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Mueller matrix polarimetry (MMP) has been demonstrated and recognized as an effective approach to attaining imaging enhancement as well as revealing polarization properties of an imaged sample. Generally, a minimum of 16 combinations of intensity-only measurements involving both linear and circular polarizations are required to completely and accurately determine the 4 × 4 Mueller matrix (MM) and comprehensively describe the polarization properties of the sample. However, broadband circular polarizations (CP) are rather difficult to obtain for design and fabrication limitations in the terahertz region, which poses a challenge to the acquisition of the 4 × 4 MM. In this circumstance, the 3 × 3 MM degradation using only linear polarizations (LP) is preferred and sufficient for characterization of non-depolarizing samples. In this paper, a multi-spectral 3 × 3 MMP system based on the THz time-domain spectroscopy (THz-TDS) is established from 0.1 to 1 THz. The system demonstrated is capable of fulfilling the accurate determination of the 3 × 3 MM. The Mueller matrix polar decomposition (MMPD), modified to be compatible with the MM degradation, is employed to explore the fine details and properties of the sample. By signal post-processing techniques, the MM elements in the time domain are retrieved, and the time dimension reflecting the depth information facilitates the 3D reconstruction of the sample. This work provides a prototype for 3D imaging of biological samples at higher frequencies in the future.
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BACKGROUND: Long non-coding RNAs (lncRNAs) are extensively intricate in the tumorigenesis and metastasis of various cancer types. Nevertheless, the detailed molecular mechanisms of lncRNA in non-small cell lung cancer (NSCLC) still remain mainly undetermined. METHODS: qPCR was performed to verify LINC00301 expression in NSCLC clinical specimens or cell lines. Fluorescence in situ hybridization (FISH) was conducted to identify the localization of LINC00301 in NSCLC cells. Chromatin immunoprecipitation (ChIP) was subjected to validate the binding activity between FOXC1 and LINC00301 promoters. RNA immunoprecipitation (RIP) was performed to explore the binding activity between LINC00301 and EZH2. RNA pull-down followed by dot-blot, protein domain mapping, and RNA electrophoresis mobility shift assay (EMSA) were conducted to identify the detailed binding regions between LINC00301 and EZH2. Alpha assay was conducted to quantitatively assess the interaction between LINC00301 and EZH2. RESULTS: LINC00301 is highly expressed in NSCLC and closely corelated to its prognosis by analyzing the relationship between differentially expressed lncRNAs and prognosis in NSCLC samples. in vitro and in vivo experiments revealed that LINC00301 facilitates cell proliferation, releases NSCLC cell cycle arrest, promotes cell migration and invasion, and suppresses cell apoptosis in NSCLC. In addition, LINC00301 increases regulatory T cell (Treg) while decreases CD8+ T cell population in LA-4/SLN-205-derived tumors through targeting TGF-ß. The transcription factor FOXC1 mediates LINC00301 expression in NSCLC. Bioinformatics prediction and in vitro experiments indicated that LINC00301 (83-123 nucleotide [nt]) can directly bind to the enhancer of zeste homolog 2 (EZH2) (612-727 amino acid [aa]) to promote H3K27me3 at the ELL protein-associated factor 2 (EAF2) promoter. EAF2 directly binds and stabilizes von Hippel-Lindau protein (pVHL), so downregulated EAF2 augments hypoxia-inducible factor 1 α (HIF1α) expression by regulating pVHL in NSCLC cells. Moreover, we also found that LINC00301 could function as a competing endogenous RNA (ceRNA) against miR-1276 to expedite HIF1α expression in the cytoplasm of NSCLC cells. CONCLUSIONS: In summary, our present research revealed the oncogenic roles of LINC00301 in clinical specimens as well as cellular and animal experiments, illustrating the potential roles and mechanisms of the FOXC1/LINC00301/EZH2/EAF2/pVHL/HIF1α and FOXC1/LINC00301/miR-1276/HIF1α pathways, which provides novel insights and potential theraputic targets to NSCLC.
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Carcinoma Pulmonar de Células não Pequenas/etiologia , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Fatores de Transcrição Forkhead/metabolismo , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Imunomodulação/genética , Neoplasias Pulmonares/etiologia , Neoplasias Pulmonares/metabolismo , RNA Longo não Codificante/genética , Microambiente Tumoral/genética , Animais , Sítios de Ligação , Carcinoma Pulmonar de Células não Pequenas/mortalidade , Carcinoma Pulmonar de Células não Pequenas/patologia , Ciclo Celular/genética , Linhagem Celular Tumoral , Metilação de DNA , Modelos Animais de Doenças , Progressão da Doença , Regulação Neoplásica da Expressão Gênica , Histonas/metabolismo , Humanos , Neoplasias Pulmonares/mortalidade , Neoplasias Pulmonares/patologia , Camundongos , Motivos de Nucleotídeos , Prognóstico , Regiões Promotoras Genéticas , Ligação Proteica , Transdução de Sinais , Subpopulações de Linfócitos T/imunologia , Subpopulações de Linfócitos T/metabolismo , Microambiente Tumoral/imunologiaRESUMO
Maspin has been identified as a tumor suppressor gene in breast cancer, but the underlying regulatory mechanisms remain unclear. In the present study, maspin pcDNA was transfected into MCF-7 cells. microRNA (miR) microarray and reverse transcription-quantitative polymerase chain reaction was used for analysis; the results demonstrated that maspin may inhibit miR-10b, miR-21 and miR-451 expression in MCF-7 cells. In addition, maspin increased the expression of certain miR-21 target genes (phosphatase and tensin homolog, programmed cell death 4 and B-cell lymphoma-2), miR-10b target gene (Homeobox D10; HOXD10) and miR-451 target gene (multidrug resistance protein 1). Furthermore, the results of the present study revealed that decreased expression of miR-21 suppressed the invasion and proliferation of MCF-7 cells. Therefore, in the present study, it was hypothesized that as a tumor-suppressor gene, the potential molecular mechanism of maspin include down-regulating the expression of miR-21 and increasing the expression of specific miR-21 target genes.
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OBJECTIVE: The present study aimed to characterize the mechanism of fluid shear stress (FSS)-induced endothelial cell (EC) injury via protein kinase C alpha (PKCα)-mediated vascular endothelial cadherin (VE-cadherin) and p120-catenin (p120ctn) expression. METHODS: We designed a T chamber system that produced stable FSS on ECs in vitro. Human umbilical vein endothelial cells (HUVECs) in which PKCα was knocked down and normal HUVECs were cultured on the coverslips. FSS was impinged on these 2 types of ECs for 0 hours and 6 hours. The morphology and density of HUVECs were evaluated, and expression levels of phosphorylated PKCα, p120-catenin (p120ctn), VE-cadherin, phosphorylated p120ctn at S879 (p-S879p120ctn), and nuclear factor kappa B (NF-κB) were analyzed by Western blot. RESULTS: HUVECs exposed to FSS were characterized by a polygonal shape and decreased cell density. The phosphorylated PKCα level was increased under FSS at 6 hours (P < 0.05). In normal HUVECs during FSS, p120ctn and VE-cadherin were decreased, whereas p-S879p120ctn and NF-κB were increased, at 6 hours (P < 0.05). In HUVECs after PKCα knockdown, p120ctn and VE-cadherin were not significantly changed (P > 0.05), p-S879p120ctn was undetectable, but NF-κB was decreased (P < 0.05) at 6 hours. CONCLUSIONS: The possible mechanism of FSS-induced EC injury may be as follows: 1) PKCα induces low expression of p120ctn, which leads to activation of NF-κB and degradation of VE-cadherin; 2) PKCα-mediated phosphorylation of p120ctn at S879 disrupts p120ctn binding to VE-cadherin.
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Antígenos CD/metabolismo , Caderinas/metabolismo , Cateninas/metabolismo , Células Endoteliais da Veia Umbilical Humana/fisiologia , Proteína Quinase C-alfa/metabolismo , Estresse Fisiológico/fisiologia , Endotélio Vascular/citologia , Endotélio Vascular/fisiologia , Técnicas de Silenciamento de Genes , Humanos , delta CateninaRESUMO
BACKGROUND: Lung cancer is still one of the most serious causes of cancer-related deaths all over the world. MicroRNAs (miRNAs) are defined as small non-coding RNAs which could play a pivotal role in post-transcriptional regulation of gene expression. Increasing evidence demonstrated dysregulation of miRNA expression associates with the development and progression of NSCLC. AIMS: To emphasize a variety of tissue-specific miRNAs, circulating miRNAs and miRNA-derived exosomes could be used as potential diagnostic and therapeutic biomarkers in NSCLC patients. MATERIALS & METHODS: In the current review, we paid attention to the significant discoveries of preclinical and clinical studies, which performed on tissue-specific miRNA, circulating miRNA and exosomal miRNA. The related studies were obtained through a systematic search of Pubmed, Web of Science, Embase. RESULTS: A variety of tissue-specific miRNAs and circulating miRNAs with high sensitivity and specificity which could be used as potential diagnostic and therapeutic biomarkers in NSCLC patients. In addition, we emphasize that the miRNA-derived exosomes become novel diagnostic biomarkers potentially in these patients with NSCLC. CONCLUSION: MiRNAs have emerged as non-coding RNAs, which have potential to be candidates for the diagnosis and therapy of NSCLC.
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Biomarcadores Tumorais/genética , Carcinoma Pulmonar de Células não Pequenas/diagnóstico , Carcinoma Pulmonar de Células não Pequenas/terapia , Regulação Neoplásica da Expressão Gênica/genética , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/terapia , MicroRNAs/genética , Animais , Carcinoma Pulmonar de Células não Pequenas/genética , Exossomos/genética , Exossomos/metabolismo , Perfilação da Expressão Gênica/métodos , Humanos , Neoplasias Pulmonares/genéticaRESUMO
OBJECTIVE: Epidemiological studies suggested that poor sleep is a potentially novel risk factor for several health outcomes currently; however, there are no validated questionnaires that can systematically measure sleep parameters within these studies. We evaluated the reliability and validity of 17-item sleep factors questionnaire (SFQ), which was developed to comprehensively assess long-term sleep habits for the Jiujiang Breast Cancer Study (JBCS), Jiujiang, China. METHODS: The participants included 100 women aged 18-74years, who were randomly selected from the JBCS project, and completed a SFQ at baseline and again 1year later, and 4 quarterly 30 consecutive days (a total of 120days) sleep diaries over this same year. Reliability was tested by comparing the 2 SFQs; validity by comparing the average measures between the SFQ and the 4 sleep diaries. RESULTS: Validity analysis showed moderate correlation (γ=0.41) for sleep duration with the adjusted concordance correlation coefficient (CCCadj) of 0.54; the weighted κ statistics indicated an excellent agreement for night/shift work and sleep medication use; fair-to-moderate for sleep quality, light at night (LAN), nighttime sleeping with light on, sleep noise and nap time; slight-to-fair for sleep quality and nighttime wakings frequency. Reliability analysis showed excellent correlation for night/shift work and sleep medication use; fair-to-moderate for LAN, nighttime wakings frequency, insomnia frequency, sleep noise and nap time; but slight-to-fair for insomnia frequency and nighttime sleeping with light on; the CCCadj for sleep duration was 0.61. CONCLUSIONS: The SFQ showed reasonable reliability and validity for sleep assessments in most domains.
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Hábitos , Prontuários Médicos/normas , Distúrbios do Início e da Manutenção do Sono/diagnóstico , Distúrbios do Início e da Manutenção do Sono/epidemiologia , Sono/fisiologia , Inquéritos e Questionários/normas , Adolescente , Adulto , Idoso , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/epidemiologia , China/epidemiologia , Estudos Epidemiológicos , Feminino , Seguimentos , Humanos , Pessoa de Meia-Idade , Reprodutibilidade dos Testes , Fatores de Risco , Fatores de Tempo , Adulto JovemRESUMO
In this study, we searched multiple databases for all relevant original articles (1996-2013). To investigate blood lead levels (BLL) and possible risk factors for lead exposure among children in China A total of 388 articles met our inclusion criteria. The overall geometric mean (GM) BLL was 71 µg/L, and the prevalence of elevated BLL (EBLL, defined as BLL â 100 µg/L) was 18.48% among children. The prevalence of EBLL remained significantly higher among boys. In children less than 6 years of age, there were significantly increasing trends in both BLL and prevalence of EBLL in an age-dependent manner. The ban on leaded gasoline significantly reduced the BLL as well as EBLL prevalence; however, children whose parents had lower educational levels or were exposed to lead in the workplace had a higher EBLL prevalence. Despite its decline over time, the average BLL among children in China remains higher than the average level most recently reported in the United States. Childhood lead poisoning remains a public health problem in China.