Does urbanization have spatial spillover effect on poverty reduction: empirical evidence from rural China

In light of a scarcity of research on the spatial effects of urbanization on poverty reduction, this study uses panel data on 30 provinces in China from 2009 to 2019 to construct a system of indices to assess poverty that spans the four dimensions of the economy, education, health, and living. We use the spatial autocorrelation test and the spatial Durbin model (SDM) to analyze the spatial effects of urbanization on poverty reduction in these different dimensions. The main conclusions are as follows: (a) China’s urbanization has the characteristics of spatial aggregation and a spatial spillover effect. (b) Different dimensions of poverty had the attributes of spatial agglomeration, and Moran’s index of a reduction in economic poverty was the highest. Under the SDM, the different dimensions of poverty also showed a significant positive spatial correlation. (c) Urbanization has a significant effect on poverty reduction along the dimensions of the economy, education, and living, but has little effect on reducing health poverty. It has a spatial spillover effect on poverty reduction in economic and living contexts. (d) There were spatial differences in the effect of urbanization on relieving economic and living-related poverty

Mitofusin 2 Participates in Mitophagy and Mitochondrial Fusion Against Angiotensin II-Induced Cardiomyocyte Injury

BackgroundMitochondrial dynamics play a critical role in mitochondrial function. The mitofusin 2 (MFN2) gene encodes a mitochondrial membrane protein that participates in mitochondrial fusion to maintain and operate the mitochondrial network. Moreover, MFN2 is essential for mitophagy. In Ang II-induced cardiac remodeling, the combined effects of MFN2-mediated mitochondrial fusion and mitophagy are unclear. This study was designed to explore a novel strategy for preventing cardiomyocyte injury via modulation of mitochondrial dynamics.MethodsWe studied the function of MFN2 in mitochondrial fusion and mitophagy in Ang II-stimulated cardiomyocyte injury. Cardiomyocyte injury experiments, including reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), and apoptosis rate of cardiomyocytes were performed. The mitochondrial morphology in cardiomyocytes was examined via transmission electron microscopy (TEM) and confocal microscopy. Autophagic levels in response to Ang II were examined by immunoblotting of autophagy-related proteins. Moreover, PINK1/MFN2/Parkin pathway-related proteins were examined.ResultsWith stimulation by Ang II, MFN2 expression was progressively reduced. MFN2 deficiency impaired mitochondrial quality, resulting in exacerbated mitochondrial damage induced by Ang II. The Ang II-induced increases in ROS production and apoptosis rate were alleviated by MFN2 overexpression. Moreover, MFN2 alleviated the Ang II-induced reduction in MMP. MFN2 promoted mitochondrial fusion, and MFN2 promoted Parkin translocation and phosphorylation, leading to mitochondrial autophagy. The effects of MFN2 overexpression were reversed by autophagy inhibitors.ConclusionMitofusin 2 promotes Parkin translocation and phosphorylation, leading to mitophagy to clear damaged mitochondria. However, the beneficial effects of MFN2 were reversed by autophagy inhibitors. Additionally, MFN2 participates in mitochondrial fusion to maintain mitochondrial quality. Thus, MFN2 participated in mitophagy and mitochondrial fusion against Ang II-induced cardiomyocyte injury

Neutral top-pion and lepton flavor violating processes

In the context of topcolor-assisted techicolor(TC2) models, we study the contributions of the neutral top-pion $\pi^{0}_{t}$ to the lepton flavor violating(LFV) processes $l_{i}\to l_{j}\gamma$ and $l_{i}\to l_{j}l_{k}l_{l}$. We find that the present experimental bound on $\mu\to e\gamma$ gives severe constraints on the free parameters of $TC2$ models. Taking into account these constraints, we consider the processes $l_{i}\to l_{j}l_{k}l_{l}$ generated by top-pion exchange at the tree-level and the one loop level, and obtain $Br(\mu\to 3e)\simeq 2.87\times 10^{-14}$, $1.1\times 10^{-15}\leq Br(\tau\to 3e)\simeq Br(\tau\to 2e\mu)\leq 4.4 \times 10^{-15}$, $3.1\times 10^{-15} \leq Br(\tau\to 2\mu e)\simeq Br(\tau\to 3\mu)\leq 1.5 \times 10^{-14}$ in most of the parameter space.Comment: latex files,16 pages, 6 figures. Submitted to Phys. Rev.

Increased uterine androgen receptor protein abundance results in implantation and mitochondrial defects in pregnant rats with hyperandrogenism and insulin resistance.

Funder: University of GothenburgIn this study, we show that during normal rat pregnancy, there is a gestational stage-dependent decrease in androgen receptor (AR) abundance in the gravid uterus and that this is correlated with the differential expression of endometrial receptivity and decidualization genes during early and mid-gestation. In contrast, exposure to 5α-dihydrotestosterone (DHT) and insulin (INS) or DHT alone significantly increased AR protein levels in the uterus in association with the aberrant expression of endometrial receptivity and decidualization genes, as well as disrupted implantation. Next, we assessed the functional relevance of the androgen-AR axis in the uterus for reproductive outcomes by treating normal pregnant rats and pregnant rats exposed to DHT and INS with the anti-androgen flutamide. We found that AR blockage using flutamide largely attenuated the DHT and INS-induced maternal endocrine, metabolic, and fertility impairments in pregnant rats in association with suppressed induction of uterine AR protein abundance and androgen-regulated response protein and normalized expression of several endometrial receptivity and decidualization genes. Further, blockade of AR normalized the expression of the mitochondrial biogenesis marker Nrf1 and the mitochondrial functional proteins Complexes I and II, VDAC, and PHB1. However, flutamide treatment did not rescue the compromised mitochondrial structure resulting from co-exposure to DHT and INS. These results demonstrate that functional AR protein is an important factor for gravid uterine function. Impairments in the uterine androgen-AR axis are accompanied by decreased endometrial receptivity, decidualization, and mitochondrial dysfunction, which might contribute to abnormal implantation in pregnant PCOS patients with compromised pregnancy outcomes and subfertility. KEY MESSAGES: The proper regulation of uterine androgen receptor (AR) contributes to a normal pregnancy process, whereas the aberrant regulation of uterine AR might be linked to polycystic ovary syndrome (PCOS)-induced pregnancy-related complications. In the current study, we found that during normal rat pregnancy there is a stage-dependent decrease in AR abundance in the gravid uterus and that this is correlated with the differential expression of the endometrial receptivity and decidualization genes Spp1, Prl, Igfbp1, and Hbegf. Pregnant rats exposed to 5α-dihydrotestosterone (DHT) and insulin (INS) or to DHT alone show elevated uterine AR protein abundance and implantation failure related to the aberrant expression of genes involved in endometrial receptivity and decidualization in early to mid-gestation. Treatment with the anti-androgen flutamide, starting from pre-implantation, effectively prevents DHT + INS-induced defects in endometrial receptivity and decidualization gene expression, restores uterine mitochondrial homeostasis, and increases the pregnancy rate and the numbers of viable fetuses. This study adds to our understanding of the mechanisms underlying poor pregnancy outcomes in PCOS patients and the possible therapeutic use of anti-androgens, including flutamide, after spontaneous conception

A novel PCR-based method for high throughput prokaryotic expression of antimicrobial peptide genes

<p>Abstract</p> <p>Background</p> <p>To facilitate the screening of large quantities of new antimicrobial peptides (AMPs), we describe a cost-effective method for high throughput prokaryotic expression of AMPs. EDDIE, an autoproteolytic mutant of the N-terminal autoprotease, Npro, from classical swine fever virus, was selected as a fusion protein partner. The expression system was used for high-level expression of six antimicrobial peptides with different sizes: Bombinin-like peptide 7, Temporin G, hexapeptide, Combi-1, human Histatin 9, and human Histatin 6. These expressed AMPs were purified and evaluated for antimicrobial activity.</p> <p>Results</p> <p>Two or four primers were used to synthesize each AMP gene in a single step PCR. Each synthetic gene was then cloned into the pET30a/His-EDDIE-GFP vector via an <it>in vivo </it>recombination strategy. Each AMP was then expressed as an Npro fusion protein in <it>Escherichia coli</it>. The expressed fusion proteins existed as inclusion bodies in the cytoplasm and the expression levels of the six AMPs reached up to 40% of the total cell protein content. On <it>in vitro </it>refolding, the fusion AMPs was released from the C-terminal end of the autoprotease by self-cleavage, leaving AMPs with an authentic N terminus. The released fusion partner was easily purified by Ni-NTA chromatography. All recombinant AMPs displayed expected antimicrobial activity against <it>E. coli</it>, <it>Micrococcus </it>luteus and <it>S. cerevisia</it>.</p> <p>Conclusions</p> <p>The method described in this report allows the fast synthesis of genes that are optimized for over-expression in <it>E. coli </it>and for the production of sufficiently large amounts of peptides for functional and structural characterization. The Npro partner system, without the need for chemical or enzymatic removal of the fusion tag, is a low-cost, efficient way of producing AMPs for characterization. The cloning method, combined with bioinformatic analyses from genome and EST sequence data, will also be useful for screening new AMPs. Plasmid pET30a/His-EDDIE-GFP also provides green/white colony selection for high-throughput recombinant AMP cloning.</p

Accelerated Iterative Learning Control of Speed Ripple Suppression for a Seeker Servo Motor

To suppress the speed ripple of a permanent magnet synchronous motor in a seeker servo system, we propose an accelerated iterative learning control with an adjustable learning interval. First, according to the error of current iterative learning for the system, we determine the next iterative learning interval and conduct real-time correction on the learning gain. For the learning interval, as the number of iterations increases, the actual interval that needs correction constantly shortens, accelerating the convergence speed. Second, we analyze the specific structure of the controller while applying reasonable assumptions pertaining to its condition. Using the &lambda;-norm, we analyze and apply our mathematical knowledge to obtain a strict mathematical proof on the P-type iterative learning control and obtain the condition of convergence for the controller. Finally, we apply the proposed method for periodic ripple inhibition of the torque rotation speed of the permanent magnet synchronous motor and establish the system model; we use the periodic load torque to simulate the ripple torque of the synchronous motor. The simulation and experimental results indicate the effectiveness of the method

An Accelerating Iterative Learning Control Based on an Adjustable Learning Interval

An iterative learning control algorithm with an adjustable interval is proposed for nonlinear systems to accelerate the convergence rate of iterative learning control. For λ-norm, the monotonic convergence of ILC was analyzed, and the corresponding convergence conditions were obtained. The results showed that the convergence rate was mainly determined by the controlled object, the control law gain, the correction factor, and the iteration interval size and that the control law gain was corrected in real time in the modified interval and the modified interval shortened as the number of iterations increased, further accelerating the convergence. The numerical simulation shows the effectiveness of the proposed method

Accelerated Iterative Learning Control of Speed Ripple Suppression for a Seeker Servo Motor

To suppress the speed ripple of a permanent magnet synchronous motor in a seeker servo system, we propose an accelerated iterative learning control with an adjustable learning interval. First, according to the error of current iterative learning for the system, we determine the next iterative learning interval and conduct real-time correction on the learning gain. For the learning interval, as the number of iterations increases, the actual interval that needs correction constantly shortens, accelerating the convergence speed. Second, we analyze the specific structure of the controller while applying reasonable assumptions pertaining to its condition. Using the &lambda;-norm, we analyze and apply our mathematical knowledge to obtain a strict mathematical proof on the P-type iterative learning control and obtain the condition of convergence for the controller. Finally, we apply the proposed method for periodic ripple inhibition of the torque rotation speed of the permanent magnet synchronous motor and establish the system model; we use the periodic load torque to simulate the ripple torque of the synchronous motor. The simulation and experimental results indicate the effectiveness of the method

Chattering-Free Sliding-Mode Control for Electromechanical Actuator with Backlash Nonlinearity

Considering the backlash nonlinearity and parameter time-varying characteristics in electromechanical actuators, a chattering-free sliding-mode control strategy is proposed in this paper to regulate the rudder angle and suppress unknown external disturbances. Different from most existing backlash compensation methods, a special continuous function is addressed to approximate the backlash nonlinear dead-zone model. Regarding the approximation error, unmodeled dynamics, and unknown external disturbances as a disturbance-like term, a strict feedback nonlinear model is established. Based on this nonlinear model, a chattering-free nonsingular terminal sliding-mode controller is proposed to achieve the rudder angle tracking with a chattering elimination and tracking dynamic performance improvement. A Lyapunov-based proof ensures the asymptotic stability and finite-time convergence of the closed-loop system. Experimental results have verified the effectiveness of the proposed method