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In order to improve the reaction efficiency and rate of Al powder with seawater, highly active Al base powder (Al-Mg-Sn-Bi alloy powder, AMSB) was prepared by adding low melting metal (Sn and Bi) by atomizing. The hydrogen generation rate and open circuit potential of AMSB alloy powder were measured by hydrogen generation test and electrochemical test, and the hydrolysis mechanism was characterized. The hydrogen generation test results show that the hydrogen generation rate of AMSB alloy powder in 3.5%(mass fraction) NaCl solution can reach 214.80 mL·min-1·g-1, and the hydrogen generation efficiency can reach 80.45%. The results of electrochemical experiments show that the addition of Sn and Bi can reduce the open circuit potential of AMSB alloy powder and promote the negative shift of the electrode potential of Al powder. The phase composition and microstructure of AMSB alloy powder before and after the reaction were characterized by XRD, XPS and SEM-EDS. Low melting point elements Sn and Bi can destroy the densification of oxide film, effectively improve the reaction efficiency of Al with water and promote the reaction process of Al and water. Moreover, the galvanic cell effect formed between Al, Sn and Bi elements is an important reason for the improvement of the hydrolysis performance of AMSB alloy powder. Therefore, the highly active Al based powder prepared has a certain application value in the field of high energy water reaction metal fuel.

The strength prediction of pervious concrete is hard to implement for the mix design due to the porous structure. This work studied the influence of the water-to-cement ratio on the fluidity, viscosity, and mechanical properties of cement paste. Then, the porosity, permeability, and compressive strength of the pervious concrete with various porosities were investigated, and the test results were fitted and analyzed. The result indicates that as the water-to-cement ratio increases, the viscosity of the cement paste reduces and the fluidity increases. The water-to-cement ratio has a negative linear relationship with net slurry strength. The porosity and permeability of pervious concrete fluctuate in accordance with the same rule as the water-to-cement ratio changes. The compressive strength of pervious concrete with varying design porosities increases initially, then declines as the water-to-cement ratio rises. According to the linear fitting analysis, when the water-to-cement ratio is constant, the permeability and compressive strength of pervious concrete have a positive and negative linear relationship with the design porosity, respectively. By analyzing the fitting results and combining the volume method of pervious concrete, a calculation method for mix proportion design is proposed to predict the strength of pervious concrete.

Cancers and neurological disorders are two major types of diseases in humans. We developed the concept called the Aberrant Cell Cycle Disease (ACCD) due to the accumulating evidence that shows that two different diseases share the common mechanism of aberrant cell cycle re-entry. The aberrant cell cycle re-entry is manifested as kinase/oncoprotein activation and tumor suppressor (TS) inactivation, which are associated with both tumor growth in cancers and neuronal death in neurological disorders. Therefore, some cancer therapies (e.g., kinase/oncogene inhibition and TS elevation) can be leveraged for neurological treatments. MicroRNA (miR/miRNA) provides a new style of drug-target binding. For example, a single tumor suppressor miRNA (TS-miR/miRNA) can bind to and decrease tens of target kinases/oncogenes, producing much more robust efficacy to block cell cycle re-entry than inhibiting a single kinase/oncogene. In this review, we summarize the miRNAs that are altered in both cancers and neurological disorders, with an emphasis on miRNA drugs that have entered into clinical trials for neurological treatment.

Excitotoxicity, a neuronal death process in neurological disorders such as stroke, is initiated by the overstimulation of ionotropic glutamate receptors. Although dysregulation of proteolytic signaling networks is critical for excitotoxicity, the identity of affected proteins and mechanisms by which they induce neuronal cell death remain unclear. To address this, we used quantitative N-terminomics to identify proteins modified by proteolysis in neurons undergoing excitotoxic cell death. We found that most proteolytically processed proteins in excitotoxic neurons are likely substrates of calpains, including key synaptic regulatory proteins such as CRMP2, doublecortin-like kinase I, Src tyrosine kinase and calmodulin-dependent protein kinase IIβ (CaMKIIβ). Critically, calpain-catalyzed proteolytic processing of these proteins generates stable truncated fragments with altered activities that potentially contribute to neuronal death by perturbing synaptic organization and function. Blocking calpain-mediated proteolysis of one of these proteins, Src, protected against neuronal loss in a rat model of neurotoxicity. Extrapolation of our N-terminomic results led to the discovery that CaMKIIα, an isoform of CaMKIIβ, undergoes differential processing in mouse brains under physiological conditions and during ischemic stroke. In summary, by identifying the neuronal proteins undergoing proteolysis during excitotoxicity, our findings offer new insights into excitotoxic neuronal death mechanisms and reveal potential neuroprotective targets for neurological disorders.

The formula of stochastic subspace identification method is deduced in details and the program is written out. The two methods are verified by a vibration test on a 5-floor rigid frame model. In this test the gauss white noise generated from a shaker table to simulate the ambient vibration on the model, and the response signals are measured. Next, the response data of experiment are processed by auto-cross spectrum density method and stochastic subspace identification method respectively, the two methods are verified by comparing with the theory result. and bearing out the superiority of stochastic subspace identification method compared to auto-cross spectrum density method.

Our previous studies demonstrated that traumatic brain injury (TBI) and ventricular administration of thrombin caused hippocampal neuron loss and cognitive dysfunction via activation of Src family kinases (SFKs). Based on SFK localization in brain, we hypothesized SFK subtypes Fyn and c-Src, as well as SFK downstream molecule Rho-associated protein kinase (ROCK), contribute to cell death and cognitive dysfunction after TBI. We administered nanoparticle wrapped small interfering RNA (siRNA)-Fyn and siRNA-c-Src, or ROCK inhibitor Y-27632 to adult rats subjected to moderate lateral fluid percussion (LFP)-induced TBI. Spatial memory function was assessed from 12 to 16 days, and NeuN stained hippocampal neurons were assessed 16 days after TBI. The combination of siRNA-Fyn and siRNA-c-Src, but neither alone, prevented hippocampal neuron loss and spatial memory deficits after TBI. The ROCK inhibitor Y-27632 also prevented hippocampal neuronal loss and spatial memory deficits after TBI. The data suggest that the combined actions of three kinases (Fyn, c-Src, ROCK) mediate hippocampal neuronal cell death and spatial memory deficits produced by LFP-TBI, and that inhibiting this pathway prevents the TBI-induced cell death and memory deficits.

Abstract Background Tissue plasminogen activator (tPA) is known to have functions beyond fibrinolysis in acute ischemic stroke, such as blood brain barrier disruption. To further delineate tPA functions in the blood, we examined the gene expression profiles induced by tPA in a rat model of ischemic stroke. Results tPA differentially expressed 929 genes in the blood of rats (p ≤ 0.05, fold change ≥ |1.2|). Genes identified had functions related to modulation of immune cells. tPA gene expression was found to be dependent on the reperfusion status of cerebral vasculature. The majority of genes regulated by tPA were different from genes regulated by ischemic stroke. Conclusions tPA modulates gene expression in the blood of rats involving immune cells in a manner that is dependent on the status of vascular reperfusion. These non-fibrinolytic activities of tPA in the blood serve to better understand tPA-related complications.

Genome-wide association studies have identified putative ischemic stroke risk genes, yet, their expression after stroke is unexplored in spite of growing interest in elucidating their specific role and identifying candidate genes for stroke treatment. Thus, we took an exploratory approach to investigate sexual dimorphism, alternative splicing, and etiology in putative risk gene expression in blood following cardioembolic, atherosclerotic large vessel disease and small vessel disease/lacunar causes of ischemic stroke in each sex compared to controls. Whole transcriptome arrays assessed 71 putative stroke/vascular risk factor genes for blood RNA expression at gene-, exon-, and alternative splicing-levels. Male (n = 122) and female (n = 123) stroke and control volunteers from three university medical centers were matched for race, age, vascular risk factors, and blood draw time since stroke onset. Exclusion criteria included: previous stroke, drug abuse, subarachnoid or intracerebral hemorrhage, hemorrhagic transformation, infection, dialysis, cancer, hematological abnormalities, thrombolytics, anticoagulants or immunosuppressants. Significant differential gene expression (fold change > |1.2|, p < 0.05, partial correlation > |0.4|) and alternative splicing (false discovery rate p < 0.3) were assessed. At gene level, few were differentially expressed: ALDH2, ALOX5AP, F13A1, and IMPA2 (males, all stroke); ITGB3 (females, cardioembolic); ADD1 (males, atherosclerotic); F13A1, IMPA2 (males, lacunar); and WNK1 (females, lacunar). GP1BA and ITGA2B were alternatively spliced in both sexes (all patients vs. controls). Six genes in males, five in females, were alternatively spliced in all stroke compared to controls. Alternative splicing and exon-level analyses associated many genes with specific etiology in either sex. Of 71 genes, 70 had differential exon-level expression in stroke patients compared to control subjects. Among stroke patients, 24 genes represented by differentially expressed exons were male-specific, six were common between sexes, and two were female-specific. In lacunar stroke, expression of 19 differentially expressed exons representing six genes (ADD1, NINJ2, PCSK9, PEMT, SMARCA4, WNK1) decreased in males and increased in females. Results demonstrate alternative splicing and sexually dimorphic expression of most putative risk genes in stroke patients' blood. Since expression was also often cause-specific, sex, and etiology are factors to consider in stroke treatment trials and genetic association studies as society trends toward more personalized medicine.

The histone deacetylase 9 (HDAC9) polymorphism rs2107595 is associated with an increased risk for large vessel atherosclerotic stroke (LVAS). In humans, there remains a need to better understand this HDAC9 polymorphism's contribution to large vessel stroke. In this pilot study, we evaluated whether the HDAC9 polymorphism rs2107595 is associated with differences in leukocyte gene expression in patients with LVAS. HDAC9 SNP rs2107595 was genotyped in 155 patients (43 LVAS and 112 vascular risk factor controls). RNA isolated from blood was processed on whole genome microarrays. Gene expression was compared between HDAC9 risk allele-positive and risk allele-negative LVAS patients and controls. Functional analysis identified canonical pathways and molecular functions associated with rs2107595 in LVAS. In HDAC9 SNP rs2107595 risk allele-positive LVAS patients, there were 155 genes differentially expressed compared to risk allele-negative patients (fold change > |1.2|, p

Intestinal metaplasia (IM) is a premalignant condition that increases the risk for subsequent gastric cancer (GC). Traditional Chinese medicine generally plays a role in the treatment of IM, and the phytochemical naringenin used in Chinese herbal medicine has shown therapeutic potential for the treatment of gastric diseases. However, naringenin's specific effect on IM is not yet clearly understood. Therefore, this study identified potential gene targets for the treatment of IM through bioinformatics analysis and experiment validation. Two genes (MTTP and APOB) were selected as potential targets after a comparison of RNA‐seq results of clinical samples, the GEO dataset (GSE78523), and naringenin‐related genes from the GeneCards database. The results of both cell and animal experiments suggested that naringenin can improve the changes in the intestinal epithelial metaplasia model via MTTP/APOB expression. In summary, naringenin likely inhibits the MTTP/APOB axis and therefore inhibits IM progression. These results support the development of naringenin as an anti‐IM agent and may contribute to the discovery of novel IM therapeutic targets. [ABSTRACT FROM AUTHOR]

Background and purposeAlthough peripheral blood mRNA and micro-RNA change after ischemic stroke, any role for long noncoding RNA (lncRNA), which comprise most of the genome and have been implicated in various diseases, is unknown. Thus, we hypothesized that lncRNA expression also changes after stroke.MethodslncRNA expression was assessed in 266 whole-blood RNA samples drawn once per individual from patients with ischemic stroke and matched with vascular risk factor controls. Differential lncRNA expression was assessed by ANCOVA (P|1.2|), principal components analysis, and hierarchical clustering on a derivation set (n=176) and confirmed on a validation set (n=90). Poststroke temporal lncRNA expression changes were assessed using ANCOVA with confounding factor correction (P|0.4|). Because sexual dimorphism exists in stroke, analyses were performed for each sex separately.ResultsA total of 299 lncRNAs were differentially expressed between stroke and control males, whereas 97 lncRNAs were differentially expressed between stroke and control females. Significant changes of lncRNA expression with time after stroke were detected for 49 lncRNAs in men and 31 lncRNAs in women. Some differentially expressed lncRNAs mapped close to genomic locations of previously identified putative stroke-risk genes, including lipoprotein, lipoprotein(a)-like 2, ABO (transferase A, α1-3-N-acetylgalactosaminyltransferase; transferase B, α1-3-galactosyltransferase) blood group, prostaglandin 12 synthase, and α-adducins.ConclusionsThis study provides evidence of altered and sexually dimorphic lncRNA expression in peripheral blood of patients with stroke compared with that of controls and suggests that lncRNAs have potential for stroke biomarker development. Some regulated lncRNA could regulate some previously identified putative stroke-risk genes.

The combination of multiple factors in marine environments can accelerate the concrete corrosion. In this work, bending fatigue load, dry–wet cycles and Cl− erosion were experimentally combined to evaluate the endurance of marine concrete incorporating nanoparticles (nano-silica (NS) and nano-titania (NT)). Dry–wet cycles of the nano-concretes were simulated in seawater (5% sodium chloride solution) and bending fatigue loads at stress levels of 0.5, 0.6, 0.7 and 0.8 were applied. The results indicated that the nanoparticles enhanced the resistance to Cl− erosion during dry–wet cycles and bending fatigue load by making the concrete more durable under coupled bending fatigue load, dry–wet cycles and Cl− erosion. The improvements were the most obvious for a NT content of 1% and a NS content of 2%, and the improvement was better with 1% NT than with 2% NS content is 2%. The free Cl− content in the concrete tension zone was larger than in the compressive zone. X-ray diffraction was used to assess the physical phases of the concretes before and after the experiments and to analyse the reasons for the increased concrete durability. The nanoparticles increases the content of hydrated calcium silicate in concrete, changed the orientation of calcium hydroxide and improved the concrete durability. [ABSTRACT FROM AUTHOR]