Analytical Cellular Pathology最新文献

{"title":"Diagnostic Accuracy of Serum P16ink4A and FOX-P3 Concentrations for Detection of Cervical Lesions Among Women Attending a Cervical Cancer Clinic in Western Uganda: A Case-Control Study.","authors":"Frank Ssedyabane, Nixon Niyonzima, Joseph Ngonzi, Josephine Nambi Najjuma, Alexcer Namuli, Christopher Okeny, Doreen Nuwashaba, Abraham Birungi, Rogers Kajabwangu, Thomas C Randall, Cesar M Castro, Hakho Lee, Deusdedit Tusubira","doi":"10.1155/ancp/1931921","DOIUrl":"10.1155/ancp/1931921","url":null,"abstract":"<p><p><b>Introduction:</b> Expression of P16ink4A and FOXP3 is correlated with the grades of cervical lesions. In this study, we determined the diagnostic accuracy of serum P16ink4A and FOXP3 concentrations for detection of cervical intraepithelial neoplasia (CIN) and cervical cancer (CC) in a rural setting in Southwestern Uganda. <b>Material and Methods:</b> CIN and CC cases (93 each before treatment), and 93 controls were identified. Clinical and demographic data were documented before quantifying serum P16ink4A and FOXP3 concentrations using quantitative ELISA kits. Cases were confirmed by cytology and/or histology. We employed descriptive statistics, cross-tabulation, and receiver operating curves (ROC) using statistical software for data science (STATA) 17. <i>p</i>-values <0.05 were considered statistically significant. <b>Results:</b> Serum FOXP3 concentration of 0.0545 ng/mL < showed moderate sensitivity (32.22% and 57.78%) for detection of CIN and CC from healthy controls, respectively. It also showed a moderately high specificity of 68.89% for detection of both CIN and CC from healthy controls (AUC-0.6014 and 0.7679, respectively). Serum P16ink4A concentration of 0.946 ng/mL < showed moderate sensitivities (50.00% and 60.00%) and specificities (56.67% and 55.56%) for the detection of CIN and CC from healthy controls, respectively (AUC-0.6085 and 0.7592, respectively). A combination of elevated serum FOXP3 and P16ink4A showed very low sensitivities of 18.89% in detecting CIN from healthy controls and 33.33% for detecting CC from healthy controls. This combination showed high specificity of 83.33% in detecting both CIN and CC from healthy controls (AUC-0.5992 and 0.7642, respectively). <b>Conclusion:</b> Although serum P16ink4A and FOXP3 concentrations showed moderate accuracy, their combination was more specific than sensitive. This combination has a high potential to be applied for diagnosis rather than screening for cervical lesions, at least in the Ugandan population. Combinations of P16ink4A and FOXP3 with other biomarkers could improve diagnostic accuracies. Additionally, studies could be conducted to assess the performance of these biomarkers in the detection of cervical lesions in specific populations, say Human Immunodeficiency Virus (HIV)-positive and HIV-negative populations.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"1931921"},"PeriodicalIF":2.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P-Selectin, Vascular Endothelial Cadherin, and Vascular Cell Adhesion Molecule-1 as Novel Biomarkers for ABO Hemolytic Disease of the Fetus and Newborn.","authors":"Weichun Tang, Linlin Zhu, Liwei Shi, Biao Gu","doi":"10.1155/ancp/9411137","DOIUrl":"https://doi.org/10.1155/ancp/9411137","url":null,"abstract":"<p><p><b>Objective:</b> This study aims to assess the potential of vascular endothelial injury markers, namely, P-selectin (PS), vascular endothelial cadherin (VE-Cad), and vascular cell adhesion molecule-1 (VCAM-1), as diagnostic and prognostic biomarkers for ABO hemolytic disease of the fetus and newborn (HDFN). <b>Methods:</b> A total of 218 pregnant women with ABO blood group incompatibility were recruited from the Third People's Hospital of Bengbu Affiliated to Bengbu Medical University. The serum levels of PS, VCAM-1, and VE-Cad were measured, and the participants were followed up until postpartum. The women were divided into an HDFN group and a control group based on the occurrence of ABO-HDFN. The correlations between the three vascular endothelial injury markers, pregnant anti-A/B antibody titers, and the occurrence and severity of HDFN were analyzed. <b>Results:</b> Compared to the control group, the levels of PS, VCAM-1, and VE-Cad were significantly elevated in the HDFN group. Additionally, these markers increased with higher IgG anti-A/B titers. For diagnosing HDFN, the area under the curve (AUC) for PS, VCAM-1, and VE-Cad were 0.826, 0.765, and 0.799, respectively. Moreover, the combined AUC of the three markers with IgG anti-A/B titers was 0.9. The levels of the three biomarkers were significantly negatively correlated with neonatal hemoglobin (Hb) and significantly positively correlated with reticulocyte percentage (Ret%), indirect bilirubin (IBIL), and lactate dehydrogenase (LDH). Univariate logistic regression indicated that increased levels of PS, VCAM-1, and VE-Cad were associated with a higher probability of ABO-HDFN. Multivariate logistic regression revealed that PS is an independent positive factor for HDFN. <b>Conclusion:</b> PS, VCAM-1, and VE-Cad provide experimental evidence for prenatal screening, diagnosis, early prevention and treatment of ABO-HDFN.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"9411137"},"PeriodicalIF":2.6,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gallic Acid Inhibits the Proliferation and Migration of Ovarian Cancer Cells via Inhibition of the PI3K-AKT Pathway and Promoting M1-Like Macrophage Polarization.","authors":"Ran Meng, Zhengmao Zhang","doi":"10.1155/ancp/3880719","DOIUrl":"https://doi.org/10.1155/ancp/3880719","url":null,"abstract":"<p><p>Ovarian cancer is one of the leading malignant women tumors that causes higher mortality, and immunotherapy has shown high potential in the treatment of advanced ovarian cancer patients by activating and mobilizing the human immune system, which can improve patient prognosis and survival. Natural compounds are a big resource for screening and finding effective lead compounds to treat diseases. Gallic acid (GA) is a natural organic acid with broad-spectrum antibacterial, antiviral, and antitumor effects. In the current study, we aim to explore the effect of GA on ovarian cancer and its underlying mechanisms. The CCK-8 assay was employed to study its anti-proliferation effect and wound healing, and transwell assay was utilized to test the GA effect on cell migration and invasion. The xenograft tumor model was used to evaluate the GA anticancer effect in vivo. The results demonstrated that GA significantly suppresses the proliferation of ovarian cancer cells both in vitro and in vivo, reduces their migration and invasion capability, and enhances macrophage cytotoxicity in the murine ID8 xenograft tumor microenvironment (TME). The mechanism study demonstrated that its anticancer effect and enhancing immunity is stem from inhibiting the PI3k-AKT pathway. In conclusion, GA plays an anticancer effect via blockage of the PI3K-AKT pathway.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"3880719"},"PeriodicalIF":2.6,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12017941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin Enhances the Chemosensitivity of Gastric Cancer to Cisplatin by Downregulating Nrf2 Level.","authors":"Guihua Duan, Min Qi, Linting Xun, Ying An, Zan Zuo, Yusi Luo, Zhengji Song","doi":"10.1155/ancp/5714423","DOIUrl":"https://doi.org/10.1155/ancp/5714423","url":null,"abstract":"<p><p>Cisplatin-based chemotherapy resistance is a common issue for cancer clinical efficacy. Metformin is being studied for its possible anticancer effect. The present study aimed to investigate whether metformin affects the chemosensitivity of gastric cancer to cisplatin and reveal the molecular mechanism. In this study, the effects of combination therapy with metformin and cisplatin on cell viability, cell apoptosis, malondialdehyde, superoxide dismutase, reactive oxygen species level, glucose uptake, lactate production, protein level, and xenograft tumor formation were analyzed in gastric cancer cells. Immunohistochemical staining was performed to detect Ki67 expression in matched tumor samples. The results showed that NCI-N87 and SNU-16 cells were most resistant and sensitive to cisplatin, respectively. Metformin treatment increased the cisplatin sensitivity of gastric cancer by inhibiting cell viability and metabolic reprogramming and promoting cell apoptosis and oxidative stress. Furthermore, overexpression of nuclear factor erythroid 2-related factor 2 (Nrf2) reversed the effects of metformin in the cisplatin sensitivity of gastric cancer by inhibiting cell viability and metabolic reprogramming and promoting cell apoptosis and oxidative stress. Metformin activated p53 and AMPK pathways in cisplatin-induced NCI-N87 cells, which were reversed by upregulating Nrf2. BAY-3827 (AMPK inhibitor) or p-nitro-Pifithrin-α (p53 inhibitor) treatments also reversed the effects of metformin increased the cisplatin sensitivity of gastric cancer by inhibiting cell viability and metabolic reprogramming and promoting cell apoptosis and oxidative stress. These results suggest that metformin significantly increases chemosensitivity of gastric cancer to cisplatin by inhibiting Nrf2 expression and metabolic reprogramming and activating oxidative stress and the pathway of p53 and AMPK.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"5714423"},"PeriodicalIF":2.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12014253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Omp34-Mediated <i>Acinetobacter baumannii</i> Invasion of Human Cervical Carcinoma Epithelial, HeLa Cells, and the Influence of Anti-Omp34 Antibodies.","authors":"Seyedeh Faezeh Hosseini, Mohammadreza Jalali Nadoushan, Zahra Fekrirad, Iraj Rasooli","doi":"10.1155/ancp/1931119","DOIUrl":"https://doi.org/10.1155/ancp/1931119","url":null,"abstract":"<p><p><i>Acinetobacter baumannii</i> is known for its ability to invade and persist within eukaryotic cells, impacting infection outcomes and disease progression. This study investigates the role of Omp34, a key outer membrane protein (Omp), in <i>A. baumannii</i> interaction with epithelial cells and the protective effects of anti-Omp34 antibodies (Abs). Omp34 is a key regulator of <i>A. baumannii</i> epithelial cell invasion, influencing bacterial adherence, internalization, and intracellular proliferation. The presence of anti-Omp34 Abs mitigates <i>A. baumannii</i>-induced cellular damage and enhances bacterial clearance. The process involved the expression and purification of Omp34, which in turn induced Abs in BALB/c mice against Omp34. The acute toxicity of Omp34 was studied through a histological analysis conducted on six distinct organs in mice. HeLa cells were infected by <i>A. baumannii</i> ATCC 19606 and a clinical strain. Various aspects of <i>A. baumannii</i> behavior with HeLa cells, including HeLa cell viability, adherence, serum resistance, cell internalization, and intracellular proliferation with and without anti-Omp34 sera. Cytoskeleton inhibitors were used to study the potential roles played in the process of <i>A. baumannii</i> invasion by microfilaments and microtubules. Omp34 effectively triggered Ab production in mice without resulting in any toxicity. The assay for serum resistance revealed potent bactericidal and antibiofilm effects on both <i>A. baumannii</i> strains. Bacterial internalization was constrained when actin polymerization was inhibited. Examination under the microscope revealed instances of adherence, alterations in the cell membrane, apoptosis, vacuolization, and cell damage. HeLa cells exposed to anti-Omp34 serum showed decreased cell damage. The results provide substantial evidence of the adherence capacity of <i>A. baumannii</i> to proliferate in the epithelial cells. In conclusion, Omp34 plays a substantial role in regulating interactions between epithelial cells and <i>A. baumannii</i>, the multifaceted nature of which intricately modifies the trajectory of infection within host cells by <i>A. baumannii</i>.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"1931119"},"PeriodicalIF":2.6,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12006715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Interplay Between Pericytes, Mesenchymal Stem Cells, and Immune Cells in the Process of Tissue Regeneration.","authors":"Vladislav Volarevic, Carl Randall Harrell, Aleksandar Arsenijevic, Valentin Djonov","doi":"10.1155/ancp/4845416","DOIUrl":"https://doi.org/10.1155/ancp/4845416","url":null,"abstract":"<p><p>Immediately after injury, damaged cells elicit tissue regeneration, a healing process that enables optimal renewal and regrowth of injured tissues. Results obtained in a large number of experimental studies suggested that the cross talk between pericytes, mesenchymal stem cells (MSC), tissue-resident stem cells, and immune cells has a crucially important role in the regeneration of injured tissues. Pericytes, MSCs, and immune cells secrete bioactive factors that influence each other's behavior and function. Immune cells produce inflammatory cytokines and chemokines that influence pericytes' migration, proliferation, and transition to MSC. MSC releases immunoregulatory factors that induce the generation of immunosuppressive phenotype in inflammatory immune cells, alleviating detrimental immune responses in injured tissues. MSC also produces various growth factors that influence the differentiation of tissue-resident stem cells into specific cell lineages, enabling the successful regeneration of injured tissues. A better understanding of molecular mechanisms that regulate crosstalk between pericytes, MSC, and immune cells in injured tissues would enable the design of new therapeutic approaches in regenerative medicine. Accordingly, in this review paper, we summarized current knowledge related to the signaling pathways that are involved in the pericytes' activation, pericytes-to-MSC transition, differentiation of tissue-resident stem cells, and MSC-dependent modulation of immune cell-driven inflammation, which are crucially responsible for regeneration of injured tissues.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"4845416"},"PeriodicalIF":2.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12003036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peroxiredoxin 1 Promotes Proinflammatory Cytokine Secretion in Human Dysplastic Oral Keratinocytes and Mouse Tongue Precancerous Tissues.","authors":"Min Zhang, Wenjing Li, Jing Li, Wenchao Wang, Lingyu Li, Yunping Lu, Min Wang, Xiaofei Tang","doi":"10.1155/ancp/6577043","DOIUrl":"10.1155/ancp/6577043","url":null,"abstract":"<p><p>Oxidative stress, a widespread phenomenon involved in many pathological conditions, may be closely related with the progression of oral leukoplakia (OLK). Under chronic inflammation, oxidative stress could stimulate the local formation of a tumor-specific microenvironment in some types of cancer, though not well defined in oral cancer even in OLK. Peroxiredoxin 1 (Prx1), a widely expressed sulfhydryl antioxidant protein, is overexpressed in various tumors and affects tumorigenesis, cell proliferation, apoptosis, invasion, and metastasis. Prx1 also acts as a potent proinflammatory factor. Nuclear factor (NF)-κB is a member of the core dimeric transcription factor family that coordinates the inflammatory response. To investigate the role of Prx1 in oxidative stress-related inflammation in OLK, a coculture model of human dysplastic oral keratinocyte (DOK) and human epidermal fibroblast (HFF) was established and stimulated with H₂O₂. Cellular reactive oxygen species (ROS) and Prx1 levels in DOK were determined via flow cytometry and western blotting, respectively. Additionally, the levels of the inflammatory factors, interleukin (IL)-6, IL-8, IL-10, and interferon (IFN)-γ, in the conditioned medium were determined via enzyme-linked immunosorbent assay (ELISA). DOK nuclear expression of NF-κB was detected via immunofluorescence assay and western blotting. Moreover, the expression levels of inflammatory factors and the nuclear expression of NF-κB were examined in 4-nitroquinoline-1-oxide (4NQO)-induced tongue precancerous tissues of mice. H₂O₂ increased Prx1 levels and nuclear expression levels of NF-κB in DOKs and mouse tongue precancerous tissues and elevated the levels of IL-6, IL-8, IL-10, and IFN-γ secreted in the culture supernatants and mouse tongue tissues. However, <i>Prx1</i> knockdown in DOK and mouse tongue tissues attenuated the upregulation of inflammatory factor and nuclear NF-κB expression levels. Overall, our results suggest that oxidative stress increases Prx1 expression, which promotes inflammatory factor expression by activating NF-κB in human DOK and mouse tongue precancerous tissues.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"6577043"},"PeriodicalIF":2.6,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recombinant Human Endostatin Suppressed the Biological Behavior of Human Umbilical Vein Endothelial Cells Under Hypoxic and Hypoxic/Starvation Conditions In Vitro.","authors":"Yongsheng Jia, Cuicui Zhang, Jimin Zhao, Chuanxiang Hu, Xiaoyong Yang, Yan Zhang","doi":"10.1155/ancp/3475731","DOIUrl":"10.1155/ancp/3475731","url":null,"abstract":"<p><p>Recombinant human endostatin (rh-endostatin) has been shown to act as an inhibitor of angiogenesis. Previous studies have indicated that rh-endostatin combined with chemotherapy can improve the objective response rate (ORR), time to progression (TTP), and clinical benefit rate (CBR) without increasing toxicity. However, this function has seldom been reported in normal cells. The aim of our study was to explore the effect of rh-endostatin on the biological behavior of human umbilical vein endothelial cells (HUVECs) under different conditions in vitro. Confluent HUVECs were cultured under normoxic, hypoxic, or hypoxic/starvation (H/S) conditions and then treated with rh-endostatin. An MTT assay was used to assess cell proliferation, and HUVEC tube formation and migration were assessed via a cell tubule formation assay and a migration assay. The expression of endoglin (CD105) was assessed by flow cytometry (FCM). Rh-endostatin inhibited the proliferation, migration, and tube formation of HUVECs under normoxic, hypoxic, and H/S conditions. Compared with that in the normoxia group, the expression of CD105 was not different in the hypoxia 24 h group, but in the starvation and hypoxia/starvation groups, the expression of CD105 was upregulated. Rh-endostatin downregulated the expression of CD105 under all the study conditions. Here we found rh-endostatin suppressed the biological behavior of HUVECs under hypoxic and H/S conditions. As the concentration increased, the effect of rh-endostatin on the biological behavior of HUVECs was not greatly enhanced. Rh-endostatin did not promote malignant biological behavior or CD105 expression. Since CD105 may induce endothelial-to-mesenchymal transition in HUVECs, we hypothesized that rh-endostatin may inhibit the malignant biological behavior of HUVECs under hypoxic conditions in vitro.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"3475731"},"PeriodicalIF":2.6,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemopreventive Potential of Paddy Waste: A Promising Approach Against Benign Prostate Hyperplasia in Spontaneously Hypertensive Rats.","authors":"Azman Seeni, Atif Amin Baig, Mogana Das Murtey","doi":"10.1155/ancp/4029625","DOIUrl":"10.1155/ancp/4029625","url":null,"abstract":"<p><p><b>Background:</b> Benign prostate hyperplasia (BPH) is common in elderly men. Previously, paddy waste (both husk and straw) reportedly had chemopreventive potential. The main aim of this study was to explore the chemopreventive properties of paddy waste against prostate disease. This study determines the antiproliferative activity of the paddy waste product in spontaneously hypertensive rats (SHRs). <b>Methods:</b> Aqueous methanol extracts of paddy husk and straw were administered to SHRs for 17 weeks via drinking water, with no observed toxicity on dietary intake, body weight, liver, or kidney. The study used 18 male SHRs to model primary hypertension and 6 male Wistar Kyoto (WKY) rats as normotensive controls. The SHRs were divided into three groups: control (<i>n</i> = 6), paddy husk treated (<i>n</i> = 6, 15 mg/kg), and paddy straw treated (<i>n</i> = 6, 15 mg/kg), with treatment delivered in drinking water. <b>Results:</b> It managed to reduce blood pressure (72.0 mmHg; <i>p</i>  < 0.01) and the size of the ventral prostate to around 0.05% (<i>p</i>  < 0.01). Histological analysis revealed antiproliferative signs such as a reduction in the number of acini (7.50; <i>p</i>  < 0.01), epithelial height (10.55 µm; <i>p</i>  < 0.01), and epithelial acinar area (18.17%; <i>p</i>  < 0.01). Aqueous methanol extracts have arrested the cell cycle by downregulating (<i>p</i>  < 0.01) proliferative marker, Ki-67, and proliferating cell nuclear antigen (PCNA). Prostate cell growth is arrested by downregulation of androgen receptor (AR) which inhibited AR mRNA transcription (RTPCR analysis) and induced cell cycle arrest at the S phase through p27 and cyclin E2 (western blot analysis). <b>Conclusion:</b> In conclusion, paddy waste product especially husk is a better chemopreventive agent against prostate disease.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"4029625"},"PeriodicalIF":2.6,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Analysis of Potential Common Pathogenic Mechanisms for COVID-19 Infection and Gastric Cancer.","authors":"Guiqian Zhang, Ning Wang, Shixun Ma, Yan Zhang, Pengxian Tao, Hui Cai","doi":"10.1155/ancp/5106674","DOIUrl":"https://doi.org/10.1155/ancp/5106674","url":null,"abstract":"<p><p>A growing body of data suggests that the prevalence of COVID-19 pneumonia in patients with stomach cancer is much higher than in the general population. However, these mechanisms are still not fully understood. After a thorough examination of shared differentially expressed genes (DEGs) for gastric cancer (GC) and COVID-19 pneumonia, we performed functional annotation, protein-protein interaction (PPI) networks, module design, and pivot gene identification. qPCR was used to verify the expression of hub genes in GC. Finally, a pivotal gene transcription factor-gene regulatory network was created and validated. According to functional enrichment analysis, common genes are mainly enriched in biological processes such as extracellular matrix tissue and extracellular structural tissue. Finally, five genes were found to be pivotal genes in the pathogenesis of GC and COVID-19 pneumonia: BGN (biglycan), UBE2C (ubiquitin-conjugating enzymes 2C), SPP1 (secreted phosphoprotein 1), THBS2 (thrombospondin 2), and COL1A1 (type I collagen alpha 1). These shared pathways and pivotal genes could provide new insights for more mechanistic studies.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"5106674"},"PeriodicalIF":2.6,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}