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1.
Artigo em Inglês | MEDLINE | ID: mdl-31529346

RESUMO

Design and synthesis of arsenic adsorbents with high performance and excellent stability has been still a significant challenge. In this study, we anchored nano-zero-valent iron (NZVI) on the surface of graphene-silica composites (GS) with high specific surface area, forming the NZVI/GS nano-composite. The prepared nano-materials were used to remove As(III) and As(V) through adsorption from aqueous solutions. The results indicated that NZVI particles were dispersed well on the surface of GS, and the NZVI/GS showed great potential to remove As(III) and As(V). Adsorption performance of NZVI/GS for As(III) and As(V) highly depended on the pH of solutions. The experimental data fitted well with the pseudo-second-order kinetic model and the Langmuir isotherm model. The calculated maximum adsorption capacities of NZVI/GS for As(III) and As(V) were up to 45.57 mg/g and 45.12 mg/g at 298 K, respectively, and the adsorption equilibrium could be reached within 60 min. The residual concentrations of As(III) and As(V) after treatment with 0.4 g/L NZVI/GS can meet with the drinking water standard of WHO when the initial concentrations were below 4 mg/L and 3 mg/L, respectively. Moreover, the as-prepared NZVI/GS had excellent anti-interference ability during the process of As removal in the presence of foreign ions. During the As removal process, As(III) was oxidized to As(V), which could be removed through adsorption by electrostatic attraction and complexation. These results indicated that the as-synthesized NZVI/GS composite is a promising adsorbent for the removal of arsenic from aqueous solutions.

2.
Mol Psychiatry ; 2019 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-31413370

RESUMO

Opioids, such as morphine, are clinic analgesics which induce euphoria. Morphine exposure modifies the excitability and functional interactions between neurons, while the underlying cellular and molecular mechanisms, especially how morphine assembles heterogeneous interneurons (INs) in prelimbic cortex (PrL) to mediate disinhibition and reward, are not clear. Using approaches of optogenetics, electrophysiology, and cell type-specific RNA-seq, we show that morphine attenuates the inhibitory synaptic transmission from parvalbumin+ (PV)-INs onto pyramidal neurons in PrL via µ-opioid receptor (MOR) in PV-INs. Meanwhile, morphine enhances the inhibitory inputs from somatostatin+ (SST)-INs onto PV-INs, and thus disinhibits pyramidal neurons via δ-opioid receptor (DOR)-dependent Rac1 upregulation in SST-INs. We show that MOR in PV-INs is required for morphine-induced behavioral sensitization, while DOR as well as Rac1 activity in SST-INs is required for morphine-induced conditioned place preference and hyper-locomotion. These results reveal that SST- and PV-INs, functioning in PrL as a disinhibitory architecture, are coordinated by morphine via different opioid receptors to disinhibit pyramidal neurons and enhance reward.

3.
Glob Chang Biol ; 25(10): 3438-3449, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31373124

RESUMO

Changes in labile carbon (LC) pools and microbial communities are the primary factors controlling soil heterotrophic respiration (Rh ) in warming experiments. Warming is expected to initially increase Rh but studies show this increase may not be continuous or sustained. Specifically, LC and soil microbiome have been shown to contribute to the effect of extended warming on Rh . However, their relative contribution is unclear and this gap in knowledge causes considerable uncertainty in the prediction of carbon cycle feedbacks to climate change. In this study, we used a two-step incubation approach to reveal the relative contribution of LC limitation and soil microbial community responses in attenuating the effect that extended warming has on Rh . Soil samples from three Tibetan ecosystems-an alpine meadow (AM), alpine steppe (AS), and desert steppe (DS)-were exposed to a temperature gradient of 5-25°C. After an initial incubation period, soils were processed in one of two methods: (a) soils were sterilized then inoculated with parent soil microbes to assess the LC limitation effects, while controlling for microbial community responses; or (b) soil microbes from the incubations were used to inoculate sterilized parent soils to assess the microbial community effects, while controlling for LC limitation. We found both LC limitation and microbial community responses led to significant declines in Rh by 37% and 30%, respectively, but their relative contributions were ecosystem specific. LC limitation alone caused a greater Rh decrease for DS soils than AMs or ASs. Our study demonstrates that soil carbon loss due to Rh in Tibetan alpine soils-especially in copiotrophic soils-will be weakened by microbial community responses under short-term warming.

4.
Int J Dev Neurosci ; 78: 28-32, 2019 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-31419477

RESUMO

Tyrosine hydroxylase (TH) deficiency is a rare autosomal recessive inborn error of dopamine transmission, which the deficient gene is at the chromosome 11, also called'Segawa Syndrome'. TH converts tyrosine into L-DOPA, which is the direct precursor of catecholamine biosynthesis. TH deficiency causes a neurological disease with primary extrapyramidal signs and a variable response to L-DOPA. We report three patients in China who were diagnosed with Tyrosine hydroxylase (TH) deficiency by genetic testing and clinical manifestations. After L-DOPA treatment, their condition had sustained improvement.

5.
J Mol Cell Biol ; 2019 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-31291646

RESUMO

High-throughput sequencing has facilitated the identification of many types of non-coding RNAs (ncRNAs) involved in diverse cellular processes. NcRNAs as epigenetic mediators play key roles in neuronal development, maintenance, and dysfunction by controlling gene expression at multiple levels. NcRNAs may not only target specific DNA or RNA for gene silence, but may also directly interact with chromatin-modifying proteins like Polycomb group (PcG) proteins to drive orchestrated transcriptional programs. Recent significant progress has been made in characterizing ncRNAs and PcG proteins involved in transcriptional, post-transcriptional, and epigenetic regulation. More importantly, dysregulation of ncRNAs, PcG proteins and interplay among them is closely associated with the pathogenesis of central nervous system (CNS) disorders. In this review, we focus on the interplay between ncRNAs and PcG proteins in CNS, and highlight the functional roles of the partnership during neural development and diseases.

6.
Plant Sci ; 286: 28-36, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31300139

RESUMO

MYB family genes act as important regulators modulating the response to abiotic stress in plants. However, much less is known about MYB proteins in cotton. Here, we found that a cotton MYB gene, GhMYB73, was induced by NaCl and abscisic acid (ABA). Silencing GhMYB73 expression in cotton increased sensitivity to salt stress. The cotyledon greening rate of Arabidopsis thaliana over-expressing GhMYB73 under NaCl or mannitol treatment was significantly enhanced during the seedling germination stage. What's more, several osmotic stress-induced genes, such as AtNHX1, AtSOS3 and AtP5CS1, were more highly induced in the over-expression lines than in wild type under salt treatment, supporting the hypothesis that GhMYB73 contributes to salinity tolerance by improving osmotic stress resistance. Arabidopsis lines over-expressing GhMYB73 had superior germination and cotyledon greening under ABA treatment, and some abiotic stress-induced genes involved in ABA pathways (AtPYL8, AtABF3, AtRD29B and AtABI5), had increased transcription levels under salt-stress conditions in these lines. Furthermore, we found that GhMYB73 physically interacts with GhPYL8 and AtPYL8, suggesting that GhMYB73 regulates ABA signaling during salinity stress response. Taken together, over-expression of GhMYB73 significantly increases tolerance to salt and ABA stress, indicating that it can potentially be used in transgenic technology approaches to improve cotton salt tolerance.


Assuntos
Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas/genética , Gossypium/fisiologia , Proteínas de Plantas/genética , Estresse Salino/genética , Fatores de Transcrição/genética , Arabidopsis/genética , Inativação Gênica , Genes myb , Gossypium/genética , Proteínas de Plantas/metabolismo , Plantas Geneticamente Modificadas/genética , Plantas Geneticamente Modificadas/metabolismo , Tolerância ao Sal/genética , Fatores de Transcrição/metabolismo
7.
Stem Cell Res ; 39: 101501, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31344652

RESUMO

GA binding protein (GABP) is a ubiquitously expressed transcription factor that regulates the development of multiple cell types, including osteoblast, hematopoietic stem cells, B cells and T cells. However, so little is known about its biological function in the development of central nervous system. In this report, we show that GABP is highly expressed in neural stem/progenitor cells (NSPCs) and down-regulated in neurons, and that GABPß1 is required for the proper proliferation of NSPCs. Knockdown of GABPα resulted in an elevated expression level of GABPß1, and GABPß1 down-regulation significantly decreased the proliferation of NSPCs, whereas GABPß2 knockdown did not result in any changes in the proliferation of NSPCs. We observed that there was nearly a 21-fold increase of the GABPß1S mRNA level in GABPß1L KO NSPCs compared to WT cells, and knocking down of GABPß1S in GABPß1L KO NSPCs could further reduce their proliferation potential. We also found that knockdown of GABPß1 promoted neuronal and astrocytic differentiation of NSPCs. Finally, we identified dozens of downstream target genes of GABPß1, which are closely associated with the cell proliferation and differentiation. Collectively, our results suggest that both GABPß1L and GABPß1S play an essential role in regulating the proper proliferation and differentiation of NSPCs.

9.
Clin Lab ; 65(6)2019 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-31232024

RESUMO

BACKGROUND: The Pentra MS CRP hematology analyzer (hereinafter the Pentra analyzer) can simultaneously provide 5-part leukocyte differential and C-reactive protein (CRP). The aim of the study was to investigate the performance of CRP determination by the Pentra analyzer. METHODS: The precision, limit of quantitation (LoQ), carryover, linearity, stability, and comparability of the Pentra analyzer were determined. The Passing-Bablok regression analysis and the Bland-Altman graphs illustrated the correlation for CRP concentration analyzed by the Pentra analyzer and BN-II analyzer. RESULTS: The within-run precision of CRP determination by the Pentra analyzer had a CV < 2.0% in peripheral blood, which met the requirements of the instructions (CV ≤ 10%). The Pentra analyzer had a total CV of 5.35% and 5.52% at a CRP concentration of 4.1 and 80 mg/L, respectively. The LoQ value for the Pentra analyzer was 0.96 mg/L. The carryover was 0.57% for peripheral blood and 0.86% for plasma by the analyzer. The stability of CRP results was good, when the anticoagulation samples were stored at room temperature or 4°C within 48 hours (deviation < 5%). The linearity range for whole blood samples was 0 - 188.13 mg/L (r² = 0.9992). There was high correlation of the CRP results analyzed with the Pentra analyzer and BN II analyzer. The Passing-Bablok regression analysis and the Bland-Altman graphs showed the bias plot display excellent agreement between the two assays (the mean value for the Pentra 2.19 mg/L and the BN-II 2.35 mg/L, n = 101). CONCLUSIONS: The results of CRP determination by the Pentra analyzer have the advantages of accuracy and reliability, and it is suitable for routine use in emergency laboratory and small to medium-size laboratories.

10.
J Mol Neurosci ; 69(2): 188-196, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31201655

RESUMO

Mutations of the CPT2 gene cause CPT2 deficiency and affect the ß-oxidation of fatty acids. This study examined the consequence of a polymorphism of rs1799822 in the CPT2 gene with respect to EV71 encephalitis in Chinese children. The study included 406 cases of both mild and severe EV71 infection diagnosed by RT-PCR, together with controls (n = 348). We used an improved multiplex ligation detection reaction technique to detect the polymorphism of rs1799822 in the CPT2 gene. The frequency of the (AG+GG) genotype and G allele in the EV71 infection group and in the severe EV71 encephalitis group was significantly lower than in the control group (p = 0.012 vs. p = 0.005, and p = 0.022 vs. p = 0.006, respectively). The frequency of the (AG+GG) genotype and G allele in the severe EV71 encephalitis group was markedly lower than in the mild EV71 encephalitis group (p = 0.045, p = 0.033). The ATP levels in the blood of the (AG+GG) genotype were distinctly higher than in the AA genotype in mild and severe EV71 encephalitis patients (P = 0.037, P = 0.040). A polymorphism of rs1799822 in the CPT2 gene is associated with the severity of EV71 encephalitis and may be one of the protection factors of severe EV71 encephalitis.

11.
Stem Cell Reports ; 13(1): 115-131, 2019 Jul 09.
Artigo em Inglês | MEDLINE | ID: mdl-31204298

RESUMO

EED (embryonic ectoderm development) is a core component of the Polycomb repressive complex 2 (PRC2) which catalyzes the methylation of histone H3 lysine 27 (H3K27) during the process of self-renewal, proliferation, and differentiation of embryonic stem cells. However, its function in the mammalian nervous system remains unexplored. Here, we report that loss of EED in the brain leads to postnatal lethality, impaired neuronal differentiation, and malformation of the dentate gyrus. Overexpression of Sox11, a downstream target of EED through interaction with H3K27me1, restores the neuronal differentiation capacity of EED-ablated neural stem/progenitor cells (NSPCs). Interestingly, downregulation of Cdkn2a, another downstream target of EED which is regulated in an H3K27me3-dependent manner, reverses the proliferation defect of EED-ablated NSPCs. Taken together, these findings established a critical role of EED in the development of hippocampal dentate gyrus, which might shed new light on the molecular mechanism of intellectual disability in patients with EED mutations.

12.
Ecology ; 100(9): e02775, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31169904

RESUMO

Changes in day (maximum temperature, TMAX ) and night temperature (minimum temperature, TMIN ) in the preseason (e.g., winter and spring) may have opposite effects on early phenophases (e.g., leafing and flowering) due to changing requirements of chilling accumulations (CAC) and heating accumulations (HAC), which could cause advance, delay or no change in early phenophases. However, their relative effects on phenology are largely unexplored, especially on the Tibetan Plateau. Here, observations were performed using a warming and cooling experiment in situ through reciprocal transplantation (2008-2010) on the Tibetan Plateau. We found that winter minimum temperature (TMIN ) warming significantly delayed mean early phenophases by 8.60 d/°C, but winter maximum temperature (TMAX ) warming advanced them by 12.06 d/°C across six common species. Thus, winter mean temperature warming resulted in a net advance of 3.46 d/°C in early phenophases. In contrast, winter TMIN cooling, on average, significantly advanced early phenophases by 5.12 d/°C, but winter TMAX cooling delayed them by 7.40 d/°C across six common species, resulting in a net delay of 2.28 d/°C for winter mean temperature cooling. The opposing effects of TMAX and TMIN warming on the early phenophases may be mainly caused by decreased CAC due to TMIN warming (5.29 times greater than TMAX ) and increased HAC due to TMAX warming (3.25 times greater than TMIN ), and similar processes apply to TMAX and TMIN cooling. Therefore, our study provides another insight into why some plant phenophases remain unchanged or delayed under climate change.

13.
Mol Nutr Food Res ; : e1801247, 2019 May 08.
Artigo em Inglês | MEDLINE | ID: mdl-31067344

RESUMO

SCOPE: Human breast milk has been shown to prevent necrotizing enterocolitis (NEC). Although exosomes have been identified in breast milk, their function and components have not been fully addressed. This study is conducted to elucidate the differences in peptidomic complexities between preterm and term milk exosomes. METHODS AND RESULTS: Breast milk samples are collected from healthy lactating mothers who have delivered term and preterm infants. Exosomes are separated and quantified. The protective effects of purified exosomes against NEC are investigated both in vitro and in vivo. The peptidomic complexities in term and preterm milk exosomes are analyzed by iTRAQ LC-MS/MS to screen differentially expressed exosomal peptides. Preterm milk exosomes administration significantly enhances proliferation and migration of intestinal epithelial cells compared with term milk exosomes. A total of 70 peptides are found to be significantly modulated in preterm milk samples compared to term milk samples. Of these, 47 peptides are upregulated, and 23 peptides are downregulated. Bioinformatics analysis suggests several potential regulatory roles of the altered peptides in intestinal epithelial cell function. CONCLUSION: These results reveal the differences for the first time in peptidomic complexities between preterm and term milk exosomes. Milk exosome administration might be a promising prevention for NEC.

14.
Appl Microbiol Biotechnol ; 103(12): 4825-4838, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31053913

RESUMO

Arginase I has been documented to impair T cell function and attenuate cellular immunity, however, there is little evidence to reveal the effect of arginase I on macrophage function. Recently, recombinant human arginase I (rhArg) has been developed for cancer therapy and is in clinical trial for hepatocellular carcinoma, whereas the potential immunosuppression induced by rhArg limited its therapeutic efficacy. To improve the clinical outcome of rhArg, addressing the immune suppression appears to be particularly important. In this study, we found that rhArg attenuated macrophage functions, including inhibiting macrophage cell proliferation, nitric oxide (NO) and reactive oxygen species (ROS) production, cytokine secretion, MHC-II surface expression, and phagocytosis, thereby inducing immunosuppression in lipopolysaccharides (LPS)/interferon-γ (IFN-γ)-activated macrophages. Notably, we observed that rhArg downregulated autophagy in activated macrophages. Moreover, application of trehalose (an autophagy inducer) significantly restored the impaired immune function in activated macrophages, suggesting the essential role of autophagy in rhArg-induced immunosuppression. To further illustrate the effect of autophagy in immunosuppression, we then observed the effect of 3-MA (an autophagy inhibitor) on the immune function of macrophages. As expected, inhibiting autophagy by 3-MA attenuated immune functions in activated macrophages. Collectively, this study elucidated that rhArg induced immunosuppression in activated macrophages via inhibiting autophagy, providing potential strategy to ameliorate the immune suppression which is of great significance to cancer therapy and facilitating the development of rhArg as a potential therapy for malignant carcinomas.


Assuntos
Arginase/imunologia , Autofagia/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Imunossupressores/farmacologia , Macrófagos/efeitos dos fármacos , Adenina/análogos & derivados , Adenina/farmacologia , Animais , Arginase/genética , Carcinoma Hepatocelular/terapia , Linhagem Celular Tumoral , Citocinas/metabolismo , Antígenos de Histocompatibilidade Classe II/metabolismo , Humanos , Neoplasias Hepáticas/terapia , Macrófagos/patologia , Camundongos , Óxido Nítrico/metabolismo , Fagocitose/efeitos dos fármacos , Células RAW 264.7 , Espécies Reativas de Oxigênio/metabolismo , Proteínas Recombinantes/imunologia , Trealose/farmacologia
15.
Neuroreport ; 30(8): 592-599, 2019 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-30969245

RESUMO

The endogenous opioid system is of great importance to normal brain functions. Opiate acts on GABAergic cells in both the ventral tegmental area and the nucleus accumbens to exert psychological effects. However, the effects of opioid signal transduction on the morphology of GABAergic interneurons (INs) of the medial prefrontal cortex (mPFC), a brain region critical for motivational and addictive behaviors, are unclear. By fluorescent dye injection and morphological reconstruction, we found that the total dendrite length and dendritic complexity of both parvalbumin (PV) INs and somatostatin (SST) INs in mPFC were significantly increased after chronic morphine administration, and such changes lasted 7 days after morphine abstinence. We then downregulated the endogenous µ-opioid and δ-opioid receptors (ORs) in the mPFC by adeno-associated virus-mediated shRNA expression. Results showed that downregulating either µ-OR or δ-OR decreased the total dendrite length and dendritic complexity of SST-INs, whereas downregulating neither µ-OR nor δ-OR affected the morphology of PV-INs. Furthermore, δ-OR but not µ-OR knockdown impaired the dendritic structure of SST-INs in the mice upon single morphine administration. Our findings indicate the differential roles of endogenous ORs in the dendritic remodeling of SST-INs and PV-INs in mPFC.

16.
Chemosphere ; 224: 588-596, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30844590

RESUMO

Tetrabromobisphenol A (TBBPA) is ubiquitous and its contents showing an increasing trend in the coastal environment. In order to investigate the effects of TBBPA on marine bivalves, juvenile manila clams Ruditapes phillipinarum were exposed to TBBPA for 28 days. The results showed that shell growth rate of juvenile clams after exposure to 62.5-1000 µg L-1 TBBPA for 28 d were significantly inhibited (p < 0.05). Then in order to link the changes in filtration rate, mRNA expression of insulin-like growth factor homologue (IGF) and tissue thyroid hormone (TH) contents to growth, juvenile clams were exposed to 62.5 and 500 µg L-1 TBBPA for 14 days. The transcriptional levels of neuroendocrine signals (NPF and insulin homologue) associated with filter feeding regulation, and genes of TH synthesis-related enzymes were also examined. The results showed that filtration rates was significantly reduced to 44.1% and 14% of controls after 14 d of exposure. In parallel, exposure to TBBPA significantly increased the expression levels of insulin which may elicit the filter feeding inhibition. TBBPA exposure caused alterations in tissue content of THs and mRNA expression of TH synthesis-related enzymes. However, the data showed increased T3 content, T3/T4 ratio and mRNA expression of IGF. These data demonstrated that the most important key event of TBBPA could be linked to growth impairment in juveniles was the reduction of filtration rate. These results provide a robust framework towards revealing the underlying mechanism of the growth inhibition caused by TBBPA on bivalves and understanding the adverse outcome pathway across taxonomic phyla.


Assuntos
Rotas de Resultados Adversos , Bivalves/crescimento & desenvolvimento , Regulação da Expressão Gênica/efeitos dos fármacos , Bifenil Polibromatos/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , Bivalves/efeitos dos fármacos , Bivalves/metabolismo , Hormônios Tireóideos/metabolismo
17.
ACS Appl Mater Interfaces ; 11(8): 8138-8147, 2019 Feb 27.
Artigo em Inglês | MEDLINE | ID: mdl-30714377

RESUMO

The regulation of oxidation levels is of great importance as an efficient way to optimize the thermoelectric (TE) performance of conducting polymers. Many efforts have been devoted to the acquisition of a high TE performance for poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS) by oxidation/reduction post treatment to achieve an effective compromise. However, a strong oxidant/reductant is usually employed to tune the TE performance of PEDOT:PSS with high electrical conductivity (σ) and Seebeck coefficient ( S), and it also presents a number of operational challenges depending on a fast reaction rate. Herein, nontoxic polyethylenimine ethoxylated (PEIE) served as a reductant to successfully realize an enhanced S for PEDOT:PSS, besides playing a significant anion-blocking role in enabling the efficient modulation of the oxidation level by sulfuric acid (H2SO4) with a longer operating time. Eventually, a good PEDOT-rich nanocrystal is achieved by a sequential dipping process in PEIE/ethylene glycol and H2SO4 solutions. The large TE power factor of 133 µW m-1 K-2 can be ascribed to the good formation of PEDOT-rich nanocrystals and an effective compromise between σ and S of PEDOT:PSS films. A mechanism was elucidated for the efficient regulation of σ and S enabling high performance of organic TE materials.

18.
Protein Cell ; 10(9): 631-648, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30788732

RESUMO

Mitochondrial dysfunctions play major roles in ageing. How mitochondrial stresses invoke downstream responses and how specificity of the signaling is achieved, however, remains unclear. We have previously discovered that the RNA component of Telomerase TERC is imported into mitochondria, processed to a shorter form TERC-53, and then exported back to the cytosol. Cytosolic TERC-53 levels respond to mitochondrial functions, but have no direct effect on these functions, suggesting that cytosolic TERC-53 functions downstream of mitochondria as a signal of mitochondrial functions. Here, we show that cytosolic TERC-53 plays a regulatory role on cellular senescence and is involved in cognition decline in 10 months old mice, independent of its telomerase function. Manipulation of cytosolic TERC-53 levels affects cellular senescence and cognition decline in 10 months old mouse hippocampi without affecting telomerase activity, and most importantly, affects cellular senescence in terc-/- cells. These findings uncover a senescence-related regulatory pathway with a non-coding RNA as the signal in mammals.

19.
Analyst ; 144(5): 1671-1678, 2019 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-30652696

RESUMO

In this work, a sensitive and selective electrochemical aptasensor for determination of microcystin-LR (MC-LR) was developed based on a dual signal amplification system consisting of a novel ternary composite and horseradish peroxidase (HRP). The ternary composite was prepared by depositing gold nanoparticles (AuNPs) on molybdenum disulfide (MoS2) covered TiO2 nanobeads (TiONBs). MoS2 nanosheet modified TiONBs provided a large surface area for immobilization of AuNPs and biomolecules. The ternary composite also possesses an improved electron transfer and catalytic capability. To construct the aptasensor, thiolated MC-LR aptamers were immobilized on the AuNP@MoS2-TiONB modified electrode through a gold-sulfur bond. Then, biotin-cDNA with a sequence complementary to the MC-LR aptamer competed with MC-LR for binding to the immobilized aptamer. The current signal catalyzed by avidin-HRP decreased with the increase of MC-LR, based on which a linear range of 0.005-30 nM and a detection limit of 0.002 nM were obtained.


Assuntos
Aptâmeros de Nucleotídeos/química , Técnicas Biossensoriais/métodos , Técnicas Eletroquímicas/métodos , Microcistinas/análise , Aptâmeros de Nucleotídeos/genética , Sequência de Bases , Benzoquinonas/química , DNA Complementar/genética , Dissulfetos/química , Água Potável/análise , Ouro/química , Peroxidase do Rábano Silvestre/química , Limite de Detecção , Nanopartículas Metálicas/química , Microcistinas/química , Molibdênio/química , Hibridização de Ácido Nucleico , Reprodutibilidade dos Testes , Rios/química , Titânio/química , Poluentes Químicos da Água/análise
20.
Chin J Integr Med ; 2019 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-30623345

RESUMO

OBJECTIVE: To investigate the inhibitory effect of Linggui Zhugan Decoction (LZD, ) on the ventricular remodeling (VR) after acute myocardial infarction (AMI) and related mRNA and proteins expression in transforming growth factor-beta 1 (TGF-ß1)/Smad signaling pathway, and explain its putative mechanism. METHODS: A VR model was generated by ligation of coronary artery in mice. Two weeks after surgery, 60 mice were randomly divided into the model group, the sham-operation group (distilled water), the positive control group (2.4 mg/kg simvastatin), and the low-, medium- and high-dose LZD groups (2.1, 4.2, 8.4 g crude drug/kg, respectively) by a random number table, 10 mice in each group. Mice in each group was treated for 4 weeks. Changes of hemodynamics indices and cardiac weight index were detected by the PowerLab data acquisition and analysis recording instrument. Morphology changes of myocardial tissue were observed by hematoxylin-eosin and Masson staining. The expressions of TGF-ß1, Smad2, Smad3, p-Smad2 and p-Smad3 in myocardial tissue were detected by Western blotting. The mRNA expressions of TGF-ß1, Smad2 and Smad3 were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expressions of matrix metalloprotein 2 (MMP2), MMP9, collagen I and collagen III were observed by immunohistochemical methods. RESULTS: VR mice showed significant dysfunction in hemodynamic indices and cardiac structure and function. Compared with the shamoperation group, myocardial tissue damage, interstitial fibrosis occurred in the model mice, left ventricular systolic pressure (LVSP), left ventricular pressure maximum contraction rate (+dp/dtmax) and left ventricular pressure maximum relaxation rate (-dp/dtmax) decreased significantly (all P<0.01), while left ventricular end-diastolic pressure (LVEDP), cardiac weight index and left ventricular weight index elevated significantly, meanwhile TGF-ß1, p-Smad2, p-Smad3, Smad2, Smad3, MMP2, MMP9, collagen I, collagen III protein expressions in myocardial tissue and TGF-ß1, Smad2 and Smad3 mRNA expressions increased significantly (all P<0.01). Compared with the model group, LZD could signififi cantly improve the pathological changes of myocardial tissue, increase LVSP, +dp/dtmax and -dp/dtmax, lower LVEDP, reduce the whole heart weight index and left ventricular weight index and inhibit the over-expressions of TGF-ß1, p-Smad2, p-Smad3, Smad2, Smad3, MMP2, MMP9, collagen I and collagen III proteins in myocardial tissue and mRNA expressions of TGF-ß1, Smad2 and Smad3 (P<0.05 or P<0.01). CONCLUSION: LZD can significantly suppress VR induced by AMI, and its underlying mechanism may be associated with its inhibitory effect on the TGF-ß1/Smad signaling pathway.

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