European Journal of Histochemistry最新文献_第10页

Dexmedetomidine attenuates neuroinflammation and microglia activation in LPS-stimulated BV2 microglia cells through targeting circ-Shank3/miR-140-3p/TLR4 axis. 右美托咪定通过靶向circ-Shank3/miR-140-3p/TLR4轴，减弱lps刺激的BV2小胶质细胞的神经炎症和小胶质细胞活化。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-07-26 DOI: 10.4081/ejh.2023.3766

Guangbao He, Yibo He, Hongwei Ni, Kai Wang, Yijun Zhu, Yang Bao

{"title":"Dexmedetomidine attenuates neuroinflammation and microglia activation in LPS-stimulated BV2 microglia cells through targeting circ-Shank3/miR-140-3p/TLR4 axis.","authors":"Guangbao He, Yibo He, Hongwei Ni, Kai Wang, Yijun Zhu, Yang Bao","doi":"10.4081/ejh.2023.3766","DOIUrl":"https://doi.org/10.4081/ejh.2023.3766","url":null,"abstract":"It has been shown that dexmedetomidine (Dex) could attenuate postoperative cognitive dysfunction (POCD) via targeting circular RNAs (circRNAs). Circ-Shank3 has been found to be involved in the neuroprotective effects of Dex against POCD. However, the role of circ-Shank3 in POCD remains largely unknown. Reverse transcription quantitative PCR (RT-qPCR) was performed to detect circ-Shank3 and miR-140-3p levels in lipopolysaccharide (LPS)-treated microglia BV-2 cells in the absence or presence of Dex. The relationship among circ-Shank3, miR-140-3p and TLR4 was confirmed by dual-luciferase reporter assay. Additionally, Western blot and immunofluorescence (IF) assays were conducted to evaluate TLR4, p65 and Iba-1 or CD11b levels in cells. In this study, we found that Dex notably decreased circ-Shank3 and TLR4 levels and elevated miR-140-3p level in LPS-treated BV2 cells. Mechanistically, circ-Shank3 harbor miR-140-3p, functioning as a miRNA sponge, and then miR-140-3p targeted the 3'-UTR of TLR4. Additionally, Dex treatment significantly reduced TLR4 level and phosphorylation of p65, and decreased the expressions of microglia markers Iba-1 and CD11b in LPS-treated BV2 cells. As expected, silenced circ-Shank3 further reduced TLR4, p65 and Iba-1 and CD11b levels in LPS-treated BV2 cells in the presence of Dex, whereas these phenomena were reversed by miR-140-3p inhibitor. Collectively, our results found that Dex could attenuate the neuroinflammation and microglia activation in BV2 cells exposed to LPS via targeting circ-Shank3/miR-140-3p/TLR4 axis. Our results might shed a new light on the mechanism of Dex for the treatment of POCD.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0b/f9/ejh-67-3-3766.PMC10476535.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10158089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA FBXO18-AS promotes gastric cancer progression by TGF-β1/Smad signaling. LncRNA FBXO18-AS通过TGF-β1/Smad信号传导促进胃癌进展。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-06-20 DOI: 10.4081/ejh.2023.3667

Yiming Zhang, Wanqiong Zheng, Liang Zhang, Yechun Gu, Lihe Zhu, Yingpeng Huang

{"title":"LncRNA FBXO18-AS promotes gastric cancer progression by TGF-β1/Smad signaling.","authors":"Yiming Zhang, Wanqiong Zheng, Liang Zhang, Yechun Gu, Lihe Zhu, Yingpeng Huang","doi":"10.4081/ejh.2023.3667","DOIUrl":"https://doi.org/10.4081/ejh.2023.3667","url":null,"abstract":"For the digestive system, there exists one common malignant tumor, known as gastric cancer. It is the third most prevalent type of tumor among different tumors worldwide. It has been reported that long noncoding RNAs (lncRNAs), participate in various biological processes of gastric cancer. However, there are still many lncRNAs with unknown functions, and we discovered a novel lncRNA designated as FBXO18-AS. Whether lncRNAFBXO18-AS participates in gastric cancer progression is still unknown. Bioinformatic analysis, immunohistochemistry, Western blotting, and qPCR were carried out to explore FBXO18-AS and TGF-β1 expression. In addition, EdU, MTS, migration and transwell assays were performed to investigate the invasion, proliferation and migration of gastric cancer in vitro. We first discovered that FBXO18-AS expression was upregulated in gastric cancer and linked to poorer outcomes among patients with gastric cancer. Then, we confirmed that FBXO18-AS promoted the proliferation, invasion, migration, and an EMT-like process in gastric cancer in vivo and in vitro. Mechanistically, FBXO18-AS was found to be involved in the progression of gastric cancer by modulating TGF-β1/Smad signaling. Therefore, it might offer a possible biomarker for gastric cancer diagnosis and an effective strategy for clinical treatment.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/99/81/ejh-67-2-3667.PMC10334307.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9829062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum - Transcription factor nuclear factor erythroid 2 p45-related factor 2 (NRF2) ameliorates sepsis-associated acute kidney injury by maintaining mitochondrial homeostasis and improving the mitochondrial function. 转录因子核因子红细胞2 p45相关因子2 (NRF2)通过维持线粒体稳态和改善线粒体功能改善脓毒症相关急性肾损伤。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-06-20 DOI: 10.4081/ejh.2023.3794

Zhijiang Chen, Huili Wang, Bin Hu, Xinxin Chen, Meiyu Zheng, Lili Liang, Juanjuan Lyu, Qiyi Zeng

引用次数: 1

Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury. 在角膜上皮损伤过程中，透明质酸钠通过下调 miR-18a 促进角膜上皮细胞的增殖、自噬和迁移。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2023-06-15 DOI: 10.4081/ejh.2023.3663

Yingzhuo Guo, Hua Wang

{"title":"Sodium hyaluronate promotes proliferation, autophagy, and migration of corneal epithelial cells by downregulating miR-18a in the course of corneal epithelial injury.","authors":"Yingzhuo Guo, Hua Wang","doi":"10.4081/ejh.2023.3663","DOIUrl":"10.4081/ejh.2023.3663","url":null,"abstract":"Corneal epithelium can resist the invasion of external pathogenic factors to protect the eye from external pathogens. Sodium hyaluronate (SH) has been confirmed to promote corneal epithelial wound healing. However, the mechanism by which SH protects against corneal epithelial injury (CEI) is not fully understood. CEI model mice were made by scratching the mouse corneal epithelium, and in vitro model of CEI were constructed via curettage of corneal epithelium or ultraviolet radiation. The pathologic structure and level of connective tissue growth factor (CTGF) expression were confirmed by Hematoxylin and Eosin staining and immunohistochemistry. CTGF expression was detected by an IHC assay. The levels of CTGF, TGF-β, COLA1A, FN, LC3B, Beclin1, and P62 expression were monitored by RT-qPCR, ELISA, Western blotting or immunofluorescence staining. Cell proliferation was detected by the CCK-8 assay and EdU staining. Our results showed that SH could markedly upregulate CTGF expression and downregulate miR-18a expression in the CEI model mice. Additionally, SH could attenuate corneal epithelial tissue injury, and enhance the cell proliferation and autophagy pathways in the CEI model mice. Meanwhile, overexpression of miR-18a reversed the effect of SHs on cell proliferation and autophagy in CEI model mice. Moreover, our data showed that SH could induce the proliferation, autophagy, and migration of CEI model cells by downregulating miR-18a. Down-regulation of miR-18a plays a significant role in the ability of SH to promote corneal epithelial wound healing. Our results provide a theoretical basis for targeting miR-18a to promote corneal wound healing.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7f/0a/ejh-67-2-3663.PMC10334306.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9772350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an in vitro model of hyperoxia-induced acute lung injury. 在体外高氧诱导急性肺损伤模型中，LncRNA gadd7通过正向调节MFN1促进线粒体膜电位下降和肺泡II型上皮细胞凋亡。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-31 DOI: 10.4081/ejh.2023.3535

Guoyue Liu, Cunzhi Yin, Mingjiang Qian, Xuan Xiao, Hang Wu, Fujian Fu

{"title":"LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an in vitro model of hyperoxia-induced acute lung injury.","authors":"Guoyue Liu, Cunzhi Yin, Mingjiang Qian, Xuan Xiao, Hang Wu, Fujian Fu","doi":"10.4081/ejh.2023.3535","DOIUrl":"10.4081/ejh.2023.3535","url":null,"abstract":"The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0e/58/ejh-67-2-3535.PMC10277814.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9670965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Proceedings of the workshop NANO23@uniVR - 8-9 June 2023, University of Verona, Italy. 研讨会记录NANO23@uniVR-2023年6月8日至9日，意大利维罗纳大学

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-31 DOI: 10.4081/ejh.2023.3778

The Scientific Committee

引用次数: 0

Metformin sensitises osteosarcoma to chemotherapy via the IGF-1R/miR-610/FEN1 pathway. 二甲双胍通过IGF-1R/miR-610/FEN1通路使骨肉瘤对化疗敏感。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-17 DOI: 10.4081/ejh.2023.3612

Suwei Dong, Yanbin Xiao, Ziqiang Zhu, Xiang Ma, Zhuohui Peng, Jianping Kang, Jianqiang Wang, Yunqing Wang, Zhen Li

{"title":"Metformin sensitises osteosarcoma to chemotherapy via the IGF-1R/miR-610/FEN1 pathway.","authors":"Suwei Dong, Yanbin Xiao, Ziqiang Zhu, Xiang Ma, Zhuohui Peng, Jianping Kang, Jianqiang Wang, Yunqing Wang, Zhen Li","doi":"10.4081/ejh.2023.3612","DOIUrl":"https://doi.org/10.4081/ejh.2023.3612","url":null,"abstract":"Metformin can enhance cancer cell chemosensitivity to anticancer drugs. IGF-1R is involved in cancer chemoresistance. The current study aimed to elucidate the role of metformin in osteosarcoma (OS) cell chemosensitivity modulation and identify its underlying mechanism in IGF-1R/miR-610/FEN1 signalling. IGF-1R, miR-610, and FEN1 were aberrantly expressed in OS and participated in apoptosis modulation; this effect was abated by metformin treatment. Luciferase reporter assays confirmed that FEN1 is a direct target of miR-610. Moreover, metformin treatment decreased IGF-1R and FEN1 but elevated miR-610 expression. Metformin sensitised OS cells to cytotoxic agents, while FEN1 overexpression partly compromised metformin's sensitising effects. Furthermore, metformin was observed to enhance adriamycin's effects in a murine xenograft model. Metformin enhanced OS cell sensitivity to cytotoxic agents via the IGF-1R/miR-610/FEN1 signalling axis, highlighting its potential as an adjuvant during chemotherapy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/47/7c/ejh-67-2-3612.PMC10230554.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9563915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High glucose inhibits neural differentiation by excessive autophagy via peroxisome proliferator-activated receptor gamma. 高糖通过过氧化物酶体增殖物激活受体γ通过过度自噬抑制神经分化。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-11 DOI: 10.4081/ejh.2023.3691

Yin Pan, Di Qiu, Shu Chen, Xiaoxue Han, Ruiman Li

{"title":"High glucose inhibits neural differentiation by excessive autophagy via peroxisome proliferator-activated receptor gamma.","authors":"Yin Pan, Di Qiu, Shu Chen, Xiaoxue Han, Ruiman Li","doi":"10.4081/ejh.2023.3691","DOIUrl":"https://doi.org/10.4081/ejh.2023.3691","url":null,"abstract":"The high prevalence of prediabetes and diabetes globally has led to the widespread occurrence of severe complications, such as diabetic neuropathy, which is a result of chronic hyperglycemia. Studies have demonstrated that maternal diabetes can lead to neural tube defects by suppressing neurogenesis during neuroepithelium development. While aberrant autophagy has been associated with abnormal neuronal differentiation, the mechanism by which high glucose suppresses neural differentiation in stem cells remains unclear. Therefore, we developed a neuronal cell differentiation model of retinoic acid induced P19 cells to investigate the impact of high glucose on neuronal differentiation in vitro. Our findings indicate that high glucose (HG) hinders neuronal differentiation and triggers excessive. Furthermore, HG treatment significantly reduces the expression of markers for neurons (Tuj1) and glia (GFAP), while enhancing autophagic activity mediated by peroxisome proliferator-activated receptor gamma (PPARγ). By manipulating PPARγ activity through pharmacological approaches and genetically knocking it down using shRNA, we discovered that altering PPARγ activity affects the differentiation of neural stem cells exposed to HG. Our study reveals that PPARγ acts as a downstream mediator in high glucose-suppressed neural stem cell differentiation and that refining autophagic activity via PPARγ at an appropriate level could improve neuronal differentiation efficiency. Our data provide novel insights and potential therapeutic targets for the clinical management of gestational diabetes mellitus.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3e/19/ejh-67-2-3691.PMC10230556.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9931775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Knockdown of ARHGAP30 inhibits ovarian cancer cell proliferation, migration, and invasiveness by suppressing the PI3K/AKT/mTOR signaling pathway. 敲低ARHGAP30通过抑制PI3K/AKT/mTOR信号通路抑制卵巢癌细胞的增殖、迁移和侵袭性。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-11 DOI: 10.4081/ejh.2023.3653

Xiaoyan Chu, Jun Lou, Yun Yi, Linlin Zhong, Ouping Huang

{"title":"Knockdown of ARHGAP30 inhibits ovarian cancer cell proliferation, migration, and invasiveness by suppressing the PI3K/AKT/mTOR signaling pathway.","authors":"Xiaoyan Chu, Jun Lou, Yun Yi, Linlin Zhong, Ouping Huang","doi":"10.4081/ejh.2023.3653","DOIUrl":"https://doi.org/10.4081/ejh.2023.3653","url":null,"abstract":"The mortality and morbidity rates of ovarian cancer (OC) are high, but the underlying mechanisms of OC have not been characterized. In this study, we determined the role of Rho GTPase Activating Protein 30 (ARHGAP30) in OC progression. We measured ARHGAP30 abundance in OC tissue samples and cells using immunohistochemistry (IHC) and RT-qPCR. EdU, transwell, and annexin V/PI apoptosis assays were used to evaluate proliferation, invasiveness, and apoptosis of OC cells, respectively. The results showed that ARHGAP30 was overexpressed in OC tissue samples and cells. Inhibition of ARHGAP30 suppressed growth and metastasis of OC cells, and enhanced apoptosis. Knockdown of ARHGAP30 in OC cells significantly inhibited the PI3K/AKT/mTOR pathway. Treatment with the PI3K/AKT/mTOR pathway inhibitor buparlisib simulated the effects of ARHGAP30 knockdown on growth, invasiveness, and apoptosis of OC cells. Following buparlisib treatment, the expression levels of p-PI3K, p-AKT, and p-mTOR were significantly decreased. Furthermore, buparlisib inhibited the effects of ARHGAP30 upregulation on OC cell growth and invasiveness. In conclusion, ARHGAP30 regulated the PI3K/AKT/mTOR pathway to promote progression of OC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3b/42/ejh-67-2-3653.PMC10230553.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9559623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus. 收缩:实验性胸腺去神经后的内在神经支配和多巴胺能标记物。

IF 2 4区生物学

European Journal of Histochemistry Pub Date : 2023-05-08 DOI: 10.4081/ejh.2023.3765

Fiorenzo Mignini, Maurizio Sabbatini, Vito D'Andrea, Carlo Cavallotti

{"title":"RETRACTION: Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus.","authors":"Fiorenzo Mignini, Maurizio Sabbatini, Vito D'Andrea, Carlo Cavallotti","doi":"10.4081/ejh.2023.3765","DOIUrl":"https://doi.org/10.4081/ejh.2023.3765","url":null,"abstract":"On behalf of the coauthors and with much regret, I must retract our publication entitled \"Intrinsic innervation and dopaminergic markers after experimental denervation in rat thymus\" published in European Journal of Histochemistry 2010;54(2):e17 for the following reason: Unfortunately, now, after thirteen years, we have realized that some microphotographs published in the paper have been processed to improve the presentation of the images. The three surviving authors of the paper agree that the processing of the presentation images is against the COPE Ethical Editorial Standard, although the presentation images do not alter the integrity of methodological procedures and the results of the research work, obtained from the direct analysis of slides under microscope and rigorous statistical analysis of data; therefore, we, the authors of the above indicated paper, request the retraction of the publication. We apologize for what happened. Maurizio Sabbatini Dip. di Scienze e Innovazione Tecnologica (DISIT) Università del Piemonte Orientale Alessandria, Italy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"67 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2023-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a2/17/ejh-67-2-3765.PMC10203977.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9519597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0