Journal of Clinical Biochemistry and Nutrition最新文献

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Association of lysophosphatidic acid molecules with liver fibrosis: different roles indicated. 溶血磷脂酸分子与肝纤维化的关系:不同的作用表明。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-11-01 Epub Date: 2023-08-18 DOI: 10.3164/jcbn.23-58
Hiroshi Tobita, Hiromichi Sakai, Akane Yamaguchi, Yoshitomo Notsu, Masatoshi Kataoka, Tomotaka Yazaki, Toru Nabika, Shunji Ishihara, Hironori Kobayashi
{"title":"Association of lysophosphatidic acid molecules with liver fibrosis: different roles indicated.","authors":"Hiroshi Tobita, Hiromichi Sakai, Akane Yamaguchi, Yoshitomo Notsu, Masatoshi Kataoka, Tomotaka Yazaki, Toru Nabika, Shunji Ishihara, Hironori Kobayashi","doi":"10.3164/jcbn.23-58","DOIUrl":"10.3164/jcbn.23-58","url":null,"abstract":"<p><p>Lysophosphatidic acid is composed of lysophosphatidic acid (LPA) molecules with varied chemical forms. The present cross-sectional study was conducted to investigate the associations of various LPA molecules with liver fibrosis. Forty-six patients affected by various types of liver disease who underwent an ultrasound-guided liver biopsy were recruited for this study. Liver fibrosis was evaluated using histological grading, as well as shear wave velocity (Vs) and serum level of type IV collagen 7S (T4c7s). Serum levels of LPA molecules were determined using liquid-chromatography tandem mass-spectrometry (LC-MSMS). Total LPA showed a significant positive association with fibrosis severity evaluated based on histological grading, Vs, and T4c7s used as parameters, following adjustment for other confounding factors, including disease type, age, gender, body mass index, and high-sensitivity C-reactive protein. This association was replicated when 16:0-LPA was substituted for total LPA. In contrast, when 20:4-LPA was substituted for total LPA, no significant association with liver fibrosis was observed. In conclusion, the degree of association varied among the different LPA molecule chemical forms, suggesting different pathophysiological roles of individual LPA molecules, although total LPA concentration was shown to be associated with liver fibrosis.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"255-261"},"PeriodicalIF":2.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361756","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
Acute effect of proprotein convertase subtilisin/kexin type 9 inhibitor on oxidized low-density lipoprotein and lipid profile in patients at cardiovascular risk. 蛋白转化酶枯草杆菌素/kexin 9型抑制剂对心血管危险患者氧化低密度脂蛋白和血脂的急性影响
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-11-01 Epub Date: 2023-09-01 DOI: 10.3164/jcbn.23-45
Yiming Li, Minni Sun, Ran Li, Min Dou, Haozhe Dong, Liqi Xue, Guoju Sun
{"title":"Acute effect of proprotein convertase subtilisin/kexin type 9 inhibitor on oxidized low-density lipoprotein and lipid profile in patients at cardiovascular risk.","authors":"Yiming Li, Minni Sun, Ran Li, Min Dou, Haozhe Dong, Liqi Xue, Guoju Sun","doi":"10.3164/jcbn.23-45","DOIUrl":"10.3164/jcbn.23-45","url":null,"abstract":"Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are a new class of potent lipid-lowering drugs. Oxidized low-density lipoprotein (ox-LDL) is the key pathogenic factor leading to atherosclerosis. However, its effect on ox-LDL levels has not been clinically reported. The clinical data of 290 very high-risk atherosclerotic cardiovascular disease (ASCVD) patients diagnosed in the First Affiliated Hospital of Zhengzhou University from May 2022 to October 2022 were collected retrospectively. According to whether evolocumab (a PCSK9 inhibitor) was used after percutaneous coronary intervention (PCI), they were divided into evolocumab group (153 cases) and statin monotherapy group (137 cases). At hospital admission, ox-LDL, total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoproteinA1 (apoA1), apolipoprotein B-100 (apoB), lipoprotein (a) [Lp(a)], and high-sensitivity reactive protein (hs-CRP) levels were collected and used as baseline data. After two weeks of treatment, ox-LDL in the evolocumab group and statin monotherapy group were significantly lower than those before treatment (p<0.05). The decrease of ox-LDL in the evolocumab group was more than in the stain monotherapy group (p<0.05). In conclusion, PCSK9 inhibitors reduce ox-LDL levels in very high-risk ASCVD patients in a short time.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"1 1","pages":"249-254"},"PeriodicalIF":2.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69361258","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
Letter to the Editor: Increased uric acid levels following fructose consumption: a biochemical perspective. 致编辑的信:果糖摄入后尿酸水平升高:生化角度。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-11-01 DOI: 10.3164/jcbn.23-72L
Sarita Anil Shinde
{"title":"Letter to the Editor: Increased uric acid levels following fructose consumption: a biochemical perspective.","authors":"Sarita Anil Shinde","doi":"10.3164/jcbn.23-72L","DOIUrl":"https://doi.org/10.3164/jcbn.23-72L","url":null,"abstract":"","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 3","pages":"262"},"PeriodicalIF":2.4,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134649006","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
TRIM62 knockdown by inhibiting the TLR4/NF-κB pathway and NLRP3 inflammasome attenuates cognitive impairment induced by diabetes in mice. 通过抑制TLR4/NF-κB通路和NLRP3炎性体,敲低TRIM62可减轻糖尿病小鼠认知功能障碍。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.22-104
Xiting Nong, Nan Li, Xiang Wang, Heng Li, Xiaoping Wu, Ming Li, Wenqing Hao, Guang Yang
{"title":"TRIM62 knockdown by inhibiting the TLR4/NF-κB pathway and NLRP3 inflammasome attenuates cognitive impairment induced by diabetes in mice.","authors":"Xiting Nong,&nbsp;Nan Li,&nbsp;Xiang Wang,&nbsp;Heng Li,&nbsp;Xiaoping Wu,&nbsp;Ming Li,&nbsp;Wenqing Hao,&nbsp;Guang Yang","doi":"10.3164/jcbn.22-104","DOIUrl":"https://doi.org/10.3164/jcbn.22-104","url":null,"abstract":"<p><p>The tripartite motif 62 is an E3 ubiquitin ligase protein that regulates cellular processes, including differentiation, immunity, development and apoptosis, leading to various disease states, such as cancer and inflammatory diseases. However, the role and mechanism of the tripartite motif 62 in the process of diabetic-induced cognitive impairment have not been reported. Therefore, the aim of this study was to investigate the role and mechanism of the tripartite motif 62 in diabetic-induced cognitive impairment. The results showed that the expression of the tripartite motif 62 was up-regulated in diabetic mice. Silencing of TRIM62 increased body weight and decreased fasting blood glucose in diabetic mice. In addition, knockdown of the tripartite motif 62 inhibited STZ-induced inflammation, apoptosis and oxidative stress. Further studies showed that the TLR4/NF-κB pathway and NLRP3 inflammasomes were involved in the regulation of diabetic mice by the tripartite motif 62. More importantly, inhibition of the tripartite motif 62 improved cognitive impairment and learning ability in mice. In conclusion, inhibition of TRIM62 inhibits STZ-induced inflammation, cell apoptosis and oxidative stress, and improves the cognitive ability of mice. Therefore, the tripartite motif 62 may be an important target for the treatment of diabetes-induced cognitive impairment.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"131-137"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a4/77/jcbn22-104.PMC10493211.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10606767","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
Involvement of proliferation of atypical hepatocytes and CDT 1 in the liver cancer of rats administered the diethylnitrosamine. 二乙基亚硝胺对肝癌大鼠非典型肝细胞和cdt1增殖的影响。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.13-16
Masahiro Ogawa, Ryota Masuzaki, Tatsuo Kanda, Hiroshi Matsumura, Hitomi Nakamura, Motomi Yamazaki, Toshikatu Shibata, Hirofumi Kogure, Mitsuhiko Moriyama
{"title":"Involvement of proliferation of atypical hepatocytes and CDT 1 in the liver cancer of rats administered the diethylnitrosamine.","authors":"Masahiro Ogawa,&nbsp;Ryota Masuzaki,&nbsp;Tatsuo Kanda,&nbsp;Hiroshi Matsumura,&nbsp;Hitomi Nakamura,&nbsp;Motomi Yamazaki,&nbsp;Toshikatu Shibata,&nbsp;Hirofumi Kogure,&nbsp;Mitsuhiko Moriyama","doi":"10.3164/jcbn.13-16","DOIUrl":"https://doi.org/10.3164/jcbn.13-16","url":null,"abstract":"<p><p>We have reported that extent of proliferation of atypical hepatocytes (POAH) in non-cancerous liver in hepatocellular carcinoma and chromatin licensing and DNA replication factor 1 (CDT1) are associated with postoperative recurrence. Here, we investigated whether extent of POAH and expression of CDT1 in liver are also associated with chemically induced liver cancer in rats. Male Fisher strain rats were orally administered diethylnitrosamine (DEN) in their drinking water and sacrificed at 6, 8, 12, or 14 weeks after start of DEN administration. We serially monitored changes in extent of POAH, CDT1 expression by immunohistochemistry (IHC), and <i>CDT1</i> mRNA expression in liver by real-time quantitative PCR. The extent of POAH in liver progressed in a time-dependent manner after start of DEN administration. CDT1 expression was higher at 8 weeks than at 6 weeks by IHC, suggesting that CDT1 expression may be a marker of POAH severity. <i>CDT1</i> mRNA expression in liver was significantly higher at 12 weeks than at 6 weeks (<i>p</i><0.0001). We found that extent of POAH and the expression of CDT1 are also important factors in the development of chemical carcinogen-induced hepatocarcinogenesis. Furthermore, the association with POAH and CDT1 expression in carcinogenic process is important regardless of the cause of hepatocarcinogenesis.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"138-144"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/60/f1/jcbn13-16.PMC10493214.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240627","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: 1
Regulation of type I IFN responses by deubiquitinating enzyme A in inflammatory bowel diseases. 去泛素化酶A在炎性肠病中对I型IFN反应的调节
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.23-24
Yasuhiro Masuta, Yasuo Otsuka, Kosuke Minaga, Hajime Honjo, Masatoshi Kudo, Tomohiro Watanabe
{"title":"Regulation of type I IFN responses by deubiquitinating enzyme A in inflammatory bowel diseases.","authors":"Yasuhiro Masuta,&nbsp;Yasuo Otsuka,&nbsp;Kosuke Minaga,&nbsp;Hajime Honjo,&nbsp;Masatoshi Kudo,&nbsp;Tomohiro Watanabe","doi":"10.3164/jcbn.23-24","DOIUrl":"https://doi.org/10.3164/jcbn.23-24","url":null,"abstract":"<p><p>The development of Inflammatory bowel disease (IBD) is driven by excessive production of pro-inflammatory cytokines including TNF-α, IL-12, and IL-23. This notion is supported by the remarkable clinical success of biologics targeting these cytokines. Recognition of cell wall components derived from intestinal bacteria by Toll-like receptors (TLRs) induces the production of these pro-inflammatory cytokines by macrophages and dendritic cells in human IBD and experimental colitis model. Although sensing of bacterial nucleic acids by endosomal TLRs, specifically TLR3, TLR7, and TLR9 leads to robust production of type I IFNs, it remains debatable whether TLR-mediated type I IFN responses are pathogenic or protective in IBD patients. Additionally, recent studies identified deubiquitinating enzyme A (DUBA) as a novel negative regulator of TLR-mediated type I IFN responses. In light of these observations and their potential applications, in this review, we summarize recent findings on the roles of type I IFN responses and DUBA-mediated negative regulation of these responses in human IBD and experimental colitis model.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"103-107"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/72/07/jcbn23-24.PMC10493212.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240625","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
TMEM189 as a target gene of MiR-499a-5p regulates breast cancer progression through the ferroptosis pathway. TMEM189作为MiR-499a-5p的靶基因通过铁下垂途径调控乳腺癌的进展。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.22-130
Dong Fan, Yue Ma, Yujuan Qi, Xiaozhou Yang, Huadong Zhao
{"title":"TMEM189 as a target gene of MiR-499a-5p regulates breast cancer progression through the ferroptosis pathway.","authors":"Dong Fan,&nbsp;Yue Ma,&nbsp;Yujuan Qi,&nbsp;Xiaozhou Yang,&nbsp;Huadong Zhao","doi":"10.3164/jcbn.22-130","DOIUrl":"https://doi.org/10.3164/jcbn.22-130","url":null,"abstract":"<p><p>MicroRNA (miR)-499a-5p has been reported to regulate the progression of various tumours. However, the role of miR-499a-5p in breast cancer is unclear. The purpose of this study was to investigate the role and mechanism of miR-499a-5p in breast cancer. The growth effect of miR-499a-5p on breast cancer cells was investigated by the CCK-8 assay, wound healing assay and Transwell invasion assay. The luciferase activity assay was used to verify the downstream targets of miR-499a-5p. The levels of GSH, MDA, and ROS were detected by kits. Quantitative real-time PCR and Western blot were used to determine the expression levels of TMEM189, COX-2, GPX4, and other related genes in cells. miR-499a-5p was down-regulated in MDA-MB-231 cells and was shown to reduced the viability, migration and invasion of MDA-MB-231 cells. Further studies revealed that TMEM189 is a target of miR-499a-5p. miR-499a-5p inhibited breast cancer cell growth by downregulating TMEM189. Furthermore, the down-regulation of TMEM189 promotes ferroptosis in breast cancer cells. The low expression of TMEM189 inhibited the development of breast cancer through the ferroptosis pathway. We have demonstrated for the first time that miR-499a-5p inhibits breast cancer progression by targeting the TMEM189-mediated ferroptosis pathway.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"154-160"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d2/79/jcbn22-130.PMC10493215.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240629","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
Metabolomics analysis of amino acid and fatty acids in colorectal cancer patients based on tandem mass spectrometry. 基于串联质谱法的结直肠癌患者氨基酸和脂肪酸代谢组学分析。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.22-110
Zhuo Zhao, Jing Bai, Chang Liu, Yansong Wang, Shuang Wang, Furong Zhao, Qiufang Gu
{"title":"Metabolomics analysis of amino acid and fatty acids in colorectal cancer patients based on tandem mass spectrometry.","authors":"Zhuo Zhao,&nbsp;Jing Bai,&nbsp;Chang Liu,&nbsp;Yansong Wang,&nbsp;Shuang Wang,&nbsp;Furong Zhao,&nbsp;Qiufang Gu","doi":"10.3164/jcbn.22-110","DOIUrl":"https://doi.org/10.3164/jcbn.22-110","url":null,"abstract":"<p><p>Metabolic differences between colorectal cancer (CRC) and NI (NI) play an important role in early diagnoses and in-time treatments. We investigated the metabolic alterations between CRC patients and NI, and identified some potential biomarkers, and these biomarkers might be used as indicators for diagnosis of CRC. In this study, there were 79 NI, 50 CRC I patients, 52 CRC II patients, 56 CRC III patients, and 52 CRC IV patients. MS-MS was used to measure the metabolic alterations. Univariate and multivariate data analysis and metabolic pathway analysis were applied to analyze metabolic data and determine differential metabolites. These indicators revealed that amino acid and fatty acids could separate these groups. Several metabolites indicated an excellent variables capability in the separation of CRC patients and NI. Ornithine, arginine, octadecanoyl carnitine, palmitoyl carnitine, adipoyl carnitine, and butyryl carnitine/propanoyl carnitine were selected to distinguish the CRC patients and NI. And methionine and propanoyl carnitine, were directly linked to different stages of CRC. Receiver operating characteristics curves and variables importance in projection both represented an excellent performance of these metabolites. In conclusion, we assessed the difference between CRC patients and NI, which supports guidelines for an early diagnosis and effective treatment.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"161-171"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/30/9a/jcbn22-110.PMC10493213.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10232123","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
Quality analysis of the clinical laboratory literature and its effectiveness on clinical quality improvement: a systematic review. 临床实验室文献的质量分析及其对提高临床质量的作用:系统综述。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 DOI: 10.3164/jcbn.23-22
Ahmed Shabbir Chaudhry, Yu Inata, Etsuko Nakagami-Yamaguchi
{"title":"Quality analysis of the clinical laboratory literature and its effectiveness on clinical quality improvement: a systematic review.","authors":"Ahmed Shabbir Chaudhry,&nbsp;Yu Inata,&nbsp;Etsuko Nakagami-Yamaguchi","doi":"10.3164/jcbn.23-22","DOIUrl":"https://doi.org/10.3164/jcbn.23-22","url":null,"abstract":"<p><p>Quality improvement in clinical laboratories is crucial to ensure accurate and reliable test results. With increasing awareness of the potential adverse effects of errors in laboratory practice on patient outcomes, the need for continual improvement of laboratory services cannot be overemphasized. A literature search was conducted on PubMed and a web of science core collection between October and February 2021 to evaluate the scientific literature quality of clinical laboratory quality improvement; only peer-reviewed articles written in English that met quality improvement criteria were included. A structured template was used to extract data, and the papers were rated on a scale of 0-16 using the Quality Improvement Minimum Quality Criteria Set (QI-MQCS). Out of 776 studies, 726 were evaluated for clinical laboratory literature quality analysis. Studies were analyzed according to the quality improvement and control methods and interventions, such as training, education, task force, and observation. Results showed that the average score of QI-MQCS for quality improvement papers from 1981-2000 was 2.5, while from 2001-2020, it was 6.8, indicating continuous high-quality improvement in the clinical laboratory sector. However, there is still room to establish a proper system to judge the quality of clinical laboratory literature and improve accreditation programs within the sector.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"108-115"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4e/27/jcbn23-22.PMC10493209.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10232118","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
NEK7 inhibition attenuates Aβ42-induced cognitive impairment by regulating TLR4/NF-κB and the NLRP3 inflammasome in mice. 通过调节TLR4/NF-κB和NLRP3炎性体,抑制NEK7可减轻Aβ42诱导的小鼠认知障碍。
IF 2.4 4区 医学
Journal of Clinical Biochemistry and Nutrition Pub Date : 2023-09-01 Epub Date: 2023-08-11 DOI: 10.3164/jcbn.22-105
Peng Li, Yifan He, Qian Yang, Hena Guo, Nini Li, Dongdong Zhang
{"title":"NEK7 inhibition attenuates Aβ<sub>42</sub>-induced cognitive impairment by regulating TLR4/NF-κB and the NLRP3 inflammasome in mice.","authors":"Peng Li, Yifan He, Qian Yang, Hena Guo, Nini Li, Dongdong Zhang","doi":"10.3164/jcbn.22-105","DOIUrl":"10.3164/jcbn.22-105","url":null,"abstract":"<p><p>NEK7 is a serine/threonine kinase that regulates cell mitosis and the activation of the nucleotide-binding oligomerization domain-like (NOD-like) receptor thermal protein domain associated protein 3 (NLRP3) inflammasome, and is related to neuroinflammation and neuronal damage. The purpose of this study was to explore the role and mechanism of NEK7 in cognitive impairment in Alzheimer's disease (AD). BV2 cells, a microglia cell line, was treated with Aβ<sub>42</sub>. NEK7 expression was measured with reverse transcription-quantitative polymerase chain reaction and Western blotting. An apoptosis kit was used to determine the apoptotic rate. APPswe/PS1dE9 (APP/PS1) transgenic mice were used as an <i>in vivo</i> AD model. The experimental mice were infected with sh-NEK7 lentivirus to downregulate NEK7. The Morris water maze was conducted to explore the effect of NEK7 downregulation on cognitive ability. The results showed that Aβ<sub>42</sub> significantly upregulated NEK7 in BV2 cells. Silencing NEK7 suppressed the decrease in BV2 viability and the increase in inflammation, oxidative stress and apoptosis induced by Aβ<sub>42</sub>. NEK7 mediated it effects through the TLR4/NF-κB signalling pathway and the NLRP3 inflammasome. Finally, inhibition of NEK7 alleviated the cognitive impairment in APP/PS1 mice. In conclusion, Silencing NEK7 suppresses Aβ<sub>42</sub>-induced cell apoptosis, inflammation and oxidative stress, and improves cognitive performance in AD mice. NEK7 may be a potential target for AD treatment.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"73 2","pages":"145-153"},"PeriodicalIF":2.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e1/bb/jcbn22-105.PMC10493210.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10240630","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
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