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INTRODUCTION: Vascular pathology is known to contribute to dementia and vascular endothelial growth factor (VEGF) is a well‐established biomarker associated with vascular alterations. Nonetheless, research findings on VEGF in Alzheimer's disease (AD) and vascular dementia (VaD) are inconsistent across various studies. METHODS: We conducted a meta‐analysis to elucidate relationships between VEGF and AD/VaD. RESULTS: Twenty‐four studies were included. Pooled data showed that both blood and cerebrospinal fluid (CSF) VEGF levels were higher in VaD patients, whereas no significant difference was found between AD patients and healthy controls. However, the correlation between blood VEGF and AD was found among studies with AD pathology verification. And blood VEGF levels were higher in AD patients than controls in "age difference < 5 years" subgroup and CSF samples for European cohorts. DISCUSSION: This study highlights that VEGF is more effective for the diagnosis of VaD and vascular factors are also an important contributor in AD. Highlights: Vascular endothelial growth factor (VEGF) levels were higher in the vascular dementia group, but not in the overall Alzheimer's disease (AD) group.Correlation between VEGF and AD was found among studies with clear AD pathological verification.Elevated VEGF in the cerebrospinal fluid might be a diagnostic marker for AD in European populations. [ABSTRACT FROM AUTHOR]

Aims: This study investigated the relationship between plasma Wnt2b levels and Alzheimer's disease (AD), and explored the effect of Wnt2b on mitochondrial dysfunction in AD. Methods: Healthy and AD subjects, AD transgenic mice, and in vitro models were used to investigate the roles of Wnt2b in abnormalities in canonical Wnt signaling and mitochondria in AD. RT‐qPCR, immunoblotting, and immunofluorescence analysis were performed to assay canonical Wnt signaling. Mitochondrial structure was analyzed by electron microscopy. Flow cytometry was used to examine the intracellular calcium and neuronal apoptosis. Results: Plasma Wnt2b levels were lower in AD patients and positively correlated with cognitive performance. Similarly, Wnt2b was reduced in the hippocampus of AD mice and in vitro models. Next, Wnt2b overexpression and recombinant Wnt2b were used to endogenously and exogenously upregulate Wnt2b levels. Upregulation of Wnt2b could effectively prevent downregulation of canonical Wnt signaling, mitochondrial dysfunction in in vitro AD models. Subsequently, intracellular calcium overload and neuronal damage were ameliorated. Conclusions: Our study highlights that Wnt2b decline is associated with cognitive impairment in AD, and upregulation of Wnt2b can exert neuroprotective effects in AD, particularly in ameliorating mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is the most common form of neurodegenerative dementia among the elderly. Excitotoxicity has been implicated as playing a dominant role in AD, especially related to the hyperactivation of excitatory neurons. Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin-dependent kinase and involved in the pathogenesis of AD, but the roles and mechanisms of DAPK1 in excitotoxicity in AD are still uncertain. Objective: We mainly explored the underlying mechanisms of DAPK1 involved in the excitotoxicity of AD and its clinical relevance. Methods: Differentiated SH-SY5Y human neuroblastoma cells, PS1 V97 L transgenic mice, and human plasma samples were used. Protein expression was assayed by immunoblotting, and intracellular calcium and neuronal damage were analyzed by flow cytometry. Plasma DAPK1 was measured by ELISA. Results: We found that DAPK1 was activated after amyloid-β oligomers (AβOs) exposure in differentiated SH-SY5Y cells. Besides, we found the phosphorylation of GluN2B subunit at Ser1303 was increased, which contributing to excitotoxicity and Ca2+ overload in SH-SY5Y cells. Inhibiting DAPK1 activity, knockdown of DAPK1 expression, and antagonizing GluN2B subunits could effectively prevent AβOs-induced activation of GluN2B subunit, Ca2+ overload, and neuronal apoptosis. Additionally, we found that DAPK1 was elevated in the brain of AD transgenic mouse and in the plasma of AD patients. Conclusion: Our finding will help to understand the mechanism of DAPK1 in the excitotoxicity in AD and provide a reference for the diagnosis and therapy of AD. [ABSTRACT FROM AUTHOR]

The global spread of colistin or carbapenem-resistant Enterobacteriaceae (CRE) has been a pressing threat to public health. Members of Enterobacteriaceae, especially Proteus mirabilis and Escherichia coli, have been prevalent foodborne pathogens and such pathogens from fresh vegetables have triggered foodborne illness in China. However, reports about CRE, especially P. mirabilis from fresh vegetables, are still lacking. In this study, we identified five blaNDM-positive P. mirabilis and five blaNDM-positive generic E. coli concurrently from five fresh vegetables in two markets from China, and four of the five E. coli also carried mcr-1. The 10 isolates were characterized with methods including antimicrobial susceptibility testing, conjugation, whole-genome sequencing and phylogenetic analysis. All 10 isolates were multidrug-resistant (MDR). blaNDM-5 in five E. coli isolates and one P. mirabilis carrying blaNDM-5 was located on similarly transferable IncX3 plasmids, while transferably untypable plasmids were the carriers of blaNDM-1 in four P. mirabilis isolates from different types of vegetables/markets. mcr-1 in the four blaNDM-5-positive E. coli was located on similarly non-conjugative IncHI2 MDR plasmids lacking transfer region. Notably, ISCR1 complex class 1 integron capable of capturing blaNDM-1 was found on all untypable plasmids from P. mirabilis, and five copies of ISCR1 complex class 1 integron containing blaNDM-1 even occurred in one P. mirabilis, which showed high-level carbapenem resistance. Plasmid and phylogenetic analysis revealed that the blaNDM-positive P. mirabilis and E. coli from fresh vegetables might be derived from animals and transmitted to humans via the food chain. The concurrence of blaNDM-positive P. mirabilis and E. coli carrying both mcr-1 and blaNDM in different types of fresh vegetables eaten raw is alarming and threatens food safety. Sustained surveillance of these foodborne pathogens among fresh vegetables is urgent to ensure the health of food consumers. We report for the first time the concurrence of blaNDM-positive P. mirabilis and mcr-1-bearing E. coli carrying blaNDM from the same fresh vegetables. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is the most common form of neurodegenerative dementia among the elderly. Excitotoxicity has been implicated as playing a dominant role in AD, especially related to the hyperactivation of excitatory neurons. Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin-dependent kinase and involved in the pathogenesis of AD, but the roles and mechanisms of DAPK1 in excitotoxicity in AD are still uncertain. Objective: We mainly explored the underlying mechanisms of DAPK1 involved in the excitotoxicity of AD and its clinical relevance. Methods: Differentiated SH-SY5Y human neuroblastoma cells, PS1 V97 L transgenic mice, and human plasma samples were used. Protein expression was assayed by immunoblotting, and intracellular calcium and neuronal damage were analyzed by flow cytometry. Plasma DAPK1 was measured by ELISA. Results: We found that DAPK1 was activated after amyloid-β oligomers (AβOs) exposure in differentiated SH-SY5Y cells. Besides, we found the phosphorylation of GluN2B subunit at Ser1303 was increased, which contributing to excitotoxicity and Ca2+ overload in SH-SY5Y cells. Inhibiting DAPK1 activity, knockdown of DAPK1 expression, and antagonizing GluN2B subunits could effectively prevent AβOs-induced activation of GluN2B subunit, Ca2+ overload, and neuronal apoptosis. Additionally, we found that DAPK1 was elevated in the brain of AD transgenic mouse and in the plasma of AD patients. Conclusion: Our finding will help to understand the mechanism of DAPK1 in the excitotoxicity in AD and provide a reference for the diagnosis and therapy of AD. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common form of neurodegenerative disease and most anti-AD drugs have failed in clinical trials; hence, it is urgent to find potentially effective drugs against AD. DL-3-n-butylphthalide (NBP) is a compound extracted from celery seed and is a multiple-target drug. Several studies have demonstrated the neuroprotective effects of NBP on cognitive impairment, but the mechanisms of NBP remains relatively unexplored. In this study, we found that NBP could alleviated the increase of intracellular Ca2+ and reversed down-regulation of Ca2+/calmodulin-dependent protein kinase alpha (CaMKIIα) signaling and rescued neuronal apoptosis in SH-SY5Y cells treated by Aβ oligomers. However, these neuroprotective effects of NBP on neuronal damage and CaMKIIα signaling were abolished when CaMKIIα expression was knocked down or its activity was inhibited. Thus, our findings suggested that CaMKIIα signaling was required for the neuroprotective effects of NBP in AD and provided an improved basis for elucidating the mechanism and treatment of NBP in AD. [ABSTRACT FROM AUTHOR]

Background: Alterations in levels of peripheral insulin-like growth factor-1 (IGF-1) in Alzheimer's disease (AD) have been reported in several studies, and results are inconsistent.Objective: We conducted a meta-analysis to investigate the relationship between peripheral and cerebrospinal fluid IGF-1 levels and AD or mild cognitive impairment (MCI).Methods: A systematic search in PubMed, Medline, Web of Science, Embase, and Cochrane Library was conducted and 18 studies were included.Results: Results of random-effects meta-analysis showed that there was no significant difference between AD patients and healthy control (17 studies; standard mean difference [SMD], -0.01; 95%CI, -0.35 to 0.32) and between MCI patients and healthy control (6 studies; SMD, -0.20; 95%CI, -0.52 to 0.13) in peripheral IGF-1 levels. Meta-regression analyses identified age difference might explain the heterogeneity (p = 0.017). However, peripheral IGF-1 levels were significantly decreased in AD subjects (9 studies; SMD, -0.44; 95%CI, -0.81 to -0.07) and MCI subjects exhibited a decreasing trend (4 studies; SMD, -0.31; 95%CI, -0.72 to 0.11) in studies with sample size≥80. Cerebrospinal fluid IGF-1 levels also significantly decreased in AD subjects (3 studies; SMD, -2.40; 95%CI, -4.36 to -0.43).Conclusion: These findings suggest that decreased peripheral and cerebrospinal fluid IGF-1 levels might be a potential marker for the cognitive decline and progression of AD. [ABSTRACT FROM AUTHOR]

Saving energy is essential for mitigating environmental harm, and convincing consumers to purchase energy-efficient products repeatedly represents a challenge for sustainable development. On the basis of motivation theory, this study developed a theoretical model to explore how the needs-based motivations (i.e., the need to feel unique and the need for social approval) of existing consumers of energy-efficient products affect their attitudes and repurchase intention of such products. People who had purchased energy-efficient products were asked to participate in a survey, and data were collected from 400 consumers. Structural equation modeling was employed for analysis. The results indicated that existing consumers of energy-efficient products who exhibited a greater need for uniqueness and social approval had a more positive attitude toward energy-efficient products. Existing consumers with a greater need for social approval exhibited an increased willingness to repurchase energy-efficient products. In addition, the attitudes of these consumers toward energy-efficient products positively influenced their repurchase intention. The aforementioned findings suggest that green marketers can encourage existing consumers to continue buying energy-efficient products by enhancing the uniqueness and social value of these products. [ABSTRACT FROM AUTHOR]

Aluminium‐based metal–organic framework (MOF) coatings on polystyrene bead surfaces were easily synthesized by reacting an intermediate metal hydroxide coating with an organic linker. Several different sizes of polystyrene beads were coated with aluminium metal hydroxide to construct Al@PS core–shell bead materials. The activated Al@PS core–shell beads were involved to make a homogenous MOF‐based layer in the presence of the organic linker. By using different sizes of the PS support the size of MOFs on the PS composites could be fine‐tuned under specific reaction conditions. MOF‐coated core–shell bead materials (Al‐1,4‐NDC@PS and MIL‐53(Al)@PS) were characterized using various analytical techniques. Al‐1,4‐NDC@PS and MIL‐53(Al)@PS were evaluated for solid‐phase microextraction (SPME) of hydrophobic polycyclic aromatic hydrocarbons (PAHs) and hydrophilic non‐steroidal anti‐inflammatory drugs (NSAIDs), respectively. Al‐1,4‐NDC@PS‐1000 displayed high extraction recoveries ranging from 79.2 % to 99.8 % in the SPME of PAHs. Meanwhile, MIL‐53(Al)@PS‐1000 showed 85.9–99.0 % extraction recoveries in the SPME of NSAIDs. These results show that the proposed approach holds potential to extract organic analytes on an industrial scale. [ABSTRACT FROM AUTHOR]

Exact solutions of the Einstein-Maxwell equations for spherically symmetric charged perfect fluid have been broadly studied so far. However, the cases with a nonzero cosmological constant are seldom focused. In the present paper, the Tolman-Oppenheimer-Volkoff (TOV) equations have been generalized from the neutral case of hydrostatic equilibrium to the charged case of hydroelectrostatic equilibrium, and base on it, for the first time we find a series of new exact solutions of Einstein-Maxwell's equations with a nonzero cosmological constant for static charged perfect fluid spheres. Moreover, two special TOV equations and two classical constant density interior solutions are also given. [ABSTRACT FROM AUTHOR]

Gravitational waves (GWs) from extra dimensions, very early universe, and some high-energy astrophysical processes might have at most six polarization states: tensor- and nontensor-mode gravitons. The peak regions or partial peak regions (of the amplitudes or energy densities) of some of such GWs are just distributed in the GHz or higher frequency band, which would be an optimal frequency band for the electromagnetic (EM) response to such high-frequency GWs (HFGWs). In this paper we investigate the EM response to the HFGWs, and for the first time we obtain the concrete form of analytic solutions of the perturbative EM fields caused by all six possible polarizations of the HFGWs in the background stable EM fields and in the proposed three dimensional synchro-resonance system (3DSR system), respectively. It is found that all such six polarizations may in principle show separability and detectability. Moreover, the detection frequency band ( ∼ 10 8 to 10 12 Hz or higher) of the signal photon fluxes by the 3DSR system and the observation frequency range ( ∼ 7 × 10 7 to 3 × 10 9 Hz) of the signals by the FAST (Five-hundred-meter Aperture Spherical Telescope, China) have a certain overlapping property, and thus their coincidence experiments in the future for observations will have high complementarity. [ABSTRACT FROM AUTHOR]