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1.
Chin Med J (Engl) ; 2021 Sep 16.
Artigo em Inglês | MEDLINE | ID: mdl-34665571

RESUMO

Backgrounds: Azithromycin mass drug administration (MDA) is a key part of the strategy for controlling trachoma. This systematic review aimed to comprehensively summarize the present studies of azithromycin MDA on trachoma; provide an overview of the impact of azithromycin MDA on trachoma in different districts; and explore the possible methods to enhance the effectiveness of azithromycin MDA in hyperendemic districts. Methods: PubMed, Embase, the Cochrane Central Register of Controlled Trials, Web of Science, and ClinicalTrials.gov were searched up to February 2021 with no language restriction. Studies reporting the effect of azithromycin MDA on trachoma were included. Mathematical modeling studies, animal studies, case reports, and reviews were excluded. The trachomatous inflammation-follicular (TF) <5.0% was used to judge the effect of azithromycin MDA on eliminating trachoma as a public health problem. Two researchers independently conducted the selection process and risk of bias assessment. Results: A total of 1543 studies were screened, of which 67 studies including 13 cluster-randomized controlled trials and 54 non-randomized studies were included. The effect of azithromycin MDA on trachoma was closely related to the baseline prevalence in districts. For the districts with baseline prevalence between 5.0% and 9.9%, a single round of MDA achieved a TF <5.0%. For the districts with baseline between 10.0% and 29.9%, annual MDA for 3 to 5 years reduced TF <5.0%. However, for the districts with high level of baseline prevalence (TF >30.0%), especially with baseline TF >50.0%, annual MDA was unable to achieve the TF <5.0% even after 5 to 7 years of treatment. Quarterly MDA is more effective in controlling trachoma in these hyperendemic districts. Conclusions: Azithromycin MDA for controlling trachoma depends on the baseline prevalence. The recommendation by the World Health Organization that annual MDA for 3 to 5 years in the districts with TF baseline >10.0% is not appropriate for all eligible districts.

2.
ACS Appl Mater Interfaces ; 13(33): 39719-39729, 2021 Aug 25.
Artigo em Inglês | MEDLINE | ID: mdl-34392680

RESUMO

In this work, cucurbiturils (CBs), a class of macrocyclic supramolecules, were observed to have an interesting peroxidase-like activity, which is metal-free, substrate-specific, thermophilic, acidophilic, and insensitive to ionic strength. By coating CBs on enzyme-encapsulated zeolitic imidazolate framework-8 (ZIF-8), a composite nanozyme was constructed, which retains the catalytic ability of CBs and enzymes and makes them cascade. On addition of the substrate, i.e., the detection target, a highly efficient cascade catalysis can be launched in all the spatial directions to generate sensitive and visible signals. Convenient detection of glucose and cholesterol as models is thereby achieved. More importantly, we have also successfully constructed a composite nanozyme-based sensor array (6 × 8 wells) and thereby achieved simultaneous colorimetric analysis of multiple samples. The concept and successful practice of the construction of the unique core-shell supramolecule/biomolecule@nanomaterial architecture provide the possibility to fabricate next-generation multifunctional materials and create new applications by integrating their unique functions.


Assuntos
Hidrocarbonetos Aromáticos com Pontes/química , Imidazóis/química , Nanocompostos/química , Peroxidases/química , Zeolitas/química , Técnicas Biossensoriais , Hidrocarbonetos Aromáticos com Pontes/metabolismo , Catálise , Colorimetria , Corantes Fluorescentes/química , Glucose Oxidase/química , Glucose Oxidase/metabolismo , Peróxido de Hidrogênio/química , Imidazóis/metabolismo , Simulação de Acoplamento Molecular , Oxirredução , Peroxidases/metabolismo , Impressão Tridimensional
3.
Aging (Albany NY) ; 13(8): 11833-11859, 2021 04 22.
Artigo em Inglês | MEDLINE | ID: mdl-33885377

RESUMO

Transcriptome differences between Hodgkin's lymphoma (HL), diffuse large B-cell lymphoma (DLBCL), and mantle cell lymphoma (MCL), which are all derived from B cell, remained unclear. This study aimed to construct lymphoma-specific diagnostic models by screening lymphoma marker genes. Transcriptome data of HL, DLBCL, and MCL were obtained from public databases. Lymphoma marker genes were screened by comparing cases and controls as well as the intergroup differences among lymphomas. A total of 9 HL marker genes, 7 DLBCL marker genes, and 4 MCL marker genes were screened in this study. Most HL marker genes were upregulated, whereas DLBCL and MCL marker genes were downregulated compared to controls. The optimal HL-specific diagnostic model contains one marker gene (MYH2) with an AUC of 0.901. The optimal DLBCL-specific diagnostic model contains 7 marker genes (LIPF, CCDC144B, PRO2964, PHF1, SFTPA2, NTS, and HP) with an AUC of 0.951. The optimal MCL-specific diagnostic model contains 3 marker genes (IGLV3-19, IGKV4-1, and PRB3) with an AUC of 0.843. The present study reveals the transcriptome data-based differences between HL, DLBCL, and MCL, when combined with other clinical markers, may help the clinical diagnosis and prognosis.


Assuntos
Biomarcadores Tumorais/genética , Doença de Hodgkin/diagnóstico , Linfoma Difuso de Grandes Células B/diagnóstico , Linfoma de Célula do Manto/diagnóstico , Modelos Genéticos , Estudos de Casos e Controles , Conjuntos de Dados como Assunto , Diagnóstico Diferencial , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Doença de Hodgkin/genética , Doença de Hodgkin/mortalidade , Humanos , Linfoma Difuso de Grandes Células B/genética , Linfoma Difuso de Grandes Células B/mortalidade , Linfoma de Célula do Manto/genética , Linfoma de Célula do Manto/mortalidade , Estadiamento de Neoplasias , Prognóstico , Intervalo Livre de Progressão , Transcriptoma/genética
4.
Oncol Rep ; 45(3): 1235-1248, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33650672

RESUMO

Breast cancer is the most common type of cancer amongst women worldwide, and numerous microRNAs (miRNAs/miRs) are involved in the initiation and progression of breast cancer. The aim of the present study was to identify hub miRNAs and determine the underlying mechanisms regulated by these miRNAs in breast cancer. Breast invasive carcinoma transcriptome data (including mRNAs and miRNAs), and clinical data were acquired from The Cancer Genome Atlas database. Differential gene expression analysis, co­expression network analysis, gene set enrichment analysis (GSEA) and prognosis analysis were used to screen the hub miRNAs and explore their functions. Functional experiments were used to determine the underlying mechanisms of the hub miRNAs in breast cancer cells. The results revealed that low miR150 expression predicted a more advanced disease stage, and was associated with a less favorable prognosis. Through the combined use of five miRNA­target gene prediction tools, 31 potential miR150 target genes were identified. GSEA revealed that low miR150 expression was associated with the upregulation of several cancer­associated signaling pathways, and the downregulation of several tumor suppressor genes. Furthermore, miR150 independently affected overall survival in patients, and interacted with its target genes to indirectly affect overall and disease­free survival. Functional experiments demonstrated that miR150 positively regulated B and T lymphocyte attenuator (BTLA), and the downregulation of miR150 and BTLA combined promoted cell migration. In conclusion, the present study revealed that low miR150 expression was associated with less favorable clinical features, upregulation of several carcinogenic signaling pathways, and poor patient survival. Additionally, a miR150­BTLA axis was suggested to regulate cell viability and migration.


Assuntos
Neoplasias da Mama/genética , Carcinogênese/genética , MicroRNAs/genética , Neoplasias da Mama/mortalidade , Neoplasias da Mama/patologia , Carcinogênese/patologia , Linhagem Celular Tumoral , Movimento Celular , Sobrevivência Celular , Feminino , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/metabolismo , Prognóstico , Receptores Imunológicos/genética , Receptores Imunológicos/metabolismo , Transdução de Sinais , Análise de Sobrevida
5.
Neurotherapeutics ; 18(2): 1064-1080, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33786807

RESUMO

Brain capillaries are crucial for cognitive functions by supplying oxygen and other nutrients to and removing metabolic wastes from the brain. Recent studies have demonstrated that constriction of brain capillaries is triggered by beta-amyloid (Aß) oligomers via endothelin-1 (ET1)-mediated action on the ET1 receptor A (ETRA), potentially exacerbating Aß plaque deposition, the primary pathophysiology of Alzheimer's disease (AD). However, direct evidence is still lacking whether changes in brain capillaries are causally involved in the pathophysiology of AD. Using APP/PS1 mouse model of AD (AD mice) relative to age-matched negative littermates, we identified that reductions of density and diameter of hippocampal capillaries occurred from 4 to 7 months old while Aß plaque deposition and spatial memory deficit developed at 7 months old. Notably, the injection of ET1 into the hippocampus induced early Aß plaque deposition at 5 months old in AD mice. Conversely, treatment of ferulic acid against the ETRA to counteract the ET1-mediated vasoconstriction for 30 days prevented reductions of density and diameter of hippocampal capillaries as well as ameliorated Aß plaque deposition and spatial memory deficit at 7 months old in AD mice. Thus, these data suggest that reductions of density and diameter of hippocampal capillaries are crucial for initiating Aß plaque deposition and spatial memory deficit at the early stages, implicating the development of new therapies for halting or curing memory decline in AD.

6.
BMC Pediatr ; 21(1): 127, 2021 03 15.
Artigo em Inglês | MEDLINE | ID: mdl-33722228

RESUMO

BACKGROUND: Enterovirus (EV) is a common cause of infection in neonates. Neonates are at high risk of enterovirus infection with serious clinical manifestations and high lethality. This review systematically summarized the clinical characteristics of neonates with severe enteroviral infection to provide evidence for the identification and treatment of severe neonatal EV infection. METHODS: PubMed, Embase, and Web of Science were searched for original studies on neonates with severe EV infections from January 1, 2000, to November 27, 2020. Two reviewers independently screened the literature, extracted the data, and performed a descriptive analysis. RESULTS: In total, 66 articles with 237 cases of severe neonatal enterovirus infection were included. All neonates developed severe complications. Among them, 46.0% neonates had hepatitis or coagulopathy, 37.1% had myocarditis, 11.0% had meningoencephalitis, and 5.9% had other complications such as hemophagocytic lymphohistiocytosis and pulmonary hemorrhage. The lethality rate of neonates with severe infection was 30.4%. The highest lethality rate was 38.6%, which was observed in neonates with myocarditis. In 70.5% neonates, the age at the onset of symptoms was less than 7 days. Coxsackievirus B infection was seen in 52.3% neonates. The most common symptoms included temperature abnormalities (127, 53.6%), rash (88, 37.1%), poor feeding (58, 24.5%), and respiratory symptoms (52, 21.9%). The main treatment included transfusion of empirical antibiotics (127, 53.6%), blood components (100, 42.2%), intravenous immunoglobulin (IVIG; 97, 40.9%), mechanical ventilation (51, 21.5%), and extracorporeal membrane oxygenation (ECMO; 43, 18.1%). Additionally, antiviral medications pleconaril (14, 5.9%) and pocapavir (3, 1.3%) were administered. CONCLUSIONS: Lethality was high in neonates with severe enterovirus infection, especially in those complicated with myocarditis. The most common symptoms included temperature abnormalities, rash, and poor feeding. The chief supportive treatment consisted of transfusion of blood components, mechanical ventilation, and ECMO. Empirical antibiotics and IVIG were widely used. Antiviral medications included pocapavir and pleconaril; however, more clinical evidence regarding their efficacy is needed.


Assuntos
Doenças Transmissíveis , Infecções por Enterovirus , Enterovirus , Oxigenação por Membrana Extracorpórea , Miocardite , Infecções por Enterovirus/complicações , Infecções por Enterovirus/diagnóstico , Infecções por Enterovirus/epidemiologia , Humanos , Recém-Nascido
7.
Sci Prog ; 104(1): 368504211001146, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33754896

RESUMO

The ubiquitin-proteasome system (UPS) plays crucial roles in numerous cellular functions. Dysfunction of the UPS shows certain correlations with the pathological changes in Alzheimer's disease (AD). This study aimed to explore the different impairments of the UPS in multiple brain regions and identify hub ubiquitin ligase (E3) genes in AD. The brain transcriptome, blood transcriptome and proteome data of AD were downloaded from a public database. The UPS genes were collected from the Ubiquitin and Ubiquitin-like Conjugation Database. The hub E3 genes were defined as the differentially expressed E3 genes shared by more than three brain regions. E3Miner and UbiBrowser were used to predict the substrate of hub E3. This study shows varied impairment of the UPS in different brain regions in AD. Furthermore, we identify seven hub E3 genes (CUL1, CUL3, EIF3I, NSMCE1, PAFAH1B1, RNF175, and UCHL1) that are downregulated in more than three brain regions. Three of these genes (CUL1, EIF3I, and NSMCE1) showed consistent low expression in blood. Most of these genes have been reported to promote AD, whereas the impact of RNF175 on AD is not yet reported. Further analysis revealed a potential regulatory mechanism by which hub E3 and its substrate genes may affect transcription functions and then exacerbate AD. This study identified seven hub E3 genes and their substrate genes affect transcription functions and then exacerbate AD. These findings may be helpful for the development of diagnostic biomarkers and therapeutic targets for AD.

8.
Anal Bioanal Chem ; 413(6): 1665-1673, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33501552

RESUMO

Acquisition of the direct electrochemical response of protein is the cornerstone for the development of the third generation of electrochemical biosensors. In this work, we developed a nanocluster-assisted protein-film voltammetry technique (NCA-PFV) which can achieve the acquisition of the electrochemical signal and maintain the activity without affecting of the protein's structure. With this strategy, a lipid bilayer membrane is used to immobilize the membrane protein so as to maintain its natural state. Copper nanoclusters with a size smaller than most proteins are then used to function at sub-protein scale and to mediate the electron hopping from the electroactive center of the electrode. As a model, the direct electrochemical signal of cyclooxygenase (COX) is successfully obtained, with a pair of well-defined redox peaks located at -0.39 mV and -0.31 mV, which characterize the heme center of the enzyme. Its catalytic activity towards the substrate arachidonic acid (AA) is also retained. The detection range for AA is 10-1000 µM and the detection limit is 2.4 µM. Electrochemical monitoring of the regulation of the catalytic activity by an inhibitor DuP-697 is also achieved. This work provides a powerful tool for the fabrication of enzyme-based electrochemical biosensors, and is also of great significance for promoting the development and application of next-generation electrochemical biosensors.


Assuntos
Técnicas Biossensoriais/métodos , Cobre/química , Eletroquímica/métodos , Heme/análise , Nanopartículas/análise , Prostaglandina-Endoperóxido Sintases/química , Ácido Araquidônico/química , Carbono/química , Catálise , Eletrodos , Heme/química , Humanos , Bicamadas Lipídicas/química , Microscopia Eletrônica de Transmissão , Nanopartículas/química , Oxirredução
9.
BMJ Open ; 11(1): e040182, 2021 01 19.
Artigo em Inglês | MEDLINE | ID: mdl-33468526

RESUMO

OBJECTIVE: Hyperbilirubinemia is one of the most common clinical symptoms in newborns. To improve patient outcomes, evidence-based and implementable guidelines are required. However, clinical guidelines may vary in quality, criteria and recommendations among regions and countries. In this study, we aimed to systematically assess the quality of guidelines using the Appraisal of Guidelines for Research & Evaluation (AGREE)-II instrument and summarise the specific recommendations for neonatal hyperbilirubinemia in order to provide suggestions for future guideline development. DESIGN: Systematic review. INTERVENTIONS: We searched the PubMed, Embase, Medline and guideline databases for relevant articles on 10 April 2020. The studies were screened by two independent reviewers according to our inclusion criteria. Two reviewers independently extracted the descriptive data. Four appraisers assessed the guidelines using the AGREE-II instrument. RESULTS: Our systematic review appraised 12 clinical practice guidelines for the diagnosis and management of neonatal hyperbilirubinemia. The 12 guidelines achieved an average score of 36%-89%. The guidelines received the highest scores for clarity of presentation and lowest scores for rigour of development. Most recommendations for diagnosis were relatively consistent, but recommendations regarding risk factors, the initiating threshold of treatment and pharmacotherapy varied. CONCLUSIONS: Our study revealed that current guidelines vary in the quality of the developing process and are inconsistent with regards to recommendations. Future guidelines should afford more attention to the quality of methodologies in guideline development, and more qualified evidence is needed to standardise the initiating threshold of treatment for neonatal hyperbilirubinemia.


Assuntos
Hiperbilirrubinemia Neonatal , Bases de Dados Factuais , Humanos , Hiperbilirrubinemia Neonatal/diagnóstico , Hiperbilirrubinemia Neonatal/terapia , Recém-Nascido
10.
Nutr Cancer ; 73(6): 983-995, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-32590916

RESUMO

This study was to screen out potential driver long non-coding RNAs (lncRNAs) in lung cancer in Xuanwei (LCXW) differently expressed mRNAs and lncRNAs were detected by gene expression microarrays in 23 paired lung adenocarcinoma and adjacent tissues. Combined bioinformatics analysis was performed to identify potential driver lncRNAs and their potential regulatory relationships. Transcriptome and clinical data in TCGA-LUAD were used as comparison and validation dataset. The comparison of LCXW and TCGA-LUAD revealed significant differences in expression of some genes, signaling pathways affected by differentially expressed genes, and the 5-year survival rate of patients. We identified 14 consistently deregulated mRNAs and 5 lncRNAs as candidate genes, which affected multiple cancer-related pathways and influenced patients' overall survival. By combined bioinformatics analysis, we further identified a potential driver lncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) and proposed its possible regulation mechanism. The low expression of FENDRR was positively correlated with Krüppel-like factor4 (KLF4), KLF4 down-regulation may loss the activation function of cyclin-dependent kinase inhibitor 1A (CDKN1A) and cyclin-dependent kinase inhibitor 1C (CDKN1C) and the inhibition function of CyclinB1 (CCNB1), eventually cause excessive cell cycle activation and lead to lung cancer. This study revealed a potential FENDRR-KLF4-cell cycle regulation axis. These results lay an important foundation for further research on the pathogenesis of LCXW and identification of potential novel biomarkers or therapeutic targets.

11.
IEEE Trans Med Imaging ; 40(3): 879-890, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33245693

RESUMO

Clusters of viral pneumonia occurrences over a short period may be a harbinger of an outbreak or pandemic. Rapid and accurate detection of viral pneumonia using chest X-rays can be of significant value for large-scale screening and epidemic prevention, particularly when other more sophisticated imaging modalities are not readily accessible. However, the emergence of novel mutated viruses causes a substantial dataset shift, which can greatly limit the performance of classification-based approaches. In this paper, we formulate the task of differentiating viral pneumonia from non-viral pneumonia and healthy controls into a one-class classification-based anomaly detection problem. We therefore propose the confidence-aware anomaly detection (CAAD) model, which consists of a shared feature extractor, an anomaly detection module, and a confidence prediction module. If the anomaly score produced by the anomaly detection module is large enough, or the confidence score estimated by the confidence prediction module is small enough, the input will be accepted as an anomaly case (i.e., viral pneumonia). The major advantage of our approach over binary classification is that we avoid modeling individual viral pneumonia classes explicitly and treat all known viral pneumonia cases as anomalies to improve the one-class model. The proposed model outperforms binary classification models on the clinical X-VIRAL dataset that contains 5,977 viral pneumonia (no COVID-19) cases, 37,393 non-viral pneumonia or healthy cases. Moreover, when directly testing on the X-COVID dataset that contains 106 COVID-19 cases and 107 normal controls without any fine-tuning, our model achieves an AUC of 83.61% and sensitivity of 71.70%, which is comparable to the performance of radiologists reported in the literature.


Assuntos
Aprendizado Profundo , Pneumonia Viral/diagnóstico por imagem , Interpretação de Imagem Radiográfica Assistida por Computador/métodos , Tomografia Computadorizada por Raios X/métodos , COVID-19/diagnóstico por imagem , Humanos , SARS-CoV-2
12.
Dev Comp Immunol ; 116: 103923, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33186561

RESUMO

Interferon regulatory factors (IRFs) are a family of transcriptional factors capable of regulating the expression of distinct subsets of interferon (IFN)-stimulated genes by binding to their promoters. IRF1 was the first member identified for its ability to regulate the IFNß gene and has now been revealed to exhibit remarkable functional diversity in the regulation of different cellular responses. In the present study, the IRF1 gene was identified and characterized in Japanese eel, Anguilla japonica (AjIRF1). The open reading frame of AjIRF1 was 804 bp in length, encoding a protein of 267 amino acids (aa) that encompasses a conserved N-terminal DNA binding domain (DBD). Sequence alignment shows the presence of six highly conserved tryptophan (W) residues in the DBD of IRF1, IRF2 and IRF11, while other IRF members have only five tryptophans. Expression analysis showed that AjIRF1 was significantly upregulated in all tested organs/tissues in response to Poly I:C stimulation or Edwardsiella tarda infection. Furthermore, the functional activity of AjIRF1 was confirmed in driving the transcription of AjIFN promoters, which depends on the highly conserved residues within DBD. Subcellular distribution analysis revealed that AjIRF1 was localized exclusively in the nucleus, which is cooperatively regulated by a bipartite NLS embedded within the DBD and a monopartite NLS located immediately downstream of the DBD. Taken together, this study presents the expression profile of AjIRF1 and defines the functional motifs required for its nuclear import and its role in activating IFN promoters, thus providing helpful information for further research on the regulatory mechanisms of teleost IRF1.

13.
ACS Sens ; 6(2): 443-449, 2021 02 26.
Artigo em Inglês | MEDLINE | ID: mdl-33369433

RESUMO

Since microbial detection is an important aspect for the prevention and control of foodborne diseases, an ideal detection system with high sensitivity, strong specificity, and timeliness is needed. Here, we proposed a fluorescent and opt-electric recording bacterial identification device (FORBID) for fully automatic real-time photoelectric sensing analysis of microbials by integrating the metabolic characteristics of microbial and selective substrate catalysis. It simplifies the testing process (one-step) and decreases the need of professional technicians. Besides, the system exhibits ultrasensitive (1 CFU/mL) and specific detection (99%) in both microbials, Escherichia coli and Pseudomonas aeruginosa. More importantly, the timeliness of this system is even better than that of the traditional culture methods. It is believed that this system can be extended to the detection of other microorganisms and provide a potential alternative for the detection of pathogens.


Assuntos
Doenças Transmitidas por Alimentos , Escherichia coli , Humanos , Pseudomonas aeruginosa , Sensibilidade e Especificidade
14.
J Appl Biomater Funct Mater ; 18: 2280800020942719, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33176539

RESUMO

This study reported about the fabrication of dentin non-collagenous proteins (dNCPs) polyelectrolyte multilayers and evaluated its osteogenic potential. The composite sandwich structure of dNCPs polyelectrolyte multilayers was generated on the surface of polycaprolactone electrospinning membranes by the Layer-by-Layer self-assembly technique. The dNCPs-coated membranes comprised the experimental group and the non-coated membranes acted as the control. Nanofiber morphologies of both membranes were observed under scanning electron microscope. The release of dNCPs was evaluated by ELISA kit. Periodontal ligament stem cells (PDLSCs) were seeded on both membranes. The morphology changes and proliferation of cells were tested. The expressions of osteogenic-related genes and proteins were evaluated by RT-PCR, alkaline phosphatase (ALP) activity assay, and immunofluorescence staining. dNCPs-coated membranes displayed significantly different fiber morphology than the non-coated membranes. A stable release of dentin phosphoprotein was maintained from day 4 to day 15 in the experimental group. Cells on dNCPs-coated membranes were found to have cuboidal or polygonal shapes. The proliferative rate of cells was significantly lower in the experimental group from day 4 to day 9 (p<0.05). However, cells on the dNCPs-coated membranes demonstrated a significantly higher ALP content and expression levels of osteogenic gene and proteins than the controls (p<0.05). These results indicated that dNCPs polyelectrolyte multilayers could induce the osteogenic differentiation of PDLSCs in vitro.

15.
Onco Targets Ther ; 13: 9929-9939, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33116577

RESUMO

Introduction: Long non-coding RNA (lncRNA) NCK1-AS1 could regulate multiple cancer progression. However, little is known regarding the roles and acting mechanisms of NCK-AS1 in gastric cancer (GC) progression. This work was aimed to explore the relationship between NCK1-AS1 and GC progression to illustrate the mechanisms of NCK1-AS1. Methods: NCK1-AS1 expression level in GC tissues and cells was measured with a quantitative real-time PCR method. In vitro experiments including cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were employed to detect biological roles of NCK1-AS1 in GC progression. In vivo experiments were performed to analyze the roles of NCK1-AS1 on GC malignant phenotype. Moreover, mechanisms behind the biological roles of NCK1-AS1 in GC were investigated using bioinformatic analysis, luciferase activity reporter assay, RNA immunoprecipitation assay, and rescue experiments. Results: NCK1-AS1 was found to have elevated expression in GC tissues and cells in comparison with normal counterparts. Loss-of-function experiments showed knockdown of NCK1-AS1 refrained GC cell proliferation, colony formation, migration, and invasion in vitro. Animal experiments showed silence of NCK1-AS1 suppresses tumor growth in vivo. Functionally, NCK1-AS1 serves as a sponge for microRNA-137 (miR-137) to upregulate nucleoporin 43 (NUP43) expression in GC. Rescue experiments proved the carcinogenic role of NCK1-AS1/miR-137/NUP43 axis in GC progression. Discussion: In conclusion, the NCK1-AS1/miR-137/NUP43 axis was identified that could contribute to GC malignancy behaviors.

16.
BMC Bioinformatics ; 21(1): 409, 2020 09 16.
Artigo em Inglês | MEDLINE | ID: mdl-32938389

RESUMO

An amendment to this paper has been published and can be accessed via the original article.

17.
Crit Rev Food Sci Nutr ; : 1-15, 2020 Aug 17.
Artigo em Inglês | MEDLINE | ID: mdl-32799539

RESUMO

Caffeinated products are frequently consumed by women of childbearing age worldwide. It still unclear that whether maternal intake of caffeine associated with an increased risk of birth defects. We searched the databases of PubMed, Embase, the Cochrane Library, and Web of Science for eligible studies through July 2020. All studies examining the association between maternal consumption of caffeine or caffeinated products and birth defects were included. Twenty-nine studies were included in this meta-analysis. Among all the birth defects, maternal caffeine consumption was associated with a higher risk of cardiovascular defects, [odds ratio (OR) 1.17; 95% confidence interval (CI), 1.07-1.28], craniofacial defects (OR 1.09; 95% CI, 1.02-1.17), alimentary tract defects (OR 1.35; 95% CI, 1.16-1.56), and abdominal-wall defects and hernia (OR 1.13; 95% CI, 1.03-1.25). No association was found between maternal caffeine intake and musculoskeletal system defects, genitourinary system defects, nervous system defects, or chromosomal abnormalities. Meanwhile, all three of the caffeine consumption categories (low, moderate, and high) were associated with a higher risk of cardiovascular defects and alimentary tract defects.

18.
Zhongguo Dang Dai Er Ke Za Zhi ; 22(8): 844-853, 2020 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-32800031

RESUMO

OBJECTIVE: To systematically summarize the clinical features of coronavirus disease 2019 (COVID-19) in children. METHODS: PubMed, Embase, Web of Science, The Cochrane Library, CNKI, Weipu Database, and Wanfang Database were searched for clinical studies on COVID-19 in children published up to May 21, 2020. Two reviewers independently screened the articles, extracted data, and assessed the risk of bias of the studies included. A descriptive analysis was then performed for the studies. Related indices between children with COVID-19 and severe acute respiratory syndromes (SARS) or Middle East respiratory syndrome (MERS) were compared. RESULTS: A total of 75 studies were included, with a total of 806 children with COVID-19. The research results showed that the age of the children ranged from 36 hours after birth to 18 years, with a male-female ratio of 1.21 : 1. Similar to SARS and MERS, COVID-19 often occurred with familial aggregation, and such cases accounted for 74.6% (601/806). The children with COVID-19, SARS, and MERS had similar clinical symptoms, mainly fever and cough. Some children had gastrointestinal symptoms. The children with asymptomatic infection accounted for 17.9% (144/806) of COVID-19 cases, 2.5% (2/81) of SARS cases, and 57.1% (12/21) of MERS cases. The children with COVID-19 and MERS mainly had bilateral lesions on chest imaging examination, with a positive rate of lesions of 63.4% (421/664) and 26.3% (5/19) respectively, which were lower than the corresponding positive rates of viral nucleic acid detection, which were 99.8% and 100% respectively. The chest radiological examination of the children with SARS mainly showed unilateral lesion, with a positive rate of imaging of 88.9% (72/81), which was higher than the corresponding positive rate of viral nucleic acid detection (29.2%). Viral nucleic acid was detected in the feces of children with COVID-19 or SARS, with positive rates of 60.2% (56/93) and 71.4% (5/7) respectively. The children with COVID-19 had a rate of severe disease of 4.6% (31/686) and a mortality rate of 0.1% (1/806), the children with SARS had a rate of severe disease of 1.5% (1/68) and a mortality rate of 0%, and those with MERS had a rate of severe disease of 14.3% (3/21) and a mortality rate of 9.5% (2/21). CONCLUSIONS: Children with COVID-19 have similar symptoms to those with SARS or MERS, mainly fever and cough. Asymptomatic infection is observed in all three diseases. Children with COVID-19 or SARS have milder disease conditions than those with MERS. COVID-19 in children often occurs with familial aggregation. Epidemiological contact history, imaging examination findings, and viral nucleic acid testing results are important bases for the diagnosis of COVID-19.


Assuntos
Infecções por Coronavirus/fisiopatologia , Pneumonia Viral/fisiopatologia , Síndrome Respiratória Aguda Grave/fisiopatologia , Síndrome Respiratória Aguda Grave/virologia , Betacoronavirus , COVID-19 , Criança , Tosse/virologia , Feminino , Febre/virologia , Humanos , Masculino , Coronavírus da Síndrome Respiratória do Oriente Médio , Pandemias , SARS-CoV-2
19.
Aging (Albany NY) ; 12(10): 9882-9914, 2020 05 27.
Artigo em Inglês | MEDLINE | ID: mdl-32461378

RESUMO

Considerable evidence suggests that metabolic abnormalities are associated with neurodegenerative diseases. This study aimed to conduct a systematic metabolic analysis of Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). Human and mouse model microarray datasets were downloaded from the Gene Expression Omnibus database. The metabolic genes and pathways were collected from the Recon 3D human metabolic model. Drug and target information was obtained from the DrugBank database. This study identified ATP1A1, ATP6V1G2, GOT1, HPRT1, MAP2K1, PCMT1 and PLK2 as key metabolic genes that were downregulated in AD, PD and HD. We screened 57 drugs that target these genes, such as digoxin, ouabain and diazoxide. This study constructed multigene diagnostic models for AD, PD and HD by using metabolic gene expression profiles in blood, all models showed high accuracy (AUC > 0.8) both in the experimental and validation sets. Furthermore, analysis of animal models showed that there was almost no consistency among the metabolic changes between mouse models and human diseases. This study systematically revealed the metabolic damage among AD, PD, and HD and uncovered the differences between animal models and human diseases. This information may be helpful for understanding the metabolic mechanisms and drug development for neurodegenerative diseases.


Assuntos
Doença de Alzheimer/genética , Fármacos do Sistema Nervoso Central/uso terapêutico , Doença de Huntington/genética , Modelos Genéticos , Doença de Parkinson/genética , Doença de Alzheimer/tratamento farmacológico , Animais , Bases de Dados Genéticas , Modelos Animais de Doenças , Regulação para Baixo/genética , Desenvolvimento de Medicamentos , Humanos , Doença de Huntington/tratamento farmacológico , Camundongos , Terapia de Alvo Molecular , Doença de Parkinson/tratamento farmacológico , Reprodutibilidade dos Testes , Transcriptoma
20.
PLoS One ; 15(4): e0230796, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32236130

RESUMO

BACKGROUND: Evidence from multiple studies suggests metabolic abnormalities play an important role in lung cancer. Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. The present study aimed to explore differences in the global metabolic response between male and female patients in LUAD and to identify the metabolic genes associated with lung cancer susceptibility. METHODS: Transcriptome and clinical LUAD data were acquired from The Cancer Genome Atlas (TCGA) database. Information on metabolic genes and metabolic subsystems were collected from the Recon3D human metabolic model. Two validation datasets (GSE68465 and GSE72094) were downloaded from the Gene Expression Omnibus (GEO) database. Differential expression analysis, gene set enrichment analysis and protein-protein interaction networks were used to identified key metabolic pathways and genes. Functional experiments were used to verify the effects of genes on proliferation, migration, and invasion in lung cancer cells in vitro. RESULTS: Samples of tumors and adjacent non-tumor tissue from both male and female patients exhibited distinct global patterns of gene expression. In addition, we found large differences in methionine and cysteine metabolism, pyruvate metabolism, cholesterol metabolism, nicotinamide adenine dinucleotide (NAD) metabolism, and nuclear transport between male and female LUAD patients. We identified 34 metabolic genes associated with lung cancer susceptibility in males and 15 in females. Most of the metabolic cancer-susceptibility genes had high prediction accuracy for lung cancer (AUC > 0.9). Furthermore, both bioinformatics analysis and experimental results showed that TAOK2 was down-regulated and ASAH1 was up-regulated in male tumor tissue and female tumor tissue in LUAD. Functional experiments showed that inhibiting ASAH1 suppressed the proliferation, migration, and invasion of lung cancer cells. CONCLUSIONS: Metabolic cancer-susceptibility genes may be used alone or in combination as diagnostic markers for LUAD. Further studies are required to elucidate the functions of these genes in LUAD.


Assuntos
Ceramidase Ácida/metabolismo , Adenocarcinoma de Pulmão/patologia , Identidade de Gênero , Predisposição Genética para Doença , Proteínas Serina-Treonina Quinases/metabolismo , Ceramidase Ácida/genética , Biomarcadores Tumorais , Feminino , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Humanos , Masculino , Redes e Vias Metabólicas/genética , Proteínas Serina-Treonina Quinases/genética
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