{"title":"Reactive oxygen species induced by indomethacin enhance accumulation of heme carrier protein 1 and hematoporphyrin accumulation <i>in vitro</i> and <i>in vivo</i> in a brain tumor model.","authors":"Hidehiro Kohzuki, Hiromu Ito, Hiromi Kurokawa, Hirofumi Matsui, Tetsuya Yamamoto, Eiichi Ishikawa","doi":"10.3164/jcbn.23-20","DOIUrl":"10.3164/jcbn.23-20","url":null,"abstract":"<p><p>Photodynamic therapy (PDT) is useful for various cancers such as high-grade glioma and cancers of other organs. However, the mechanism of tumor-specific accumulation of porphyrin is not clear. The authors previously reported that heme carrier protein 1 (HCP1) contributes to the transport of porphyrins; specifically, we showed that the production of cancer-specific reactive oxygen species from mitochondria (mitROS) leads in turn to enhanced HCP1 expression. Indomethacin (IND), a non-steroidal anti-inflammatory drug, increases ROS production by affecting mitochondrial electron transfer system. In the present work, the authors investigated the effect of pretreatment with IND on cancer-specific porphyrin accumulation, using both a glioma cell line and a rat brain tumor model. This work demonstrated that exposure of a rat glioma cell to IND results in increased generation of cancer-specific mitROS and accumulation of HCP1 expression and porphyrin concentration. Additionally, systemic dosing of a brain tumor animal model with IND resulted in elevated cellular accumulation of porphyrin in tumor cell. This is an effect not seen with normal brain tissue. Thus, the administration of IND increases intracellular porphyrin concentrations in tumor cell without exerting harmful effects on normal brain tissue, and increased porphyrin concentration in tumor cell may lead to improved PDT effect.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"207-212"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141156176","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}
{"title":"Crosstalk between oxygen signaling and iron metabolism in renal interstitial fibroblasts.","authors":"Norio Suzuki, Yuma Iwamura, Koichiro Kato, Hirotaka Ishioka, Yusuke Konta, Koji Sato, Nao Uchida, Noa Koida, Hiroki Sekine, Tetsuhiro Tanaka, Naonori Kumagai, Taku Nakai","doi":"10.3164/jcbn.24-8","DOIUrl":"10.3164/jcbn.24-8","url":null,"abstract":"<p><p>To maintain the oxygen supply, the production of red blood cells (erythrocytes) is promoted under low-oxygen conditions (hypoxia). Oxygen is carried by hemoglobin in erythrocytes, in which the majority of the essential element iron in the body is contained. Because iron metabolism is strictly controlled in a semi-closed recycling system to protect cells from oxidative stress caused by iron, hypoxia-inducible erythropoiesis is closely coordinated by regulatory systems that mobilize stored iron for hemoglobin synthesis. The erythroid growth factor erythropoietin (EPO) is mainly secreted by interstitial fibroblasts in the renal cortex, which are known as renal EPO-producing (REP) cells, and promotes erythropoiesis and iron mobilization. Intriguingly, EPO production is strongly induced by hypoxia through iron-dependent pathways in REP cells. Here, we summarize recent studies on the network mechanisms linking hypoxia-inducible EPO production, erythropoiesis and iron metabolism. Additionally, we introduce disease mechanisms related to disorders in the network mediated by REP cell functions. Furthermore, we propose future studies regarding the application of renal cells derived from the urine of kidney disease patients to investigate the molecular pathology of chronic kidney disease and develop precise and personalized medicine for kidney disease.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"179-184"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154200","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}
{"title":"Sebacic acid, a royal jelly-containing fatty acid, decreases LPS-induced IL-6 mRNA expression in differentiated human THP-1 macrophage-like cells.","authors":"Erika Ogawa, Nobuko Suzuki, Tetsuro Kamiya, Hirokazu Hara","doi":"10.3164/jcbn.23-16","DOIUrl":"10.3164/jcbn.23-16","url":null,"abstract":"<p><p>Macrophages produce many inflammatory mediators, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), in innate immune responses. However, excess production of these mediators by activated macrophages triggers deleterious effects, leading to disorders associated with inflammation. Royal jelly (RJ), a milky-white substance secreted by worker bees, contains unique fatty acids, including 10-hydroxy-2-decenoic acid (10H2DA) and sebacic acid (SA). 10H2DA has been reported to have various biological functions, such as anti-inflammation. However, the anti-inflammatory effect of SA is not fully understood. In this study, we investigated the effects of SA on lipopolysaccharide (LPS)-induced cytokine expression using differentiated human THP-1 macrophage-like cells. SA dose-dependently decreased LPS-induced mRNA expression of IL-6, but not TNF-α and IL-1β. SA suppressed the phosphorylation of signal transducers and activators of transcription 1 (STAT1) and STAT3, but hardly affected the activation of JNK, p38, or NF-κB. In addition, SA decreased LPS-induced interferon-β (IFN-β) expression, and the addition of IFN-β restored the inhibition by SA of LPS-induced STAT activation and IL-6 expression. Furthermore, SA suppressed LPS-induced nuclear translocation of interferon regulatory factor 3 (IRF3), a transcription factor responsible for IFN-β expression. Taken together, we conclude that SA selectively decreases LPS-induced expression of IL-6 mRNA through inhibition of the IRF3/IFN-β/STAT axis.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"192-198"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154661","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}
{"title":"Availability of dietary secoisolariciresinol diglucoside on borderline blood cholesterol level in men: a randomized, parallel, controlled, double-blinded clinical trial.","authors":"Kouta Ookoshi, Kento Sawane, Satoshi Fukumitsu, Kazuhiko Aida","doi":"10.3164/jcbn.23-122","DOIUrl":"10.3164/jcbn.23-122","url":null,"abstract":"<p><p>Borderline low-density lipoprotein cholesterol levels (120-139 mg/dl) increase the risk of cardiovascular disease. Therefore, the use of functional dietary nutrients is expected to control blood low-density lipoprotein cholesterol levels. This study aimed to evaluate the effect of dietary secoisolariciresinol diglucoside on blood cholesterol in healthy adults with borderline low-density lipoprotein cholesterol levels. A randomized, parallel, controlled, double-blinded clinical trial was performed for participants with borderline low-density lipoprotein cholesterol levels, for 12 weeks with secoisolariciresinol diglucoside (60 mg/day) or placebo. Lipid profile [low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio, total cholesterol, and triglycerides] and liver disease risk markers were measured at weeks 0, 4, 8, and 12. Analyzing 36 participants in each group revealed a significant interaction between treatment and time, indicating reduced low-density lipoprotein cholesterol (<i>p</i> = 0.049) and total cholesterol (<i>p</i> = 0.020) levels in secoisolariciresinol diglucoside-receiving men but not women. However, no significant differences were observed in other markers regardless of gender. The results suggest that a daily intake of 60 mg of secoisolariciresinol diglucoside lowers low-density lipoprotein cholesterol and total cholesterol levels in men with borderline low-density lipoprotein cholesterol, proposing secoisolariciresinol diglucoside potential as a functional dietary nutrient for cardiovascular disease prevention. This study was registered in the UMIN-CTR database (UMIN000046202).</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"261-266"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154182","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}
{"title":"Efficacy evaluation of upper gastrointestinal endoscopy screening for secondary prevention of gastric cancer using the standardized detection ratio during a medical check-up in Japan.","authors":"Chieko Tanaka, Koji Otani, Mitsuhiro Tamoto, Hisako Yoshida, Yuji Nadatani, Masaki Ominami, Shusei Fukunaga, Shuhei Hosomi, Noriko Kamata, Fumio Tanaka, Koichi Taira, Tatsuo Kimura, Shinya Fukumoto, Toshio Watanabe, Yasuhiro Fujiwara","doi":"10.3164/jcbn.24-28","DOIUrl":"10.3164/jcbn.24-28","url":null,"abstract":"<p><p>We used standardized detection ratio to evaluate the quality of nasal upper gastrointestinal endoscopy screening for the secondary prevention of gastric cancer, and examined the gastric cancer risk in the era of total <i>Helicobacter pylori</i> (<i>H. pylori</i>) eradication. We performed 21,931 upper gastrointestinal endoscopies, 77 subjects were diagnosed with gastric cancer. Of these, 28 had gastric cancer after <i>H. pylori</i> eradication, 47 had gastric cancer with <i>H. pylori</i>-positive or others, and 2 had <i>H. pylori</i>-negative gastric cancer. The Standardized detection ratios for men and women were 5.33 and 4.82, respectively. Multivariable logistic regression analyses performed exclusively on first endoscopy subjects, excluding <i>H. pylori</i>-negative gastric cancer, revealed that smoking was a risk factor for developing gastric cancer (adjusted odds ratio, 3.31; 95% confidence interval, 1.65-6.64; <i>p</i> = 0.001). A statistically significant interaction was found between daily alcohol consumpption and <i>H. pylori</i> eradication on gastric cancer development (<i>p</i> = 0.005). In conclusion, relatively high standardized detection ratio values suggest that an appropriate endoscopic diagnosis of gastric cancer should be performed during a medical check-up. Smoking is a risk factor for developing gastric cancer, and continued alcohol consumption suggests a possible risk for developing gastric cancer after <i>H. pylori</i> eradication.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"253-260"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154434","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}
{"title":"Nutritional roles and therapeutic potentials of dietary sphingomyelin in brain diseases.","authors":"Shoug Alashmali","doi":"10.3164/jcbn.23-97","DOIUrl":"10.3164/jcbn.23-97","url":null,"abstract":"<p><p>Sphingolipids have recently gained interest as potential players in variety of diseases due to their import roles in human body particularly, the brain. As sphingomyelin is the most common type of sphingolipids, deficits in its distribution to brain cells may contribute to neurological anomalies. However, data is limited regarding the impact of different levels of dietary sphingomyelin intake on neural function especially if this approach can boost cognition and prevent neurological disorders. This review evaluates the effect of dietary sphingomyelin and its metabolites (ceramide and sphingosine-1-phosphate) in animal models and in humans, with a primary focus on its impact on brain health. Additionally, it proposes multiple neuroenhancing effects of sphingomyelin-rich diet. This presents an opportunity to stimulate further research that aims to determine the therapeutic value of dietary sphingomyelin in preventing, improving or slowing the progression of central nervous system disorders.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"185-191"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154699","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}
{"title":"Involvement of α-klotho in growth hormone (GH) signaling.","authors":"Megumi Koike, Tetsuhiko Sato, Yuji Shiozaki, Aoi Komiya, Mizuki Miura, Ayami Higashi, Akane Ishikawa, Kaori Takayanagi, Minori Uga, Ken-Ichi Miyamoto, Hiroko Segawa","doi":"10.3164/jcbn.23-127","DOIUrl":"10.3164/jcbn.23-127","url":null,"abstract":"<p><p>Growth hormone (GH) exerts multiple effects on different organs directly or via its main mediator, insulin-like growth factor1 (IGF1). In this study, we focused on the novel relationship between GH action and the antiaging hormone α-klotho. Immunofluorescent staining of α-klotho was observed in the renal distal tubules and pituitary glands of somatostatin- and GH-positive cells in wild-type (WT) mice. Treatment of 4-week-old WT mice with GH increased IGF1 mRNA expression in the pituitary gland, liver, heart, kidney, and bone but increased α-klotho mRNA expression only in the pituitary gland, kidney, and bone. Increased α-klotho protein levels were observed in the kidney but not in the pituitary gland. No induction of α-klotho RNA expression by GH was observed in juvenile mice with kidney disease, indicating GH resistance. Furthermore, GH and α-klotho supplementation in HEK293 cells transfected with GHR increased Janus kinase 2 mRNA (a GH downstream signal) expression compared to supplementation with GH alone. In conclusion, we suggest that 1) the kidney is the main source of secreted α-klotho, which is detected in blood by the downstream action of GH, 2) α-klotho induction by GH is resistant in kidney disease, and 3) α-klotho might be an enhanced regulator of GH signaling.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"221-229"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154538","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}
{"title":"Effect of high-amylose rice \"Hoshinishiki\" on postprandial glucose levels measured by continuous glucose monitoring in patients with diabetes.","authors":"Jia Li, Koutatsu Maruyama, Satoshi Minakuchi, Kumiko Toshimitu, Ryoichi Kawamura, Yasunori Takata, Haruhiko Osawa","doi":"10.3164/jcbn.23-75","DOIUrl":"10.3164/jcbn.23-75","url":null,"abstract":"<p><p>We examined the effect of consuming Hoshinishiki, a type of high-amylose rice, on postprandial glucose as measured by continuous glucose monitoring in diabetes patients. A single-blinded clinical trial involving 11 hospitalized patients diagnosed with type 1 or type 2 diabetes was performed. The patients consumed high-amylose rice for 2 days (days 2 and 4 of the study) and control rice for 2 days (days 1 and 3 of the study). Linear mixed models were used to test the effects on the 24-h mean glucose levels, time in range (TIR), incremental area under the curve of glucose levels at 2 h after meals, the average glucose levels at 1, 2, and 3 h after meals, and the maximum glucose levels within 3 h. The results showed that the consumption of high-amylose rice led to significantly lower 24-h mean glucose levels, levels at 2 and 3 h after a meal, and postprandial glucose peak levels within 3 h, as well as significantly higher TIR. A similar trend was observed when the analysis was restricted to patients with type 2 diabetes. These results suggest that high-amylose rice may be a more beneficial staple food for glycemic control than regular rice.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"230-234"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154348","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}
{"title":"Porphyromonas gingivalis lipopolysaccharide regulates cell proliferation, apoptosis, autophagy in esophageal squamous cell carcinoma via TLR4/MYD88/JNK pathway.","authors":"Chi Lu, Zhiguo Chen, Hongda Lu, Ke Zhao","doi":"10.3164/jcbn.22-138","DOIUrl":"10.3164/jcbn.22-138","url":null,"abstract":"<p><p>The study aimed to explore the impact and potential mechanism of Porphyromonas gingivalis lipopolysaccharide (LPS-PG) on esophageal squamous cell carcinoma (ESCC) cell behavior. ESCC cells from the Shanghai Cell Bank were used, and TLR4, MYD88, and JNK interference vectors were constructed using adenovirus. The cells were divided into six groups: Control, Model, Model + radiotherapy + LPS-PG, Model + radiotherapy + 3-MA, Model + radiotherapy + LPS-PG + 3-MA, and Model + radiotherapy. Various radiation doses were applied to determine the optimal dose, and a radioresistant ESCC cell model was established and verified. CCK8 assay measured cell proliferation, flow cytometry and Hoechst 33258 assay assessed apoptosis, and acridine orange fluorescence staining tested autophagy. Western blot analyzed the expression of LC3II, ATG7, P62, and p-ULK1. Initially, CCK8 and acridine orange fluorescence staining identified optimal LPS-PG intervention conditions. Results revealed that 10 ng/ml LPS-PG for 12 h was optimal. LPS-PG increased autophagy activity, while 3-MA decreased it. LPS-PG + 3-MA group exhibited reduced autophagy. LPS-PG promoted proliferation and autophagy, inhibiting apoptosis in radioresistant ESCCs. LPS-PG regulated TLR4/MYD88/JNK pathway, enhancing ESCC autophagy, proliferation, and radioresistance. In conclusion, LPS-PG, through the TLR4/MYD88/JNK pathway, promotes ESCC proliferation, inhibits apoptosis, and enhances radioresistance by inducing autophagy.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 3","pages":"213-220"},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11111472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154654","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}
{"title":"Crosstalk between NOD2 and TLR2 suppresses the development of TLR2-mediated experimental colitis.","authors":"Natsuki Okai, Yasuhiro Masuta, Yasuo Otsuka, Akane Hara, Sho Masaki, Ken Kamata, Kosuke Minaga, Hajime Honjo, Masatoshi Kudo, Tomohiro Watanabe","doi":"10.3164/jcbn.23-87","DOIUrl":"10.3164/jcbn.23-87","url":null,"abstract":"<p><p>Nucleotide-binding oligomerization domain 2 (NOD2) is an intracellular sensor for muramyl dipeptide (MDP), a degradation product of bacterial cell wall peptidoglycan (PGN). PGN stimulates cell-surface Toll-like receptor 2 (TLR2) independently of NOD2, indicating the presence of crosstalk between extracellular TLR2 and intracellular NOD2 upon exposure to PGN. NOD2-deficient mice were sensitive, while TLR2-deficient mice were resistant to experimental colitis induced by intrarectal administration of PGN. Severe colitis in NOD2-deficient mice was accompanied by increased expression of nuclear factor-kappa B-dependent cytokines and decreased expression of autophagy-related 16-like 1 (ATG16L1). MDP activation of NOD2 enhanced autophagy mediated by TLR2 in human dendritic cells. mRNA expression of TLR2 tended to be higher in the colonic mucosa of patients with active ulcerative colitis compared to that of those in remission. Induction of remission was associated with increased mRNA expression of ATG16L1 in both ulcerative colitis and Crohn's disease patients. Conversely, mRNA expression of receptor-interacting serine/threonine-protein kinase 2 was higher in the inflammatory colonic mucosa of patients with active disease than in the non-inflamed mucosa of patients in remission, in both ulcerative colitis and Crohn's disease. These findings highlight the role of NOD2-TLR2 crosstalk in the immunopathogenesis of colitis.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"74 2","pages":"146-153"},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10948350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140174902","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}