{"title":"Challenging diagnosis in pulmonary nut carcinoma: A report of two cases with different histopathologic and molecular features and a novel <i>NUTM1::SPECC1</i> gene fusion.","authors":"Ling Xie, Jie Chen, Fei Ke, YanYing Zheng, Hui Li","doi":"10.14670/HH-18-905","DOIUrl":"https://doi.org/10.14670/HH-18-905","url":null,"abstract":"<p><strong>Background: </strong>NUT carcinoma (NC), formerly known as NUT midline carcinoma, is a rare but highly aggressive cancer. It is a poorly differentiated carcinoma characterized by rearrangements of the <i>NUTM1</i> (nuclear protein in Testis) gene with a member of the bromodomain-containing protein (<i>BRD</i>) family gene, usually <i>BRD4</i>. There is limited knowledge about primary pulmonary NC till now. It is probably underestimated or underdiagnosed because of its poorly differentiated character, misleading immunophenotype, and wide range of differential diagnoses.</p><p><strong>Method: </strong>We report here two cases of pulmonary NC with different clinicopathological and molecular presentations to draw attention to some atypical clinicopathologic features that can help clinicians and pathologists consider this rare entity.</p><p><strong>Results: </strong>The first case shows a nested pattern with small, uniform, blue epithelioid cells and aberrant expression of neuroendocrine markers, which has a known <i>BRD3::NUTM1</i> fusion accompanied by a novel <i>IGR</i> (downstream ROR2)<i>::NUTM1</i> fusion. The second case demonstrates solid sheets and cords of eosinophilic epithelioid-polygonal cells with a mucoid stroma and TTF1 expression, which has a novel <i>SPECC1::NUTM1</i> gene fusion accompanied by <i>TP53</i> and <i>JAK1</i> gene oncogenic variants.</p><p><strong>Conclusion: </strong>As a result, our study contributes to expanding the variant spectrum of the <i>NUTM1</i> gene. NUT carcinoma with different fusion partners seems to have unique clinicopathological characteristics, yet more cases need to accumulate experience.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18905"},"PeriodicalIF":2.5,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729967","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":"Cocaine abuse and its impact on the thymus and spleen.","authors":"Toshihiko Aki, Kana Unuma","doi":"10.14670/HH-18-904","DOIUrl":"https://doi.org/10.14670/HH-18-904","url":null,"abstract":"<p><p>Cocaine is a psychostimulant abused worldwide. Its pharmacotoxicological properties are derived mainly from its impact on the neurotransmission of sympathomimetic nerves. Cocaine enhances and prolongs the neurotransmission of monoamines, such as dopamine, serotonin, and adrenaline, which are responsible not only for cocaine's euphoric effects, but also its cardiovascular toxicity. In addition to these effects on central as well as peripheral nerves, immunosuppression is also implicated in cocaine toxicity. The thymus and spleen are lymphoid organs that are essential in lymphocyte maturation and erythrocyte homeostasis. Reductions in thymus and spleen size, which are observed under both physiological and pathological conditions, are known as thymic involution and splenic contraction, respectively. These phenomena are also observed in experimental animal models of binge cocaine abuse. In this brief review, we describe the mechanisms of cocaine toxicity, thymic involution, and splenic contraction, followed by discussions about the possible role of the latter two phenomena in cocaine intoxication.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18904"},"PeriodicalIF":2.5,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718701","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}
Jinhui Kang, Jun Wen, Huifang Chen, Cui Zhu, Yinshan Bai
{"title":"Progress of research on engineered extracellular vesicles from different sources for disease treatment.","authors":"Jinhui Kang, Jun Wen, Huifang Chen, Cui Zhu, Yinshan Bai","doi":"10.14670/HH-18-903","DOIUrl":"https://doi.org/10.14670/HH-18-903","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are lipid bilayer nanoparticles that encapsulate proteins, lipids, nucleic acids, and small molecules and display low immunogenicity, high stability, and cross-species transmission. By applying engineering technologies, the surface of EVs can be modified and loaded with cargo with therapeutic properties. Thus, engineered EVs can play important roles in preventing and treating various diseases. However, many challenges and uncertainties are faced in the clinical translation of EVs. In this review, we comprehensively analyzed the types of EVs derived from animal cells, plant cells, and microorganisms and summarized their biological properties and potential for engineering modifications. Furthermore, we also explored their therapeutic potential and discussed recent advancements in relevant clinical trials, aiming to provide scientific guidance for future research on the engineering of EVs and precision treatment of clinical diseases.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18903"},"PeriodicalIF":2.5,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709527","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":"Astragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1 <i>in vitro</i> and <i>in vivo</i>.","authors":"Bensong Duan, Zhewei Bao, Jingya Yang, Zhenzhen Wang, Aoxiang Li, Jin Yang, Mengke Lv, Haibin Zhang","doi":"10.14670/HH-18-902","DOIUrl":"https://doi.org/10.14670/HH-18-902","url":null,"abstract":"<p><strong>Background: </strong>Astragaloside IV (AS-IV) has demonstrated a protective effect against gastrointestinal tract injury induced by various factors. However, its potential mechanism against chronic atrophic gastritis (CAG) remains unknown.</p><p><strong>Purpose: </strong>The objective of the present study was to investigate the impact of AS-IV on CAG and elucidate its molecular mechanism.</p><p><strong>Methods: </strong>The mRNA and protein levels of protease-activated receptor-1 (PAR-1) and related proteins were assessed using reverse transcription-polymerase chain reaction and western blot analyses, respectively. In addition, the levels of inflammatory factors were measured via enzyme-linked immunosorbent assay in GES-1 cells following treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The CAG model was established in rats induced with MNNG and concurrently treated with AS-IV for 10 weeks. Subsequently, serum samples were collected to assess the expression levels of proteins reflecting inflammatory markers. The gastric tissue sections were used for hematoxylin and eosin staining, immunohistochemical analysis, and the assessment of p-NF-κB p65 and PAR-1 signaling.</p><p><strong>Results: </strong><i>In-vitro</i> experiments demonstrated that the mRNA levels of PAR-1 were upregulated following treatment with AS-IV and MNNG. Conversely, inhibition of PAR-1 expression reversed the therapeutic effects of AS-IV on MNNG-treated GES-1 cells, leading to increased expression of cyclooxygenase-2 and p-NF-κB p65. In addition, PAR-1 inhibition notably reversed MNNG-induced inflammatory factors, including IL increase. <i>In-vivo</i> experimental validation further confirmed that the upregulation of PAR-1 expression following treatment with AS-IV exerted a protective effect on the gastric mucosa of CAG rats.</p><p><strong>Conclusion: </strong>In conclusion, the findings of the present study suggested that AS-IV exhibited therapeutic efficacy against CAG induced by MNNG; its mechanism may be closely associated with the thrombin/PAR-1 signaling pathway. The present study provides a theoretical foundation for further exploration of the pharmacological effects of AS-IV on the treatment of human CAG.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18902"},"PeriodicalIF":2.5,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700373","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}
Charlotte Schubert, Theresa Vilsmaier, Falk Batz, Vincent Cavaillès, Sophie Sixou, Thomas Kolben, Sarah Meister, Christina Buschmann, Friederike Hagemann, Sven Mahner, Melitta B Köpke, Nina Ditsch, Udo Jeschke, Alaleh Zati Zehni
{"title":"A low nuclear-to-cytoplasmic ratio of VDR expression is an independent prognostic marker in breast cancer.","authors":"Charlotte Schubert, Theresa Vilsmaier, Falk Batz, Vincent Cavaillès, Sophie Sixou, Thomas Kolben, Sarah Meister, Christina Buschmann, Friederike Hagemann, Sven Mahner, Melitta B Köpke, Nina Ditsch, Udo Jeschke, Alaleh Zati Zehni","doi":"10.14670/HH-18-901","DOIUrl":"https://doi.org/10.14670/HH-18-901","url":null,"abstract":"<p><p>The aim of this retrospective study was to analyze the prognostic value of cytoplasmic versus nuclear expression of the vitamin D receptor (VDR) in breast cancer (BC) tissue samples and to relate the results to clinicopathological parameters. VDR expression was assessed in 319 primary breast cancer patients using the Remmele and Stegner immunoreactive scoring (IRS) system. Follow-up data were obtained from the Munich Cancer Registry. The correlation with overall survival (OS) and disease-free survival (DFS) was calculated using univariate and multivariate analyses. Correlation analysis revealed a correlation between nuclear VDR expression and improved outcomes for both OS (<i>p</i>=0.004) and DFS (<i>p</i>=0.001). Conversely, cytoplasmic VDR expression was significantly associated with a shorter OS (<i>p</i>=0.003) and DFS (<i>p</i><0.001). Additionally, both cytoplasmic and nuclear VDR expression were found to be independent markers of DFS (<i>p</i><0.001; <i>p</i>=0.021) when examined alongside clinicopathological parameters. Moreover, nuclear VDR expression was positively associated with lower lymph node invasion (pN; <i>p</i>=0.01). For triple-negative patients, cytoplasmic VDR expression was found to have a significant inverse correlation with DFS (<i>p</i><0.001). Lastly, the ratio of VDR nuclear/cytoplasmic was identified as an auxiliary independent marker of DFS and OS. These findings strongly indicate that the subcellular localization of VDR is crucial in determining BC prognosis. The expression of nuclear VDR appears to have a protective effect, while cytoplasmic VDR is associated with a more aggressive disease course. The data may help identify subgroups of patients with high-risk BC, possibly leading to specific options for targeted tumor therapy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18901"},"PeriodicalIF":2.5,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691978","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}
Pratima Chaudhary, Pragya Yadav, Partha Pratim Manna
{"title":"Tumoricidal potential of binary therapy in lymphoma: Role of DC-NK cross-talk and checkpoint inhibitors.","authors":"Pratima Chaudhary, Pragya Yadav, Partha Pratim Manna","doi":"10.14670/HH-18-900","DOIUrl":"https://doi.org/10.14670/HH-18-900","url":null,"abstract":"<p><p>Lymphoma is a common type of cancer that occurs in humans. Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma (NHL) subtype and is characterized by high clinical and biological heterogeneity. The tumor microenvironment (TME) in lymphoma is critical for the initiation, progression, and metastasis of tumors and influences the therapeutic efficiency of chemotherapy or immunotherapy, including cell therapy or appropriate combinations of therapeutics. The role of effector immune cells in the development and progression of DLBCL is complex and involves reciprocal interactions between tumor cells, adaptive and innate immune cells, their soluble mediators, and structural components present in the TME. Recruitment of immune cells in the TME and their distinct effects on tumor progression and therapeutic outcomes in the presence of therapy have decisive effects on the outcome of therapy. In this review, we discuss the application and implications of binary therapy involving suboptimal-dose chemotherapy and adoptive cell therapy on the basis of our recent findings on γc cytokine-aided cross-talk between dendritic cells and natural killer cells in therapy against experimental murine lymphoma. This novel therapeutic protocol induces a healing response in experimental lymphoma by downregulating FOXP3 and programmed cell death protein 1. We discuss the various aspects of binary therapy covering multiple issues, including the participation of cell subsets and checkpoint inhibitors in the treatment of malignant lymphoma. These new therapies involve the induction of adoptive cell therapy through the passive transfer of immunologic effectors in addition to a suboptimal dose of adriamycin (doxorubicin hydrochloride) to increase the ability of the immune system to react against tumor antigens, inducing the destruction of tumor cells.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18900"},"PeriodicalIF":2.5,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663573","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":"ITGAX promotes Th17-cell differentiation and drives pathogenesis in pediatric ulcerative colitis.","authors":"Wanying Xie, Dong Zhan","doi":"10.14670/HH-18-899","DOIUrl":"https://doi.org/10.14670/HH-18-899","url":null,"abstract":"<p><strong>Background: </strong>Pediatric ulcerative colitis (UC) is an inflammatory bowel disease characterized by dysregulated immune responses and intestinal inflammation, often more severe than adult-onset UC. Th17 cells play a crucial role in UC pathogenesis but the mechanisms regulating their differentiation and recruitment in pediatric UC remain incompletely understood.</p><p><strong>Methods: </strong>Transcriptomic analysis of pediatric UC patients and weighted gene co-expression network analysis (WGCNA) were performed to identify key dysregulated genes. The functional role of the candidate gene <i>ITGAX</i> was investigated using <i>in vitro</i> Th17 differentiation assays with siRNA knockdown and an in vivo dextran sodium sulfate (DSS)-induced UC mouse model with intrarectal siRNA administration.</p><p><strong>Results: </strong>WGCNA identified <i>ITGAX, SOCS3, CXCL1, CASP1</i>, and <i>CXCL11</i> as core upregulated genes in pediatric UC, with <i>ITGAX</i> being a novel candidate regulator of Th17 cells. ITGAX knockdown in naive CD4+ T cells impaired Th17 differentiation and IL-17A production <i>in vitro</i>. In the DSS-induced UC mouse model, intrarectal ITGAX siRNA ameliorated colonic inflammation and ulceration, suppressed IL-17A levels, and selectively reduced the expansion of IFNγ-IL-17<sup>+</sup> Th17 cells in the colon.</p><p><strong>Conclusion: </strong>ITGAX is a key promoter of Th17-cell differentiation and expansion, contributing to the pathogenesis of pediatric UC. Targeting ITGAX may represent a potential therapeutic strategy for pediatric UC by modulating aberrant Th17 responses.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18899"},"PeriodicalIF":2.5,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656581","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}
Inka Rantala, Hanna-Riikka Teppo, Jonas Händelin, Janette Kemppainen, Riina K Ollikainen, Outi Kuittinen, Milla E L Kuusisto
{"title":"Oxidative stress markers 8-OHdG, Trx-1, and Prx6 are expressed in seminoma and are connected to TXNDC2, 3, and 6 expression levels.","authors":"Inka Rantala, Hanna-Riikka Teppo, Jonas Händelin, Janette Kemppainen, Riina K Ollikainen, Outi Kuittinen, Milla E L Kuusisto","doi":"10.14670/HH-18-898","DOIUrl":"10.14670/HH-18-898","url":null,"abstract":"<p><p>Testis-specific thioredoxins (TXNDCs) and oxidative stress have not been studied before in seminoma. We studied the immunohistochemical (IHC) expression of 8-OHdG, Prx6, Trx-1, TXNDC2, 3, and 6 in 25 testicular seminoma and 24 control samples. We retrospectively collected patient details and treatments from hospital records and combined them with IHC results. In normal testis, IHC expression of 8-OHdG, Prx6, TXNDC2, and 3 was higher than in seminoma samples (<i>p</i><0.001 each), and the absence of n8-OHdG (<i>p</i>=0.002) and nTXNDC2 expression (<i>p</i>=0.044) was clinically associated with elevated lactate dehydrogenase levels. On the contrary, Trx-1 and TXNDC6 were overexpressed in seminoma samples (<i>p</i>=0.035 and <i>p</i><0.001, respectively), and TXNDC6 was negatively associated with age over 40 (<i>p</i>=0.036). Concordant with the IHC expression, <i>PRDX6</i> mRNA levels were downregulated with a fold change of -2517.4 (<i>p</i><0.001), and <i>TXN</i> mRNA levels were upregulated with a fold change of 11637.4 (<i>p</i>=0.008) in seminoma samples compared with healthy controls. The oxidative stress markers studied had a correlation between the nuclear and cytoplasmic localization, a mutual correlation in expression between different markers, and mutual protein-protein interactions according to STRING Enrichment analysis. Our results show that oxidative stress markers and their expression in seminoma differ from that in normal testis tissue. Trx-1 and cTXNDC6 are seemingly overexpressed in seminoma, which might indicate their relevance in seminoma biology.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18898"},"PeriodicalIF":2.5,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648420","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":"Cytoskeleton proteins, the structural basis of T-lymphocyte and TEC restructure during rapid thymus regeneration.","authors":"Xunuo Wen, Jianli Gao","doi":"10.14670/HH-18-897","DOIUrl":"https://doi.org/10.14670/HH-18-897","url":null,"abstract":"<p><p>Thymus regeneration is the main way for humans to combat immune degeneration and immunosenescence. The interesting cycle of thymus degeneration and regeneration achieves the renewal of adaptive immunity, which is crucial for reconstructing cellular immunity. Rapid thymic regeneration is the main renewal mode after various acute stress-induced thymic involutions, such as radiation, immunosuppressants, and starvation. The cytoskeleton is a key regulator of immune response by affecting the structure and function of immune cells. Our team has conducted years of research on rapid thymic regeneration and found that some types of cytoskeletal proteins, such as F-actin/G-actin, the Thymosin β family, ERM (Ezrin/Radixin/Moesin), and WAVE2, play a critical role in the spatial development of thymic epithelial cells (TECs), and finally regulate the regeneration of the thymus by modulating the skeleton of TECs and T lymphocytes. Here, we summarize the current understanding of cytoskeleton proteins and cell restructure of TECs or T lymphocytes and its relationship with the regeneration of the thymus.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18897"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624472","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":"Diversity and dynamics of fish ovaries: Insights into reproductive strategies, hormonal regulation, and ovarian development.","authors":"Doaa M Mokhtar","doi":"10.14670/HH-18-802","DOIUrl":"10.14670/HH-18-802","url":null,"abstract":"<p><p>Fish ovaries exhibit a remarkable diversity in shape, size, and organization, reflecting the myriad reproductive strategies employed by different species. This review delves into the intricate biology of fish ovaries, highlighting their structural diversity and the hormonal regulation that governs ovarian development and oocyte maturation. Key hormones include pituitary gonadotropins (GTHs) and maturation-inducing hormones (MIHs), which initiate oocyte growth and maturation. GTHs stimulate ovarian production of estradiol-17β and 17α,20β-DP, which induce oocyte maturation via MPF formation. Sex steroids like estrogens and progestogens, synthesized from cholesterol, play crucial roles. Other hormones, including growth hormone, prolactin, thyroid hormones, IGFs, ACTH, and melatonin, influence ovarian activity. The review also explores the varied reproductive strategies among fish, including oviparity and viviparity, and discusses how environmental factors like water temperature and photoperiod influence ovarian histology. Understanding the complex interplay between these factors is essential for advancing fisheries management, conservation, and aquaculture practices. Additionally, the evolutionary trajectory of fish ovaries underscores their adaptation to diverse ecological niches, contributing to the survival and reproductive success of fish species. The ovarian stroma provides structural support and houses various cell types, including dendritic cells (DCs), endocrine cells, and telocytes, contributing to follicle growth and hormone production, essential for reproductive success in fish. Fish ovaries are a crucial aspect of fish biology, with their structure and function intricately regulated by hormonal, environmental, and seasonal factors.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"283-295"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286030","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}