Researchers Database

Tsuji Ai

    Faculty Division of Human Life and Environmental Sciences Research Group of Food Science and Nutrition Assistant Professor
Last Updated :2021/10/25



  • Doctor of Philosophy

Research Areas

  • Humanities & social sciences, Home economics, lifestyle science

Research Experience

  • Apr. 2019 Mar. - 2021, 神戸学院大学 非常勤講師
  • Apr. 2018, 奈良女子大学 生活環境学部 食物栄養学科・助教
  • Apr. 2019 Mar. - 2020, 神戸常磐大学 非常勤講師
  • Apr. 2017 Mar. - 2018, 辻製菓専門学校 非常勤講師
  • Oct. 2016 Mar. - 2018, 神戸学院大学 栄養学部 食品機能学部門・博士研究員
  • Apr. 2016 Sep. - 2016, 神戸大学 科学技術イノベーション研究科・学術研究員


  • Apr. 2013, Mar. - 2016, 滋賀県立大学大学院, 人間文化学研究科, 生活文化学専攻
  • Apr. 2011, Mar. - 2013, 滋賀県立大学大学院, 人間文化学研究科, 生活文化学専攻
  • Apr. 2007, Mar. - 2011, 滋賀県立大学, 人間文化学部, 生活文化学科 食生活コース

Published Papers

  • Role of tumor suppressor molecules in genomic perturbations and damaged DNA repair involved in the pathogenesis of cancer and neurodegeneration (Review).

    Satoru Matsuda; Mutsumi Murakami; Yuka Ikeda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi

    Genomic perturbations due to inaccurate DNA replication, including inappropriate chromosomal segregation often underlie the development of cancer and neurodegenerative diseases. The incidence of these two diseases increases with age and exhibits an inverse association. Therefore, elderly subjects with cancer exhibit a reduced risk of a neurodegenerative disease, and vice versa. Both of these diseases are associated with aging and share several risk factors. Cells have multiple mechanisms to repair DNA damage and inaccurate replication. Previous studies have demonstrated that tumor suppressor proteins serve a critical role in the DNA damage response, which may result in genomic instability and thus induction of cellular apoptosis. Tumor suppressor genes, such as phosphatase and tensin homologue deleted on chromosome 10 (PTEN), breast cancer susceptibility gene 1 (BRCA1) and TP53 reduce genomic susceptibility to cancer by repairing the damaged DNA. In addition, these genes work cooperatively to ensure the inhibition of the development of several types of cancer. PTEN, BRCA1 and TP53 have been recognized as the most frequently deleted and/or mutated genes in various types of human cancer. Recently, tumor suppressor genes have also been shown to be involved in the development of neurodegenerative diseases. The present review summarizes the recent findings of the functions of these tumor suppressors that are associated with genomic stability, and are involved in carcinogenic and neurodegenerative cell signaling. A summary is presented regarding the interactions of these tumor suppressors with their partners which results in transduction of downstream signals. The implications of these functions for cancer and neurodegenerative disease-associated biology are also highlighted., Spandidos Publications, Sep. 2020, Biomedical reports, 13 (3), 10 - 10, True, doi;pubmed;pmc

    Scientific journal

  • Special bioactive compounds and functional foods may exhibit neuroprotective effects in patients with dementia (Review).

    Mutsumi Murakami; Yuka Ikeda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda

    Dementia is a failure of cognitive ability characterized by severe neurodegeneration in select neural systems, and Alzheimer's disease (AD) is the most common type of neurodegenerative disease. Although numerous studies have provided insights into the pathogenesis of AD, the underlying signaling and molecular pathways mediating the progressive decline of cognitive function remain poorly understood. Recent progress in molecular biology has provided an improved understanding of the importance of molecular pathogenesis of AD, and has proposed an association between DNA repair mechanisms and AD. In particular, the fundamental roles of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and breast cancer gene 1 (BRCA1) tumor suppressors have been shown to regulate the pathogenesis of neurodegeneration. Consequently, onset of neurodegenerative diseases may be deferred with the use of dietary neuroprotective agents which alter the signaling mediated by the aforementioned tumor suppressors. In a healthy neuron, homeostasis of key intracellular molecules is of great importance, and preventing neuronal apoptosis is one of the primary goals of treatments designed for dementia-associated diseases. In the present review, progress into the understanding of dietary regulation for preventing or limiting development of dementia is discussed with a focus on the modulatory roles of PTEN and BRCA1 signaling., Aug. 2020, Biomedical reports, 13 (2), 1 - 1, True, doi;pubmed;pmc

    Scientific journal

  • Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling.

    Yuka Ikeda; Mutsumi Murakami; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda

    Fatty liver disease (FLD) is characterized by accumulation of excess fat in the liver. The underlying molecular mechanism associated with the progression of the disease has been in elusive. Hepatocellular demise due to increased oxidative stress resulting in an inflammatory response may be a key feature in FLD. Recent advances in molecular biology have led to an improved understanding of the molecular pathogenesis, suggesting a critical association between the PI3K/AKT/PTEN signaling pathway and FLD. In particular, PTEN has been associated with regulating the pathogenesis of hepatocyte degeneration. Given the function of mitochondria in reactive oxygen species (ROS) generation and the initiation of oxidative stress, the mitochondrial antioxidant network is of interest. It is vital to balance the activity of intracellular key molecules to maintain a healthy liver. Consequently, onset of FLD may be delayed using dietary protective agents that alter PTEN signaling and reduce ROS levels. The advancement of research on dietary regulation with a focus on modulatory roles in ROS generation and PTEN associated signaling is summarized in the current study, supporting further preventive and therapeutic exploration., Jun. 2020, Biomedical reports, 12 (6), 295 - 302, True, doi;pubmed;pmc

    Scientific journal

  • Effects of Biotin Deficiency on the Urinary Excretion of B-Group Vitamins in Mice

    Tsuji Ai; Tsuji A; Shibata K

    Mar. 2019, J Clin Nutr Metab, 3 (1)

  • Roles of PI3K/AKT/GSK3 Pathway Involved in Psychiatric Illnesses.

    Satoru Matsuda; Yuka Ikeda; Mutsumi Murakami; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi

    Psychiatric illnesses may be qualified to the cellular impairments of the function for survival or death in neurons, which may consequently appear as abnormalities in the neuroplasticity. The molecular mechanism has not been well understood, however, it seems that PI3K, AKT, GSK3, and their downstream molecules have crucial roles in the pathogenesis. Through transducing cell surviving signal, the PI3K/AKT/GSK3 pathway may organize an intracellular central network for the action of the synaptic neuroplasticity. In addition, the pathways may also regulate cell proliferation, cell migration, and apoptosis. Several lines of evidence have supported a role for this signaling network underlying the development and treatment for psychiatric illnesses. Indeed, the discovery of molecular biochemical phenotypes would represent a breakthrough in the research for effective treatment. In this review, we summarize advances on the involvement of the PI3K/AKT/GSK3 pathways in cell signaling of neuronal cells. This study may provide novel insights on the mechanism of mental disorder involved in psychiatric illnesses and would open future opportunity for contributions suggesting new targets for diagnostic and/or therapeutic procedures., 13 Feb. 2019, Diseases (Basel, Switzerland), 7 (1), True, doi;pubmed;pmc

    Scientific journal

  • By using either endogenous or transplanted stem cells, which could you prefer for neural regeneration?

    Satoru Matsuda; Yukie Nakagawa; Kumi Amano; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi

    Oct. 2018, Neural regeneration research, 13 (10), 1731 - 1732, True, doi;pubmed;pmc

    Scientific journal

  • Binding of Catechins to Staphylococcal Enterotoxin A.

    Yuko Shimamura; Mio Utsumi; Chikako Hirai; Shogo Nakano; Sohei Ito; Ai Tsuji; Takeshi Ishii; Takahiro Hosoya; Toshiyuki Kan; Norio Ohashi; Shuichi Masuda

    Staphylococcal enterotoxin A (SEA) is a toxin protein, and is the most common cause of staphylococcal food poisoning. Polyphenols, such as catechins, are known to interact with proteins. In this study, we investigated the binding of catechins to SEA using SPR (Biacore), Fourier transform infrared spectroscopy (FT-IR), isothermal titration calorimetry (ITC), and protein-ligand docking. We found that (−)-epigallocatechin gallate (EGCG) could strongly bind to SEA. According to thermodynamic parameters, a negative ΔG indicated that the interaction between EGCG and SEA was spontaneous, and the electrostatic force accompanied by hydrophobic binding forces may play a major role in the binding. Data from Western blot analysis and docking simulation suggest that the hydroxyl group at position 3 of the galloyl group in the catechin structure was responsible for binding affinity with the Y91 of the A-6 region of SEA active sites. Our results provide further understanding of the binding interactions between catechins and SEA, and the inhibition of toxin activities by catechins., 09 May 2018, Molecules (Basel, Switzerland), 23 (5), True, doi;pubmed;pmc

    Scientific journal

  • Implications of PI3K/AKT/PTEN Signaling on Superoxide Dismutases Expression and in the Pathogenesis of Alzheimer's Disease.

    Satoru Matsuda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Atsuko Nakanishi; Toshiyuki Murai

    Alzheimer’s disease is a neurodegenerative sickness, where the speed of personal disease progression differs prominently due to genetic and environmental factors such as life style. Alzheimer’s disease is described by the construction of neuronal plaques and neurofibrillary tangles composed of phosphorylated tau protein. Mitochondrial dysfunction may be a noticeable feature of Alzheimer’s disease and increased production of reactive oxygen species has long been described. Superoxide dismutases (SODs) protect from excess reactive oxygen species to form less reactive hydrogen peroxide. It is suggested that SODs can play a protective role in neurodegeneration. In addition, PI3K/AKT pathway has been shown to play a critical role on the neuroprotection and inhibiting apoptosis via the enhancing expression of the SODs. This pathway appears to be crucial in Alzheimer’s disease because it is related to the tau protein hyper-phosphorylation. Dietary supplementation of several ordinary compounds may provide a novel therapeutic approach to brain disorders by modulating the function of the PI3K/AKT pathway. Understanding these systems may offer a better efficacy of new therapeutic approaches. In this review, we summarize recent progresses on the involvement of the SODs and PI3K/AKT pathway in neuroprotective signaling against Alzheimer’s disease., 20 Apr. 2018, Diseases (Basel, Switzerland), 6 (2), True, doi;pubmed;pmc

  • Effects of Mild and Severe Vitamin B1 Deficiencies on the Meiotic Maturation of Mice Oocytes.

    Ai Tsuji; Toshinobu Nakamura; Katsumi Shibata

    We investigated the effects of vitamin B1 deficiency on the meiosis maturation of oocytes. Female Crl:CD1 (ICR) mice were fed a 20% casein diet (control group) or a vitamin B1-free diet (test group). The vitamin B1 concentration in ovary was approximately 30% lower in the test group than in the control group. Oocyte meiosis was not affected by vitamin B1 deficiency when the deficiency was not accompanied by body weight loss. On the contrary, frequency of abnormal oocyte was increased by vitamin B1 deficiency when deficiency was accompanied by body weight loss (referred to as severe vitamin B1 deficiency; frequency of abnormal oocyte, 13.8% vs 43.7%, P = .0071). The frequency of abnormal oocytes was decreased by refeeding of a vitamin B1-containing diet (13.9% vs 22.9%, P = .503). These results suggest that severe vitamin B1 deficiency inhibited meiotic maturation of oocytes but did not damage immature oocytes., 2017, Nutrition and metabolic insights, 10, 1178638817693824 - 1178638817693824, True, doi;pubmed;pmc

  • High-dose thiamine prevents brain lesions and prolongs survival of Slc19a3-deficient mice.

    Kaoru Suzuki; Kenichiro Yamada; Yayoi Fukuhara; Ai Tsuji; Katsumi Shibata; Nobuaki Wakamatsu

    SLC19A3 deficiency, also called thiamine metabolism dysfunction syndrome-2 (THMD2; OMIM 607483), is an autosomal recessive neurodegenerative disorder caused by mutations in SLC19A3, the gene encoding thiamine transporter 2. To investigate the molecular mechanisms of neurodegeneration in SLC19A3 deficiency and whether administration of high-dose thiamine prevents neurodegeneration, we generated homozygous Slc19a3 E314Q knock-in (KI) mice harboring the mutation corresponding to the human SLC19A3 E320Q, which is associated with the severe form of THMD2. Homozygous KI mice and previously reported homozygous Slc19a3 knock-out (KO) mice fed a thiamine-restricted diet (thiamine: 0.60 mg/100 g food) died within 30 and 12 days, respectively, with dramatically decreased thiamine concentration in the blood and brain, acute neurodegeneration, and astrogliosis in the submedial nucleus of the thalamus and ventral anterior-lateral complex of the thalamus. These findings may bear some features of thiamine-deficient mice generated by pyrithiamine injection and a thiamine-deficient diet, suggesting that the primary cause of THMD2 could be thiamine pyrophosphate (TPP) deficiency. Next, we analyzed the therapeutic effects of high-dose thiamine treatment. When the diet was reverted to a conventional diet (thiamine: 1.71 mg/100 g food) after thiamine restriction, all homozygous KO mice died. In contrast, when the diet was changed to a high-thiamine diet (thiamine: 8.50 mg/100 g food) after thiamine restriction, more than half of homozygous KO mice survived, without progression of brain lesions. Unexpectedly, when the high-thiamine diet of recovered mice was reverted to a conventional diet, some homozygous KO mice died. These results showed that acute neurodegeneration caused by thiamine deficiency is preventable in most parts, and prompt high-dose thiamine administration is critical for the treatment of THMD2. However, reduction of thiamine should be performed carefully to prevent recurrence after recovery of the disease., 2017, PloS one, 12 (6), e0180279, True, doi;pubmed;pmc

  • Folic Acid Deficiency Does Not Adversely Affect Oocyte Meiosis in Mice.

    Ai Tsuji; Rina Noguchi; Toshinobu Nakamura; Katsumi Shibata

    Spindle defect and chromosome misalignment occuring in oocyte meiosis induce nondisjunction. Nondisjunction causes Down syndrome, also known as trisomy 21. Folic acid (FA) is an essential nutrient composition for fetal growth and development. It has been reported that FA nutritional status is associated with the risk of Down syndrome. However, to our knowledge, little is known about the effect of FA deficiency on abnormal oocytes (spindle defects, chromosome misalignments and immature oocyte) in vivo. In the present study, we investigate the effects of FA deficiency on oocyte meiosis in female mice. In order to induce FA deficiency in mice, female Crl:CD1 mice were fed a FA-free diet for 58 d. The diet also contained an antibiotic which has functions on limiting FA formation by intestinal microorganisms. The level of FA deficiency was determined by measuring the concentration of FA in the liver, hemocyte, uterus, ovary, and urine. FA concentrations in these samples from the FA-deficient group were 50-90% lower. Despite this, the frequency of abnormal oocytes was no different between the FA-deficient and control groups (20.0% vs 14.6%). According to the past research, FA transporter was strongly expressed in oocytes. Hence, it is possible that FA-free diets may not affect the concentration of oocyte FA in mice. To sum up these data, our study concluded that FA deficiency did not adversely affect oocyte meiosis., 2016, Journal of nutritional science and vitaminology, 62 (6), 375 - 379, False, doi;pubmed

  • Biotin-deficient diet induces chromosome misalignment and spindle defects in mouse oocytes.

    Ai Tsuji; Toshinobu Nakamura; Katsumi Shibata

    Increased abnormal oocytes due to meiotic chromosome misalignment and spindle defects lead to elevated rates of infertility, miscarriage, and trisomic conceptions. Here, we investigated the effect of biotin deficiency on oocyte quality. Three-week-old female ICR mice were fed a biotin-deficient or control diet (0, 0.004 g biotin/kg diet) for 21 days. On day 22, these mouse oocytes were analyzed by immunofluorescence. Due to biotin, undernutrition increased the frequency of abnormal oocytes (the biotin deficient vs. control: 40 vs. 16%). Next, the remaining mice in the biotin-deficient group were fed a control or biotin-deficient diet from day 22 to 42. Although biotin nutritional status in the recovery group was restored, the frequency of abnormal oocytes in the recovery group was still higher than that in the control group (48 vs. 18%). Our results indicate that steady, sufficient biotin intake is required for the production of high-quality oocytes in mice., 2015, Bioscience, biotechnology, and biochemistry, 79 (2), 292 - 9, True, doi;pubmed

  • Effects of Fatty Liver Induced by Excess Orotic Acid on B-Group Vitamin Concentrations of Liver, Blood, and Urine in Rats.

    Katsumi Shibata; Nobuya Morita; Tomoyo Kawamura; Ai Tsuji; Tsutomu Fukuwatari

    Fatty liver is caused when rats are given orotic acid of the pyrimidine base in large quantities. The lack of B-group vitamins suppresses the biosynthesis of fatty acids. We investigated how orotic acid-induced fatty liver affects the concentrations of liver, blood, and urine B-group vitamins in rats. The vitamin B6 and B12 concentrations of liver, blood, and urine were not affected by orotic acid-induced fatty liver. Vitamin B2 was measured only in the urine, but was unchanged. The liver, blood, and urine concentrations of niacin and its metabolites fell dramatically. Niacin and its metabolites in the liver, blood, and urine were affected as expected. Although the concentrations of vitamin B1, pantothenic acid, folate, and biotin in liver and blood were decreased by orotic acid-induced fatty liver, these urinary excretion amounts showed a specific pattern toward increase. Generally, as for the typical urinary excretion of B-group vitamins, these are excreted when the body is saturated. However, the ability to sustain vitamin B1, pantothenic acid, folate, and biotin decreased in fatty liver, which is hypothesized as a specific phenomenon. This metabolic response might occur to prevent an abnormally increased biosynthesis of fatty acids by orotic acid., 2015, Journal of nutritional science and vitaminology, 61 (5), 355 - 61, False, doi;pubmed

  • L-tryptophan metabolism in pregnant mice fed a high L-tryptophan diet and the effect on maternal, placental, and fetal growth.

    Ai Tsuji; Chifumi Nakata; Mitsue Sano; Tsutomu Fukuwatari; Katsumi Shibata

    Excess L-tryptophan (L-Trp) in the diet decreases fetal body weight. However, the relationship between L-Trp concentration and its effects on maternal, placental, and fetal growth are not well-understood. We investigated the effects of excess L-Trp intake on maternal, placental, and fetal growth. Female mice were fed a 20% casein diet (control diet) or control diet plus 2% or 5% L-Trp during gestation. Pup weights did not differ between the control (L-Trp intake: 0.04 g/kg body weight (BW)/day) and 2% L-Trp groups (L-Trp intake: 3.3 g/kg BW/day), but were significantly lower in the 5% L-Trp group (L-Trp intake: 7.0 g/kg BW/day) than in the control and 2% L-Trp groups. These results show that less than 3.3 g/kg BW/day L-Trp intake in pregnant mice during gestation does not affect fetal growth or L-Trp homeostasis in the placenta or fetus., 2013, International journal of tryptophan research : IJTR, 6, 21 - 33, True, doi;pubmed;pmc

  • Save Children from Mortal Shock of COVID-19

    Satoru Matsuda; Yuka Ikeda; Mutsumi Murakami; Ai Tsuji

    2020, Journal of Advances in Medicine and Medical Research, 32 (8), 23 - 25

    Scientific journal

  • Gut in Mind!

    Behavioral Health Forecast

    2020, Journal of Psychiatry and Behavioral Health Forecast, 3 (1), 1 - 2

    Scientific journal

  • COVID-19, an infertility risk?

    Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Satoru Matsuda

    2020, Clinical Obstetrics, Gynecology and Reproductive Medicine, 6, 1

    Scientific journal

  • Prevention in Daily Life against Progression of COVID-19.

    Mutsumi Murakami; Yuka Ikeda; Ai Tsuji; Satoru Matsuda

    2020, International journal of preventive medicine, 11, 99 - 99, True, doi;pubmed;pmc

    Scientific journal

  • d-Leucine protects oocytes from chronic psychological stress in mice.

    Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Yasuko Kitagishi; Satoru Matsuda

    Purpose: Psychological stress could negatively influence female reproductive ability. d-Leucine (d-Leu) is a d-type amino acid found in foods and mammalian tissues. We have examined the protective effects of d-Leu on oocyte abnormality induced by psychological stress. Methods: Female mice (6-week-old) were divided into three groups: control, restraint stress (RS), and RS/d-Leu. The RS and RS/d-Leu mice were holed for 3 hours daily during 14 days. RS/d-Leu mice were fed 0.3% d-Leu diet. The oocyte maturation failure was analyzed by shapes of spindles and chromosomes. In addition, levels of heme-oxygenase-1 (HO-1) and superoxide dismutase (SOD) expression in the ovaries were also examined. Whether d-Leu reduces the generation of reactive oxygen species (ROS) in cultured cells, K562 cells were treated with d-Leu, and then ROS in K562 were analyzed. Results: Oocyte maturation failure was increased in RS mice. d-Leu reduced abnormal oocytes to control level. The expression levels of HO-1 and SOD2 increased in RS/d-Leu mice compared to those of RS mice. ROS levels were decreased in K562 cells with d-Leu in a dose-dependent manner. Conclusions: We concluded that d-Leu protects oocytes from psychological stress through the induction of HO-1 and SOD2 expression then by reducing oxidative stress., Oct. 2021, Reproductive medicine and biology, 20 (4), 477 - 484, False, doi;pubmed;pmc

    Scientific journal


  • Novel mechanism responsible for regulation of branched-chain alpha-ketoacid dehydrogenase kinase

    Yoshiharu Shimomura; Yusuke Kondo; Rina Ito; Ai Tsuji; Katsumi Shibata; Yasuyuki Kitaura

    FEDERATION AMER SOC EXP BIOL, Apr. 2016, FASEB JOURNAL, 30, web_of_science

    Summary international conference

  • ビタミン欠乏が卵母細胞の質におよぼす影響

    辻愛; 中村肇伸; 柴田克己

    2017, 日本農芸化学会大会講演要旨集(Web), 2017, j_global

  • 低葉酸栄養状態では卵子の質は劣化しない

    辻愛; 野口里奈; 中村肇伸; 柴田克己

    2016, 日本栄養・食糧学会大会講演要旨集, 70th, j_global

  • Vitamin B1栄養が卵子の質におよぼす影響

    辻愛; 中村肇伸; 柴田克己

    2015, 日本栄養・食糧学会近畿支部大会および公開シンポジウム講演抄録集, 54th, j_global

  • マウスにおけるビオチン欠乏は卵子の染色体および紡錘体形成異常を増加させる

    柴田克己; 辻愛; 中村肇伸

    2015, ビタミン, 89 (8), j_global


  • ビオチン欠乏および再摂取が卵子中脂肪滴、卵巣中脂質代謝におよぼす影響

    辻 愛; 樺澤 理紗子; 池田 祐香; 中川 友希江; 村上 睦美; 北岸 靖子; 松田 覚

    第93回日本生化学会, Sep. 2020

  • 慢性的心因性ストレスの生体への影響とその保護に働く食品成分

    池田 祐香; 村上 睦美; 北岸 靖子; 辻 愛; 松田 覚

    第93回日本生化学会, Sep. 2020

  • ビオチン欠乏による減数分裂異常とその要因の解明

    第92回日本生化学会(横浜), 19 Sep. 2019

  • 脂質代謝に関与する食成分が卵子の健康に及ぼす影響

    、第92回日本生化学会(横浜), 19 Sep. 2019

  • 非アルコール性脂肪性肝疾患(NAFLD)におけるD-Trp摂取の影響

    第92回日本生化学会(横浜), 18 Sep. 2019

  • ビオチン欠乏食が尿中水溶性ビタミン排泄量に及ぼす影響

    Tsuji Ai; Ai Tsuji; Katsumi Shiabta

    第57回日本栄養・食糧学会 近畿支部大会, Dec. 2018, 畿央大学(奈良)

  • オウバク成分は非アルコール性脂肪肝疾患(NAFLD)改善に関与するか?

    Tsuji Ai

    第91回日本生化学会大会, Sep. 2018, 京都

  • 脂肪性肝障害に対する少量アセトアルデヒド摂取の影響

    Tsuji Ai

    第91回日本生化学会大会, Sep. 2018

  • 渋味を呈するポリフェノールの分子特性解析

    Tsuji Ai

    日本農芸化学会2018年度大会, 2018

  • ウーロンホモビスフラバン類の消化管タンパク質に対する強力な修飾作用

    Tsuji Ai

    第 22回日本フードファクター学会学術集会, 2017

  • ビタミン欠乏が卵母細胞の質におよぼす影響

    Tsuji Ai

    日本農芸化学会2017年度大会, 2017

  • フラボノイドの分子会合に寄与する構造特性

    Tsuji Ai

    日本農芸化学会2017年度大会, 2017

  • 日本ヨモギエタノール抽出物が糖尿病モデルマウスにおよぼす影響

    Tsuji Ai

    第496回日本農芸化学会 近畿支部大会, 2016

  • 低葉酸栄養状態では卵子の質は劣化しない

    Tsuji Ai

    第70回日本栄養・食糧学会大会, 2016

  • L-Tryptophan metabolism in pregnant mice fed a high L-tryptophan diet and the effect on maternal, placental, and fetal growth.

    Tsuji Ai

    ISTRY 2015, 2015

  • マウスにおけるビオチン欠乏は卵子の質を劣化させる

    Tsuji Ai

    第13回 日本栄養改善学会近畿支部学術総会, 2014

  • ストレス保護に関与する食品成分の検討

    池田祐香; 岡本恵実; 宮原朋佳; 中川友希江; 村上睦美; 辻愛; 北岸靖子; 松田 覚

    第74回日本栄養・食糧学会, 2020, 2020, rm:research_project_id

  • Lipid droplets in oocyte were decreased by biotin-deficiency.

    辻愛; 樺澤理紗子; 池田祐香; 中川友希江; 村上睦美; 北岸靖子; 松田覚

    第74回日本栄養・食糧学会, 2020, 2020, rm:research_project_id

Association Memberships

  • 日本栄養・食糧学会

  • 日本栄養改善学会

  • 農芸化学会

  • 日本フードファクター学会

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