Histology and histopathology最新文献

{"title":"CORM-3 mitigates hypoxia/reoxygenation-induced injury in neonatal rat cardiomyocytes by regulating Mitochondrial-Mediated apoptosis and complex IV activity.","authors":"Fang Du, Qingsheng Niu, Xiaojuan Yang, Junwei Zheng, Xiaohong Wang","doi":"10.14670/HH-18-941","DOIUrl":"10.14670/HH-18-941","url":null,"abstract":"<p><strong>Background: </strong>Myocardial ischemia-reperfusion injury (MIRI) is a major contributor to myocardial infarction and leads to significant myocardial dysfunction. Mitochondria, crucial for cellular energy production, are particularly susceptible to damage during ischemia/reperfusion (I/R) events. Carbon monoxide-releasing molecule-3 (CORM-3), a water-soluble compound that releases carbon monoxide (CO), has demonstrated multiple protective effects against I/R injury. Mitochondria are recognized as selective targets for CO's protective actions in cells.</p><p><strong>Purpose: </strong>This study aimed to explore whether CORM-3 mitigates cardiomyocyte injury during hypoxia/reoxygenation (H/R) by regulating the mitochondrial-mediated apoptosis pathway and mitochondrial respiration.</p><p><strong>Methods: </strong>Neonatal rat cardiomyocytes were cultured and randomly assigned into four groups: control group, H/R group (hypoxia for three hours followed by reoxygenation for six hours), CORM-3 group, and inactivated CORM-3 (iCORM-3) group. CORM-3 and iCORM-3 (12.5 µmol/L) were administered at the onset of hypoxia. Mitochondrial ultrastructure was assessed using transmission electron microscopy. The protein levels of caspase-3, caspase-9, mitochondrial cytochrome c, and cytosolic cytochrome c were analyzed via western blot. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) were measured by flow cytometry. ATP levels were quantified using an ATP Assay Kit, and mitochondrial respiratory chain complex IV activity was determined using a cytochrome oxidase activity colorimetric assay kit.</p><p><strong>Results: </strong>CORM-3 effectively reduced myocardial mitochondrial structural damage induced by H/R and downregulated the expression of caspase-3, caspase-9, and cytosolic cytochrome c. Moreover, CORM-3 inhibited cytochrome c release from mitochondria and enhanced mitochondrial membrane potential. Additionally, CORM-3 diminished ROS production and increased the activity of mitochondrial respiratory complex IV in cardiomyocytes. CORM-3 also alleviated the decline in ATP levels following H/R. The protective effects were lost when using inactivated CORM-3 (iCORM-3), suggesting that CO is the active mediator.</p><p><strong>Conclusion: </strong>The results indicate that CORM-3 effectively alleviates myocardial injury during H/R by inhibiting mitochondria-mediated apoptosis and enhancing mitochondrial respiratory function.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18941"},"PeriodicalIF":2.5,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215704","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 redefinition of prognosis: Invasive carcinoma with metastasis originating from microglandular adenosis.","authors":"Dan Chen, Xiaochun Fei","doi":"10.14670/HH-18-940","DOIUrl":"https://doi.org/10.14670/HH-18-940","url":null,"abstract":"<p><strong>Aim: </strong>To investigate the clinicopathological features, immunophenotype, diagnosis, and prognosis of invasive carcinoma originating from microglandular adenosis.</p><p><strong>Methods: </strong>Two cases of invasive carcinoma originating from microadenosis were analyzed in the Department of Pathology of the Ruijin Hospital affiliated with the Medical College of Shanghai Jiaotong University. Histopathological morphology, immunohistochemical staining, and prognosis were observed.</p><p><strong>Results: </strong>(1) Histopathological morphology: microscopically, the tumor showed small clusters and nests of infiltrative growth; a few areas showed tubules, and some eosinophilic secretions were observed in the lumen. (2) Immunohistochemistry and molecular genetics: Case 1 was partly positive for S-100, positive for SOX-10, and negative for ER, PR, and HER2 (2+). The result of HER2 gene amplification was negative. Breast and liver tissue lesions in Case 2 were positive for S-100 and SOX-10 but negative for ER and HER2. PR was positive in the liver lesions but showed moderate to strong expression in approximately 80% of the staining. Myoepithelial markers (p63 and calponin) showed loss of myoepithelium around the nests of invasive cancers. TP53 (R213Ter) showed somatic gene variations, and no exon amplification or deletion was detected in BRCA1/2.</p><p><strong>Conclusion: </strong>Invasive carcinoma originating from microadenosis has the same immunophenotype as microadenosis, and its prognosis is difficult to determine.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18940"},"PeriodicalIF":2.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208384","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":"Intraductal carcinoma of the prostate: A comprehensive literature review focused on grading challenges and controversies.","authors":"Ioanna-Maria Grypari, Angeliki Pomoni, Vasiliki Tzelepi","doi":"10.14670/HH-18-939","DOIUrl":"https://doi.org/10.14670/HH-18-939","url":null,"abstract":"<p><p>Intraductal carcinoma of the prostate (IDC-P) is characterized by neoplastic cell proliferation within pre-existing ducts or acini, exhibiting architectural and cytological atypia exceeding that of high-grade prostatic intraepithelial neoplasia. Its presence in needle biopsies and prostatectomies is associated with adverse clinical and pathological features, including large tumor volume, high grade, advanced stage, early biochemical recurrence, and intrinsic resistance to systemic therapy. Although rare, IDC-P can occasionally occur without concurrent invasive cancer or be associated with low-grade prostate cancer. Molecularly, IDC-P resembles its associated invasive carcinoma, sharing alterations typical of high-grade aggressive tumors. These findings support the hypothesis that IDC-P arises from the retrograde spread of invasive carcinoma, with ducts providing a protective niche against the tumor microenvironment. In contrast, isolated IDC-P and IDC-P associated with low-grade invasive carcinoma may represent precursor lesions. IDC-P must be distinguished from other intraductal lesions, both benign and malignant, particularly in needle biopsies, as its detection impacts therapeutic decisions. While grading does not apply to isolated IDC-P, there is an ongoing debate regarding IDC-P with synchronous invasive cancer. The International Society of Urological Pathology (2019) recommends incorporating IDC-P into Gleason score calculations, whereas the Genitourinary Pathology Society advises against grading it at all. Both approaches have merit, but further validation studies focusing on cases where IDC-P inclusion alters the final grade, though uncommon, are warranted.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18939"},"PeriodicalIF":2.5,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198905","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":"High histamine expression by early-stage squamous cell carcinoma of the tongue is associated with a poor prognosis.","authors":"Satoshi Kimura, Hirotsugu Noguchi, Hiroaki Sato, Shohei Shimajiri, Toshiyuki Nakayama","doi":"10.14670/HH-18-938","DOIUrl":"https://doi.org/10.14670/HH-18-938","url":null,"abstract":"<p><strong>Background: </strong>Although not widely known, several types of cancers express histamine. Squamous cell carcinoma (SCC) of the tongue is one such cancer, and histamine expression is associated with the tumor microenvironment. Our aim was to examine whether histamine expression is a useful prognostic factor for tongue SCC.</p><p><strong>Methods: </strong>Histamine cannot be accurately measured directly because it is rapidly degraded after secretion. Therefore, L-histidine decarboxylase (HDC), an enzyme that synthesizes histamine in a single step, was used to estimate histamine secretion. In a retrospective study, tongue SCC samples from patients were immunohistochemically stained for HDC; the staining intensity was semi-quantified and evaluated relative to indices used in histopathological diagnosis.</p><p><strong>Results: </strong>High expression of HDC was associated with the worst tumor invasion and tumor budding. Overall survival curves revealed that patients with tongue SCC showing high HDC expression had a poor prognosis.</p><p><strong>Conclusion: </strong>The expression of histamine may be a prognostic indicator for tongue SCC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18938"},"PeriodicalIF":2.5,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180800","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":"HMMR inhibition by 4-methylumbelliferone is effective in preclinical hepatocellular carcinoma models.","authors":"Ying Zhu, Ge Sang Wang Dui, Suo Lang Bai Ma, Ci Yang, Wen Xu, Jianguo Xu","doi":"10.14670/HH-18-937","DOIUrl":"https://doi.org/10.14670/HH-18-937","url":null,"abstract":"<p><p>The poor prognosis of hepatocellular carcinoma (HCC), especially in advanced stages, underscores the need for new therapeutic strategies. In this study, we show that hyaluronan-mediated motility receptor (HMMR) is highly expressed in HCC tumors compared with normal liver tissues. Knockdown of HMMR using siRNA significantly reduced cell proliferation and migration in both parental and doxorubicin-resistant HCC cell lines without inducing apoptosis. Similarly, treatment with 4-Methylumbelliferone (4-MU), a pharmacological HMMR inhibitor, led to dose-dependent decreases in proliferation and migration <i>in vitro</i>. <i>In vivo</i>, 4-MU treatment significantly inhibited tumor growth in a HepG2 xenograft model, resulting in a 44% reduction in tumor volume by day 20 and an 80% decrease in HMMR expression in tumor tissues. These results demonstrate that HMMR promotes growth and migration in HCC, and targeting HMMR effectively inhibits both parental and drug-resistant HCC cells. Additionally, our findings suggest that 4-MU, an approved drug for biliary tract disorders, holds promise as a repurposed therapeutic candidate for HCC treatment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18937"},"PeriodicalIF":2.5,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173402","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":"Ion channels and actin: A tale of two friends.","authors":"Federico Sesti, Elena Forzisi","doi":"10.14670/HH-18-936","DOIUrl":"https://doi.org/10.14670/HH-18-936","url":null,"abstract":"<p><p>An increasing number of studies highlight ion channels as multifunctional proteins involved in diverse cellular processes, including proliferation, differentiation, adhesion, migration, morphology, and programmed cell death (apoptosis). Given these broad roles, it is not surprising that ion channels interact closely with actin-a ubiquitous cytoskeletal component that participates in a vast array of biological functions. Ion channels depend on the actin cytoskeleton for essential activities such as trafficking to and from the plasma membrane. Conversely, actin dynamics are often modulated by ion channels during various cellular events. In this review, we provide an overview of the field and discuss key examples that reveal emerging patterns in the bidirectional interactions between ion channels and the actin cytoskeleton.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18936"},"PeriodicalIF":2.5,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158396","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":"Tuoli Xiaodu powder ameliorated 5-fluorouracil-induced intestinal injury by reducing intes-tinal inflammation, oxidative stress, and intestinal flora imbalance.","authors":"Yongjun Wu, Ling Jiang, Wanrou Jiang, Wanyi Zhang, Wenjuan Zheng, Hongjie Huang, Yu Xia, Xiuyun He, Chaofu Zhu","doi":"10.14670/HH-18-935","DOIUrl":"https://doi.org/10.14670/HH-18-935","url":null,"abstract":"<p><p>Chemotherapy-induced diarrhea (CID) is a common adverse event in cancer patients treated with 5-fluorouracil (5-FU). This study aimed to investigate the potential protective effects of Tuoli Xiaodu (TLXD) powder on CID and to explore its possible mechanisms. Mice with CID induced by 5-FU were randomly divided into seven groups: Blank group, CID group, positive drug (loperamide) group, and TLXD powder low, medium, and high groups. The degree of diarrhea, tumor growth, intestinal barrier damage, intestinal inflammation, oxidative stress, and gut microbiota diversity were assessed. The study showed that TLXD powder significantly inhibited diarrhea and tumor growth in 5-FU-induced CID mice. H&E staining and western blot showed that TLXD powder improved the intestinal mucosa and intestinal permeability of 5-FU-induced CID mice. Furthermore, TLXD powder elicited a reduction in the expres-sion of inflammatory factors within the intestinal tract of mice with CID while simultaneously augment-ing the expression of anti-inflammatory factors and maintaining a balanced Th17/Treg ratio. TLXD pow-der decreased intestinal oxidative stress and intestinal epithelial cell ferroptosis and activated the Nrf2/HO-1 signaling axis in CID mice. The results of the gut flora analysis showed that TLXD powder improved the intestinal flora structure of CID mice. TLXD powder significantly reduced the proportion of Proteobacteria, Actinobacteria, Deferribacteres, and TM7 at the phylum level and Desulfovibrio, Mucis-pirillum, Adlercreutzia, and Odoribacter at the genus level. These findings provide a new therapeutic approach for the management of CID in cancer patients treated with 5-FU.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18935"},"PeriodicalIF":2.5,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150319","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":"Engineering vascular grafts from decellularized plants: Advances and challenges.","authors":"Nick Merna","doi":"10.14670/HH-18-934","DOIUrl":"https://doi.org/10.14670/HH-18-934","url":null,"abstract":"<p><p>Small-caliber vascular grafts (<6 mm diameter) are critical for coronary and peripheral bypass surgeries, yet developing functional substitutes remains challenging. Autologous vessels are ideal but often unavailable or of poor quality. Synthetic grafts, such as expanded polytetrafluoroethylene (ePTFE) and Dacron, have high failure rates in small diameters due to thrombosis, intimal hyperplasia, and compliance mismatch. Tissue-engineered vascular grafts (TEVGs) aim to overcome these issues by providing a biocompatible scaffold with an endothelial lining. Decellularized plant tissues have recently gained attention as natural scaffolds for TEVGs due to their structural similarity to human vasculature. Leaves and stems provide an extracellular matrix (ECM) primarily composed of cellulose, which is biocompatible, porous, and non-thrombogenic. These scaffolds are cost-effective, scalable, and ethically uncontroversial. Decellularized parsley stems or leatherleaf leaves, for instance, can be recellularized with endothelial and smooth muscle cells (SMCs) to create small-diameter grafts that support endothelialization and withstand physiological pressures. Perfusion bioreactors further enhance the functionality of plant-based grafts by simulating physiological conditions. Pulsatile flow and pressure stimulate endothelial cell alignment, reducing thrombogenicity, while mechanical stimulation promotes SMC maturation and ECM deposition, improving graft strength and compliance. This review summarizes recent advances in plant-based vascular grafts and perfusion bioreactor conditioning, compares their performance to conventional grafts, and highlights remaining challenges. Decellularized plant scaffolds, with their inherent vascular architecture and biocompatibility, show promise as natural templates for small-caliber vascular grafts. However, further research is needed to address key challenges such as standardization, mechanical optimization, and long-term <i>in vivo</i> validation to facilitate their clinical application.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18934"},"PeriodicalIF":2.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142448","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":"ENO3 regulates ferroptosis by interaction with PKM2 to promote the progression of metabolic dysfunction-associated steatotic liver disease.","authors":"Zhenzi Cao, Xue Li, Qian Hao, Jing Liu, Minghao Li, Baoding Li, Shengjuan Hu, Yanling Li, Xiaofei Li, Yuanyuan Tang, Fuliang Pan, Yanxia Liu, Min Niu","doi":"10.14670/HH-18-933","DOIUrl":"https://doi.org/10.14670/HH-18-933","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder characterized by excessive lipid accumulation in the liver. The glycolytic enzyme enolase 3 (ENO3) is reported to be most significantly elevated in the analysis of MASLD-related sequencing results based on the GEO database. However, the specific mechanism by which ENO3 regulates MASLD is not fully understood.</p><p><strong>Objective: </strong>To investigate the role and possible molecular mechanism of ENO3 in MASLD.</p><p><strong>Methods: </strong>The expression of ENO3 and PKM2 in the liver tissues of control and MASLD rats was detected by immunohistochemistry and western blot. <i>In vitro</i> studies involved treating THLE-2 cells with free fatty acids (FFA) and Ferrostatin-1 (Fer-1), as well as manipulating ENO3 expression via small interfering RNA (siRNA) and overexpression plasmids, and manipulating PKM2 expression via siRNA. Fat accumulation was assessed using Oil Red O staining and measurements of intracellular total cholesterol (TC) and triglycerides (TG). Ferroptosis markers, including SLC7A11, GPX4, Fe²⁺, and malondialdehyde (MDA), were evaluated. Protein-protein interactions between ENO3 and PKM2 were examined using co-immunoprecipitation (Co-IP) and immunofluorescence.</p><p><strong>Results: </strong>MASLD liver tissues exhibited significantly higher levels of ENO3 and PKM2. Silencing ENO3 in FFA-treated THLE-2 cells reduced fat accumulation, downregulated PKM2 expression, and decreased ferroptosis markers. Conversely, ENO3 overexpression promoted fat accumulation and ferroptosis, which were mitigated by Fer-1 or si-PKM2. Co-IP and immunofluorescence confirmed the physical interaction and co-localization of ENO3 and PKM2 in THLE-2 cells.</p><p><strong>Conclusions: </strong>ENO3 interacted with PKM2 to regulate ferroptosis and further promoted the progression of MASLD.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18933"},"PeriodicalIF":2.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119609","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":"Extracellular vesicles derived from different brain tissue cells: A potential therapeutic measure for hypoxic-ischemic brain injury in immature brains.","authors":"Yitong Guan, Lijun Yang, Hong Cui","doi":"10.14670/HH-18-932","DOIUrl":"https://doi.org/10.14670/HH-18-932","url":null,"abstract":"<p><p>Neonatal hypoxic-ischemic encephalopathy and neonatal acute ischemic stroke are common causes of hypoxic-ischemic brain injury (HIBI) in the neonatal period, which may lead to permanent neurological sequelae. It is difficult to distinguish the two in the early stage. As a timely brain protection measure, hypothermia is still the standard treatment, but its efficacy in the treatment of immature brain injury is still controversial. The underlying pathophysiological mechanisms and effective treatment strategies of neonatal hypoxic-ischemic brain damage (HIBD) have been an active area of research. Extracellular vesicles (EVs), a class of nanoscale membranous structures, play a critical role in intercellular communication by facilitating the transfer of bioactive molecules or engaging in receptor-mediated interactions. Recent studies have demonstrated that various cell types within brain tissue, including neurons, astrocytes, microglia, endothelial cells, and stem cells, secrete substantial amounts of EVs. These vesicles carry diverse cargo, such as microRNAs, DNA, and proteins, which exert regulatory effects on recipient cells within the brain, thereby mediating neuroprotective effects. These effects include enhancing synaptic plasticity, modulating neuroinflammation, promoting angiogenesis, and regulating cellular autophagy, collectively contributing to neuroprotection. This review aims to summarize the functional characteristics of EVs derived from different cell types within the brain and to highlight recent advancements in this field. By providing insights into the role of EVs in HIBI, it seeks to provide novel insights and references for understanding the pathogenesis of neonatal HIBI and exploring innovative therapeutic approaches.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18932"},"PeriodicalIF":2.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110427","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}