Delay-Dependent Stability of Single-Loop Controlled Grid-Connected Inverters with LCL Filters

LCL filters have been widely used for grid-connected inverters. However, the problem that how time delay affects the stability of digitally controlled grid-connected inverters with LCL filters has not been fully studied. In this paper, a systematic study is carried out on the relationship between the time delay and stability of single-loop controlled grid-connected inverters that employ inverter current feedback (ICF) or grid current feedback (GCF). The ranges of time delay for system stability are analyzed and deduced in the continuous s-domain and discrete z-domain. It is shown that in the optimal range, the existence of time delay weakens the stability of the ICF loop, whereas a proper time delay is required for the GCF loop. The present work explains, for the first time, why different conclusions on the stability of ICF loop and GCF loop have been drawn in previous studies. To improve system stability, a linear predictor-based time delay reduction method is proposed for ICF, while a time delay addition method is used for GCF. A controller design method is then presented that guarantees adequate stability margins. The delay-dependent stability study is verified by simulation and experiment

The APC Algorithm of Solving Large-Scale Linear Systems: A Generalized Analysis

A new algorithm called accelerated projection-based consensus (APC) has recently emerged as a promising approach to solve large-scale systems of linear equations in a distributed fashion. The algorithm adopts the federated architecture, and attracts increasing research interest; however, it's performance analysis is still incomplete, e.g., the error performance under noisy condition has not yet been investigated. In this paper, we focus on providing a generalized analysis by the use of the linear system theory, such that the error performance of the APC algorithm for solving linear systems in presence of additive noise can be clarified. We specifically provide a closed-form expression of the error of solution attained by the APC algorithm. Numerical results demonstrate the error performance of the APC algorithm, validating the presented analysis.Comment: 6 pages, 3 figure

Selective unresponsiveness to the inhibition of p38 MAPK activation by cAMP helps L929 fibroblastoma cells escape TNF-α-induced cell death

<p>Abstract</p> <p>Background</p> <p>The cyclic AMP (cAMP) signaling pathway has been reported to either promote or suppress cell death, in a cell context-dependent manner. Our previous study has shown that the induction of dynein light chain (DLC) by cAMP response element-binding protein (CREB) is required for cAMP-mediated inhibition of mitogen-activated protein kinase (MAPK) p38 activation in fibroblasts, which leads to suppression of NF-κB activity and promotion of tumor necrosis factor-α (TNF-α)-induced cell death. However, it remains unknown whether this regulation is also applicable to fibroblastoma cells.</p> <p>Methods</p> <p>Intracellular cAMP was determined in L929 fibroblastoma cells after treatment of the cells with various cAMP elevation agents. Effects of cAMP in the presence or absence of the RNA synthesis inhibitor actinomycin D or small interfering RNAs (siRNAs) against CREB on TNF-α-induced cell death in L929 cells were measured by propidium iodide (PI) staining and subsequent flow cytomety. The activation of p38 and c-Jun N-terminal protein kinase (JNK), another member of MAPK superfamily, was analyzed by immunoblotting. JNK selective inhibitor D-JNKi1 and p38 selective inhibitor SB203580 were included to examine the roles of JNK and p38 in this process. The expression of DLC or other mediators of cAMP was analyzed by immunoblotting. After ectopic expression of DLC with a transfection marker GFP, effects of cAMP on TNF-α-induced cell death in GFP+ cells were measured by PI staining and subsequent flow cytomety.</p> <p>Results</p> <p>Elevation of cAMP suppressed TNF-α-induced necrotic cell death in L929 fibroblastoma cells via CREB-mediated transcription. The pro-survival role of cAMP was associated with selective unresponsiveness of L929 cells to the inhibition of p38 activation by cAMP, even though cAMP significantly inhibited the activation of JNK under the same conditions. Further exploration revealed that the induction of DLC, the major mediator of p38 inhibition by cAMP, was impaired in L929 cells. Enforced inhibition of p38 activation by using p38 specific inhibitor or ectopic expression of DLC reversed the protection of L929 cells by cAMP from TNF-α-induced cell death.</p> <p>Conclusion</p> <p>These data suggest that the lack of a pro-apoptotic pathway in tumor cells leads to a net survival effect of cAMP.</p

Auxin depletion from leaf primordia contributes to organ patterning

Stem cells are responsible for organogenesis, but it is largely unknown whether and how information from stem cells acts to direct organ patterning after organ primordia are formed. It has long been proposed that the stem cells at the plant shoot apex produce a signal, which promotes leaf adaxial-abaxial (dorsoventral) patterning. Here we show the existence of a transient low auxin zone in the adaxial domain of early leaf primordia. We also demonstrate that this adaxial low auxin domain contributes to leaf adaxial-abaxial patterning. The auxin signal is mediated by the auxin-responsive transcription factor MONOPTEROS (MP), whose constitutive activation in the adaxial domain promotes abaxial cell fate. Furthermore, we show that auxin flow from emerging leaf primordia to the shoot apical meristem establishes the low auxin zone, and that this auxin flow contributes to leaf polarity. Our results provide an explanation for the hypothetical meristem-derived leaf polarity signal. Opposite to the original proposal, instead of a signal derived from the meristem, we show that a signaling molecule is departing from the primordium to the meristem to promote robustness in leaf patterning

Pathogenic alpha-synuclein aggregates preferentially bind to mitochondria and affect cellular respiration

Abstract Misfolded alpha-synuclein (αSyn) is a major constituent of Lewy bodies and Lewy neurites, which are pathological hallmarks of Parkinson’s disease (PD). The contribution of αSyn to PD is well established, but the detailed mechanism remains obscure. Using a model in which αSyn aggregation in primary neurons was seeded by exogenously added, preformed αSyn amyloid fibrils (PFF), we found that a majority of pathogenic αSyn (indicated by serine 129 phosphorylated αSyn, ps-αSyn) was membrane-bound and associated with mitochondria. In contrast, only a minuscule amount of physiological αSyn was mitochondrial bound. In vitro, αSyn PFF displayed a stronger binding to purified mitochondria than did αSyn monomer, revealing a preferential mitochondria binding by aggregated αSyn. This selective mitochondrial ps-αSyn accumulation was confirmed in other neuronal and animal αSyn aggregation models that do not require exogenously added PFF and, more importantly, in postmortem brain tissues of patients suffering from PD and other neurodegenerative diseases with αSyn aggregation (α-synucleinopathies). We also showed that the mitochondrial ps-αSyn accumulation was accompanied by defects in cellular respiration in primary neurons, suggesting a link to mitochondrial dysfunction. Together, our results show that, contrary to physiological αSyn, pathogenic αSyn aggregates preferentially bind to mitochondria, indicating mitochondrial dysfunction as the common downstream mechanism for α-synucleinopathies. Our findings suggest a plausible model explaining the formation and the peculiar morphology of Lewy body and reveal that disrupting the interaction between ps-αSyn and the mitochondria is a therapeutic target for α-synucleinopathies.https://deepblue.lib.umich.edu/bitstream/2027.42/148288/1/40478_2019_Article_696.pd

Cofactor Molecules Maintain Infectious Conformation and Restrict Strain Properties in Purified Prions

Prions containing misfolded prion protein (PrP(Sc)) can be formed with cofactor molecules using the technique of serial protein misfolding cyclic amplification. However, it remains unknown whether cofactors materially participate in maintaining prion conformation and infectious properties. Here we show that withdrawal of cofactor molecules during serial propagation of purified recombinant prions caused adaptation of PrP(Sc) structure accompanied by a reduction in specific infectivity of >10(5)-fold, to undetectable levels, despite the ability of adapted “protein-only” PrP(Sc) molecules to self-propagate in vitro. We also report that changing only the cofactor component of a minimal reaction substrate mixture during serial propagation induced major changes in the strain properties of an infectious recombinant prion. Moreover, propagation with only one functional cofactor (phosphatidylethanolamine) induced the conversion of three distinct strains into a single strain with unique infectious properties and PrP(Sc) structure. Taken together, these results indicate that cofactor molecules can regulate the defining features of mammalian prions: PrP(Sc) conformation, infectivity, and strain properties. These findings suggest that cofactor molecules likely are integral components of infectious prions

The effect of symmetrically tilt grain boundary of aluminum on hydrogen diffusion

High-strength aluminum alloys are widely used in industry. Hydrogen embrittlement greatly reduces the performance and service safety of aluminum alloys. The hydrogen traps in alumi-num profoundly affect the hydrogen embrittlement of aluminum. Here, we took a coinci-dence-site lattice (CSL) symmetrically tilted grain boundary (STGB) Σ5(120)[001] as an example to carry out molecular dynamics (MD) simulations of hydrogen diffusion in aluminum at dif-ferent temperatures, and to obtain results and rules consistent with the experiment. At 700 K, three groups of MD simulations with concentrations of 0.5, 2.5 and 5 atomic % hydrogen (at. % H) were carried out for STGB models at different angles. By analyzing the simulation results and the MSD curves of hydrogen atoms, we found that, in the low hydrogen concentration of STGB models, the grain boundaries captured hydrogen atoms and hindered their movement. In high-hydrogen-concentration models, the diffusion rate of hydrogen atoms was not affected by the grain boundaries. The analysis of the simulation results showed that the diffusion of hydro-gen atoms at the grain boundary is anisotropic