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1.
J Phys Condens Matter ; 32(1): 015702, 2020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-31519019

RESUMO

We measure planar Hall effect (PHE) and longitudinal anisotropic magnetoresistance (AMR) with a magnetic field rotating in the a-b plane in the type-II Dirac semimetal PdTe2. The measured PHE and AMR curves can be fitted by the theoretical equations; however, a detailed analysis of the extracted data demonstrates that the parameter related to PHE and AMR has no relationship with the chiral anomaly due to the absence of negative longitudinal magnetoresistance (MR) when the electric and magnetic fields are parallel to each other. Meanwhile, we prove that the origin of PHE in PdTe2 is the anisotropic orbital MR. Our work suggests that negative longitudinal MR is necessary to identify chiral anomaly, and we cannot in general use PHE as a signal for the presence of the chiral anomaly in Dirac/Weyl semimetals.

2.
Cell Rep ; 29(10): 3331-3348.e7, 2019 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-31801093

RESUMO

Metformin is the front-line treatment for type 2 diabetes worldwide. It acts via effects on glucose and lipid metabolism in metabolic tissues, leading to enhanced insulin sensitivity. Despite significant effort, the molecular basis for metformin response remains poorly understood, with a limited number of specific biochemical pathways studied to date. To broaden our understanding of hepatic metformin response, we combine phospho-protein enrichment in tissue from genetically engineered mice with a quantitative proteomics platform to enable the discovery and quantification of basophilic kinase substrates in vivo. We define proteins whose binding to 14-3-3 are acutely regulated by metformin treatment and/or loss of the serine/threonine kinase, LKB1. Inducible binding of 250 proteins following metformin treatment is observed, 44% of which proteins bind in a manner requiring LKB1. Beyond AMPK, metformin activates protein kinase D and MAPKAPK2 in an LKB1-independent manner, revealing additional kinases that may mediate aspects of metformin response. Deeper analysis uncovered substrates of AMPK in endocytosis and calcium homeostasis.

3.
Int J Mol Sci ; 20(21)2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31683916

RESUMO

Although metabolic perturbations are sensitive indicators for low-dose toxic effects, the metabolic mechanisms affected by rac-metalaxyl and metalaxyl-M in mammals from a metabolic profiling perspective remain unclear. In this study, the metabolic perturbations and toxic effects of rac-metalaxyl and metalaxyl-M in mice were carefully investigated using integrative nuclear magnetic resonance (NMR) and ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) based metabolomics. Histopathology, NMR-based untargeted urine profile, multivariate pattern recognition, metabolite identification, pathway analysis, UPLC-MS/MS based targeted serum amino acids, and tryptophan pathway analysis were determined after rac-metalaxyl and metalaxyl-M exposure, individually. Histopathology indicated that metalaxyl-M induced greater hepatocellular inflammatory, necrosis, and vacuolation in mice than rac-metalaxyl at the same exposure dosage. The metabolic perturbations induced by rac-metalaxyl and metalaxyl-M were directly separated using partial least-squares discriminant analysis (PLS-DA). Furthermore, metabolite identification and pathway analysis indicated that rac-metalaxyl mainly induced ten urine metabolite changes and four pathway fluctuations. However, metalaxyl-M induced 19 urine metabolite changes and six pathway fluctuations. Serum amino acids and tryptophan pathway metabolite changes induced by rac-metalaxyl and metalaxyl-M were also different even at the same exposure level. Such results may provide specific insight into the metabolic perturbations and toxic effects of rac-metalaxyl and metalaxyl-M, and contribute to providing available data for health risk assessments of rac-metalaxyl and metalaxyl-M at a metabolomics level.

4.
Psychiatry Res ; : 112690, 2019 Nov 12.
Artigo em Inglês | MEDLINE | ID: mdl-31757642

RESUMO

OBJECTIVE: We aimed to study the association among venlafaxine antidepressive outcome, NR3C2 gene polymorphisms and the change of two neuroendocrine hormones during treatment. METHODS: 195 Chinese Han major depressive disorder (MDD) patients were recruited and received a 6-week venlafaxine treatment in this study. Adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH) levels were measured at the beginning and at the end of treatment. Six single-nucleotide polymorphisms (SNPs) (NR3C2: rs1512325, rs1512342, rs2070951; NR3C1: rs6191, rs6196, rs10482614) were selected for high-throughput SNP genotyping. Allele and genotype frequencies of them were compared between remission and non-remission groups. RESULTS: We found that genotype frequency of the rs1512325 located in the NR3C2 gene was significantly different between remission and non-remission groups respectively (p < 0.05). Meanwhile, the frequency of the rs1512325 C-allele was significantly lower (p < 0.05) in remission group. The TSH concentration significantly increased after venlafaxine treatment in remission group (p < 0.05). CONCLUSION: The rs1512325 in NR3C2 gene and TSH concentration may be related to venlafaxine treatment outcome in Chinese Han MDD patients.

6.
Nat Genet ; 51(12): 1670-1678, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31740837

RESUMO

Schizophrenia is a debilitating psychiatric disorder with approximately 1% lifetime risk globally. Large-scale schizophrenia genetic studies have reported primarily on European ancestry samples, potentially missing important biological insights. Here, we report the largest study to date of East Asian participants (22,778 schizophrenia cases and 35,362 controls), identifying 21 genome-wide-significant associations in 19 genetic loci. Common genetic variants that confer risk for schizophrenia have highly similar effects between East Asian and European ancestries (genetic correlation = 0.98 ± 0.03), indicating that the genetic basis of schizophrenia and its biology are broadly shared across populations. A fixed-effect meta-analysis including individuals from East Asian and European ancestries identified 208 significant associations in 176 genetic loci (53 novel). Trans-ancestry fine-mapping reduced the sets of candidate causal variants in 44 loci. Polygenic risk scores had reduced performance when transferred across ancestries, highlighting the importance of including sufficient samples of major ancestral groups to ensure their generalizability across populations.

7.
Neural Netw ; 122: 163-173, 2019 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-31683144

RESUMO

Visual development during early childhood is a vital process. Examining the visual acuity of children is essential for early detection of visual abnormalities, but performing visual examination in children is challenging. Here, we developed a human-in-the-loop deep learning (DL) paradigm that combines traditional vision examination and DL with integration of software and hardware, thus facilitating the execution of vision examinations, offsetting the shortcomings of human doctors, and improving the abilities of both DL and doctors to evaluate the vision of children. Because this paradigm contains two rounds (a human round and DL round), doctors can learn from DL and the two can mutually supervise each other such that the precision of the DL system in evaluating the visual acuity of children is improved. Based on DL-based object localization and image identification, the experiences of doctors and the videos captured in the first round, the DL system in the second round can simulate doctors in evaluating the visual acuity of children with a final accuracy of 75.54%. For comparison, we also assessed an automatic deep learning method that did not consider the experiences of doctors, but its performance was not satisfactory. This entire paradigm can evaluate the visual acuity of children more accurately than humans alone. Furthermore, the paradigm facilitates automatic evaluation of the vision of children with a wearable device.

8.
Med Hypotheses ; 135: 109438, 2019 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-31739077

RESUMO

Bone augmentation is increasingly important in implantology. Bone substitute materials exert essential roles during bone augmentation process. However, accelerating bone substitute materials remodeling and acquiring high bone architecture quality was still the challenges of bone augmentation. Accumulated studies had suggested osteoclasts is the key cell type to resorb bone or bone substitute materials. Our previous study and other studies suggested osteoclasts contributed to bone formation by promoting osteoblast function and facilitate angiogenesis. We hypothesized that bone substitute materials loaded osteoclastogenic cytokines or osteoclast progenitors will help to bone substitute materials rapid remodeling and subsequent bone formation. Our hypothesis could help to lessen long-term post-bone augmentation period and acquire better bone quality for osseointegration.

9.
Biochim Biophys Acta Mol Cell Biol Lipids ; 1865(2): 158535, 2019 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-31678621

RESUMO

OBJECTIVE: Angiopoietin-1 (Ang-1), a secreted protein, mainly regulates angiogenesis. Ang-1 has been shown to promote the development of atherosclerosis, whereas little is known about its effects on lipid metabolism and inflammation in this process. METHOD: Ang-1 was transfected into ApoE-/- mice via lentiviral vector or incubated with THP-1 derived macrophages. Oil red O and HE staining were performed to measure the size of atherosclerotic plaques in ApoE-/- mice. Immunofluorescence was employed to show the expression of target proteins in aorta. [3H] labeled cholesterol was performed to examine the efficiency of cholesterol efflux and reverse cholesterol transport (RCT) both in vivo and vitro. Western blot and qPCR were used to quantify target proteins both in vivo and vitro. ELISA detected the levels of pro-inflammatory cytokines in mouse peritoneal macrophage. RESULTS: Our data showed that Ang-1 augmented atherosclerotic plaques formation and inhibited cholesterol efflux. The binding of Ang-1 to Tie2 resulted in downregulation of LXRα, ABCA1 and ABCG1 expression via inhibiting the translocation of TFE3 into nucleus. In addition, Ang-1 decreased serum HDL-C levels and reduced reverse cholesterol transport (RCT) in ApoE-/- mice. Furthermore, Ang-1 induced lipid accumulation followed by increasing TNF-α, IL-6, IL-1ß,and MCP-1 produced by MPMs, as well as inducing M1 phenotype macrophage marker iNOS and CD86 expression in aorta of ApoE-/- mice. CONCLUSION: Ang-1 has an adverse effect on cholesterol efflux by decreasing the expression of ABCA1 and ABCG1 via Tie2/TFE3/LXRα pathway, thereby promoting inflammation and accelerating atherosclerosis progression.

10.
PLoS One ; 14(11): e0224819, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31697777

RESUMO

OBJECTIVE: In recent years, virtual reality (VR) has been tested as a therapeutic tool in neurorehabilitation research. However, the impact effectiveness of VR technology on for Parkinson's Disease (PD) patients is still remains controversial unclear. In order to provide a more scientific basis for rehabilitation of PD patients' modality, we conducted a systematic review of VR rehabilitation training for PD patients and focused on the improvement of gait and balance. METHODS: An comprehensive search was conducted using the following databases: PubMed, Web of Science, Cochrane Library, CINHAL, Embase and CNKI (China National Knowledge Infrastructure).Articles published before 30 December 2018 and of a randomized controlled trial design to study the effects of VR for patients with PD were included. The study data were pooled and a meta-analysis was completed. This systematic review was conducted in accordance with the PRISMA guideline statement and was registered in the PROSPERO database (CRD42018110264). RESULTS: A total of sixteen articles involving 555 participants with PD were included in our analysis. VR rehabilitation training performed better than conventional or traditional rehabilitation training in three aspects: step and stride length (SMD = 0.72, 95%CI = 0.40,1.04, Z = 4.38, P<0.01), balance function (SMD = 0.22, 95%CI = 0.01,0.42, Z = 2.09, P = 0.037), and mobility(MD = -1.95, 95%CI = -2.81,-1.08, Z = 4.41, P<0.01). There was no effect on the dynamic gait index (SMD = -0.15, 95%CI = -0.50,0.19, Z = 0.86, P = 0.387), and gait speed (SMD = 0.19, 95%CI = -0.03,0.40, Z = 1.71, P = 0.088).As for the secondary outcomes, compared with the control group, VR rehabilitation training demonstrated more significant effects on the improvement of quality of life (SMD = -0.47, 95%CI = -0.73,-0.22, Z = 3.64, P<0.01), level of confidence (SMD = -0.73, 95%CI = -1.43,-0.03, Z = 2.05, P = 0.040), and neuropsychiatric symptoms (SMD = -0.96, 95%CI = -1.27,-0.65, Z = 6.07, P<0.01), while it may have similar effects on global motor function (SMD = -0.50, 95%CI = -1.48,0.48, Z = 0.99, P = 0.32), activities of daily living (SMD = 0.25, 95%CI = -0.14,0.64, Z = 1.24, P = 0.216), and cognitive function (SMD = 0.21, 95%CI = -0.28,0.69, Z = 0.84, P = 0.399).During the included interventions, four patients developed mild dizziness and one patient developed severe dizziness and vomiting. CONCLUSIONS: According to the results of this study, we found that VR rehabilitation training can not only achieve the same effect as conventional rehabilitation training. Moreover, it has better performance on gait and balance in patients with PD. Taken together, when the effect of traditional rehabilitation training on gait and balance of PD patients is not good enough, we believe that VR rehabilitation training can at least be used as an alternative therapy. More rigorous design of large-sample, multicenter randomized controlled trials are needed to provide a stronger evidence-based basis for verifying its potential advantages.

11.
J Med Genet ; 2019 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-31704776

RESUMO

BACKGROUND: Abnormal pronuclear formation during fertilisation and subsequent early embryonic arrest results in female infertility. In recent years, with the prevalence of assisted reproductive technology, a few genes have been identified that are involved in female infertility caused by abnormalities in oocyte development, fertilisation and embryonic development. However, the genetic factors responsible for multiple pronuclei formation during fertilisation and early embryonic arrest remain largely unknown. OBJECTIVE: We aim to identify genetic factors responsible for multiple pronuclei formation during fertilisation or early embryonic arrest. METHODS: Whole-exome sequencing was performed in a cohort of 580 patients with abnormal fertilisation and early embryonic arrest. Effects of mutations were investigated in HEK293T cells by western blotting and immunoprecipitation, as well as minigene assay. RESULTS: We identified a novel homozygous missense mutation (c.397T>G, p.C133G) and a novel homozygous donor splice-site mutation (c.546+5G>A) in the meiotic gene REC114. REC114 is involved in the formation of double strand breaks (DSBs), which initiate homologous chromosome recombination. We demonstrated that the splice-site mutation affected the normal alternative splicing of REC114, while the missense mutation reduced the protein level of REC114 in vitro and resulted in the loss of its function to protect its partner protein MEI4 from degradation. CONCLUSIONS: Our study has identified mutations in REC114 responsible for human multiple pronuclei formation and early embryonic arrest, and these findings expand our knowledge of genetic factors that are responsible for normal human female meiosis and fertility.

12.
J Craniofac Surg ; 30(8): 2451-2455, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31689729

RESUMO

OBJECTIVE: To evaluate the morphological changes of the upper airway of patients with skeletal Class III malocclusion after undergoing bilateral mandibular ramus dislocated mandibular retrogression (SSRO) or SSRO combined with Le Fort I maxillary osteotomy and 3-dimensional imaging. METHODS: All previous studies related to the upper airway in patients with skeletal class III malocclusion and orthognathic surgery were collected from the PubMed, EMB, Cochrane Library, Web of science, ClinicalKey, EBSCO, Weipu, Wanfang, China National Knowledge Infrastructure, and Chinese BioMedical Literature databases. The search date ends in August 2017. RevMan5.3 software was used to perform a meta-analysis related to upper airway morphology. Ten studies were included. RESULTS: The meta-analysis showed that 6 months after SSRO, CV1, and CV2 did not change significantly (P >0.05), whereas CV3 and CV4 narrowed (P <0.05) and remained narrow after 1 year (P <0.05). (CV1,CV2,CV3,CV4: Plans parallel to the FH plane passing through the most anterior inferior point of the anterior arch of the atlas, the 2nd cervical vertebra, the 3rd cervical vertebra, the 4th cervical vertebra.) There was no significant change in nasopharyngeal volume or laryngeal pharyngeal volume (P >0.05), but oropharyngeal volume and total volume decreased (P ≤0.01). Six months after SSRO combined with Le Fort I maxillary osteotomy, the minimum cross-sectional area of the upper airway was smaller (P <0.05), there was no significant change in nasopharyngeal volume or oropharyngeal volume (P >0.05), and oropharynx volume and total volume decreased (P <0.05). CONCLUSIONS: Single and double jaw surgery has no significant effect on nasopharynx and oropharynx, but reduces laryngopharynx and total volume; however, whether this will result in postoperative obstructive sleep apnea-hypopnea syndrome or become ameliorated over time requires more in-depth study and a longer period of clinical observation.

13.
Nat Commun ; 10(1): 5070, 2019 Nov 07.
Artigo em Inglês | MEDLINE | ID: mdl-31699980

RESUMO

ß-Adrenergic receptor (ß-AR) signaling is a pathway controlling adaptive thermogenesis in brown or beige adipocytes. Here we investigate the biological roles of the transcription factor Foxp1 in brown/beige adipocyte differentiation and thermogenesis. Adipose-specific deletion of Foxp1 leads to an increase of brown adipose activity and browning program of white adipose tissues. The Foxp1-deficient mice show an augmented energy expenditure and are protected from diet-induced obesity and insulin resistance. Consistently, overexpression of Foxp1 in adipocytes impairs adaptive thermogenesis and promotes diet-induced obesity. A robust change in abundance of the ß3-adrenergic receptor (ß3-AR) is observed in brown/beige adipocytes from both lines of mice. Molecularly, Foxp1 directly represses ß3-AR transcription and regulates its desensitization behavior. Taken together, our findings reveal Foxp1 as a master transcriptional repressor of brown/beige adipocyte differentiation and thermogenesis, and provide an important clue for its targeting and treatment of obesity.

14.
Artigo em Inglês | MEDLINE | ID: mdl-31724280

RESUMO

Herein, a sensitive amine-responsive disassembly of self-assembled Au(I)-Cu(I) double salts was observed and its utilization for the synergistic catalysis was further enlightened. Investigation of the disassembly of [Au(NHC)2][CuI2] revealed the contribution of Cu-assisted ligand exchange of N-heterocyclic carbene (NHC) by amine in [Au(NHC)2]+ and the capacity of [CuI2]- on the oxidative step. By integrating the implicative information coded in the responsive behaviour and inherent catalytic functions of d10 metal complexes, we have developed a novel catalyst for the oxidative carbonylation of amines. The advantages of this protocol were clearly reflected on mild reaction condtion and the significantly expanded scope (51 examples); both primary and steric secondary amines can be employed as substrates. The cooperative reactivity from Au and Cu centers, as an indispensable prerequisite for the excellent catalytic performance, was validated in the synthesis of (un)symmetric ureas and carbamates.

15.
Commun Biol ; 2: 390, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31667364

RESUMO

Adolescent idiopathic scoliosis is the most common spinal disorder in adolescents with a prevalence of 0.5-5.2% worldwide. The traditional methods for scoliosis screening are easily accessible but require unnecessary referrals and radiography exposure due to their low positive predictive values. The application of deep learning algorithms has the potential to reduce unnecessary referrals and costs in scoliosis screening. Here, we developed and validated deep learning algorithms for automated scoliosis screening using unclothed back images. The accuracies of the algorithms were superior to those of human specialists in detecting scoliosis, detecting cases with a curve ≥20°, and severity grading for both binary classifications and the four-class classification. Our approach can be potentially applied in routine scoliosis screening and periodic follow-ups of pretreatment cases without radiation exposure.

16.
Oncogene ; 2019 Oct 28.
Artigo em Inglês | MEDLINE | ID: mdl-31659254

RESUMO

Discerning oncogenic drivers from passengers remain a major effort in understanding of the essence of the initiation and development of hepatocellular carcinoma (HCC), which is the most common primary liver malignancy and the third leading cause of cancer mortality worldwide. Here we report that ZNF774, a novel zinc-finger protein, inhibits the proliferation and invasion of HCC cells. Molecular characterization of this protein indicated that ZNF774 acts as a transcription repressor, and interrogation of ZNF774 interactome by affinity purification-coupled mass spectrometry revealed that ZNF774 is physically associated with the Mi-2/nucleosome remodeling and deacetylase (NuRD) complex in cells. Genome-wide identification of the transcriptional targets of the ZNF774/NuRD complex by ChIP-seq indicated that ZNF774 represses a cohort of genes including NOTCH2 that are critically involved in the growth and mobility of HCC. We demonstrated that the ZNF774/NuRD complex inhibits the proliferation and invasion of HCC cells in vitro and suppresses HCC growth and metastasis in vivo. Importantly, the expression of ZNF774 is significantly downregulated in HCC, and low ZNF774 expression strongly correlated with high NOTCH2 expression, advanced pathological stages, and poor overall survival of the patients. Together, these results uncover a key role for the ZNF774/NuRD-NOTCH2 axis in hepatocarcinogenesis.

17.
J Lipid Res ; 60(12): 2020-2033, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31662443

RESUMO

CXC chemokine ligand 12 (CXCL12) is a member of the CXC chemokine family and mainly acts on cell chemotaxis. CXCL12 also elicits a proatherogenic role, but the molecular mechanisms have not been fully defined yet. We aimed to reveal if and how CXCL12 promoted atherosclerosis via regulating lipid metabolism. In vitro, our data showed that CXCL12 could reduce ABCA1 expression, and it mediated cholesterol efflux from THP-1-derived macrophages to apoA-I. Data from the luciferase reporter gene and chromatin immunoprecipitation assays revealed that transcription factor 21 (TCF21) stimulated the transcription of ABCA1 via binding to its promoter region, which was repressed by CXCL12. We found that CXCL12 increased the levels of phosphorylated glycogen synthase kinase 3ß (GSK3ß) and the phosphorylation of ß-catenin at the Thr120 position. Inactivation of GSK3ß or ß-catenin increased the expression of TCF21 and ABCA1. Further, knockdown or inhibition of CXC chemokine receptor 4 (CXCR4) blocked the effects of CXCL12 on TCF21 and ABCA1 expression and the phosphorylation of GSK3ß and ß-catenin. In vivo, the overexpression of CXCL12 in Apoe-/- mice via lentivirus enlarged the atherosclerotic lesion area and increased macrophage infiltration in atherosclerotic plaques. We further found that the overexpression of CXCL12 reduced the efficiency of reverse cholesterol transport and plasma HDL-C levels, decreased ABCA1 expression in the aorta and mouse peritoneal macrophages (MPMs), and suppressed cholesterol efflux from MPMs to apoA-I in Apoe-/- mice. Collectively, these findings suggest that CXCL12 interacts with CXCR4 and then activates the GSK-3ß/ß-cateninT120/TCF21 signaling pathway to inhibit ABCA1-dependent cholesterol efflux from macrophages and aggravate atherosclerosis. Targeting CXCL12 may be a novel and promising strategy for the prevention and treatment of atherosclerotic cardiovascular diseases.

18.
Pest Manag Sci ; 2019 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-31595658

RESUMO

BACKGROUND: Precise regulation of oogenesis is crucial to female reproduction. Seventy percent of pests belong to lepidopteran species, so it would be interesting to explore the highly conserved genes involved in oogenesis that do not affect growth and development in the lepidopteran model, Bombyx mori. This can provide potential target genes for pest control and promote the development of insect sterility technology. RESULTS: In lepidopteran species, ovarian serine protease (Osp), which encodes a member of the serine protease family, is essential for oogenesis. In this study, we used transgenic CRISPR/Cas9 technology to obtain Osp mutants in the model lepidopteran insect Bombyx mori and in the lepidopteran agricultural pest Spodoptera litura. Sequence analysis of mutants revealed an array of deletions in Osp loci in both species. We found that the deletion of Osp resulted in female sterility, whereas male fertility was not affected. Although B. mori and S. litura mutant females mated normally, they laid fewer eggs than wild-type females and eggs did not hatch. CONCLUSION: Osp is crucial for female reproductive success in two species of Lepidoptera. As the Osp gene is highly conserved in insect species, this gene is a potential molecular target for genetic-based pest management. © 2019 Society of Chemical Industry.

19.
ACS Appl Mater Interfaces ; 11(45): 42751-42759, 2019 Nov 13.
Artigo em Inglês | MEDLINE | ID: mdl-31626529

RESUMO

The domain morphology in the growth of transition-metal dichalcogenides (TMDCs) is mostly triangular but rarely dendritic. Here, we report a robust chemical vapor deposition method to fabricate atomic-thin 2H-phase MoS2 dendrites on several single-crystalline substrates with different lattice structures, such as rutile-TiO2(001), SrTiO3(001), and sapphire(0001). It is found that by tuning the concentration of Mo adatoms, the morphology of MoS2 domains on these substrates evolves from tridentate dendrites at a low Mo concentration to semicompact fractal domains at an intermediate Mo concentration, and to a compact triangular shape at a high Mo concentration. First-principles calculations reveal that the edge diffusion barrier of Mo is comparable to the attachment barrier, inhibiting fast Mo atom diffusion along the edge. Kinetics Monte Carlo simulations with varying Mo concentrations well reproduce the experimental results. Our combined experimental and theoretical analyses evidently show that the growth of MoS2 dendritic domains at a low Mo concentration is a nonequilibrium process, which is dominated by the kinetics of Mo adatoms. Our study presents an effective route to control the morphology of TMDCs by simply tuning the transition-metal adatom concentration.

20.
Environ Pollut ; 255(Pt 2): 113330, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31606662

RESUMO

2,6-Di-tert-butyl-hydroxytotulene (BHT), as a significant synthetic phenolic antioxidant (SPA), has received increasing attention in the environmental field. In the present study, the BHT is confirmed to be mainly distributed in the liquid phase in the environment base on the Aspen PLUS simulation results. The mechanism and kinetics of BHT transformation initiated by OH radicals were conducted in aquatic environment using density functional theory (DFT) method. Briefly, seven initiation reactions and three detailed transformation pathways of BHT were reported. The H atoms in the t-butyl and methyl group were found more favorable to be abstracted. The C1 site of the BHT was susceptible to addition by OH radicals. Rate constants of different initial reactions were calculated and they were inhibited by temperature rise. Meanwhile, the acute and chronic toxicities of BHT and its metabolites were evaluated at three different trophic levels using the ECOSAR program. During the degradation process, the toxicities of these metabolites gradually decreased, but the toxicities of the final product 2,6-di-tert-butyl-2,5-cyclohexadien-1,4-dione (BHT-Q) were significantly increased. These results could help to reveal the transformation mechanism and risk assessment of BHT in aquatic environment, and further design the experimental and industrial applications of SPAs.

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