General physiology and biophysics最新文献_第2页

Co-expression and interaction network analysis identifies neutrophil-related genes as the core mediator of atrial fibrillation. 共表达和相互作用网络分析确定中性粒细胞相关基因是心房颤动的核心介质。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2024004

Shaolan Liang, Xiaoxue Zhang, Jia Chen, Yongcong He, Jun Lai

{"title":"Co-expression and interaction network analysis identifies neutrophil-related genes as the core mediator of atrial fibrillation.","authors":"Shaolan Liang, Xiaoxue Zhang, Jia Chen, Yongcong He, Jun Lai","doi":"10.4149/gpb_2024004","DOIUrl":"https://doi.org/10.4149/gpb_2024004","url":null,"abstract":"Atrial fibrillation (AF) is the most common cardiac arrhythmia and can cause serious complications. Several studies have shown that neutrophils may influence AF progression. However, the key genes related to neutrophils in AF have not been fully elucidated. Here, we downloaded microarray expression data of AF, and screened differentially expressed genes. Key immune cells in AF were identified by immune cell infiltration analysis. Weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) analysis were used to construct gene co-expression modules and identify hub genes. The association between key genes and neutrophils was then verified. Our results showed that 303 differentially expressed genes (DEGs) were screened in AF and sinus rhythm (SR), of which 194 were up-regulated and 109 were down-regulated. DEGs were mainly enriched in functions and pathways of neutrophil activation and biological functions of neutrophil activation-mediated immune response. Immune infiltration analysis revealed elevated levels of neutrophil infiltration in AF. WGCNA analysis revealed that the modules in dark red were associated with neutrophils. PPI analysis of these modules yielded 10 hub genes. S100A12, FCGR3B and S100A8 are 3 potential key genes related to neutrophils in AF, which are significantly positively correlated with neutrophils. These genes deserve further investigation and may be potential therapeutic targets for AF.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Quercetin decreases fructose drinking in model of fructose-induced insulin resistance. Unexpected uric acid and TBARS lowering effect of methyl cellulose vehicle and fructose combination. 槲皮素能降低果糖诱导的胰岛素抵抗模型中的果糖饮用量甲基纤维素载体和果糖组合具有意想不到的降低尿酸和 TBARS 的效果。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2024003

Goran Koricanac, Jana Hricoviniova, Snjezana Romic, Viktoria Dobrocsyova, Mojca Stojiljkovic, Katarina Krskova, Tamara Ivkovic, Stefan Zorad

{"title":"Quercetin decreases fructose drinking in model of fructose-induced insulin resistance. Unexpected uric acid and TBARS lowering effect of methyl cellulose vehicle and fructose combination.","authors":"Goran Koricanac, Jana Hricoviniova, Snjezana Romic, Viktoria Dobrocsyova, Mojca Stojiljkovic, Katarina Krskova, Tamara Ivkovic, Stefan Zorad","doi":"10.4149/gpb_2024003","DOIUrl":"https://doi.org/10.4149/gpb_2024003","url":null,"abstract":"The aim of this study was to improve insulin sensitivity in fructose-treated animals by ingestion of flavonoid quercetin. Several signs of insulin resistance have been developed in rats by drinking 10% fructose solution for 9 weeks. The effect of 6-week-gavage-administrated quercetin (20 mg/kg/day in 1% methyl cellulose solution) was monitored. Rats of the control groups received methyl cellulose vehicle as well. The most striking result of the quercetin treatment was the normalization of the fructose solution drinking to the level of drinking water intake. In addition, quercetin supplementation considerably decreased the plasma glucose and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) index in rats consuming fructose. Surprisingly, fructose ingestion did not elevate plasma uric acid, thiobarbituric acid reactive substances, nitrotyrosine, or advanced glycation end products fluorescence. Instead, a reduction of the above parameters was observed. In summary, these results indicate that quercetin supplementation reduces fructose drinking and decreases plasma glucose and the HOMA-IR index. Furthermore, methyl cellulose, in combination with fructose, causes uric acid - lowering, antioxidant and anti-glycation effects. Thus, methyl cellulose possibly shifts fructose metabolism in favor of the utilization of antioxidant features of fructose. Our results call for using methyl cellulose in sweetened beverages and other sweetened food.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Putative identification of proopiomelanocortin and neuropeptide-Y neurons of the arcuate nucleus by their response to leptin: in vivo electrophysiology study in male and female rats. 通过弓状核神经元对瘦素的反应推测识别前绒毛膜促皮质素和神经肽-Y神经元：雌雄大鼠体内电生理学研究。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 Epub Date: 2024-02-22 DOI: 10.4149/gpb_2024002

Daniil Grinchii, Viera Kominkova, Eliyahu Dremencov

{"title":"Putative identification of proopiomelanocortin and neuropeptide-Y neurons of the arcuate nucleus by their response to leptin: in vivo electrophysiology study in male and female rats.","authors":"Daniil Grinchii, Viera Kominkova, Eliyahu Dremencov","doi":"10.4149/gpb_2024002","DOIUrl":"10.4149/gpb_2024002","url":null,"abstract":"The arcuate nucleus (ARN) of the hypothalamus is involved in multiple biological functions, such as feeding, sexual activity, and the regulation of the cardiovascular system. It was reported that leptin increased c-Fos expression in the proopiomelanocortin (POMC)- and decreased it in the neuropeptide-Y (NPY)-positive neurons of the ARN, suggesting that it stimulates the former, and inhibits the later. This study aimed at the direct electrophysiological examination of the effect of leptin on ARN neurons and to investigate potential sex-dimorphic changes. Wistar rats were anesthetized with urethane and the electrodes were inserted into the ARN. After a spontaneous active neuron was recorded for at least one minute, leptin was administered intravenously, and the firing activity of the same neuron was recorded for two additional minutes. It was found that approximately half of the ARN neurons had an excitatory, and another half an inhibitory response to the leptin administration. The excitability of the neurons with excitatory response to leptin was not different between the sexes. The average firing rate of the neurons with inhibitory response to leptin in females was, however, significantly lower comparing to the males. The obtained results demonstrate that the ARN neurons with stimulatory response to leptin are POMC and those with inhibitory response are NPY neurons. NPY Y1 receptor be might responsible, at least in part, for the sex differences in the excitability of the neurons putatively identified as NPY neurons.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ampelopsin facilitates diabetic wound healing and keratinocyte cell progression by inhibiting the NLRP3 inflammasome pathway in macrophages. 安泼辣素通过抑制巨噬细胞中的 NLRP3 炎性体通路，促进糖尿病伤口愈合和角质细胞进展。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2023039

Qiong Zhou, Geng Cheng

{"title":"Ampelopsin facilitates diabetic wound healing and keratinocyte cell progression by inhibiting the NLRP3 inflammasome pathway in macrophages.","authors":"Qiong Zhou, Geng Cheng","doi":"10.4149/gpb_2023039","DOIUrl":"10.4149/gpb_2023039","url":null,"abstract":"Ampelopsin (AMP) had a wound-healing effect in rat skin wounds with or without purulent infection. However, the role of AMP in diabetic wound healing remains poorly defined. Wounds were created on the dorsal skin of type 2 diabetic mouse model, and the histological features of wounds were examined by hematoxylin and eosin (HE) staining. Caspase-1 activity and the secretion of inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Cell viability and migration were examined through cell counting kit-8 (CCK-8) and wound healing assays, respectively. AMP facilitated wound healing in vivo. AMP notably facilitated platelet endothelial cell adhesion molecule-31 (CD31), collagen type I alpha 1 chain (COL1A1), and alpha-smooth muscle actin (α-SMA), and inhibited matrix metallopeptidase 9 (MMP9) and cyclooxygenase 2 (Cox2) expression in diabetic wounds. The inflammasome pathway was implicated in skin injury. AMP inhibited pro-inflammatory factor secretions and NLR family pyrin domain containing 3 (NLRP3) inflammasome pathway in diabetic wounds and high glucose-treated THP-1 macrophages. AMP-mediated NLRP3 inflammasome inhibition in THP-1 macrophages increased cell viability and migratory capacity in HaCaT cells. AMP facilitated diabetic wound healing and increased keratinocyte cell viability and migratory ability by inhibiting the NLRP3 inflammasome pathway in macrophages.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141074939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CCCTC-binding factor suppresses alpha-2-macroglobulin transcription to improve vascular endothelial cell functions in lower extremity arteriosclerosis obliterans. CCCTC结合因子可抑制α-2-巨球蛋白转录，从而改善下肢动脉硬化闭塞症的血管内皮细胞功能。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2024005

Tianmin He, Mengqiang You, Huixin Zhu, Peng Chen, Shanhong Fang

{"title":"CCCTC-binding factor suppresses alpha-2-macroglobulin transcription to improve vascular endothelial cell functions in lower extremity arteriosclerosis obliterans.","authors":"Tianmin He, Mengqiang You, Huixin Zhu, Peng Chen, Shanhong Fang","doi":"10.4149/gpb_2024005","DOIUrl":"10.4149/gpb_2024005","url":null,"abstract":"Vascular endothelial cell functions affect lower extremity arteriosclerosis obliterans (LEASO), while alpha-2-macroglobulin (A2M) and CCCTC-binding factor (CTCF) are closely related to the function of such cells. This paper aims to identify the influences of CTCF on vascular endothelial cells in LEASO by regulating A2M. A rat model of LEASO was established to measure intima-media ratio, blood lipid, and inflammatory factor levels. By constructing LEASO cell models, cell viability and apoptosis were assayed, while autophagy-related proteins, CTCF and A2M levels in femoral artery tissues and HUVECs were determined. The transcriptional regulation of CTCF on A2M was verified. In LEASO rat models, femoral artery lumen was narrowed and endothelial cells were disordered; levels of total cholesterol, IL-1, and TNF-α enhanced, and HDL-C decreased, with strong expression of A2M and low expression of CTCF. The viability of ox-LDL-treated HUVECs was decreased, together with higher apoptosis, lower LC3II/I expression, and higher p62 expression, which were reversed by sh-A2M transfection. Overexpression of CTCF inhibited A2M transcription, promoted the viability and autophagy of HUVECs, and decreased apoptosis. Collectively, CTCF improves the function of vascular endothelial cells in LEASO by inhibiting A2M transcription.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

KRAS depletion suppresses ferroptosis and affects Hippo pathway in cataract. 抑制 KRAS 可抑制白内障中的铁蛋白沉积并影响 Hippo 通路。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2024009

Hongda Jiang, Yinggui Yu, Yu Yan

{"title":"KRAS depletion suppresses ferroptosis and affects Hippo pathway in cataract.","authors":"Hongda Jiang, Yinggui Yu, Yu Yan","doi":"10.4149/gpb_2024009","DOIUrl":"10.4149/gpb_2024009","url":null,"abstract":"Cataract, a painless and progressive disorder is manifested as the opacification of the lens that represents the most significant cause of blindness worldwide. The objective of this study is to unveil the function of Kirsten rat sarcoma (KRAS) and potential action mechanisms against cataract. The ferroptosis-associated differentially expressed genes (DEGs) and pivot genes were extracted through the comprehensive bioinformatics methods. Erastin was applied for inducing ferroptosis in hydrogen peroxide (H2O2)-treated SRA01/04 cells, and validated by detecting content of intracellular iron, glutathione (GSH), malondialdehyde (MDA). Additionally, the effects of KRAS deficiency on ferroptosis were determined by functional assays. The proteins expression related to ferroptosis and Hippo pathway were determined by Western blotting. A total of 73 ferroptosis-related DEGs were discovered, and 6 critical core genes were confirmed upregulation in cataract cell model. The H2O2-treated SRA01/04 cells exhibited decrease of cell viability and proliferation, iron accumulation, MDA increase, GSH consumption, rise of COX2 and decline of GPX4, with further aggravated under erastin treatment, while the phenomena were improved by KRAS knockdown. Additionally, KRAS deficiency was involved in the Hippo signalling pathway activation. Downregulation of KRAS might restrain ferroptosis and affect Hippo pathway in cataract.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Trivalent anions as probes of the CFTR channel pore. 作为 CFTR 通道孔探针的三价阴离子。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2024-05-01 DOI: 10.4149/gpb_2024007

Paul Linsdell

{"title":"Trivalent anions as probes of the CFTR channel pore.","authors":"Paul Linsdell","doi":"10.4149/gpb_2024007","DOIUrl":"10.4149/gpb_2024007","url":null,"abstract":"The cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel uses positively charged amino-acid side-chains to form binding sites for permeating anions. These binding sites have been investigated experimentally using a number of anionic probes. Mutations that alter the distribution of positive and negative charges within the pore have differential effects on the binding of monovalent versus divalent anions. This study uses patch clamp recording from wild-type and pore-mutant forms of CFTR to investigate small trivalent anions (Co(NO2)63-, Co(CN)3- and IrCl63-) as potential probes of anion binding sites. These anions caused weak block of Cl- permeation in wild-type CFTR (Kd ≥ 700 μM) when applied to the intracellular side of the membrane. Mutations that increase the density of positive charge within the pore (E92Q, I344K, S1141K) increased the binding affinity of these anions 80-280-fold, and also greatly increased the voltage-dependence of block, consistent with fixed charges in the pore affecting monovalent : multivalent anion selectivity. However, high-affinity pore block by Co(NO2)63-apparently did not alter channel gating, a hallmark of high-affinity binding of divalent Pt(NO2)42- ions within the pore. This work increases the arsenal of probes available to investigate anion binding sites within Cl- channel pores.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Daidzein protects endothelial cells against high glucose-induced injury through the dual-activation of PPARα and PPARγ. 通过 PPARα 和 PPARγ 的双重激活，Daidzein 可保护内皮细胞免受高血糖诱导的损伤。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023041

Xuemei Yang, Xinhui Jiang, Changqing Liu, Chuang Yang, Sheng Yao, Hongmei Qiu, Junxia Yang, Ke Wu, Hong Liao, Qingsong Jiang

{"title":"Daidzein protects endothelial cells against high glucose-induced injury through the dual-activation of PPARα and PPARγ.","authors":"Xuemei Yang, Xinhui Jiang, Changqing Liu, Chuang Yang, Sheng Yao, Hongmei Qiu, Junxia Yang, Ke Wu, Hong Liao, Qingsong Jiang","doi":"10.4149/gpb_2023041","DOIUrl":"10.4149/gpb_2023041","url":null,"abstract":"Endothelial damage caused by persistent glucose and lipid metabolism disorders is the main reason of diabetic vascular diseases. Daidzein exerts positive effects on vascular dysfunction. Peroxisome proliferator-activated receptors (PPARs) regulate critically glucose and lipid metabolism. However, the interaction of daidzein to PPARs is still insufficiently explored. In this study, the cell proliferation was detected by EdU. The intrinsic activity and binding affinity of daidzein for human PPARs (hPPARs) were estimated by transactivation reporter gene test and HPLC-UV method, respectively. Daidzein significantly reversed high glucose (HG, at 30 mmol/l)-induced injury in HUVECs, which was inhibited by both PPARα and PPARγ antagonist, but no PPARβ antagonist. Daidzein selectively activated hPPARα and hPPARγ1, but weakly hPPARβ. Additionally, daidzein also bound to both hPPARα and hPPARγ1. The findings suggested that daidzein may be a PPARα and PPARγ dual-agonist. The amelioration of daidzein on HUVECs from hyperglycemia may be mediated by the activation of PPARα and PPARγ receptors.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TRIM67 interacts with ENAH to regulate the apoptosis and autophagy of lung cancer cells. TRIM67 与ENAH相互作用，调节肺癌细胞的凋亡和自噬。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023037

Rui Liu, Kun Miao, Ling Gao, Ling He

引用次数: 0

The role of endoplasmic reticulum stress-related genes in the diagnosis and subtyping of non-alcoholic fatty liver disease. 内质网应激相关基因在非酒精性脂肪肝的诊断和亚型分类中的作用。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2024-03-01 DOI: 10.4149/gpb_2023042

Zihao Guo, Xiaoxiao Yu, Zhihao Fang, Kai Yang, Changxu Liu, Zhichao Dong, Chang Liu

{"title":"The role of endoplasmic reticulum stress-related genes in the diagnosis and subtyping of non-alcoholic fatty liver disease.","authors":"Zihao Guo, Xiaoxiao Yu, Zhihao Fang, Kai Yang, Changxu Liu, Zhichao Dong, Chang Liu","doi":"10.4149/gpb_2023042","DOIUrl":"10.4149/gpb_2023042","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide. Chronic activation of endoplasmic reticulum stress (ERS) in hepatocytes may promote the development of NAFLD, yet endoplasmic reticulum stress-related genes (ERSGs) have not been studied in NAFLD. Our aim is to study the relationship between ERSGs and the immune microenvironment of NAFLD patients and to construct predictive models. We screened 48 endoplasmic reticulum stress-related differentially expressed genes (ERSR-DEGs) using data from two GEO datasets and the GeneCards database. Enrichment analysis revealed that ERSR-DEGs are closely associated with immune-related pathways and functions. The immune infiltration profile of NAFLD was obtained by single sample gene set enrichment analysis (ssGSEA). There were significant differences in immune cell infiltration and immune function between NAFLD group and control group. Using 113 NAFLD samples, we explored two molecular clusters based on ERSR-DEGs. A five-gene SVM model was selected as the best machine learning model, and a nomogram based on five-gene SVM model showed good predictive efficiency. The mRNA expression levels of POR, PPP1R15A, FOS and FAS were significantly different between NAFLD mice and healthy mice. In conclusion, ERS is closely associated with the development of NAFLD. We established a promising and SVM-based predictive model to assess the risk of disease in patients with ERS subtypes and NAFLD.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0