Thermal Error Compensation of the Wear-Depth Real-Time Detecting of Self-Lubricating Spherical Plain Bearings

The spherical plain bearing test bench is a necessary detecting equipment in the research process of self?lubricating spherical plain bearings. The varying environmental temperatures cause the thermal deformation of the wear?depth detecting system of bearing test benches and then a ect the accuracy of the wear?depth detecting data. However, few researches about the spherical plain bearing test benches can be found with the implementation of the detect?ing error compensation. Based on the self?made modular spherical plain bearing test bench, two main causes of ther?mal errors, the friction heat of bearings and the environmental temperature variation, are analysed. The thermal errors caused by the friction heat of bearings are calculated, and the thermal deformation of the wear?depth detecting sys?tem caused by the varying environmental temperatures is detected. In view of the above results, the environmental temperature variation is the main cause of the two error factors. When the environmental temperatures rise is 10.3 °C, the thermal deformation is approximately 0.01 mm. In addition, the comprehensive compensating model of the thermal error of the wear?depth detecting system is built by multiple linear regression(MLR) and time series analysis. Compared with the detecting data of the thermal errors, the comprehensive compensating model has higher fitting precision, and the maximum residual is only 1 μm. A comprehensive compensating model of the thermal error of the wear?depth detecting system is proposed, which provides a theoretical basis for the improvement of the real?time wear?depth detecting precision of the spherical plain bearing test bench.

Inhibitory effect of baicalein on mice tremor induced by oxotremorine and mechanisms

OBJECTIVE To investigate the anti-tremor effect and mechanism of baicalein on oxotremorine-induced muscle tremor in mice.METHODS The acute model of muscular tremor was induced by intraperitoneal injection of oxotremorine,and the latency,duration and frequency of muscle tremor in mice were measured immediately;the saliva of mice was measured to reflect the correlation between tremor and peripheral nerve function;the aim of this study was to determine the content of MDA and the activity of GSH-PX,and to investigate the anti-oxidation of mice with tremor model.The activity of acetylcholinesterase(AchE)and acetylcholine transferase(ChA T)can indirectly reflect the level of acetylcholine in the brain.The level of monoamine neurotransmitters in brain tissue was determined by high performance liquid chromatography(HPLC-ECD).RESULTS The animals in the model group appeared obvious tremoring,salivating and erecting and other symptoms.Compared to the model group,there was no obvious inhibitory effect on the administration of each dose.After 7,14,21 and 28 d of continuous administration,the latency,duration and tremor frequency of tremor mice were significantly shortened,the levels of acetylcholine were significantly decreased,the changes of DOPAC and DA neurotransmitters in the brain of model group were recovered,regulate the dynamic balance of acetylcholine and dopamine in the brain.CONCLUSION Long-term administration can improve the tremor behavior of mice,the mechanismmay be related to the regulation of neurotransmittersin brain.

铂片电极表面芥子气伏安行为研究

本文探究了芥子气(HD)在铂片电极表面的电化学行为。循环伏安(CV)结果展现了两个分隔良好的氧化峰,不同扫描速率的CV曲线表明氧化峰电流和峰电势均与扫描速率呈一定的线性关系,证明了该氧化过程为动力学控制的不可逆过程,同时计算了氧化过程转移的电子数和相关参数。以HD在铂片上的电化学行为为基础,采用傅里叶红外光谱(FT-IR)和电化学对比实验解释了CV曲线中两个氧化峰相对应的氧化过程,HD连续电化学氧化为二氯二乙基亚砜和二氯二乙基砜,为鉴别两种氧化产物提供了新的策略。方波伏安法(SWV)结果表明:HD浓度为2.5×10^(-5)~6.0×10^(-4) mol·L^(-1)时与峰电流呈线性关系,检测限为2.15×10^(-5) mol·L^(-1),该方法无需电极材料修饰,简单易得,且稳定性好,抗干扰能力强。通过研究HD在铂片电极表面的电化学行为,为其电化学传感提供基础。下一步工作应以负载型铂纳米粒子和多维载体为出发点,提高其检测能力。

VRK2 is involved in the innate antiviral response by promoting mitostress-induced mtDNA release

Mitochondrial stress (mitostress) triggered by viral infection or mitochondrial dysfunction causes the release of mitochondrial DNA (mtDNA) into the cytosol and activates the cGAS-mediated innate immune response. The regulation of mtDNA release upon mitostress remains uncharacterized. Here, we identified mitochondria-associated vaccinia virus-related kinase 2 (VRK2) as a key regulator of this process. VRK2 deficiency inhibited the induction of antiviral genes and caused earlier and higher mortality in mice after viral infection. Upon viral infection, VRK2 associated with voltage-dependent anion channel 1 (VDAC1) and promoted VDAC1 oligomerization and mtDNA release, leading to the cGAS-mediated innate immune response. VRK2 was also required for mtDNA release and cGAS-mediated innate immunity triggered by nonviral factors that cause Ca^(2+) overload but was not required for the cytosolic nucleic acid-triggered innate immune response. Thus, VRK2 plays a crucial role in the mtDNA-triggered innate immune response and may be a potential therapeutic target for infectious and autoimmune diseases associated with mtDNA release.

Inhibitory effect of H_(3+x)PMo_(12-x)V_xO_(40)-Ton the self-polymerization of methyl methacrylate

In this work,a series of molybdovanadophosphoric heteropoly acid quaternary ammonium salts H_(3+x)PMo_(12 -x)V_xO40-T were synthesized and employed as a reaction inhibitor in the selfpolymerization of methyl methacrylate(MMA).The polymerization inhibition effect of H_(3+x)PMoPMo_(12 -x)V_xO40-T)with different number of vanadium atoms and reaction dosages was investigated using differential scanning calorimetry(DSC).It shows that the inhibitory effect was improved with the increasing dosages of H_(3+x)PMoPMo_(12 -x)V_xO40-T),and the polymerization inhibition was also affected by the number of vanadium atoms in the H_(3+x)PMo_(12 -x)V_xO40-T .Furthermore,cyclic voltammograms(CV)was used to probe the mechanism of the inhibition reaction with H3+xPMo12xVxO40-T.The result of CV indicates that the inhibition reaction is an oxidation–reduction reaction.H_(3+x)PMo_(12 -x)V_xO40-T can react directly with the MMA monomer radicals,which eliminated the MMA monomers,and therefore the self-polymerization of the MMA can be effectively inhibited by H_(3+x)PMo_(12 -x)V_xO40-T.

CdS quantum dot sensitized p-type NiO as photocathode with integrated cobaloxime in photoelectrochemical cell for water splitting

CdS sensitized NiO electrode was used as the photoactive cathode in a photoelectrochemical cell for water splitting,avoiding the use of a sacrificial electron donor.Photocurrent increment under visible light irradiation was observed after integration of[Co(dmgH)_2(4-Me-py)Cl](1) to the photocathode,suggesting 1 could accept electrons from photoexcited CdS for water reduction and NiO could move the holes in the valence band of CdS to anode for water oxidation.

Enhanced performance of ruthenium dye-sensitized solar cell by employing an organic co-adsorbent of N,N'-bis((pyridin-2-yl)(methyl)methylene)-o-phenylenediamine

A pyridine-anchor co-adsorbent of N,N'-bis((pyridin-2-yl)(methyl) methylene)-o-phenylenediamine(named BPPI) is prepared and employed as co-adsorbent in dye-sensitized solar cells(DSSCs). The prepared co-adsorbent could overcome the deficiency of N719 absorption in the low wavelength region of visible spectrum, offset competitive visible light absorption of I_3^-, enhance the spectral responses of the co-adsorbed TiO_2 film in region from 300 nm to 750 nm, suppress charge recombination, prolong electron lifetime, and decrease the total resistance of DSSCs. The optimized cell device co-sensitized by BPPI/N719 dye gives a short circuit current density of 12.98 m A cm^(-2), an open circuit voltage of 0.73 V,and a fill factor of 0.66 corresponding to an overall conversion efficiency of 6.22% under standard global AM 1.5 solar irradiation, which is much higher than that of device solely sensitized by N719(5.29%)under the same conditions. Mechanistic investigations are carried out by various spectral and electrochemical characterizations.

Estrogen receptorα-mediated signaling inhibits type I interferon response to promote breast carcinogenesis

Estrogen receptorα(ERα)is an important driver and therapeutic target in∼70%of breast cancers.How ERαdrives breast carcinogenesis is not fully understood.In this study,we show that ERαis a negative regulator of type I interferon(IFN)response.Activation of ERαby its natural ligand estradiol inhibits IFN-β-induced transcription of downstream IFN-stimulated genes(ISGs),whereas ERαdeficiency or the stimulation with its antagonist fulvestrant has opposite effects.Mechanistically,ERαinduces the expression of the histone 2A variant H2A.Z to restrict the engagement of the IFN-stimulated gene factor 3(ISGF3)complex to the promoters of ISGs and also interacts with STAT2 to disrupt the assembly of the ISGF3 complex.These two events mutually lead to the inhibition of ISG transcription induced by type I IFNs.In a xenograft mouse model,fulvestrant enhances the ability of IFN-βto suppress ERα^(+)breast tumor growth.Consistently,clinical data analysis reveals that ERα^(+)breast cancer patients with higher levels of ISGs exhibit higher long-term survival rates.Taken together,our findings suggest that ERαinhibits type I IFN response via two distinct mechanisms to promote breast carcinogenesis.