Journal of Molecular Histology最新文献

{"title":"Dendritic pathology and overexpression of MAP2 in Purkinje cells from mice inoculated with rabies virus","authors":"Andrés Obdulio Porras,&nbsp;María Paula Morales,&nbsp;Gerardo Santamaría,&nbsp;Orlando Torres-Fernández","doi":"10.1007/s10735-024-10348-5","DOIUrl":"10.1007/s10735-024-10348-5","url":null,"abstract":"<div><p>The effect of rabies virus infection on dendritic morphology and on the expression of the MAP2 protein in Purkinje cells in the cerebellum of mice was studied. ICR mice were inoculated with rabies virus, and six days later, the mice were sacrificed, the cerebellum was removed and processed for Golgi-Cox staining or MAP2 immunohistochemistry. Infection with rabies virus altered the dendritic pattern of Purkinje cells ranged from moderate changes to accentuated retraction in the dendritic tree of some Purkinje cells. The loss of dendritic branches in the samples of mice infected with RABV was also reflected in a decrease in intersections quantified using the Sholl technique, thus suggesting dendritic pathology. Immunoreactivity to MAP2 protein in the molecular layer of the cerebellum of control mice was mainly distributed in dendrites of Purkinje cells. Some somas were faintly stained. In infected mice immunoreactivity to MAP2 was intense in somas and dendrites of Purkinje cells and in some interneurons. These results are consistent with similar findings we previously reported for the cerebral cortex and spinal cord of rabies-infected mice. But they differ from studies in other pathologies where an association between dendritic pathology and loss of MAP2 immunoreactivity has been found. Our studies in rabies contribute to suggestion that MAP2 overexpression may also be associated with alterations in dendritic morphology. MAP2 protein contributes to maintaining cytoskeleton stability. However, in rabies, increased MAP2 expression here only determined by immunohistochemistry could destabilize the cytoskeleton of dendrites. Golgi staining is considered the gold standard for the study of dendritic morphology. Its association with changes in MAP2 expression appears to provide molecular support for the concept of dendritic pathology. These results contribute to the understanding of the effect of rabies virus infection on dendritic morphology. They therefore reinforce the idea that rabies not only has a dysfunctional effect on neurons, as some authors claim, but also affects their structure.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142890084","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":"Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the immune system maternal-fetal interface during palatal development","authors":"Wang Yongkai,&nbsp;Zhang Shuhui,&nbsp;Ma Li","doi":"10.1007/s10735-024-10331-0","DOIUrl":"10.1007/s10735-024-10331-0","url":null,"abstract":"<div><p>2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an important environmental pollutant that disturbs the immune balance of the maternal-fetal interface (MFI) and is also a common environmental factor for the formation of cleft palate (CP). Therefore, the purpose is to investigate whether TCDD can cause CP by disrupting the immune balance of the maternal-fetal interface. Fifteen C57BL/6J mice were randomly assigned to three groups: control group, TCDD group, and TCDD plus Freund’s complete adjuvant (FCA) (TCDD + FCA) group. Peripheral blood, placentas, and palatal tissues were collected for H&amp;E, flow cytometry, and ELISA. In the TCDD group, the placental diameter, the number of placental labyrinth vessels, and the area of sponge layer cells were all significantly reduced. At embryonic day (E) 17.0, there was a significant decrease in T-helper 1 (Th1) and Th2 cells in the peripheral blood of pregnant mice. Additionally, the levels of interferon-γ (IFN-γ) and interleukin-4 (IL-4), particularly IL-4, were significantly decreased. However, after treatment with FCA, the distance between the palatal shelves was reduced, and the placental weight, the number of labyrinth vessels, and the area of the cavernous cells in the placenta also increased. The number of Th1 and Th2 cells significantly increased, returning to the levels observed in the control group, with a more pronounced increase in the number of Th2 cells. In conclusion, TCDD may induce CP by disrupting the homeostasis of the MFI. The precise mechanisms by which TCDD impacts the immune system at the MFI require further investigation.2,3,7,8-四氯二苯并-对二恶英 （TCDD） 是一种重要的环境污染物，会扰乱母胎界面 （MFI） 的免疫平衡，也是形成腭裂 （CP） 的常见环境因素。因此，目的是研究 TCDD 是否可以通过破坏母胎界面的免疫平衡来引起 CP。将 15 只 C57BL/6J 小鼠随机分为 3 组：对照组、TCDD 组和 TCDD 加弗氏完全佐剂 （FCA） （TCDD + FCA） 组。收集外周血、胎盘和腭组织用于 H&amp;E、流式细胞术和 ELISA。TCDD 组胎盘直径、胎盘迷路血管数量和海绵层细胞面积均显著减少。在胚胎第 17.0 天 （E） 时，妊娠小鼠外周血中的 T 辅助细胞 1 （Th1） 和 Th2 细胞显著减少。此外，干扰素-γ （IFN-γ） 和白细胞介素-4 （IL-4），特别是 IL-4 的水平显着降低。然而，用 FCA 处理后，腭架之间的距离减小，胎盘重量、迷路血管的数量和胎盘中海绵状细胞的面积也增加。Th1 和 Th2 细胞的数量显著增加，恢复到对照组观察到的水平，Th2 细胞的数量增加更明显。总之，TCDD 可能通过破坏 MFI 的稳态来诱导 CP。TCDD 影响 MFI 免疫系统的确切机制需要进一步研究。</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-024-10331-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889855","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":"Bolanthus turcicus: a promising antidiabetic with in-vitro antioxidant, enzyme inhibitory and antiadipogenic activities","authors":"Sibel Özdaş,&nbsp;İpek Canatar,&nbsp;Gizem Ece Derici,&nbsp;Murat Koç","doi":"10.1007/s10735-024-10283-5","DOIUrl":"10.1007/s10735-024-10283-5","url":null,"abstract":"<div><p>It is crucial to investigate new anti-diabetic agents and therapeutic approaches targeting molecules in potential signaling pathways for the treatment of Type 2 diabetes mellitus (T2DM). The objective of the study was to investigate the total phenolic content, antioxidant capacity, α-glucosidase, and α-amylase inhibitory activities of <i>Bolanthus turcicus</i> (<i>B. turcicus</i>), as well as their cytotoxic, anti-adipogenic, anti-diabetic, apoptotic, and anti-migration potential on adipocytes. <i>B. turcicus</i> samples were extracted with methanol (MeOH), ethyl acetate (EA) and aqueous (Aq) solvents. The MeOH extract had the highest phenolic content (81.14 mg GAE/g), followed by EA (74.93 mg GAE/g) and Aq (51.09 mg GAE/g). All extracts exhibited dose-dependent increases in α-glycosidase and α-amylase inhibitory activity. <i>B. turcicus</i> extracts showed cytotoxic effect on adipocytes with IC₅₀ values of MeOH (141.0 µg/mL) &lt; Aq (155.3 µg/mL) &lt; EA (199.5 µg/mL). Furthermore, <i>B. turcicus</i> extracts reduced lipid droplet formation and adipocyte diameter size. All extracts altered cell morphology to resemble fibroblasts. <i>B. turcicus</i> extracts exhibited anti-migratory effect delaying wound healing for up to 96 h. The <i>B. turcicus</i> extracts showed a pro-apoptotic effects on adipocytes by increasing Caspase-3 enzyme activity and the population of DAPI-positive cell with apoptotic nuclear-morphology. <i>B. turcicus</i> extracts upregulated the expression of the <i>Glut-4</i> gene at the mRNA, protein and intracellular level in adipocytes. In conclusion, our findings indicate that <i>B. turcicus</i> not only exhibits strong antioxidant properties and enzyme inhibitory activities but also exerts significant anti-adipogenic and pro-apoptotic effects in adipocytes, thereby providing a comprehensive mechanism through which it may contribute to the management of T2DM. These effects highlight the potential of <i>B. turcicus</i> as a therapeutic agent for improving glucose homeostasis and insulin sensitivity.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889582","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":"Effects of Moringa oleifera extract on biochemical and histological parameters of sodium valproate induced lungs damage","authors":"Umar Faruk Magaji,&nbsp;Pınar Koroglu,&nbsp;Melis Coremen,&nbsp;Omur Karabulut Bulan,&nbsp;Ozlem Sacan,&nbsp;Refiye Yanardag","doi":"10.1007/s10735-024-10345-8","DOIUrl":"10.1007/s10735-024-10345-8","url":null,"abstract":"<div><p>Sodium valproate– a salt of valproic acid (VPA), is an anticonvulsant used in the treatment of epilepsy and a range of psychiatric conditions that include panic attacks, anxiety, post-traumatic stress, migraine and bipolar disorder etc. VPA can cause direct damage to many tissues due to accumulation of toxic metabolites. Nowadays, phytochemicals are amongst the best options for the treatment of diseases. <i>Moringa oleifera</i> is a popular plant in the tropics owing to its numerous pharmacological and phytochemical properties such as antiproliferative, hepatoprotective, anti-inflammatory, and cardioprotective effects. In the present study, the protective effects of Moringa ethanol extract on oxidative lung damage caused by VPA was assessed biochemically and histologically. Sprague Dawley female rats were divided into 4 groups: Control, Moringa extract (M), sodium valproate (V), and sodium valproate + Moringa extract (V + M). Doses of sodium valproate and Moringa extract (dissolved in physiological saline) were given at 500 mg/kg b.w. and 300 mg/kg b.w. for 15 days, respectively. The rats were sacrificed on the 16th day, lung tissues collected biochemical parameters (glutathione level, antioxidant enzyme activities, oxidative stress biomarker and inflammatory proteins) and histopathological findings obtained from the study indicated increased damage in lung tissue of the valproate administered group. The damage was prevented/decreased upon administration of Moringa to the valproate rats. The present findings revealed that Moringa extract had a protective and therapeutic effect against VPA induced lung damage. Moringa extract demonstrated an ameliorative effect on histopathological and biochemical parameters in valproate induced lung damage.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889581","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":"Silencing miR-126-5p protects trabecular meshwork cells against chronic oxidative injury by upregulating HSPB8 to activate PI3K/AKT pathway","authors":"Tianqi Jia,&nbsp;Yujia Guo,&nbsp;Xiaolong Zhao","doi":"10.1007/s10735-024-10337-8","DOIUrl":"10.1007/s10735-024-10337-8","url":null,"abstract":"<div><p>Chronic oxidative stress (COS) is related to the pathophysiology of the trabecular meshwork (TM) in glaucoma. MicroRNAs (miRNAs) have a key role in the oxidative stress-mediated glaucoma. This work investigated the function of miR-126-5p in human trabecular meshwork cells (TMCs) under chronic oxidative stress (COS). The miR-126-5p inhibitor was transfected into TMCs to assess the function of miR-126-5p. The targets of miR-126-5p were predicted by bioinformatic analysis. A luciferase assay was applied to test the relationship between miR-126-5p and its target. Cell proliferation was assessed using MTT. Flow cytometry and TUNEL were used for the assessment of apoptosis. We found that the miR-126-5p level was elevated in TMCs exposed to COS. MiR-126-5p inhibitor markedly promoted TMC proliferation and inhibited the increases in apoptosis and extracellular matrix (ECM) proteins induced by COS. Heat shock protein B8 (HSPB8) was identified to be targeted by miR-126-5p. MiR-126-5p inhibitor restored the expression level of HSPB8 in TMCs under COS. Additionally, miR-126-5p depletion activated PI3K/AKT signaling in TMCs by upregulating HSPB8. HSPB8 downregulation or LY294002 treatment prevented the effects mediated by miR-126-5p inhibition on apoptosis and ECM in COS-treated TMCs. Overall, silencing miR-126-5p protects TMCs against COS-induced injury by upregulating HSPB8 to activate PI3K/AKT signaling.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889583","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":"Signaling pathway regulators in preimplantation embryos","authors":"Narges Karami,&nbsp;Adeleh Taei,&nbsp;Poopak Eftekhari-Yazdi,&nbsp;Fatemeh Hassani","doi":"10.1007/s10735-024-10338-7","DOIUrl":"10.1007/s10735-024-10338-7","url":null,"abstract":"<div><p>Embryonic development during the preimplantation stages is highly sensitive and critically dependent on the reception of signaling cues. The precise coordination of diverse pathways and signaling factors is essential for successful embryonic progression. Even minor disruptions in these factors can result in physiological dysfunction, fetal malformations, or embryonic arrest. This issue is particularly evident in assisted reproductive technologies, such as in vitro fertilization, where embryonic arrest is frequently observed. A detailed understanding of these pathways enhances insight into the fundamental mechanisms underlying cellular processes and their contributions to embryonic development. The significance of elucidating signaling pathways and their regulatory factors in preimplantation development cannot be overstated. The application of this knowledge in laboratory settings has the potential to support strategies for modeling developmental stages and diseases, drug screening, therapeutic discovery, and reducing embryonic arrest. Furthermore, using various factors, small molecules, and pharmacological agents can enable the development or optimization of culture media for enhanced embryonic viability. While numerous pathways influence preimplantation development, this study examines several critical signaling pathways in this contex.</p><h3>Graphical abstract</h3>\u0000<div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889578","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":"Oxidative stress and its role in recurrent pregnancy loss: mechanisms and implications","authors":"Xiaoyu Zhang,&nbsp;Jiawei Gao,&nbsp;Liuxin Yang,&nbsp;Xiaoling Feng,&nbsp;Xingxing Yuan","doi":"10.1007/s10735-024-10332-z","DOIUrl":"10.1007/s10735-024-10332-z","url":null,"abstract":"<div><p>Recurrent pregnancy loss (RPL) is the occurrence of two or more consecutive miscarriages before 20 weeks of gestation. Recent research has increasingly focused on the role of oxidative stress in RPL, providing insights into its underlying mechanisms and potential therapeutic targets. Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, leading to cellular damage and inflammation. Oxidative stress has been implicated in disrupting placental blood flow, inducing apoptosis in fetal and placental cells, and exacerbating inflammatory responses, all of which can contribute to pregnancy loss. Elevated levels of ROS have been associated with compromised placental function, impaired fetal development, and increased risk of RPL. Additionally, oxidative stress can modulate maternal immune responses, potentially leading to immune-related pregnancy complications. This review synthesizes current evidence on the mechanisms by which oxidative stress contributes to RPL and highlights emerging research on potential interventions, including antioxidant therapies and lifestyle modifications. Understanding these mechanisms is crucial for developing effective preventive and therapeutic strategies to reduce the risk of RPL and improve pregnancy outcomes. Future research should focus on elucidating the specific pathways involved and exploring novel treatments aimed at mitigating oxidative damage during pregnancy.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889904","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":"USP37 promotes diffuse large B-cell lymphoma progression by deubiquitinating and stabilizing c-myc","authors":"Ying Li,&nbsp;Wei Wang,&nbsp;Lingjie Sun,&nbsp;Junxia Huang,&nbsp;Xiaolin Ma,&nbsp;Saisai Li,&nbsp;Xue Shi","doi":"10.1007/s10735-024-10323-0","DOIUrl":"10.1007/s10735-024-10323-0","url":null,"abstract":"<div><p>A poorer prognosis is thought to be associated with “double expressor lymphomas,” which are a subtype of diffuse large B cell lymphomas (DLBCL) that co-express MYC and BCL2. While the role of ubiquitin-specific peptidase 37 (USP37) in lung cancer, where it mediates the deubiquitination and stabilization of c-myc, has been well-documented, its involvement in DLBCL remains unexplored. The use of RT-PCR, immunohistochemistry, or WB test allowed for the detection of elevated USP37 in DLBCL tissues and cells. In order to understand the function of USP37 in DLBCL, keloid DLBCL cells were transfected with si-USP37 using Lipofectamine 3000. When tested on DLBCL cells, USP37 increased cell proliferation and inhibited cell cycle progression. USP37 controls the process of deubiquitination to stabilise c-myc proteins. The overexpression of c-Myc facilitated cell proliferation and prevented the cell cycle of DLBCL cells stimulated by si-USP37, which should be taken into consideration. Furthermore, USP37 depletion consistently hinders the development of tumour xenografts in mouse models. Overexpressing c-myc, however, may partially counteract this impact. The data show that USP37 may be a potential therapeutic target for DLBCL, and that it may enhance the course of the disease by deubiquitinating c-myc via direct interactions with c-myc.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889746","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":"Inhibitory effect of andrographolide on the expression of key regulatory genes in Staphylococcus epidermidis biofilm formation","authors":"Kangjian Zhang,&nbsp;Qing Li,&nbsp;Chengxia Gong,&nbsp;Huihui Mao,&nbsp;Daobin Han","doi":"10.1007/s10735-024-10295-1","DOIUrl":"10.1007/s10735-024-10295-1","url":null,"abstract":"<div><p>The purpose of this study was to explore the inhibitory effect of andrographolide on the expression of key regulatory genes involved in the biofilm formation of <i>Staphylococcus epidermidis</i> (SE). Taking the film-producing strain <i>Staphylococcus epidermidis</i> SE1457 as the research object, the effect of andrographolide on the formation of <i>Staphylococcus epidermidis</i> biofilms was analyzed via crystal violet staining, and biofilm models of SE adhesion, aggregation and maturity were established in vitro. RT‒PCR was used to detect the effects of the expression of icaA-, atlE-, aap- and luxS-related genes of andrographolide on biofilm formation in SE. Congo red qualitative test to evaluate the ability of andrographolide to inhibit biofilm formation of <i>Staphylococcus epidermidis</i>. Compared with that of the control group, the light absorption value of the low- and high-concentration andrographolide groups was significantly lower, and the light absorption value of the high-concentration andrographolide group was significantly lower than that of the low-concentration andrographolide group. The levels of key genes involved in the adhesion, aggregation and maturation of icaA, atlE, aap and luxS in group C were greater than those in group B. The biofilm-forming ability of SE in group A was strong, and the colonies were obviously black. The colony in the direction of the arrow in group B was red, and the SE biofilm was inhibited. Most of the colonies in group C were red. SE biofilms were significantly inhibited. Andrographolide inhibits SE biofilm formation, and its mechanism may involve inhibition of the expression of the related genes icaA, atlE, aap and luxS.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875197","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":"Exploration of plasma tryptophan levels along with Ki-67 expression binomial investigation for forecasting tumor aggressiveness within invasive ductal breast cancer","authors":"Takwa Salmi,&nbsp;Djilali Ameur,&nbsp;Majda Dali-Sahi,&nbsp;Joanna Dib,&nbsp;Nawel Amraoui,&nbsp;Youssouf Kachekouche,&nbsp;Nouria Dennouni-Medjati","doi":"10.1007/s10735-024-10333-y","DOIUrl":"10.1007/s10735-024-10333-y","url":null,"abstract":"<div><p>Ki-67 is a histological marker indicating cancer aggressiveness, while tryptophan (TRP) depletion modulates immune responses, including tumor aggressiveness. The study evaluates Ki-67's predictive value in relation to plasma TRP levels in invasive ductal carcinoma of breast cancer, aiming to improve understanding of tumor characteristics and clinical behavior. A study involving 165 women, measured plasma TRP levels and Ki-67 and analyzed their relationship with tumor aggressiveness markers using statistical analyses and predictive models. Our study highlighted a significant correlation between decreased plasma levels of TRP and a high mitotic index, measured by the Ki-67 marker (Pearson correlation coefficient r = − 0.402; p = 0.011). Tryptophan levels below 40 µmol/L were associated with a Ki-67 level above 15%, suggesting more active tumor growth in patients. Additionally, several risk factors for BC were identified within the studied population. The demographic and clinical characteristics of the participants include an average age of 63 years, plasma glucose levels above 1.2 g/L, and plasma TRP levels below 40 µmol/L, which are associated with an increased risk of BC. Furthermore, various polynomial logistic regression models indicate that TRP levels may be predicted based on Ki-67 expression, providing a promising approach to refine prognostic assessments. The study showed a correlation between low levels of tryptophan (TRP) and a high Ki-67 mitotic index in breast cancer patients, particularly in invasive ductal carcinoma, which is strongly linked to the aggressiveness of the disease. The integration of these markers into routine practice remains a technical and economic challenge.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142870412","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}