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1.
Int J Mol Sci ; 20(21)2019 Oct 28.
Artigo em Inglês | MEDLINE | ID: mdl-31661866

RESUMO

Lateral organ boundaries domain (LBD) proteins belong to a particular class of transcription factors of lateral organ boundary (LOB) specific domains that play essential roles in plant growth and development. However, a potato phylogenetic analysis of the LBD family has not been fully studied by scholars and researchers. In this research, bioinformatics methods and the growth of potatoes were used to identify 43 StLBD proteins. We separated them into seven subfamilies: Ia, Ib, Ic, Id, Ie, IIa and IIb. The number of amino acids encoded by the potato LBD family ranged from 94 to 327. The theoretical isoelectric point distribution ranged from 4.16 to 9.12 Kda, and they were distributed among 10 chromosomes. The results of qRT-PCR showed that the expression levels of StLBD2-6 and StLBD3-5 were up-regulated under drought stress in the stem. The expression levels of StLBD1-5 and StLBD2-6 were down-regulated in leaves. We hypothesized that StLBD1-5 was down-regulated under drought stress, and that StLBD2-6 and StLBD3-5 up-regulation might help to maintain the normal metabolism of potato and enhance the potatoes' resistance to drought.

2.
Gigascience ; 8(10)2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31574156

RESUMO

BACKGROUND: The African eggplant (Solanum aethiopicum) is a nutritious traditional vegetable used in many African countries, including Uganda and Nigeria. It is thought to have been domesticated in Africa from its wild relative, Solanum anguivi. S. aethiopicum has been routinely used as a source of disease resistance genes for several Solanaceae crops, including Solanum melongena. A lack of genomic resources has meant that breeding of S. aethiopicum has lagged behind other vegetable crops. RESULTS: We assembled a 1.02-Gb draft genome of S. aethiopicum, which contained predominantly repetitive sequences (78.9%). We annotated 37,681 gene models, including 34,906 protein-coding genes. Expansion of disease resistance genes was observed via 2 rounds of amplification of long terminal repeat retrotransposons, which may have occurred ∼1.25 and 3.5 million years ago, respectively. By resequencing 65 S. aethiopicum and S. anguivi genotypes, 18,614,838 single-nucleotide polymorphisms were identified, of which 34,171 were located within disease resistance genes. Analysis of domestication and demographic history revealed active selection for genes involved in drought tolerance in both "Gilo" and "Shum" groups. A pan-genome of S. aethiopicum was assembled, containing 51,351 protein-coding genes; 7,069 of these genes were missing from the reference genome. CONCLUSIONS: The genome sequence of S. aethiopicum enhances our understanding of its biotic and abiotic resistance. The single-nucleotide polymorphisms identified are immediately available for use by breeders. The information provided here will accelerate selection and breeding of the African eggplant, as well as other crops within the Solanaceae family.

3.
BMJ Open ; 9(10): e029929, 2019 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-31640996

RESUMO

OBJECTIVES: To explore the association between the number of teeth and frailty among older Chinese adults using a nationally representative sample. DESIGN: Cross-sectional analysis was carried out using the 2014 wave data from the Chinese Longitudinal Healthy Longevity Survey, which used a targeted random-sampling design. SETTING: This research was conducted in communities from nearly half of the counties and cities in 22 out of 31 provinces throughout China. PARTICIPANTS: Of the 6934 interviewees aged ≥65 years, the final analysis included 3635 older adults who had completed the 2014 wave survey on the variables included in the study. PRIMARY AND SECONDARY OUTCOME MEASURES: Outcome variables included frailty, measured by the Frailty Index, and number of teeth. Covariates included demographic characteristics (ie, age, sex, co-residence, marital status, years of education and financial support), body mass index (BMI) and health behaviours (ie, smoking, drinking and exercise). A univariate logistic regression was used to test the factors associated with frailty. A multiple logistic regression model was used, using the frailty score as the dependent variable and the number of teeth together with significant covariates as the independent variables. RESULTS: The prevalence of frailty was 27.68%. The mean number of teeth present was 9.23 (SD=10.03). The multiple logistic regression showed that older adults' demographic variables, health behaviours, BMI, tooth number and chewing pain were significantly associated with frailty. After adjusting for the covariates, older adults with fewer teeth had significantly higher odds of frailty than those with 20 or more teeth (no teeth: OR=2.07, 95% CI 1.53 to 2.80; 1 to 10 teeth: OR=1.77, 95% CI 1.31 to 2.38), except for older adults with 11 to 20 teeth (OR=1.30, 95% CI 0.93 to 1.82). CONCLUSIONS: The presence of fewer teeth is significantly associated with frailty status among older Chinese adults. Future studies are needed to explain the specific mechanisms underlying how oral health status is associated with frailty.

4.
IEEE Trans Cybern ; 49(12): 4271-4281, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31502955

RESUMO

In this paper, the event-based controller synthesis problem for networked control systems under the resilient event-triggering communication scheme (RETCS) and periodic denial-of-service (DoS) jamming attacks is studied. First, a new periodic RETCS is designed under the assumption that the DoS attacks imposed by power-constrained pulsewidth-modulated jammers are partially identified, that is, the period of the jammer and a uniform lower bound on the jammer's sleeping periods are known. Second, a new state error-dependent switched system model is constructed, including the impacts of the RETCS and DoS attacks. According to this new model, the exponential stability criteria are derived by using the piecewise Lyapunov functional. In these criteria, the relationship among DoS parameters, the triggering parameters, the sampling period, and the decay rate is quantitatively characterized. Then, a criterion is also proposed to obtain the explicit expressions of the triggering parameter and event-based state feedback controller gain simultaneously. Finally, the obtained theoretical results are verified by a satellite yaw-angles control system.

5.
Virol Sin ; 2019 Sep 24.
Artigo em Inglês | MEDLINE | ID: mdl-31552609

RESUMO

Beak and feather disease virus (BFDV) is an infectious agent responsible for feather degeneration and beak deformation in birds. In March 2017, an epidemic of psittacine beak and feather disease (PBFD) struck a farm in Fuzhou in the Fujian Province of southeast China, resulting in the death of 51 parrots. In this study, the disease was diagnosed and the pathogen was identified by PCR and whole genome sequencing. A distinct BFDV strain was identified and named as the FZ strain. This BFDV strain caused severe disease symptoms and pathological changes characteristic of typical PBFD in parrots, for example, loss of feathers and deformities of the beak and claws, and severe pathological changes in multiple organs of the infected birds. Phylogenetic analysis showed that the FZ strain was more closely related to the strain circulating in New Caledonia than the strains previously reported in China. Nucleotide homology between the FZ strain and other 43 strains of BFDV ranged from 80.0% to 92.0%. Blind passage experiment showed that this strain had limited replication capability in SPF Chicken Embryos and DF-1 Cells. Furthermore, the capsid (Cap) gene of this FZ strain was cloned into the pGEX-4T-1 expression vector to prepare the polyclonal anti-Cap antibody. Western blotting analysis using the anti-Cap antibody further confirmed that the diseased parrots were infected with BFDV. In this study, a PBFD and its pathogen was identified for the first time in Fujian Province of China, suggesting that future surveillance of BFDV should be performed.

6.
Mol Genet Genomic Med ; 7(11): e923, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31503426

RESUMO

BACKGROUND: Pediatric myelodysplastic syndromes (MDS) display clonal genomic instability that can lead to acquisition of other hematological disorders, usually by loss of heterozygosity. Immunodeficiency caused by uniparental disomy (UPD) has not previously been reported. METHODS: We investigated a 13-year-old boy who suffered from recurrent infections and pancytopenia for 1 year. Both the comet assay and chromosome breakage analysis were normal, but the bone marrow showed evidence of dysplasia characteristic of MDS. With his normal sister as donor, he underwent failed hematopoietic stem cell transplantation (HSCT) with reduced intensity conditioning (RIC) followed by successful HSCT with myeloablative conditioning (MAC). We used single nucleotide polymorphism (SNP) array, targeted gene panel, and whole exome sequencing to investigate the etiology of his disease. RESULTS: The molecular analyses revealed multiple regions of homozygosity, one region encompassing a homozygous missense variant of recombination activating gene 1 (RAG1) which was previously associated with severe immunodeficiency in infancy. This RAG1 mutation was heterozygous in the proband's fingernail DNA, but was changed to homozygous in the proband's marrow by somatic acquisition of UPD event. No other pathogenic driver mutation for MDS-related genes was identified. CONCLUSION: The hematological phenotype, somatic genomic instability, and response to HSCT MAC but not HSCT RIC deduced to a diagnosis of MDS type refractory cytopenia of children in this patient. His immunodeficiency was secondary to MDS due to somatic acquisition of homozygosity for known pathogenic RAG1 mutation.

7.
Neuroimage ; 202: 116074, 2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31386919

RESUMO

Landmarks and path integration cues are two important sources of spatial information for navigation. For example, both can be used to compute positional information, which, in rodents, has been related to computations in the entorhinal cortex. In humans, however, if and how the entorhinal cortex supports landmark-based navigation and path integration is poorly understood. To address this important question, we developed a novel spatial navigation task in which participants learned a target location and judged relative positions of test locations in relation to the target. Landmarks and path integration cues were dissociated, and their reliability levels were manipulated. Using fMRI adaptation, we investigated whether spatial distances among the test locations were encoded in the BOLD responses, separately for landmarks and self-motion cues. The results showed that the anterior-lateral entorhinal cortex adapted to the distance between successively visited test locations when landmarks were used for localization, meaning that its activation decreased as the distance between the currently occupied location and the preceding location decreased. In contrast, the posterior-medial entorhinal cortex adapted to between-location distance when path integration cues were used for localization. In addition, along with the hippocampus and the precuneus, both entorhinal subregions showed stronger activation in correct trials than incorrect trials, regardless of cue type and reliability level. Together, these findings suggest that subdivisions of entorhinal cortex encode fine-grained spatial information for different spatial cues, which provides important insights into how the entorhinal cortex supports different modes of spatial navigation.

8.
Biochem Biophys Res Commun ; 518(2): 219-226, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31434611

RESUMO

Mycobacterium tuberculosis (MTB) infection could induce death of host human macrophages, promoting bacterial spread. In the current study we tested the potential role of microRNA-579 (miR-579) in the death of macrophages infected with MTB. In the primary human macrophages MTB infection induced upregulation of miR-579 but downregulation of its mRNA targets, SIRT1 and PDK1, which were accompanied by significant macrophage death and apoptosis. miR-579 inhibition, by its anti-sense sequence, restored SIRT1-PDK1 expression and significantly attenuated MTB-induced cytotoxicity and apoptosis in human macrophages. Conversely, ectopic overexpression of miR-579 further downregulated SIRT1-PDK1 expression and exacerbated MTB-induced cytotoxicity in human macrophages. Further studies showed that cPWWP2A, the miR-579's endogenous sponge circRNA, was downregulated in MTB-infected macrophages. Conversely, forced overexpression of cPWWP2A, by a recombinant adeno-associated virus construct, reversed MTB-induced miR-579 upregulation and macrophage cytotoxicity. Taken together, our results show that miR-579 upregulation mediates MTB-induced macrophage cytotoxicity. Targeting cPWWP2A-miR-579 axis could be a novel strategy to protect human macrophages from MTB infection.

9.
Circ Res ; 125(6): 590-605, 2019 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-31318658

RESUMO

RATIONALE: Endothelial dysfunction results in sustained and chronic vascular inflammation, which is central to atherosclerotic diseases. However, transcriptional regulation of vascular endothelial inflammation has not been well clarified. OBJECTIVE: This study aims to explore Foxp (forkhead box P) transcription factor 1 in regulation of endothelial homeostasis, atherogenesis, and its mechanisms. METHODS AND RESULTS: To assess the importance of Foxp1 in atherosclerosis, Foxp1 expression was analyzed in human coronary artery and mouse artery, and we observed significant downregulation of Foxp1 in atherosclerotic and atherosusceptible endothelium. Endothelial-specific Foxp1 knockout mice (Foxp1ECKO) were bred onto ApoeKO mice to generate endothelial Foxp1-deletion hyperlipidemic model Foxp1ECKO;ApoeKO, which displayed significant increases in atherosclerotic lesion formation in aortas and aortic roots with enhanced monocyte adhesion, migration, and infiltration into the vascular wall and formation of inflammatory lipid-laden macrophages. In contrast, endothelial-specific Foxp1 overexpression mice Foxp1ECTg;ApoeKO exhibited reduced atherosclerotic lesion formation with less monocyte infiltration. Foxp1 was further identified as a gatekeeper of vessel inflammation by direct regulation of endothelial inflammasome components, including Nlrp3 (NLR [nucleotide-binding and leucine-rich repeat immune receptors] family pyrin domain containing 3), caspase-1, and IL (interleukin)-1ß. Moreover, endothelial Foxp1 was found to be regulated by Klf2 (Kruppel-like factor 2). Oscillatory shear stress downregulated Foxp1 expression via repressing Klf2 expression in endothelium, and, therefore, promoted endothelial inflammasome activation, leading to atherosclerotic lesion formation. Simvastatin upregulated the reduced expression of Klf2 and Foxp1 in atherosusceptible vascular endothelium and alleviated vascular inflammation contributing to its inhibitory effect in atherosclerosis. CONCLUSIONS: These data are the first in vivo experimental validation of an atheroprotective role of endothelial Klf2 and Foxp1, which reveals a Klf2-Foxp1 transcriptional network in endothelial cells as a novel regulator of endothelial inflammasome activation for atherogenesis, therefore, provides opportunities for therapeutic intervention of atherosclerotic diseases and uncovers a novel atheroprotective mechanism for simvastatin.

10.
Menopause ; 26(10): 1171-1177, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31188285

RESUMO

OBJECTIVE: Recent studies show that vitamin D (VitD) deficiency is associated with metabolic syndrome (MetS). Current evidence suggests that estrogen and VitD have similar physiological functions and potentially interact with bone health. We investigated the association between estradiol (E2) and 25-hydroxyvitamin-D [25(OH)D] with MetS and its components in Chinese postmenopausal women. METHODS: In this cross-sectional study, we examined 616 postmenopausal women (aged 49-86 y) from southern China who were not taking estrogen and VitD/calcium supplements. At the end of data collection, serum E2 and 25(OH)D were measured for each participant. MetS was defined according to the 2006 International Diabetes Federation standard. RESULTS: There was a positive correlation between 25(OH)D and E2. Higher 25(OH)D was associated with a favorable lipid profile, blood pressure, and glucose level. E2 was negatively associated with cholesterol, triglycerides, and blood pressure. The odds ratio for MetS was 2.19 (95% CI, 1.19-4.01, P value for trend=0.009) for deficient compared with sufficient women after multivariable adjustment. This association remained unchanged after further adjusting for E2 levels. After stratified analysis by VitD status, low E2 increased MetS risk in women with VitD deficiency (odds ratio = 3.49, 95% CI, 1.45-8.05 for the lowest vs the highest tertile). CONCLUSIONS: These results suggest a synergistic role of VitD and E2 deficiency in MetS in Chinese postmenopausal women.

11.
Graefes Arch Clin Exp Ophthalmol ; 257(8): 1813, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31165246

RESUMO

The article "A comparison of risk factors for age-related macular degeneration and polypoidal choroidal vasculopathy in Chinese patients" has been retracted.

12.
Circulation ; 140(8): 665-680, 2019 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-31177814

RESUMO

BACKGROUND: Pathological cardiac fibrosis and hypertrophy, the common features of left ventricular remodeling, often progress to heart failure. Forkhead box transcription factor P1 (Foxp1) in endothelial cells (ECs) has been shown to play an important role in heart development. However, the effect of EC-Foxp1 on pathological cardiac remodeling has not been well clarified. This study aims to determine the role of EC-Foxp1 in pathological cardiac remodeling and the underlying mechanisms. METHODS: Foxp1 EC-specific loss-of-function and gain-of-function mice were generated, and an angiotensin II infusion or a transverse aortic constriction operation mouse model was used to study the cardiac remodeling mechanisms. Foxp1 downstream target gene transforming growth factor-ß1 (TGF-ß1) was confirmed by chromatin immunoprecipitation and luciferase assays. Finally, the effects of TGF-ß1 blockade on EC-Foxp1 deletion-mediated profibrotic and prohypertrophic phenotypic changes were further confirmed by pharmacological inhibition, more specifically by RGD-peptide magnetic nanoparticle target delivery of TGF-ß1-siRNA to ECs. RESULTS: Foxp1 expression is significantly downregulated in cardiac ECs during angiotensin II-induced cardiac remodeling. EC-Foxp1 deletion results in severe cardiac remodeling, including more cardiac fibrosis with myofibroblast formation and extracellular matrix protein production, as well as decompensated cardiac hypertrophy and further exacerbation of cardiac dysfunction on angiotensin II infusion or transverse aortic constriction operation. In contrast, EC-Foxp1 gain of function protects against pathological cardiac remodeling and improves cardiac dysfunction. TGF-ß1 signals are identified as Foxp1 direct target genes, and EC-Foxp1 deletion upregulates TGF-ß1 signals to promote myofibroblast formation through fibroblast proliferation and transformation, resulting in severe cardiac fibrosis. Moreover, EC-Foxp1 deletion enhances TGF-ß1-promoted endothelin-1 expression, which significantly increases cardiomyocyte size and reactivates cardiac fetal genes, leading to pathological cardiac hypertrophy. Correspondingly, these EC-Foxp1 deletion-mediated profibrotic and prohypertrophic phenotypic changes and cardiac dysfunction are normalized by the blockade of TGF-ß1 signals through pharmacological inhibition and RGD-peptide magnetic nanoparticle target delivery of TGF-ß1-siRNA to ECs. CONCLUSIONS: EC-Foxp1 regulates the TGF-ß1-endothelin-1 pathway to control pathological cardiac fibrosis and hypertrophy, resulting in cardiac dysfunction. Therefore, targeting the EC-Foxp1-TGF-ß1-endothelin-1 pathway might provide a future novel therapy for heart failure.

13.
Mol Ther Nucleic Acids ; 17: 92-101, 2019 May 24.
Artigo em Inglês | MEDLINE | ID: mdl-31234009

RESUMO

The aim of this study was to explore the roles of the long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) on cisplatin resistance in ovarian cancer and the underlying mechanisms. We investigated the expression of lncRNAs in 3 paired cisplatin-sensitive and cisplatin-resistant tissues of ovarian cancer by microarray analysis. The qRT-PCR analysis was to investigate the expression pattern of UCA1 in cisplatin-resistant ovarian cancer patient tissues and cell lines. Then we examined the effects of UCA1 on cisplatin resistance in vitro and in vivo. In this study, UCA1 was observed to be upregulated in cisplatin-resistant patient tissues and cell lines. Knockdown of UCA1 inhibited cell proliferation and promoted the cisplatin-induced cell apoptosis in ovarian cancer cells. Then we demonstrated that repressed UCA1 promoted the miR-143 expression and miR-143 could bind to the predicted binding site of UCA1. Furthermore, we found that miR-143 displayed its role via modulating the FOSL2 expression. Importantly, we demonstrated that UCA1 was upregulated in serum exosomes from cisplatin-resistant patients. In summary, our study demonstrated that UCA1 modulates cisplatin resistance through the miR-143/FOSL2 pathway in ovarian cancer.

14.
iScience ; 16: 106-121, 2019 May 16.
Artigo em Inglês | MEDLINE | ID: mdl-31154207

RESUMO

Growth hormone (GH) binds to its receptor (growth hormone receptor [GHR]) to exert its pleiotropic effects on growth and metabolism. Disrupted GH/GHR actions not only fail growth but also are involved in many metabolic disorders, as shown in murine models with global or tissue-specific Ghr deficiency and clinical observations. Here we constructed an adipose-specific Ghr knockout mouse model Ad-GHRKO and studied the metabolic adaptability of the mice when stressed by high-fat diet (HFD) or cold. We found that disruption of adipose Ghr accelerated dietary obesity but protected the liver from ectopic adiposity through free fatty acid trapping. The heat-producing brown adipose tissue burning and white adipose tissue browning induced by cold were slowed in the absence of adipose Ghr but were recovered after prolonged cold acclimation. We conclude that at the expense of excessive subcutaneous fat accumulation and lower emergent cold tolerance, down-tuning adipose GHR signaling emulates a healthy obesity situation which has metabolic advantages against HFD.

15.
Int J Obes (Lond) ; 2019 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-31209269

RESUMO

BACKGROUND/OBJECTIVES: Pentraxin 3 (PTX3) has been characterized as a soluble and multifunctional pattern recognition protein in the regulation of innate immune response. However, little is known about its role in adipose tissue inflammation and obesity. Herein, we investigated the role of PTX3 in the regulation of lipopolysaccharide (LPS)-induced inflammation in adipocytes and adipose tissue, as well as high-fat diet (HFD)-induced metabolic inflammation in obesity. METHODS: Ptx3 knockdown 3T3-L1 Cells were generated using shRNA for Ptx3 gene and treated with different inflammatory stimuli. For the in vivo studies, Ptx3 knockout mice were treated with 0.3 mg/kg of LPS for 6 h. Adipose tissues were collected for gene and protein expression by qPCR and western blotting, respectively. Ptx3 knockout mice were fed with HFD for 12 week since 6 week of age. RESULTS: We observed that the expression of PTX3 in adipose tissue and serum PTX3 were markedly increased in response to LPS administration. Knocking down Ptx3 in 3T3-L1 cells reduced adipogenesis and caused a more profound and sustained upregulation of proinflammatory gene expression and signaling pathway activation during LPS-stimulated inflammation in 3T3-L1 adipocytes. In vivo studies showed that PTX3 deficiency significantly exacerbated the LPS-induced upregulation of inflammatory genes and downregulation of adipogeneic genes in visceral and subcutaneous adipose tissue of mice. Accordingly, LPS stimulation elicited increased activation of nuclear factor-κB (NF-κB) and p44/42 MAPK (Erk1/2) signaling pathways in visceral and subcutaneous adipose tissue. The expression of PTX3 in adipose tissue was also induced by HFD, and PTX3 deficiency led to the upregulation of proinflammatory genes in visceral adipose tissue of HFD-induced obese mice. CONCLUSIONS: Our results suggest a protective role of PTX3 in LPS- and HFD-induced sustained inflammation in adipose tissue.

16.
Mol Immunol ; 112: 10-21, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31075558

RESUMO

Extracellular adenosine triphosphate (eATP), released following inflammatory stimulation or infection, is a potent signaling molecule in activating innate immune responses in fish. However, the regulation of eATP-mediated innate immunity in fish remains unknown. Ecto-nucleoside triphosphate diphosphohydrolase 1 (CD39) is a critical molecular switch for controlling the ATP levels in the extracellular space. CD39 plays a key role in regulating eATP-activated innate immune responses through the phosphohydrolysis of pro-inflammatory eATP to inactive AMP. Here, we identified and characterized a CD39 homolog (namely, poCD39) in the Japanese flounder Paralichthys olivaceus and analyzed its regulatory role in eATP-mediated innate immunity. Real-time quantitative PCR analysis revealed that poCD39 is ubiquitously present in all tested normal tissues with dominant expression in enriched Japanese flounder head kidney macrophages (HKMs). Immune challenge experiments demonstrated that poCD39 expression was upregulated by inflammatory stimulation and Edwardsiella tarda infection. Biochemical and immunofluorescence analysis revealed that poCD39 is a functional glycosylated membrane protein for the hydrolysis of eATP. Inhibition of poCD939 activity with the ecto-NTPDase inhibitor ARL 67156 resulted in increased IL-1beta gene expression and ROS production in Japanese flounder HKMs. In contrast, overexpression of poCD39 in Japanese flounder FG-9307 cells reduced eATP-induced pro-inflammatory cytokine IL-1beta gene expression. Finally, poCD39 expression was significantly induced by eATP stimulation in the HKMs, suggesting that eATP may provide a feedback mechanism for transcriptional regulation of fish CD39. Taken together, we identified and characterized a functional fish CD39 protein involved in regulating eATP-mediated innate immune responses in fish.


Assuntos
Trifosfato de Adenosina/imunologia , Antígenos CD/imunologia , Apirase/imunologia , Linguado/imunologia , Imunidade Inata/imunologia , Monofosfato de Adenosina/imunologia , Animais , Edwardsiella tarda/imunologia , Infecções por Enterobacteriaceae/imunologia , Infecções por Enterobacteriaceae/microbiologia , Infecções por Enterobacteriaceae/veterinária , Proteínas de Peixes/imunologia , Linguado/microbiologia , Regulação da Expressão Gênica/imunologia , Rim Cefálico/imunologia , Rim Cefálico/microbiologia , Inflamação/imunologia , Inflamação/microbiologia , Japão , Macrófagos/imunologia , Macrófagos/microbiologia , Espécies Reativas de Oxigênio/imunologia , Transcrição Genética/imunologia , Regulação para Cima/imunologia
17.
Dis Markers ; 2019: 8282414, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31089399

RESUMO

Objective: The synaptic adhesion-like molecule (SALM) family is largely restricted to neural tissues and is involved in the regulation of neurite outgrowth and synapse formation. However, the expression of SALM3 in gastric cancer (GC) and its clinical significance remain unclear. The aim of the present study was to investigate the prognostic value of SALM3 in patients with GC. Patients and Methods: Expression of SALM3 was validated by tissue microarrays from 730 GC patients and statistically assessed for correlations with the clinical parameters and the prognosis of the patients. The transcriptional and survival data of SALM3 in GC patients were also mined through the Oncomine and Kaplan-Meier Plotter databases. Results: SALM3 is overexpressed in the tumor cells and fibroblasts of clinical GC tissues, and a high level of SALM3 was significantly associated with tumor invasive characteristics. Cox proportional hazards univariate and multivariate regression analyses revealed SALM3 expression in tumor cells or stroma as an independent prognostic factor in the overall survival rate of GC patients. Furthermore, the survival of GC patients with high SALM3 expression in both tumor cells and fibroblasts was significantly poorer than that of the other groups. Oncomine and Kaplan-Meier Plotter analyses further confirmed high levels of SALM3 expression in GC, and high levels of SALM3 expression were associated with shorter survival in patients. Conclusion: SALM3 may be a prognostic factor for GC and may potentially be a high-priority therapeutic target.


Assuntos
Biomarcadores Tumorais/genética , Glicoproteínas de Membrana/genética , Proteínas do Tecido Nervoso/genética , Neoplasias Gástricas/metabolismo , Biomarcadores Tumorais/metabolismo , Células Cultivadas , Feminino , Fibroblastos/metabolismo , Humanos , Masculino , Glicoproteínas de Membrana/metabolismo , Pessoa de Meia-Idade , Proteínas do Tecido Nervoso/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia
18.
Stem Cell Res ; 38: 101441, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31082678

RESUMO

Production of 3-dimensional neural progenitor cultures from human pluripotent stem cells offers the potential to generate large numbers of cells. We utilised our nanobridge system to generate 3D hPSC aggregates for differentiation towards the neural lineage, and investigate the ability to passage aggregates while maintaining cells at a stem/progenitor stage. Over 38 days, aggregate cultures exhibited upregulation and maintenance of neural-associated markers and demonstrated up to 10 fold increase in cell number. Aggregates undergoing neural induction in the presence or absence of nanobridges demonstrated no differences in marker expression, proliferation or viability. However, aggregates formed without nanobridges were statistically significantly fewer and smaller by passage 3. Organoids, cultured from aggregates, and treated with retinoic acid or rock inhibitor demonstrated terminal differentiation as assessed by immunohistochemistry. These data demonstrate that nanobridge 3D hPSC can differentiate to neural stem/progenitor cells, and be maintained at this stage through serial passaging and expansion.

19.
Sci Rep ; 9(1): 6926, 2019 May 06.
Artigo em Inglês | MEDLINE | ID: mdl-31061448

RESUMO

The present study evaluated the growth response and sugar accumulation of lettuce exposed to different lighting modes of red and blue LED light based on the same daily light integral (7.49 µmol·m-2). Six lighting treatments were performed, that were monochromatic red light (R), monochromatic blue light (B), simultaneous red and blue light as the control (RB, R:B = 1:1), mixed modes of R, B and RB (R/RB/B, 4 h R to 4 h RB and then 4 h B), and alternating red and blue light with alternating intervals of 4 h and 1 h respectively recorded as R/B(4 h) and R/B(1 h). The Results showed that different irradiation modes led to obvious morphological changes in lettuce. Among all the treatments, the highest fresh and dry weight of lettuce shoot were both detected with R/B(1 h), significantly higher than the other treatments. Compared with plants treated with RB, the contents of fructose, glucose, crude fiber as well as the total sweetness index (TSI) of lettuce were significantly enhanced by R treatment; meanwhile, monochromatic R significantly promoted the activities of sucrose degrading enzymes such as acid invertase (AI) and neutral invertase (NI), while obviously reduced the activity of sucrose synthesizing enzyme (SPS). Additionally. The highest contents of sucrose and starch accompanied with the strongest activity of SPS were detected in plants treated with R/B(1 h). The alternating treatments R/B(4 h) and R/B(1 h) inhibited the activity of SS, while enhanced that of SPS compared with the other treatments, indicating that different light environment might influence sugar compositions via regulating the activities of sucrose metabolism enzymes. On the whole, R/B(1 h) was the optimal lighting strategy in terms of lettuce yield, taste and energy use efficiency in the present study.

20.
J Contin Educ Nurs ; 50(6): 275-281, 2019 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-31136671

RESUMO

BACKGROUND: Nurses' level of knowledge about pain management directly determines the steps of implementation of clinical pain policies. METHOD: This study surveyed 2,882 pediatric nurse practitioners from six children's hospitals using demographics and pain management questionnaires, as well as the Chinese version questionnaire of the Pediatric Nurse Practitioners' Knowledge and Attitudes Survey Regarding Pain (PNKAS) via the WeChat application. RESULTS: The total score on the PNKAS was 14.88 ± 3.58 for the pediatric nurse practitioners. Multiple regression results showed the main factors influencing the PNKAS score related to position, the frequency of receiving training pain-related knowledge, and working department, which could account for 35.1% of the total variance. CONCLUSION: Pediatric nurse practitioners from pediatric hospitals were not found to have sufficient knowledge or an appropriate attitude regarding pain management. A new standardized training project of pain management that is closely related to clinical practice for children should be conducted in the future. [J Contin Educ Nurs. 2019;50(6):275-281.].

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