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BACKGROUND: Insulin resistance (IR) can increase atherosclerotic and cardiovascular risk by inducing endothelial dysfunction, decreasing nitric oxide (NO) production, and accelerating arterial inflammation. The aim is to determine the mechanism by which insulin action and NO production in endothelial cells can improve systemic bioenergetics and decrease atherosclerosis via differentiation of perivascular progenitor cells (PPCs) into brown adipocytes (BAT). METHODS: Studies used various endothelial transgenic and deletion mutant ApoE-/- mice of insulin receptors, eNOS (endothelial NO synthase) and ETBR (endothelin receptor type B) receptors for assessments of atherosclerosis. Cells were isolated from perivascular fat and micro-vessels for studies on differentiation and signaling mechanisms in responses to NO, insulin, and lipokines from BAT. RESULTS: Enhancing insulin's actions on endothelial cells and NO production in ECIRS1 transgenic mice reduced body weight and increased systemic energy expenditure and BAT mass and activity by inducing differentiation of PPCs into beige/BAT even with high-fat diet. However, positive changes in bioenergetics, BAT differentiation from PPCs and weight loss were inhibited by N(gamma)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of eNOS, in ECIRS1 mice and eNOSKO mice. The mechanism mediating NO's action on PPC differentiation into BAT was identified as the activation of solubilized guanylate cyclase/PKGIα (cGMP protein-dependent kinase Iα)/GSK3ß (glycogen synthase kinase 3ß) pathways. Plasma lipidomics from ECIRS1 mice with NO-induced increased BAT mass revealed elevated 12,13-diHOME production. Infusion of 12,13-diHOME improved endothelial dysfunction and decreased atherosclerosis, whereas its reduction had opposite effects in ApoE-/-mice. CONCLUSIONS: Activation of eNOS and endothelial cells by insulin enhanced the differentiation of PPC to BAT and its lipokines and improved systemic bioenergetics and atherosclerosis, suggesting that endothelial dysfunction is a major contributor of energy disequilibrium in obesity.
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Tecido Adiposo Marrom , Aterosclerose , Tecido Adiposo Marrom/metabolismo , Animais , Apolipoproteínas E/metabolismo , Aterosclerose/genética , Aterosclerose/metabolismo , Aterosclerose/prevenção & controle , Células Endoteliais/metabolismo , Insulina/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Óxido Nítrico/metabolismoRESUMO
Subcellular compartmentalization ensures orderly and efficient intracellular metabolic activities in eukaryotic life. Investigation of the subcellular metabolome could provide in-depth insight into cellular biological activities. However, the sensitive measurement of multi-subcellular metabolic profiles is still a significant challenge. Herein, we present a comprehensive subcellular fractionation, characterization, and metabolome analysis strategy. First, six subcellular fractions including nuclei, mitochondria, lysosomes, peroxisomes, microsomes, and cytoplasm were generated from a single aliquot of liver homogenate. Then, a dansyl-labeling-assisted liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for measuring 151 amino/phenol- or carboxyl-containing metabolites in the subcellular fractions was established and validated. Last, the strategy was applied to a rat model of carbon tetrachloride (CCl4)-induced acute liver injury (ALI). The metabolic profile of individual organelles was compared with that of the liver. Interestingly, many unique changes were observed specifically in organelles, while the liver failed to capture these changes. This result indicates that metabolic investigation at the tissue level might lead to erroneous results due to the leveling effect. Our study demonstrates a feasible approach for the broad-spectrum-targeted metabolic profiling of multi-subcellular fractions, which can be of great use in driving our further understanding of intracellular metabolic activities in various physical and pathological conditions.
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Metaboloma , Espectrometria de Massas em Tandem , Animais , Ratos , Cromatografia Líquida/métodos , Espectrometria de Massas em Tandem/métodos , Metabolômica/métodos , Núcleo Celular , Marcação por IsótopoRESUMO
Rumination is closely linked to the onset and maintenance of major depressive disorder (MDD). Prior neuroimaging studies have identified the association between self-reported rumination trait and the functional coupling among a network of brain regions using resting-state functional magnetic resonance imaging (MRI). However, little is known about the underlying neural circuitry mechanism during active rumination in MDD. Degree centrality (DC) is a simple metric to denote network integration, which is critical for higher-order psychological processes such as rumination. During an MRI scan, individuals with MDD (N = 45) and healthy controls (HC, N = 46) completed a rumination state task. We examined the interaction effect between the group (MDD vs. HC) and condition (rumination vs. distraction) on vertex-wise DC. We further characterized the identified brain region's functional involvement with Neurosynth and BrainMap. Network-wise seed-based functional connectivity (FC) analysis was also conducted for the identified region of interest. Finally, exploratory correlation analysis was conducted between the identified region of interest's network FCs and self-reported in-scanner affect levels. We found that a left superior frontal gyrus (SFG) region, generally overlapped with the frontal eye field, showed a significant interaction effect. Further analysis revealed its involvement with executive functions. FCs between this region, the frontoparietal, and the dorsal attention network (DAN) also showed significant interaction effects. Furthermore, its FC to DAN during distraction showed a marginally significant negative association with in-scanner affect level at the baseline. Our results implicated an essential role of the left SFG in the rumination's underlying neural circuitry mechanism in MDD and provided novel evidence for the conceptualization of rumination in terms of impaired executive control.
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Transtorno Depressivo Maior , Humanos , Encéfalo/diagnóstico por imagem , Córtex Pré-Frontal , Função Executiva , Lobo Frontal , Imageamento por Ressonância Magnética , Mapeamento EncefálicoRESUMO
Metallic elements play a pivotal role in maternal and fetal health. Metals can cross the placental barrier and be absorbed by fetuses, where they may affect closure of the neural tube during embryonic development. Neural tube defects (NTDs), which result from aberrant closure of the neural tube three to four weeks post-conception, have a multifactorial and complex etiology that combines genetic variants and environmental exposure. Recent advances in population-level association studies have investigated the link between maternal environmental exposure and NTDs, particularly the influence of metals on the incidence of NTDs. Herein, we present a broad and qualitative review of current literature on the association between maternal and prenatal metal exposure via the maternal peripheral blood, amniotic fluid, placenta, umbilical cord, and maternal hair, and the risk of developing NTDs. Specifically, we identify the various aggravating or attenuating effects of metallic exposure on the risk of NTD formation. This review provides novel insights into the association between environmental metals and NTDs and has important applications for NTD prevention and mitigating environmental exposure to metals.
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Defeitos do Tubo Neural , Efeitos Tardios da Exposição Pré-Natal , Humanos , Feminino , Gravidez , Placenta , Defeitos do Tubo Neural/induzido quimicamente , Defeitos do Tubo Neural/epidemiologia , Defeitos do Tubo Neural/genética , Tubo Neural , FetoRESUMO
BACKGROUND: Extensive research into psychoneuroimmunology has led to substantial advances in our understanding of the reciprocal interactions between the central nervous system and the immune system in neuropsychiatric disorders. To date, inflammation has been implicated in the pathogenesis of depression and anxiety. The immunomodulating effects of antidepressants on depression have been reported, however, there is no evidence of the similar effects of antidepressants on anxiety. The aim of the study was to investigate the effects of selective serotonin reuptake inhibitors (SSRIs) on peripheral inflammatory cytokines in patients with first episode generalized anxiety disorder (GAD). METHODS: A prospective cohort design was employed: 42 patients with first episode GAD were treated with either escitalopram or sertraline for 12â¯weeks. Anxiety was measured by the Generalized Anxiety Disorder Scale and the State Trait Anxiety Inventory, serum pro-inflammatory cytokine levels were measured by the enzyme-linked immunosorbent assay (ELISA), and CRP determined by an immunoturbidimetric method before and after SSRIs treatment RESULTS: Baseline levels of anxiety and pro-inflammatory cytokines including IL-1α, IL-6, IL-8, IL-12, IFN-γ, and CRP were significantly reduced after treatment of SSRIs (pâ¯<â¯0.05 in all cases). In addition, the change of anxiety measures co-vary with the change of peripheral cytokine levels (pâ¯<â¯0.05 in all cases). The regression model revealed that log transformed baseline levels of CRP and IL-6 predicted treatment response (pâ¯<â¯0.05 in both cases). CONCLUSIONS: This study is the first to investigate the effects of SSRIs on pro-inflammatory cytokines in patients with first episode GAD. The findings indicate moderate acute anti-inflammatory effects of SSRIs in GAD, and suggest that these anti-inflammatory effects may underlie anxiolytic effects of SSRIs. The study also indicates that serum levels of CRP and IL-6 may predict treatment response. However, data from randomized controlled trials is warranted to confirm these findings.
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Transtornos de Ansiedade/tratamento farmacológico , Transtornos de Ansiedade/imunologia , Inibidores Seletivos de Recaptação de Serotonina/uso terapêutico , Adulto , Idoso , Ansiolíticos , Antidepressivos/uso terapêutico , Ansiedade/sangue , Ansiedade/tratamento farmacológico , Transtornos de Ansiedade/sangue , Proteína C-Reativa/análise , Citalopram/uso terapêutico , Estudos de Coortes , Citocinas/efeitos dos fármacos , Depressão/tratamento farmacológico , Transtorno Depressivo/tratamento farmacológico , Feminino , Humanos , Interleucina-12/análise , Interleucina-12/sangue , Interleucina-6/análise , Interleucina-6/sangue , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Sertralina/uso terapêuticoRESUMO
RATIONALE: Activation of monocytes/macrophages by hyperlipidemia associated with diabetes mellitus and obesity contributes to the development of atherosclerosis. PKCδ (protein kinase C δ) expression and activity in monocytes were increased by hyperlipidemia and diabetes mellitus with unknown consequences to atherosclerosis. OBJECTIVE: To investigate the effect of PKCδ activation in macrophages on the severity of atherosclerosis. METHODS AND RESULTS: PKCδ expression and activity were increased in Zucker diabetic rats. Mice with selective deletion of PKCδ in macrophages were generated by breeding PKCδ flox/flox mice with LyzM-Cre and ApoE-/- mice (MPKCδKO/ApoE-/- mice) and studied in atherogenic (AD) and high-fat diet (HFD). Mice fed AD and HFD exhibited hyperlipidemia, but only HFD-fed mice had insulin resistance and mild diabetes mellitus. Surprisingly, MPKCδKO/ApoE-/- mice exhibited accelerated aortic atherosclerotic lesions by 2-fold versus ApoE-/- mice on AD or HFD. Splenomegaly was observed in MPKCδKO/ApoE-/- mice on AD and HFD but not on regular chow. Both the AD or HFD increased macrophage number in aortic plaques and spleen by 1.7- and 2-fold, respectively, in MPKCδKO/ApoE-/- versus ApoE-/- mice because of decreased apoptosis (62%) and increased proliferation (1.9-fold), and not because of uptake, with parallel increased expressions of inflammatory cytokines. Mechanisms for the increased macrophages in MPKCδKO/ApoE-/- were associated with elevated phosphorylation levels of prosurvival cell-signaling proteins, Akt and FoxO3a, with reduction of proapoptotic protein Bim associated with PKCδ induced inhibition of P85/PI3K. CONCLUSIONS: Accelerated development of atherosclerosis induced by insulin resistance and hyperlipidemia may be partially limited by PKCδ isoform activation in the monocytes, which decreased its number and inflammatory responses in the arterial wall.
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Apoptose/fisiologia , Aterosclerose/metabolismo , Dieta Hiperlipídica/efeitos adversos , Hiperlipidemias/metabolismo , Macrófagos/metabolismo , Proteína Quinase C-delta/metabolismo , Animais , Aterosclerose/etiologia , Aterosclerose/patologia , Ativação Enzimática/fisiologia , Hiperlipidemias/etiologia , Hiperlipidemias/patologia , Resistência à Insulina/fisiologia , Isoenzimas/metabolismo , Macrófagos/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Ratos , Ratos ZuckerRESUMO
OBJECTIVE: The objective of this study is to evaluate whether exogenously induced hyperinsulinemia may increase the development of atherosclerosis. APPROACH AND RESULTS: Hyperinsulinemia, induced by exogenous insulin implantation in high-fat fed (60% fat HFD) apolipoprotein E-deficient mice (ApoE-/-) mice, exhibited insulin resistance, hyperglycemia, and hyperinsulinemia. Atherosclerosis was measured by the accumulation of fat, macrophage, and extracellular matrix in the aorta. After 8 weeks on HFD, ApoE-/- mice were subcutaneously implanted with control (sham) or insulin pellet, and phlorizin, a sodium glucose cotransporters inhibitor (1/2)inhibitor, for additional 8 weeks. Intraperitoneal glucose tolerance test showed that plasma glucose levels were lower and insulin and IGF-1 (insulin-like growth factor-1) levels were 5.3- and 3.3-fold higher, respectively, in insulin-implanted compared with sham-treated ApoE-/- mice. Plasma triglyceride, cholesterol, and lipoprotein levels were decreased in mice with insulin implant, in parallel with increased lipoprotein lipase activities. Atherosclerotic plaque by en face and complexity staining showed significant reductions of fat deposits and expressions of vascular adhesion molecule-1, tumor necrosis factor-α, interleukin 6, and macrophages in arterial wall while exhibiting increased activation of pAKT and endothelial nitric oxide synthase (P<0.05) comparing insulin-implanted versus sham HFD ApoE-/- mice. No differences were observed in atherosclerotic plaques between phlorizin-treated and sham HFD ApoE-/- mice, except phlorizin significantly lowered plasma glucose and glycated hemoglobin levels while increased glucosuria. Endothelial function was improved only by insulin treatment through endothelial nitric oxide synthase/nitric oxide activations and reduced proinflammatory (M1) and increased anti-inflammatory (M2) macrophages, which were inhibited by endothelial nitric oxide synthase inhibitor. CONCLUSIONS: Exogenous insulin decreased atherosclerosis by lowering inflammatory cytokines, macrophages, and plasma lipids in HFD-induced hyperlipidemia, insulin resistant and mildly diabetic ApoE-/- mice.
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Aterosclerose/prevenção & controle , Citocinas/sangue , Diabetes Mellitus/tratamento farmacológico , Endotélio Vascular/efeitos dos fármacos , Hipoglicemiantes/administração & dosagem , Mediadores da Inflamação/sangue , Inflamação/prevenção & controle , Insulina/administração & dosagem , Lipídeos/sangue , Animais , Anti-Inflamatórios/administração & dosagem , Aterosclerose/sangue , Aterosclerose/patologia , Aterosclerose/fisiopatologia , Biomarcadores/sangue , Glicemia/efeitos dos fármacos , Glicemia/metabolismo , Diabetes Mellitus/sangue , Diabetes Mellitus/patologia , Diabetes Mellitus/fisiopatologia , Dieta Hiperlipídica , Modelos Animais de Doenças , Implantes de Medicamento , Endotélio Vascular/metabolismo , Endotélio Vascular/patologia , Endotélio Vascular/fisiopatologia , Hipoglicemiantes/efeitos adversos , Inflamação/sangue , Inflamação/patologia , Inflamação/fisiopatologia , Resistência à Insulina , Macrófagos/efeitos dos fármacos , Macrófagos/metabolismo , Camundongos Knockout para ApoE , Florizina/farmacologia , Placa AteroscleróticaRESUMO
The biodegradable, nontoxic, and renewable carboxymethyl cellulose (CMC) hydrogel has been developed into a green adsorbent. However, the weak chemical interaction limits its adsorption capability and reusability. This work incorporated lignin with complex structure and ZnO nanoparticles with photocatalytic properties into CMC hydrogel beads to improve the removal of methylene blue (MB) through chemical interaction. Scanning electron microscopic images and Fourier-transform infrared spectra confirmed the compatibility between lignin and ZnO nanoparticles as well as the increment of active sites for dye removal. The MB adsorption on CMC hydrogel beads was more significantly affected by the temperate and initial concentration compared to contact time, pH, and adsorbent dosage. The MB adsorption capacity of CMC hydrogel was improved to 276.79 mg/g after incorporating lignin and ZnO nanoparticles. The adsorption followed the pseudo-second-order kinetic model and Langmuir isotherm model, indicating chemical adsorption. After 6 cycles, the adsorption capacity was reduced by about 15 %. The UV irradiation could recover and improve MB adsorption capacity of CMC hydrogel beads containing ZnO nanoparticles due to the introduction of reactive oxygen species.
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Carboximetilcelulose Sódica , Hidrogéis , Lignina , Azul de Metileno , Óxido de Zinco , Azul de Metileno/química , Óxido de Zinco/química , Carboximetilcelulose Sódica/química , Adsorção , Lignina/química , Catálise , Hidrogéis/química , Cinética , Concentração de Íons de Hidrogênio , Poluentes Químicos da Água/química , Purificação da Água/métodos , Processos FotoquímicosRESUMO
Chronic complications of diabetes are due to myriad disorders of numerous metabolic pathways that are responsible for most of the morbidity and mortality associated with the disease. Traditionally, diabetes complications are divided into those of microvascular and macrovascular origin. We suggest revising this antiquated classification into diabetes complications of vascular, parenchymal, and hybrid (both vascular and parenchymal) tissue origin, since the profile of diabetes complications ranges from those involving only vascular tissues to those involving mostly parenchymal organs. A major paradigm shift has occurred in recent years regarding the pathogenesis of diabetes complications, in which the focus has shifted from studies on risks to those on the interplay between risk and protective factors. While risk factors are clearly important for the development of chronic complications in diabetes, recent studies have established that protective factors are equally significant in modulating the development and severity of diabetes complications. These protective responses may help explain the differential severity of complications, and even the lack of pathologies, in some tissues. Nevertheless, despite the growing number of studies on this field, comprehensive reviews on protective factors and their mechanisms of action are not available. This review thus focused on the clinical, biochemical, and molecular mechanisms that support the idea of endogenous protective factors, and their roles in the initiation and progression of chronic complications in diabetes. In addition, this review also aimed to identify the main needs of this field for future studies.
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Diabetes Mellitus Tipo 2 , Diabetes Mellitus , Angiopatias Diabéticas , Humanos , Fatores de Proteção , Angiopatias Diabéticas/complicações , Diabetes Mellitus/etiologia , Fatores de Risco , Diabetes Mellitus Tipo 2/complicaçõesRESUMO
AIMS: Increased prevalence of acute myocardial infarction related to diabetes and insulin resistance is associated with elevated risk for unstable atherosclerotic plaques, which are characterized by reduced vascular smooth muscle cells (VSMC) and extracellular matrix (ECM) and increased inflammation. Thus, insulin resistance may reduce plaque stability as deleting insulin receptors (IR) in VSMC decreased their proliferation and enhanced apoptosis. METHODS AND RESULTS: Direct effects of insulin on VSMC to alter plaque composition were studied using mice with double knockout of ApoE and IR genes in VSMC with SMIRKO/ApoE-/- and Myh11-CreERT2EYFP+/ApoE-/- and Myh11-CreERT2EYFP+IRKO/ApoE-/- mice, which were also used for lineage tracing studies. Compared to ApoE-/- mice, SMIRKO/ApoE-/-- mice exhibited more atherosclerotic plaques, which contained less VSMC and collagen, but increased levels of VSMC apoptosis and necrotic areas. Lineage tracing studies showed that Icam1+ Vcam1+ VSMC was inflammatory VSMC, which increased in aortas of Myh11-CreERT2EYFP+IRKO/ApoE-/- mice compared to control mice. Isolated VSMC lacking IR expressed higher inflammatory cytokines than cells with IR. Cell based studies indicated that insulin's anti-apoptotic and pro-proliferative effects in VSMC were mediated via activation of IR/Akt pathway, which were decreased in VSMC from SMIRKO or high fat diet (HFD) mice. Analysis of IR targets that regulated inflammatory cytokines in VSMC showed that thrombospondin 1 (Thbs1) and Mmp2 were consistently increased with loss of IR. Insulin inhibited Thbs1 expression, but not Mmp2, by p-Akt/p-FoxO1 pathways in VSMC from ApoE-/- mice, which was impaired in cells from SMIRKO/ApoE-/-- mice. Thbs1 further induced Icam1 and Mmp2 expressions in VSMC. CONCLUSIONS: Insulin via IR has significant actions in VSMC to decrease inflammation, apoptosis and ECM turnover via the activation of Akt and FoxO1 pathways. Inhibition of insulin actions and related pathways related to insulin resistance and diabetes may contribute to the formation of unstable atherosclerotic plaques.
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Instant dark tea (IDT), prepared by liquid-state fermentation using Aspergillus niger, is known for its high theabrownins content and lipid-lowering effect. To explore the impact of fungal fermentation on IDT compositions and its pancreatic lipase inhibitory ability (PLIA), untargeted and targeted metabolomic analysis were applied to track the changes of metabolites over a 9-day fermentation period, and correlation analysis was then conducted between metabolites and PLIA of IDT. There were 54 differential metabolites exhibited significant changes from day 3 to day 5 of fermentation. The concentrations of theabrownins and caffeine increased during fermentation, while phenols and free amino acids decreased. The PLIA of IDT samples significantly increased from day 5 to day 9 of fermentation. Theabrownins not only positively correlated with the PLIA but also exhibited a high inhibition rate. These findings provide a theoretical basis to optimize the production of IDT as functional food ingredient.
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BACKGROUND: Accumulating evidence suggests that the inflammatory cytokine interleukin-6 (IL-6) contributes to the pathophysiology of psychiatric disorders. However, there was no study concerning the relationship between IL-6 concentrations and clinical features in the chronic phase of early-onset schizophrenia (EOS). AIM: To investigate the relationship between serum IL-6 concentration and the clinical features of EOS. METHODS: We measured serum IL-6 Levels from 74 patients with chronic schizophrenia, including 33 with age at onset < 21 years (EOS group) and 41 with onset ≥ 21 years in [adult-onset schizophrenia (AOS) group], and from 41 healthy controls. Symptom severities were evaluated using the Positive and Negative Syndrome Scale (PANSS). RESULTS: Serum IL-6 concentrations were higher in both EOS and AOS groups than healthy controls (F = 22.32, P < 0.01), but did not differ significantly between EOS and AOS groups (P > 0.05) after controlling for age, body mass index, and other covariates. Negative symptom scores were higher in the EOS group than the AOS group (F = 6.199, P = 0.015). Serum IL-6 concentrations in the EOS group were negatively correlated with both total PANSS-negative symptom score (r = -0.389, P = 0.032) and avolition/asociality subscore (r = -0.387, P = 0.026). CONCLUSION: Patients with EOS may have more severe negative symptoms than those with adult-onset schizophrenia during the chronic phase of the illness. IL-6 signaling may regulate negative symptoms and its avolition/asociality subsymptoms among the early-onset chronic schizophrenic patients.
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Purpose: The purpose of this study is to examine how risks and benefits affect users' privacy-related decision-making processes. Design/methods/approach: This study collected and analyzed the neural activity processes of users' privacy-related decisions when faced with personalized services with different risks and benefits through an ERP experiment that included 40 participants. Findings/results: The findings show that users subconsciously categorize personalized services based on benefit; Privacy calculus affects privacy decision by influencing the allocation of cognitive resources for personalized service, and the scarcity of cognitive resources increases the degree of privacy disclosure; Emotional change in privacy decision is the result of many factors, not the result of privacy risk alone. Originality/Discussion: This study provides a new perspective to explain the process of privacy decision-making, and a new approach to investigate the privacy paradox.
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Although anionic polyelectrolyte hydrogel beads offer attractive adsorption of cationic dyes, phosphate adsorption is limited by electrostatic interactions. In this work, carboxymethyl cellulose (CMC)/sodium alginate (SA) hydrogel beads were modified with calcium carbonate (CaCO3) and/or bentonite (Be). The compatibility between CaCO3 and Be was proven by the homogeneous surface, as shown in the scanning electron microscopic images. Fourier-transform infrared and X-ray diffraction spectra further confirmed the existence of inorganic filler in the hydrogel beads. Although CMC/SA/Be/CaCO3 hydrogel beads attained the highest methylene blue and phosphate adsorption capacities (142.15 MB mg/g, 90.31 P mg/g), phosphate adsorption was significantly improved once CaCO3 nanoparticles were incorporated into CMC/SA/CaCO3 hydrogel beads. The kinetics of MB adsorption by CMC/SA hydrogel beads with or without inorganic fillers could be described by the pseudo-second-order model under chemical interactions. The phosphate adsorption by CMC/SA/Be/CaCO3 hydrogel beads could be explained by the Elovich model due to heterogeneous properties. The incorporation of Be and CaCO3 also improved the phosphate adsorption through chemical interaction since Langmuir isotherm fitted the phosphate adsorption by CMC/SA/Be/CaCO3 hydrogel beads. Unlike MB adsorption, the reusability of these hydrogel beads in phosphate adsorption reduced slightly after 5 cycles.
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Fosfatos , Poluentes Químicos da Água , Carboximetilcelulose Sódica/química , Bentonita/química , Alginatos/química , Poluentes Químicos da Água/química , Hidrogéis/química , Adsorção , Cinética , Concentração de Íons de HidrogênioRESUMO
This study aimed to evaluate the associations of baseline high-sensitivity C-reactive protein (Hs-CRP) and its change with subsequent cognitive decline and cognitive impairment. Data for this study were obtained from the China Health and Retirement Longitudinal Study, a national community-based prospective cohort study. Hs-CRP level and cognitive function were measured repeatedly over a 7-year follow-up. Linear mixed models and cox proportional hazard models were used to evaluate the associations. The study comprised 7385 participants (50.67% women, mean age 59.08 ± 8.86 years) with baseline Hs-CRP ranging from 0.03 to 178.10 mg/L (median: 1.01 mg/L, IQR: 0.55-2.11 mg/L). During a median of 5.79 years follow-up, the highest quartile of the Hs-CRP group showed a faster rate of cognitive decline (-0.0053 SD/year, p = 0.006) and a higher risk of cognitive impairment (HR 1.0814, p = 0.044) than those in the lowest quartile. Individuals in the elevated group of Hs-CRP change had a significantly faster cognitive decline (-0.0070 SD/year, p = 0.016) compared with those in the stable group. In this study, significant longitudinal associations between baseline Hs-CRP, elevated Hs-CRP, and long-term cognitive deterioration were observed. Hs-CRP level could perhaps serve as a predictor for cognitive deterioration in middle-aged and older adults.
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Fermented tea (FT) using a single Eurotium cristatum strain can produce a pleasant fungal-flowery aroma, which is similar to the composite aroma characteristic of minty, flowery, and woody aromas, but its molecular basis is not yet clear. In this study, solvent-assisted flavor evaporation and gas chromatography-mass spectrometry/olfactometry were applied to isolate and identify volatiles from the FT by E. cristatum. The application of an aroma extract dilution analysis screened out 43 aroma-active compounds. Quantification revealed that there were 11 odorants with high odor threshold concentrations. Recombination and omission tests revealed that nonanal, methyl salicylate, decanoic acid, 4-methoxybenzaldehyde, α-terpineol, phenylacetaldehyde, and coumarin were the major odorants in the FT. Addition tests further verified that methyl salicylate, 4-methoxybenzaldehyde, and coumarin were the key odorants for fungal-flowery aroma, each corresponding to minty, woody, and flowery aromas, respectively. 4-Methoxybenzaldehyde and coumarin were newly found odorants for fungal-flowery aroma in FT, and 4-methoxybenzaldehyde had not been reported as a tea volatile compound before. This finding may guide future industrial production optimization of FT with improved flavor.
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Odorantes , Compostos Orgânicos Voláteis , Odorantes/análise , Olfato , Aromatizantes/análise , Compostos Orgânicos Voláteis/análise , Olfatometria , Cumarínicos/análise , CháRESUMO
Insulin resistance and hyperglycemia are risk factors for periodontitis and poor wound healing in diabetes, which have been associated with selective loss of insulin activation of the PI3K/Akt pathway in the gingiva. This study showed that insulin resistance in the mouse gingiva due to selective deletion of smooth muscle and fibroblast insulin receptor (SMIRKO mice) or systemic metabolic changes induced by a high-fat diet (HFD) in HFD-fed mice exacerbated periodontitis-induced alveolar bone loss, preceded by delayed neutrophil and monocyte recruitment and impaired bacterial clearance compared with their respective controls. The immunocytokines, CXCL1, CXCL2, MCP-1, TNFα, IL-1ß, and IL-17A, exhibited delayed maximal expression in the gingiva of male SMIRKO and HFD-fed mice compared with controls. Targeted overexpression of CXCL1 in the gingiva by adenovirus normalized neutrophil and monocyte recruitment and prevented bone loss in both mouse models of insulin resistance. Mechanistically, insulin enhanced bacterial lipopolysaccharide-induced CXCL1 production in mouse and human gingival fibroblasts (GFs), via Akt pathway and NF-κB activation, which were reduced in GFs from SMIRKO and HFD-fed mice. These results provided the first report that insulin signaling can enhance endotoxin-induced CXCL1 expression to modulate neutrophil recruitment, suggesting CXCL1 as a new therapeutic direction for periodontitis or wound healing in diabetes. ARTICLE HIGHLIGHTS: The mechanism for the increased risks for periodontitis in the gingival tissues due to insulin resistance and diabetes is unclear. We investigated how insulin action in gingival fibroblasts modulates the progression of periodontitis in resistance and diabetes. Insulin upregulated the lipopolysaccharide-induced neutrophil chemoattractant, CXCL1, production in gingival fibroblasts via insulin receptors and Akt activation. Enhancing CXCL1 expression in the gingiva normalized diabetes and insulin resistance-induced delays in neutrophils recruitment and periodontitis. Targeting dysregulation of CXCL1 in fibroblasts is potentially therapeutic for periodontitis and may also improve wound healing in insulin resistance and diabetes.
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Diabetes Mellitus , Resistência à Insulina , Insulinas , Periodontite , Animais , Humanos , Masculino , Camundongos , Quimiocina CXCL1 , Resistência à Insulina/genética , Insulinas/uso terapêutico , Lipopolissacarídeos , Infiltração de Neutrófilos , Periodontite/tratamento farmacológico , Periodontite/metabolismo , Fosfatidilinositol 3-Quinases , Proteínas Proto-Oncogênicas c-aktRESUMO
Nutritional deficiency is prevalent among the elderly, and it is associated with many adverse health consequences. China is rapidly moving toward an aging society with a large population; however, evidence on the epidemiological trends in nutritional deficiency among the Chinese elderly is limited. Data on the incidence of nutritional deficiency among Chinese adults aged 65 years or above from 1990 to 2019 were extracted from the Global Burden of Disease 2019 database. We used the joinpoint regression method to estimate the average annual percentage change (AAPC) and to describe trend patterns. Age, period, and cohort effects were determined using age-period-cohort models. From 1990 to 2019, the incidence of vitamin A deficiency and iodine deficiency among Chinese older adults decreased from 1784.12 and 8.20 to 304.27 and 7.26 per 100,000, with AAPCs of -0.41 (-0.44, -0.38)% and -5.86 (-6.29, -5.43)%, respectively. A continually increasing trend was seen for incidence rates of protein-energy malnutrition, from 1342.02 to 2275.87 per 100,000 person-years, with an AAPC of 1.70 (1.40, 2.01)%. These trends were more pronounced among men than women. A strong age effect and birth cohort effect were present. Specifically, the population that was older or born later had a lower incidence of deficiencies in vitamin A and iodine but a higher incidence of protein-energy malnutrition. The results show a substantial reduction in vitamin A and iodine deficiencies among the Chinese elderly, and health policies and public awareness are needed to address the burden of protein-energy malnutrition in this population.
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Iodo , Desnutrição , Desnutrição Proteico-Calórica , Idoso , Masculino , Humanos , Feminino , Vitamina A , Carga Global da Doença , China/epidemiologia , Incidência , Desnutrição/epidemiologiaRESUMO
Leaders are critical to a team or organization, their behavior affects employees' psychology and their work effort, and then affects the efficiency and innovation of the team or organization. Previous studies have focused on the role model of leaders, ignoring the guiding role of leaders with different efforts. This paper introduces leader decision-making into the game of public goods to investigate the exemplary role of leaders in behavior decision-making. It divides them into three types by setting the investment amount of leaders to explore the mechanism of leaders' influence in behavior decision-making and behavior change of team members when facing the transformation of leaders with different investment types. This research can provide a significant reference value for enterprises and social organizations on how to play the role of leaders.
RESUMO
A large number of scholars have conducted detailed studies on the effectiveness of commercial advertising by using neuroimaging methods, but only a few scholars have used this method to study the effectiveness of public service announcements (PSAs). To research the relationship between the effectiveness of PSAs and the audience's implicit awareness, functional near-infrared spectroscopy (fNIRS) was employed to record the neural activity data of participants in this study. The results showed that there was a correlation between activation of dorsolateral prefrontal cortex (dlPFC) and the effectiveness of PSAs; The activation of the dlPFC could also be used as an indicator to represent the appeal of advertising content. The results means that neuroimaging tool can also be used to investigate the effectiveness of PSAs, not just commercial advertisements and a few PSAs study, and that neural activity can predict and improve the effectiveness of PSAs before they are released.