Tokushima University / Educator and Researcher Directory --- Sakurai, Akiko

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Academic Paper (Judged Full Paper):

1.	Akiko Sakurai, Hiroyuki Ono, Arisa Ochi, Motokazu Matsuura, Sakiya Yoshimoto, Seiji Kishi, Taichi Murakami, Tatsuya Tominaga, Kojiro Nagai, Hideharu Abe and Toshio Doi : Involvement of Elf3 on Smad3 activation-dependent injuries in podocytes and excretion of urinary exosome in diabetic nephropathy., PLoS ONE, Vol.14, No.5, 2019. (Summary) Diabetic nephropathy (DN) is among the most serious complications of diabetes mellitus, and often leads to end-stage renal disease ultimately requiring dialysis or renal transplantation. The loss of podocytes has been reported to have a role in the onset and progression of DN. Here, we addressed the activation mechanism of Smad3 signaling in podocytes. Expression of RII and activation of Smad3 were induced by AGE exposure (P<0.05). Reduction of the activation of RII-Smad3 signaling ameliorated podocyte injuries in Smad3-knockout diabetic mice. The bone morphogenetic protein 4 (BMP4) significantly regulated activation of RII-Smad3 signalings (P<0.05). Moreover, the epithelium-specific transcription factor, Elf3was induced by AGE stimulation and, subsequently, upregulated RII expression in cultured podocytes. Induction of Elf3 and activation of RII-Smad3 signaling, leading to a decrease in WT1 expression, were observed in podocytes in diabetic human kidneys. Moreover, AGE treatment induced the secretion of Elf3-containing exosomes from cultured podocytes, which was dependent on the activation of the TGF-β-Smad3 signaling pathway. In addition, exosomal Elf3 protein in urine could be measured only in urinary exosomes from patients with DN. The appearance of urinary exosomal Elf3 protein in patients with DN suggested the existence of irreversible injuries in podocytes. The rate of decline in the estimated Glomerular Filtration Rate (eGFR) after measurement of urinary exosomal Elf3 protein levels in patients with DN (R2 = 0.7259) might be useful as an early non-invasive marker for podocyte injuries in DN. (Tokushima University Institutional Repository) ● Metadata: 114344 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0216788 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31150422 ● Search Scopus @ Elsevier (PMID): 31150422 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0216788 (Tokushima University Institutional Repository: 114344, DOI: 10.1371/journal.pone.0216788, PubMed: 31150422)
2.	Hideharu Abe, Akiko Sakurai and Arisa Ochi : Induction of steady-state glomeruloid sphere by self-assembly from human embryonic kidney cells., Biochemical and Biophysical Research Communications, Vol.508, No.2, 654-659, 2018. (Summary) The glomerulus is a network of capillaries known as a tuft, located at the beginning of a nephron in the kidney. Here we describe a novel method for the induction of a macroscopically visible three-dimensional glomerulus-like sphere (GLS). This procedure did not require any additional cytokines and completed the formation of spheres within 24 h. After the formation was complete, GLS maintained a steady state for at least five days without proliferation and without a decrease in viability. Therefore, this procedure assists various assays for a prolong period of time. Overall, our protocol allows for a very simple mixing of cells from different sources to obtain fine-grained and highly dispersed GLSs. The kidney filtration barrier is a unique structure characterized by a complex three-dimensional framework of podocytes and endothelial cells. GLS exhibited the induction of many podocyte-specific gene profiles similar to those in adult human kidneys, suggesting that the sphere formation process is important for the maturation of podocytes. Focal segmental glomerulosclerosis (FSGS) is one of the major causes of steroid-resistant nephrotic syndrome, and some circulating permeability factors in the patient's serum FSGS have been implicated in the pathogenesis of the disease. Serum from patients with FSGS induced the collapse of GLS, which imitates the appearance of glomerulosclerosis in patients. In conclusion, the investigation and use of GLS may provide a novel method to elucidate the molecular mechanisms underlying complicated and unexplained events in glomeruli in a similar condition in adult kidneys. (Keyword) Cells, Cultured / Glomerulosclerosis, Focal Segmental / Humans / Kidney Glomerulus (Tokushima University Institutional Repository) ● Metadata: 115014 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2018.11.160 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30522864 ● Search Scopus @ Elsevier (PMID): 30522864 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2018.11.160 (Tokushima University Institutional Repository: 115014, DOI: 10.1016/j.bbrc.2018.11.160, PubMed: 30522864)
3.	Hideharu Abe, Akiko Sakurai, Hiroyuki Ono, Sanae Hayashi, Sakiya Yoshimoto, Arisa Ochi, Sayo Ueda, Kenji Nishimura, Eriko Shibata, Masanori Tamaki, Fumi Kishi, Seiji Kishi, Taichi Murakami, Kojiro Nagai and Toshio Doi : Urinary Exosomal mRNA of WT1 as Diagnostic and Prognostic Biomarker for Diabetic Nephropathy, The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 208-215, 2018. (Summary) Diabetic nephropathy (DN) is the major cause of end-stage renal failure and is associated with increased morbidity and mortality as compared to other causes of renal disease. Albuminuria is often the first clinical indicator of the presence of DN. However, albuminuria or proteinuria is a common symptom in patients with various renal disorders. Therefore, specific biomarkers for the diagnosis of DN are required. A primary hallmark of DN is the progressive damage and death of glomerular podocytes, resulting in the leaking of proteins into the urine. Urinary exosomes released by podocytes are microvesicles containing information of the originated cells. Podocyte-derived signal transduction factors (PDSTFs) are good candidates to assess podocyte injuries. The profile of PDSTFs in urinary exosomes from patients with DN is different from that from patients with minimal change nehrotic syndrome. In addition, PDSTFs molecules in exosomes were derived from primary murine podocytes under high glucose conditions. Among PDSTFs in urinary exosomes, Wilms tumor 1 (WT1) levels reflected damage of diabetic glomeruli in the patients. Urinary exosomal WT1 can predict the decline in eGFR for the following several years. In conclusion, urinary exosomal WT1 is a useful biomarker to improve risk stratification in patients with DN. J. Med. Invest. 65:208-215, August, 2018. (Keyword) Adolescent / Adult / Biomarkers / Case-Control Studies / Cells, Cultured / Diabetic Nephropathies / Exosomes / Genes, Wilms Tumor / Genetic Markers / Humans / Middle Aged / Nephrosis, Lipoid / Podocytes / Prognosis / RNA, Messenger / WT1 Proteins / Young Adult (Tokushima University Institutional Repository) ● Metadata: 112239 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.208 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282862 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054429444 (Tokushima University Institutional Repository: 112239, DOI: 10.2152/jmi.65.208, PubMed: 30282862, Elsevier: Scopus)
4.	Hiroyuki Ono, Hideharu Abe, Akiko Sakurai, Arisa Ochi, Tatsuya Tominaga, Masanori Tamaki, Seiji Kishi, Taichi Murakami, Kojiro Nagai, Masayuki Kohashi and Toshio Doi : Novel Interplay Between Smad1 and Smad3 Phosphorylation via AGE Regulates the Progression of Diabetic Nephropathy., Scientific Reports, Vol.8, No.1, 2018. (Summary) ; db/db mice and probucol-treated db/db mice, which was consistent with the attenuation of ECM overproduction. These results indicate that Smad3 expression and activation or probucol treatment alters Smad1 phosphorylation, thus suggesting new molecular mechanisms underlying DN development and progression. (Tokushima University Institutional Repository) ● Metadata: 112878 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-018-28439-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30002389 ● Search Scopus @ Elsevier (PMID): 30002389 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-28439-1 (Tokushima University Institutional Repository: 112878, DOI: 10.1038/s41598-018-28439-1, PubMed: 30002389)
5.	Hideharu Abe, Akiko Sakurai and Toshio Doi : Probucol modulates Nrf2 function and ameliorates diabetic nephropathy in db/db mice., Medical Research Archives, Vol.10, No.4, 1-16, 2017. (Link to Publication Site) ● Publication site (DOI): 10.18103/mra.v4i8.935 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.18103/mra.v4i8.935 (DOI: 10.18103/mra.v4i8.935)
6.	Motokazu Matsuura, Hideharu Abe, Tatsuya Tominaga, Akiko Sakurai, Taichi Murakami, Seiji Kishi, Yoshimi Bando, Jun Minakuchi, Kojiro Nagai and Toshio Doi : A Novel Method of DAPI Staining for Differential Diagnosis of Renal Amyloidosis., The Journal of Medical Investigation : JMI, Vol.64, No.3.4, 217-221, 2017. (Summary) Amyloidosis is often overlooked because its clinical manifestations can mimic those of more-common diseases. It is important to get a precise diagnosis as early as possible for the prevention of further organ damages. Amyloidosis is a disorder caused by deposition of insoluble abnormal amyloid. The kidney is a frequent site of amyloid deposition. The amyloid fibrils have a characteristic appearance and generate birefringence under polarized light when stained with the Congo red dye. Classification of amyloidosis is based on the precursor protein that forms the amyloid fibrils and the distribution of amyloid deposits as either systemic or localized. Involvement of amyloid fibrils in kidneys mainly occurs as amyloid light-chain (AL) or amyloid A (AA) amyloidosis. The potassium permanganate method with Congo red staining was once used widely to discriminate AL and AA amyloidoses, but this method has a problem of false positive results. We found that extracellular and cytoplasmic glomerular 4', 6-diamidino-2-phenylindole (DAPI)-positive areas were clearly consistent with amyloid deposition in AL amyloidosis. In contrast, the overlapping staining was not seen in AA amyloidosis. Therefore, we propose that DAPI staining readily distinguishes AL renal amyloidosis from AA renal amyloidosis as a simple and reproducible histochemical method. J. Med. Invest. 64: 217-221, August, 2017. (Keyword) Amyloidosis / Kidney Diseases / Serum Amyloid A Protein / Staining and Labeling (Tokushima University Institutional Repository) ● Metadata: 111119 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.217 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954985 ● Search Scopus @ Elsevier (PMID): 28954985 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.217 (Tokushima University Institutional Repository: 111119, DOI: 10.2152/jmi.64.217, PubMed: 28954985)
7.	Takahiro Hirano, Taichi Murakami, Hiroyuki Ono, Akiko Sakurai, Tatsuya Tominaga, Toshikazu Takahashi, Kojiro Nagai, Toshio Doi and Hideharu Abe : A Novel Interaction between FLICE-Associated Huge Protein (FLASH) and E2A Regulates Cell Proliferation and Cellular Senescence via Tumor Necrosis Factor (TNF)-Alpha-p21WAF1/CIP1 Axis., PLoS ONE, Vol.10, No.7, e0133205, 2015. (Summary) Dysregulation of the cell proliferation has been implicated in the pathophysiology of a number of diseases. Cellular senescence limits proliferation of cancer cells, preventing tumorigenesis and restricting tissue damage. However, the role of cellular senescence in proliferative nephritis has not been determined. The proliferative peak in experimental rat nephritis coincided with a peak in E2A expression in the glomeruli. Meanwhile, E12 (an E2A-encoded transcription factor) did not promote proliferation of Mesangial cells (MCs) by itself. We identified caspase-8-binding protein FLICE-associated huge protein (FLASH) as a novel E2A-binding partner by using a yeast two-hybrid screening. Knockdown of FLASH suppressed proliferation of MCs. This inhibitory effect was partially reversed by the knockdown of E2A. In addition, the knockdown of FLASH induced cyclin-dependent kinase inhibitor p21WAF1/CIP1 (p21) expression, but did not affect p53 expression. Furthermore, overexpression of E12 and E47 induced p21, but not p53 in MCs, in the absence of FLASH. We also demonstrated that E2A and p21 expression at the peak of proliferation was followed by significant induction of FLASH in mesangial areas in rat proliferative glomerulonephritis. Moreover, we revealed that FLASH negatively regulates cellular senescence via the interaction with E12. We also demonstrated that FLASH is involved in the TNF--induced p21 expressions. These results suggest that the functional interaction of E2A and FLASH play an important role in cell proliferation and cellular senescence via regulation of p21 expression in experimental glomerulonephritis. (Tokushima University Institutional Repository) ● Metadata: 114923 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0133205 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26208142 ● Summary page in Scopus @ Elsevier: 2-s2.0-84941908247 (Tokushima University Institutional Repository: 114923, DOI: 10.1371/journal.pone.0133205, PubMed: 26208142, Elsevier: Scopus)

Academic Paper (Unrefereed Paper):

1.	Keiko Kataoka, Hideyuki Nemmoto, Akiko Sakurai, Koji Yasutomo and Masataka Shikanai : Preventive effect of fermented brown rice and rice bran on spontaneous type 1 diabetes in NOD female mice, Journal of Functional Foods, Vol.78, 104356, 2021. (Tokushima University Institutional Repository) ● Metadata: 116549 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jff.2021.104356 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85099455517 (Tokushima University Institutional Repository: 116549, DOI: 10.1016/j.jff.2021.104356, Elsevier: Scopus)

Proceeding of International Conference:

1.	Misato Moriki, Akiko Sakurai and Keiko Kataoka : High-fat high-sucrose diet induced fatty liver disease and gut microbiota in obese mice., Technological Competency as Caring in the Health Sciences (2018), Aug. 2018. (Keyword) gut microbiota / culture-independent analysis / obecity / non-alcoholic fatty liver disease / high-fat high-sucrose diet

Proceeding of Domestic Conference:

1.	Sayuko Kagawa, ISHIKAWA Ryuji, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : 出生後の児の便中細菌叢および有機酸濃度の経時的変化と影響要因, 第96回日本細菌学会総会, Mar. 2023.
2.	Masanobu Miyashiro, RYUYA Wakabayashi, Akiko Sakurai and Tatsuya Tominaga : 腎脂質代謝異常とERストレスの作用機序について「ApoE欠損動脈硬化症モデルマウスでの検討」, 第46回徳島県医学検査学会, Dec. 2022.
3.	Miku Shimomura, Himari Usuki, Sayuko Kagawa, ISHIKAWA Ryuji, Akiko Sakurai and Keiko Kataoka : 食餌誘導性NASHモデルマウスの腸内細菌叢の16Sメタゲノム解析の試み, 第46回徳島県医学検査学会, Dec. 2022.
4.	Sayuko Kagawa, Miku Shimomura, Himari Usuki, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : ヒトの腸内細菌叢の形成過程における腸内環境の変化, 第46回徳島県医学検査学会, Dec. 2022.
5.	Himari Usuki, Miku Shimomura, Sayuko Kagawa, Akiko Sakurai and Keiko Kataoka : 高脂肪特殊飼料摂取におけるNASHモデルマウス肝臓組織の線維化・炎症関連遺伝子発現レベルの検討, 第46回徳島県医学検査学会, Dec. 2022.
6.	越智ありさ, Akiko Sakurai, 太田浩二, 飛永恭兵, RYUYA Wakabayashi, Shu Wakino, Koichi Ute and Tatsuya Tominaga : A new purification method for exosome, using highly water-absorbing polymer., 第45回日本分子生物学会年会, Dec. 2022.
7.	RYUYA Wakabayashi, Akiko Sakurai, 越智ありさ and Tatsuya Tominaga : 腎硬化症における小胞体ストレス分子メカニズムの解析, 第45回日本分子生物学会年会, Dec. 2022.
8.	RYUYA Wakabayashi, Akiko Sakurai, 越智ありさ and Tatsuya Tominaga : 小胞体ストレス誘導下における腎線維化とBMP4/CHOPの機能解析, 第95回日本生化学会大会, Nov. 2022.
9.	松田修己, 東野乃, 田中莉乃, Akiko Sakurai and Keiko Kataoka : NASHモデルマウスにおける幼若期の抗菌薬暴露が腸内環境に及ぼす影響, 第95回日本細菌学会総会, Mar. 2022.
10.	SATOH Tomomi, Yuka Hiroshima, Akikazu Murakami, Hideki Fujii, Akiko Sakurai, Keiko Kataoka and Keiji Murakami : カタラーゼをコードするkatA/katB遺伝子が及ぼす緑膿菌の抗菌薬抵抗性における影響, 第45回徳島県医学検査学会, Dec. 2021.
11.	Rino Tanaka, Yoshimi Matsuda, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : ヒトの腸内細菌叢の形成過程における菌叢構成および便中有機酸濃度の変化について, 第45回徳島県医学検査学会, Dec. 2021.
12.	Yoshimi Matsuda, Rino Tanaka, Nono Higashi, Akiko Sakurai and Keiko Kataoka : NASHモデルマウスにおける離乳までの時期の抗菌薬曝露が腸内環境に及ぼす影響, 第45回徳島県医学検査学会, Dec. 2021.
13.	Ryuya Wakabayashi, Kanako Tamura, Akiko Sakurai and Tatsuya Tominaga : 腎線維化病変発症機序の解析, 第45回徳島県医学検査学会, Dec. 2021.
14.	Kanako Tamura, Ryuya Wakabayashi, Akiko Sakurai and Tatsuya Tominaga : 血管内皮特異的BMP4発現マウスへの高脂肪食負荷による影響について, 第45回徳島県医学検査学会, Dec. 2021.
15.	Nono Higashi, Rino Tanaka, Yoshimi Matsuda, Akiko Sakurai and Keiko Kataoka : 高脂肪特殊飼料摂取におけるNASHモデルマウス肝臓組織の線維化の検討, 第45回徳島県医学検査学会, Dec. 2021.
16.	Nozomi Fujimoto, Miyu Higasa, Akiko Sakurai and Keiko Kataoka : 非アルコール性脂肪肝炎モデルマウスにおける幼若期の抗菌薬暴露の影響, 第94回日本細菌学会総会, Mar. 2021.
17.	Chihiro Yoshimoto, Sonoka Aibara, Teruyuki Nagai, Wako Matsuda, 大西幸代, Tomoyo Hara, 中村信元, Kumiko Kagawa, Hirokazu Miki, Masahiro Abe, Akiko Sakurai, Mai Kanai and Itsuro Endo : 血液悪性腫瘍化学療法入院中の骨格筋量の減少ビタミンD充足との関連, 第44回徳島県医学検査学会, Dec. 2020.
18.	Sonoka Aibara, Teruyuki Nagai, Wako Matsuda, Chihiro Yoshimoto, 大西幸代, Tomoyo Hara, Mai Kanai, Itsuro Endo, Hirokazu Miki and Akiko Sakurai : 多発性骨髄腫に対するゾレドロン酸の治療経験, 第44回徳島県医学検査学会, Dec. 2020.
19.	Wako Matsuda, Sonoka Aibara, Teruyuki Nagai, Chihiro Yoshimoto, 金島慶太, 大西幸代, Tomoyo Hara, Akiko Sakurai, Mai Kanai and Itsuro Endo : 原発性骨粗鬆症におけるビタミンD充足の検討, 第44回徳島県医学検査学会, Dec. 2020.
20.	Makoto Ogasa, Akiko Sakurai, Keiko Kataoka, 越智ありさ and Hideharu Abe : ヒト尿沈渣中のCXC Chemokine Receptor遺伝子発現について, 第44回徳島県医学検査学会, Dec. 2020.
21.	Kiyoe Kurahashi, 村井純平, 堀太貴, Ryohei Sumitani, Takeshi Harada, Shingen Nakamura, Mai Kanai, Akiko Sakurai, 原倫世, 桝田志保, Sumiko Yoshida, Itsuro Endo, 松本俊夫, Masahiro Abe and Seiji Fukumoto : 高1,25(OH)2D血症による高Ca血症を来したホジキンリンパ腫の一例, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 150, Oct. 2020. (Keyword) Calcitriol Dacarbazine(治療的利用) Doxorubicin(治療的利用) Hodgkin病(合併症,病理学,薬物療法) Vinblastine(治療的利用) *高カルシウム血症(病因,病理学,薬物療法) 免疫組織化学 Brentuximab Vedotin(治療的利用) ヒト高齢者(65~79) 男
22.	黒田大智, 水本健斗, Akiko Sakurai, Mai Kanai, 大西幸代, 松岡飛翔 and Itsuro Endo : 鉄剤投与によるFGF23関連低リン血症モデル作成の試み, 第43回徳島県医学検査学会, Dec. 2019.
23.	菊池結愛, 坂井ちか, Akiko Sakurai, Mai Kanai, 大西幸代, Masahiro Abe and Itsuro Endo : TAK1阻害による炎症性サイトカイン誘導性筋萎縮の改善, 第43回徳島県医学検査学会, Dec. 2019.
24.	水本健斗, 菊池結愛, Kiyoe Kurahashi, Akiko Sakurai, Mai Kanai, 大西幸代 and Itsuro Endo : カルシウム感知受容体活性型変異における耐糖能異常, 第43回徳島県医学検査学会, Dec. 2019.
25.	坂井ちか, 菊池結愛, 黒田大智, Akiko Sakurai, Mai Kanai, 大西幸代 and Itsuro Endo : 副腎皮質機能低下症・不全症のカットオフ値設定の試み, 第43回徳島県医学検査学会, Dec. 2019.
26.	Keisuke Teramoto, Nozomi Fujimoto, Rina Murata, Akiko Sakurai and Keiko Kataoka : 高脂肪高ショ糖食の摂取によるマウスの腸内細菌叢の変化とマウス週齢との関連について, 第43回徳島県医学検査学会, Dec. 2019.
27.	Rio Tanaka, Miho Tamaki, Keisuke Teramoto, Nozomi Fujimoto, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : 乳児の腸内細菌叢におけるBifidobacterium属の変動と分娩様式の違いとの関連について, 第43回徳島県医学検査学会, Dec. 2019.
28.	Miho Tamaki, Rio Tanaka, Keisuke Teramoto, Nozomi Fujimoto, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : 出生後1年までの乳児の腸内細菌叢の変化と環境要因の関連について, 第43回徳島県医学検査学会, Dec. 2019.
29.	Eishi Higuchi, Nozomi Fujimoto, Rina Murata, Akiko Sakurai and Keiko Kataoka : 2型糖尿病モデルマウスに対する玄米発酵食品の発症抑制効果-膵臓組織でのインスリンと関連タンパク質の発現量の比較-, 第43回徳島県医学検査学会, Dec. 2019.
30.	越智ありさ, Hideharu Abe and Akiko Sakurai : iPS細胞を用いない，腎臓病治療薬HTPのための腎糸球体スフェロイド開発, 第42回日本分子生物学会年会, Dec. 2019.
31.	Akiko Sakurai, 越智ありさ and Hideharu Abe : ポドサイト障害における尿中バイオマーカーWT1・CXCR4による各種腎疾患の評価, 第66回日本臨床検査医学会学術集会, Nov. 2019.
32.	Keiko Kataoka, Misato Moriki, Akiko Sakurai, Haruyuki Imaohji and Tomomi Kuwahara : Feeding style of high fat high sucrose diet affects gut environment and nonalcoholic fatty liver disease in mice., The 92nd Annual Meeting of Japanese Society for Bacteriology, Apr. 2019.
33.	Arisa Ochi, Akiko Sakurai and Hideharu Abe : iPS/ES細胞を用いない，糸球体スフェロイド作成, 第258回徳島医学会学術集会, Feb. 2019.
34.	木村優里, 高橋寛典, 松島滉海, Akiko Sakurai, Mai Kanai and Itsuro Endo : TAK1阻害による炎症性サイトカイン誘導性サルコペ二ア改善の可能性, 第42回徳島県医学検査学会, Dec. 2018.
35.	Hiromi Matsushima, Yuri Kimura, 高橋寛典, Akiko Sakurai, Mai Kanai, Takeshi Kondo, 桝田志保, Tomoteru Kishimoto and Itsuro Endo : hCG, FSH製剤の併用によりパートナーの妊娠，健常児正常出産が確認された低ゴナドトロピン性男背性性腺機能低下症の2例, 第42回徳島県医学検査学会, Dec. 2018.
36.	Shimpei Morino, Misato Moriki, Akiko Sakurai and Keiko Kataoka : 1型糖尿病に対する玄米発酵食品の発症抑制効果∼モデルマウスにおける膵臓細胞のアポトーシス抑制とインスリン発現レベルの検討∼, 第42回徳島県医学検査学会, Dec. 2018.
37.	Rina Murata, Keiji Murakami, Hideki Fujii, 佐藤雅美, 笹田倫子, 井上みなみ, 平尾早紀, 別所将弘, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 呼吸器感染症患者由来緑膿菌の抗菌薬抵抗性と抗酸化能の関連について, 第42回徳島県医学検査学会, Dec. 2018.
38.	Shiho Takemasa, Minami Urushihara, Misato Moriki, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : 分娩様式と栄養方法が出生後の腸内菌叢に及ぼす影響について, 第42回徳島県医学検査学会, Dec. 2018.
39.	Minami Urushihara, Shiho Takemasa, Misato Moriki, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : 分娩様式と栄養方法が出生後の腸内環境に及ぼす影響について, 第42回徳島県医学検査学会, Dec. 2018.
40.	Misato Moriki, Yuri Morimoto, Akiko Sakurai and Keiko Kataoka : The timing of high-fat high-sucrose diet intake affects gut microbiota and fatty liver disease in mice., 第22回腸内細菌学会, May 2018. (Keyword) gut microbiota / high-fat high-sucrose diet / fatty liver disease
41.	岡諭紀, Mai Kanai, Akiko Sakurai and Itsuro Endo : 免疫チェックポイント阻害薬で中枢性副腎不全を来した2例, 第41回徳島県医学検査学会, Dec. 2017.
42.	野原圭一郎, 岡諭紀, 藤田幸那, Mai Kanai, Akiko Sakurai and Itsuro Endo : デノスマブによる対糖能改善, 第41回徳島県医学検査学会, Dec. 2017.
43.	Narumi Senoh, Chiaki Matsuda, Yuri Morimoto, Misato Moriki, Akiko Sakurai and Keiko Kataoka : 高脂肪高ショ糖食摂取マウスの脂肪組織および肝臓細胞での遺伝子発現に対する玄米発酵食品の影響, 第41回徳島県医学検査学会, Dec. 2017.
44.	Ryo Kuge, Chiaki Matsuda, Yuri Morimoto, Misato Moriki, Akiko Sakurai and Keiko Kataoka : 2型糖尿病モデルマウスに対する玄米発酵食品摂取の効果-免疫組織染色を用いた膵臓PDX-1発現分布の検討-, 第41回徳島県医学検査学会, Dec. 2017.
45.	Chiaki Matsuda, Yuri Morimoto, Misato Moriki, Akiko Sakurai and Keiko Kataoka : 1型糖尿病にたいする玄米発酵食品の発症抑制効果-モデルマウスにおける膵臓遺伝子発現レベルの検討-, 第41回徳島県医学検査学会, Dec. 2017.
46.	藤田結衣, Tatsuya Tominaga, Akiko Sakurai, Kojiro Nagai, Hideharu Abe and Toshio Doi : BMP4シグナルが作用するポドサイト障害発生機序の解析, 第255回徳島医学会学術集会, Aug. 2017.
47.	Shoto Ogawa, Shinichi Fujie, Keiji Murakami, Takashi Amoh, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 緑膿菌オートインデューサー類似化合物が抗菌薬抵抗性に及ぼす影響, 第40回徳島県医学検査学会, Dec. 2016.
48.	Mayuko Gohji, Keiko Komatsu, Yuri Morimoto, Akiko Sakurai and Keiko Kataoka : 1型糖尿病に対する玄米発酵食品の発症抑制効果-モデルマウスにおける膵臓PDX-1発現レベルの検討-, 第40回徳島県医学検査学会, Dec. 2016.
49.	Keiko Komatsu, Mayuko Gohji, Yuri Morimoto, Keiko Kataoka and Akiko Sakurai : 高脂肪高ショ糖食摂取マウスの血中レジスチン濃度に対する玄米発酵食品の影響, 第40回徳島県医学検査学会, Dec. 2016.
50.	Hiromi Nakagawa, Tatsuya Tominaga, Akiko Sakurai, Yui Fujita, Hideharu Abe, Kojiro Nagai and Toshio Doi : ポドサイトへのBMP4過剰発現による腎組織への影響, 徳島県臨床検査技師会誌第40回徳島県医学検査学会抄録集, 28, Dec. 2016.
51.	Yuri Morimoto, Akiko Sakurai and Keiko Kataoka : 高脂肪食により誘導される生活習慣病のリスクに対する玄米発酵食品の影響, 第11回日本臨床検査学教育学会学術大会, Sep. 2016.
52.	Motokazu Matsuura, Sakiya Yoshimoto, Akiko Sakurai, Taichi Murakami, Kojiro Nagai, Hideharu Abe and Toshio Doi : DAPIはAL型アミロイド腎症の診断に有用かもしれない, Sep. 2016.
53.	Tatsuya Shirai, Yuri Morimoto, Akiko Sakurai and Keiko Kataoka : 食事誘導性肥満マウスの腸内菌叢に対する玄米発酵食品投与の影響, 第39回徳島県医学検査学会, Dec. 2015.
54.	Ayumi Yoshida, Mai Ueta, Keiji Murakami, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 緑膿菌におけるストレス応答と抗菌薬抵抗性について, 第39回徳島県医学検査学会, Dec. 2015.
55.	Mai Ueta, Ayumi Yoshida, Keiji Murakami, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : リボザイムを応用したcyclic-di-GMPの定量法の開発, 第39回徳島県医学検査学会, Dec. 2015.
56.	Akiko Sakurai, Hideharu Abe, Tatsuya Tominaga, 三好雅士 and Toshio Doi : 糖尿病のポドサイト障害におけるCXCR7シグナル異常, 中四国支部医学検査学会(第48回), Nov. 2015.
57.	Hiroyuki Ono, 平野隆弘, Akiko Sakurai, 新井美存, 上田紗代, Eriko Shibata, Sakiya Yoshimoto, Masanori Tamaki, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Toshio Doi and Hideharu Abe : E2A新規結合分子FLASHによるTNFα-p21制御と細胞増殖・老化の調整による腎炎の修復機構, 第6回分子腎臓フォーラム, Sep. 2015.
58.	小野広幸, 平野隆弘, Akiko Sakurai, 新井美存, 上田紗代, 柴田恵理子, Sakiya Yoshimoto, 田蒔昌憲, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Toshio Doi and Hideharu Abe : E2A新規結合分子FLASHによるTNFα-p21制御と細胞増殖・老化の調整による腎炎の修復機構, 第6回分子腎臓フォーラム, Sep. 2015.
59.	Hiroyuki Ono, 平野隆弘, Akiko Sakurai, 新井美存, 上田紗代, Eriko Shibata, Sakiya Yoshimoto, Masanori Tamaki, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Toshio Doi and Hideharu Abe : E2A新規結合因子FLASHによるTNFα-P21制御と細胞増殖・老化の調整による腎炎の修復機構, 第58回日本腎臓学会学術総会, Jun. 2015.
60.	小野広幸, 平野隆弘, Akiko Sakurai, 新井美存, 上田紗代, 柴田恵理子, Sakiya Yoshimoto, 田蒔昌憲, Motokazu Matsuura, Taichi Murakami, Kojiro Nagai, Toshio Doi and Hideharu Abe : E2A新規結合因子FLASHによるTNFα-P21制御と細胞増殖・老化の調整による腎炎の修復機構, 第58回日本腎臓学会学術総会, Jun. 2015.
61.	Yukari Yoshikawa, Shoko Kannuki, Keiji Murakami, Yoichiro Miyake, 畑美智子, 佐藤雅美, 笹田倫子, 香川葉子, 菅崎幹樹, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 本院で分離されたST-8型MRSAについて, 第38回徳島県医学検査学会, Dec. 2014.
62.	Shoko Kannuki, Yukari Yoshikawa, Keiji Murakami, Yoichiro Miyake, Hideaki Maseda, 畑美智子, 佐藤雅美, 笹田倫子, 香川葉子, 菅崎幹樹, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 臨床および環境分離緑膿菌における病原性について, 第38回徳島県医学検査学会, Dec. 2014.
63.	Mai Matsumoto, Takakazu Kinugawa, Ken Saito, Yurie Tamai, Yuki Horike, Aya Matsura and Akiko Sakurai : 若年健常者におけるTpTeの分布と性差に関する検討, 徳島県臨床検査技師会誌, 22, Dec. 2014. (Keyword) TpTe間隔 / 心拍変動解析 / 自律神経機能
64.	Takakazu Kinugawa, Mai Matsumoto, Ken Saito, Yurie Tamai, Yuki Horike, Aya Matsura and Akiko Sakurai : 自己回帰モデルを用いた短時間心拍変動解析の検討, 徳島県臨床検査技師会誌, 21, Dec. 2014. (Keyword) 自己回帰モデル / 心拍変動解析 / 自律神経機能
65.	Chihiro Itami, Akiko Sakurai and Keiko Kataoka : 高脂肪高ショ糖食がマウス腸内菌叢に及ぼす影響について, Dec. 2014.
66.	Akiko Sakurai, Hideharu Abe, Kojiro Nagai, Taichi Murakami, Naoko Abe and Toshio Doi : 糖尿病のポドサイト障害におけるBMP-CXCR7シグナル異常の検出法, 第61回日本臨床検査医学会学術集会, Nov. 2014.
67.	Hideharu Abe, 小野広幸, 平野隆弘, Akiko Sakurai and Toshio Doi : FlashとE2Aの新規相互作用はTNF-α-p21によって細胞増殖と細胞老化を制御する, 第37回日本分子生物学会年会, Nov. 2014.
68.	Akiko Sakurai, 林早苗, Tatsuya Tominaga, 藤田結衣, Naoko Abe, Toshio Doi and Hideharu Abe : 糖尿病性腎症におけるmiR-21のポドサイトに対するPDCD4制御を介した抗アポトーシス効果, 第36回日本分子生物学会年会, Dec. 2013.
69.	Fujita Yui, Akiko Sakurai, Tatsuya Tominaga, Hayashi Sanae, Naoko Abe, Toshio Doi and Hideharu Abe : Multiple regulatory pathways of BMP-Smad axis through a sclerosis-specific basic HLH transcription factor in diabetic nephropathy., 第86回日本生化学会大会, Sep. 2013.
70.	白水裕也, 星野佑太, 西田みなみ, 曽宮葉子, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Yoichiro Miyake, Akiko Sakurai, 佐藤雅美, 岡本貴子, 香川葉子 and 畑美智子 : 緑膿菌臨床分離株における抗菌薬耐性のメカニズム, 第36回徳島県医学検査学会, Dec. 2012.
71.	星野佑太, 白水裕也, 西田みなみ, 曽宮葉子, Chieko Matsuura, Tsuneko Ono, Keiji Murakami, Yoichiro Miyake, Akiko Sakurai, 佐藤雅美, 岡本貴子, 香川葉子 and 畑美智子 : 緑膿菌臨床分離株における抗菌薬抵抗性と病原因子について, 第36回徳島県医学検査学会, Dec. 2012.

Et cetera, Workshop:

1.	Miyu Higasa, Yuma Takemoto, Nozomi Fujimoto, Rina Murata, Akiko Sakurai and Keiko Kataoka : NASHモデルマウスにおける離乳までの時期の抗菌薬暴露の影響について, 第44回徳島県医学検査学会, Dec. 2020.
2.	Saho Yamanaka, Rina Murata, Keiji Murakami, Yuka Hiroshima, Hideki Fujii, Akiko Sakurai and Keiko Kataoka : 緑膿菌の抗菌薬抵抗性に関与する二成分制御系について, 第44回徳島県医学検査学会, Dec. 2020.
3.	Yuma Takemoto, Miyu Higasa, Nozomi Fujimoto, Toshiyuki Yasui, Akiko Sakurai and Keiko Kataoka : 乳児の腸内細菌叢における Bifidobacterium 属の変動について, 第44回徳島県医学検査学会, Dec. 2020.
4.	Mizuki Abe, Narumi Senoh, Keiji Murakami, Takashi Amoh, Hideki Fujii, 佐藤雅美, 笹田倫子, 菅崎幹樹, 森本悠里, 平尾早紀, Akiko Sakurai and Keiko Kataoka : オートインデューサーアナログ(AIA)の緑膿菌に及ぼす影響, 第41回徳島県医学検査学会, Dec. 2017.
5.	Shinichi Fujie, Shoto Ogawa, Keiji Murakami, Takashi Amoh, Yoichiro Miyake, 佐藤雅美, 笹田倫子, 菅崎幹樹, 香川葉子, Yuri Morimoto, Momoyo Azuma, Akiko Sakurai and Keiko Kataoka : 呼吸器由来緑膿菌における病原性と抗菌薬抵抗性との関連について, 第40回徳島県医学検査学会, Dec. 2016.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Stability of gut microbiota and its relationship with a risk of nonalcoholic fatty liver disease. (Project/Area Number: 22K11725 )
ポドサイトの活性化シグナルの解析による各種腎障害の鑑別法の開発 (Project/Area Number: 21K07367 )
Intervention to gut microbiota and reduction of the risk of non-alcoholic steatohepatitis. (Project/Area Number: 19K11719 )
糖尿病における進行性腎障害の病態特異的バイオマーカー樹立と修復機構解明 (Project/Area Number: 18K08245 )
Identification of specific podocyte-damaging molecules in diabetic nephropathy and establishment of urinary biomarkers (Project/Area Number: 18K07415 )
The timing of high-fat high-sucrose diet intake affects gut microbiota and fatty liver disease in mice (Project/Area Number: 15K00820 )
Development and Establishment of therapeutic target molecules as podocyte failure markers in diabetic nephropathy (Project/Area Number: 25893155 )
Search by Researcher Number (70707900)

Assistant Professor : Sakurai, Akiko

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)