Nan fang yi ke da xue xue bao = Journal of Southern Medical University最新文献

{"title":"[A dual-domain cone beam computed tomography reconstruction framework with improved differentiable domain transform for cone-angle artifact correction].","authors":"S Peng, Y Wang, Z Bian, J Ma, J Huang","doi":"10.12122/j.issn.1673-4254.2024.06.21","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.21","url":null,"abstract":"<p><strong>Objective: </strong>We propose a dual-domain cone beam computed tomography (CBCT) reconstruction framework DualCBR-Net based on improved differentiable domain transform for cone-angle artifact correction.</p><p><strong>Methods: </strong>The proposed CBCT dual-domain reconstruction framework DualCBR-Net consists of 3 individual modules: projection preprocessing, differentiable domain transform, and image post-processing. The projection preprocessing module first extends the original projection data in the row direction to ensure full coverage of the scanned object by X-ray. The differentiable domain transform introduces the FDK reconstruction and forward projection operators to complete the forward and gradient backpropagation processes, where the geometric parameters correspond to the extended data dimension to provide crucial prior information in the forward pass of the network and ensure the accuracy in the gradient backpropagation, thus enabling precise learning of cone-beam region data. The image post-processing module further fine-tunes the domain-transformed image to remove residual artifacts and noises.</p><p><strong>Results: </strong>The results of validation experiments conducted on Mayo's public chest dataset showed that the proposed DualCBR-Net framework was superior to other comparison methods in terms of artifact removal and structural detail preservation. Compared with the latest methods, the DualCBR-Net framework improved the PSNR and SSIM by 0.6479 and 0.0074, respectively.</p><p><strong>Conclusion: </strong>The proposed DualCBR-Net framework for cone-angle artifact correction allows effective joint training of the CBCT dual-domain network and is especially effective for large cone-angle region.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[High expression of the stemness-associated molecule Nanog in esophageal squamous cell carcinoma tissues promotes tumor invasion and metastasis by activating the TGF-β signaling pathway].","authors":"C Sun, S Zheng, M Li, M Yang, M Qin, Y Xu, W Liang, J Hu, L Wang, F Li, H Zhou, L Yang","doi":"10.12122/j.issn.1673-4254.2024.06.23","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.23","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the expression of Nanog and its regulatory relationship with MMP-2/MMP-9 proteins in esophageal squamous cell carcinoma (ESCC).</p><p><strong>Methods: </strong>We detected Nanog and MMP-2/MMP-9 protein expressions in 127 ESCC tissues and 82 adjacent normal tissues using immunohistochemistry and explored their correlations with the clinicopathological parameters and prognosis of the patients. GEO database was utilized to analyze the pathways enriched with the stemness-related molecules including Nanog, and TIMER online tool was used to analyze the correlations among TβR1, MMP-2, and MMP-9 in esophageal cancer.</p><p><strong>Results: </strong>Nanog and MMP-2/MMP-9 proteins were significantly upregulated in ESCC tissues and positively intercorrelated. Their expression levels were closely correlated with infiltration depth and lymph node metastasis of ESCC but not with age, gender, or tumor differentiation. The patients with high expressions of Nanog and MMP-2/MMP-9 had significantly shorter survival time. Bioinformatics analysis showed enrichment of stemness-associated molecules in the TGF-β signaling pathway, and the expressions of MMP-2/MMP-9 and TβR1 were positively correlated. In cultured ESCC cells, Nanog knockdown significantly decreased the expression of TβR1, p-Smad2/3, MMP-2, and MMP-9 and strongly inhibited cell migration.</p><p><strong>Conclusion: </strong>The high expressions of Nanog, MMP-2, and MMP-9, which are positively correlated, are closely related with invasion depth, lymph node metastasis, and prognosis of ESCC. Nanog regulates the expressions of MMP-2/MMP-9 proteins through the TGF-β signaling pathway, and its high expression promotes migration of ESCC cells.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Prediction of risk of in-hospital death in patients with chronic heart failure complicated by lung infections using interpretable machine learning].","authors":"C Shen, S Wang, R Zhou, Y Wang, Q Gao, X Chen, S Yang","doi":"10.12122/j.issn.1673-4254.2024.06.15","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.15","url":null,"abstract":"<p><strong>Objective: </strong>To predict the risk of in-hospital death in patients with chronic heart failure (CHF) complicated by lung infections using interpretable machine learning.</p><p><strong>Methods: </strong>The clinical data of 1415 patients diagnosed with CHF complicated by lung infections were obtained from the MIMIC-IV database. According to the pathogen type, the patients were categorized into bacterial pneumonia and non-bacterial pneumonia groups, and their risks of in-hospital death were compared using Kaplan-Meier survival curves. Univariate analysis and LASSO regression were used to select the features for constructing LR, AdaBoost, XGBoost, and LightGBM models, and their performance was compared in terms of accuracy, precision, F1 value, and AUC. External validation of the models was performed using the data from eICU-CRD database. SHAP algorithm was applied for interpretive analysis of XGBoost model.</p><p><strong>Results: </strong>Among the 4 constructed models, the XGBoost model showed the highest accuracy and F1 value for predicting the risk of in-hospital death in CHF patients with lung infections in the training set. In the external test set, the XGBoost model had an AUC of 0.691 (95% <i>CI</i>: 0.654-0.720) in bacterial pneumonia group and an AUC of 0.725 (95% <i>CI</i>: 0.577-0.782) in non-bacterial pneumonia group, and showed better predictive ability and stability than the other models.</p><p><strong>Conclusion: </strong>The overall performance of the XGBoost model is superior to the other 3 models for predicting the risk of in-hospital death in CHF patients with lung infections. The SHAP algorithm provides a clear interpretation of the model to facilitate decision-making in clinical settings.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Dexmedetomidine inhibits ferroptosis of human renal tubular epithelial cells by activating the Nrf2/HO-1/GPX4 pathway].","authors":"F Zhang, G Liu","doi":"10.12122/j.issn.1673-4254.2024.06.14","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.14","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the protective effect of dexmedetomidine (DEX) against erastin-induced ferroptosis in human renal tubular epithelial cells (HK-2 cells) and explore the underlying mechanism.</p><p><strong>Methods: </strong>HK-2 cells were treated with erastin alone or in combination with different concentrations (2.5, 5.0 and 10 μmol/L) of DEX, and the changes in cell viability were observed using CCK-8 assay. To explore the mechanism by which DEX inhibits erastin-induced ferroptosis, HK-2 cells were treated with erastin, erastin+10 μmol/L DEX, or erastin+10 μmol/L DEX+ML385 (a Nrf2 inhibitor), after which the cell viability was assessed. The level of intracellular Fe²⁺ was detected by cell ferrous iron colorimetric assay kit, and flow cytometry was performed to detect reactive oxygen species (ROS); MDA and reduced glutathione assay kits were used to detect the contents of MDA and GSH in the cells; The expressions of Nrf2, HO-1 and GPX4 proteins were detected by Western blotting.</p><p><strong>Results: </strong>Erastin treatment significantly inhibited the viability of the cells, decreased GSH content, and increased intracellular levels of Fe²⁺, ROS and MDA. The combined treatment with 10 μmol/L DEX markedly increased the viability of the cells, increased GSH content, reduced the levels of Fe²⁺, ROS and MDA, and upregulated the protein expressions of Nrf2, HO-1 and GPX4 in the cells. The application of ML385 obviously blocked the protective effect of DEX and caused significant inhibition of the Nrf2/HO-1/GPX4 pathway, decreased the cell viability and GSH content, and increased the levels of Fe²⁺, ROS and MDA in HK-2 cells.</p><p><strong>Conclusion: </strong>The protective effect of DEX against erastin-induced ferroptosis of HK-2 cells is probably mediated by activation of the Nrf2/HO-1/GPX4 pathway to inhibit oxidative stress.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Aqueous extract of Chuan Xiong Rhizoma enhances inhibitory effect of temozolomide against brain metastasis of melanoma in mice].","authors":"Q Zhao, Z Zhang, X Zhou, X Rong, X Liu, X Zhao, H Wang, J Pang, S Li, X Li","doi":"10.12122/j.issn.1673-4254.2024.06.09","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.09","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of the aqueous extract of Chuan Xiong Rhizoma (CR) on brain metastasis of melanoma B16F10 cells in mice.</p><p><strong>Methods: </strong>C57BL/6J mouse models of brain metastasis of melanoma were established by ultrasound-guided intraventricular injection of Luc-labeled B16F10 cells, and brain tumor growth was monitored by in vivo imaging. The mouse models were then randomized for daily gavage of saline or aqueous extract of CR (equivalent crude drug concentration of 1 mg/g). Behavioral tests were used to evaluate the neuroprotective effects of CR in the tumor-bearing mice, and the changes in proteins associated with blood-brain barrier integrity, neuronal cell proliferation and apoptosis, and microglial cell apoptosis and activation were observed using immunofluorescence assay. The efficacy of CR combined with temozolomide (25 mg/kg) against brain metastases of B16F10 cells was observed by <i>in vivo</i> imaging.</p><p><strong>Results: </strong>CR-treated mouse models did not show obvious progression of brain metastases and had a reduced rate of body weight loss and lowered protein expressions of ZO-1, claudin-5, occludin, P-gp, TNF-α, AQP4 and PDGFRβ. In the behavioral tests, the CR-treated mice showed prolonged stay on the wooden stick with a shortened time of sticky stick removal. Immunofluorescence assay showed increased proliferation and decreased apoptosis of neuronal cells and microglia in CR-treated mice. CR treatment significantly increased the levels of CD86, CD206, IL-4 and IL-10 and decreased the levels of CD163 and IL-1β in the microenvironment of brain metastases. The mice receiving combined treatments with CR and temozolomide showed significantly lower intensity of fluorescent signals in the brain than those treated with temozolomide alone.</p><p><strong>Conclusion: </strong>CR does not promote brain metastasis of melanoma while inducing opening of the blood-brain barrier, and its combined use with TMZ results in enhanced inhibition against brain metastasis of melanoma B16F10 cells in mice.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Recombinant <i>Schistosoma japonicum</i> cystatin alleviates acute liver injury in mice by inhibiting endoplasmic reticulum stress, inflammation and hepatocyte apoptosis].","authors":"L Lu, X Yang, H Zhang, Y Liang, X Shi, X Zhou","doi":"10.12122/j.issn.1673-4254.2024.06.13","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.13","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the protective effect of recombinant <i>Schistosoma japonicum</i> cystatin (rSj-Cys) against acute liver injury induced by lipopolysaccharide (LPS) and D-GalN in mice.</p><p><strong>Methods: </strong>Adult male C57BL/6J mice with or without LPS/D-GaIN-induced acute liver injury were given intraperitoneal injections of rSj-Cys or PBS 30 min after modeling (<i>n</i>=18), and serum and liver tissues samples were collected from 8 mice in each group 6 h after modeling. The survival of the remaining 10 mice in each group within 24 h was observed. Serum levels of ALT, AST, TNF-α and IL-6 of the mice were measured, and liver pathologies was observed with HE staining. The hepatic expressions of macrophage marker CD68, Bax, Bcl-2 and endoplasmic reticulum stress (ERS)-related proteins were detected using immunohistochemistry or immunoblotting, and TUNEL staining was used to detect hepatocyte apoptosis.</p><p><strong>Results: </strong>The survival rates of PBS- and rSj-Cys-treated mouse models of acute liver injury were 30% and 80% at 12 h and were 10% and 60% at 24 h after modeling, respectively; no death occurred in the two control groups within 24 h. The mouse models showed significantly increased serum levels of AST, ALT, IL-6 and TNF-α and serious liver pathologies with increased hepatic expressions of CD68 and Bax, lowered expression of Bcl-2, increased hepatocyte apoptosis, and up-regulated expressions of ERS-related signaling pathway proteins GRP78, CHOP and NF-κB p-p65. Treatment of the mouse models significantly lowered the levels of AST, ALT, IL-6 and TNF-α, alleviated liver pathologies, reduced hepatic expressions of CD68, Bax, GRP78, CHOP and NF-κB p-p65, and enhanced the expression of Bcl-2. In the normal control mice, rSj-Cys injection did not produce any significant changes in these parameters compared with PBS.</p><p><strong>Conclusion: </strong>rSj-Cys alleviates LPS/D-GalN-induced acute liver injury in mice by suppressing ERS, attenuating inflammation and inhibiting hepatocyte apoptosis.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Exogenous leptin improves cerebral ischemia-reperfusion-induced glutamate excitotoxic injury in mice by up-regulating GLT-1 and GLAST expression in astrocytes].","authors":"J Chen, C Liu, C Wang, L Li, W Tao, J Xun, H Tang, L Huang","doi":"10.12122/j.issn.1673-4254.2024.06.08","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.08","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the protective effect of exogenous leptin against focal cerebral ischemia-reperfusion (I/R) injury in mice and explore the underlying mechanism.</p><p><strong>Methods: </strong>A total of 100 C57BL/6 mice were randomly divided into 5 groups, including a sham-operated group, cerebral I/R model group, and 3 leptin treatment groups with intraperitoneal injections of 0.5, 1.0 or 2.0 leptin immediately after occlusion of the internal carotid artery. At 24 h after reperfusion, neurological function scores of the mice were assessed, and TTC staining was used to determine the area of cerebral infarction. The pathological changes in the cortical brain tissue of the mice were observed using HE staining, and degenerative damage of the cortical neurons were assessed with Fluoro-Jade C staining. The expression of glial fibrillary acidic protein in cortical brain tissues was detected using immunohistochemistry and Western blotting. In another 45 C57BL/6 mice with sham operation, I/R modeling, or leptin (1 mg/kg) treatment, glutamic acid in the cortical brain tissue was detected using glutamate assay, and cortical glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) protein expressions were detected using immunohistochemistry.</p><p><strong>Results: </strong>Compared with the I/R model mice, the leptin-treated mice had significantly lower neurological deficit scores, smaller cerebral infarct area, milder pathologies in the cortical brain tissue, and lessened cortical neuronal damage with normal morphology and less excessive proliferation of the astrocytes. Leptin treatment significantly up-regulated the expressions of GLT-1 and GLAST and lowered the content of glutamic acid in the brain tissue of the I/R mice.</p><p><strong>Conclusion: </strong>Exogenous leptin has obvious neuroprotective effect against cerebral I/R injury in mice, mediated probably by controlling excessive astrocyte proliferation and up-regulating cortical GLT-1 and GLAST expressions to reduce glutamate-mediated excitotoxic injury of the astrocytes.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Overexpression of CDHR2 inhibits proliferation of breast cancer cells by inhibiting the PI3K/Akt pathway].","authors":"J Fang, L Liu, J Lin, F Chen","doi":"10.12122/j.issn.1673-4254.2024.06.12","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.12","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the mechanism by which CDHR2 overexpression inhibits breast cancer cell growth and cell cycle pragression <i>via</i> the PI3K/Akt signaling pathway.</p><p><strong>Methods: </strong>Bioinformatic analysis was performed to investigate CDHR2 expression in breast cancer and its correlation with survival outcomes of the patients. Immunohistochemistry was used to examine CDHR2 expressions in surgical specimens of tumor and adjacent tissues from 10 patients with breast cancer. CDHR2 expression levels were also detected in 5 breast cancer cell lines and a normal human mammary epithelial cell line using qRT-PCR and Western blotting. Breast cancer cell lines MDA-MB-231 and MCF7 with low CDHR2 expression were transfected with a CDHR2-overexpressing plasmid, and the changes in cell proliferation and cell cycle were evaluated using CCK-8 assay, EdU assay, and cell cycle assay; the changes in expressions of PI3K/Akt signaling pathway and cell cycle pathway proteins were detected with Western blotting.</p><p><strong>Results: </strong>Bioinformatic analysis showed low CDHR2 expression level in both breast cancer and adjacent tissues without significant difference between them (<i>P</i> > 0.05), but breast cancer patients with a high expression of CDHR2 had a more favorable prognosis. Immunohistochemistry, qRT-PCR and Western blotting showed that the expression of CDHR2 was significantly down-regulated in breast cancer tissues and breast cancer cells (<i>P</i> < 0.01), and its overexpression strongly inhibited cell proliferation, caused cell cycle arrest, and significantly inhibited PI3K and Akt phosphorylation and the expression of cyclin D1.</p><p><strong>Conclusion: </strong>Overexpression of CDHR2 inhibits proliferation and causes cell cycle arrest in breast cancer cells possibly by inhibiting the PI3K/Akt signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Solasonine promotes apoptosis of non-small cell lung cancer cells by regulating the Bcl-2/Bax/caspase-3 pathway].","authors":"G Chen, X Liao, P Sun, H Cen, S Shu, B Li, J Li","doi":"10.12122/j.issn.1673-4254.2024.06.11","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.11","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of solasonine, an active component of <i>Solanum nigrum</i>, on proliferation and apoptosis of non-small cell lung cancer PC9 cells.</p><p><strong>Methods: </strong>PC9 cells were treated with 2, 5, 10, 15, 20, or 25 μmol/L solasonine, and the changes in cell proliferation were examined using CCK-8 assay. Tetramethyl rhodamine ethyl ester (TMRE) was used to detect the changes in mitochondrial membrane potential, and caspase-3/7 detection kit and GreenNuc^TM caspase-3/Annexin V-mCherry kit for live cell were used to analyze the changes in caspase-3 of the cells. Annexin V-FITC/PI double staining was employed to analyze the apoptosis rate of the cells. The effect of PTEN inhibitors on solasonine-induced cell apoptosis was examined by detecting apoptosis-related protein expressions using Western blotting.</p><p><strong>Results: </strong>Solasonine treatment for 24, 48, and 72 h significantly lowered the viability of PC9 cells. The cells treated with solasonine for 24 h showed significantly decreased mitochondrial membrane potential and increased cell apoptosis with enhanced caspase-3/7 and caspase-3 activities and expression of cleaved caspase-3. Solasonine treatment significantly decreased phosphorylation levels of PI3K and Akt, increased the protein expressions of PTEN and Bax, and lowered the expression of Bcl-2 protein in the cells.</p><p><strong>Conclusion: </strong>Solasonine inhibits proliferation and induces apoptosis of PC9 cells by regulating the Bcl-2/Bax/caspase-3 pathway and its upstream proteins.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Carrier screening for 223 monogenic diseases in Chinese population: a multi-center study in 33 104 individuals].","authors":"W Hou, X Fu, X Xie, C Zhang, J Bian, X Mao, J Wen, C Luo, H Jin, Q Zhu, Q Qi, Y Qian, J Yuan, Y Zhao, A Yin, S Li, Y Jiang, M Zhang, R Xiao, Y Lu","doi":"10.12122/j.issn.1673-4254.2024.06.01","DOIUrl":"10.12122/j.issn.1673-4254.2024.06.01","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the epidemiological characteristics and mutation spectrum of monogenic diseases in Chinese population through a large-scale, multicenter carrier screening.</p><p><strong>Methods: </strong>This study was conducted among a total of 33 104 participants (16 610 females) from 12 clinical centers across China.Carrier status for 223 genes was analyzed using high-throughput sequencing and different PCR methods.</p><p><strong>Results: </strong>The overall combined carrier frequency was 55.58% for 197 autosomal genes and 1.84% for 26 X-linked genes in these participants.Among the 16 669 families, 874 at-risk couples (5.24%) were identified.Specifically, 584 couples (3.50%) were at risk for autosomal genes, 306(1.84%) for X-linked genes, and 16 for both autosomal and X-linked genes.The most frequently detected autosomal at-risk genes included GJB2(autosomal recessive deafness type 1A, 393 couples), HBA1/HBA2(α-thalassemia, 36 couples), PAH (phenylketonuria, 14 couples), and SMN1(spinal muscular atrophy, 14 couples).The most frequently detected X-linked at-risk genes were G6PD (G6PD deficiency, 236 couples), DMD (Duchenne muscular dystrophy, 23 couples), and FMR1(fragile X syndrome, 17 couples).After excluding GJB2 c.109G>A, the detection rate of at-risk couples was 3.91%(651/16 669), which was lowered to 1.72%(287/16 669) after further excluding G6PD.The theoretical incidence rate of severe monogenic birth defects was approximately 4.35‰(72.5/16 669).Screening for a battery of the top 22 most frequent genes in the at-risk couples could detect over 95% of at-risk couples, while screening for the top 54 genes further increased the detection rate to over 99%.</p><p><strong>Conclusion: </strong>This study reveals the carrier frequencies of 223 monogenic genetic disorders in the Chinese population and provides evidence for carrier screening strategy development and panel design tailored to the Chinese population.In carrier testing, genetic counseling for specific genes or gene variants can be challenging, and the couples need to be informed of these difficulties before testing and provided with options for not screening these genes or gene variants.</p>","PeriodicalId":18962,"journal":{"name":"Nan fang yi ke da xue xue bao = Journal of Southern Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11237288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141559209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}