ZmELP1, an Elongator complex subunit, is required for the maintenance of histone acetylation and RNA Pol II phosphorylation in maize kernels.

The Elongator complex was originally identified as an interactor of hyperphosphorylated RNA polymerase II (RNAPII) in yeast and has histone acetyltransferase (HAT) activity. However, the genome-wide regulatory roles of Elongator on transcriptional elongation and histone acetylation remain unclear. We characterized a maize miniature seed mutant, mn7 and map-based cloning revealed that Mn7 encodes one of the subunits of the Elongator complex, ZmELP1. ZmELP1 deficiency causes marked reductions in the kernel size and weight. Molecular analyses showed that ZmELP1 interacts with ZmELP3, which is required for H3K14 acetylation (H3K14ac), and Elongator complex subunits interact with RNA polymerase II (RNAPII) C-terminal domain (CTD). Genome-wide analyses indicated that loss of ZmELP1 leads to a significant decrease in the deposition of H3K14ac and the CTD of phosphorylated RNAPII on Ser2 (Ser2P). These chromatin changes positively correlate with global transcriptomic changes. ZmELP1 mutation alters the expression of genes involved in transcriptional regulation and kernel development. We also showed that the decrease of Ser2P depends on the deposition of Elongator complex-mediated H3K14ac. Taken together, our results reveal an important role of ZmELP1 in the H3K14ac-dependent transcriptional elongation, which is critical for kernel development.

HEAT SHOCK PROTEIN 90.6 interacts with carbon and nitrogen metabolism components during seed development.

Carbon and nitrogen are the two main nutrients in maize (Zea mays L.) kernels, and kernel filling and metabolism determine seed formation and germination. However, the molecular mechanisms underlying the relationship between kernel filling and corresponding carbon and nitrogen metabolism remain largely unknown. Here, we found that HEAT SHOCK PROTEIN 90.6 (HSP90.6) is involved in both seed filling and the metabolism processes of carbon and nitrogen. A single-amino acid mutation within the HATPase_c domain of HSP90.6 led to small kernels. Transcriptome profiling showed that the expression of amino acid biosynthesis- and carbon metabolism-related genes was significantly downregulated in the hsp90.6 mutant. Further molecular evidence showed strong interactions between HSP90.6 and the 26S proteasome subunits REGULATORY PARTICLE NON-ATPASE6 (RPN6) and PROTEASOME BETA SUBUNITD2 (PBD2). The mutation of hsp90.6 significantly reduced the activity of the 26S proteasome, resulting in the accumulation of ubiquitinated proteins and defects in nitrogen recycling. Moreover, we verified that HSP90.6 is involved in carbon metabolism through interacting with the 14-3-3 protein GENERAL REGULATORY FACTOR14-4 (GF14-4). Collectively, our findings revealed that HSP90.6 is involved in seed filling and development by interacting with the components controlling carbon and nitrogen metabolism.

The Ca2+ Sensor SCaBP3/CBL7 Modulates Plasma Membrane H+-ATPase Activity and Promotes Alkali Tolerance in Arabidopsis.

Saline-alkali soil is a major environmental constraint impairing plant growth and crop productivity. In this study, we identified a Ca2+ sensor/kinase/plasma membrane (PM) H+-ATPase module as a central component conferring alkali tolerance in Arabidopsis (Arabidopsis thaliana). We report that the SCaBP3 (SOS3-LIKE CALCIUM BINDING PROTEIN3)/CBL7 (CALCINEURIN B-LIKE7) loss-of-function plants exhibit enhanced stress tolerance associated with increased PM H+-ATPase activity and provide fundamental mechanistic insights into the regulation of PM H+-ATPase activity. Consistent with the genetic evidence, interaction analyses, in vivo reconstitution experiments, and determination of H+-ATPase activity indicate that interaction of the Ca2+ sensor SCaBP3 with the C-terminal Region I domain of the PM H+-ATPase AHA2 (Arabidopsis thaliana PLASMA MEMBRANE PROTON ATPASE2) facilitates the intramolecular interaction of the AHA2 C terminus with the Central loop region of the PM H+-ATPase to promote autoinhibition of H+-ATPase activity. Concurrently, direct interaction of SCaPB3 with the kinase PKS5 (PROTEIN KINASE SOS2-LIKE5) stabilizes the kinase-ATPase interaction and thereby fosters the inhibitory phosphorylation of AHA2 by PKS5. Consistently, yeast reconstitution experiments and genetic analysis indicate that SCaBP3 provides a bifurcated pathway for coordinating intramolecular and intermolecular inhibition of PM H+-ATPase. We propose that alkaline stress-triggered Ca2+ signals induce SCaBP3 dissociation from AHA2 to enhance PM H+-ATPase activity. This work illustrates a versatile signaling module that enables the stress-responsive adjustment of plasma membrane proton fluxes.

Maize PPR278 Functions in Mitochondrial RNA Splicing and Editing.

Pentatricopeptide repeat (PPR) proteins are a large protein family in higher plants and play important roles during seed development. Most reported PPR proteins function in mitochondria. However, some PPR proteins localize to more than one organelle; functional characterization of these proteins remains limited in maize (Zea mays L.). Here, we cloned and analyzed the function of a P-subfamily PPR protein, PPR278. Loss-function of PPR278 led to a lower germination rate and other defects at the seedling stage, as well as smaller kernels compared to the wild type. PPR278 was expressed in all investigated tissues. Furthermore, we determined that PPR278 is involved in the splicing of two mitochondrial transcripts (nad2 intron 4 and nad5 introns 1 and 4), as well as RNA editing of C-to-U sites in 10 mitochondrial transcripts. PPR278 localized to the nucleus, implying that it may function as a transcriptional regulator during seed development. Our data indicate that PPR278 is involved in maize seed development via intron splicing and RNA editing in mitochondria and has potential regulatory roles in the nucleus.

Decomposition-Coordination of Double-Layer MPC for Constrained Systems.

Large-scale industrial processes usually adopt centralized control and optimization methods. However, with the growth of the scale of industrial processes leading to increasing computational complexity, the online optimization capability of the double-layer model predictive control algorithm is challenged, exacerbating the difficulty of the widespread implementation of this algorithm in the industry. This paper proposes a distributed double-layer model predictive control algorithm based on dual decomposition for multivariate constrained systems to reduce the computational complexity of process control. Firstly, to solve the problem that the original dual decomposition method does not apply to constrained systems, two improved dual decomposition model prediction control methods are proposed: the dual decomposition method based on the quadratic programming in the subsystem and the dual decomposition method based on constraint zones, respectively. It is proved that the latter will certainly converge to the constraint boundaries with appropriate convergence factors for the controlled variables. The online optimization ability of the proposed two methods is compared in discussion and simulation, concluding that the dual decomposition method based on the constraint zones exhibits superior online optimization ability. Further, a distributed double-layer model predictive control algorithm with dual decomposition based on constraint zones is proposed. Different from the objective function of the original dual decomposition model predictive control, the proposed algorithm's dynamic control-layer objective function simultaneously tracks the steady-state optimization values of the controlled and manipulated variables, giving the optimal solution formulation of the optimization problem consisting of this objective function and the constraints. The algorithm proposed in this paper achieves the control goals while significantly reducing the computational complexity and has research significance for promoting the industrial implementation of double-layer model predictive control.

Hybrid Beamforming Design for Self-Interference Cancellation in Full-Duplex Millimeter-Wave MIMO Systems with Dynamic Subarrays.

Full-duplex (FD) millimeter-wave (mmWave) multiple-input multiple-output (MIMO) communication is a promising solution for the extremely high-throughput requirements in future cellular systems. The hybrid beamforming structure is preferable for its low hardware complexity and low power consumption with acceptable performance. In this paper, we introduce the hardware efficient dynamic subarrays to the FD mmWave MIMO systems and propose an effective hybrid beamforming design to cancel the self-interference (SI) in the considered system. First, assuming no SI, we obtain the optimal fully digital beamformers and combiners via the singular value decomposition of the uplink and downlink channels and the water-filling power allocation. Then, based on the obtained fully digital solutions, we get the dynamic analog solutions and digital solutions using the Kuhn-Munkres algorithm-aided dynamic hybrid beamforming design. Finally, we resort to the null space projection method to cancel the SI by projecting the obtained digital beamformer at the base station onto the null space of the equivalent SI channel. We further analyze the computational complexity of the proposed method. Numerical results demonstrate the superiority of the FD mmWave MIMO systems with the dynamic subarrays using the proposed method compared to the systems with the fixed subarrays and the half-duplex mmWave communications. When the number of RF chains is 6 and the signal-to-noise ratio is 10 dB, the proposed design outperforms the FD mmWave MIMO systems with fixed subarrays and the half-duplex mmWave communications, respectively, by 22.4% and 47.9% in spectral efficiency and 19.9% and 101% in energy efficiency.

VAMP711 Is Required for Abscisic Acid-Mediated Inhibition of Plasma Membrane H+-ATPase Activity.

Drought stress is a limiting environmental factor that affects plant growth and development. The plant hormone abscisic acid (ABA) plays an important role in plant drought responses. Previous studies have indicated that ABA inhibits plasma membrane H+-ATPase (PM H+-ATPase) activity, and the decrease in PM H+-ATPase activity promotes stomatal closure under drought stress, thereby reducing water loss. However, the underlying molecular mechanisms are not well understood. In this study, we found that in Arabidopsis (Arabidopsis thaliana), ABA induces an N-ethylmaleimide-sensitive factor attachment protein receptor protein, namely, VESICLE-ASSOCIATED MEMBRANE PROTEIN 711 (VAMP711), to interact with the Arabidopsis PM H+-ATPases AHA1 and AHA2. The interaction occurs at their C-termini and inhibits PM H+-ATPase activity. Deletion of VAMP711 in Arabidopsis results in a higher PM H+-ATPase activity and slower stomatal closure in response to ABA and drought treatments. In addition, overexpression of VAMP711 partially rescues the drought-sensitive phenotype of ost2-2D, a mutation in AHA1 resulting in a constitutive activated PM H+-ATPase. Our results demonstrate that VAMP711 is involved in regulating ABA-mediated inhibition of PM H+-ATPase activity and stomatal closure in response to drought stress.

[In-Situ Analysis of Solid Steel Samples with Remote Double-Pulse Laser-Induced Breakdown Spectroscopy System].

In order to realize real-time, online monitoring of the component of steel and other metal smelting process, we designed a remote double-pulse laser-induced breakdown spectroscopy (LIBS) analysis system which can realize non-contact remote measurement and component analysis for long distance sample. The paper first tests the system on solid standard steel samples, which provides basis for online monitoring the component of molten steel. The experimental results show：laser focal spot is about 1mm in long distance; double-pulse ablation depth is deeper than single pulse's; the optimum delay of double-pulse is non-consistent in different distances; the enhancement effect of double- pulse in 3.1 m is better than that in 2.1 m，and the maximum enhancement is 5.19 of Ti(Ⅰ) 319.99 nm; the calibration curve of R2 is about 0.99, RSD being less than 5%, RMSE being less than 0.021%, LOD being less than 500 ppm for most elements in 2.1 m, which is better than that in 3.1 m.

[Quantitative analysis of alloy steel based on laser induced breakdown spectroscopy with partial least squares method].

In the present paper both the partial least squares (PLS) method and the calibration curve (CC) method are used to quantitatively analyze the laser induced breakdown spectroscopy data obtained from the standard alloy steel samples. Both the major and trace elements were quantitatively analyzed. By comparing the results of two different calibration methods some useful results were obtained: for major elements, the PLS method is better than the CC method in quantitative analysis; more importantly, for the trace elements, the CC method can not give the quantitative results due to the extremely weak characteristic spectral lines, but the PLS method still has a good ability of quantitative analysis. And the regression coefficient of PLS method is compared with the original spectral data with background interference to explain the advantage of the PLS method in the LIBS quantitative analysis. Results proved that the PLS method used in laser induced breakdown spectroscopy is suitable for quantitative analysis of trace elements such as C in the metallurgical industry.

Linkage of Blood MALT1 with CD4+ T Cell Subset, Inflammation, Lipid, and Its Potency as a Biomarker for Predicting Major Adverse Cardiovascular Events in Coronary Heart Disease Patients.

OBJECTIVE: Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) promotes CD4+ T cell differentiation, vascular inflammation, and atherogenesis to engage in coronary heart disease (CHD) progression. This study intended to explore the correlation of blood MALT1 with clinical characteristics, CD4+ T cell subset and prognosis in CHD patients. METHODS: MALT1 in peripheral blood mononuclear cells of 258 CHD patients and 50 healthy controls (HCs) was determined by RT-qPCR. Additionally, blood T helper (Th)1, Th2, Th17, and regulatory T (Treg) cells were measured through flow cytometry; major adverse cardiovascular events (MACE) were recorded during the routine follow up in CHD patients. RESULTS: Blood MALT1 was elevated in CHD patients compared to HCs. Interestingly, blood MALT1 positively associated with hyperlipidemia, triglyceride, C-reactive protein, and Gensini score in CHD patients. It also negatively linked with Th2 cells, Treg cells, and positively related to Th17 cells but not Th1 cells in CHD patients. More importantly, MACE-free survival was shortened in CHD patients with high blood MALT1 compared to those with low blood MALT1 (cut off by the median) while less significance was observed when cut off by quartiles. Separately, blood MALT1 was elevated in CHD patients occurred MACE within 1-year, 2-year, 3-year, and 4-year duration compared to those who did not. CONCLUSION: Blood MALT1 links with unbalanced CD4+ T-cell subset, elevated inflammation, and coronary-artery stenosis serving as a candidate biomarker for predicting MACE risk in CHD patients.

A New Approach to Modeling Ultrashort Channel Ballistic Nanowire GAA MOSFETs.

We propose a numerical compact model for describing the drain current in ballistic mode by using an expression to represent the transmission coefficients for all operating regions. This model is based on our previous study of an analytic compact model for the subthreshold region in which the DIBL and source-to-drain tunneling effects were both taken into account. This paper introduces an approach to establishing the smoothing function for expressing the critical parameters in the model's overall operating regions. The resulting compact model was tested in a TCAD NEGF simulation, demonstrating good consistency.

In silico identification of common and specific signatures in coronary heart diseases.

Coronary heart disease (CHD) is on the increase in developing countries, where lifestyle choices such as smoking, bad diet, and no exercise contribute and increase the incidence of high blood pressure and high cholesterol levels to cause CHD. Through utilization of a biomarker-based approach for developing interventions, the aim of the study was to identify differentially expressed genes (DEGs) and their association and impact on various bio-targets. The microarray datasets of both healthy and CHD patients were analyzed to identify the DEGs and their interactions using Gene Ontology, PANTHER, Reactome, and STRING (for the possible associated genes with multiple targets). Our data mining approach suggests that the DEGs were associated with molecular functions, including protein binding (75%) and catalytic activity (56%); biological processes such as cellular process (83%), biological regulation (57%), and metabolic process (44%); and cellular components such as cell (65%) and organelle (58%); as well as other associations including apoptosis, inflammatory, cell development and metabolic pathways. The molecular functions were further analyzed, and protein binding in particular was analyzed using network analysis to determine whether there was a clear association with CHD and disease. The ingenuity pathway analysis revealed pathways related to cell cholesterol biosynthesis, the immune system including cytokinin signaling, in which, the understanding of DEGs is crucial to predict the advancement of preventive strategies. Results of the present study showed that, there is a need to validate the top DEGs to rule out their molecular mechanism in heart failure caused by CHD.

Long non-coding RNA HULC exerts oncogenic activity on papillary thyroid cancer in vitro and in vivo.

Thyroid cancer is a frequently happened malignancy in human endocrine system. Papillary thyroid cancer (PTC) presents 70-80% of all thyroid cancer cases. Herein, we probed the possible oncogenic function of long non-coding RNA (lncRNA) highly up-regulated in liver cancer (HULC) in PTC. First, the HULC and microRNA-106a (miR-106a) expressions in PTC tissues and cells were tested. Plasmids or miRNAs transfections were done for altering HULC and miR-106a expressions. Then, cells viability and apoptosis, along with cell proliferative, migratory and invasive abilities, were tested, respectively. The PI3K/AKT and Wnt/ß-catenin pathways activities were measured. Finally, the animal model of PTC was constructed and the tumour volumes and weights were gauged. We discovered that HULC and miR-106a had relative high expression levels in PTC tissues and cells. HULC overexpression enhanced TPC-1 cells viability and cell proliferative, migratory and invasive abilities. Silencing HULC induced TPC-1 cell apoptosis. miR-106a engaged in the oncogenic impacts of HULC. Moreover, HULC overexpression boosted PI3K/AKT and Wnt/ß-catenin pathways activities via raising miR-106a expression. Besides, HULC overexpression enhanced the volumes and weights of PTC tumours. To sum up, HULC exhibited oncogenic function on PTC in vitro and in vivo.

Regulation of plasma membrane H+-ATPase activity by the members of the V-SNARE VAMP7C family in arabidopsis thaliana.

The plasma membrane (PM) H+-ATPase plays an important role in response to environmental stress, such as salt-alkaline stress. We have reported that the N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein Vesicle-associated membrane protein 711 (VAMP711) is involved in drought stress by regulating PM H+-ATPase activity directly. In this study, we report that VAMP7C (VAMP711-14) represses PM H+-ATPase activity in response to high-pH stress. The Arabidopsis PM H+-ATPase AHA2 interacts with VAMP7C. The longin domain of VAMP711 interacts with AHA2 to inhibit PM H+-ATPase activity on the plasma membrane. The alkaline phenotype of vamp711 and vamp711 vamp712 vamp713 triple mutants suggested that VAMP7C was functionally redundant in regulating PM H+-ATPase activity in response to high-pH stress.

Calcium-activated 14-3-3 proteins as a molecular switch in salt stress tolerance.

Calcium is a universal secondary messenger that triggers many cellular responses. However, it is unclear how a calcium signal is coordinately decoded by different calcium sensors, which in turn regulate downstream targets to fulfill a specific physiological function. Here we show that SOS2-LIKE PROTEIN KINASE5 (PKS5) can negatively regulate the Salt-Overly-Sensitive signaling pathway in Arabidopsis. PKS5 can interact with and phosphorylate SOS2 at Ser294, promote the interaction between SOS2 and 14-3-3 proteins, and repress SOS2 activity. However, salt stress promotes an interaction between 14-3-3 proteins and PKS5, repressing its kinase activity and releasing inhibition of SOS2. We provide evidence that 14-3-3 proteins bind to Ca2+, and that Ca2+ modulates 14-3-3-dependent regulation of SOS2 and PKS5 kinase activity. Our results suggest that a salt-induced calcium signal is decoded by 14-3-3 and SOS3/SCaBP8 proteins, which selectively activate/inactivate the downstream protein kinases SOS2 and PKS5 to regulate Na+ homeostasis by coordinately mediating plasma membrane Na+/H+ antiporter and H+-ATPase activity.

Pregabalin can decrease acute pain and morphine consumption in laparoscopic cholecystectomy patients: A meta-analysis of randomized controlled trials.

BACKGROUND: Pregabalin has been used as an adjunct for the management of acute pain in laparoscopic cholecystectomy. This meta-analysis aimed to illustrate the efficacy and safety of pregabalin for pain management following laparoscopic cholecystectomy. METHODS: In March 2017, a systematic computer-based search was conducted in PubMed, EMBASE, Web of Science, Cochrane Database of Systematic Reviews, and Google databases. Data on patients prepared for laparoscopic cholecystectomy in studies that compared pregabalin versus placebo were retrieved. The primary endpoints were the visual analog scale (VAS) score with rest or mobilization at 6, 12, and 24 hours and total morphine consumption. The secondary outcomes were the morphine-related complications (i.e., nausea, vomiting, dizziness, somnolence, headache, pruritus, urine retention, respiratory depression, and blurred vision). Continuous outcomes were expressed as the weighted mean difference (WMD) with a corresponding 95% confidence interval (CI), and discontinuous outcomes were expressed as a risk ratio (RR) with a corresponding 95% CI. RESULTS: Twelve clinical studies with 938 patients (gabapentin group = 536, control group = 402) were ultimately included in the meta-analysis. Pregabalin was associated with reduced pain scores with rest at 6, 12, and 24 hours, which corresponded to a reduction of 11.27 points at 6 hours, 9.46 points at 12 hours, and 3.99 points at 24 hours on a 100-point VAS. Moreover, pregabalin was associated with reduced pain scores with mobilization at 6, 12, and 24 hours, which corresponded to a reduction of 8.74 points, 5.80 points and 6.37 points at 6, 12, and 24 hours, respectively, on a 110-point VAS. Furthermore, pregabalin reduced the occurrence of nausea and vomiting. There were no significant differences in the occurrence of respiratory depression, pruritus, dizziness, blurred vision, and headache. CONCLUSIONS: Pregabalin was efficacious in the reduction of postoperative pain, total morphine consumption, and morphine-related complications following laparoscopic cholecystectomy. In addition, a high dose of pregabalin was more effective than a low dose. The dose of pregabalin differed across the studies, and the heterogeneity was large. More studies are needed to verify the optimal dose of pregabalin in laparoscopic cholecystectomy patients.

O-6-methylguanine-DNA methyltransferase gene promoter methylation and lung cancer risk: A meta-analysis.

OBJECTIVE: To evaluate O-6-methylguanine-DNA methyltransferase (MGMT) gene promoter methylation pattern in tumor tissue and autologous controls (plasma, normal lung tissue, and bronchial lavage fluid [BLF]) in patients with nonsmall cell lung cancer (NSCLC). MATERIALS AND METHODS: We electronic searched the MEDLINE and CNKI databases to find the open published studies related to MGMT gene promoter hypermethylation in NSCLC patients. The odds ratio (OR) for hypermethylation in plasma, BLF, and tissue was pooled by fixed or random effect model according to the statistical heterogeneity across the included studies. RESULTS: After searching the related databases, we finally included 13 studies in this meta-analysis. The hypermethylation rate of tumor tissue, plasma, BLF, and control tissue of MGMT gene in NSCLC patients were 0.34 ± 0.20, 0.18 ± 0.14, and 0.39 ± 0.23; the statistical heterogeneity across the studies was evaluated by Chi-square and I2-test. Moreover, no statistical heterogeneity was existed in the aspects of hypermethylation for plasma, BLF, and tissue (P < 0.05). Meta-analysis showed the hypermethylation rate in tumor tissue was significantly higher than normal lung tissue (OR = 4.18, 95% CI: 2.76-6.32) and plasma (OR = 2.37, 95% CI: 1.49-3.75) in NSCLC patients. However, for BLF (OR = 2.05, 95% CI: 0.88-4.78), the hypermethylation rate was not statistical different (P > 0.05). CONCLUSION: Hypermethylation rate in MGMT gene promoter of cancer tissue was statistical higher than autologous controls which indicated that MGMT may play an important in the cancer development.