Kyoko iwasaki biography sampler
Age-related change in mammographic breast density of women without history of breast cancer over a 10-year retrospective study
Introduction
In Japan, the incidence rate of breast cancer has increased year by year (Katanoda et al., 2021), whereas the mortality rate has tended to level off since 2010. This contrasts with Western countries, where the mortality rate has leveled off or decreased since 2000 (Henley et al., 2020; Huang et al., 2021). Effective prevention of breast cancer is to identify women at increased risk. Although age, family history, reproductive factors, estrogen and lifestyle are established risk factors for breast cancer (Britt, Cuzick & Phillips, 2020), breast density has especially attracted attention. Globally, research on dense breasts began in the 1970s (Wolfe, 1976; Wolfe, 1977), and numerous studies have been reported since the 1990s (Boyd et al., 1998; Warner et al., 1992; Szklo, Salane & Wolfe, 1991). In Japan, there has been a high level of interest in dense breasts since around 2016 with the enactment of the Breast Density Notification Law in the US (Kasahara, 2019).
Breast densities fall into four categories by the ratio of mammary glands to fat in the breast tissue. The definition of a dense breast in Japan is a breast that is classified as Category 3 (heterogeneously dense) or Category 4 (extremely dense) according to the four breast density categories defined by the Breast Imaging Reporting and Data System (BI-RADS) (Mendelson, 2003; Japan Radiological Society & Japanese Society of Radiological Technology, 2021). Dense breast is known to increase the risk of breast cancer and decrease the detection rate of lesions on mammographic images (Boyd et al., 2007; Kerlikowske et al., 2007; Wong et al., 2011). The case-control studies on dense breasts have been conducted in Japan, and a trend toward an increased risk of developing the disease has been reported (Nagata et al., 2005; Kotsuma et al., 2008; Nishiyama et al., Pharmacogenomic/pharmacokinetic assessment of a four-probe cocktail for CYPs and OATPs following oral microdosing DOI 10.5414/CP201763 We have previously shown that a 28-amino acid peptide derived from the BRC4 motif of BRCA2 tumor suppressor inhibits selectively human RAD51 recombinase (HsRad51). With the aim of designing better inhibitors for cancer treatment, we combined an in silico docking approach with in vitro biochemical testing to construct a highly efficient chimera peptide from eight existing human BRC motifs. We built a molecular model of all BRC motifs complexed with HsRad51 based on the crystal structure of the BRC4 motif-HsRad51 complex, computed the interaction energy of each residue in each BRC motif, and selected the best amino acid residue at each binding position. This analysis enabled us to propose four amino acid substitutions in the BRC4 motif. Three of these increased the inhibitory effect in vitro, and this effect was found to be additive. We thus obtained a peptide that is about 10 times more efficient in inhibiting HsRad51−ssDNA complex formation than the original peptide. The human RAD51 protein (HsRad51a) is crucial for DNA repair processes that are based on homologous recombination between damaged loci and their undamaged copies in sister chromatids. The protein is thus involved in the repair of a double-stranded break, the most severe DNA damage. Efficient DNA repair is usually beneficial for living organisms. However, in the case of cancer cells, their efficient DNA repair opposes the action of radio- and chemotherapies based on DNA damaging agents. Rad51 is often overexpressed in cancer cells, and its cellular amount is correlated in some way to resistance to anticancer treatment and to the degree of cancer advancement. Rad51 is thus a potential target for cancer treatment. In fact, inhibiting the cellular expression of Rad51 directly by antisense or siRNA or indirectly by affecting the regulatory protein is found to slow down tumor development and increase survival time in mice besides increasing the efficiency of radio Task force talk/archives Related talk/archives Can anyone substantiate or refute the kanji-etymology related claim here. It would be especially helpful if someone would post the alleged pre-modernization version of the kanji 鬼. I would have assumed that if there was a kyūjitai version of 鬼 it would be noted in its wiktionary entry, which led me to doubt the claim. Thank you, Bradford4413:00, 2 October 2007 (UTC) Ok, I was bored at work, so I went roving throught the Kukishinryu page. Here's the part in Japanese, corresponding to the claim: The same part in English from the same site: Int. Journal of Clinical Pharmacology and Therapeutics, Volume 50 - October (689 - 700)
Ichiro Ieiri, Masato Fukae, Kazuya Maeda, Yukie Ando, Miyuki Kimura, Takeshi Hirota, Takeshi Nakamura, Kazuhide Iwasaki, Shunji Matsuki, Kyoko Matsuguma, Eri Kanda, Mariko Deguchi, Shin Irie, Yuichi Sugiyama
Department of Clinical Pharmacokinetics, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Laboratory of Molecular Pharmacokinetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Kyushu Clinical Pharmacology Research Clinic, Fukuoka, and Business Development Division, Contract Research Company, Shin Nippon Biomedical Laboratories, Ltd, Osaka, Japan Abstract
Objectives: To test whether the multiple phenotype and genotype relationships established using therapeutic dose, can be reproduced following oral microdosing using substrates of CYP2C9 (warfarin and glibenclamide), CYP2C19 (lansoprazole), CYP2D6 (dextromethorphan), and OATPs (glibenclamide). Methods: A cocktail of test drugs was administered orally under the microdose in liquid or capsule form, and then a therapeutic dose of dextromethorphan was administered to 17 healthy subjects whose genotypes for CYPs and OATPs had been prescreened. Concentrations of the drugs and their metabolites were measured by LC-MS/MS. Results: The AUC and t1/2 of glibenclamide following the microdosing tended to be higher and longer, respectively, in CYP2C9*1/*3 than CYP2C9*1/*1 subjects. In contrast, there were no significant differences in any of the pharmacokinetic parameters for warfarin between the two genotypes. For CYP2D6 following the therapeutic dose, there was good concordance between genotype and phenotype; however, such relat Abstract
Introduction
Wikipedia talk:WikiProject Japan/Archive/October 2007
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