Folia neuropathologica最新文献

{"title":"Possible association between cerebral white matter atrophy and impaired performance of activities of daily living in patients with Parkinson's disease.","authors":"Zhi-Hao Lu,&nbsp;Yang-Kun Chen,&nbsp;Xiao-Li Fu,&nbsp;Qi-Ting Chen,&nbsp;Shu-Lan Yuan","doi":"10.5114/fn.2023.127651","DOIUrl":"10.5114/fn.2023.127651","url":null,"abstract":"<p><strong>Introduction: </strong>The contribution of brain abnormalities in patients with Parkinson's disease (PD) to impaired functional status remains uncertain. Our study assessed whether global and regional brain structural abnormalities are associated with impaired performance of activities of daily living (ADL) in PD patients.</p><p><strong>Material and methods: </strong>A retrospective analysis was conducted of 46 patients with PD, recruited prospectively from a movement disorder clinic. Motor impairment and disability were assessed using the Hoehn and Yahr (H-Y) scale and Unified Parkinson's Disease Rating Scale Part III (UPDRS-III). Cognitive status was evaluated with Montreal Cognitive Assessment (MoCA). The performance of ADL was indexed by the sum score of the Physical Self-Maintenance Scale (PSMS) and Lawton Instrumental ADL scale. Brain magnetic resonance imaging (MRI) was performed to assess white matter hyperintensities and medial temporal lobe atrophy (MTLA). Global brain atrophy, indexed by the relative grey matter volume (RGM), relative white matter volume (RWM) and average cortical thickness of the whole brain, was quantified by voxel-based morphometry (VBM).</p><p><strong>Results: </strong>The ADL score (where higher scores indicate poorer performance) negatively correlated with RWM (where greater volume indicates less severe atrophy; r = -0.41, p = 0.004) and RGM (where greater volume indicates less severe atrophy; r = -0.43, p = 0.003) but not with the average cortical thickness ( r = -0.16, p = 0.29). With ADL score as the dependent variable in a linear regression model, H-Y stage and RWM significantly correlated with the ADL score after adjusting for age and MoCA score, and together accounted for 51% of the variance therein. RGM was not significantly correlated with the ADL score after adjusting for age and MoCA score.</p><p><strong>Conclusions: </strong>Cerebral white matter atrophy may be associated with the performance of ADL in patients with PD, indicating an important role of white matter impairment in their functional status.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 3","pages":"266-272"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41196294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"5-HT and S100β values in evaluating severity of cognitive impairment after traumatic brain injury.","authors":"Guan Jin,&nbsp;Yanhao Yang,&nbsp;Feng Bi,&nbsp;Mingyan Yang,&nbsp;Yinhua Ma","doi":"10.5114/fn.2023.125119","DOIUrl":"https://doi.org/10.5114/fn.2023.125119","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of the study was to investigate the relationship between serum serotonin (5-HT) and central nervous system specific protein S100b application value in evaluating the severity of cognitive impairment after traumatic brain injury (TBI).</p><p><strong>Material and methods: </strong>102 patients with TBI treated in Jilin Neuropsychiatric Hospital from June 2018 to October 2020 were selected. According to Montreal Cognitive Assessment (MoCA) scale, patients were tested for cognitive function from multiple levels, such as attention, executive function, memory, and language. Patients with cognitive impairment were included into study group ( n = 64), and those without cognitive impairment were assigned to control group ( n = 58). Serum 5-HT and S100b were compared between the two groups with b level. Serum 5-HT and S100b were analyzed by receiver operating characteristic curve (ROC), b application value judging cognitive impairment.</p><p><strong>Results: </strong>Serum 5-HT and S100b levels in the study group were significantly higher than those in the control group ( p < 0.05). In serum 5-HT and S100b, there was a significant negative correlation with a MoCA score ( r = -0.527, r = -0.436; p < 0.05, p < 0.05). Combined detection of serum 5-HT and S100b's area under ROC curve (AUC) was 0.810 (95% CI: 0.742-0.936, p < 0.05), sensitivity was 0.842, and specificity was 0.813.</p><p><strong>Conclusions: </strong>Serum 5-HT and S100b levels are closely related to the cognitive function of TBI patients. Combined detection is helpful to improve the accuracy of predicting cognitive impairment.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 1","pages":"47-52"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9742713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The neuroprotective effect of Dl-3-n-butylphthalide in epileptic rats via inhibiting endoplasmic reticulum stress.","authors":"Shuang Tian,&nbsp;Zhenzhen Qu,&nbsp;Huifang Cao,&nbsp;Xiaoli Niu,&nbsp;Qi Qiao,&nbsp;Bing Zhang,&nbsp;Lijing Jia,&nbsp;Weiping Wang","doi":"10.5114/fn.2022.123516","DOIUrl":"https://doi.org/10.5114/fn.2022.123516","url":null,"abstract":"<p><strong>Introduction: </strong>The purpose of this study is to investigate whether Dl-3-n-Butylphthalide (NBP) has a neuroprotective effect on pilocarpine-induced epileptic (EP) rats through endoplasmic reticulum stress (ERS)-mediated apoptosis.</p><p><strong>Material and methods: </strong>The Sprague-Dawley rats were divided into four groups: control (CON), EP, EP + NBP 60 (NBP 60 mg/kg) and EP + NBP 120 (NBP 120 mg/kg) groups. After the successful establishment of the temporal lobe EP model using the lithium-pilocarpine, the rats were given NBP for 28 consecutive days in EP + NBP 60 and EP + NBP 120 groups. Then, the spontaneous recurrent seizure (SRS) latency, SRS frequency and seizure duration were observed in each group. In order to observe the abnormal discharge of rats, the intracranial electrodes were implanted to monitor the electroencephalogram. Nissl staining was used to observe the damage to the hippocampal CA1 neurons, TUNEL staining was employed to observe hippocampal neuronal apoptosis. Western blot was used to detect the expression of ERS and ERS-mediated apoptotic proteins.</p><p><strong>Results: </strong>NBP 60 and NBP 120 decreased SRS frequency (all p < 0.05), shortened seizure duration (all p < 0.05), and reduced the abnormal discharge of the brain. Nissl staining and TUNEL staining results show that NBP protected the hippocampal neurons from damage (all p < 0.05) and inhibited hippocampal neuronal apoptosis in EP rats (all p < 0.05). NBP 60 and NBP 120 could reduce ERS and ERS-mediated apoptotic protein expression in EP rats (all p < 0.05). In addition, the therapeutic effect of NBP on epilepsy in rats is dose-dependent. The SRS frequency of the EP + NBP 120 group was lower, and the seizure duration was shorter than in the EP + NBP 60 group (all p < 0.05), and there were more neurons in the EP + NBP 120 group than in the EP + NBP 60 group ( p < 0.05).</p><p><strong>Conclusions: </strong>NBP had a significant neuroprotective effect in EP rats. Large doses of NBP are more effective than low doses. The mechanism may be associated with the inhibition of ERS and ERS-mediated apoptosis.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 2","pages":"185-195"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10017136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of long non-coding RNA LINC00941 suppressed cell proliferation, colony-formation, and migration of human glioblastoma cell lines.","authors":"Yuan Wang,&nbsp;Shuwei Wang,&nbsp;Haibo Wang,&nbsp;Di Zhao,&nbsp;Haoliang Zhang,&nbsp;Huan Liu,&nbsp;Jianzhong Cui,&nbsp;Kaijie Wang","doi":"10.5114/fn.2023.126894","DOIUrl":"https://doi.org/10.5114/fn.2023.126894","url":null,"abstract":"<p><strong>Introduction: </strong>Glioblastoma (GBM) represents the most common and lethal type of primary brain tumour in adults, and due to its high invasiveness, treatment of GBM remains challenging. This work is aimed to elucidate the role of LINC00941 in GBM.</p><p><strong>Material and methods: </strong>Expression of LINC00941 in two GBM cell lines U251 and U87-MG was knocked down using siRNA. Cell proliferation and colony-formation ability of LINC00941 knockdown were examined. Apoptosis of the knockdown was evaluated using flow cytometry, with the levels of Bax, Bcl-2, cleaved caspase-3, and phosphorylation of ERK and Akt to be examined using western blotting. Migration and invasion of the knockdown was studied using transwell assays.</p><p><strong>Results: </strong>Expression of LINC00941 was significantly elevated in GBM compared to non-tumour tissues ( p < 0.01). Statistical analysis on the expression data further revealed the negative correlation between LINC00941 and miR-526b-5p ( r = 0.7494, p < 0.001). LINC00941 was successfully knocked down with RNA interference in U251 and U87-MG. The knockdown significantly suppressed cell proliferation and the ability to form colonies. Percentage of apoptotic cells was elevated by the knockdown in both cell lines as evidenced by flow cytometric analysis, which was accompanied by a significant decrease in Bcl-2 and substantial increases in Bax and cleaved caspase-3. Phosphorylation of ERK and Akt was also enhanced in both cell lines by the knockdown. In addition, knockdown of LINC00941 suppressed migration of both cell lines across transwell membrane and matrigel.</p><p><strong>Conclusions: </strong>LINC00941 is overexpressed in GBM, exhibiting important roles in cell proliferation and survival, migration and invasion.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 2","pages":"209-216"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of synthetic ligand of PPARα in regulation of transcription of genes related to mitochondria biogenesis and dynamic in an animal model of Alzheimer's disease.","authors":"Sylwia Żulińska,&nbsp;Anna K Strosznajder,&nbsp;Joanna B Strosznajder","doi":"10.5114/fn.2023.129195","DOIUrl":"https://doi.org/10.5114/fn.2023.129195","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptors α (PPARα) are members of the nuclear receptors family and a very potent transcription factor engaged in the regulation of lipid and energy metabolism. Recent data suggest that PPARα could play an important role in the pathomechanism of Alzheimer's disease (AD) and other neuropsychiatric disorders. This study focused on the effect of a synthetic ligand of PPARα, GW7647 on the transcription of genes encoding proteins of mitochondria biogenesis and dynamics in the brain of AD mice. The experiments were carried out using 12-month-old female FVB-Tg mice with the V717I mutation of amyloid precursor protein (APP + ) and mice without the transgene (APP - ). Moreover, APP + and APP - mice were treated for 14 days with GW7647 administered subcutaneously with a dose 5 mg/kg b.w. Brain cortex was used and qRT-PCR was performed. Our data indicated that GW7647 upregulated the expression of genes encoding proteins of mitochondria biogenesis in ADTg mice. GW7647 enhanced the level of mRNA of Ppargc1, Nrf2 and Tfam in APP + as compared to APP - mice treated with GW7647. Moreover, our studies demonstrated that GW7647 had no effect on genes that regulate mitochondria fission and fusion of ADTg mice as correlated to mice without the transgene. Our results indicate that the ligand of PPARα, GW7647 may exert a promising neuroprotective effect through the regulation of transcription of genes coding proteins of mitochondria biogenesis. These data suggest that activation of PPARα at an early stage of AD could be a helpful strategy for slowing the progression of neurodegeneration.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 2","pages":"138-143"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10017137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-484 promotes the malignant progression of glioma by inhibiting CDKN2A expression.","authors":"Yingrui Gu,&nbsp;Hongbing Lei,&nbsp;Peipei Ma,&nbsp;Yi Chen","doi":"10.5114/fn.2023.130002","DOIUrl":"https://doi.org/10.5114/fn.2023.130002","url":null,"abstract":"<p><strong>Introduction: </strong>Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) is involved in glioma progression, but the specific molecular mechanism of CDKN2A in glioma cell migration and invasion needs to be further explored.</p><p><strong>Material and methods: </strong>Data related to CDKN2A expression and glioma overall survival were obtained from The Cancer Genome Atlas (TCGA) database. Then, CDKN2A expression in glioma tissues/cells or paracancer tissues/astrocytes was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or Western blot. Afterwards, Wound healing, Transwell and tube formation assay were performed to identify the invasion, migration and angiogenesis of glioma cells, respectively. TargetScan database predicted the targeted binding between miR-484 and CDKN2A, which was verified by dual luciferase reporter gene assay. Western blot and qRT-PCR were performed to detect the expression of VEGF, E-cadherin, N-cadherin and Vimentin in glioma cells.</p><p><strong>Results: </strong>CDKN2A was low-expressed in glioma tissue/cells as compared to paracancer tissue/astrocytes, and was strongly associated to the poor prognosis of glioma. Further studies found that down-regulation of CDKN2A could promote migration, invasion and angiogenesis of glioma cells. Besides, miR-484 was high-expressed in glioma cells compared to astrocytes. Up-regulation of miR-484 could enhance migration, invasion and angiogenesis of glioma cells. In addition, up-regulated miR-484 suppressed the expression of E-cadherin, and promoted the expression of N-cadherin, Vimentin and VEGF. However, there was negative regulation of miR-484 and CDKN2A, and CDKN2A could partially offset the effect of miR-484.</p><p><strong>Conclusions: </strong>MiR-484 promoted cell migration, invasion and angiogenesis by inhibiting CDKN2A expression.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 3","pages":"249-265"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41196292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor","authors":"Yuhao Peng, Xiaoling Hu, Haifeng He, Xinting Zhou, Zhonghui Luo","doi":"10.5114/fn.2023.131556","DOIUrl":"https://doi.org/10.5114/fn.2023.131556","url":null,"abstract":"AMA Peng Y, Hu X, He H, Zhou X, Luo Z. Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131556. APA Peng, Y., Hu, X., He, H., Zhou, X., & Luo, Z. (2023). Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131556 Chicago Peng, Yuhao, Xiaoling Hu, Haifeng He, Xinting Zhou, and Zhonghui Luo. 2023. \"Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor\". Folia Neuropathologica. doi:10.5114/fn.2023.131556. Harvard Peng, Y., Hu, X., He, H., Zhou, X., and Luo, Z. (2023). Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131556 MLA Peng, Yuhao et al. \"Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.131556. Vancouver Peng Y, Hu X, He H, Zhou X, Luo Z. Dexmedetomidine promotes the functional recovery of mice after acute ischemic stroke via activation of the α2-adrenoceptor. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131556.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"47 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136302706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway","authors":"Yuan Gao, Jiang Liu, Xiaoyan Wang, Qiang Meng","doi":"10.5114/fn.2023.131191","DOIUrl":"https://doi.org/10.5114/fn.2023.131191","url":null,"abstract":"AMA Gao Y, Liu J, Wang X, Meng Q. Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131191. APA Gao, Y., Liu, J., Wang, X., & Meng, Q. (2023). Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131191 Chicago Gao, Yuan, Jiang Liu, Xiaoyan Wang, and Qiang Meng. 2023. \"Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway\". Folia Neuropathologica. doi:10.5114/fn.2023.131191. Harvard Gao, Y., Liu, J., Wang, X., and Meng, Q. (2023). Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131191 MLA Gao, Yuan et al. \"Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.131191. Vancouver Gao Y, Liu J, Wang X, Meng Q. Vanillin attenuates oxidative stress and neurochemical balance in MPTP-induced Parkinson’s disease mice by regulating the TLR-4 inflammatory pathway. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131191.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"96 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135496322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours","authors":"Michał Sobstyl, Ewa Nagańska, Piotr Glinka, Teresa Wierzba-Bobrowicz, Albert Acewicz, Aleksandra Kuls-Oszmaniec","doi":"10.5114/fn.2023.131640","DOIUrl":"https://doi.org/10.5114/fn.2023.131640","url":null,"abstract":"AMA Sobstyl M, Nagańska E, Glinka P, Wierzba-Bobrowicz T, Acewicz A, Kuls-Oszmaniec A. Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131640. APA Sobstyl, M., Nagańska, E., Glinka, P., Wierzba-Bobrowicz, T., Acewicz, A., & Kuls-Oszmaniec, A. (2023). Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131640 Chicago Sobstyl, Michał, Ewa Nagańska, Piotr Glinka, Teresa Wierzba-Bobrowicz, Albert Acewicz, and Aleksandra Kuls-Oszmaniec. 2023. \"Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours\". Folia Neuropathologica. doi:10.5114/fn.2023.131640. Harvard Sobstyl, M., Nagańska, E., Glinka, P., Wierzba-Bobrowicz, T., Acewicz, A., and Kuls-Oszmaniec, A. (2023). Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. https://doi.org/10.5114/fn.2023.131640 MLA Sobstyl, Michał et al. \"Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours.\" Folia Neuropathologica, 2023. doi:10.5114/fn.2023.131640. Vancouver Sobstyl M, Nagańska E, Glinka P, Wierzba-Bobrowicz T, Acewicz A, Kuls-Oszmaniec A. Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and consistence of meningioma – a case of collision tumours. Folia Neuropathologica. 2023. doi:10.5114/fn.2023.131640.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"37 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136007887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00470 represses cell autophagy and cisplatin sensitivity of glioma via suppressing PTEN expression.","authors":"Biyin Chen,&nbsp;Wenwu Wang,&nbsp;Fangfeng Lin,&nbsp;Shuping Shi,&nbsp;Shunjie Ou,&nbsp;Yunqiu Yu","doi":"10.5114/fn.2023.125327","DOIUrl":"https://doi.org/10.5114/fn.2023.125327","url":null,"abstract":"<p><strong>Introduction: </strong>Glioma is one of primary brain tumours which has the worst clinical prognoses of patients. As an alternative chemotherapeutic drug for malignant glioma, the therapeutic effect of cisplatin (CDDP) is devastatingly affected due to resistance in patients. In this study, we investigated the effect of LINC00470/PTEN on the CDDP sensitivity of glioma cells.</p><p><strong>Material and methods: </strong>Differentially expressed lncRNAs and the downstream regulators in glioma tissue were obtained via bioinformatics analysis. LINC00470 and PTEN mRNA expression levels were detected using qRT-PCR. IC50 values of glioma cells were examined using Cell Counting Kit-8 (CCK-8). Cell apoptosis was revealed by flow cytometry. The expression level of autophagy-related protein was detected by western blot. Intracellular autophagosome formation was detected by immunofluorescence staining, and the methylation level of PTEN promoter was detected via methylation-specific PCR (MSP).</p><p><strong>Results: </strong>Through the above steps, we found that LINC00470 was highly expressed in glioma cells, and the survival rate of patients was reduced in the presence of high expression of LINC00470. Silenced LINC00470 promoted LC3 II expression and autophagosome formation, and facilitated cell apoptosis to inhibit resistance to CDDP. While silenced PTEN could successfully reverse the previous effects on glioma cells.</p><p><strong>Conclusions: </strong>Based on the above, LINC00470 repressed cell autophagy by constraining PTEN, thereby enhancing CDDP resistance of glioma cells.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"61 1","pages":"88-96"},"PeriodicalIF":2.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9398471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}