Acta histochemica最新文献

{"title":"Corrigendum to \"Protective effect of FXN overexpression on ferroptosis in L-Glu-induced SH-SY5Y cells\" [Acta Histochem. 126 (2024) 152135].","authors":"Mengran Wang, Tingting Xuan, Haining Li, Jing An, Tianhui He, Jiang Cheng","doi":"10.1016/j.acthis.2024.152192","DOIUrl":"https://doi.org/10.1016/j.acthis.2024.152192","url":null,"abstract":"","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339039","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}

{"title":"Nrf2: A critical participant in regulation of apoptosis, ferroptosis, and autophagy in gastric cancer","authors":"LiJie Tang,&nbsp;DongXiu He,&nbsp;Bo Su","doi":"10.1016/j.acthis.2024.152203","DOIUrl":"10.1016/j.acthis.2024.152203","url":null,"abstract":"<div><div>Nuclear factor erythroid 2-related factor-2 (Nrf2) is a specific transcription factor that maintains redox homeostasis by regulating the expression of anti-oxidative stress-related genes. Hyperactivation of Nrf2 is involved in tumor progression and is associated with chemoresistance in a large number of solid tumors. Programmatic cell death (PCD), such as apoptosis, ferroptosis, and autophagy, plays a crucial role in tumor development and chemotherapy sensitivity. Accumulating evidence suggests that some anti-tumor compounds and genes can induce massive production of reactive oxygen species (ROS) via inhibiting Nrf2 expression, which exacerbates oxidative stress and promotes Gastric cancer (GC) cell death, thereby enhancing the sensitivity of GC cells to chemotherapy-induced PCD. In this review, we summarize the role of antitumor drugs in interfering in three different types of PCD (apoptosis, ferroptosis, and autophagy) in GC cells by modulating Nrf2 expression, as well as the molecular mechanisms through which targeting Nrf2 brings about PCD and chemosensitivity. It is reasonable to believe that Nrf2 serves as a potential therapeutic target, and targeting Nrf2 by drug or gene regulation could provide a new strategy for the treatment of GC.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328207","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}

{"title":"Early PSA-NCAM reduction in the dentate gyrus and impaired plasticity in the Alzheimer´s disease 3xTg-mice model","authors":"J.J. Rodríguez ,&nbsp;E. Gardenal ,&nbsp;F. Zallo ,&nbsp;J. Cabot ,&nbsp;X. Busquets","doi":"10.1016/j.acthis.2024.152194","DOIUrl":"10.1016/j.acthis.2024.152194","url":null,"abstract":"<div><p>Neurodegenerative diseases such as Alzheimer´s (AD) and physiological ageing are characterized by a decline in neurogenesis and in the polysialylated isoforms of neural cell adhesion molecule (PSA-NCAM) expression within the hippocampus and specifically in the dentate gyrus (DG). In the 3xTG-AD mouse model, which mimics the human disease in both pathological and behavioral features, this decline in PSA-NCAM is associated with the presence of Aβ plaques at 9 months and Tau tangles at 12–15 months. In this work we studied the presence of PSA-NCAM at early ages (1–6 months) in the same model. Our results demonstrated that even as early as the first month of age there is a strong decrease in PSA-NCAM dendritic tree mainly altering the molecular layer (MolL) coverage affecting the synaptic plasticity and furthermore confirmed by the reduction of PSA-NCAM area density (Sv) in the 3xTG-AD. Similar and more marked early changes were seen during aging in both NTG and 3xTg-AD animals. Our results demonstrate for the first time a precipitate decrease of PSA-NCAM cells at such very early phases of the disease. This result suggests an early effect of the disease in the progression of immature and pluripotent cells resulting in an ulterior and early diminution of neurogenesis and therefore an impaired hippocampal cellular and synaptic plasticity.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142243148","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}

{"title":"Maternal hyperglycemia affects cell proliferation signalling and stromal organization in the prostate of neonatal and juvenile rat offspring","authors":"Luiz Felipe Fernandes Peixoto ,&nbsp;Laura Eduarda Dinato Sudário ,&nbsp;Marina das Graças Carneiro e Silva ,&nbsp;Fernanda Naves Araújo do Prado Mascarenhas ,&nbsp;Elusca Helena Muniz ,&nbsp;Renata Graciele Zanon ,&nbsp;Daniele Lisboa Ribeiro","doi":"10.1016/j.acthis.2024.152193","DOIUrl":"10.1016/j.acthis.2024.152193","url":null,"abstract":"<div><p>Gestational diabetes mellitus is a common medical complication during pregnancy. It creates a hyperglycemic environment and impacts offspring development, increasing the risk of long-term complications, including obesity, impaired glucose metabolism and cardiovascular disease. The impact of gestational diabetes on the prostates of adult offspring has already been described; however, it is not known whether these effects are due only to the maternal condition or whether the offspring develop them throughout life. This investigation evaluated the prostates of neonatal and juvenile offspring of hyperglycemic rats due to diabetes. Diabetes was induced with streptozotocin (50 mg/kg, ip) in pregnant Wistar rats and the prostates of 7- or 30-day-old pups from healthy (PC7, PC30) or diabetic (PD7, PD30) mothers were evaluated. We found reduced body weight in pups of PD7 and PD30 and prostate weight in PD30. Prostate branching was not affected, but a reduction in apoptotic levels was associated with impaired acinar bud canalization in neonates. Additionally, PD7 presented reduced ERK1/2 phosphorylation, cell proliferation and collagen, but fibroblasts were increased. In PD30, there was a reduction in the area of the secretory epithelium and stroma, but the luminal area was increased. Moreover, fibroblasts, smooth muscle cells, collagen and metalloproteinase 2 were decreased in these juvenile pups. These data indicate that maternal hyperglycemia inactivates an important cell proliferation signaling pathway in the prostate in the first postnatal days (which is restored in the juvenile period), but it was not sufficient to avoid epithelial and stromal atrophy. This effect on postnatal gland development may impact the reproductive capacity of the prostate in adult life.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142149449","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}

{"title":"A set of pretreatment reagents including improved formula fixation and decalcification facilitating immunohistochemistry and DNA analyses of formalin-fixed paraffin-embedded bone marrow trephine biopsy","authors":"Ting Sun ,&nbsp;Liming Xu ,&nbsp;Hongtian Yao ,&nbsp;Jing Zhao ,&nbsp;Zhen Chen ,&nbsp;Zexin Chen ,&nbsp;Bo Wang ,&nbsp;Wei Ding","doi":"10.1016/j.acthis.2024.152188","DOIUrl":"10.1016/j.acthis.2024.152188","url":null,"abstract":"<div><p>Bone marrow biopsy depends on tissue morphology, immunohistochemical staining, and moleculardetection. Tissue pretreatment is required for bone marrow samples, from clinical specimen acquisition to pathological reporting, but during the process, proteins and nucleic acids are often altered because of the acid in fixation and decalcification solutions. In our study, we present an easy and effective pretreatment protocol and compared this novel pretreatment protocol (Set 2) with an existing traditional pretreatment process (Set 1) using tissue morphology, IHC staining, and molecular pathological analyses. Granulocytic IHC markers showed more intensive staining in samples of Set 2 than in those of Set 1. The Set 2 protocol provided a higher DNA yield and less fragmentation; moreover, samples processed with the Set 2 protocol could be subsequently used in FISH and DNA sequencing assays. Our optimized novel pretreatment protocol could better protect proteins and DNA molecules while maintaining good cell morphology compared to traditional pretreatment The novel pretreatment reagents could role as a reference by more laboratories for pretreating bone marrow biopsy samples and scientific research.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144911","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}

{"title":"Paracrine signalling in breast cancer: Insights into the tumour endothelial phenotype","authors":"Atarah Rass ,&nbsp;Carla Eksteen ,&nbsp;Anna-Mart Engelbrecht","doi":"10.1016/j.acthis.2024.152191","DOIUrl":"10.1016/j.acthis.2024.152191","url":null,"abstract":"<div><p>Tumour endothelial cells (TECs) are genetically and phenotypically distinct from their normal, healthy counterparts and provide various pro-tumourigenic effects. This study aimed to investigate the impact of conditioned media (CM) from non-tumourigenic MCF-12A breast epithelial cells as well as from MCF-7 and MDA-MB-231 breast cancer cells on human umbilical vein endothelial cells (HUVECs). Significant increases in cell viability were observed across all breast CM groups compared to controls, with notable differences between the MCF-12A, MCF-7, and MDA-MB-231 groups. Despite increased viability, no significant differences in MCM2 expression, a marker of cell proliferation, were detected. Morphological changes in HUVECs, including elongation, lumen formation, and branching, were more pronounced in breast cancer CM groups, especially in the MDA-MB-231 CM group. qPCR and Western blot analyses showed increased expression of TEC markers such as MDR1, LOX, and TEM8 in HUVECs treated with MCF-12A CM. The MCF-7 CM group significantly enhanced HUVEC migratory activity compared to MCF-12A CM, as evidenced by a scratch assay. These findings underscore distinct angiogenic responses elicited by non-tumourigenic and tumourigenic breast epithelial cells, with tumourigenic cells inducing a hyperactivated angiogenic response. The study highlights the differential effects of breast cancer cell paracrine signalling on endothelial cells and suggests the need for further investigation into TEC markers' role in both physiological and tumour angiogenesis.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S006512812400059X/pdfft?md5=85680f7e54fc6e034bcef4d9085b736d&pid=1-s2.0-S006512812400059X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142094833","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}

{"title":"Human umbilical cord mesenchymal stem cells-derived exosomes attenuate burn-induced acute lung injury via inhibiting ferroptosis","authors":"Lin Li ,&nbsp;Qin-qin Song ,&nbsp;Shuang-ru Li ,&nbsp;Zhi-gang Jia ,&nbsp;Xing‑chen Sun ,&nbsp;Yu‑ting Zhao ,&nbsp;Jia-bin Deng ,&nbsp;Jun-jun Wu ,&nbsp;Tao Ni ,&nbsp;Ji-song Liu","doi":"10.1016/j.acthis.2024.152189","DOIUrl":"10.1016/j.acthis.2024.152189","url":null,"abstract":"<div><p>Our previous study has shown that exosomes derived from human umbilical cord mesenchymal stem cells (hUCMSCs-exo) alleviated burn-induced acute lung injury (ALI). In this study, we explored a novel mechanism by which hUCMSCs-exo contributed to the inhibition of burn-induced ALI. The ALI rat model with severe burn was established for the <em>in vivo</em> experiments, and rats PMVECs were stimulated with the serum from burn-induced ALI rats for the <em>in vitro</em> experiments. The pathological changes of lung tissues were evaluated by HE staining; the cell viability was measured using CCK-8; the iron level and Fe²⁺ concentration were assessed using Iron Assay Kit and Fe²⁺ fluorescence detection probe; the mRNA expression of SLC7A11 and GPX4 were measured by qRT-PCR; the protein levels of SLC7A11, GPX4, Nrf2 and HO-1 were detected by western blot. Both the <em>in vivo</em> and <em>in vitro</em> experiments revealed that ferroptosis was significantly induced in burn-induced ALI, which as verified by increased iron level and Fe²⁺ concentration, and decreased SLC7A11 and GPX4 mRNA and protein levels. Furthermore, both hUCMSCs-exo and Fer-1 (the inhibitor of ferroptosis) alleviated lung inflammation and up-regulated protein levels of Nrf2 and HO-1 in the lung tissues of burn-induced ALI rats. These results suggested that hUCMSCs-exo exhibited a protective role against burn-induced ALI by inhibiting ferroptosis, partly owing to the activation of Nrf2/HO-1 pathway, thus providing a novel therapeutic strategy for burn-induced ALI.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142087770","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}

{"title":"RGS1 targeted by miR-191-3p inhibited the stemness properties of esophageal cancer cells by suppressing CXCR4/PI3K/AKT signaling","authors":"Jing Xun ,&nbsp;Yuan Ma ,&nbsp;Botao Wang ,&nbsp;Xiaolin Jiang ,&nbsp;Bin Liu ,&nbsp;Ruifang Gao ,&nbsp;Qiongli Zhai ,&nbsp;Runfen Cheng ,&nbsp;Xueliang Wu ,&nbsp;Yu Wu ,&nbsp;Qi Zhang","doi":"10.1016/j.acthis.2024.152190","DOIUrl":"10.1016/j.acthis.2024.152190","url":null,"abstract":"<div><h3>Background</h3><p>Esophageal cancer is one of the most common malignant tumors in the world. It is urgent to prevent the development and progression of esophageal cancer. Cancer stem cells (CSCs) were reported to have the ability to initiate tumorigenesis, and reducing the stem cell-like characteristics of tumors is an important strategy to inhibit the occurrence and development of tumors. miRNAs are key regulators of the stemness of cancer. Here, we aimed to investigate the role and regulatory mechanism of miR-191-3p in the stemness properties of esophageal cancer cells.</p></div><div><h3>Methods</h3><p>Esophageal cancer cells with stable expression of miR-191-3p were established by lentivirus system. CCK-8 assay, transwell assay<strong>,</strong> wound healing assay were used to evaluate the effect of miR-191-3p on proliferation and metastasis of esophageal cancer cells. The expression of stemness-related markers (NANOG, OCT4, SOX2), ALDH activity, sphere-forming assay and subcutaneous tumor model in nude mice were performed to evaluate the stemness properties of esophageal cancer cells <em>in vitro</em> and <em>in vivo</em>. Dual-luciferase reporter assay was used to verify the molecular mechanism.</p></div><div><h3>Result</h3><p>Here we found that overexpression of miR-191-3p promoted the stemness properties of esophageal cancer cells <em>in vitro</em> and <em>in vivo</em>, including increasing esophageal cancer cell proliferation and metastasis ability, the expression of stemness-related markers NANOG, OCT4, and SOX2, ALDH activity, the number of spheres formed and tumor growth. Bioinformatic analysis and dual-luciferase assay demonstrated that regulator of G protein signaling 1 (RGS1) was the directed target gene of miR-191-3p and attenuated the promotion effect of miR-191-3p on the stemness of esophageal cancer cells. Furthermore, we found that RGS1 knockdown activated the PI3K/AKT pathway by negatively regulating CXCR4 to promote the stemness of esophageal cancer cells.</p></div><div><h3>Conclusions</h3><p>Our findings revealed that RGS1 targeted by miR-191-3p inhibited the stemness of esophageal cancer cells by suppressing the CXCR4/PI3K/AKT pathway, which provide potential prognostic markers and therapeutic targets in the future.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0065128124000588/pdfft?md5=9a42e6ff9fd33276cd17e59dd8234b62&pid=1-s2.0-S0065128124000588-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142034910","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}

{"title":"ACOT7 positively regulated by CREB1 promotes the progression of cutaneous melanoma","authors":"Ni Tang,&nbsp;Yunhui Li,&nbsp;Junchi Tang,&nbsp;Juexin Chen,&nbsp;Lili Chen,&nbsp;Lin Dang","doi":"10.1016/j.acthis.2024.152186","DOIUrl":"10.1016/j.acthis.2024.152186","url":null,"abstract":"<div><p>Cutaneous melanoma (cM) is a prevalent invasive cancer resulting from the malignant transformation of melanocytes. At present, the primary treatment for melanoma is surgical resection, which is not appropriate for patients with metastasis. Therefore, it is necessary to identify effective therapeutic targets for the early diagnosis and treatment of metastatic melanoma. Acyl-CoA thioesterase 7 (ACOT7) has been reported to be involved in the progression of multiple cancer, while its role in melanoma has not been extensively researched. Through gain-of-function and loss-of-function experiments, ACOT7 was identified as a tumor promoter that facilitates the progression of melanoma cells. Cell proliferation was promoted by overexpressing ACOT7 in M14 cells, and was suppressed by silencing ACOT7 in MeWo cells. Knockdown of ACOT7 induced cell cycle arrest by increasing the expressions of cyclin dependent kinase inhibitor 1B (P27) and cyclin dependent kinase inhibitor 1 A (P21), while simultaneously reducing proliferating cell nuclear antigen (PCNA) expression. Upregulation of ACOT7 promoted the cell cycle of melanoma cells. Additionally, apoptosis was induced by the absence of ACOT7 through activating caspase-3 and poly (ADP-ribose) polymerase (PARP). The metastatic and invasive capacity of melanoma cells was significantly enhanced by the overexpression of ACOT7 and inhibited by the downregulation of ACOT7. Moreover, the cAMP responsive element binding protein 1 (CREB1) positively regulates ACOT7 expression by binding to its promoter region. A decrease of cell proliferation, migration and invasion, as well as an increase of cell apoptosis induced by silencing CREB1 were obviously reversed by ACOT7. In summary, ACOT7 transcriptionally activated by CREB1 elevates the progression of cM.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141979583","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}

{"title":"Localization of EFA6A, an exchange factor for Arf6, in Z-lines and sarcoplasmic reticulum membranes in addition to myofilaments in I-domains of skeletal myofibers of peri-natal mice","authors":"Surang Chomphoo ,&nbsp;Hiroyuki Sakagami ,&nbsp;Hisatake Kondo ,&nbsp;Wiphawi Hipkaeo","doi":"10.1016/j.acthis.2024.152187","DOIUrl":"10.1016/j.acthis.2024.152187","url":null,"abstract":"<div><p>Membrane trafficking and actin-remodeling are critical for well-maintained integrity of the cell organization and activity, and they require Arf6 (ADP ribosylation factor 6) activated by GEF (guanine nucleotide exchange factor) including EFA6 (exchange factor for Arf6). In the present immuno-electron microscopic study following previous immunohistochemical study by these authors (Chomphoo et al., 2020) of <em>in situ</em> skeletal myoblasts and myotubes of pre-and perinatal mice, the immunoreactivity for EFA6A was found to be localized at Z-bands and sarcoplasmic reticulum (SR) membranes in I-domains as well as I-domain myofilaments of skeletal myofibers of perinatal mice. Based on the previous finding that EFA6 anchored on the neuronal postsynaptic density via α-actinin which is known to be shared by muscular Z-bands, the present finding suggests that EFA6A is also anchored on Z-bands via α-actinin and involved in the membrane trafficking and actin-remodeling in skeletal myofibers. The localization of EFA6A-immunoreactivity in I-domain SR suggests a differential function in the membrane traffic between the I- and A-domain intracellular membranes in perinatal skeletal myofibers.</p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141911325","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}