Cytotechnology最新文献_第6页

Degranulation of RBL-2H3 rat basophilic leukemia cells is synergistically inhibited by combined treatment with nobiletin and lactoferrin 联合使用金霉素和乳铁蛋白可协同抑制 RBL-2H3 大鼠嗜碱性粒细胞的脱颗粒作用

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-04-04 DOI: 10.1007/s10616-024-00625-2

Kaho Miyake, Mamoru Tanaka, Sayaka Yokoyama, Lu Rui, Ayaka Koida, Hana Kozai, Takeaki Okamoto

{"title":"Degranulation of RBL-2H3 rat basophilic leukemia cells is synergistically inhibited by combined treatment with nobiletin and lactoferrin","authors":"Kaho Miyake, Mamoru Tanaka, Sayaka Yokoyama, Lu Rui, Ayaka Koida, Hana Kozai, Takeaki Okamoto","doi":"10.1007/s10616-024-00625-2","DOIUrl":"https://doi.org/10.1007/s10616-024-00625-2","url":null,"abstract":"The aim of this study was to elucidate the anti-allergic effects of polymethoxyflavonoids in combination with milk proteins and the mechanism of inhibition. Three polymethoxyflavonoids and two milk proteins were exposed to the rat basophilic leukemia cell line RBL-2H3. β-hexosaminidase was used as an indicator of degranulation inhibition. The mechanism of inhibition was examined by measuring intracellular Ca2+ levels and western blot method. In the degranulation inhibition test with polymethoxyflavonoids and milk proteins alone, nobiletin was the strongest inhibitor in the polymethoxyflavonoid group and lactoferrin in the milk protein group. Next, co-stimulation with nobiletin and lactoferrin showed stronger synergistic degranulation inhibition than treatment with nobiletin or lactoferrin alone. Western blot analysis showed that co-stimulation with nobiletin and lactoferrin significantly downregulated the induction of phospholipase Cγ 1 phosphorylation. The degranulation response in RBL-2H3 cells was synergistically suppressed by co-stimulation of nobiletin and lactoferrin acting on both Ca2+-dependent and Ca2+-independent pathways.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"2011 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140603472","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

LncRNA MIR181A2HG negatively regulates human keratinocytes proliferation by binding SRSF1 LncRNA MIR181A2HG 通过结合 SRSF1 负向调节人类角朊细胞的增殖

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-03-26 DOI: 10.1007/s10616-024-00621-6

{"title":"LncRNA MIR181A2HG negatively regulates human keratinocytes proliferation by binding SRSF1","authors":"","doi":"10.1007/s10616-024-00621-6","DOIUrl":"https://doi.org/10.1007/s10616-024-00621-6","url":null,"abstract":"<h3>Abstract</h3> Psoriasis is a common chronic inflammatory skin disease. Abnormal proliferation of keratinocytes plays an important role in the pathogenesis of psoriasis. Long non-coding RNAs (lncRNAs) are involved in the regulation of a variety of cell biological processes. The purpose of this study was to investigate the potential role of lncRNA MIR181A2HG in the proliferation of human keratinocytes. qRT-PCR and Western blotting were performed to measure the expression levels of MIR181A2HG, SRSF1, KRT6, and KRT16 in tissue specimens and HaCaT keratinocytes. The effects of MIR181A2HG on HaCaT keratinocytes proliferation were evaluated using Cell Counting Kit-8 (CCK-8) assays, 5-Ethynyl-2’-deoxyuridine (EdU) incorporation, and cell-cycle assays. RNA pulldown-mass spectrometry (MS) was applied to identify the proteins interacting with MIR181A2HG. RNA pull-down-Western blotting and RNA immunoprecipitation coupled with real-time quantitative reverse transcription-PCR (RIP-qRT-PCR) assays were used to determine the interactions between MIR181A2HG and its RNA-binding proteins (RBPs). MIR181A2HG was down-regulated in psoriasis tissues. MIR181A2HG overexpression induced G0/G1 and G2/M phase cell cycle arrest and decreased the protein levels of KRT6, KRT16, Cyclin D1, CDK4, and Cyclin A2 in HaCaT keratinocytes. MIR181A2HG knockdown showed the opposite effect. By using RNA pulldown-MS, 356 proteins were identified to interact with MIR181A2HG potentially. Bioinformatics analysis showed that NOP56 and SRSF1 may be RNA binding proteins (RBPs) that may be interact with MIR181A2HG. Furthermore, by using RNA pull-down-Western blotting and RIP-qRT-PCR, SRSF1 was determined to interact with MIR181A2HG. Moreover, silencing of SRSF1 inhibited keratinocytes proliferation, which could be reversed with the knockdown of MIR181A2HG. Our findings indicated that MIR181A2HG can negatively regulate HaCaT keratinocytes proliferation by binding SRSF1, suggesting that MIR181A2HG and SRSF1 may serve as potential targets for the treatment of psoriasis.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"1 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140302196","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

Schizandrin A enhances the sensitivity of gastric cancer cells to 5-FU by promoting ferroptosis 五味子异黄酮 A 通过促进铁变态反应增强胃癌细胞对 5-FU 的敏感性

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-03-25 DOI: 10.1007/s10616-024-00623-4

{"title":"Schizandrin A enhances the sensitivity of gastric cancer cells to 5-FU by promoting ferroptosis","authors":"","doi":"10.1007/s10616-024-00623-4","DOIUrl":"https://doi.org/10.1007/s10616-024-00623-4","url":null,"abstract":"<h3>Abstract</h3> Schizandrin A (Sch A) exert anticancer and multidrug resistance-reversing effects in a variety of tumors, but its effect on 5-fluorouracil (5-Fu) in gastric cancer (GC) cells remains unclear. The aim of the present study was to examine the resistance-reversing effect of Schizandrin A and assess its mechanisms in 5-Fu-resistant GC cells.5-Fu-sensitive GC cells were treated with 5-Fu and 5-Fu-resistant GC cells AGS/5-Fu and SGC7901/5-Fu were were established. These cells were stimulated with Schizandrin A alone or co-treated with 5-Fu and their effect on tumor cell growth, proliferation, migration, invasion and ferroptosis-related metabolism were investigated both in vitro and in vivo. A number of additional experiments were conducted in an attempt to elucidate the molecular mechanism of increased ferroptosis. The results of our study suggest that Schizandrin A in combination with 5-Fu might be useful in treating GC by reverse drug resistance. It was shown that Schizandrin A coadministration suppressed metastasis and chemotherapy resistance in 5-Fu-resistant GC cells through facilitating the onset of ferroptosis, which is an iron-dependent form of cell death, which was further demonstrated in a xenograft nude mouse model. Mechanistically, Schizandrin A co-administration synergistically increased the expression of transferin receptor, thus iron accumulates within cells, leading to lipid peroxidation, which ultimately results in 5-Fu-resistant GC cells death. The results of this study have provided a novel strategy for increasing GC chemosensitivity, indicating Schizandrin A as a novel ferroptosis regulator. Mechanistically, ferroptosis is induced by Schizandrin A coadministration via increasing transferrin receptor expression.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"97 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140302189","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

Anti-cancer drug-mediated increase in mitochondrial mass limits the application of metabolic viability-based MTT assay in cytotoxicity screening 抗癌药物介导的线粒体质量增加限制了基于代谢活力的 MTT 检测在细胞毒性筛选中的应用

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-03-21 DOI: 10.1007/s10616-024-00618-1

Abhishek Kumar, Yogesh Rai, Anant Narayan Bhatt

{"title":"Anti-cancer drug-mediated increase in mitochondrial mass limits the application of metabolic viability-based MTT assay in cytotoxicity screening","authors":"Abhishek Kumar, Yogesh Rai, Anant Narayan Bhatt","doi":"10.1007/s10616-024-00618-1","DOIUrl":"https://doi.org/10.1007/s10616-024-00618-1","url":null,"abstract":"The high-throughput metabolic viability-based colorimetric MTT test is commonly employed to screen the cytotoxicity of different chemotherapeutic drugs. The assay assumes a cell density-dependent linear correlation with the MTT spectral absorbance. Therefore, the present study aimed to compare the cytotoxicity assessment between the MTT assay and gold standard cell number enumeration. The cytotoxicity was induced by Cisplatin, Etoposide, and Doxorubicin in human lung epithelial adenocarcinoma cells (A549) and cervix carcinoma (HeLa) cell lines. The mitochondrial mass was estimated, and immunoblotting of succinate dehydrogenase (SDH-A) was performed following drug treatment in both cell lines. Student’s t-test paired analysis was employed to calculate the significance of the results, where the value p < 0.05 was considered statistically significant. The drug-induced cytotoxic response estimated by MTT absorbance did not show any significant difference with respect to control, and no correlation was observed with the enumerated cell number in both A549 and HeLa cells. Interestingly, per-cell metabolic viability was found to be increased by 1.18 to 3.26-fold (p < 0.05) following drug treatment. Further, mechanistic investigation revealed a drug concentration-dependent significant increase in mitochondrial mass (1.21 to 4.2-fold) and upregulation of SDH protein (50–70%) as well as enzymatic activity with respect to control in both A549 and Hela cells. The limitation of the MTT assay for drug-induced cytotoxicity assessment is due to increased mitochondrial mass and SDH upregulation in surviving cells, leading to enhanced formazan formation. This leads to a lack of correlation between cell number and MTT spectral absorbance, suggesting that the MTT assay may provide an erroneous conclusion for cytotoxicity assessment.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"21 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140205647","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

Immature mandarin orange extract increases the amount of hyaluronic acid in human skin fibroblast and keratinocytes 未成熟柑橘提取物能增加人体皮肤成纤维细胞和角质细胞中的透明质酸含量

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-27 DOI: 10.1007/s10616-024-00615-4

Tomoko Furukawa, Chisako Yokono, Yoshihiro Nomura

引用次数: 0

LncRNA HOTAIR accelerates free fatty acid-induced inflammatory response in HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA LncRNA HOTAIR通过招募SRSF1稳定MLXIPL mRNA，加速游离脂肪酸诱导的HepG2细胞炎症反应

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-20 DOI: 10.1007/s10616-023-00614-x

Bo Guo, Shengzhe Yan, Lei Zhai, Yanzhen Cheng

{"title":"LncRNA HOTAIR accelerates free fatty acid-induced inflammatory response in HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA","authors":"Bo Guo, Shengzhe Yan, Lei Zhai, Yanzhen Cheng","doi":"10.1007/s10616-023-00614-x","DOIUrl":"https://doi.org/10.1007/s10616-023-00614-x","url":null,"abstract":"LncRNA HOTAIR has been reported to be associated with metabolic diseases of the liver. However, the effect of HOTAIR on non-alcoholic fatty liver disease (NAFLD) inflammation and its potential mechanism have not been reported. Genes and proteins expression were detected by qRT-PCR and Western blot respectively. The level of inflammatory cytokines was assessed by ELISA. HepG2 cell viability was detected by MTT assay. TG level and lipid accumulation were measured by Assay Kit and Oil red O staining, respectively. Direct binding relationship between HOTAIR and Serine/arginine splicing factor 1 (SRSF1), SRSF1 and MLX interacting protein like (MLXIPL) were confirmed by RNA-pull down and RIP assay. HOTAIR was highly expressed in free fatty acids (FFA)-treated HepG2 cells. HOTAIR knockdown alleviated FFA-induced inflammation of HepG2 cells. Then further analysis showed that HOTAIR and SRSF1 had a mutual binding relationship, and HOTAIR maintained MLXIPL mRNA stability via recruiting SRSF1 in HepG2 cells. Moreover, the inhibitory effect of HOTAIR knockdown on FFA-induced inflammation in HepG2 cells was reversed by MLXIPL overexpression. HOTAIR accelerates inflammation of FFA-induced HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA, which will help to find new effective strategies for NAFLD therapy.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"30 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139928339","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

Ionic composition of Shotokuseki extract alters cell differentiation and lipid metabolism in three-dimensional cultured human epidermis 麝香石竹提取物的离子成分可改变三维培养人表皮的细胞分化和脂质代谢

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-16 DOI: 10.1007/s10616-024-00616-3

Kei Tsukui, Masamitsu Suzuki, Miyu Amma, Yoshihiro Tokudome

{"title":"Ionic composition of Shotokuseki extract alters cell differentiation and lipid metabolism in three-dimensional cultured human epidermis","authors":"Kei Tsukui, Masamitsu Suzuki, Miyu Amma, Yoshihiro Tokudome","doi":"10.1007/s10616-024-00616-3","DOIUrl":"https://doi.org/10.1007/s10616-024-00616-3","url":null,"abstract":"Corneocytes and intercellular lipids form the stratum corneum. The content and composition of intercellular lipids in the stratum corneum significantly affect skin barrier function. The purpose of this study was to demonstrate the effect of Shotokuseki extract (SE) on intercellular lipid production and metabolism in human three-dimensional cultured human epidermis. SE or ion mixtures containing five common ions were applied to three-dimensional cultured human epidermis for 2–8 days for each assay. The mRNA expression levels of epidermal differentiation markers and lipid metabolism genes were quantified by real-time PCR. After extraction of lipids from the epidermis, ceramide, sphingosine, free fatty acids, and cholesterol were quantified by LC-MS/MS, GC-MS, or HPLC. The results showed that the application of SE increased the gene expression levels of epidermal differentiation markers keratin10 and transglutaminase. Elongation of very long-chain fatty acids protein 3, serine palmitoyl transferase, ceramide synthase 3, and acid ceramidase mRNA expression levels increased and fatty acid synthase mRNA expression decreased. The content of each lipid, [EOS] ceramide decreased and total sphingosine content increased on day 4. On day 8 of application, ceramide [NDS], [NP], and [EODS] increased and total free fatty acid content decreased. These results show that SE alters the lipid composition of the epidermis, increasing ceramides and decreasing free fatty acids in the epidermis. The composition of the ions in the SE may be responsible for the changes in lipid composition. These behaviors were different from those observed when the ion mixture was applied.<h3 data-test=\"abstract-sub-heading\">Graphical abstract</h3>\u0000","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"22 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139763009","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

Therapeutic potential of exosome derived from hepatocyte growth factor-overexpressing adipose mesenchymal stem cells in TGFβ1-stimulated hepatic stellate cells 肝细胞生长因子过表达脂肪间充质干细胞衍生的外泌体对 TGFβ1 刺激的肝星状细胞的治疗潜力

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-15 DOI: 10.1007/s10616-023-00611-0

{"title":"Therapeutic potential of exosome derived from hepatocyte growth factor-overexpressing adipose mesenchymal stem cells in TGFβ1-stimulated hepatic stellate cells","authors":"","doi":"10.1007/s10616-023-00611-0","DOIUrl":"https://doi.org/10.1007/s10616-023-00611-0","url":null,"abstract":"<h3>Abstract</h3> Cirrhosis is a familiar end-stage of multiple chronic liver diseases. The gene-modified mesenchymal stem cells (MSCs) have become one of the most promising schemes for the treatment of cirrhosis. MSCs exhibit their therapeutic role mainly by secreting hepatocyte growth factor (HGF). The aim of this research was to probe the anti-fibrosis role of exosomes secreted by HGF modified-mouse adipose MSCs (ADMSCs) on activated hepatic stellate cells (HSCs) and to preliminarily explore the possible mechanism. Firstly, mouse ADMSCs were isolated and identified. Quantitative real-time polymerase chain reaction verified the transfection efficiency of ADMSC transfected with HGF lentivirus. Exosomes derived from ADMSC transfecting negative control/HGF (ADMSCNC-Exo/ADMSCHGF-Exo) were extracted by density gradient centrifugation. HSCs were allocated to the control, TGF-β, TGF-β + ADMSC-Exo, TGF-β + ADMSCNC-Exo, and TGF-β + ADMSCHGF-Exo groups. Moreover, all mice were distributed to the control, CCl4 (40% CCl4 in olive oil), CCl4+ADMSC-Exo, CCl4+ADMSCNC-Exo, and CCl4+ADMSCHGF-Exo groups. Exosomes derived from ADMSCs with or without HGF transfection suppressed HSC activation, as evidenced by attenuating cell viability and cell cycle arrest at S phase but inducing apoptosis. Moreover, ADMSC-Exo, ADMSCNC-Exo, and ADMSCHGF-Exo effectively repressed the gene and protein levels of α-SMA, Col-I, Rho A, Cdc42, and Rac1 in TGF-β-treated HSCs, and ADMSCHGF-Exo had the best effect. ADMSCHGF-Exo had a stronger regulatory effect on serum liver index than ADMSCNC-Exo in CCl4-induced mice. In conclusion, ADMSCHGF-Exo alleviated liver fibrosis by weakening the Rho pathway, thus reducing collagen production.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"11 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139763364","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

miR-92a-3p promotes pulmonary fibrosis progression by regulating KLF2-mediated endothelial-to-mesenchymal transition miR-92a-3p 通过调控 KLF2 介导的内皮细胞向间质转化促进肺纤维化进展

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-15 DOI: 10.1007/s10616-024-00617-2

Sisi Pang, Bo Chen, Yan Li, Shuangshuang Wu, Lei Chen

引用次数: 0

NEAT1 promotes the progression of prostate cancer by targeting the miR-582-5p/EZH2 regulatory axis NEAT1 通过靶向 miR-582-5p/EZH2 调控轴促进前列腺癌的进展

IF 2.2 4区生物学

Cytotechnology Pub Date : 2024-02-14 DOI: 10.1007/s10616-023-00612-z

Weiqiang Xu, Yu Wu, Guoxi Zhang

{"title":"NEAT1 promotes the progression of prostate cancer by targeting the miR-582-5p/EZH2 regulatory axis","authors":"Weiqiang Xu, Yu Wu, Guoxi Zhang","doi":"10.1007/s10616-023-00612-z","DOIUrl":"https://doi.org/10.1007/s10616-023-00612-z","url":null,"abstract":"<h3>Abstract</h3> In several forms of malignant tumors, nuclear enriched abundant transcript 1 (NEAT1), a lncRNA, has been identified to play an important role. NEAT1’s regulation patterns in prostate cancer (PCa) are, however, mainly unknown. This study was aimed to evaluate and study the roles and regulatory mechanisms of NEAT1 in PCa. NEAT1, miR-582-5p, and enhancer of zeste homolog 2 (EZH2) expression were detected by qRT-PCR. The PCa cells’ invasive, migrative, and proliferative activities in vitro were assessed using transwell migration and invasion, wound-healing, cloning creation, and CCK-8 assays. In the present study, impaired proliferative, migrative, and invasive capacities were observed in the NEAT1-deficient PCa (PC3 and LNCaP) cells. Further mechanistic studies found that NEAT1 performs its function through sponging miR-582-5p. Furthermore, EZH2 was confirmed to be the downstream target gene of miRNA-582-5p. The impaired progression caused by NEAT1 deficiency in PCa cells was significantly restored by the inhibition of miR-582-5p, while these effects were largely abolished by the deletion of EZH2. Finally, the xenograft nude mouse model showed that knocking down the expression of NEAT1 suppressed the growth of PCa. In conclusion, NEAT1 promotes the progression of PCa by controlling the miR-582-5p and miR-582-5p-mediated EZH2.","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"43 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139762891","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