著者
鈴木 円 Madoka SUZUKI 昭和女子大学初等教育学科
出版者
光葉会
雑誌
學苑 = GAKUEN (ISSN:13480103)
巻号頁・発行日
vol.892, pp.83-95, 2015-02-01

The term Spartan education, translated into Japanese as "Suparuta kyoiku" is widely used nowadays to mean "severe education." This paper reviews 12 Japanese books or articles on Spartan education published from the 1870s to the 1970s and examines how the authors have understood Spartan education and in what context they have used the term. The above materials, published from the early Meiji to post-war period, suggest that Japanese learned about the education system of ancient Sparta from Western academic sources. However, after the influential bestseller, Shintaro Ishihara's Suparuta Kyoiku(Spartan Education; A book for raising tough kids), was published, leading Japanese educators seem to have begun using the term "Suparuta kyoiku" to mean Japanese militaristic education. Historically, Western classical scholars have acknowledged the value of Spartan public education in contrast to Athenian individualistic education. However, Japanese educators seem to have failed to understand the value of Spartan education because of the change in the understanding of the term "Suparuta kyoiku." The author concludes that educators ought to have used that term with that original sense in mind.
著者
Shuya Ishii Madoka Suzuki Shin’ichi Ishiwata Masataka Kawai
出版者
The Biophysical Society of Japan
雑誌
Biophysics and Physicobiology (ISSN:21894779)
巻号頁・発行日
vol.16, pp.28-40, 2019 (Released:2019-02-02)
参考文献数
77

The majority of hypertrophic cardiomyopathy (HCM) is caused by mutations in sarcomere proteins. We examined tropomyosin (Tpm)’s HCM mutants in humans, V95A and D175N, with in vitro motility assay using optical tweezers to evaluate the effects of the Tpm mutations on the actomyosin interaction at the single molecular level. Thin filaments were reconstituted using these Tpm mutants, and their sliding velocity and force were measured at varying Ca2+ concentrations. Our results indicate that the sliding velocity at pCa ≥8.0 was significantly increased in mutants, which is expected to cause a diastolic problem. The velocity that can be activated by Ca2+ decreased significantly in mutants causing a systolic problem. With sliding force, Ca2+ activatable force decreased in V95A and increased in D175N, which may cause a systolic problem. Our results further demonstrate that the duty ratio determined at the steady state of force generation in saturating [Ca2+] decreased in V95A and increased in D175N. The Ca2+ sensitivity and cooperativity were not significantly affected by the mutations. These results suggest that the two mutants modulate molecular processes of the actomyosin interaction differently, but to result in the same pathology known as HCM.
著者
Hideki Itoh Kotaro Oyama Madoka Suzuki Shin’ichi Ishiwata
出版者
日本生物物理学会
雑誌
BIOPHYSICS (ISSN:13492942)
巻号頁・発行日
vol.10, pp.109-119, 2014 (Released:2014-12-17)
参考文献数
41
被引用文献数
5 7

Temperature-sensitive Ca2+ dynamics occur primarily through transient receptor potential channels, but also by means of Ca2+ channels and pumps on the endoplasmic reticulum membrane. As such, cytoplasmic Ca2+ concentration ([Ca2+]cyt) is re-equilibrated by changes in ambient temperature. The present study investigated the effects of heat pulses (heating duration: 2 s or 150 s) on [Ca2+]cyt in single WI-38 fibroblasts, which are considered as normal cells. We found that Ca2+ burst occurred immediately after short (2 s) heat pulse, which is similar to our previous report on HeLa cells, but with less thermosensitivity. The heat pulses originated from a focused 1455-nm infrared laser light were applied in the vicinity of cells under the optical microscope. Ca2+ bursts induced by the heat pulse were suppressed by treating cells with inhibitors for sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) or inositol trisphosphate receptor (IP3R). Long (150 s) heat pulses also induced Ca2+ bursts after the onset of heating and immediately after re-cooling. Cells were more thermosensitive at physiological (37°C) than at room (25°C) temperature; however, at 37°C, cells were responsive at a higher temperature (ambient temperature+heat pulse). These results strongly suggest that the heat pulse-induced Ca2+ burst is caused by a transient imbalance in Ca2+ flow between SERCA and IP3R, and offer a potential new method for thermally controlling Ca2+-regulated cellular functions.