المؤلفون: Takeuchi, Masayoshi, Suzuki, Hirokazu, Takeda, Kenji, Sakai-Sakasai, Akiko

المساهمون: Japan Society for the Promotion of Science

المصدر: Medical Hypotheses ; volume 183, page 111248 ; ISSN 0306-9877

مصطلحات موضوعية: General Medicine

الإتاحة: https://doi.org/10.1016/j.mehy.2023.111248Test
https://api.elsevier.com/content/article/PII:S030698772300244X?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S030698772300244X?httpAccept=text/plainTest

المؤلفون: Takeuchi, Masayoshi, Fujiwara, Naoki, Kuwayama, Takanori, Nakagawa, Satoshi, Iimura, Soshi, Matsuishi, Satoru, Yamakawa, Youichi, Kontani, Hiroshi, Hosono, Hideo

مصطلحات موضوعية: Condensed Matter - Superconductivity

الوصف: An iron-based superconductor LaFeAsO$_{1-x}$H$_x$ (0 $\leq x \leq$ 0.6) undergoes two antiferromagnetic (AF) phases upon H doping. We investigated the second AF phase ($x$=0.6) using NMR techniques under pressure. At pressures up to 2 GPa, the ground state is a spin-density-wave state with a large gap; however, the gap closes at 4.0 GPa, suggesting a pressure-induced quantum critical point. Interestingly, the gapped excitation coexists with gapless magnetic fluctuations at pressures between 2 and 4 GPa. This coexistence is attributable to the lift up of the $d_{xy}$ orbital to the Fermi level, a Lifshitz transition under pressure.

الوصول الحر: http://arxiv.org/abs/1905.06606Test

المؤلفون: Mao, Ziling, Baker, Jacqueline Roshelli, Takeuchi, Masayoshi, Hyogo, Hideyuki, Tjønneland, Anne, Eriksen, Anne Kirstine, Severi, Gianluca, Rothwell, Joseph, Laouali, Nasser, Katzke, Verena, Kaaks, Rudolf, Schulze, Matthias B., Palli, Domenico, Sieri, Sabina, de Magistris, Maria Santucci, Tumino, Rosario, Sacerdote, Carlotta, Derksen, Jeroen W.G., Gram, Inger T., Skeie, Guri, Sandanger, Torkjel M., Quirós, Jose Ramón, Crous-Bou, Marta, Sánchez, Maria Jose, Amiano, Pilar, Colorado-Yohar, Sandra M., Guevara, Marcela, Harlid, Sophia, Johansson, Ingegerd, Perez-Cornago, Aurora, Freisling, Heinz, Gunter, Marc, Weiderpass, Elisabete, Heath, Alicia K., Aglago, Elom, Jenab, Mazda, Fedirko, Veronika

المصدر: Mao , Z , Baker , J R , Takeuchi , M , Hyogo , H , Tjønneland , A , Eriksen , A K , Severi , G , Rothwell , J , Laouali , N , Katzke , V , Kaaks , R , Schulze , M B , Palli , D , Sieri , S , de Magistris , M S , Tumino , R , Sacerdote , C , Derksen , J W G , Gram , I T , Skeie , G , Sandanger , T M , Quirós , J R , Crous-Bou ....

مصطلحات موضوعية: advanced glycation end products, colorectal cancer, glyceraldehyde-derived advanced glycation end products, mortality, prospective study

الوصف: Glyceraldehyde-derived advanced glycation end products (glycer-AGEs) could contribute to colorectal cancer development and progression due to their pro-oxidative and pro-inflammatory properties. However, the association of glycer-AGEs with mortality after colorectal cancer diagnosis has not been previously investigated. Circulating glycer-AGEs were measured by competitive ELISA. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) for associations of circulating glycer-AGEs concentrations with CRC-specific and all-cause mortality among 1034 colorectal cancer (CRC) cases identified within the European Prospective Investigation into Cancer and Nutrition (EPIC) study between 1993 and 2013. During a mean of 48 months of follow-up, 529 participants died (409 from CRC). Glycer-AGEs were statistically significantly positively associated with CRC-specific (HRQ5 vs Q1 = 1.53, 95% CI: 1.04-2.25, Ptrend = .002) and all-cause (HRQ5 vs Q1 = 1.62, 95% CI: 1.16-2.26, Ptrend < .001) mortality among individuals with CRC. There was suggestion of a stronger association between glycer-AGEs and CRC-specific mortality among patients with distal colon cancer (per SD increment: HRproximal colon = 1.02, 95% CI: 0.74-1.42; HRdistal colon = 1.51, 95% CI: 1.20-1.91; Peffect modification = .02). The highest HR was observed among CRC cases in the highest body mass index (BMI) and glycer-AGEs category relative to lowest BMI and glycer-AGEs category for both CRC-specific (HR = 1.78, 95% CI: 1.02-3.01) and all-cause mortality (HR = 2.15, 95% CI: 1.33-3.47), although no statistically significant effect modification was observed. Our study found that prediagnostic circulating glycer-AGEs are positively associated with CRC-specific and all-cause mortality among individuals with CRC. Further investigations in other populations and stratifying by tumor location and BMI are warranted. ; Glyceraldehyde-derived advanced glycation end products (glycer-AGEs) could ...

وصف الملف: application/pdf

الإتاحة: https://doi.org/10.1002/ijc.34449Test
https://curis.ku.dk/portal/da/publications/prediagnostic-serum-glyceraldehydederived-advanced-glycation-end-products-and-mortality-among-colorectal-cancer-patientsTest(e34cd835-f142-47a4-8c39-e8e3a4b5f631).html
https://curis.ku.dk/ws/files/359550389/IKM_Intl_Journal_of_Cancer_2023_Mao_Pre_diagnostic_Serum_Glyceraldehyde_Derived_Advanced_Glycation_End_Products_and.pdfTest

المؤلفون: Ooi, Hayahide, Furukawa, Ayako, Takeuchi, Masayoshi, Koriyama, Yoshiki

المصدر: International Journal of Molecular Sciences; Jul2024, Vol. 25 Issue 13, p7409, 14p

مستخلص: Advanced glycation end-products (AGEs) form through non-enzymatic glycation of various proteins. Optic nerve degeneration is a frequent complication of diabetes, and retinal AGE accumulation is strongly linked to the development of diabetic retinopathy. Type 2 diabetes mellitus is a major risk factor for Alzheimer's disease (AD), with patients often exhibiting optic axon degeneration in the nerve fiber layer. Notably, a gap exists in our understanding of how AGEs contribute to neuronal degeneration in the optic nerve within the context of both diabetes and AD. Our previous work demonstrated that glyceraldehyde (GA)-derived toxic advanced glycation end-products (TAGE) disrupt neurite outgrowth through TAGE–β-tubulin aggregation and tau phosphorylation in neural cultures. In this study, we further illustrated GA-induced suppression of optic nerve axonal elongation via abnormal β-tubulin aggregation in mouse retinas. Elucidating this optic nerve degeneration mechanism holds promise for bridging the knowledge gap regarding vision loss associated with diabetes mellitus and AD. [ABSTRACT FROM AUTHOR]

: Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Sakai-Sakasai, Akiko, Takeda, Kenji, Suzuki, Hirokazu, Takeuchi, Masayoshi

المصدر: Biomolecules (2218-273X); Feb2024, Vol. 14 Issue 2, p202, 15p

مصطلحات موضوعية: ADVANCED glycation end-products, RECEPTOR for advanced glycation end products (RAGE), PYRIDINIUM compounds, FRUCTOSE, SUGAR, GLUCOSE metabolism

مستخلص: Advanced glycation end-products (AGEs) have recently been implicated in the onset/progression of lifestyle-related diseases (LSRDs); therefore, the suppression of AGE-induced effects may be used in both the prevention and treatment of these diseases. Various AGEs are produced by different biological pathways in the body. Glyceraldehyde (GA) is an intermediate of glucose and fructose metabolism, and GA-derived AGEs (GA-AGEs), cytotoxic compounds that accumulate and induce damage in mammalian cells, contribute to the onset/progression of LSRDs. The following GA-AGE structures have been detected to date: triosidines, GA-derived pyridinium compounds, GA-derived pyrrolopyridinium lysine dimers, methylglyoxal-derived hydroimidazolone 1, and argpyrimidine. GA-AGEs are a key contributor to the formation of toxic AGEs (TAGE) in many cells. The extracellular leakage of TAGE affects the surrounding cells via interactions with the receptor for AGEs. Elevated serum levels of TAGE, which trigger different types of cell damage, may be used as a novel biomarker for the prevention and early diagnosis of LSRDs as well as in evaluations of treatment efficacy. This review provides an overview of the structures of GA-AGEs. [ABSTRACT FROM AUTHOR]

: Copyright of Biomolecules (2218-273X) is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Yasuda, Yuushi, Aoki, Hirofumi, Fujita, Wataru, Fujibayashi, Kousuke, Wakasa, Minoru, Kawai, Yasuyuki, Nakanishi, Hiroaki, Saito, Kazuyuki, Takeuchi, Masayoshi, Kajinami, Kouji

المساهمون: Grants-in-Aid from the Japan Society for the Promotion of Science

المصدر: Scandinavian Cardiovascular Journal ; volume 56, issue 1, page 208-216 ; ISSN 1401-7431 1651-2006

الإتاحة: https://doi.org/10.1080/14017431.2022.2095013Test

المؤلفون: Ooi, Hayahide, Nasu, Ryuto, Furukawa, Ayako, Takeuchi, Masayoshi, Koriyama, Yoshiki

المساهمون: Japan Society for the Promotion of Science

المصدر: Frontiers in Pharmacology ; volume 13 ; ISSN 1663-9812

مصطلحات موضوعية: Pharmacology (medical), Pharmacology

الوصف: Diabetes mellitus (DM) has been identified as a risk factor for the onset and progression of Alzheimer’s disease (AD). In our previous study, we demonstrated that glyceraldehyde (GA)-derived toxic advanced glycation end-products (toxic AGEs, TAGE) induced similar alterations to those observed in AD. GA induced dysfunctional neurite outgrowth via TAGE-β-tubulin aggregation, which resulted in the TAGE-dependent abnormal aggregation of β-tubulin and tau phosphorylation in human neuroblastoma SH-SY5Y cells. However, the effects of inhibitors of AGE formation on dysfunctional neurite outgrowth caused by GA-induced abnormalities in the aggregation of β-tubulin and tau phosphorylation remain unknown. Aminoguanidine (AG), an AGE inhibitor, and pyridoxamine (PM), a natural form of vitamin B 6 (VB 6 ), are effective AGE inhibitors. Therefore, the present study investigated whether AG or PM ameliorate TAGE-β-tubulin aggregation and the suppression of neurite outgrowth by GA. The results obtained showed that AG and PM inhibited the formation of TAGE-β-tubulin, mitigated the GA-induced suppression of neurite outgrowth, and reduced GA-mediated increases in tau phosphorylation levels. Collectively, these results suggest the potential of AG and PM to prevent the DM-associated onset and progression of AD.

الإتاحة: https://doi.org/10.3389/fphar.2022.921611Test

المؤلفون: Takeda, Kenji, Sakai-Sakasai, Akiko, Kajinami, Kouji, Takeuchi, Masayoshi

المصدر: Cells (2073-4409); Dec2023, Vol. 12 Issue 24, p2838, 26p

مصطلحات موضوعية: CHECKPOINT kinase 1, GLATIRAMER acetate, ADVANCED glycation end-products, RECEPTOR for advanced glycation end products (RAGE)

مستخلص: Advanced glycation end-products (AGEs), formed through glyceraldehyde (GA) as an intermediate in non-enzymatic reactions with intracellular proteins, are cytotoxic and have been implicated in the pathogenesis of various diseases. Despite their significance, the mechanisms underlying the degradation of GA-derived AGEs (GA-AGEs) remain unclear. In the present study, we found that N-terminal checkpoint kinase 1 cleavage products (CHK1-CPs) and their mimic protein, d270WT, were degraded intracellularly post-GA exposure. Notably, a kinase-dead d270WT variant (d270KD) underwent rapid GA-induced degradation, primarily via the ubiquitin–proteasome pathway. The high-molecular-weight complexes formed by the GA stimulation of d270KD were abundant in the RIPA-insoluble fraction, which also contained high levels of GA-AGEs. Immunoprecipitation experiments indicated that the high-molecular-weight complexes of d270KD were modified by GA-AGEs and that p62/SQSTM1 was one of its components. The knockdown of p62 or treatment with chloroquine reduced the amount of high-molecular-weight complexes in the RIPA-insoluble fraction, indicating its involvement in the formation of GA-AGE aggregates. The present results suggest that the ubiquitin–proteasome pathway and p62 play a role in the degradation and aggregation of intracellular GA-AGEs. This study provides novel insights into the mechanisms underlying GA-AGE metabolism and may lead to the development of novel therapeutic strategies for diseases associated with the accumulation of GA-AGEs. [ABSTRACT FROM AUTHOR]

: Copyright of Cells (2073-4409) is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Takino, Jun-ichi, Sato, Takuma, Kanetaka, Takumi, Okihara, Kasumi, Nagamine, Kentaro, Takeuchi, Masayoshi, Hori, Takamitsu

المساهمون: Japan Society for the Promotion of Science

المصدر: Scientific Reports ; volume 11, issue 1 ; ISSN 2045-2322

مصطلحات موضوعية: Multidisciplinary

الوصف: Advanced glycation end-products (AGEs) are formed by the non-enzymatic reaction of sugars and proteins. Among the AGEs, glyceraldehyde-derived toxic AGEs (TAGE) are associated with various diseases, including diabetic complications such as diabetic retinopathy (DR). The risk of developing DR is strongly associated with poor glycemic control, which causes AGE accumulation and increases AGE-induced vascular permeability. We previously reported that Ras guanyl nucleotide releasing protein 2 (RasGRP2), which activates small G proteins, may play an essential role in the cell response to toxicity when exposed to various factors. However, it is not known whether RasGRP2 prevents the adverse effects of TAGE in vascular endothelial cells. This study observed that TAGE enhanced vascular permeability by disrupting adherens junctions and tight junctions via complex signaling, such as ROS and non-ROS pathways. In particular, RasGRP2 protected adherens junction disruption, thereby suppressing vascular hyper-permeability. These results indicate that RasGRP2 is an essential protective factor of vascular permeability and may help develop novel therapeutic strategies for AGE-induced DR.

الإتاحة: https://doi.org/10.1038/s41598-021-82619-0Test
https://www.nature.com/articles/s41598-021-82619-0.pdfTest
https://www.nature.com/articles/s41598-021-82619-0Test

المؤلفون: Jinno, Masao, Nagai, Ryoji, Takeuchi, Masayoshi, Watanabe, Aiko, Teruya, Koji, Sugawa, Hikari, Hatakeyama, Naohisa, Jinno, Yuichi

المصدر: Reproductive Biology and Endocrinology ; volume 19, issue 1 ; ISSN 1477-7827

مصطلحات موضوعية: Developmental Biology, Endocrinology, Reproductive Medicine, Obstetrics and Gynecology

الوصف: Background Advanced glycation end-products (AGE), which accumulate with insulin resistance and aging, impair folliculogenesis and may decrease endometrial receptivity. Hishi ( Trapa bispinosa Roxb.) extract, a safe herbal medicine, strongly inhibits AGE formation in vitro . We determined whether Hishi lowers AGE and increases live births in older assisted reproductive technology (ART) patients. Methods This prospective randomized open-label controlled trial included 64 patients 38 to 42 years old undergoing ART with or without Hishi extract between June 11, 2015 and July 12, 2019. None had over 2 ART failures, diabetes, uterine anomalies, or exhausted ovarian reserve. After allocation, the Hishi group received Hishi extract (100 mg/day) until late pregnancy or failure. The control group received no extract. Both groups underwent 1 cycle of conventional infertility treatment; 1 long-protocol cycle of ovarian stimulation, oocyte retrieval, in vitro fertilization/intracytoplasmic sperm injection, and fresh embryo transfer (ET); and, if needed, cryopreserved ET until live birth or embryo depletion. Serum AGE were measured before and during ART, as were AGE in follicular fluid (FF). Results Cumulative live birth rate among 32 Hishi patients was 47%, significantly higher than 16% among 31 controls (p<0.01; RR, 4.6; 95% CI, 1.4 – 15.0; 1 control dropped out). Live birth rate per ET, including fresh and cryopreserved, was significantly higher with Hishi (28% in 47 ET vs. 10% in 49 ET; p<0.05; RR, 3.4; 95% CI, 1.1-10.4). Among variables including age, day-3 FSH, anti-Müllerian hormone, and Hishi, logistic regression identified only Hishi as significantly associated with increased cumulative live birth (p<0.05; OR, 5.1; 95% CI, 1.4 - 18.3). Hishi significantly enhanced oocyte developmental potential, improved endometrial receptivity in natural cycles, and decreased AGE in serum and FF. Larger serum AGE decreases with Hishi were associated with more oocytes becoming day-2 embryos. Conclusions Hishi ...

الإتاحة: https://doi.org/10.1186/s12958-021-00832-yTest