236 research outputs found
Toxic wavelength of blue light changes as insects grow
<div><p>Short-wavelength visible light (blue light: 400–500 nm) has lethal effects on various insects, such as fruit flies, mosquitoes, and flour beetles. However, the most toxic wavelengths of blue light might differ across developmental stages. Here, we investigate how the toxicity of blue light changes with the developmental stages of an insect by irradiating <i>Drosophila melanogaster</i> with different wavelengths of blue light. Specifically, the lethal effect on eggs increased at shorter light wavelengths (i.e., toward 405 nm). In contrast, wavelengths from 405 to 466 nm had similar lethal effects on larvae. A wavelength of 466 nm had the strongest lethal effect on pupae; however, mortality declined as pupae grew. A wavelength of 417 nm was the most harmful to adults at low photon flux density, while 466 nm was the most harmful to adults at high photon flux density. These findings suggest that, as the morphology of <i>D</i>. <i>melanogaster</i> changes with growth, the most harmful wavelength also changes. In addition, our results indicated that reactive oxygen species influence the lethal effect of blue light. Our findings show that blue light irradiation could be used as an effective pest control method by adjusting the wavelength to target specific developmental stages.</p></div
Gutenberg-Richter’s law in sliding friction of gels
We report on experimental studies of spatio-temporally heterogeneous stick-slip motions in the sliding friction between a hard polymethyl methacrylate (PMMA, plexiglass) block and a soft poly-dimethyl siloxane (PDMS, silicone) gel plate. We perform experiments on two PDMS gels with different viscoelastic properties. For the less viscous gel, large and rapid events are preceded by an alternation of active and less active periods. For the more viscous gel, successive slow slip events take place continuously. The probability distributions of the force drop, a quantity analogous to seismic moment, obey a power law similar to Gutenberg-Richter's empirical law for the frequency-size statistics of earthquakes, and the exponents of the power law vary with the plate velocity and the viscosity of the gel. We propose a simple model to explain the dependence of the power law exponent on the plate velocity, which agrees with experimental results
\u3cem\u3eMycobacterium avium\u3c/em\u3e subsp. \u3cem\u3eparatuberculosis\u3c/em\u3e lipophilic antigen causes Crohn’s disease-type necrotizing colitis in Mice
Background: A 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced murine colitis model was developed to investigate the pathogenesis and to evaluate a method of treating human Crohn’s disease. This experimental model rapidly induces colitis similar to human Crohn’s disease lesion in a reproducible manner. However, natural exposure of the human digestive tract to TNBS is unrealistic. A novel animal model based on realistic data is eagerly anticipated in future research on pathogenesis of CD. Method: We evaluated the potency of Map antigen molecules in an effort to develop a novel colitis model using a more realistic source than TNBS. We prepared the Map antigen by ethanol extraction and developed a mouse model in a manner similar to that of the well-known TNBS-induced colitis in mice. In the experiment, seven days after subcutaneous (SC) injection of the antigen into normal C57BL/6 mice, the same antigen in 50% ethanol was injected into the colon by the transanal route with a fine cannula. Results: On the fifth day after the transanal injection, histopathological examination revealed full-thickness necrotizing colitis with erosion and ulcers; severe infiltration with neutrophils, lymphocytes, macrophages, and perforation. However, no change was detected with each single Map-antigen injection. Conclusion: The present results provide a novel animal model for research on CD and may be the key to clarifying the relationship between CD and Map. This is the first evidence that mycobacterium antigen induces necrotizing colitis
Mycalolide-B, a novel and specific inhibitor of actomyosin ATPase isolated from marine sponge
AbstractA toxin isolated from marine sponge, mycalolide-B, inhibited smooth muscle contractions without changing cytosolic Ca2+ levels. It also inhibited Ca2+-induced contraction in permeabilized smooth muscles. In native actomyosin prepared from chicken gizzard, mycalolide-B inhibited superprecipitation and Mg2+-ATPase activity stimulated by Ca2+ without changing myosin light chain phosphorylation. In the permeabilized muscle and native actomyosin preparation thiophosphorylated with ATPγS, mycalolide-B inhibited ATP-induced contraction and Mg2+-ATPase activity, respectively, in the absence of Ca2+. Mycalolide-B also inhibited Mg2+-ATPase activity of skeletal muscle native actomyosin. Mycalolide-B had no effect on calmodulin-stimulated (Ca2+Mg2+)-ATPase activity of erythrocyte membranes. These results suggest that mycalolide-B selectively inhibits actin—myosin interaction
Salvage brachytherapy for seminal vesicle recurrence after initial brachytherapy for prostate cancer: a case report
BACKGROUND: To report the efficacy and safety of salvage brachytherapy for seminal vesicle recurrence after initial brachytherapy in a patient with prostate cancer. As far as we know, this is a first report of salvage brachytherapy for seminal vesicle recurrence in Japan. CASE PRESENTATION: A 70-year-old Japanese man with low-risk prostate cancer received low-dose-rate brachytherapy. Forty-two months after the seed implantation, he showed biochemical recurrence based on the nadir + 2 ng/mL definition. The prostate specific antigen (PSA) level was 5.11 ng/mL at 58 months after seed implantation. A saturation biopsy of the prostate showed no recurrence. Systemic screening also showed no distant metastases. However, T2-weighted magnetic resonance imaging (MRI) demonstrated a low intensity area at the base of the right seminal vesicle, which was strongly suggestive of recurrence. Sixty months after the initial therapy, a seminal vesicle biopsy confirmed recurrence with a Gleason score of 4 + 3 before salvage brachytherapy was performed. The prescribed dose was 145 Gy, the same as the dose of the initial therapy. One month later, the PSA level had rapidly declined to 0.898 ng/mL without androgen deprivation therapy. Ten months after the salvage brachytherapy, the PSA level reached 0.078 ng/mL. No adverse events were seen during the follow-up period. CONCLUSIONS: We experienced a patient who was successfully treated with salvage brachytherapy for seminal vesicle recurrence. Salvage brachytherapy is one of the promising therapeutic options for recurrence after initial brachytherapy
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