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The growing number of industrial carbon emissions have resulted in a significant increase in the greenhouse gas carbon dioxide (CO2), which, in turn, will have a major impact on climate change. Therefore, the reduction, storage, and reuse of CO2 is an important concern in modern society. Calcium oxide (CaO) is known to be an excellent adsorbent of CO2 in a high-temperature environment. However, since deterioration of the adsorbent is likely to occur after repeated cycles of adsorption under high temperature conditions, it would be desirable to mitigate this phenomenon, in order to maintain the stability of CaO. In the present study, common eggshell waste was used as the starting material. The main component of eggshell waste is calcium carbonate (CaCO3), which was purified to produce CaO. Different surfactants and amino-containing polymers were added to synthesize CaO-based adsorbents with different configurations and pore sizes. The amount of CO2 adsorbed was determined using a thermogravimetric analyzer (TGA). The results showed that the CO2 adsorption capacity of the synthetic CaO recovered from purified eggshell waste could reach 0.6 g-CO2/g-sorbent, indicating a good adsorption capacity. CaO modified with a dopamine-containing polymer was shown to have an adsorption capacity of 0.62 g-CO2/g-sorbent. Moreover, it showed an excellent adsorption capacity of 0.40 g-CO2/g-sorbent, even after 10 cycles of CO2 adsorption. The present study suggests that using eggshell waste to synthesize CaO-based adsorbents for effective CO2 adsorption can not only reduce environmental waste, but also have the potential to capture greenhouse gas CO2 emissions, which conforms to the principles of green chemistry.
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Dióxido de Carbono , Gases de Efeito Estufa , Adsorção , Animais , Compostos de Cálcio , Casca de Ovo , ÓxidosRESUMO
Imbalanced splicing of premessenger RNA is typical of tumorous malignancies, and the regulatory mechanisms involved in several tumorigenesis-associated splicing events are identified. Elevated expression of serine-arginine protein kinase 1 (SRPK1) may participate in the pathway responsible for the dysregulation of splicing events in malignant tumor cells. In this study, we observed a correlation between the cytoplasmic accumulation of RNA-binding motif protein 4 (RBM4) and up-regulated SRPK1 in breast cancer cells. The production of the IR-B and MCL-1S transcripts was induced separately by the overexpression of RBM4 and SRPK1 gene silencing. Overexpressed RBM4 simultaneously bound to the CU-rich elements within the MCL-1 exon2 and the downstream intron, which subsequently facilitated the exclusion of the regulated exon. Breast cancer cells are deprived of apoptotic resistance through the RBM4-mediated up-regulation of the IR-B and MCL-1S transcripts. These findings suggest that the splicing events regulated by the SRPK1-RMB4 network may contribute to tumorigenesis through altered sensitivity to apoptotic signals in breast cancer cells.
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Apoptose , Neoplasias da Mama/genética , Neoplasias da Mama/patologia , Proteínas Serina-Treonina Quinases/metabolismo , Splicing de RNA/genética , RNA Mensageiro/genética , Proteínas de Ligação a RNA/metabolismo , Western Blotting , Mama/metabolismo , Neoplasias da Mama/metabolismo , Carcinoma Ductal de Mama/genética , Carcinoma Ductal de Mama/metabolismo , Carcinoma Ductal de Mama/patologia , Proliferação de Células , Células Cultivadas , Ensaio de Desvio de Mobilidade Eletroforética , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Técnicas Imunoenzimáticas , Proteína de Sequência 1 de Leucemia de Células Mieloides/genética , Gradação de Tumores , Invasividade Neoplásica , Estadiamento de Neoplasias , Fosforilação , Proteínas Serina-Treonina Quinases/genética , RNA Interferente Pequeno/genética , Proteínas de Ligação a RNA/genética , Ativação TranscricionalRESUMO
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.
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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 V97âL 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-ß oligomers (AßOs) 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 AßOs-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.
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Doença de Alzheimer , Neuroblastoma , Idoso , Animais , Humanos , Camundongos , Doença de Alzheimer/genética , Peptídeos beta-Amiloides/metabolismo , Cálcio/metabolismo , Proteínas Quinases Associadas com Morte Celular/genética , Camundongos Transgênicos , Receptores de N-Metil-D-Aspartato/metabolismoRESUMO
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.
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Lung cancer is the leading cause of cancer deaths worldwide, and squamous cell carcinoma (SQC) is Taiwan's second most common lung carcinoma histotype. This study aimed to investigate changes in the long-term trend of the SQC incidence rate in Taiwan. SQC cases between 1985 and 2019 were adopted from Taiwan's Cancer Registry System; the age-adjusted incidence rate was calculated using the World Standard Population in 2000. The long-term trends of the age, period, and birth cohort effect of SQC incidence rates were estimated using the SEER Age-Period-Cohort Web Tool. The results revealed that the incidence of lung carcinoma in Taiwan increased, while the incidence of SQC exhibited a slight decrease during this study period. The age rate ratio (ARR) of the incidence rate in men declined gradually, and the period effect changed more slowly for women than men. The cohort effect formed a bimodal curve. The annual percentage change results for women indicated that the ARR decreased from 1.652 (95% confidence interval (CI): 1.422, 1.9192) at 30 to 34 years to 0.559 (95% CI: 0.4988, 0.6265) at 75 to 79 years; the period effect decreased from 1.2204 (95% CI: 1.1148, 1.336) in 1995 to 1999 to 0.608 (95% CI: 0.5515, 0.6704) in 2015 to 2019, with a greater decline in the later period. The cohort effect was unimodal, with the SQC risk value peaking in the 1915 birth cohort and exhibiting a steady decline thereafter. The results of this study suggest that a decrease in the smoking rate may be the reason for the decline in the incidence of SQC, and we observed a similar trend between SQC and the smoking rate in men.
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Carcinoma Pulmonar de Células não Pequenas , Carcinoma de Células Escamosas , Neoplasias Pulmonares , Masculino , Humanos , Feminino , Incidência , Taiwan/epidemiologia , Carcinoma de Células Escamosas/epidemiologia , Carcinoma de Células Escamosas/patologia , Neoplasias Pulmonares/epidemiologia , Neoplasias Pulmonares/patologia , Pulmão/patologiaRESUMO
The widespread presence of carbapenem-resistant Enterobacteriaceae (CRE) and mcr-positive Escherichia coli (MCREC) poses a huge threat to both animal and human health. River water environments are vital reservoirs of antibiotic resistance genes, however, the prevalence and characteristics of CRE and MCREC from large-scale rivers in China have not been reported. In the current study, we sampled 86 rivers from four cities in Shandong Province, China in 2021 and analyzed the prevalence of CRE and MCREC. The blaNDM/blaKPC-2/mcr-positive isolates were characterized with methods including PCR, antimicrobial susceptibility testing, conjugation, replicon typing, whole-genome sequencing and phylogenetic analysis. We found that the prevalence of CRE and MCREC in 86 rivers was 16.3% (14/86) and 27.9% (24/86), respectively and eight rivers carried both mcr-1 and blaNDM/blaKPC-2. A total of 48 Enterobacteriaceae isolates (10 ST11 Klebsiella pneumoniae with blaKPC-2, 12 blaNDM-positive E. coli and 26 MCREC carrying only mcr-1) were obtained in this study and 47 displayed multidrug resistance (MDR). Notably, 10 of the 12 blaNDM-positive E. coli isolates also harbored the mcr-1 gene. The blaKPC-2 gene was located within mobile element ISKpn27-blaKPC-2-ISKpn6 on novel F33:A-:B- non-conjugative MDR plasmids in ST11 K. pneumoniae. The dissemination of blaNDM was mediated by transferable MDR IncB/O plasmids or IncX3 plasmids while mcr-1 was primarily disseminated by highly similar IncI2 plasmids. Notably, these waterborne IncB/O, IncX3 and IncI2 plasmids were all highly similar to previously identified plasmids from animal and human isolates. A phylogenomic analysis revealed that the CRE and MCREC isolates from water environments might be derived from animals and trigger infections in humans. The high prevalence of CRE and MCREC in large-scale environmental rivers is alarming and needs sustained surveillance due to the potential risk for transmission to humans via the food chain (irrigation) or direct contact.
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Enterobacteriáceas Resistentes a Carbapenêmicos , Enterobacteriaceae , Animais , Humanos , Enterobacteriaceae/genética , Colistina/farmacologia , Enterobacteriáceas Resistentes a Carbapenêmicos/genética , Escherichia coli/genética , Rios , Prevalência , Filogenia , beta-Lactamases/genética , Testes de Sensibilidade Microbiana , Antibacterianos/farmacologia , Plasmídeos , Klebsiella pneumoniae/genética , Genômica , Água , China/epidemiologiaRESUMO
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.
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Doença de Alzheimer , Mitocôndrias , Fármacos Neuroprotetores , Animais , Camundongos , Peptídeos beta-Amiloides/metabolismo , Cálcio , Modelos Animais de Doenças , Camundongos Transgênicos , Mitocôndrias/metabolismo , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Regulação para Cima , HumanosRESUMO
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 Aß 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.
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Doença de Alzheimer , Benzofuranos , Doenças Neurodegenerativas , Fármacos Neuroprotetores , Doença de Alzheimer/metabolismo , Benzofuranos/farmacologia , Benzofuranos/uso terapêutico , Humanos , Doenças Neurodegenerativas/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêuticoRESUMO
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 (pâ=â0.017). 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.
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Doença de Alzheimer/líquido cefalorraquidiano , Doença de Alzheimer/diagnóstico , Fator de Crescimento Insulin-Like I/líquido cefalorraquidiano , Doença de Alzheimer/epidemiologia , Biomarcadores/líquido cefalorraquidiano , HumanosRESUMO
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.
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BACKGROUND: Late-onset poststroke seizure is highly associated with epilepsy but the incidence of it is variable due to different definition and follow-up time. We conducted a meta-analysis to determine the incidence of poststroke seizure and analyze the discrepancies among published studies. METHODS: We searched the literature for relevant articles published in English between January 1, 1990, and December 31, 2014, by using the following search terms: "seizures after stroke," "poststroke seizures," "epilepsy after stroke," "poststroke epilepsy," "incidence," and "follow-up." Reference lists of the relevant articles were reviewed to identify eligible studies not captured by these terms. RESULTS: Seven relevant cohort studies were identified and analyzed. Incidence density was defined as the number of episodes per 100 person-years. Using the definition of late-onset poststroke seizure as seizure occurring 14â¯days after a stroke, the incidence density was 1.12 (0.95-1.32) per 100 person-years. For poststroke seizures occurring 7â¯days after the stroke, the incidence density increased to 3.22 (2.94-3.52) per 100 person-years. CONCLUSION: Our results are relevant to the epidemiology of late-onset poststroke seizure, with 14â¯days being the ideal cutoff time point. The pooled incidence density of late-onset poststroke seizure was 1.12 per 100 person-years in 4 cohort studies.