Universal N2O Reaction Gas To Remove Spectral Interferences of Nonmetallic Impurity Elements by Inductively Coupled Plasma Tandem Mass Spectrometry Analysis of High-Purity Magnesium Alloys.

Using N2O as a universal reaction gas, a new strategy was proposed for the highly sensitive interference-free simultaneous determination of nonmetallic impurity elements in high-purity magnesium (Mg) alloys by ICP-MS/MS. In the MS/MS mode, through O-atom and N-atom transfer reactions, 28Si+ and 31P+ were converted to the oxide ions 28Si16O2+ and 31P16O+, respectively, while 32S+ and 35Cl+ were converted to the nitride ions 32S14N+ and 14N35Cl+, respectively. The ion pairs formed via the 28Si+ → 28Si16O2+, 31P+ → 31P16O+, 32S+ → 32S14N+, and 35Cl+ → 14N35Cl+ reactions by the mass shift method could eliminate spectral interferences. Compared with the O2 and H2 reaction modes, the present approach delivered much higher sensitivity and lower limit of detection (LOD) of the analytes. The accuracy of the developed method was evaluated via standard addition method and comparative analysis by sector field ICP-MS (SF-ICP-MS). The study indicates that in the MS/MS mode, use of N2O as reaction gas can provide interference-free conditions and sufficiently low LODs for analytes. The LODs of Si, P, S, and Cl could reach down to 17.2, 4.43, 10.8, and 31.9 ng L-1, respectively, and the recoveries were in the range of 94.0-106%. The determination results of the analytes were consistent with those obtained by SF-ICP-MS. This study presents a systematic method for the precise and accurate quantification of Si, P, S, and Cl in high-purity Mg alloys by ICP-MS/MS. The developed method provides valuable reference that can be expanded and applied to other fields.

Combined processing strategy based on magnetorheological finishing for monocrystalline silicon x-ray mirrors.

Higher requirements for monocrystalline silicon x-ray mirrors have been put forward with the development of synchrotron radiation optics. The existing processing technologies limit their efficiency while achieving high-precision manufacturing of x-ray mirrors. Hence, this paper formulates a processing strategy of employing magnetorheological finishing (MRF) to make the precision of x-ray mirrors fully meet the standard. The combination of fine polishing and super-smooth processing can effectively improve the surface quality of mirrors. The residual error, wavefront gradient, and surface roughness of the mirror can reach 7.2 nm, 0.42 µrad, and 0.28 nm, respectively, after several iterations. The research not only indicates that MRF can replace the existing manufacturing method and greatly improve processing efficiency, but also provides technical support for optimizing the processing route of x-ray mirrors.

Analysis of the smoothing characteristics and shape-retaining ability of conformal vibration polishing and suppression strategy for full-spatial frequency errors of optics.

Conformal vibration polishing (CVP) employing flexible polishing tools is expected to be an efficient means of optical processing, and all current research on it is limited to planar components. Hence, the smoothing characteristics of the middle spatial frequency (MSF) errors and the ability to maintain the surface shape of different types of optics in CVP are analyzed. A combined processing method based on magnetorheological finishing and CVP for full-spatial frequency errors is proposed and verified by experiment. The peak-to-valley value, MSF errors, and surface roughness of the large-diameter component can reach 75 nm, 1.1 nm, and 0.37 nm after 9 h of processing. The research not only demonstrates the excellent removal characteristics of CVP and the effectiveness of the proposed method but also provides an additional choice for the high-precision manufacturing of optics.

Chemical constituents from the stems of Acanthopanax senticosus with their cytotoxic activities.

A new coumestan named 7,5'-dihydroxy-4'-(3''-hydroxy-3''-methyl-trans-isobut-1''-enyl) coumestan (1), together with five known compounds (2-6), was isolated from the EtOAc-soluble extract of the stems of Acanthopanax senticosus. Their structures were elucidated based on extensive spectroscopic analyses. All the isolates were evaluated for in vitro cytotoxic activities against four human cancer cells including HepG2, A549, HeLa and MCF-7. Among them, the new compound 1 was found to exhibit significant cytotoxic activity on HeLa cells with IC50 value of 6.5 µM.

Frequency division combined machining method to improve polishing efficiency of continuous phase plate by bonnet polishing.

Continuous phase plate (CPP), as a key diffractive optical element, is difficult to manufacture owing to its random and small features. In this paper, a novel frequency division combined machining (FDCM) method was proposed to improve polishing efficiency of CPP by optimizing the tool influence functions (TIFs) over targeted frequency bands. In addition, the convergence rate of power spectral density (CR-PSD) was proposed to evaluate the correct ability of TIF in different frequency bands, and to determine the division frequency for the combined processing. Through simulation verification, the combined processing with optimized TIFs by FDCM enabled high precision in less total time than that with single TIF processing. The experimental results verified that the method could imprint a 300 × 300 mm CPP with residual root-mean-square 24.7 nm after approximately 6-h bonnet polishing. Comparing the focal spots of designed and fabricated CPPs, the deviation of their energy concentration within 500 microns is only 0.22%. Hence, bonnet polishing using the FDCM is a new technical option for the production of large-aperture CPPs. Furthermore, the FDCM method shows a significant increase in efficiency, and it could be a generic method for CPP processing through other technologies, including magnetorheological and ion beam finishing.

Smoothing process of conformal vibration polishing for mid-spatial frequency errors: characteristics research and guiding prediction.

By combining the conformal polishing method with short stroke vibration, a novel, to the best of our knowledge, conformal vibration polishing (CVP) method is proposed. The CVP method is expected to be an efficient means of optical processing by its high material removal rate and smoothing characteristics of mid-spatial frequency (MSF) errors. A quantitative time-domain smoothing model and a convergence factor (${\rm CF}_C$) are presented based on the research of smoothing characteristics. The motion mechanism, material removal ability, solution, and expansion of the smoothing model are demonstrated theoretically and experimentally. The experimental results exhibited good agreement with the theoretical predictions for the proposed method. The research provides a certain theoretical foundation for parameter selection and process optimization of the CVP method.

Planetary Gearbox Dynamic Modeling Considering Bearing Clearance and Sun Gear Tooth Crack.

Planetary gearbox systems are critical mechanical components in heavy machinery such as wind turbines. They may suffer from various failure modes, due to the harsh working environment. Dynamic modeling is a useful method to support early fault detection for enhancing reliability and reducing maintenance costs. However, reported studies have not considered the sun gear tooth crack and bearing clearance simultaneously to analyze their combined effect on vibration characteristics of planetary gearboxes. In this paper, a dynamic model is developed for planetary gearboxes considering the clearance of planet gear, sun gear, and carrier bearings, as well as sun gear tooth crack levels. Bearing forces are calculated considering bearing clearance, and the dynamic model equations are updated accordingly. The results reveal that the combination of bearing clearances can affect the vibration response with sun gear tooth crack by increasing the kurtosis. It is found that the effect of planet gear bearing clearance is very small, while the sun gear and carrier bearing clearance has clear impact on the vibration responses. These findings suggest that the incorporation of bearing clearance is important for planetary gearbox dynamic modeling.

Chemical constituents from Maackia amurensis and their anti-inflammatory and antioxidant activities.

A new flavonoid named (2S)-7,4'-dimethoxyl-6-(2″,3″-epoxy-3″-methylbutyl)flavanone (1), along with five known compounds (2-6), were isolated from the EtOAc-soluble extract of the stem bark of Maackia amurensis. Their structures were elucidated on the basis of spectroscopic methods. All compounds were evaluated for anti-inflammatory and antioxidant activities in vitro. Among them, compound 5 showed the highest inhibitory activity on NO production in RAW264.7 cells stimulated by LPS with IC50 value of 59.0 ± 1.5 µM. Meanwhile, compounds 1-6 exhibited varying antioxidant activities through DPPH, ABTS free radical-scavenging and FRAP assays.

Decreased cpg15 augments oxidative stress in sleep deprived mouse brain.

Sleep deprivation (SD) has detrimental effects on the physiological function of the brain. However, the underlying mechanism remains elusive. In the present study, we investigated the expression of candidate plasticity-related gene 15 (cpg15), a neurotrophic gene, and its potential role in SD using a REM-SD mouse model. Immunofluorescent and Western blot analysis revealed that the expression of cpg15 protein decreased in the hippocampus, ventral group of the dorsal thalamus (VENT), and somatosensory area of cerebral cortex (SSP) after 24-72 h of REM-SD, and the oxidative stress in these brain regions was increased in parallel, as indicated by the ratio of glutathione (GSH) to its oxidative product (GSSG). Over-expression of cpg15 in thalamus, hippocampus, and cerebral cortex mediated by AAV reduced the oxidative stress in these regions, indicating that the decrease of cpg15 might be a cause that augments oxidative stress in the sleep deprived mouse brain. Collectively, the results imply that cpg15 may play a protective function in the SD-subjected mouse brain via an anti-oxidative function. To our knowledge, this is the first time to provide evidences in the role of cpg15 against SD-induced oxidative stress in the brain.

Evaluation and compensation of a kinematic error to enhance prepolishing accuracy for large aspheric surfaces by robotic bonnet technology.

To obtain an economical uniform polishing method, it is effective to combine robot technology with bonnet polishing technology and apply it to the precision processing of large aspheric surfaces. However, the large robotic kinematic error causes significant deterioration to the surface shape of aspheric optics during robotic bonnet polishing (R-BP). To address this problem, research on the evaluation and compensation of the kinematic error was conducted to enhance the prepolishing accuracy on large aspheric surfaces by R-BP. Firstly, a precession control model of R-BP applied to the polishing of large aspheric surfaces was proposed. Then, an evaluation and compensation method of a robot kinematic error was presented based on machining errors. At last, it had been verified by experiments that at the removal depth of 2.5 µm, the variation of surface shape was reduced from 0.42 µm to 0.11 µm after compensation. Meanwhile, the change rate was reduced from 16.8% to 4.4%. Hence, the effectiveness of evaluation and compensation method to improve the prepolishing accuracy was verified, which is beneficial to implement mass production of high-precision large aspheric surfaces with low cost.

Serum Amyloid A is a Novel Inflammatory Biomarker in Polycystic Ovary Syndrome.

BACKGROUND: Serum amyloid A (SAA) is considered a biomarker of inflammation; however, the SAA levels in polycystic ovary syndrome (PCOS) are still uncertain. METHODS: In this study, SAA, glucose, insulin, C-reactive protein (CRP), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total testosterone concentrations were measured in 82 women with PCOS and 60 healthy controls. RESULTS: The median concentration of SAA was 5.000 mg/L (IQR: 2.825 - 5.400) in women with PCOS, which was significantly higher than that of controls (3.700 mg/L, IQR: 2.825 - 5.400, p = 0.025). SAA was only positively associated with the CRP (r = 0.303, p = 0.006). No significant association was observed between SAA and body mass index (BMI), total testosterone, or insulin resistance (IR). CONCLUSIONS: SAA levels were increased in women with PCOS, and SAA may be a potential inflammatory biomarker for PCOS.

Decreased Serum Kruppel-Like Factor 7 Level is Positively Associated with Low-Density Lipoprotein Cholesterol Level in Women with Polycystic Ovary Syndrome.

BACKGROUND: Kruppel-like factor 7 (KLF7) is associated with type 2 diabetes and obesity; however, at present the KLF7 level in polycystic ovary syndrome (PCOS) remains unreported. METHODS: In this study, serum KLF7, glucose, insulin, C-reactive protein (CRP), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total testosterone concentrations were measured in 65 women with PCOS and 61 healthy controls. RESULTS: Body mass index (BMI) in PCOS and the control group were all < 25 kg/m2. The median concentration of KLF7 was 3.630 ng/mL [interquartile range (IQR): 1.547 - 7.172] in women with PCOS, which was significantly lower than that of controls (5.282 ng/mL, IQR: 3.128 - 11.263, p = 0.003). The KLF7 level was positively correlated with low-density lipoprotein cholesterol (LDL-C) (r = 0.261, p = 0.018). No significant association was observed between KLF7 and the BMI, total testosterone, and insulin resistance (IR). CONCLUSIONS: The KLF7 level decreased in women with PCOS. KLF7 may represent a new therapeutic target in the treatment of PCOS.

Time-varying tool influence function model of bonnet polishing for aspheric surfaces.

For bonnet polishing of an aspheric surface, the tool influence function (TIF) is inevitably time varying, induced by the different surface curvatures on the aspheric surface. Accordingly, this paper investigated how the surface curvature affects the bonnet-workpiece contact area, and then presented a time-varying TIF model. The time-varying TIF was modeled based on the finite element analysis and kinematics analysis methods, and validated by experiments. The experimental results exhibited good agreement with the theoretical results. The proposed method can forecast the TIF for different polishing positions on aspheric surfaces, and provide the theoretical foundation for dynamic compensation of aspheric surface polishing.

Investigation of subsurface damage density and morphology impact on the laser-induced damage threshold of fused silica.

The laser-induced damage threshold (LIDT) of fused silica is affected by laser field intensity modulation and laser energy absorption. In this paper, the subsurface damage (SSD) density and morphology are detected by the small-angle taper polishing method. The modulation effect of SSD morphology on the incident laser/electric field is analyzed by the finite difference time domain (FDTD) simulation. Finally, the LIDT of the taper polished surface is tested to analyze the relationship among LIDT, SSD density, and SSD morphology, and the results show a high correlation. A reliable regression model is obtained based on the results, which shows that LIDT is inversely proportional to SSD density and the light intensity enhancement factor (LIEF).

Soluble cpg15 from Astrocytes Ameliorates Neurite Outgrowth Recovery of Hippocampal Neurons after Mouse Cerebral Ischemia.

The present study focuses on the function of cpg15, a neurotrophic factor, in ischemic neuronal recovery using transient global cerebral ischemic (TGI) mouse model and oxygen-glucose deprivation (OGD)-treated primary cultured cells. The results showed that expression of cpg15 proteins in astrocytes, predominantly the soluble form, was significantly increased in mouse hippocampus after TGI and in the cultured astrocytes after OGD. Addition of the medium from the cpg15-overexpressed astrocytic culture into the OGD-treated hippocampal neuronal cultures reduces the neuronal injury, whereas the recovery of neurite outgrowths of OGD-injured neurons was prevented when cpg15 in the OGD-treated astrocytes was knocked down, or the OGD-treated-astrocytic medium was immunoadsorbed by cpg15 antibody. Furthermore, lentivirus-delivered knockdown of cpg15 expression in mouse hippocampal astrocytes diminishes the dendritic branches and exacerbates injury of neurons in CA1 region after TGI. In addition, treatment with inhibitors of MEK1/2, PI3K, and TrkA decreases, whereas overexpression of p-CREB, but not dp-CREB, increases the expression of cpg15 in U118 or primary cultured astrocytes. Also, it is observed that the Flag-tagged soluble cpg15 from the astrocytes transfected with Flag-tagged cpg15-expressing plasmids adheres to the surface of neuronal bodies and the neurites. In conclusion, our results suggest that the soluble cpg15 from astrocytes induced by ischemia could ameliorate the recovery of the ischemic-injured hippocampal neurons via adhering to the surface of neurons. The upregulated expression of cpg15 in astrocytes may be activated via MAPK and PI3K signal pathways, and regulation of CREB phosphorylation.SIGNIFICANCE STATEMENT Neuronal plasticity plays a crucial role in the amelioration of neurological recovery of ischemic injured brain, which remains a challenge for clinic treatment of cerebral ischemia. cpg15 as a synaptic plasticity-related factor may participate in promoting the recovery process; however, the underlying mechanisms are still largely unknown. The objective of this study is to reveal the function and mechanism of neuronal-specific cpg15 expressed in astrocytes after ischemia induction, in promoting the recovery of injured neurons. Our findings provided new mechanistic insight into the neurological recovery, which might help develop novel therapeutic options for cerebral ischemia via astrocytic-targeting interference of gene expression.

MicroRNA-365 modulates astrocyte conversion into neuron in adult rat brain after stroke by targeting Pax6.

Reactive astrocytes induced by ischemia can transdifferentiate into mature neurons. This neurogenic potential of astrocytes may have therapeutic value for brain injury. Epigenetic modifications are widely known to involve in developmental and adult neurogenesis. PAX6, a neurogenic fate determinant, contributes to the astrocyte-to-neuron conversion. However, it is unclear whether microRNAs (miRs) modulate PAX6-mediated astrocyte-to-neuron conversion. In the present study we used bioinformatic approaches to predict miRs potentially targeting Pax6, and transient middle cerebral artery occlusion (MCAO) to model cerebral ischemic injury in adult rats. These rats were given striatal injection of glial fibrillary acidic protein targeted enhanced green fluorescence protein lentiviral vectors (Lv-GFAP-EGFP) to permit cell fate mapping for tracing astrocytes-derived neurons. We verified that miR-365 directly targets to the 3'-UTR of Pax6 by luciferase assay. We found that miR-365 expression was significantly increased in the ischemic brain. Intraventricular injection of miR-365 antagomir effectively increased astrocytic PAX6 expression and the number of new mature neurons derived from astrocytes in the ischemic striatum, and reduced neurological deficits as well as cerebral infarct volume. Conversely, miR-365 agomir reduced PAX6 expression and neurogenesis, and worsened brain injury. Moreover, exogenous overexpression of PAX6 enhanced the astrocyte-to-neuron conversion and abolished the effects of miR-365. Our results demonstrate that increase of miR-365 in the ischemic brain inhibits astrocyte-to-neuron conversion by targeting Pax6, whereas knockdown of miR-365 enhances PAX6-mediated neurogenesis from astrocytes and attenuates neuronal injury in the brain after ischemic stroke. Our findings provide a foundation for developing novel therapeutic strategies for brain injury.

Effect of temperature on surface error and laser damage threshold for self-healing BK7 glass.

Cracks caused during the lapping and polishing process can decrease the laser-induced damage threshold (LIDT) of the BK7 glass optical elements, which would shorten the lifetime and limit the output power of the high-energy laser system. When BK7 glass is heated under appropriate conditions, the surface cracks can exhibit a self-healing phenomenon. In this paper, based on thermodynamics and viscous fluid mechanics theory, the mechanisms of crack self-healing are explained. The heat-healing experiment was carried out, and the effect of water was analyzed. The multi-spatial-frequency analysis was used to investigate the effect of temperature on surface error for self-healing BK7 glass, and the lapped BK7 glass specimens before and after heat healing were detected by an interferometer and atomic force microscopy. The low-spatial-frequency error was analyzed by peak to valley and root mean square, the mid-spatial-frequency error was analyzed by power spectral density, and the high-spatial-frequency error was analyzed by surface roughness. The results showed that the optimal heating temperature for BK7 was 450°C, and when the heating temperature was higher than the glass transition temperature (555°C), the surface quality decreased a lot. The laser damage test was performed, and the specimen heated at 450°C showed an improvement in LIDT.

Striatal astrocytes transdifferentiate into functional mature neurons following ischemic brain injury.

To determine whether reactive astrocytes stimulated by brain injury can transdifferentiate into functional new neurons, we labeled these cells by injecting a glial fibrillary acidic protein (GFAP) targeted enhanced green fluorescence protein plasmid (pGfa2-eGFP plasmid) into the striatum of adult rats immediately following a transient middle cerebral artery occlusion (MCAO) and performed immunolabeling with specific neuronal markers to trace the neural fates of eGFP-expressing (GFP(+)) reactive astrocytes. The results showed that a portion of striatal GFP(+) astrocytes could transdifferentiate into immature neurons at 1 week after MCAO and mature neurons at 2 weeks as determined by double staining GFP-expressing cells with ßIII-tubulin (GFP(+)-Tuj-1(+)) and microtubule associated protein-2 (GFP(+)-MAP-2(+)), respectively. GFP(+) neurons further expressed choline acetyltransferase, glutamic acid decarboxylase, dopamine receptor D2-like family proteins, and the N-methyl-D-aspartate receptor subunit R2, indicating that astrocyte-derived neurons could develop into cholinergic or GABAergic neurons and express dopamine and glutamate receptors on their membranes. Electron microscopy analysis indicated that GFP(+) neurons could form synapses with other neurons at 13 weeks after MCAO. Electrophysiological recordings revealed that action potentials and active postsynaptic currents could be recorded in the neuron-like GFP(+) cells but not in the astrocyte-like GFP(+) cells, demonstrating that new GFP(+) neurons possessed the capacity to fire action potentials and receive synaptic inputs. These results demonstrated that striatal astrocyte-derived new neurons participate in the rebuilding of functional neural networks, a fundamental basis for brain repair after injury. These results may lead to new therapeutic strategies for enhancing brain repair after ischemic stroke.

Splicing factor NSSR1 reduces neuronal injury after mouse transient global cerebral ischemia.

This study focuses on the function of NSSR1, a splicing factor, in neuronal injury in the ischemic mouse brain using the transient global cerebral ischemic mouse model and the cultured cells treated with oxygen-glucose deprivation (OGD). The results showed that the cerebral ischemia triggers the expression of NSSR1 in hippocampal astrocytes, predominantly the dephosphorylated NSSR1 proteins, and the Exon3 inclusive NCAM-L1 variant and the Exon4 inclusive CREB variant. While in the hippocampus of astrocyte-specific NSSR1 conditional knockdown (cKD) mice, where cerebral ischemia no longer triggers NSSR1 expression in astrocytes, the expression of Exon3 inclusive NCAM-L1 variant and Exon4 inclusive CREB variant were no longer triggered as well. In addition, the injury of hippocampal neurons was more severe in astrocyte-specific NSSR1 cKD mice compared with in wild-type mice after brain ischemia. Of note, the culture media harvested from the astrocytes with overexpression of NSSR1 or the Exon3 inclusive NCAM-L1 variant, or Exon4 inclusive CREB variant were all able to reduce the neuronal injury induced by OGD. The results provide the evidence demonstrating that: (1) Splicing factor NSSR1 is a new factor involved in reducing ischemic injury. (2) Ischemia induces NSSR1 expression in astrocytes, not in neurons. (3) NSSR1-mediated pathway in astrocytes is required for reducing ischemic neuronal injury. (4) NCAM-L1 and CREB are probably mediators in NSSR1-mediated pathway. In conclusion, our results suggest for the first time that NSSR1 may provide a novel mechanism for reducing neuronal injury after ischemia, probably through regulation on alternative splicing of NCAM-L1 and CREB in astrocytes.

Regulation of RAGE splicing by hnRNP A1 and Tra2ß-1 and its potential role in AD pathogenesis.

The receptor for advanced glycation end products (RAGE) gene expresses two major alternative splicing isoforms, full-length membrane-bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis, either via interaction of mRAGE with ß-amyloid peptide (Aß) or inhibition of the mRAGE-activated signaling pathway. In the present study, we showed that heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and Transformer2ß-1 (Tra2ß-1) were involved in the alternative splicing of mRAGE and esRAGE. Functionally, two factors had an antagonistic effect on the regulation. Glucose deprivation induced an increased ratio of mRAGE/esRAGE via up-regulation of hnRNP A1 and down-regulation of Tra2ß-1. Moreover, the ratios of mRAGE/esRAGE and hnRNP A1/Tra2ß-1 were increased in peripheral blood mononuclear cells from AD patients. The results provide a molecular basis for altered splicing of mRAGE and esRAGE in AD pathogenesis. The receptor for advanced glycation end products (RAGE) gene expresses two major alternative splicing isoforms, membrane-bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis. Mechanism for imbalanced expression of these two isoforms in AD brain remains elusive. We proposed here a hypothetic model to illustrate that impaired glucose metabolism in AD brain may increase the expression of splicing protein hnRNP A1 and reduce Tra2ß-1, which cause the imbalanced expression of mRAGE and esRAGE.