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The goal of this study was to establish a comprehensive growth index (CGI) of grassland vegetation for monitor the overall condition of the grassland. Taking the desert grassland in Otuoke Banner, Ordos City, Inner Mongolia as the research object, this study integrates five indicators. First, the optimal band of the unmanned aerial vehicle hyperspectral data is optimized using the correlation analysis, successive projection algorithm (SPA), optimum index factor method, and band combination index method. A dual-band spectral index in good correlation with the CGI is then constructed in the optimal band. Afterwards, a CGI characterization model is established in accordance with the partial least squares regression (PLSR) algorithm and its accuracy is analyzed. Finally, the CGI of the study area is estimated. The experimental results are as follows. 1) The R2of models built using the training samples of the spectral indices corresponding to the optimal spectra screened by the SPA method was 0.7835, RMSE was 0.0712, and RE was 6.89%, less than 10%. The R2 of the Validation samples was 0.7698, RMSE was 0.0471, and RE was 6.36%, less than 10%, highest precision. 2) Models were built using the spectral indices corresponding to the optimal spectra screened by the SPA method, and the CGImean values were inverted. A comparison of the meanmeasured CGI values of the sample quadrat of the test area showed that the mean relative error was 3.82%. The results show that the vegetation growth of desert-steppe grasslands can be adequatelymonitored, providing technical support for the rapid and accurate diagnosis of grassland conditions. However, there are still shortcomings in this study. 1) The research area for this study was mainly in the desert steppe in Otuoke Banner, Ordos, hence the relevance and universality of the findings need to be verified, and subsequent experiments need to be carried out on desert steppes in other regions or even other types of grasslands to test the universality of the model. 2) In this study, the influence of soil background and litter on the spectral reflectance is not considered in depth. In addition, the influence of sensor observation angle and solar elevation angle on the inversion model demands further investigation efforts. [ABSTRACT FROM AUTHOR]

Monolayer (ML) MoS2 is one of the most extensively studied two-dimensional (2D) semiconductors. However, it suffers from low carrier mobility and pervasive Schottky contact with metal electrodes. 2D semiconductor Bi2O2S, a sulfur analogue of 2D Bi2O2Se, has been prepared recently. ML fully hydrogen-passivated Bi2O2S2 (Bi2O2S2H2) posseses a comparable band gap (1.92 eV) with ML MoS2 (1.8 eV), but probably has a better device performance than ML MoS2. Based on the density functional theory, the electron and hole mobilities of ML Bi2O2S2H2 at 300 K are calculated to be 16 447–26 699 and 264–968 cm² V−1 s−1, respectively. Then we firstly characterize the contact properties of ML half hydrogen-passivated Bi2O2S2 (Bi2O2S2H) with four bulk metal electrodes (Ti, Sc, Pd, and Pt) based on ab initio quantum transport simulation. In the lateral direction, a p-type Schottky contact is found in Pd and Pt electrodes, and the corresponding hole Schottky barrier heights (SBHs) are 0.54 and 0.99 eV, respectively. Remarkably, a coveted n-type Ohmic contact appears in Sc and Ti electrodes. Finally, the current on–off ratio of the ML hydrogen-passivated Bi2O2S2 field effect transistor with a Ti electrode reaches 105. Hence, the good intrinsic properties, contact properties, and large switching ability put ML hydrogen-passivated Bi2O2S2 in the rank of potential channel candidates for post-silicon era field effect transistors. [ABSTRACT FROM AUTHOR]

OBJECTIVES: The aim of this study was to explore the predictors of the improvement in moderate ischaemic mitral regurgitation (IMR) after off-pump coronary artery bypass grafting (OPCAB) focusing on left ventricular (LV) dyssynchrony. METHODS: A prospective study was performed among 135 patients (age at surgery, mean ± SD: 67.0 ± 8.2 years, 33.3% women) with prior myocardial infarction and moderate IMR undergoing OPCAB from 2008 to 2015. Preoperative and follow-up clinical and echocardiographic parameters were analysed, focusing on LV global/regional dyssynchrony. Patients were grouped by IMR at 1 year postoperatively: improved group with no or mild IMR (n = 61) and failure group with moderate or severe IMR (n = 67). Data were compared between groups to explore the predictors of IMR improvement after OPCAB. RESULTS: Seven patients who died before the 1-year postoperative assessment were excluded. At the 1-year follow up, there were 61 patients in the improved group and 67 patients in the failure group. Preoperatively, the improved group had smaller LV global dyssynchrony, LV regional dyssynchrony (papillary muscle systolic dyssynchrony; improved group versus failure group: 48.5 ± 4.5 ms vs 57.1 ± 3.9 ms; P < 0.001) and greater LV ejection fraction (improved group versus failure group: 44.7 ± 5.0% vs 36.7 ± 6.7%; P < 0.001) than the failure group. Papillary muscle systolic dyssynchrony (odds ratio 1.556, 95% confidence interval 1.313-1.845; P < 0.001) and preoperative ejection fraction (odds ratio 0.799, 95% confidence interval 0.691-0.924; P = 0.002) were independent predictors of moderate IMR improvement after OPCAB. CONCLUSIONS: In the selected patients, preoperative moderate IMR could be relieved by coronary artery bypass grafting. Greater ejection fraction and absence of LV regional dyssynchrony may predict the improvement in moderate IMR after coronary artery bypass grafting, suggesting that LV dyssynchrony especially regional dyssynchrony and preserved ventricular function would be important to the outcome of patients with moderate IMR. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is characterized by the progressive loss of select neuronal populations, but the prodeath genes mediating the neurodegenerative processes remain to be fully elucidated. Trib3 (tribbles pseudokinase 3) is a stress-induced gene with proapoptotic activity that was previously described as highly activated at the transcriptional level in a 6-hydroxydopamine (6-OHDA) cellular model of PD. Here, we report that Trib3 immunostaining is elevated in dopaminergic neurons of the substantia nigra pars compacta (SNpc) of human PD patients. Trib3 protein is also upregulated in cellular models of PD, including neuronal PC12 cells and rat dopaminergic ventral midbrain neurons treated with 6-OHDA, 1-methyl-4-phenylpyridinium (MPP+), or α-synuclein fibrils (aSYN). In the toxin models, Trib3 induction is substantially mediated by the transcription factors CHOP and ATF4. Trib3 overexpression is sufficient to promote neuronal death; conversely, Trib3 knockdown protects neuronal PC12 cells as well as ventral midbrain dopaminergic neurons from 6-OHDA, MPP+, or aSYN. Mechanism studies revealed that Trib3 physically interacts with Parkin, a prosurvival protein whose loss of function is associated with PD. Elevated Trib3 reduces Parkin expression in cultured cells; and in the SNpc of PD patients, Parkin levels are reduced in a subset of dopaminergic neurons expressing high levels of Trib3. Loss of Parkin at least partially mediates the prodeath actions of Trib3 in that Parkin knockdown in cellular PD models abolishes the protective effect of Trib3 downregulation. Together, these findings identify Trib3 and its regulatory pathways as potential targets to suppress the progression of neuron death and degeneration in PD. [ABSTRACT FROM AUTHOR]

Embedding transition-metal (TM) atoms into nonmagnetic nanomaterials is an efficient way to induce magnetism. Using first-principles calculations, we systematically investigated the structural stability and magnetic properties of TM atoms from Sc to Zn embedded into silicene with single vacancy (SV) and double vacancies (DV). The binding energies for different TM atoms correlate with the TM d-shell electrons. Sc, Ti, and Co show the largest binding energies of as high as 6 eV, while Zn has the lowest binding energy of about 2 eV. The magnetic moment of silicene can be modulated by embedding TM atoms from V to Co, which mainly comes from the 3d orbitals of TM along with partly contributions from the neighboring Si atoms. Fe atom on SV and Mn atom on DV have the largest magnetic moment of more than 3 μB. In addition, we find that doping of N or C atoms on the vacancy site could greatly enhance the magnetism of the systems. Our results provide a promising approach to design silicene-based nanoelectronics and spintronics device. [ABSTRACT FROM AUTHOR]

Background: Embryonic stem cells (ESCs) are pluripotent stem cells and can differentiate into cardiomyocytes when cultured in appropriate conditions. The function of hypoxia-inducible factors (HIFs) has been identified in directing the formation of cardiac lineages. The purpose of this study was to investigate the ability of HIF2α to induce differentiation of ESCs into cardiomyocytes and to explore the potential underlying molecular mechanisms. Methods: Cardiac differentiation from mouse ESCs was analyzed using the "hanging drop" method, and success was determined by assaying the numbers of beating embryoid bodies and the expression level of cardiac markers. The expression of HIF2α was then manipulated during cardiac differentiation with piggyBac transposon and the lentivirus system. The underlying mechanism was finally examined via administering selective inhibitors of the Wnt/β-catenin signaling pathway. Results: Overexpressing HIF2α can significantly drive mouse ESCs to form cardiomyocytes. Contrarily, knockdown of HIF2α inhibits the emergence of cardiac cells. In addition, the cardiomyogenesis-promoting effect of HIF2α occurred by increasing the protein level of β-catenin, an effector that contributes to cardiac differentiation at an early stage of ESC differentiation. Conclusion: HIF2α has a cardiomyogenesis-promoting effect in ESCs via enhancing the activation of the Wnt/β-catenin signaling pathway. Our results may be beneficial for generating and applying cardiomyocytes from ESCs safely and effectively in the future. [ABSTRACT FROM AUTHOR]

This study aimed to determine the performance and long-term outcomes of therapeutic ERCP in very old patients. Patients aged or over 90 (Group A, n = 78) and consecutive sex-matched controls (Group B, n = 312) under 65 selected were compared. More patients in Group A had chronic concomitant diseases, but the success and complication rates were comparable. The follow-up of 61 patients (78.2%) in Group A were done, with a mean period of 27.5 (3-54) months. Seven patients survived; the main causes of death for the other patients were concomitant diseases (n = 43) and primary diseases (n = 11). In patients with choledocholithiasis, cases with complete extractions of stones in bile ducts survived longer than those without (30 vs. 24 months, P , 0.001). Therapeutic ERCP in patients aged 90 years or older is effective and safe. In patients with choledocholithiasis, complete clearance of stones is associated with longer survival time. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a common neurodegenerative disorder, for which there are no effective disease-modifying therapies. The transcription factor ATF4 (activating transcription factor 4) is induced by multiple PD-relevant stressors, such as endoplasmic reticulum stress and oxidative damage. ATF4 may exert either protective or deleterious effects on cell survival, depending on the paradigm. However, the role of ATF4 in the pathogenesis of PD has not been explored. We find that ATF4 levels are increased in neuromelanin-positive neurons in the substantia nigra of a subset of PD patients relative to controls. ATF4 levels are also upregulated in neuronal PC12 cells treated with the dopaminergic neuronal toxins 6-hydroxydopamine (6-OHDA) and l-methyl-4-phenylpyridinium (MPP+). To explore the role of ATF4 in cell survival in PD-relevant contexts, we either silenced or overexpressed ATF4 in cellular models of PD. In neuronal PC 12 cells, silencing of ATF4 enhanced cell death in response to either 6-OHDA or MPP +. Conversely, overexpression of ATF4 reduced cell death caused by dopaminergic neuronal toxins. ATF4 was also protective against 6-OHDA-induced death of cultured mouse ventral midbrain dopaminergic neurons. We further show that parkin, a gene associated with autosomal recessive PD, plays a critical role in ATF4-mediated protection. After treatment with 6-OHDA or MPP+, parkin protein levels fall, despite an increase in mRNA levels. ATF4 silencing exacerbates the toxin-induced reduction of parkin, whereas ATF4 overexpression partially preserves parkin levels. Finally, parkin silencing blocked the protective capacity of ATF4. These results indicate that ATF4 plays a protective role in PD through the regulation of parkin. [ABSTRACT FROM AUTHOR]

Maintenance of the Golgi apparatus (GA) structure and function depends on Golgi matrix proteins. The posttranslational modification of Golgi proteins such as phosphorylation of members of the golgin and GRASP families is important for determining Golgi architecture. Some Golgi proteins including golgin-84 are also known to be methylated, but the function of golgin methylation remains unclear. Here, we show that the protein arginine methyltransferase 5 (PRMT5) localizes to the GA and forms complexes with several components involved in GA ribbon formation and vesicle tethering. PRMT5 interacts with the golgin GM130, and depletion of PRMT5 causes defects in Golgi ribbon formation. Furthermore, PRMT5 methylates N-terminal arginines in GM130, and such arginine methylation appears critical for GA ribbon formation. Our findings reveal a molecular mechanism by which PRMT5-dependent arginine methylation of GM130 controls the maintenance of GA architecture. [ABSTRACT FROM AUTHOR]