Acta histochemica最新文献

{"title":"Metabolic shift as a compensatory response to impaired hippocampal neurogenesis after developmental exposure to sodium fluoride in rats","authors":"Momoka Shobudani ,&nbsp;Yuri Sakamaki ,&nbsp;Ayumi Karasawa ,&nbsp;Ryota Ojiro ,&nbsp;Xinyu Zou ,&nbsp;Qian Tang ,&nbsp;Shunsuke Ozawa ,&nbsp;Meilan Jin ,&nbsp;Toshinori Yoshida ,&nbsp;Makoto Shibutani","doi":"10.1016/j.acthis.2024.152204","DOIUrl":"10.1016/j.acthis.2024.152204","url":null,"abstract":"<div><div>Fluoride affects neurodevelopment in children. In this study, we examined the effects of developmental exposure to sodium fluoride (NaF) on hippocampal neurogenesis in rats. Dams were given drinking water containing NaF at 0 (untreated controls), 30 or 100 ppm from gestational day 6 to day 21 post-delivery upon weaning, and offspring were reared until postnatal day (PND) 77. On PND 21, NaF at 100 ppm altered the numbers in subpopulations of granule cell lineages, including a decrease in type-3 neural progenitor cells (NPCs), as well as a compensatory increase in type-1 neural stem cells (NSCs) and type-2a NPCs. NaF exposure tended to increase GluR2⁺ mossy cells in the hilus of the dentate gyrus (DG) in a dose-dependent manner, suggesting that NaF exposure induces a compensatory neurogenic response. NaF also caused a dose-dependent increase in ARC⁺ granule cells, and it upregulated <em>Ptgs2</em> in the DG at 100 ppm, suggesting that NaF exposure increases synaptic plasticity in granule cells. NaF at 100 ppm upregulated granule cell lineage marker genes (<em>Nes</em>, <em>Eomes</em> and <em>Rbfox3</em>) and an anti-apoptotic gene (<em>Bcl2</em>), suggesting ameliorating responses against the impaired neurogenesis during NaF exposure. Moreover, NaF at 100 ppm downregulated oxidative phosphorylation-related genes (<em>Atp5f1b</em> and <em>Sdhd</em>) and upregulated a glycolysis-related gene (<em>Hk3</em>), suggesting a metabolic shift in cells undergoing neurogenesis. By PND 77, the changes in granule cell lineages were no longer detected, and GABAergic interneuron marker genes (<em>Calb2</em> and <em>Reln</em>) were upregulated, suggesting a persistent protective response in granule cell lineages. Together, these findings suggest that developmental NaF exposure causes transient disruption of hippocampal neurogenesis, which in turn induces a metabolic shift as a compensatory response.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152204"},"PeriodicalIF":2.3,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441519","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":"Renal expression of autophagy markers in diabetic kidney of PUFA-supplemented rats","authors":"Ivan Brdar ,&nbsp;Tomislav Mašek ,&nbsp;Anita Racetin ,&nbsp;Marija Jurić ,&nbsp;Katarina Vukojević ,&nbsp;Ivana Bočina ,&nbsp;Natalija Filipović","doi":"10.1016/j.acthis.2024.152206","DOIUrl":"10.1016/j.acthis.2024.152206","url":null,"abstract":"<div><div>Diabetic nephropathy is the leading cause of end-stage kidney disease, and the association between impaired autophagy and kidney structure damage in diabetes is well known. Diets enriched with polyunsaturated fatty acids (PUFAs) have been the subject of numerous studies on preventing and treating various metabolic disorders. The results of these studies suggest that n-3 PUFA may have a renoprotective effect, reducing the structural damage to the kidneys associated with DM. We hypothesized that the activation of autophagy partly mediates the potential protective effect of n-3 PUFA on diabetic kidneys. Wistar rats were randomly divided into four groups according to the type of diet: control (C) and diabetic (STZ) groups received food including 0.5 % linseed oil and 2 % sunflower oil with an n-6/n-3 ratio of 7; the STZ+N6 group received a diet with 2.5 % sunflower oil with an n-6/n-3 ratio of 60; and the STZ+N3 group received a diet containing 2.5 % fish oil with an n-6/n-3 ratio of 1, with the addition of eicosapentaenoic acid (EPA) and 19 % docosahexaenoic acid (DHA). All rats, except for those in the C group, had diabetes induced by an intraperitoneal injection of streptozotocin. We conducted histological and immunohistochemical assessments to determine the effects of different n-6/n-3 PUFA dietary ratios on the expression levels of different autophagy markers in the kidney of the rats. The results indicate significant effects of n-3 and n-6 PUFA supplementation on the expression of different autophagy markers in the renal cortex of the diabetic rats. In particular, n-6 PUFA supplementation increased LC3B expression while simultaneously decreasing Rab7 expression; meanwhile, n-3 PUFA supplementation resulted in a decreased expression of LAMP2A and Rab7. Moreover, n-3 PUFA supplementation prevented an increase in BECL1 and p62, that was observed in kidneys from diabetic and diabetic n-3 supplemented animals. These results point to the complex interactions of fatty acids and autophagy during the development of diabetic kidney disease, which should be taken into account in future therapeutic approaches.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152206"},"PeriodicalIF":2.3,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142434520","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":"Immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2) in the rat carotid body","authors":"Hiroki Saito,&nbsp;Takuya Yokoyama ,&nbsp;Nobuaki Nakamuta,&nbsp;Yoshio Yamamoto","doi":"10.1016/j.acthis.2024.152205","DOIUrl":"10.1016/j.acthis.2024.152205","url":null,"abstract":"<div><div>The carotid body is a hypoxia-sensitive chemoreceptor that induces sensory long-term facilitation after exposure to chronic intermittent hypoxia. However, the mechanisms underlying synaptic plasticity in the carotid body remain unknown. In the present study, we examined the immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2), which are candidate molecules involved in the modulation of synaptic transmission. Dot-like CB1 immunoreactivity was distributed in the perinuclear cytoplasm of chemoreceptor cells immunoreactive for the catecholamine-synthesizing enzymes, tyrosine hydroxylase and dopamine beta-hydroxylase. Furthermore, CB1 immunoreactivity was observed in sensory nerve endings immunoreactive for P2X₃ purinoceptors that colocalized with vesicular glutamate transporter 2. On the other hand, immunoreactivity for CB2 was mainly distributed in chemoreceptor cells, and was weakly observed in sensory nerve endings immunoreactive for P2X₂ purinoceptors. The present results suggest that CB1 and CB2 regulate the release of catecholamines and glutamate from chemoreceptor cells and sensory nerve endings, respectively. Therefore, CB1 and CB2 may be involved in synaptic plasticity in the carotid body.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152205"},"PeriodicalIF":2.3,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142434521","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":"Corrigendum to “Protective effect of FXN overexpression on ferroptosis in L-Glu-induced SH-SY5Y cells” [Acta Histochem. 126 (2024) 152135]","authors":"Mengran Wang ,&nbsp;Tingting Xuan ,&nbsp;Haining Li ,&nbsp;Jing An ,&nbsp;Tianhui He ,&nbsp;Jiang Cheng","doi":"10.1016/j.acthis.2024.152192","DOIUrl":"10.1016/j.acthis.2024.152192","url":null,"abstract":"","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"126 8","pages":"Article 152192"},"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":"126 8","pages":"Article 152203"},"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":"126 8","pages":"Article 152194"},"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":"126 8","pages":"Article 152193"},"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":"126 8","pages":"Article 152188"},"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":"126 5","pages":"Article 152191"},"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":"126 5","pages":"Article 152189"},"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}