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A method was developed for the simultaneous analysis of trace arsine and phosphine in ethylene and propylene products by gas chromatography-atomic emission spectroscopy detector and the chromatographic analysis conditions were optimized, and the detection limit, linear range, recovery rate and repeatability of the method were investigated. The results showed that the detection limit of the method for arsine was as low as 0.02 mL/m3, the linear correlation coefficient was more than 0.999 in the volume concentration range of 0.02~2 090 mL/m3, the recovery rate was 87.60% and the relative standard deviation of the 3 parallel measurements was 1.83%. The detection limit of phosphine was as low as 0.03 mL/m3, the correlation coefficient was greater than 0.999 in the volume concentration range of 0.03~3 010 mL/m3, the recovery rate was 106.13% and the relative standard deviation of the 3 parallel measurements was 3.39%. The method can be used as a control analysis method for trace arsine and phosphine in ethylene and propylene products.

Objective To explore the feasibility of genetic marker detection of semen-specific coding region single nucleotide polymorphism （cSNP） based on SNaPshot technology in semen stains and mixed body fluid identification. Methods Genomic DNA （gDNA） and total RNA were extracted from 16 semen stains and 11 mixtures composed of semen and venous blood, and the total RNA was reverse transcribed into complementary DNA （cDNA）. The cSNP genetic markers were screened on the validated semen-specific mRNA coding genes. The cSNP multiplex detection system based on SNaPshot technology was established, and samples were genotyped by capillary electrophoresis （CE）. Results A multiplex detection system containing 5 semen-specific cSNPs was successfully established. In 16 semen samples, except the cSNP located in the TGM4 gene showed allele loss in cDNA detection results, the gDNA and cDNA typing results of other cSNPs were highly consistent. When detecting semen-venous blood mixtures, the results of cSNP typing detected were consistent with the genotype of semen donor and were not interfered by the genotype of venous blood donor. Conclusion The method of semen-specific cSNPs detection by SNaPshot technology method can be applied to the genotyping of semen （stains） and provide information for determining the origin of semen in mixed body fluids （stains）.

Abstract Neuroinflammation occurs early in Alzheimer’s disease (AD). The initial stage of AD is related to glial dysfunction, which contributes to impairment of Aβ clearance and disruption of synaptic connection. CEBPβ, a member of the CCAAT-enhancer-binding protein (CEBP) family, modulates the expression of inflammation-associated genes, and its expression is elevated in brains undergoing degeneration and injured brains. However, the mechanism underlying CEBPβ-mediated chronic inflammation in AD is unclear. In this study, we observed that increases in the levels of nuclear CEBPβ facilitated the interaction of CEBPβ with the NFκB p65 subunit, increasing the transcription of proinflammatory cytokines in the APP/PS1 mouse brain. Oral administration of nanocarrier-packaged carnosic acid (CA) reduced the aberrant activation of microglia and astrocytes and diminished mature IL-1β, TNFα and IL-6 production in the APP/PS1 mouse brain. CA administration reduced β-amyloid (Aβ) deposition and ameliorated cognitive impairment in APP/PS1 mice. We observed that CA blocked the interaction of CEBPβ with NFκB p65, and chromatin immunoprecipitation revealed that CA reduced the transcription of the NFκB target genes TNFα and IL-6. We confirmed that CA alleviated inflammatory mediator-induced neuronal degeneration and reduced Aβ secretion by inhibiting the CEBPβ-NFκB signalling pathway in vitro. Sulfobutyl ether-beta-cyclodextrin (SBEβCD) was used as the encapsulation agent for the CA-loaded nanocarrier to overcome the poor water solubility and enhance the brain bioavailability of CA. The CA nanoparticles (NPs) had no obvious toxicity. We demonstrated a feasible SBEβCD-based nanodelivery system targeting the brain. Our data provide experimental evidence that CA-loaded NPs are potential therapeutic agents for AD treatment.

Aims: To explore the co‐occurrence of urinary incontinence and frailty by testing the roles of depression and activity engagement guided by the mechanisms of common cause and interaction pathways. Design: A secondary analysis of a 1‐year three‐wave panel data collected from older nursing home residents in China. Methods: Changes in depression and activity engagement were regressed on urinary incontinence and frailty incidence underpinned by the common cause mechanism of chronic conditions co‐occurrence, and these changes were also taken as mediators linking from frailty to urinary incontinence incidence supported by the interaction pathways' mechanism. Results: A total of 348 older adults were included in this study, and 55.7% were women. The co‐occurrence of urinary incontinence and frailty was found in 16.7% of the participants at baseline. Older adults with sole frailty at baseline had almost twice the rate of incident urinary incontinence (32.7%) compared with those without (16.7%) over a 1‐year period. The subsample analyses showed that changes in depression and activity engagement failed to significantly predict the incidence of urinary incontinence and frailty. The mediating roles of these changes linking frailty to urinary incontinence incidence were also not statistically significant. Conclusion: The co‐occurrence of urinary incontinence and frailty is prevalent in older nursing home residents. Older adults with frailty at baseline are more likely to develop urinary incontinence a year later. The common cause and interaction pathways mechanisms for the co‐occurrence of urinary incontinence and frailty were not verified with changes in depression and activity engagement. Implications for the Profession and/or Patient Care: The phenomenon of urinary incontinence and frailty co‐occurrence should be given extreme emphasis. Although statistically significant findings on the roles of depression and activity engagement were not inferred, this study provides multiple possibilities for future studies to test and depict a clear picture of this co‐occurrence. Impact: What problem did the study address? This study was designed to test the roles of depression and activity engagement in predicting the incidence of urinary incontinence and frailty, and the mediating roles in linking frailty to urinary incontinence incidence.What were the main findings? Despite the methodological pitfalls in literature have been addressed, neither depression nor activity engagement would significantly predict the incidence of urinary incontinence and frailty in older adults. Their mediating roles in linking frailty to urinary incontinence incidence were also not significant.Where and on whom will the research have an impact? Our findings add important pieces of evidence to promote researchers' understanding and provide an important basis for untangling the puzzle of urinary incontinence and frailty co‐occurrence. Reporting Method: The report of this study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement guidelines. Patient or Public Contribution: No patient or public contribution. [ABSTRACT FROM AUTHOR]

C36H52Ag2N10O8S2, orthorhombic, Pna21 (no. 33), a = 11.7911(16) Å, b = 31.310(5) Å, c = 10.6883(11) Å, V = 3945.9(9) Å3, Z = 4, Rgt(F) = 0.0353, wRref(F2) = 0.0784, T = 293(2) K.

Background: Oxidative stress is an early event in the development of Alzheimer's disease (AD) and maybe a pivotal point of interaction governing AD pathogenesis; oxidative stress contributes to metabolism imbalance, protein misfolding, neuroinflammation and apoptosis. Excess reactive oxygen species (ROS) are a major contributor to oxidative stress. As vital sources of ROS, mitochondria are also the primary targets of ROS attack. Seeking effective avenues to reduce oxidative stress has attracted increasing attention for AD intervention. Methods: We developed liposome‐packaged Ligustilide (LIG) and investigated its effects on mitochondrial function and AD‐like pathology in the APPswe/PS1dE9 (APP/PS1) mouse model of AD, and analyzed possible mechanisms. Results: We observed that LIG‐loaded liposome (LIG‐LPs) treatment reduced oxidative stress and β‐amyloid (Aβ) deposition and mitigated cognitive impairment in APP/PS1 mice. LIG management alleviated the destruction of the inner structure in the hippocampal mitochondria and ameliorated the imbalance between mitochondrial fission and fusion in the APP/PS1 mouse brain. We showed that the decline in cAMP‐dependent protein kinase A (PKA) and A‐kinase anchor protein 1 for PKA (AKAP1) was associated with oxidative stress and AD‐like pathology. We confirmed that LIG‐mediated antioxidant properties and neuroprotection were involved in upregulating the PKA/AKAP1 signaling in APPswe cells in vitro. Conclusion: Liposome packaging for LIG is relatively biosafe and can overcome the instability of LIG. LIG alleviates mitochondrial dysfunctions and cognitive impairment via the PKA/AKAP1 signaling pathway. Our results provide experimental evidence that LIG‐LPs may be a promising agent for AD therapy. [ABSTRACT FROM AUTHOR]