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1.
Appl Microbiol Biotechnol ; 105(20): 7695-7708, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34586458

RESUMO

Fipronil is a broad-spectrum phenyl-pyrazole insecticide that is widely used in agriculture. However, in the environment, its residues are toxic to aquatic animals, crustaceans, bees, termites, rabbits, lizards, and humans, and it has been classified as a C carcinogen. Due to its residual environmental hazards, various effective approaches, such as adsorption, ozone oxidation, catalyst coupling, inorganic plasma degradation, and microbial degradation, have been developed. Biodegradation is deemed to be the most effective and environmentally friendly method, and several pure cultures of bacteria and fungi capable of degrading fipronil have been isolated and identified, including Streptomyces rochei, Paracoccus sp., Bacillus firmus, Bacillus thuringiensis, Bacillus spp., Stenotrophomonas acidaminiphila, and Aspergillus glaucus. The metabolic reactions of fipronil degradation appear to be the same in different bacteria and are mainly oxidation, reduction, photolysis, and hydrolysis. However, the enzymes and genes responsible for the degradation are somewhat different. The ligninolytic enzyme MnP, the cytochrome P450 enzyme, and esterase play key roles in different strains of bacteria and fungal. Many unanswered questions exist regarding the environmental fate and degradation mechanisms of this pesticide. The genes and enzymes responsible for biodegradation remain largely unexplained, and biomolecular techniques need to be applied in order to gain a comprehensive understanding of these issues. In this review, we summarize the literature on the degradation of fipronil, focusing on biodegradation pathways and identifying the main knowledge gaps that currently exist in order to inform future research. KEY POINTS: • Biodegradation is a powerful tool for the removal of fipronil. • Oxidation, reduction, photolysis, and hydrolysis play key roles in the degradation of fipronil. • Possible biochemical pathways of fipronil in the environment are described.


Assuntos
Inseticidas , Poluentes do Solo , Streptomyces , Animais , Aspergillus , Biodegradação Ambiental , Pirazóis/análise , Coelhos , Poluentes do Solo/análise , Stenotrophomonas
2.
Int J Med Sci ; 18(13): 2897-2904, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34220316

RESUMO

Background: The detectable component of triglyceride-rich lipoproteins (TGRLs), remnant lipoprotein cholesterol (RLP-c), has been proven being correlated with the progression of atherosclerosis and myocardial infarction. However, when taken as a risk predictor, the prognostic and diagnostic potential of RLP-c remains controversial in studies. In this study, we evaluated the hypothesis that atherogenic lipoprotein-cholesterol (AL-c), representing the sum of RLP-c and the sd-LDL-c, to the HDL-c ratio, could represent a better predictive indicator than RLP-c alone in ST-segment elevation myocardial infarction (STEMI). Methods: The 316 consecutive patients suffering from persistent chest discomfort admitted to the Shanghai General Hospital between January 2018 and June 2018 were enrolled. 149 STEMI patients (62% men, mean age 69.6 ± 13.3 years) were included as the study cohort. The AL-c/HDL-c ratio was calculated on admission in a cohort of electrocardiogram-confirmed STEMI patients and compared to other lipid profiles as a predictive indicator. Results: The AL-c/HDL-c ratio was significantly increased in STEMI patients compared with apparently healthy adults (0.93; IQR [0.71-1.18] vs 0.70; IQR [0.45-1.04]; p < 0.001). Gender dependency existed, and the male and female patients had median AL-c/HDL-c ratios of 1.01 and 0.79, respectively (p < 0.001). Compared to RLP-c, the AL-c/HDL-c ratio had a better prognostic value to predict STEMI risk in both sexes (AUC of 0.672 with a sensitivity of 0.794 in males and 0.613 with a sensitivity of 0.684 in females). Conclusions: The AL-c/HDL-c ratio could represent a convenient and sensitive biomarker for screening and predicting STEMI risk.

3.
Cell Prolif ; 54(8): e13088, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34240781

RESUMO

OBJECTIVES: Breast cancer-amplified sequence 3 (BCAS3) was initially found to be amplified in human breast cancer (BRCA); however, there has been little consensus on the functions of BCAS3 in breast tumours. MATERIALS AND METHODS: We analysed BCAS3 expression in BRCA using bio-information tools. Affinity purification and mass spectrometry were employed to identify BCAS3-associated proteins. GST pull-down and ubiquitination assays were performed to analyse the interaction mechanism between BCAS3/p53 and CUL4A-RING E3 ubiquitin ligase (CRL4A) complex. BCAS3 was knocked down individually or in combination with p53 in MCF-7 cells to further explore the biological functions of the BCAS3/p53 axis. The clinical values of BCAS3 for BRCA progression were evaluated via semiquantitative immunohistochemistry (IHC) analysis and Cox regression. RESULTS: We reported that the expression level of BCAS3 in BRCA was higher than that in adjacent normal tissues. High BCAS3 expression promoted growth, inhibited apoptosis and conferred chemoresistance in breast cancer cells. Mechanistically, BCAS3 overexpression fostered BRCA cell growth by interacting with the CRL4A complex and promoting ubiquitination and proteasomal degradation of p53. Furthermore, BCAS3 could regulate cell growth, apoptosis and chemoresistance through a p53-mediated mechanism. Clinically, BCAS3 overexpression was significantly correlated with a malignant phenotype. Moreover, higher expression of BCAS3 correlates with shorter overall survival (OS) in BRCA. CONCLUSIONS: The functional characterization of BCAS3 offers new insights into the oncogenic properties and chemotherapy resistance in breast cancer.


Assuntos
Neoplasias da Mama/patologia , Proteínas de Neoplasias/metabolismo , Proteína Supressora de Tumor p53/metabolismo , Apoptose , Neoplasias da Mama/metabolismo , Neoplasias da Mama/mortalidade , Linhagem Celular Tumoral , Núcleo Celular/metabolismo , Proliferação de Células , Proteínas Culina/metabolismo , Resistencia a Medicamentos Antineoplásicos , Feminino , Humanos , Pessoa de Meia-Idade , Proteínas de Neoplasias/antagonistas & inibidores , Proteínas de Neoplasias/genética , Prognóstico , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Taxa de Sobrevida , Proteína Supressora de Tumor p53/antagonistas & inibidores , Proteína Supressora de Tumor p53/genética , Ubiquitina-Proteína Ligases/metabolismo , Ubiquitinação
4.
Sci Rep ; 11(1): 14894, 2021 07 21.
Artigo em Inglês | MEDLINE | ID: mdl-34290269

RESUMO

Roux-en-Y gastric bypass (RYGB) has been demonstrated to be the most effective treatment for morbid obesity, yet the impact of RYGB on intestinal permeability is not fully known. In this work, we subjected obese mice to RYGB and sham operation procedures. Serum lipopolysaccharide (LPS) level, inflammatory cytokines and intestinal permeability were measured at 8 weeks post surgery. In contrast to sham surgery, RYGB reduced body weight, improved glucose tolerance and insulin resistance, and decreased serum levels of LPS, IL6 and TNFα. Intestinal permeability of the common limb and colon was significantly improved in the RYGB group compared to the sham group. The mRNA levels of IL1ß, IL6, and TLR4 in the intestine were significantly decreased in the RYGB group compared with the sham group. The expression levels of intestinal islet-derived 3ß (REG3ß), islet-derived 3γ (REG3γ) and intestinal alkaline phosphatase (IAP) were higher in the RYGB group than in the sham group. In conclusion, in a diet-induced obesity (DIO) mouse model, both decreased intestinal permeability and attenuated systemic inflammation after RYGB surgery were associated with improved innate immunity, which might result from enhanced production of IAP and antimicrobial peptides.

6.
J Hazard Mater ; 418: 126294, 2021 09 15.
Artigo em Inglês | MEDLINE | ID: mdl-34102366

RESUMO

We prepared a single-atom Fe catalyst supported on an oxygen-doped, nitrogen-rich carbon support (SAFe-OCN) for degrading a broad spectrum of contaminants of emerging concern (CECs) by activating peroxides such as peroxymonosulfate (PMS). In the SAFe-OCN/PMS system, most selected CECs were amenable to degradation and high-valent Fe species were present for oxidation. Moreover, SAFe-OCN showed excellent performance for contaminant degradation in complex water matrices and high stability in oxidation. Specifically, SAFe-OCN, with a catalytic center of Fe coordinated with both nitrogen and oxygen (FeNxO4-x), showed 5.13-times increased phenol degradation kinetics upon activating PMS compared to the catalyst where Fe was only coordinated with nitrogen (FeN4). Molecular simulations suggested that FeNxO4-x, compared to FeN4, was an excellent multiple-electron donor and it could potential-readily form high-valent Fe species upon oxidation. In summary, the single-atom Fe catalyst enables efficient, robust, and sustainable water and wastewater treatment, and molecular simulations highlight that the electronic nature of Fe could play a key role in determining the activity of the single-atom catalyst.


Assuntos
Ferro , Peróxidos , Carbono , Catálise , Oxirredução
7.
J Med Virol ; 93(10): 5825-5832, 2021 10.
Artigo em Inglês | MEDLINE | ID: mdl-34061377

RESUMO

The coronavirus disease 2019 (COVID-19) pandemic has focused attention on the need to develop effective therapeutics against the causative pathogen, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and also against other pathogenic coronaviruses. In this study, we report on a kind of bisbenzylisoquinoline alkaloid, neferine, as a pan-coronavirus entry inhibitor. Neferine effectively protected HEK293/hACE2 and HuH7 cell lines from infection by different coronaviruses pseudovirus particles (SARS-CoV-2, SARS-CoV-2 [D614G, N501Y/D614G, 501Y.V1, 501Y.V2, 501Y.V3 variants], SARS-CoV, MERS-CoV) in vitro, with median effect concentration (EC50 ) of 0.13-0.41 µM. Neferine blocked host calcium channels, thus inhibiting Ca2+ -dependent membrane fusion and suppressing virus entry. This study provides experimental data to support the fact that neferine may be a promising lead for pan-coronaviruses therapeutic drug development.


Assuntos
Antivirais/farmacologia , Benzilisoquinolinas/farmacologia , Cálcio/metabolismo , SARS-CoV-2/efeitos dos fármacos , Internalização do Vírus/efeitos dos fármacos , COVID-19/virologia , Linhagem Celular , Coronavirus/efeitos dos fármacos , Coronavirus/fisiologia , Células HEK293 , Humanos , Isoquinolinas/farmacologia , Fenóis/farmacologia , SARS-CoV-2/fisiologia
8.
ACS Appl Mater Interfaces ; 13(25): 30205-30212, 2021 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-34137259

RESUMO

Bioskins possess a great ability to detect and deliver external mechanical or temperature stimuli into identifiable signals such as color changes. However, the integration of visualization with simultaneous detection of multiple complex external stimuli in a single biosensor device remains a challenge. Here we propose an all-solution-processed bioinspired stretchable electronic skin with interactive color changes and four-mode sensing properties. The fabricated biosensor demonstrates sensitive responses to various stimuli including pressure, strain, voltage, and temperature. Sensing visualization is realized by color changes of the e-skin from brown to green and finally bright yellow as a response to intensified external stimuli, suggesting great application potential in military defense, healthcare monitoring, and smart bionic skin.


Assuntos
Colorimetria/instrumentação , Dispositivos Eletrônicos Vestíveis , Colorimetria/métodos , Desenho de Equipamento , Humanos , Pressão , Temperatura
9.
Front Cell Infect Microbiol ; 11: 642500, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34041042

RESUMO

Background: The aim of this study was to explore potential risk factors for cytomegalovirus (CMV) reactivation and their impact on liver failure patient outcomes. Methods: A 10-year retrospective case-control study was conducted in adult participants, who were diagnosed with liver failure and had undergone CMV DNA tests. CMV reactivation cases were matched with controls at a 2:1 ratio based on age, sex, and year of admission. Univariate and multivariate analyses were used to explore risk factors for CMV reactivation. Results: Between January 2011 and April 2020, 198 adult patients with liver failure and available CMV DNA test results were enrolled into the study. Among them, 33 patients had detectable CMV DNA in their plasma (16.7%). Clinical manifestations and liver function were comparable between the CMV reactivation and non-reactivation groups. However, CMV reactivation may triple mortality in patients with liver failure. We found that nearly 50% of patients in the CMV-positive group received glucocorticoids, compared to 13.6% in the CMV-negative group (P=0.000). The median total glucocorticoid dose included 836.5 mg of methylprednisolone (IQR 308.7-1259.0 mg) in the CMV-positive group, which was significantly higher than that in the CMV-negative group. A multivariate analysis revealed that glucocorticoid use significantly increased the risk of CMV reactivation (adjusted OR, 4.84; 95% CI, 1.61-14.49; P=0.005). Patients with CMV reactivation tended to be associated with higher white cell counts (adjusted OR, 1.21; 95% CI, 1.08-1.36; P=0.002). Conclusions: High intravenous glucocorticoid doses may be the most important risk factor for CMV reactivation in liver failure.


Assuntos
Infecções por Citomegalovirus , Falência Hepática , Adulto , Estudos de Casos e Controles , Citomegalovirus , Humanos , Estudos Retrospectivos , Ativação Viral
10.
FASEB J ; 35(6): e21664, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-34042215

RESUMO

The pluripotency gene regulatory network of porcine induced pluripotent stem cells(piPSCs), especially in epigenetics, remains elusive. To determine the biological function of epigenetics, we cultured piPSCs in different culture conditions. We found that activation of pluripotent gene- and pluripotency-related pathways requires the erasure of H3K9 methylation modification which was further influenced by mouse embryonic fibroblast (MEF) served feeder. By dissecting the dynamic change of H3K9 methylation during loss of pluripotency, we demonstrated that the H3K9 demethylases KDM3A and KDM3B regulated global H3K9me2/me3 level and that their co-depletion led to the collapse of the pluripotency gene regulatory network. Immunoprecipitation-mass spectrometry (IP-MS) provided evidence that KDM3A and KDM3B formed a complex to perform H3K9 demethylation. The genome-wide regulation analysis revealed that OCT4 (O) and SOX2 (S), the core pluripotency transcriptional activators, maintained the pluripotent state of piPSCs depending on the H3K9 hypomethylation. Further investigation revealed that O/S cooperating with histone demethylase complex containing KDM3A and KDM3B promoted pluripotency genes expression to maintain the pluripotent state of piPSCs. Together, these data offer a unique insight into the epigenetic pluripotency network of piPSCs.


Assuntos
Regulação da Expressão Gênica no Desenvolvimento , Redes Reguladoras de Genes , Células-Tronco Pluripotentes Induzidas/metabolismo , Histona Desmetilases com o Domínio Jumonji/metabolismo , Fator 3 de Transcrição de Octâmero/metabolismo , Fatores de Transcrição SOXB1/metabolismo , Animais , Metilação de DNA , Epigênese Genética , Células-Tronco Pluripotentes Induzidas/citologia , Histona Desmetilases com o Domínio Jumonji/genética , Fator 3 de Transcrição de Octâmero/genética , Fatores de Transcrição SOXB1/genética , Suínos
11.
Protein Expr Purif ; 185: 105893, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-33933613

RESUMO

MAP30 (Momordica antiviral protein 30kD) is a single-chain Ⅰ-type ribosome inactivating protein with a variety of biological activities, including anti-tumor ability. It was reported that MAP30 would serve as a novel and relatively safe agent for prophylaxis and treatment of liver cancer. To determine whether adding two tumor targeting peptides could improve the antitumor activities of MAP30, we genetically modified MAP30 with an RGD motif and a EGFRi motif, which is a ligand with high affinity for αvß3 integrins and with high affinity for EGFR. The recombinant protein ELRL-MAP30 (rELRL-MAP30) containing a GST-tag was expressed in E. coli. The rELRL-MAP30 was highly expressed in the soluble fraction after induction with 0.15 mM IPTG for 20 h at 16 °C. The purified rELRL-MAP30 appeared as a band on SDS-PAGE. It was identified by western blotting. Cytotoxicity of recombinant protein to HepG2, MDA-MB-231, HUVEC and MCF-7 cells was detected by MTT analysis. Half maximal inhibitory concentration (IC50) values were 54.64 µg/mL, 70.13 µg/mL, 146 µg/mL, 466.4 µg/mL, respectively. Proliferation inhibition assays indicated that rELRL-MAP30 could inhibit the growth of Human liver cancer cell HepG2 effectively. We found that rELRL-MAP30 significantly induced apoptosis in liver cancer cells, as evidenced by nuclear staining of DAPI. In addition, rELRL-MAP30 induced apoptosis in human liver cancer HepG2 cells by up-regulation of Bax as well as down-regulation of Bcl-2. Migration of cell line were markedly inhibited by rELRL-MAP30 in a dose-dependent manner compared to the recombinant MAP30 (rMAP30). In summary, the fusion protein displaying extremely potent cytotoxicity might be highly effective for tumor therapy.

12.
Appl Microbiol Biotechnol ; 105(11): 4369-4381, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34021814

RESUMO

The herbicide butachlor has been used in huge quantities worldwide, affecting various environmental systems. Butachlor residues have been detected in soil, water, and organisms, and have been shown to be toxic to these non-target organisms. This paper briefly summarizes the toxic effects of butachlor on aquatic and terrestrial animals, including humans, and proposes the necessity of its removal from the environment. Due to long-term exposure, some animals, plants, and microorganisms have developed resistance toward butachlor, indicating that the toxicity of this herbicide can be reduced. Furthermore, we can consider removing butachlor residues from the environment by using such butachlor-resistant organisms. In particular, microbial degradation methods have attracted much attention, with about 30 kinds of butachlor-degrading microorganisms have been found, such as Fusarium solani, Novosphingobium chloroacetimidivorans, Chaetomium globosum, Pseudomonas putida, Sphingomonas chloroacetimidivorans, and Rhodococcus sp. The metabolites and degradation pathways of butachlor have been investigated. In addition, enzymes associated with butachlor degradation have been identified, including CndC1 (ferredoxin), Red1 (reductase), FdX1 (ferredoxin), FdX2 (ferredoxin), Dbo (debutoxylase), and catechol 1,2 dioxygenase. However, few reviews have focused on the microbial degradation and molecular mechanisms of butachlor. This review explores the biochemical pathways and molecular mechanisms of butachlor biodegradation in depth in order to provide new ideas for repairing butachlor-contaminated environments. KEY POINTS: • Biodegradation is a powerful tool for the removal of butachlor. • Dechlorination plays a key role in the degradation of butachlor. • Possible biochemical pathways of butachlor in the environment are described.


Assuntos
Herbicidas , Acetanilidas , Biodegradação Ambiental , Chaetomium , Fusarium , Herbicidas/toxicidade , Humanos , Redes e Vias Metabólicas , Sphingomonadaceae , Sphingomonas
13.
Zool Res ; 42(3): 377-388, 2021 May 18.
Artigo em Inglês | MEDLINE | ID: mdl-33998185

RESUMO

LIN28A, an RNA-binding protein, plays an important role in porcine induced pluripotent stem cells (piPSCs). However, the molecular mechanism underlying the function of LIN28A in the maintenance of pluripotency in piPSCs remains unclear. Here, we explored the function of LIN28A in piPSCs based on its overexpression and knockdown. We performed total RNA sequencing (RNA-seq) of piPSCs and detected the expression levels of relevant genes by quantitative real-time polymerase chain reaction (qRT-PCR), western blot analysis, and immunofluorescence staining. Results indicated that piPSC proliferation ability decreased following LIN28A knockdown. Furthermore, when LIN28A expression in the shLIN28A2 group was lower (by 20%) than that in the negative control knockdown group ( shNC), the pluripotency of piPSCs disappeared and they differentiated into neuroectoderm cells. Results also showed that LIN28A overexpression inhibited the expression of DUSP (dual-specificity phosphatases) family phosphatases and activated the mitogen-activated protein kinase (MAPK) signaling pathway. Thus, LIN28A appears to activate the MAPK signaling pathway to maintain the pluripotency and proliferation ability of piPSCs. Our study provides a new resource for exploring the functions of LIN28A in piPSCs.


Assuntos
Fosfatases de Especificidade Dupla/metabolismo , Células-Tronco Pluripotentes Induzidas/fisiologia , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Proteínas de Ligação a RNA/metabolismo , Animais , Proliferação de Células , Fosfatases de Especificidade Dupla/genética , Técnicas de Silenciamento de Genes , Células HEK293 , Humanos , Sistema de Sinalização das MAP Quinases/fisiologia , Quinases de Proteína Quinase Ativadas por Mitógeno/genética , Proteínas de Ligação a RNA/genética , Suínos
14.
J Plant Physiol ; 260: 153390, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33667937

RESUMO

To maximize breeding and exploitation of disease resistance traits for managing apple replant disease (ARD), it is of great importance to understand the mechanisms of apple root resistance. Currently, little is known about the functions of the specific genes that confer resistance traits in apple root. In this study, molecular, biochemical, and genetic approaches allowed an in-depth understanding of the role of the MdPR4 gene in the defense response of apple root. The MdPR4 encoding gene showed upregulation following ARD pathogen inoculation in our previous transcriptome data. Subcellular localization analyses revealed that MdPR4 is localized on the plasma membrane, endoplasmic reticulum, and apoplast, which is mainly determined by its signal peptide. Molecular docking analysis between MdPR4 protein with chitin molecule and in vitro MdPR4 chitin affinity assay proved its chitin-binding ability, which provided evidence for its role in chitin-mediated immune responses. Purified MdPR4 protein and MdPR4 overexpressed apple callus inhibited spore germination and mycelial growth of ARD-related Fusarium spp. pathogens. These data support the conclusion that MdPR4 is a chitin-binding protein in apple vegetative tissues that may play an important role in defense activation in response to ARD pathogen infection.


Assuntos
Fusarium/fisiologia , Malus/imunologia , Proteínas de Membrana/genética , Doenças das Plantas/imunologia , Imunidade Vegetal/genética , Proteínas de Plantas/genética , Quitina/metabolismo , Fusarium/crescimento & desenvolvimento , Regulação da Expressão Gênica de Plantas/imunologia , Malus/genética , Proteínas de Membrana/imunologia , Proteínas de Membrana/metabolismo , Simulação de Acoplamento Molecular , Micélio/crescimento & desenvolvimento , Micélio/fisiologia , Doenças das Plantas/microbiologia , Proteínas de Plantas/imunologia , Proteínas de Plantas/metabolismo , Esporos Fúngicos/crescimento & desenvolvimento
15.
Sci Adv ; 7(5)2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33571113

RESUMO

The growth of the Tibetan Plateau throughout the past 66 million years has profoundly affected the Asian climate, but how this unparalleled orogenesis might have driven vegetation and plant diversity changes in eastern Asia is poorly understood. We approach this question by integrating modeling results and fossil data. We show that growth of north and northeastern Tibet affects vegetation and, crucially, plant diversity in eastern Asia by altering the monsoon system. This northern Tibetan orographic change induces a precipitation increase, especially in the dry (winter) season, resulting in a transition from deciduous broadleaf vegetation to evergreen broadleaf vegetation and plant diversity increases across southeastern Asia. Further quantifying the complexity of Tibetan orographic change is critical for understanding the finer details of Asian vegetation and plant diversity evolution.

16.
Plant Sci ; 304: 110747, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33568292

RESUMO

Anthocyanin provides a red color for apple and health benefit for human. To better understand the molecular mechanisms of regulating apple color formation, we analyzed 27 transcriptomes of fruit skin from three cultivars 'Huashuo' (red-skinned), 'Hongcuibao' (red-skinned), and 'Golden Delicious' (yellow-skinned) at 0, 2, and 6 days after bag removal. Using pairwise comparisons and weighted gene co-expression network analyses (WGCNA), we constructed 17 co-expression modules. Among them, a specific module was negatively correlated to anthocyanin accumulation. The genes in the module are enriched in flavonoid biosynthesis pathways. These pathway genes were used to construct gene co-expression network of anthocyanin accumulation. Finally, a R2R3-MYB repressor designated MdMYB28 was identified as a key hub gene in the anthocyanin metabolism network. During the anthocyanin accumulation of apple fruit skin reaching a peak, MdMYB28 expression level was negatively correlated with the anthocyanin content. MdMYB28 was shown to directly bind to the promoter of MdMYB10 in yeast one-hybrid analyses. Over-expression of MdMYB28 decreased the anthocyanin biosynthesis in tobacco flower petals, suggesting that MdMYB28 acts as a negatively regulator of anthocyanin biosynthesis.


Assuntos
Flavonoides/metabolismo , Frutas/metabolismo , Genes de Plantas/genética , Malus/genética , Epiderme Vegetal/metabolismo , Antocianinas/metabolismo , Regulação da Expressão Gênica de Plantas , Malus/metabolismo , Filogenia , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Proteínas de Plantas/fisiologia , Plantas Geneticamente Modificadas , Reação em Cadeia da Polimerase em Tempo Real , Análise de Sequência de DNA , Tabaco , Transcriptoma , Técnicas do Sistema de Duplo-Híbrido
17.
Stem Cell Res Ther ; 12(1): 149, 2021 02 25.
Artigo em Inglês | MEDLINE | ID: mdl-33632325

RESUMO

BACKGROUND: Patients with coronary artery disease (CAD) are characterized by a decline in vascular regeneration, which is related to the dysfunction of endothelial progenitor cells (EPCs). G-protein-coupled receptor 4 (GPR4) is a proton-sensing G-protein-coupled receptor (GPCR) that contributes to neovascularization in acidic microenvironments. However, the role of GPR4 in regulating the angiogenic capacity of EPCs from CAD patients in response to acidity generated in ischemic tissue remains completely unclear. METHODS: The angiogenic capacity of EPCs collected from CAD patients and healthy subjects was evaluated in different pH environments. The GPR4 function of regulating EPC-mediated angiogenesis was analyzed both in vitro and in vivo. The downstream mechanisms were further investigated by genetic overexpression and inhibition. RESULTS: Acidic environment prestimulation significantly enhanced the angiogenic capacity of EPCs from the non-CAD group both in vivo and in vitro, while the same treatment yielded the opposite result in the CAD group. Among the four canonical proton-sensing GPCRs, GPR4 displays the highest expression in EPCs. The expression of GRP4 was markedly lower in EPCs from CAD patients than in EPCs from non-CAD individuals independent of acid stimulation. The siRNA-mediated knockdown of GPR4 with subsequent decreased phosphorylation of STAT3 mimicked the impaired function of EPCs from CAD patients at pH 6.4 but not at pH 7.4. Elevating GPR4 expression restored the neovessel formation mediated by EPCs from CAD patients in an acidic environment by activating STAT3/VEGFA signaling. Moreover, the beneficial impact of GPR4 upregulation on EPC-mediated angiogenic capacity was abrogated by blockade of the STAT3/VEGFA signaling pathway. CONCLUSIONS: Our present study demonstrated for the first time that loss of GPR4 is responsible for the decline in proton sensing and angiogenic capacity of EPCs from CAD patients. Augmentation of GPR4 expression promotes the neovessel formation of EPCs by activating STAT3/VEGF signaling. This finding implicates GPR4 as a potential therapeutic target for CAD characterized by impaired neovascularization in ischemic tissues.


Assuntos
Doença da Artéria Coronariana , Células Progenitoras Endoteliais , Células Cultivadas , Doença da Artéria Coronariana/genética , Humanos , Neovascularização Fisiológica , Receptores Acoplados a Proteínas G/genética , Fator de Transcrição STAT3/genética , Transdução de Sinais , Fator A de Crescimento do Endotélio Vascular
18.
Nanoscale ; 2021 Jan 04.
Artigo em Inglês | MEDLINE | ID: mdl-33393574

RESUMO

Biocompatible materials have received increasing attention as one of the most important building blocks for flexible and transient memories. Herein, a fully biocompatible resistive switching (RS) memory electronic composed of a carbon dot (CD)-polyvinyl pyrrolidone (PVP) nanocomposite and a silver nanowire (Ag NW) network buried in a flexible gelatin film is introduced with promising nonvolatile RS characteristics for flexible and transient memory applications. The fabricated device exhibited a rewritable flash-type memory behavior, such as low operation voltage (≈ -1.12 V), high ON/OFF ratio (>102), long retention time (over 104 s), and small bending radius (15 mm). As a proof of degradability, this transient memory can dissolve completely within 90 s after being immersed into deionized water at 55 °C; it can decompose naturally in soil within 6 days. This fully biocompatible memory electronic paves a novel way for flexible and wearable green electronics.

19.
Angew Chem Int Ed Engl ; 60(15): 8505-8509, 2021 Apr 06.
Artigo em Inglês | MEDLINE | ID: mdl-33484217

RESUMO

The formation of high-nuclearity silver(I) clusters remains elusive and their potential applications are still underdeveloped. Herein, we firstly prepared a chain-like thiolated AgI complex {[Ag18 (St Bu)10 (NO3 )8 (CH3 CN)2 (H2 O)2 ] ⋅ [Ag18 (St Bu)10 (NO3 )8 (CH3 CN)6 ]}n (abbreviated as Ag18 ) in which two similar Ag18 clusters are assembled by NO3 - anions. The solution containing Ag18 reacted with hydrogen sulfide with controlled concentration, promptly producing another identifiable and bright red-emitting high-nuclearity silver(I) cluster, Ag62 (S)13 (St Bu)32 (NO3 )4 (abbreviated as Ag62 ). We tracked the transformation using time-dependent electrospray ionization mass spectrometry (ESI-MS), UV/Vis absorption and photoluminescence spectra. Based on this cluster transformation, we further developed an ultra-sensitive turn-on sensor detecting H2 S gas with an ultrafast response time (30 s) at a low detection limit (0.13 ppm). This work opens a new way of understanding the growth of metal clusters and developing their luminescent sensing applications.

20.
Clin Microbiol Infect ; 27(7): 1000-1006, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33421578

RESUMO

OBJECTIVES: Delay in diagnosis of tuberculosis (TB) is an important but under-appreciated problem. Our study aimed to analyse the patient pathway and possible risk factors of long diagnostic delay (LDD). METHODS: We enrolled 400 new bacteriologically diagnosed patients with pulmonary TB from 20 hospitals across China. LDD was defined as an interval between the initial care visit and the confirmation of diagnosis exceeding 14 days. Its potential risk factors were investigated by multivariate logistic regression and multilevel logistic regression. Hospitals in China were classified by increasing size, from level 0 to level 3. TB laboratory equipment in hospitals was also evaluated. RESULTS: The median diagnostic delay was 20 days (IQR: 7-72 days), and 229 of 400 patients (57.3%, 95%CI 52.4-62.1) had LDD; 15% of participants were diagnosed at the initial care visit. Compared to level 0 facilities, choosing level 2 (OR 0.27, 95%CI 0.12-0.62, p 0.002) and level 3 facilities (OR 0.34, 95%CI 0.14-0.84, p 0.019) for the initial care visit was independently associated with shorter LDD. Equipping with smear, culture, and Xpert at initial care visit simultaneously also helped to avoid LDD (OR 0.28, 95%CI 0.09-0.82, p 0.020). The multilevel logistic regression yielded similar results. Availability of smear, culture, and Xpert was lower in level 0-1 facilities than in level 2-3 facilities (p < 0.001, respectively). CONCLUSIONS: Most patients failed to be diagnosed at the initial care visit. Patients who went to low-level facilities initially had a higher risk of LDD. Improvement of TB laboratory equipment, especially at low-level facilities, is urgently needed.

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