=== Generating (published_papers) ===
=== Generating (research_interests) ===
=== Generating (teaching_experience) ===
=== Generating (misc) ===
=== Generating (research_projects) ===
=== Generating (presentations) ===
==== begin registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/published_papers-propagate.jsonl) ====
line:1, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/39796581","label":"url"},{"@id":"https://www.scopus.com/pages/publications/85214514845","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=418513","label":"url"}],"paper_title":{"en":"Ghrelin Promotes Lipid Uptake into White Adipose Tissue via Endothelial Growth Hormone Secretagogue-Receptor in Mice","ja":"Ghrelin Promotes Lipid Uptake into White Adipose Tissue via Endothelial Growth Hormone Secretagogue-Receptor in Mice"},"authors":{"en":[{"name":"Urai Hidenori"},{"name":"Azegami Tatsuhiko"},{"name":"Komatsu Motoaki"},{"name":"Takahashi Rina"},{"name":"Kubota Yoshiaki"},{"name":"Hasegawa Kazuhiro"},{"name":"Tokuyama Hirofumi"},{"name":"Wakino Shu"},{"name":"Hayashi Kaori"},{"name":"Kanda Takeshi"},{"name":"Itoh Hiroshi"}],"ja":[{"name":"Urai Hidenori"},{"name":"Azegami Tatsuhiko"},{"name":"Komatsu Motoaki"},{"name":"Takahashi Rina"},{"name":"Kubota Yoshiaki"},{"name":"長谷川 一宏"},{"name":"Tokuyama Hirofumi"},{"name":"𦚰野 修"},{"name":"Hayashi Kaori"},{"name":"Kanda Takeshi"},{"name":"Itoh Hiroshi"}]},"description":{"en":"Background/Objectives: Endothelial peroxisome proliferator-activated receptor gamma (PPARγ) regulates adipose tissue by facilitating lipid uptake into white adipocytes, but the role of endothelial lipid transport in systemic energy balance remains unclear. Ghrelin conveys nutritional information through the central nervous system and increases adiposity, while deficiency in its receptor, growth hormone secretagogue-receptor (GHSR), suppresses adiposity on a high-fat diet. This study aims to examine the effect of ghrelin/GHSR signaling in the endothelium on lipid metabolism. Methods: We compared the effects of ghrelin on adiposity and lipid uptake into adipocytes in wild-type and GHSR-null mice. Transgenic mice expressing GHSR selectively in endothelial cells were also generated and compared with global GHSR-null and wild-type mice. The impact of ghrelin on lipid uptake-related genes was assessed in cultured endothelial cells. Results: Ghrelin increased adiposity and triglyceride clearance in wild-type but not in GHSR-null mice. GHSR-null mice showed higher serum triglyceride after olive oil gavage and lower white adipose tissue (WAT) weight on a high-fat diet, suggesting impaired lipid uptake. Restoring GHSR expression in endothelial cells increased lipoprotein lipase activity, lipid uptake into WAT, and WAT weight. Ghrelin enhanced free fatty acid uptake and the expression of lipid uptake genes in cultured endothelial cells, whereas these effects were absent in GHSR-null mice-derived endothelial cells. Knockdown of PPARγ revealed that ghrelin/GHSR signaling in endothelial cells promoted lipid uptake via endothelial PPARγ. Conclusions: Endothelial GHSR is key for regulating lipid metabolism via PPARγ in response to ghrelin and for the role of endothelium in regulating white adipocyte metabolism. Targeting endothelial ghrelin signaling may be a promising therapeutic approach for managing excessive adiposity and associated metabolic disorders.","ja":"Background/Objectives: Endothelial peroxisome proliferator-activated receptor gamma (PPARγ) regulates adipose tissue by facilitating lipid uptake into white adipocytes, but the role of endothelial lipid transport in systemic energy balance remains unclear. Ghrelin conveys nutritional information through the central nervous system and increases adiposity, while deficiency in its receptor, growth hormone secretagogue-receptor (GHSR), suppresses adiposity on a high-fat diet. This study aims to examine the effect of ghrelin/GHSR signaling in the endothelium on lipid metabolism. Methods: We compared the effects of ghrelin on adiposity and lipid uptake into adipocytes in wild-type and GHSR-null mice. Transgenic mice expressing GHSR selectively in endothelial cells were also generated and compared with global GHSR-null and wild-type mice. The impact of ghrelin on lipid uptake-related genes was assessed in cultured endothelial cells. Results: Ghrelin increased adiposity and triglyceride clearance in wild-type but not in GHSR-null mice. GHSR-null mice showed higher serum triglyceride after olive oil gavage and lower white adipose tissue (WAT) weight on a high-fat diet, suggesting impaired lipid uptake. Restoring GHSR expression in endothelial cells increased lipoprotein lipase activity, lipid uptake into WAT, and WAT weight. Ghrelin enhanced free fatty acid uptake and the expression of lipid uptake genes in cultured endothelial cells, whereas these effects were absent in GHSR-null mice-derived endothelial cells. Knockdown of PPARγ revealed that ghrelin/GHSR signaling in endothelial cells promoted lipid uptake via endothelial PPARγ. Conclusions: Endothelial GHSR is key for regulating lipid metabolism via PPARγ in response to ghrelin and for the role of endothelium in regulating white adipocyte metabolism. Targeting endothelial ghrelin signaling may be a promising therapeutic approach for managing excessive adiposity and associated metabolic disorders."},"publication_date":"2024-12","publication_name":{"en":"Nutrients","ja":"Nutrients"},"volume":"17","number":"1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/nu17010146"],"issn":["2072-6643"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://tokushima-u.repo.nii.ac.jp/records/2012210","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38928090","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=410124","label":"url"}],"paper_title":{"en":"Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1.","ja":"Deficiency Causes Mitoribosome Excess in Diabetic Nephropathy Mediated by Transcriptional Repressor HIC1."},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"Sakamaki Yusuke"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"Sakamaki Yusuke"},{"name":"𦚰野 修"}]},"description":{"en":"overexpression preserved mitoribosomal function, suggesting its protective role in DN.","ja":"overexpression preserved mitoribosomal function, suggesting its protective role in DN."},"publication_date":"2024-06-09","publication_name":{"en":"International Journal of Molecular Sciences","ja":"International Journal of Molecular Sciences"},"volume":"25","number":"12","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/ijms25126384"],"issn":["1422-0067"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://tokushima-u.repo.nii.ac.jp/records/2012209","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38587753","label":"url"},{"@id":"https://www.scopus.com/pages/publications/85189697626","label":"url"},{"@id":"https://www.scopus.com/pages/publications/85196749614","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=410122","label":"url"}],"paper_title":{"en":"Ability of NAD and Sirt1 to epigenetically suppress albuminuria.","ja":"Ability of NAD and Sirt1 to epigenetically suppress albuminuria."},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"Shibata Eriko"},{"name":"Inagaki Taizo"},{"name":"Minato Masanori"},{"name":"Yamaguchi Sumiyo"},{"name":"Shimizu Ikuko"},{"name":"Miyakami Shinji"},{"name":"Tada Miho"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"柴田 恵理子"},{"name":"稲垣 太造"},{"name":"湊 将典"},{"name":"Yamaguchi Sumiyo"},{"name":"清水 郁子"},{"name":"Miyakami Shinji"},{"name":"多田 美穂"},{"name":"𦚰野 修"}]},"description":{"en":"The time for diabetic nephropathy (DN) to progress from mild to severe is long. Thus, methods to continuously repress DN are required to exert long-lasting effects mediated through epigenetic regulation. In this study, we demonstrated the ability of nicotinamide adenine dinucleotide (NAD) and its metabolites to reduce albuminuria through Sirt1- or Nampt-dependent epigenetic regulation. We previously reported that proximal tubular Sirt1 was lowered before glomerular Sirt1. Repressed glomerular Sirt1 was found to epigenetically elevate Claudin-1. In addition, we reported that proximal tubular Nampt deficiency epigenetically augmented TIMP-1 levels in Sirt6-mediated pathways, leading to type-IV collagen deposition and diabetic fibrosis. Altogether, we propose that the Sirt1/Claudin-1 axis may be crucial in the onset of albuminuria at the early stages of DN and that the Nampt/Sirt6/TIMP-1 axis promotes diabetic fibrosis in the middle to late stages of DN. Finally, administration of NMN, an NAD precursor, epigenetically potentiates the regression of the onset of DN to maintain Sirt1 and repress Claudin-1 in podocytes, suggesting the potential use of NAD metabolites as epigenetic medications for DN.","ja":"The time for diabetic nephropathy (DN) to progress from mild to severe is long. Thus, methods to continuously repress DN are required to exert long-lasting effects mediated through epigenetic regulation. In this study, we demonstrated the ability of nicotinamide adenine dinucleotide (NAD) and its metabolites to reduce albuminuria through Sirt1- or Nampt-dependent epigenetic regulation. We previously reported that proximal tubular Sirt1 was lowered before glomerular Sirt1. Repressed glomerular Sirt1 was found to epigenetically elevate Claudin-1. In addition, we reported that proximal tubular Nampt deficiency epigenetically augmented TIMP-1 levels in Sirt6-mediated pathways, leading to type-IV collagen deposition and diabetic fibrosis. Altogether, we propose that the Sirt1/Claudin-1 axis may be crucial in the onset of albuminuria at the early stages of DN and that the Nampt/Sirt6/TIMP-1 axis promotes diabetic fibrosis in the middle to late stages of DN. Finally, administration of NMN, an NAD precursor, epigenetically potentiates the regression of the onset of DN to maintain Sirt1 and repress Claudin-1 in podocytes, suggesting the potential use of NAD metabolites as epigenetic medications for DN."},"publication_date":"2024-04-08","publication_name":{"en":"Clinical and Experimental Nephrology","ja":"Clinical and Experimental Nephrology"},"volume":"28","number":"7","starting_page":"599","ending_page":"607","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10157-024-02502-w"],"issn":["1437-7799"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37199399","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=400706","label":"url"}],"paper_title":{"en":"PCK1 Protects against Mitoribosomal Defects in Diabetic Nephropathy in Mouse Models.","ja":"PCK1 Protects against Mitoribosomal Defects in Diabetic Nephropathy in Mouse Models."},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Sakamaki Yusuke"},{"name":"Tamaki Masanori"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"Sakamaki Yusuke"},{"name":"田蒔 昌憲"},{"name":"𦚰野 修"}]},"description":{"en":"PCK1 preserves mitoribosomal function and may play a novel protective role in DN.","ja":"PCK1 preserves mitoribosomal function and may play a novel protective role in DN."},"publication_date":"2023-05-18","publication_name":{"en":"Journal of the American Society of Nephrology","ja":"Journal of the American Society of Nephrology"},"volume":"34","number":"8","starting_page":"1343","ending_page":"1365","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1681/ASN.0000000000000156"],"issn":["1533-3450"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33795425","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=400909","label":"url"}],"paper_title":{"en":"Pre-emptive Short-term Nicotinamide Mononucleotide Treatment in a Mouse Model of Diabetic Nephropathy.","ja":"Pre-emptive Short-term Nicotinamide Mononucleotide Treatment in a Mouse Model of Diabetic Nephropathy."},"authors":{"en":[{"name":"Yasuda Itaru"},{"name":"Hasegawa Kazuhiro"},{"name":"Sakamaki Yusuke"},{"name":"Muraoka Hirokazu"},{"name":"Kawaguchi Takahisa"},{"name":"Kusahana Ei"},{"name":"Ono Takashi"},{"name":"Kanda Takeshi"},{"name":"Tokuyama Hirobumi"},{"name":"Wakino Shu"},{"name":"Itoh Hiroshi"}],"ja":[{"name":"Yasuda Itaru"},{"name":"長谷川 一宏"},{"name":"Sakamaki Yusuke"},{"name":"Muraoka Hirokazu"},{"name":"Kawaguchi Takahisa"},{"name":"Kusahana Ei"},{"name":"Ono Takashi"},{"name":"Kanda Takeshi"},{"name":"Tokuyama Hirobumi"},{"name":"𦚰野 修"},{"name":"Itoh Hiroshi"}]},"description":{"en":"The activation of NAD+-dependent deacetylase, Sirt1, by the administration of nicotinamide mononucleotide (NMN) ameliorates various aging-related diseases. Diabetic db/db mice were treated with NMN transiently for 2 weeks and observed for effects on diabetic nephropathy (DN). At 14 weeks after the treatment period, NMN attenuated the increases in urinary albumin excretion in db/db mice without ameliorating hemoglobin A1c levels. Short-term NMN treatment mitigated mesangium expansion and foot process effacement, while ameliorating decreased Sirt1 expression and increased claudin-1 expression in the kidneys of db/db mice. This treatment also improved the decrease in the expression of H3K9me2 and DNMT1. Short-term NMN treatment also increased kidney concentrations of NAD+ and the expression of Sirt1 and nicotinamide phosphoribosyltransferase (Nampt), and it maintained nicotinamide mononucleotide adenyltransferase1 (Nmnat1) expression in the kidneys. In addition, survival rates improved after NMN treatment. Short-term NMN treatment in early-stage DN has remote renal protective effects through the upregulation of Sirt1 and activation of the NAD+ salvage pathway, both of which indicate NMN legacy effects on DN.","ja":"The activation of NAD+-dependent deacetylase, Sirt1, by the administration of nicotinamide mononucleotide (NMN) ameliorates various aging-related diseases. Diabetic db/db mice were treated with NMN transiently for 2 weeks and observed for effects on diabetic nephropathy (DN). At 14 weeks after the treatment period, NMN attenuated the increases in urinary albumin excretion in db/db mice without ameliorating hemoglobin A1c levels. Short-term NMN treatment mitigated mesangium expansion and foot process effacement, while ameliorating decreased Sirt1 expression and increased claudin-1 expression in the kidneys of db/db mice. This treatment also improved the decrease in the expression of H3K9me2 and DNMT1. Short-term NMN treatment also increased kidney concentrations of NAD+ and the expression of Sirt1 and nicotinamide phosphoribosyltransferase (Nampt), and it maintained nicotinamide mononucleotide adenyltransferase1 (Nmnat1) expression in the kidneys. In addition, survival rates improved after NMN treatment. Short-term NMN treatment in early-stage DN has remote renal protective effects through the upregulation of Sirt1 and activation of the NAD+ salvage pathway, both of which indicate NMN legacy effects on DN."},"publication_date":"2021-04-01","publication_name":{"en":"Journal of the American Society of Nephrology","ja":"Journal of the American Society of Nephrology"},"volume":"32","number":"6","starting_page":"1355","ending_page":"1370","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1681/ASN.2020081188"],"issn":["1533-3450"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"6000007612","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://tokushima-u.repo.nii.ac.jp/records/2011234","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33452384","label":"url"},{"@id":"https://www.scopus.com/pages/publications/85099472433","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=400911","label":"url"}],"paper_title":{"en":"Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells.","ja":"Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells."},"authors":{"en":[{"name":"Kawaguchi Takahisa"},{"name":"Hasegawa Kazuhiro"},{"name":"Yasuda Itaru"},{"name":"Muraoka Hirokazu"},{"name":"Umino Hiroyuki"},{"name":"Tokuyama Hirobumi"},{"name":"Hashiguchi Akinori"},{"name":"Wakino Shu"},{"name":"Itoh Hiroshi"}],"ja":[{"name":"Kawaguchi Takahisa"},{"name":"長谷川 一宏"},{"name":"Yasuda Itaru"},{"name":"Muraoka Hirokazu"},{"name":"Umino Hiroyuki"},{"name":"Tokuyama Hirobumi"},{"name":"Hashiguchi Akinori"},{"name":"𦚰野 修"},{"name":"Itoh Hiroshi"}]},"description":{"en":"Diabetic nephropathy (DN) is accompanied by characteristic changes in the glomerulus, but little is known about the effect of diabetes on parietal epithelial cells (PECs). In this study, a descriptive analysis of PECs was undertaken in diabetic db/db mice and in diabetic patients. PEC hypertrophy was significantly more prominent in diabetic mice than in nondiabetic mice, and this was evident even at the early stage. Additionally, the number of vacuoles in PECs was markedly increased in diabetic mice, suggesting the presence of cellular injury in PECs in DN. Although rare, binuclear cells were observed in mice with early diabetes. In cultured PECs, a high glucose condition, compared with normal glucose condition, induced cellular hypertrophy and apoptosis. Flow cytometry showed that some PECs in the G0 phase reentered the cell cycle but got arrested in the S phase. Finally, in human diabetic subjects, hypertrophy and vacuolization were observed in the PECs. Our data showed that PECs undergo substantial changes in DN and may participate in rearrangement for differentiation into podocytes.","ja":"Diabetic nephropathy (DN) is accompanied by characteristic changes in the glomerulus, but little is known about the effect of diabetes on parietal epithelial cells (PECs). In this study, a descriptive analysis of PECs was undertaken in diabetic db/db mice and in diabetic patients. PEC hypertrophy was significantly more prominent in diabetic mice than in nondiabetic mice, and this was evident even at the early stage. Additionally, the number of vacuoles in PECs was markedly increased in diabetic mice, suggesting the presence of cellular injury in PECs in DN. Although rare, binuclear cells were observed in mice with early diabetes. In cultured PECs, a high glucose condition, compared with normal glucose condition, induced cellular hypertrophy and apoptosis. Flow cytometry showed that some PECs in the G0 phase reentered the cell cycle but got arrested in the S phase. Finally, in human diabetic subjects, hypertrophy and vacuolization were observed in the PECs. Our data showed that PECs undergo substantial changes in DN and may participate in rearrangement for differentiation into podocytes."},"publication_date":"2021-01-15","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"11","number":"1","starting_page":"1515","ending_page":"1515","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-021-81027-8"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
==== end registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/published_papers-propagate.jsonl, QEpmlp8Bn_HdSsNVNxm7) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/376686/researchmap/misc-propagate.jsonl) ====
line:1, {"insert":{"user_id":"6000007612","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://tokushima-u.repo.nii.ac.jp/records/2012211","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390299528381041664/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=410125","label":"url"}],"paper_title":{"en":"特集 糖尿病性腎症研究の最前線 糖尿病性腎症の発症機序 糖尿病性腎症におけるミトコンドリアの役割","ja":"特集 糖尿病性腎症研究の最前線 糖尿病性腎症の発症機序 糖尿病性腎症におけるミトコンドリアの役割"},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"Shibata Eriko"},{"name":"Minato Masanori"},{"name":"Inagaki Taizo"},{"name":"清水 郁子"},{"name":"山口 純代"},{"name":"宮上 慎司"},{"name":"多田 美穂"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"柴田 恵理子"},{"name":"湊 将典"},{"name":"稲垣 太造"},{"name":"清水 郁子"},{"name":"山口 純代"},{"name":"宮上 慎司"},{"name":"多田 美穂"},{"name":"𦚰野 修"}]},"publication_date":"2024-02-25","publication_name":{"en":"Kidney and Dialysis","ja":"腎と透析"},"volume":"96","number":"2","starting_page":"159","ending_page":"164","languages":["jpn"],"invited":true,"identifiers":{"doi":["10.24479/kd.0000001187"],"issn":["0385-2156"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"6000007612","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://cir.nii.ac.jp/crid/1390862168254226944/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=410126","label":"url"}],"paper_title":{"en":"特集 血液透析患者の血圧を再考する 5.透析患者の至適血圧-腹膜透析も含む","ja":"特集 血液透析患者の血圧を再考する 5.透析患者の至適血圧-腹膜透析も含む"},"authors":{"en":[{"name":"Wakino Shu"},{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"Shibata Eriko"}],"ja":[{"name":"𦚰野 修"},{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"柴田 恵理子"}]},"publication_date":"2024-02-10","publication_name":{"en":"The Japanese Journal of Clinical Dialysis","ja":"臨床透析"},"volume":"40","number":"2","starting_page":"155","ending_page":"163","languages":["jpn"],"identifiers":{"doi":["10.19020/cd.0000002887"],"issn":["0910-5808"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"6000007612","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://search.jamas.or.jp/link/ui/2023126589","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1520013962704009344/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=401012","label":"url"}],"paper_title":{"en":"近位尿細管から見た糖尿病性腎臓病と肥満関連腎症","ja":"近位尿細管から見た糖尿病性腎臓病と肥満関連腎症"},"authors":{"en":[{"name":"Wakino Shu"},{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"}],"ja":[{"name":"𦚰野 修"},{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"}]},"publication_date":"2023-02","publication_name":{"en":"Cardioangiology","ja":"循環器内科"},"volume":"93","number":"2","starting_page":"182","ending_page":"189","languages":["jpn"],"identifiers":{"issn":["1884-2909"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"6000007612","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://cir.nii.ac.jp/crid/1390016195131521024/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=400712","label":"url"}],"paper_title":{"en":"【急性腎障害(AKI)】AKIの病態とその対応 手術とAKI","ja":"【急性腎障害(AKI)】AKIの病態とその対応 手術とAKI"},"authors":{"en":[{"name":"Tamaki Masanori"},{"name":"Hasegawa Kazuhiro"},{"name":"Wakino Shu"}],"ja":[{"name":"田蒔 昌憲"},{"name":"長谷川 一宏"},{"name":"𦚰野 修"}]},"publication_date":"2023-01-25","publication_name":{"en":"Kidney and Dialysis","ja":"腎と透析"},"volume":"94","number":"1","starting_page":"83","ending_page":"86","languages":["jpn"],"identifiers":{"doi":["10.24479/kd.0000000586"],"issn":["0385-2156"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"6000007612","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://cir.nii.ac.jp/crid/1520011108762623872/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=401037","label":"url"}],"paper_title":{"en":"【ポドサイトパチー】糖尿病性腎症におけるポドサイト傷害の見える化へ迫る最新論文","ja":"【ポドサイトパチー】糖尿病性腎症におけるポドサイト傷害の見える化へ迫る最新論文"},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"𦚰野 修"}]},"publication_date":"2022-06","publication_name":{"en":"Nephrology","ja":"腎臓内科"},"volume":"15","number":"6","starting_page":"659","ending_page":"664","languages":["jpn"],"identifiers":{"issn":["2435-1903"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"6000007612","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://cir.nii.ac.jp/crid/1520292395539278336/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=391084","label":"url"}],"paper_title":{"en":"ミトコンドリアとSIRT1/NMNと腎臓病","ja":"ミトコンドリアとSIRT1/NMNと腎臓病"},"authors":{"en":[{"name":"Hasegawa Kazuhiro"},{"name":"Tamaki Masanori"},{"name":"坂巻 裕介"},{"name":"Wakino Shu"}],"ja":[{"name":"長谷川 一宏"},{"name":"田蒔 昌憲"},{"name":"坂巻 裕介"},{"name":"𦚰野 修"}]},"publication_date":"2022-05","publication_name":{"en":"Nephrology","ja":"腎臓内科"},"volume":"15","number":"5","starting_page":"551","ending_page":"557","languages":["jpn"],"identifiers":{"issn":["2435-1903"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
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