Journal of Clinical Biochemistry and Nutrition最新文献_第2页

Capturing systemic inflammation in a nonhuman primate using a new leukocyte activity assessment system. 使用新的白细胞活性评估系统捕获非人灵长类动物的全身炎症。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-09-01 Epub Date: 2025-06-11 DOI: 10.3164/jcbn.25-65

Kozo Takeuchi, Shigeyuki Yamamoto, Yukiko Hatano, Dai Fukumoto, Takeharu Kakiuchi, Yoshiyuki Shimizu, Kimiko Kazumura

{"title":"Capturing systemic inflammation in a nonhuman primate using a new leukocyte activity assessment system.","authors":"Kozo Takeuchi, Shigeyuki Yamamoto, Yukiko Hatano, Dai Fukumoto, Takeharu Kakiuchi, Yoshiyuki Shimizu, Kimiko Kazumura","doi":"10.3164/jcbn.25-65","DOIUrl":"10.3164/jcbn.25-65","url":null,"abstract":"We developed an optical system that simultaneously monitors leukocytes producing the reactive oxygen species (ROS) superoxide and hypochlorite ions using only a few microliters of whole blood. Here, we report the first use of this system to measure circulating blood from a nonhuman primate. This observational pilot study involved rhesus monkeys recruited for a different purpose, brain positron emission tomography in the conscious state. The results indicated that (1) surgical inflammation influences the total ROS produced by leukocytes per unit of time; (2) blood analysis of a septic rhesus monkey exhibited a characteristic pattern of leukocyte ROS production; and (3) a strong positive correlation was observed between leukocyte ROS production and neutrophil counts at normal C-reactive protein (CRP) levels, which decreased under abnormal CRP levels. These findings suggest that the system can capture systemic inflammation in non-human primates and highlight the importance of monitoring leukocyte ROS production to understand inflammatory status. The difficulty of identifying subjective symptoms in veterinary medicine highlights the importance of technologies for easily and objectively monitor animals' physical conditions. Further analyses, including studies with larger animal populations and comparisons with conventional biomarkers, are needed to determine the specific inflammatory status reflected in leukocyte ROS production.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 2","pages":"162-173"},"PeriodicalIF":1.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Poricoic acid a inhibits mitochondrial dysfunction in myocardial infarction by activating SIRT3. 茯苓酸a通过激活SIRT3抑制心肌梗死线粒体功能障碍。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-09-01 Epub Date: 2025-04-19 DOI: 10.3164/jcbn.24-208

Jinzhu Yin, Qu Jin, Zhaozheng Liu

{"title":"Poricoic acid a inhibits mitochondrial dysfunction in myocardial infarction by activating SIRT3.","authors":"Jinzhu Yin, Qu Jin, Zhaozheng Liu","doi":"10.3164/jcbn.24-208","DOIUrl":"10.3164/jcbn.24-208","url":null,"abstract":"Acute myocardial infarction (MI) is the most severe clinical manifestation of ischemic heart disease. Despite this, the mechanisms that disrupt mitochondrial homeostasis and contribute to cardiomyocyte loss during MI are poorly understood, emphasizing the urgent need for new therapeutic interventions. Poricoic acid A (PAA), the principal active component of pachymaria, possesses a range of pharmacological effects. However, the specific role and mechanisms by which PAA addresses mitochondrial dysfunction in MI remain unclear. This study aims to elucidate the impact of PAA on MI and uncover its potential regulatory mechanisms. We developed MI cell models using mouse primary cardiomyocytes incubated in a Forma Steri-Cult chamber containing 1% oxygen, 94% nitrogen, and 5% carbon dioxide. Our results demonstrate that PAA significantly improves cardiomyocyte injury in hypoxia-induced mouse primary cardiomyocytes. Furthermore, PAA activates the AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1-alpha/Sirtuin 3 (AMPK/PGC-1α/SIRT3) signaling pathway in hypoxia-induced mouse primary cardiomyocytes. PAA enhances the oxidative stress response in hypoxia-induced mouse primary cardiomyocytes by activating SIRT3. Additionally, it improves mitochondrial dysfunction in these cardiomyocytes and reduces apoptosis by activating SIRT3. In summary, PAA inhibits mitochondrial dysfunction associated with MI by activating SIRT3, indicating its promise as a therapeutic agent for MI.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 2","pages":"136-143"},"PeriodicalIF":1.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Relationship between serum pyridoxal 5'-phosphate concentration and cognitive function in older Japanese. 老年日本人血清吡哆醛5′-磷酸浓度与认知功能的关系。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-02-20 DOI: 10.3164/jcbn.24-233

Kotaro Itoh, Akiko Kuwabara, Rei Otsuka, Taiki Sugimoto, Takashi Sakurai, Shumpei Niida, Misora Ao, Kiyoshi Tanaka, Shigeo Takenaka, Hiroaki Kanouchi

{"title":"Relationship between serum pyridoxal 5'-phosphate concentration and cognitive function in older Japanese.","authors":"Kotaro Itoh, Akiko Kuwabara, Rei Otsuka, Taiki Sugimoto, Takashi Sakurai, Shumpei Niida, Misora Ao, Kiyoshi Tanaka, Shigeo Takenaka, Hiroaki Kanouchi","doi":"10.3164/jcbn.24-233","DOIUrl":"10.3164/jcbn.24-233","url":null,"abstract":"Deficiency of pyridoxal 5'-phosphate (PLP) causes neurological abnormalities. The decline in blood PLP concentration has been associated with the onset of dementia, but no studies have been conducted on Japanese. This study aimed to determine the relationship between serum PLP concentration and Alzheimer's disease (AD) in older Japanese individuals. A total of 266 participants, 84 healthy participants, 87 participants with mild cognitive impairment (MCI), and 95 patients with AD were randomly selected from those who visited the National Center for Geriatrics and Gerontology for Longevity Sciences. Serum PLP concentration was significantly lower in the AD compared to the NC. Participants were divided into quartiles (Q1-Q4). The relationship between quartiles of serum PLP concentration and cognitive function was analyzed using logistic regression analyses adjusted with covariate factors (sex, age, number of applicable frailty evaluations, APOE4, educational level, albumin, homocysteine, vitamin B1, B12, and folate). The odds ratios (ORs) for MCI or AD were significantly lower for Q3 and Q4 compared to Q1, and the ORs (95% CI) for Q3 and Q4 were 0.40 (0.16-0.98) and 0.37 (0.13-0.99), respectively. Lower serum PLP concentration is independently related to the incidence of MCI or AD. Further research is needed to clarify the causal relationship.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"79-84"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TFAP2C activates PTGES through the NOTCH3 signaling pathway to affect gefitinib resistance in lung adenocarcinoma. TFAP2C通过NOTCH3信号通路激活PTGES，影响肺腺癌患者吉非替尼耐药。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-04-25 DOI: 10.3164/jcbn.24-104

Junmeng Xiao, Jianwei Cao, Lei Zhu, Jianbin Hou

{"title":"TFAP2C activates PTGES through the NOTCH3 signaling pathway to affect gefitinib resistance in lung adenocarcinoma.","authors":"Junmeng Xiao, Jianwei Cao, Lei Zhu, Jianbin Hou","doi":"10.3164/jcbn.24-104","DOIUrl":"10.3164/jcbn.24-104","url":null,"abstract":"Lung adenocarcinoma (LUAD) is one of the primary culprits of cancer-related deaths. Current treatment modalities for LUAD have certain limitations, necessitating innovating effective LUAD treatment strategies. Prostaglandin E synthase (PTGES) and TF activating protein 2C (TFAP2C) in the process of drug resistance in LUAD are less studied and need further in-depth research. This study aimed to investigate the specific molecular mechanisms of PTGES and TFAP2C in gefitinib resistance in LUAD. The results indicated that PTGES and TFAP2C were considerably overexpressed in LUAD tissues and cells. Chromatin immunoprecipitation and dual luciferase assay validated that TFAP2C targeted the PTGES promoter region. In addition, gene set enrichment analysis results demonstrated the notable enrichment of PTGES in the NOTCH3 signaling pathway. Overexpression of PTGES remarkably enhanced the viability of PC-9/GR (gefitinib-resistant) cells and their response to gefitinib resistance, which was reversed by the addition of a NOTCH3 inhibitor. Furthermore, overexpressing PTGES upon the TFAP2C silence restored the great inhibition effect conferred by TFAP2C silence in PC-9/GR cells on cell viability and cell response to gefitinib resistance. This study confirmed that TFAP2C can transcriptionally activate PTGES through the NOTCH3 signaling pathway to enhance the response of LUAD cells to gefitinib resistance, proffering a new approach for the treatment of gefitinib resistance in LUAD cells.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"1-9"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kurarinone activates the Nrf-2/HO-1 signaling pathway and alleviates high glucose-induced ferroptosis in HK2 cells. Kurarinone激活Nrf-2/HO-1信号通路，缓解高糖诱导的HK2细胞铁下垂。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-04-16 DOI: 10.3164/jcbn.24-210

Chunmei Ma

引用次数: 0

Erratum. 勘误表。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 DOI: 10.3164/jcbn.24-178_Erratum2

引用次数: 0

Simple method for estimating low muscle mass in persons with bioelectrical impedance analysis measurement difficulties. 有生物电阻抗分析测量困难的人低肌肉量的简单估计方法。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-20 DOI: 10.3164/jcbn.25-13

Hirohito Sasaki, Osamu Yamamura, Hidenori Onishi, Hiromasa Tsubouchi, Yasutaka Mizukami, Masafumi Kubota, Ryouko Ikeda, Naohiro Konoshita, Tokuharu Tanaka, Takahiro Kishimoto, Koji Kobayashi, Hiroyuki Hayashi, Yasuhiro Nishiyama

{"title":"Simple method for estimating low muscle mass in persons with bioelectrical impedance analysis measurement difficulties.","authors":"Hirohito Sasaki, Osamu Yamamura, Hidenori Onishi, Hiromasa Tsubouchi, Yasutaka Mizukami, Masafumi Kubota, Ryouko Ikeda, Naohiro Konoshita, Tokuharu Tanaka, Takahiro Kishimoto, Koji Kobayashi, Hiroyuki Hayashi, Yasuhiro Nishiyama","doi":"10.3164/jcbn.25-13","DOIUrl":"10.3164/jcbn.25-13","url":null,"abstract":"Bioelectrical impedance analysis cannot be used to measure muscle mass in some individuals. We aimed to determine cutoff values for low skeletal muscle mass index in sarcopenia diagnosis, based on the fat-free muscle mass index estimated using body fat percentage prediction equations, without relying on bioelectrical impedance analysis. The study included 564 residents from Wakasa, Fukui Prefecture, with a mean age of 76.0 ± 7.1 years. Body composition assessments using bioelectrical impedance analysis were conducted. Three prediction equations for body fat percentage (Ito et al., Deurenberg et al., and Gallagher et al.'s model for Asians) were applied. The cutoff value of the fat-free muscle mass index corresponding to low skeletal muscle mass index in sarcopenia diagnostic criteria was determined using receiver operating characteristic curves. Receiver operating characteristic curve analysis showed that the formula by Ito et al. yielded the highest area under the curve for estimating low skeletal muscle mass index in men, at 0.83. In women, the formulas by Ito et al. and Gallagher et al. performed similarly, each achieving an area under the curve of 0.779. The fat-free muscle mass index estimated using the body fat prediction formulas appear to be useful for screening low skeletal muscle mass index.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"91-98"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The revelation of UCHL1 in malignant epithelial cells of TNBC reinforcing cisplatin resistance by modulating ferroptosis based on single-cell transcriptome data. 基于单细胞转录组数据的TNBC恶性上皮细胞中UCHL1通过调节铁凋亡增强顺铂耐药的揭示。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-15 DOI: 10.3164/jcbn.24-206

Huan Li, Shaojun Chen, Haiqin Hou, Zhuoying Li, Yiming Zhang, Wenxia Zhang

{"title":"The revelation of UCHL1 in malignant epithelial cells of TNBC reinforcing cisplatin resistance by modulating ferroptosis based on single-cell transcriptome data.","authors":"Huan Li, Shaojun Chen, Haiqin Hou, Zhuoying Li, Yiming Zhang, Wenxia Zhang","doi":"10.3164/jcbn.24-206","DOIUrl":"10.3164/jcbn.24-206","url":null,"abstract":"Chemotherapy resistance is a key obstacle in the treatment of triple-negative breast cancer (TNBC). Single-cell RNA sequencing (scRNA-seq) plays a pivotal part in revealing the mechanism of drug resistance in tumors. This work aimed to explore the molecular events driving TNBC resistance based on scRNA-seq data. Breast cancer (BC) scRNA-seq data GSE176078 was sourced from the GEO database. Nine TNBC samples were analyzed. The cellular composition and differentially expressed genes of TNBC were clarified through dimension reduction, clustering, and cell annotation. Drug-resistant and sensitive epithelial cell clusters in malignant epithelial cells were identified, with their heterogeneity analyzed. Key genes driving drug-resistant epithelium were screened and KEGG enrichment analysis was undertaken. The expression of Ubiquitin Carboxy-Terminal Hydrolase L1 (UCHL1) in TNBC was examined. The effect and molecular mechanism of UCHL1 on cisplatin (CDDP) resistance in TNBC was confirmed by constructing CDDP-resistant cell lines. We successfully identified resistant and sensitive cell clusters in malignant epithelial cells of TNBC and screened for the greatly upregulated gene UCHL1 in the resistant epithelium. KEGG analysis revealed its enrichment in the ferroptosis signaling pathway. Further analyses demonstrated the upregulation of UCHL1 in CDDP-resistant TNBC cells. Knocking down UCHL1 potentiated the sensitivity of TNBC cells to CDDP treatment and reinforced ferroptosis. The ferroptosis inhibitor Ferrostatin-1 reversed the inhibitory effect of UCHL1 knockdown on CDDP resistance. UCHL1 reinforces CDDP resistance in TNBC by suppressing ferroptosis. The study brings new insights into the drug-resistance mechanism of TNBC.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"18-29"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sanguinarine attenuates hypoxia/reoxygenation-triggered H9c2 cell injury through activation of the Nrf2/NLRP3 pathway. 血根碱通过激活Nrf2/NLRP3通路减轻缺氧/再氧化引发的H9c2细胞损伤。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-04-11 DOI: 10.3164/jcbn.24-235

Bo Qiu, Xin Li, Wenna Wang

{"title":"Sanguinarine attenuates hypoxia/reoxygenation-triggered H9c2 cell injury through activation of the Nrf2/NLRP3 pathway.","authors":"Bo Qiu, Xin Li, Wenna Wang","doi":"10.3164/jcbn.24-235","DOIUrl":"10.3164/jcbn.24-235","url":null,"abstract":"Myocardial ischemia/reperfusion injury (MI/RI) is a prevalent condition encountered by many patients with ischemic heart disease, which can badly influence the health of patients and even do harm their lives. Sanguinarine (SA), one active ingredient separated from the poppy family, and exhibits anti-oxidant, anti-tumor, and anti-inflammation properties. However, the precise regulatory impacts and associated mechanisms of SA in the progression of MI/RI remain largely elusive. In this study, firstly, H9c2 cells were treated by hypoxia/reoxygenation (HR) to mimic MI/RI cell model. It was uncovered that SA strengthened HR-mediated cell viability of H9c2 cells. Following HR treatment, there was an increase in the production of inflammatory markers (TNF-α, IL-1β, and IL-6), whereas this effect was mitigated after SA treatment. The oxidative stress was heightened after HR treatment, but this phenomenon was offset after SA treatment. SA activated the Nrf2/NLRP3 pathway and relieved proptosis. At last, through rescue assays, it was demonstrated that SA improved HR-triggered inflammation and oxidative stress through Nrf2 pathway. SA also modulated HR-triggered cell viability, inflammation, and oxidative stress in rat primary cardiomyocytes. In summary, our findings indicate that SA protects against HR-induced H9c2 cell injury through activation of the Nrf2/NLRP3 pathway. This discovery suggests that SA may be one helpful drug for ameliorating MI/RI.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"37-44"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Seven days of piceatannol supplementation exerted no effect on fat metabolism at rest, during and after exercise. 在休息、运动期间和运动后，补充7天皮杉醇对脂肪代谢没有影响。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2025-07-01 Epub Date: 2025-03-11 DOI: 10.3164/jcbn.25-2

Nobukazu Kasai, Kanon Hayashi, Masaki Kito, Takuma Morishima

{"title":"Seven days of piceatannol supplementation exerted no effect on fat metabolism at rest, during and after exercise.","authors":"Nobukazu Kasai, Kanon Hayashi, Masaki Kito, Takuma Morishima","doi":"10.3164/jcbn.25-2","DOIUrl":"10.3164/jcbn.25-2","url":null,"abstract":"Piceatannol is a type of polyphenol that is abundantly obtained from passion fruit. The present study aimed to determine the effect of 7 days of piceatannol supplementation on fat metabolism at rest, during and after low-intensity aerobic exercise. This randomized, double-blind, and crossover study included eight physically active male participants. The participants completed two experimental trials: placebo and piceatannol. They ingested either a placebo or piceatannol tablets containing 0 or 10 ‍mg of piceatannol for seven consecutive days. The participants visited the laboratory at 8:00 am after seven days. In the following baseline measurements, the participants performed 60 ‍min of pedaling exercise at 30% of their maximum oxygen uptake. Respiratory gas and blood samples were collected before, during, and after the exercise. No significant differences were found between the trials in oxygen uptake, carbon dioxide output, ventilation, and respiratory exchange ratio either at rest and during and after exercise. Similarly, serum growth hormone, cortisol, insulin, free fatty acid, glycerol, acetoacetic acid, 3-hydroxybutyric acid, and ketone body responses exhibited no significant differences between trials. These results indicate that the 7-day piceatannol supplementation did not promote fat metabolism at rest and during and after low-intensity aerobic exercise.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"77 1","pages":"85-90"},"PeriodicalIF":1.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0