Computed tomography (CT) is essential for radiotherapy simulation and dose calculation, which rely on the relationship between CT number and relative electron density (RED). Tube voltage (kVp) and current (mAs) affect CT numbers and may impact Monitor Unit (MU) accuracy if calibration curves do not match scan parameters.
Purpose
To evaluate the effects of varying kVp and mAs on the CT number–RED relationship, image quality, and MU calculation accuracy, and to establish kVp-specific calibration curves for clinical use.
Methods
A 64-slice CT simulator scanned an electron density phantom at kVp of 80, 100, 120, and 140 kVp with fixed 100 mAs. The phantom was then rescanned at each kVp setting with mAs values of 100, 200, 300, and 400. CT numbers from 13 inserts (RED range: 0.20–6.92) were averaged over three repeated scans to generate CT number–RED calibration curves, which were imported into the treatment planning system (TPS). MU deviations under matched and mismatched calibration conditions were evaluated using thorax phantom scans and 3D conformal radiotherapy (3D-CRT) plans. Image quality was assessed using the Catphan 604 phantom according to AAPM TG-66 guidelines.
Results
Varying kVp caused noticeable CT number changes, especially in high-density materials (up to ±806 HU). In contrast, mAs had smaller effects (≤60 HU at 80 kVp; <30 HU at ≥100 kVp). MU deviations from mismatched curves stayed within 0.72 %, below the ±2 % tolerance from IAEA TECDOC 1583. Image quality assessment showed consistent uniformity (±4 HU), noise (3.78–4.62 HU), spatial resolution of 6 lp/cm, and CNR >1.2 across all kVp settings, aligning with AAPM TG-66 criteria.
Conclusions
kVp-specific calibration curves improve MU calculation accuracy. Adjusting kVp based on patient size helps optimize image quality and calibration stability. Both 100 and 140 kVp are viable alternatives to 120 kVp for CT simulation.
{"title":"Effect of tube voltage and current on CT number–relative electron density calibration and radiotherapy dose calculation accuracy","authors":"Kamonrat Sueangamiam , Kritsada Prasomsap , Sarinya Yenprasert , Adjima Titalakkana , Nattakarn Kittiva","doi":"10.1016/j.jrras.2025.102151","DOIUrl":"10.1016/j.jrras.2025.102151","url":null,"abstract":"<div><h3>Background</h3><div>Computed tomography (CT) is essential for radiotherapy simulation and dose calculation, which rely on the relationship between CT number and relative electron density (RED). Tube voltage (kVp) and current (mAs) affect CT numbers and may impact Monitor Unit (MU) accuracy if calibration curves do not match scan parameters.</div></div><div><h3>Purpose</h3><div>To evaluate the effects of varying kVp and mAs on the CT number–RED relationship, image quality, and MU calculation accuracy, and to establish kVp-specific calibration curves for clinical use.</div></div><div><h3>Methods</h3><div>A 64-slice CT simulator scanned an electron density phantom at kVp of 80, 100, 120, and 140 kVp with fixed 100 mAs. The phantom was then rescanned at each kVp setting with mAs values of 100, 200, 300, and 400. CT numbers from 13 inserts (RED range: 0.20–6.92) were averaged over three repeated scans to generate CT number–RED calibration curves, which were imported into the treatment planning system (TPS). MU deviations under matched and mismatched calibration conditions were evaluated using thorax phantom scans and 3D conformal radiotherapy (3D-CRT) plans. Image quality was assessed using the Catphan 604 phantom according to AAPM TG-66 guidelines.</div></div><div><h3>Results</h3><div>Varying kVp caused noticeable CT number changes, especially in high-density materials (up to ±806 HU). In contrast, mAs had smaller effects (≤60 HU at 80 kVp; <30 HU at ≥100 kVp). MU deviations from mismatched curves stayed within 0.72 %, below the ±2 % tolerance from IAEA TECDOC 1583. Image quality assessment showed consistent uniformity (±4 HU), noise (3.78–4.62 HU), spatial resolution of 6 lp/cm, and CNR >1.2 across all kVp settings, aligning with AAPM TG-66 criteria.</div></div><div><h3>Conclusions</h3><div>kVp-specific calibration curves improve MU calculation accuracy. Adjusting kVp based on patient size helps optimize image quality and calibration stability. Both 100 and 140 kVp are viable alternatives to 120 kVp for CT simulation.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102151"},"PeriodicalIF":2.5,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1016/j.jrras.2025.102154
Yingjia Mao , Hao Yu , Rong Yu , Hongmei Niu , Xin Deng , Qing Qi , Xiang Li , Fuqian Zhao , Daofu Shen , Lei Wang
Background
The lack of early diagnostic markers often leads to the late diagnosis of lung cancer. Although LRG1 was identified in the serum of metastatic patients, its functional role and diagnostic potential remain largely unexplored. We hypothesize that LRG1 promotes lung cancer progression via immune modulation and enhances metastatic potential.
Methods
We analyzed the relationship between LRG1 expression and survival outcomes using TCGA data. Immune cell relevance was assessed using the TIMER and TISCH databases. The functional effects of LRG1 on lung cancer cell proliferation and migration were investigated using CCK-8, EdU, scratch assays, and Western blot. Peripheral serum was collected from healthy controls (n = 15), non-metastatic groups (n = 13), and metastatic groups (n = 56). Serum LRG1 levels were detected by ELISA, and its diagnostic value was evaluated using ROC curve analysis.
Results
High LRG1 expression is associated with poor prognosis and is linked to macrophage and neutrophil infiltration. In vitro functional studies have shown that LRG1 promotes lung cancer cell proliferation and migration. Furthermore, serum LRG1 levels are significantly elevated in patients with metastatic lung cancer, and LRG1 demonstrates high diagnostic accuracy across all disease stages. In metastatic patients, LRG1 showed promising potential for early detection in LUAD patients (AUC = 0.74) and LUSC patients (AUC = 0.69), showing high levels in LUAD patients (AUC = 0.75) and LUSC patients (AUC = 0.73).
Conclusion
Our study has revealed the potential of LRG1 as a novel biomarker for early diagnosis and recurrence monitoring of lung cancer. It has diagnostic value in early-stage disease and prognostic value in late-stage disease. However, further investigation into its mechanistic role is warranted.
{"title":"LRG1 protein is a novel prognostic indicator for patients with non-small cell lung cancer","authors":"Yingjia Mao , Hao Yu , Rong Yu , Hongmei Niu , Xin Deng , Qing Qi , Xiang Li , Fuqian Zhao , Daofu Shen , Lei Wang","doi":"10.1016/j.jrras.2025.102154","DOIUrl":"10.1016/j.jrras.2025.102154","url":null,"abstract":"<div><h3>Background</h3><div>The lack of early diagnostic markers often leads to the late diagnosis of lung cancer. Although LRG1 was identified in the serum of metastatic patients, its functional role and diagnostic potential remain largely unexplored. We hypothesize that LRG1 promotes lung cancer progression via immune modulation and enhances metastatic potential.</div></div><div><h3>Methods</h3><div>We analyzed the relationship between LRG1 expression and survival outcomes using TCGA data. Immune cell relevance was assessed using the TIMER and TISCH databases. The functional effects of LRG1 on lung cancer cell proliferation and migration were investigated using CCK-8, EdU, scratch assays, and Western blot. Peripheral serum was collected from healthy controls (n = 15), non-metastatic groups (n = 13), and metastatic groups (n = 56). Serum LRG1 levels were detected by ELISA, and its diagnostic value was evaluated using ROC curve analysis.</div></div><div><h3>Results</h3><div>High LRG1 expression is associated with poor prognosis and is linked to macrophage and neutrophil infiltration. In vitro functional studies have shown that LRG1 promotes lung cancer cell proliferation and migration. Furthermore, serum LRG1 levels are significantly elevated in patients with metastatic lung cancer, and LRG1 demonstrates high diagnostic accuracy across all disease stages. In metastatic patients, LRG1 showed promising potential for early detection in LUAD patients (AUC = 0.74) and LUSC patients (AUC = 0.69), showing high levels in LUAD patients (AUC = 0.75) and LUSC patients (AUC = 0.73).</div></div><div><h3>Conclusion</h3><div>Our study has revealed the potential of LRG1 as a novel biomarker for early diagnosis and recurrence monitoring of lung cancer. It has diagnostic value in early-stage disease and prognostic value in late-stage disease. However, further investigation into its mechanistic role is warranted.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102154"},"PeriodicalIF":2.5,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1016/j.jrras.2025.102153
Yanhao Li , Wei Qu , Zhijun Zhu
Background
Hepatic carcinosarcoma (HCS) is an exceptionally rare (<0.1 % of primary liver malignancies) but highly aggressive tumor with a dismal prognosis. The clinical manifestations of HCS are similar to those of hepatocellular carcinoma (HCC), and the current diagnosis relies on surgical pathological results.
Case summary
We report a case of HCS, a poorly differentiated hepatocellular carcinoma (HCC) mixed with osteosarcoma components in a 53-year-old male patient. The patient had a giant (approximately 20 cm) cystic-solid mass in the right hepatic lobe, which was evident on ultrasonography and CT scans. A puncture biopsy of the lesion suggested hepatocellular carcinoma. He received liver transplantation (LT) after 1 session of hepatic artery embolization with doxorubicin-loaded beads (DEB-TACE). Postoperative pathology and immunohistochemistry of the mass, which was surgically removed, suggested primary hepatic carcinosarcoma containing poorly differentiated HCC and osteosarcoma components. Hepatic osteosarcoma reoccurred 14 days after LT, resulting in significant compression and narrowing of the hepatic segment of the inferior vena cava. Unfortunately, the patient died of multiple organ failure caused by tumor reoccurence 24 days after transplantation.
Conclusion
This case suggests that a diagnosis of HCS, even when meeting standard oncological criteria, should warrant extreme caution and potentially contraindicate liver transplantation due to the high risk of immediate, lethal recurrence. For localized disease, radical surgical resection combined with adjuvant therapy might be considered, though the optimal treatment strategy remains undefined.
{"title":"Poorly differentiated hepatic carcinosarcoma with osteosarcoma components rapidly relapsed after liver Transplantation:A case report and literature review","authors":"Yanhao Li , Wei Qu , Zhijun Zhu","doi":"10.1016/j.jrras.2025.102153","DOIUrl":"10.1016/j.jrras.2025.102153","url":null,"abstract":"<div><h3>Background</h3><div>Hepatic carcinosarcoma (HCS) is an exceptionally rare (<0.1 % of primary liver malignancies) but highly aggressive tumor with a dismal prognosis. The clinical manifestations of HCS are similar to those of hepatocellular carcinoma (HCC), and the current diagnosis relies on surgical pathological results.</div></div><div><h3>Case summary</h3><div>We report a case of HCS, a poorly differentiated hepatocellular carcinoma (HCC) mixed with osteosarcoma components in a 53-year-old male patient. The patient had a giant (approximately 20 cm) cystic-solid mass in the right hepatic lobe, which was evident on ultrasonography and CT scans. A puncture biopsy of the lesion suggested hepatocellular carcinoma. He received liver transplantation (LT) after 1 session of hepatic artery embolization with doxorubicin-loaded beads (DEB-TACE). Postoperative pathology and immunohistochemistry of the mass, which was surgically removed, suggested primary hepatic carcinosarcoma containing poorly differentiated HCC and osteosarcoma components. Hepatic osteosarcoma reoccurred 14 days after LT, resulting in significant compression and narrowing of the hepatic segment of the inferior vena cava. Unfortunately, the patient died of multiple organ failure caused by tumor reoccurence 24 days after transplantation.</div></div><div><h3>Conclusion</h3><div>This case suggests that a diagnosis of HCS, even when meeting standard oncological criteria, should warrant extreme caution and potentially contraindicate liver transplantation due to the high risk of immediate, lethal recurrence. For localized disease, radical surgical resection combined with adjuvant therapy might be considered, though the optimal treatment strategy remains undefined.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102153"},"PeriodicalIF":2.5,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-27DOI: 10.1016/j.jrras.2025.102137
Shihua Zhang , Kejin Li , Yan Chen , Yusong Liu , Lin Wang , Limao Xu
Purpose
This study aimed to elucidate the molecular mechanism by which simvastatin promotes ferroptosis in colorectal cancer cells, focusing on its targeting of HMGCR, suggesting that simvastatin-induced ferroptosis is associated with mevalonate pathway suppression.
Methods
Cell proliferation was evaluated after exposure to various concentrations of simvastatin. The expression of GPX4 and HMGCR was quantified using RT-qPCR and western blotting following treatment with simvastatin alone or combined with the ferroptosis inhibitor ferrostatin-1 (Fer-1). Apoptosis was analyzed by flow cytometry. In addition, intracellular reactive oxygen species (ROS), malondialdehyde (MDA), and ferrous iron (Fe2+) levels were determined to assess metabolic alterations induced by simvastatin.
Results
Treatment with 20 μM simvastatin for 72 h significantly inhibited the proliferation of HCT116 and HCT15 cells, and reduced both mRNA and protein levels of GPX4 and HMGCR. Simvastatin also increased overall cell death, as detected by Annexin V/PI staining, and the rescue by Fer-1 supports ferroptosis as the primary mechanism. Co-treatment with Fer-1 attenuated these effects by restoring GPX4 expression and reducing apoptosis, ROS, MDA, and Fe2+ levels.
Conclusion
Simvastatin induces ferroptosis in HCT116 and HCT15 cells by enhancing lipid peroxidation and oxidative stress. The inhibitory influence of Fer-1 on these changes underscores the pivotal involvement of ferroptosis in simvastatin's antitumor effect. Overall, the results highlight simvastatin as a potential therapeutic option for colorectal cancer management.
{"title":"Simvastatin induces ferroptosis of colorectal cancer cells and is associated with mevalonate pathway inhibition","authors":"Shihua Zhang , Kejin Li , Yan Chen , Yusong Liu , Lin Wang , Limao Xu","doi":"10.1016/j.jrras.2025.102137","DOIUrl":"10.1016/j.jrras.2025.102137","url":null,"abstract":"<div><h3>Purpose</h3><div>This study aimed to elucidate the molecular mechanism by which simvastatin promotes ferroptosis in colorectal cancer cells, focusing on its targeting of HMGCR, suggesting that simvastatin-induced ferroptosis is associated with mevalonate pathway suppression.</div></div><div><h3>Methods</h3><div>Cell proliferation was evaluated after exposure to various concentrations of simvastatin. The expression of GPX4 and HMGCR was quantified using RT-qPCR and western blotting following treatment with simvastatin alone or combined with the ferroptosis inhibitor ferrostatin-1 (Fer-1). Apoptosis was analyzed by flow cytometry. In addition, intracellular reactive oxygen species (ROS), malondialdehyde (MDA), and ferrous iron (Fe<sup>2+</sup>) levels were determined to assess metabolic alterations induced by simvastatin.</div></div><div><h3>Results</h3><div>Treatment with 20 μM simvastatin for 72 h significantly inhibited the proliferation of HCT116 and HCT15 cells, and reduced both mRNA and protein levels of GPX4 and HMGCR. Simvastatin also increased overall cell death, as detected by Annexin V/PI staining, and the rescue by Fer-1 supports ferroptosis as the primary mechanism. Co-treatment with Fer-1 attenuated these effects by restoring GPX4 expression and reducing apoptosis, ROS, MDA, and Fe<sup>2+</sup> levels.</div></div><div><h3>Conclusion</h3><div>Simvastatin induces ferroptosis in HCT116 and HCT15 cells by enhancing lipid peroxidation and oxidative stress. The inhibitory influence of Fer-1 on these changes underscores the pivotal involvement of ferroptosis in simvastatin's antitumor effect. Overall, the results highlight simvastatin as a potential therapeutic option for colorectal cancer management.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102137"},"PeriodicalIF":2.5,"publicationDate":"2025-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-26DOI: 10.1016/j.jrras.2025.102118
Xiao Yan , Shuang Miao , Bozhen Fan , Zeyu Xu , Yunzhi Zhao , Chenyue Yuan , Ziliang Wang , Yongning Sun
Background
Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regualtors in cancer biology, including ovarian cancer (OC). Analysis of the OC cohort in the Cancer Genome Atlas (TCGA) revealed that LINC011123 is significantly upregulated in OC compared to normal ovarian tissue. Nonetheless, the functional consequence of this upregulation and the underlying mechanism of LINC01123 in OC remain unclear. We hypothesized that elevated LINC01123 exerts an oncogenic function.
Methods
RNA sequencing datasets from TCGA were analyzed to identify the RNAs with differential expression in OC tissues relative to standard ovarian tissue. The role of LINC01123 in regulating cell proliferation, migration, and autophagy was defined through functional experiments including wound healing, transwell, and western blotting in vitro, and a xenograft mouse model in vivo. LINC01123 regulation underwent investigation using RNA pulldown and mass spectrometry, RNA immunoprecipitation, luciferase reporter assays, and so on.
Results
LINC01123 is one of the most highly increased lncRNAs in OC specimens compared to non-cancerous ovarian tissue. Downregulation of LINC01123 functioned to suppress proliferation and cellular migration. RNA pulldown and gene set enrichment analysis suggested that the amount of LINC01123 positively correlated with genes involved in autophagy. LINC01123 promoted autophagy by promoting ATG13 expression. Further mechanistic studies showed that LINC01123 directly binds to p65 to activate ATG13 transcription, promoting autophagy and facilitating OC tumorigenesis.
Conclusion
Our results uncovered the oncogenic function and mechanism of LINC01123 in OC. LINC01123 associates with p65, augmenting autophagy, which in turn facilitates tumor metastasis within OC cells by increasing ATG13 expression. LINC01123 is a potential therapeutic target for OC patients.
{"title":"LINC01123 drives autophagy-mediated promotion of ovarian tumor metastasis through the p65/ATG13 pathway","authors":"Xiao Yan , Shuang Miao , Bozhen Fan , Zeyu Xu , Yunzhi Zhao , Chenyue Yuan , Ziliang Wang , Yongning Sun","doi":"10.1016/j.jrras.2025.102118","DOIUrl":"10.1016/j.jrras.2025.102118","url":null,"abstract":"<div><h3>Background</h3><div>Long non-coding RNAs (lncRNAs) are increasingly recognized as critical regualtors in cancer biology, including ovarian cancer (OC). Analysis of the OC cohort in the Cancer Genome Atlas (TCGA) revealed that LINC011123 is significantly upregulated in OC compared to normal ovarian tissue. Nonetheless, the functional consequence of this upregulation and the underlying mechanism of LINC01123 in OC remain unclear. We hypothesized that elevated LINC01123 exerts an oncogenic function.</div></div><div><h3>Methods</h3><div>RNA sequencing datasets from TCGA were analyzed to identify the RNAs with differential expression in OC tissues relative to standard ovarian tissue. The role of LINC01123 in regulating cell proliferation, migration, and autophagy was defined through functional experiments including wound healing, transwell, and western blotting <em>in vitro</em>, and a xenograft mouse model <em>in vivo</em>. LINC01123 regulation underwent investigation using RNA pulldown and mass spectrometry, RNA immunoprecipitation, luciferase reporter assays, and so on.</div></div><div><h3>Results</h3><div>LINC01123 is one of the most highly increased lncRNAs in OC specimens compared to non-cancerous ovarian tissue. Downregulation of LINC01123 functioned to suppress proliferation and cellular migration. RNA pulldown and gene set enrichment analysis suggested that the amount of LINC01123 positively correlated with genes involved in autophagy. LINC01123 promoted autophagy by promoting ATG13 expression. Further mechanistic studies showed that LINC01123 directly binds to p65 to activate ATG13 transcription, promoting autophagy and facilitating OC tumorigenesis.</div></div><div><h3>Conclusion</h3><div>Our results uncovered the oncogenic function and mechanism of LINC01123 in OC. LINC01123 associates with p65, augmenting autophagy, which in turn facilitates tumor metastasis within OC cells by increasing ATG13 expression. LINC01123 is a potential therapeutic target for OC patients.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102118"},"PeriodicalIF":2.5,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-26DOI: 10.1016/j.jrras.2025.102115
Fang Wang , Rui Dai
Background
Naringenin, a natural flavonoid, has various pharmacological effects. However, the function of naringenin in cardiac inflammation remains unclear. This study investigated whether naringenin alleviates cardiac inflammatory induced by lipopolysaccharide (LPS).
Methods
Naringenin's regulatory targets in inflammation and apoptosis were investigated using network pharmacology and molecular docking. LPS activated H9c2 cardiomyocytes, which were then treated with naringenin.
Results
Naringenin (20 or 40 μM) reduced the expression of cytokine induced by LPS (P < 0.05). In LPS-induced cells treated with naringenin (20 μM), the nuclear translocation of p65 was inhibited, concomitantly with a significant reduction in IκBα degradation. TUNEL staining revealed that naringenin (20 μM) significantly reduced apoptosis triggered by LPS (P < 0.05). Naringenin (20 μM) also significantly decreased the expression level of Bax and cleaved-caspase 3, and significantly elevated Bcl-2 expression.
Conclusion
Naringenin may be able to attenuate H9c2 cardiomyocyte inflammation and apoptosis induced by LPS.
{"title":"Naringenin attenuates inflammation and apoptosis in lipopolysaccharide-induced H9c2 cardiomyocytes","authors":"Fang Wang , Rui Dai","doi":"10.1016/j.jrras.2025.102115","DOIUrl":"10.1016/j.jrras.2025.102115","url":null,"abstract":"<div><h3>Background</h3><div>Naringenin, a natural flavonoid, has various pharmacological effects. However, the function of naringenin in cardiac inflammation remains unclear. This study investigated whether naringenin alleviates cardiac inflammatory induced by lipopolysaccharide (LPS).</div></div><div><h3>Methods</h3><div>Naringenin's regulatory targets in inflammation and apoptosis were investigated using network pharmacology and molecular docking. LPS activated H9c2 cardiomyocytes, which were then treated with naringenin.</div></div><div><h3>Results</h3><div>Naringenin (20 or 40 μM) reduced the expression of cytokine induced by LPS (P < 0.05). In LPS-induced cells treated with naringenin (20 μM), the nuclear translocation of p65 was inhibited, concomitantly with a significant reduction in IκBα degradation. TUNEL staining revealed that naringenin (20 μM) significantly reduced apoptosis triggered by LPS (P < 0.05). Naringenin (20 μM) also significantly decreased the expression level of Bax and cleaved-caspase 3, and significantly elevated Bcl-2 expression.</div></div><div><h3>Conclusion</h3><div>Naringenin may be able to attenuate H9c2 cardiomyocyte inflammation and apoptosis induced by LPS.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102115"},"PeriodicalIF":2.5,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-25DOI: 10.1016/j.jrras.2025.102139
Xin Lian, Jiafeng Ding, Ting Chen, Xiaofen Wu
Background
This study aimed to investigate the role of bufalin in inhibiting the osteogenic differentiation of human renal interstitial fibroblasts (hRIFs) and explore its potential mechanism through the OCT4/BMP2/Smads signaling axis.
Methods
Osteogenic differentiation of hRIFs was induced via osteogenic medium (OM), and this osteogenic differentiation was evaluated via alizarin red staining for calcium nodule formation, cobalt chloride staining for alkaline phosphatase activity, and Western blotting (WB) analysis for the expression of key osteogenic protein. Then, differentiated osteoblasts were treated with various concentrations of bufalin, and cell viability was assessed via the MTT assay to determine the optimal concentration. To investigate whether the inhibitory effect of bufalin on osteogenic differentiation involves the OCT4/BMP2/Smads signaling pathway, Western blot analysis, OCT4 overexpression, and BMP2-targeting short hairpin RNA (sh-BMP2) were used.
Results
OM successfully induced osteogenic differentiation in hRIFs and this differentiation was inhibited by bufalin. Mechanistically, bufalin suppressed OCT4 expression and consequently inhibited BMP2/Smads pathway activation. Notably, OCT4 upregulation reversed the inhibitory effects of bufalin on hRIF growth and osteoblast differentiation. Conversely, BMP2 downregulation counteracted the pro-osteogenic effects induced by OCT4 upregulation in bufalin-treated cells.
Conclusion
Bufalin inhibits the osteogenic differentiation in hRIFs, via a mechanism involving the downregulation the OCT4/BMP2/Smads pathway. These findings reveal that bufalin plays an important regulatory role in the osteogenic differentiation of hRIFs, which may provide a theoretical foundation for future research into the treatment of Randall's plaque formation.
{"title":"Bufalin inhibits the osteogenic differentiation of renal interstitial fibroblasts through the OCT4/BMP2/Smads signaling axis","authors":"Xin Lian, Jiafeng Ding, Ting Chen, Xiaofen Wu","doi":"10.1016/j.jrras.2025.102139","DOIUrl":"10.1016/j.jrras.2025.102139","url":null,"abstract":"<div><h3>Background</h3><div>This study aimed to investigate the role of bufalin in inhibiting the osteogenic differentiation of human renal interstitial fibroblasts (hRIFs) and explore its potential mechanism through the OCT4/BMP2/Smads signaling axis.</div></div><div><h3>Methods</h3><div>Osteogenic differentiation of hRIFs was induced via osteogenic medium (OM), and this osteogenic differentiation was evaluated via alizarin red staining for calcium nodule formation, cobalt chloride staining for alkaline phosphatase activity, and Western blotting (WB) analysis for the expression of key osteogenic protein. Then, differentiated osteoblasts were treated with various concentrations of bufalin, and cell viability was assessed via the MTT assay to determine the optimal concentration. To investigate whether the inhibitory effect of bufalin on osteogenic differentiation involves the OCT4/BMP2/Smads signaling pathway, Western blot analysis, OCT4 overexpression, and BMP2-targeting short hairpin RNA (sh-BMP2) were used.</div></div><div><h3>Results</h3><div>OM successfully induced osteogenic differentiation in hRIFs and this differentiation was inhibited by bufalin. Mechanistically, bufalin suppressed OCT4 expression and consequently inhibited BMP2/Smads pathway activation. Notably, OCT4 upregulation reversed the inhibitory effects of bufalin on hRIF growth and osteoblast differentiation. Conversely, BMP2 downregulation counteracted the pro-osteogenic effects induced by OCT4 upregulation in bufalin-treated cells.</div></div><div><h3>Conclusion</h3><div>Bufalin inhibits the osteogenic differentiation in hRIFs, via a mechanism involving the downregulation the OCT4/BMP2/Smads pathway. These findings reveal that bufalin plays an important regulatory role in the osteogenic differentiation of hRIFs, which may provide a theoretical foundation for future research into the treatment of Randall's plaque formation.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102139"},"PeriodicalIF":2.5,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Indonesia is committed to achieving net zero greenhouse gas emissions by 2060. To meet this objective, a diversified energy strategy is needed, which includes the deployment of nuclear power plants in addition to other renewable energy sources. It is planned that the first NPP in Indonesia will be introduced in 2032 or no later than 2034, with a target of approximately 31 GWe by 2060. To meet this demand, various reactor types will be considered based on geographical and demographic conditions, including Small Modular Reactors (SMRs). One potential site, Pantai Gosong in West Kalimantan, is currently under evaluation. An important aspect of site evaluation is the radiological safety assessment for accident conditions. The assessment includes the air concentration and ground deposition of several isotopes, individual effective doses, and early countermeasures. Site-specific meteorological data, were taken from the relevant national agencies. This study focuses on assessing radiation doses and formulating early countermeasure strategies, specifically for shelter management, in response to a hypothetical accident involving an SMR at the site, based on two potential release scenarios. Simulations were conducted using PC-Cosyma code. The sheltering pattern generated by the PC Cosyma is displayed using GIS and combined with settlement area, existing buildings suifigura for shelter, and the road network. Simulation results show that the calculated individual effective doses to the public remain well below reference levels. Nevertheless, a cautious approach to early countermeasures must be applied by implementing sheltering within a specific radius. This strategy aims to reduce the risk of radiation exposure while also preparing for potential subsequent actions, such as evacuation or the distribution of stable iodine (KI) tablets, if necessary. Proposed special protection zones within a 2 km radius can be established for immediate response measures. The existing public facilities are adequate to shelter the population within a 2 km radius. However, the presence of arterial roads within this area poses a potential risk of radiation exposure. Thus, alternative routes outside the 2 km radius should be suggested to enable effective traffic management in the event of an emergency.
{"title":"Sheltering management to protect the population: A case study of radiological impact assessment under a postulated accident condition in Indonesia's first NPP site","authors":"Yarianto Sugeng Budi Susilo , Muhammad Budi Setiawan , Jaja Sukmana , Anik Purwaningsih , Khusnul Khotimah , Djarot Sulistio Wisnubroto , Mohammad Dhandhang Purwadi , Anis Rohanda , Hery Adrial , Heni Susiati , Erlan Dewita , Totti Tjiptosumirat , Ferly Hermana , Wahyu Retno Prihatiningsih , Murdahayu Makmur , June Mellawati , Sunarko Sunarko , Suparman Suparman , Roziq Himawan , Dede Sutarya","doi":"10.1016/j.jrras.2025.102125","DOIUrl":"10.1016/j.jrras.2025.102125","url":null,"abstract":"<div><div>Indonesia is committed to achieving net zero greenhouse gas emissions by 2060. To meet this objective, a diversified energy strategy is needed, which includes the deployment of nuclear power plants in addition to other renewable energy sources. It is planned that the first NPP in Indonesia will be introduced in 2032 or no later than 2034, with a target of approximately 31 GWe by 2060. To meet this demand, various reactor types will be considered based on geographical and demographic conditions, including Small Modular Reactors (SMRs). One potential site, Pantai Gosong in West Kalimantan, is currently under evaluation. An important aspect of site evaluation is the radiological safety assessment for accident conditions. The assessment includes the air concentration and ground deposition of several isotopes, individual effective doses, and early countermeasures. Site-specific meteorological data, were taken from the relevant national agencies. This study focuses on assessing radiation doses and formulating early countermeasure strategies, specifically for shelter management, in response to a hypothetical accident involving an SMR at the site, based on two potential release scenarios. Simulations were conducted using PC-Cosyma code. The sheltering pattern generated by the PC Cosyma is displayed using GIS and combined with settlement area, existing buildings suifigura for shelter, and the road network. Simulation results show that the calculated individual effective doses to the public remain well below reference levels. Nevertheless, a cautious approach to early countermeasures must be applied by implementing sheltering within a specific radius. This strategy aims to reduce the risk of radiation exposure while also preparing for potential subsequent actions, such as evacuation or the distribution of stable iodine (KI) tablets, if necessary. Proposed special protection zones within a 2 km radius can be established for immediate response measures. The existing public facilities are adequate to shelter the population within a 2 km radius. However, the presence of arterial roads within this area poses a potential risk of radiation exposure. Thus, alternative routes outside the 2 km radius should be suggested to enable effective traffic management in the event of an emergency.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102125"},"PeriodicalIF":2.5,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-23DOI: 10.1016/j.jrras.2025.102141
Tenghong Rong , Jingqi Sun
Introduction/objective
Medical image segmentation can raise the diagnostic efficiency of doctors and reduce their burden, which is of great significance. To raise the accuracy of medical image segmentation and solve the problem of scarce medical image data, corresponding segmentation algorithms are designed separately.
Methods
Firstly, a cascaded knowledge dissemination network model is designed to raise the accuracy of medical image segmentation through the collaborative work of three task subnets: initial segmentation, lesion classification, and fine segmentation, combined with a feature fusion module. Secondly, a semi-supervised segmentation model based on pseudo label guided feature aggregation network is designed, innovatively introducing pseudo label guided feature enhancement module and multi-scale multi-stage feature aggregation module, optimizing the teacher-student network architecture, and fully utilizing unlabeled data to supplement training samples, in order to solve the problem of data scarcity.
Results
The findings denoted that the average multi-category accuracy and segmentation accuracy of the cascaded knowledge dissemination network model were 86.7 % and 99.4 %. On the molecular nucleus segmentation dataset, when the proportion of annotated data was 10 % and 50 %, the maximum intersection to union ratios of the semi supervised segmentation model were 0.859 and 0.867, respectively.
Discussion
It can be seen that the cascaded knowledge dissemination network model has a segmentation accuracy of over 99.0 % on medical images, which can effectively improve the segmentation accuracy of medical images. The semi supervised segmentation model also has good intersection to union ratio and Dice coefficient in low annotated data ratios, and can complete segmentation tasks in medical image data scarcity. The two medical image segmentation models designed in the research have good effectiveness.
Conclusion
The contribution of the research is the design of a semi supervised model consisting of a cascaded knowledge dissemination network model and a pseudo label guided feature aggregation network, which improves the accuracy of medical image segmentation and solves the problem of data scarcity.
{"title":"Design of CKDNet and PMGFANet segmentation models for medical images considering accuracy improvement and data scarcity resolution","authors":"Tenghong Rong , Jingqi Sun","doi":"10.1016/j.jrras.2025.102141","DOIUrl":"10.1016/j.jrras.2025.102141","url":null,"abstract":"<div><h3>Introduction/objective</h3><div>Medical image segmentation can raise the diagnostic efficiency of doctors and reduce their burden, which is of great significance. To raise the accuracy of medical image segmentation and solve the problem of scarce medical image data, corresponding segmentation algorithms are designed separately.</div></div><div><h3>Methods</h3><div>Firstly, a cascaded knowledge dissemination network model is designed to raise the accuracy of medical image segmentation through the collaborative work of three task subnets: initial segmentation, lesion classification, and fine segmentation, combined with a feature fusion module. Secondly, a semi-supervised segmentation model based on pseudo label guided feature aggregation network is designed, innovatively introducing pseudo label guided feature enhancement module and multi-scale multi-stage feature aggregation module, optimizing the teacher-student network architecture, and fully utilizing unlabeled data to supplement training samples, in order to solve the problem of data scarcity.</div></div><div><h3>Results</h3><div>The findings denoted that the average multi-category accuracy and segmentation accuracy of the cascaded knowledge dissemination network model were 86.7 % and 99.4 %. On the molecular nucleus segmentation dataset, when the proportion of annotated data was 10 % and 50 %, the maximum intersection to union ratios of the semi supervised segmentation model were 0.859 and 0.867, respectively.</div></div><div><h3>Discussion</h3><div>It can be seen that the cascaded knowledge dissemination network model has a segmentation accuracy of over 99.0 % on medical images, which can effectively improve the segmentation accuracy of medical images. The semi supervised segmentation model also has good intersection to union ratio and Dice coefficient in low annotated data ratios, and can complete segmentation tasks in medical image data scarcity. The two medical image segmentation models designed in the research have good effectiveness.</div></div><div><h3>Conclusion</h3><div>The contribution of the research is the design of a semi supervised model consisting of a cascaded knowledge dissemination network model and a pseudo label guided feature aggregation network, which improves the accuracy of medical image segmentation and solves the problem of data scarcity.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102141"},"PeriodicalIF":2.5,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-23DOI: 10.1016/j.jrras.2025.102140
Mingqin Zhang , Jin Xu , Dongyi Yang , Jiabin Wang , Sha Luo , Yiping Wang
Background
Ischemic stroke (IS) is implicated in disruptions of mitochondrial energy metabolism and ferroptosis. However, the underlying mechanisms remain elusive.
Methods
Three stroke-related transcriptome datasets (GSE22255, GSE58294, and GSE16561) were retrieved from the GEO database. A series of bioinformatic analyses were conducted, including differential expression analysis, functional enrichment, and protein–protein interaction (PPI) network construction. We further applied random forest modeling and single-cell sequencing to screen mitochondrial energy metabolism- and ferroptosis-related genes. The diagnostic value and immune correlations of these genes were further validated. We constructed an IS model in HT22 cells with OGD/R induction and employed IDH2 overexpression by transfection for subsequent functional validation.
Results
8 differentially expressed genes (DEGs) were identified (MGST1, ACSL1, PDK4, IDH2, ECH1, GPX4, BCAT2, PARK7). Functional enrichment analysis revealed their involvement in pathways like pyruvate metabolism and immune response regulation. In the random forest model, IDH2 showed a promising diagnostic value in the external validation set (AUC = 0.682). Single-cell analysis identified specific expression of IDH2 in glial cells and MGST1 in astrocytes, with both genes showing a notable correlation to macrophage infiltration. Notably, IDH2 expression was markedly reduced in IS cell models, and its overexpression significantly improved mitochondrial energy metabolism and inhibited ferroptosis.
Conclusion
This study elucidated the critical roles of mitochondrial energy metabolism–ferroptosis–related genes in IS and highlights IDH2 as a key candidate for disease diagnosis and potential therapeutic intervention. And its overexpression significantly improved mitochondrial energy metabolism and inhibited ferroptosis, suggesting a protective mechanistic role.
{"title":"Integrated bioinformatic analysis and experimental validation identify IDH2 as a key mitochondrial energy metabolism-ferroptosis biomarker in ischemic stroke","authors":"Mingqin Zhang , Jin Xu , Dongyi Yang , Jiabin Wang , Sha Luo , Yiping Wang","doi":"10.1016/j.jrras.2025.102140","DOIUrl":"10.1016/j.jrras.2025.102140","url":null,"abstract":"<div><h3>Background</h3><div>Ischemic stroke (IS) is implicated in disruptions of mitochondrial energy metabolism and ferroptosis. However, the underlying mechanisms remain elusive.</div></div><div><h3>Methods</h3><div>Three stroke-related transcriptome datasets (GSE22255, GSE58294, and GSE16561) were retrieved from the GEO database. A series of bioinformatic analyses were conducted, including differential expression analysis, functional enrichment, and protein–protein interaction (PPI) network construction. We further applied random forest modeling and single-cell sequencing to screen mitochondrial energy metabolism- and ferroptosis-related genes. The diagnostic value and immune correlations of these genes were further validated. We constructed an IS model in HT22 cells with OGD/R induction and employed IDH2 overexpression by transfection for subsequent functional validation.</div></div><div><h3>Results</h3><div>8 differentially expressed genes (DEGs) were identified (MGST1, ACSL1, PDK4, IDH2, ECH1, GPX4, BCAT2, PARK7). Functional enrichment analysis revealed their involvement in pathways like pyruvate metabolism and immune response regulation. In the random forest model, IDH2 showed a promising diagnostic value in the external validation set (AUC = 0.682). Single-cell analysis identified specific expression of IDH2 in glial cells and MGST1 in astrocytes, with both genes showing a notable correlation to macrophage infiltration. Notably, IDH2 expression was markedly reduced in IS cell models, and its overexpression significantly improved mitochondrial energy metabolism and inhibited ferroptosis.</div></div><div><h3>Conclusion</h3><div>This study elucidated the critical roles of mitochondrial energy metabolism–ferroptosis–related genes in IS and highlights IDH2 as a key candidate for disease diagnosis and potential therapeutic intervention. And its overexpression significantly improved mitochondrial energy metabolism and inhibited ferroptosis, suggesting a protective mechanistic role.</div></div>","PeriodicalId":16920,"journal":{"name":"Journal of Radiation Research and Applied Sciences","volume":"19 1","pages":"Article 102140"},"PeriodicalIF":2.5,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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