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1.
Front Neurosci ; 16: 892022, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35784838

RESUMO

Objective: To investigate the potential pathogenic mechanism of temporal lobe epilepsy with hippocampal sclerosis (TLE+HS) by analyzing the expression profiles of microRNA/ mRNA/ lncRNA/ DNA methylation in brain tissues. Methods: Brain tissues of six patients with TLE+HS and nine of normal temporal or parietal cortices (NTP) of patients undergoing internal decompression for traumatic brain injury (TBI) were collected. The total RNA was dephosphorylated, labeled, and hybridized to the Agilent Human miRNA Microarray, Release 19.0, 8 × 60K. The cDNA was labeled and hybridized to the Agilent LncRNA+mRNA Human Gene Expression Microarray V3.0,4 × 180K. For methylation detection, the DNA was labeled and hybridized to the Illumina 450K Infinium Methylation BeadChip. The raw data was extracted from hybridized images using Agilent Feature Extraction, and quantile normalization was performed using the Agilent GeneSpring. P-value < 0.05 and absolute fold change >2 were considered the threshold of differential expression data. Data analyses were performed using R and Bioconductor. BrainSpan database was used to screen for signatures that were not differentially expressed in normal human hippocampus and cortex (data from BrainSpan), but differentially expressed in TLE+HS' hippocampus and NTP' cortex (data from our cohort). The strategy "Guilt by association" was used to predict the prospective roles of each important hub mRNA, miRNA, or lncRNA. Results: A significantly negative correlation (r < -0.5) was found between 116 pairs of microRNA/mRNA, differentially expressed in six patients with TLE+HS and nine of NTP. We examined this regulation network's intersection with target gene prediction results and built a lncRNA-microRNA-Gene regulatory network with structural, and functional significance. Meanwhile, we found that the disorder of FGFR3, hsa-miR-486-5p, and lnc-KCNH5-1 plays a key vital role in developing TLE+HS.

2.
mSystems ; 6(4): e0074821, 2021 Aug 31.
Artigo em Inglês | MEDLINE | ID: mdl-34427528

RESUMO

Culturing unculturable bacteria is a classic microbiology challenge; to successfully culture unculturable bacteria, microbiologists work hard to create hundreds of culture conditions. To improve the success rate and efficiency of culturing a broad spectrum of environmental microbes, it is helpful to know more about the microbial community composition. Shortening the amount of time spent sequencing, analyzing sequencing data, and predicting suitable culture conditions seems to be a critical step for improving knowledge of microbes in environmental samples and expanding culture collections. In this commentary, we introduce potential strategies using rapid and portable sequencing devices to help scientists design and plan for specific microbial culture media on their way back to the laboratory. Rapid metagenomic sequencing approaches and real-time analysis make it possible to choose microbes we are interested in and discover novel microbes in environments for cultivation.

3.
Oncol Rep ; 32(5): 2104-10, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25175832

RESUMO

A number of microRNAs have been identified to be important regulators of tumorigenesis. Previous research has shown that miR-124 is abundantly expressed in normal brain tissue; however, only a few reports have focused on the biological impact of miR-124 on glioma cells, and the underlying mechanisms need to be elucidated. Therefore, we investigated the effect of miR-124a on glioma cell proliferation and invasion; furthermore, the underlying molecular mechanism was examined. The present study demonstrated that miR-124a expression was downregulated in human glioma tissues, and its expression level was negatively correlated with the pathological grade of the glioma. Restoration of miR-124a inhibited glioma cell proliferation and invasion in vitro. Furthermore, we found that miR-124a directly targeted and suppressed IQ motif containing GTPase activating protein 1 (IQGAP1), a well-known regulator of actin dynamics and cell motility. RNA interference assay showed that IQGAP1 knockdown led to downregulation of ß-catenin and downstream cyclin D1. Taken together, our study revealed that miR-124a could inhibit glioma cell proliferation and invasion by blocking the expression of the IQGAP1 gene and downstream ß-catenin and cyclin D1. This research may provide a useful molecular therapy for gliomas.


Assuntos
Glioma/patologia , MicroRNAs/genética , Proteínas Ativadoras de ras GTPase/genética , Proteínas Ativadoras de ras GTPase/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Glioma/genética , Glioma/metabolismo , Humanos , Invasividade Neoplásica , beta Catenina/genética , beta Catenina/metabolismo
4.
Med Oncol ; 30(1): 372, 2013 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-23315217

RESUMO

Moesin, a member of the ERM family, acts as a linker between the actin cytoskeleton and the plasma membrane and plays a key role in the control of cell morphology, motility, adhesion and other processes of tumourigenesis. The expression pattern and clinical significance of moesin in astrocytoma remain unknown. In this study, we used RT-PCR to systematically investigate the expression of moesin in 49 astrocytomas of different pathological grade and 6 normal brain tissues. We found that the mRNA expression levels of moesin in astrocytomas were significantly higher in comparison with normal brain tissues. Furthermore, moesin up-regulation was correlated with pathological grade of astrocytomas. Subsequently, we tested 112 astrocytomas and 14 normal brain tissues by immunohistochemistry. Similar results were also confirmed. Univariate and multivariate survival analysis were used to determine the correlations of moesin expression with overall survival and progression-free survival. Our results showed the expression of moesin was strongly negatively correlated with the patient progression-free survival and overall survival. These results suggest moesin protein involved in the genesis and progression of astrocytomas and might be regarded as an independent predictor of poor prognosis.


Assuntos
Astrocitoma/metabolismo , Biomarcadores Tumorais/análise , Neoplasias Encefálicas/metabolismo , Proteínas dos Microfilamentos/biossíntese , Adolescente , Adulto , Idoso , Astrocitoma/mortalidade , Astrocitoma/patologia , Neoplasias Encefálicas/mortalidade , Neoplasias Encefálicas/patologia , Criança , Pré-Escolar , Intervalo Livre de Doença , Feminino , Humanos , Imuno-Histoquímica , Masculino , Proteínas dos Microfilamentos/análise , Pessoa de Meia-Idade , Gradação de Tumores , RNA Mensageiro/análise , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Resultado do Tratamento , Adulto Jovem
5.
J Clin Neurosci ; 19(12): 1700-5, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23084350

RESUMO

Aldehyde dehydrogenase 1 (ALDH1), a detoxifying enzyme, is a stem-like cell marker, but its expression pattern and clinical significance in astrocytoma remain unclear. In this study, we used immunohistochemical analysis to systematically investigate the expression of ALDH1 in 76 astrocytomas of different pathological grade and seven samples of normal brain tissues. We found that ALDH1 was expressed in some of the astrocytomas but was not detected in normal brain tissues. The proportion of ALDH1-expressing cells was positively correlated with the pathological grade of the astrocytomas, but not with patient age, sex or tumor size. We also collected detailed follow-up data and analyzed the correlation of ALDH1 expression with overall survival (OS) and progression-free survival (PFS) using univariate and multivariate analysis. We found that the proportion of ALDH1-positive cells was an independent prognostic factor for PFS and OS. These results show that ALDH1 is expressed in astrocytoma, and that its expression is correlated with pathological grade and patient survival.


Assuntos
Astrocitoma/enzimologia , Astrocitoma/patologia , Neoplasias Encefálicas/enzimologia , Neoplasias Encefálicas/patologia , Isoenzimas/biossíntese , Retinal Desidrogenase/biossíntese , Adolescente , Adulto , Família Aldeído Desidrogenase 1 , Astrocitoma/mortalidade , Biomarcadores Tumorais/análise , Neoplasias Encefálicas/mortalidade , Intervalo Livre de Doença , Feminino , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Gradação de Tumores , Prognóstico , Modelos de Riscos Proporcionais , Resultado do Tratamento , Adulto Jovem
6.
Turk Neurosurg ; 22(5): 547-57, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23015330

RESUMO

AIM: We present the long-term outcomes as well as their correlation with tumor size in 127 consecutive patients harboring large MSWM after microsurgical treatment. MATERIAL AND METHODS: The retrospective analysis of clinical data and follow-up data of 127 microsurgical treated patients with MSWM was performed. The mean maximum diameter of tumors was 5.2cm (ranged 1.5-10.0cm). RESULTS: 104 cases (81.9%) achieved gross total resection. There was no operative mortality. Detailed follow-up data was available in 120 cases for a mean duration of 81.6 months (12-216 months). The permanent morbidity was 14.2%. The mean KPS score 1 year after surgery was 90.6 (ranged 60-100). Among 74 patients of preoperative visual acuity (VA) impairment, postoperative VA improved in 42 cases (56.8%), unchanged in 30 (40.5%), and deteriorated in 2 (2.7%). MR images revealed tumor recurrence after total resection in 10 cases (10.2%) and tumor progression after subtotal resection in 10 cases (45.5%). CONCLUSION: Tumor recurrence was the major risk in the long run, thus the initial surgery was extremely important and hence should be aggressive. The size of tumor affected the extent of tumor removal determining clinical outcomes including VA improvement and KPS score immediately after surgery; however, it was not correlated with long-term overall outcomes.


Assuntos
Meningioma/patologia , Meningioma/cirurgia , Microcirurgia/métodos , Procedimentos Neurocirúrgicos/métodos , Neoplasias Cranianas/patologia , Neoplasias Cranianas/cirurgia , Osso Esfenoide/patologia , Osso Esfenoide/cirurgia , Adolescente , Adulto , Idoso , Criança , Progressão da Doença , Feminino , Seguimentos , Humanos , Avaliação de Estado de Karnofsky , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia , Exame Neurológico , Complicações Pós-Operatórias/epidemiologia , Qualidade de Vida , Estudos Retrospectivos , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Adulto Jovem
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