9 plays a protective role in the lungs at an early stage of infection prior to the entry of circulating inflammatory cells. Alveolar as well as bone marrow-derived macrophages deficient in either TLR9 or the myeloid adaptor differentiation protein MyD88 were impaired in pneumococcal uptake and in pneumococcal killing. Our data suggest that in the airways, pneumococcal infection triggers a TLR9 and MyD88-dependent activation of phagocytic activity from resident macrophages leading to an early clearance of bacteria from the lower respiratory tract.

Animals↗

Explosive fragmentation of a thin ceramic tube using pulsed power.

This study experimentally examined the explosive fragmentation of thin ceramic tubes using pulsed power. A thin ceramic tube was threaded on a thin copper wire, and high voltage was applied to the wire using a pulsed power generator. This melted the wire and the resulting vapor put pressure on the ceramic tube, causing it to fragment. We examined the statistical properties of the fragment mass distribution. The cumulative fragment mass distribution obeyed the double exponential or power law with exponential decay. Both distributions agreed well with the experimental data. Finally, we obtained universal scaling for fragmentation, which is applicable to both impact and explosive fragmentation.

Journal Article↗

Adding problem-based learning tutorials to a traditional lecture-based curriculum: a pilot study in a dental school.

This article reports on the implementation of a problem-based learning (PBL) tutorial in our advanced program for second year students within an existing curriculum. The program was opened on the last 5 days of the summer vacation and students could volunteer to be part of the group. Students separated themselves into small groups by random sampling. The PBL tutorials were done during the first 3 days for medical problems according to our original scenarios (based on medical cases), and during the last 2 days, students made presentations of their learning outcomes, using information technology (IT) by themselves. Throughout this program, students were expected to engage in self-learning, except for a 1(1/2)-h group session with a tutor. Assessment was done by attendance at a group session and by portfolio analysis. Following the portfolio analysis, students identified the number of learning issues (group A, 26 +/- 7 issues; group B, 20 +/- 3 issues; group C, 21 +/- 7 issues). Research, by questionnaire, revealed that 84% of the students were strongly interested in each scenario and 95% of the students felt familiar with each scenario. The levels of satisfaction with the tutor were different in the three groups. All of the students were comfortable in the discussion room and IT center. These results suggested that PBL tutorials are supported by the scenario, the tutor, and the location of the group session, as well as by self-learning. Moreover, one of the most important factors for a PBL tutorial that the student is ready for the free discussions and has enough time for individual self-learning.

Computer-Assisted Instruction↗

Myeloid differentiation factor 88-dependent signalling controls bacterial growth during colonization and systemic pneumococcal disease in mice.

The Toll-like receptors (TLRs) and the myeloid differentiation factor 88 (MyD88) are key players in the activation of the innate immune defence during microbial infections. Using different murine infection models, we show that MyD88-dependent signalling is crucial for the activation of the innate immune defence against Streptococcus pneumoniae. Our data demonstrate that both local and systemic inflammatory response to S. pneumoniae depends on the presence of MyD88 to clear bacterial colonization of the upper respiratory tract and to prevent pulmonary and systemic infection in mice. Finally, we described a strong correlation between enhanced bacterial growth in the bloodstream of MyD88-deficient mice and the inability to lower the serum iron concentration in response to infection.

Adaptor Proteins, Signal Transducing↗

Crossover of weighted mean fragment mass scaling in two-dimensional brittle fragmentation.

We performed vertical and horizontal sandwich two-dimensional brittle fragmentation experiments. The weighted mean fragment mass was scaled using the multiplicity mu. The scaling exponent crossed over at log(10) mu(c) approximately equal to -1.4 . In the small mu (<< mu(c) ) regime, the binomial multiplicative (BM) model was suitable and the fragment mass distribution obeyed log-normal form. However, in the large mu (>> mu(c) ) regime, in which a clear power-law cumulative fragment mass distribution was observed, it was impossible to describe the scaling exponent using the BM model. We also found that the scaling exponent of the cumulative fragment mass distribution depended on the manner of impact (loading conditions): it was 0.5 in the vertical sandwich experiment and approximately 1.0 in the horizontal sandwich experiment.

Journal Article↗

Scaling of impact fragmentation near the critical point.

We investigated two-dimensional brittle fragmentation with a flat impact experimentally, focusing on the low-impact-energy region near the fragmentation-critical point. We found that the universality class of fragmentation transition disagreed with that of percolation. However, the weighted mean mass of the fragments could be scaled using the pseudo-control-parameter multiplicity. The data for highly fragmented samples included a cumulative fragment mass distribution that clearly obeyed a power law. The exponent of this power law was 0.5 and it was independent of sample size. The fragment mass distributions in this regime seemed to collapse into a unified scaling function using weighted mean fragment mass scaling. We also examined the behavior of higher-order moments of the fragment mass distributions, and obtained multiscaling exponents that agreed with those of the simple biased cascade model.

Journal Article↗

Asymptotic function for multigrowth surfaces using power-law noise.

Numerical simulations are used to investigate the multiaffine exponent alpha(q) and multigrowth exponent beta(q) of ballistic deposition growth for noise obeying a power-law distribution. The simulated values of beta(q) are compared with the asymptotic function beta(q)=1/q that is approximated from the power-law behavior of the distribution of height differences over time. They are in good agreement for large q. The simulated alpha(q) is found in the range 1/q< or =alpha(q)< or =2/(q+1). This implies that large rare events tend to break the Kardar-Parisi-Zhang universality scaling law at higher order q.

Journal Article↗

Intracellular production and extracellular release of oxygen radicals by PMNs and oxidative stress on PMNs during phagocytosis of periodontopathic bacteria.

In this study we investigated intracellular and extracellular oxygen radical production by polymorphonuclear leukocytes (PMNs) during the phagocytosis of periodontopathic bacteria. In in vitro assays, bacteria of the species Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Fusobacterium nucleatum were phagocytosed at 37 degrees C for 4 h by purified peripheral human PMNs from healthy subjects (n = 6). Superoxide production during phagocytosis was determined by flow cytometry and with a fluorescence/luminescence microplate reader. After phagocytosis, oxidative stress was determined by flow cytometry. Both the intracellular and extracellular oxygen radical production by PMNs phagocytosing F. nucleatum was significantly greater than that of PMNs phagocytosing P. gingivalis and A. actinomycetemcomitans ( P < 0.01 by the Mann-Whitney test). Moreover, after 4 h of incubation, the oxidative stress of PMNs phagocytosing F. nucleatum was significantly greater than that of PMNs phagocytosing P. gingivalis and A. actinomycetemcomitans. We conclude that a high level of superoxide production by PMNs may damage not only periodontopathic bacteria but also PMNs themselves, and may be correlated with the destruction of periodontal tissue.

Aggregatibacter actinomycetemcomitans↗