Forebrain E-I balance controlled in cognition through coordinated inhibition and inhibitory transcriptome mechanism

IntroductionForebrain neural networks are vital for cognitive functioning, and their excitatory-inhibitory (E-I) balance is governed by neural homeostasis. However, the homeostatic control strategies and transcriptomic mechanisms that maintain forebrain E-I balance and optimal cognition remain unclear.MethodsWe used patch-clamp and RNA sequencing to investigate the patterns of neural network homeostasis with suppressing forebrain excitatory neural activity and spatial training.ResultsWe found that inhibitory transmission and receptor transcription were reduced in tamoxifen-inducible Kir2.1 conditional knock-in mice. In contrast, spatial training increased inhibitory synaptic connections and the transcription of inhibitory receptors.DiscussionOur study provides significant evidence that inhibitory systems play a critical role in the homeostatic control of the E-I balance in the forebrain during cognitive training and E-I rebalance, and we have provided insights into multiple gene candidates for cognition-related homeostasis in the forebrain

Direct Torque Control System and Sensorless Technique of Permanent Magnet Synchronous Motor

AbstractThe direct torque control theory has achieved great success in the control of induction motors. However, in the DTC drive system of Permanent Magnet Synchronous Machine (PMSM) proposed a few years ago, there are many basic theoretical problems that must be clarified. This paper describes an investigation about the effect of the zero voltage space vectors in the DTC system of PMSM and points out that if using the zero voltage space vectors rationally, not only can the DTC system be driven successfully but also the torque ripple is reduced and the performance of the system is improved. This paper also studies the sensorless technique in the DTC system of PMSM and configures the DTC system of PMSM with sensorless technique including zero voltage space vectors. Numerical simulations and experimental tests have proved the theory correct. In the condition of sensorless, the DTC system of PMSM is wide-rangely speed adjusting, and the ratio of speed adjustment is 1:100

Protective effect of Yiguanjian decoction against DNA damage on concanavalin A-induced liver injury mice model

AbstractObjectiveTo investigate the inhibitory effect of Yiguanjian decoction (YD) on DNA damage in Concanavalin A (Con A)-induced liver injury mice model and to explain the possible mechanism.MethodsTotally 120 male BALB/c mice were randomly divided into 6 groups, 20 mice each: normal group, model group, Bifendate group, YD low dose group, YD middle dose group and YD high dose group. Except normal group, liver injury model induced by Con A was established. While modeling, each mouse in YD group was given YD (0.4 mL/20 g per day) by intragastric administration (0.13 g YD for YD low dose group; 0.26 g for YD middle dose group; 0.52 g for YD high dose group). Bifendate group was given Bifendate (0.2 g·kg−1·d−1) by gavage. Normal group and model group were fed with same volume of physiological saline daily. After 8 weeks, the serum alanine transaminase (ALT) and aspartate transaminase (AST) were tested. The hematoxylin-eosin staining was used to evaluate the grade of liver inflammation and liver fibrosis stage. Hepatocellular DNA damage was detected by single cell gel electrophoresis technology. The protein expression of tumor necrosis factor-α (TNF-α), Bax and MutT Homolog 1 (MTH1) was detected by western blotting and enzyme linked immunosorbent assay. Bax mRNA and MTH1 mRNA were detected by Real-time Polymerase Chain Reaction (PCR).ResultsYD can improve the degree of liver inflammation and fibrosis in the liver of chronic hepatitis mice, the dose effect relationship is remarkable (P < 0.05). YD can reduce liver cell DNA damage. The difference between YD middle dose group and model group was statistically significant (P < 0.05). YD middle dose group had decreased the protein expression of TNF-α in the mice liver of immunological liver injury (P < 0.05). YD can increase the protein expression of Bax (P < 0.05). Compared with normal group, the protein expression of MTH1 was decreased (P < 0.05), but there was no statistical significance between YD group and model group (P > 0.05). YD can increase the mRNA expression of Bax and MTH1 (both P < 0.05).ConclusionYD can effectively inhibit the DNA damage in immunological liver injury mice, the mechanism may be that it can decrease the TNF-α and increase the Bax and MTH1 expression

Detection of entangled states supported by reinforcement learning

Discrimination of entangled states is an important element of quantum enhanced metrology. This typically requires low-noise detection technology. Such a challenge can be circumvented by introducing nonlinear readout process. Traditionally, this is realized by reversing the very dynamics that generates the entangled state, which requires a full control over the system evolution. In this work, we present nonlinear readout of highly entangled states by employing reinforcement learning (RL) to manipulate the spin-mixing dynamics in a spin-1 atomic condensate. The RL found results in driving the system towards an unstable fixed point, whereby the (to be sensed) phase perturbation is amplified by the subsequent spin-mixing dynamics. Working with a condensate of 10900 {87}^Rb atoms, we achieve a metrological gain of 6.97 dB beyond the classical precision limit. Our work would open up new possibilities in unlocking the full potential of entanglement caused quantum enhancement in experiments

Effects of Intake Components and Stratification on the Particle and Gaseous Emissions of a Diesel Engine

It is of great significance to improve the performance of diesel engines by adjusting the intake components and their distribution. In this work, various proportions of exhaust gas recirculation (EGR) gas and oxygen (O2) have been introduced to the intake charge of a diesel engine and the effects of different intake components and stratification conditions on pollutant emissions, especially for particles, have been explored. The results show that the introduction of O2 into the intake charge is beneficial to alleviate the deterioration of particles and hydrocarbon (HC) emissions caused by high EGR rates. Compared with the pure air intake condition, the introduction of moderate O2 at high EGR rate conditions can simultaneously reduce nitrogen oxides (NOx) and particles, when the intake oxygen content (IOC) is 0.2 and the EGR rate is 20%, the NOx and particles are reduced by 45.66% and 66.49%, respectively. It is worth noting that different intake components have a significant impact on the particle size distribution (PSD) of diesel engines. In addition, the in-cylinder O2 concentration distribution formed by the stratified intake is advantageous for further improving the combined effect of NOx, particles and HC emissions relative to the homogeneous intake. At a condition of 0.2 IOC and 20% EGR rate, the NOx, particles, and HC emissions are about 8.8%, 14.3%, and 26% lower than that of intake components nonstratification, respectively

Targeting USP1-dependent KDM4A protein stability as a potential prostate cancer therapy

The histone demethylase lysine-specific demethylase 4A (KDM4A) is reported to be overexpressed and plays a vital in multiple cancers through controlling gene expression by epigenetic regulation of H3K9 or H3K36 methylation marks. However, the biological role and mechanism of KDM4A in prostate cancer (PC) remain unclear. Herein, we reported KDM4A expression was upregulation in phosphatase and tensin homolog knockout mouse prostate tissue. Depletion of KDM4A in PC cells inhibited their proliferation and survival in vivo and vitro. Further studies reveal that USP1 is a deubiquitinase that regulates KDM4A K48-linked deubiquitin and stability. Interestingly, we found c-Myc was a key downstream effector of the USP1-KDM4A/androgen receptor axis in driving PC cell proliferation. Notably, upregulation of KDM4A expression with high USP1 expression was observed in most prostate tumors and inhibition of USP1 promotes PC cells response to therapeutic agent enzalutamide. Our studies propose USP1 could be an anticancer therapeutic target in PC