RESUMEN
Epstein-Barr virus (EBV) infection is prevalent in global population and associated with multiple malignancies and autoimmune diseases. During the infection, EBV-harbored or infected cell-expressing antigen could elicit a variety of antibodies with significant role in viral host response and pathogenesis. These antibodies have been extensively evaluated and found to be valuable in predicting disease diagnosis and prognosis, exploring disease mechanisms, and developing antiviral agents. In this review, we discuss the versatile roles of EBV antibodies as important biomarkers for EBV-related diseases, potential driving factors of autoimmunity, and promising therapeutic agents for viral infection and pathogenesis.
Asunto(s)
Enfermedades Autoinmunes , Infecciones por Virus de Epstein-Barr , Esclerosis Múltiple , Humanos , Infecciones por Virus de Epstein-Barr/diagnóstico , Infecciones por Virus de Epstein-Barr/tratamiento farmacológico , Infecciones por Virus de Epstein-Barr/complicaciones , Herpesvirus Humano 4 , Anticuerpos Antivirales , Enfermedades Autoinmunes/complicaciones , Antivirales/uso terapéuticoRESUMEN
Metallic zinc is regarded as an ideal anode material for high-energy aqueous zinc ion batteries owing to its high theoretical capacity, low cost, and abundant resource. However, the undesirable dendrite formation and side reactions occurring on Zn anode during the long-term cycling process seriously restrict the electrochemical performance of the device. Herein, 1-hydroxy ethylidene-1,1-diphosphonic acid (HEDP) is used as electrolyte additive to release the chemical corrosion and hydrogen evolution occurring on Zn anode based on the absorption of HEDP on the Zn foil. Moreover, the strong coordination of HEDP with Zn2+ can balance ion flux at the electrode/electrolyte interface, thus inducing uniform Zn deposition. Thereby, Zn anode exhibits a prolonged cycle life of reversible Zn plating/stripping under different current densities (2800 h at 2 mA cm-2 , 1 mAh cm-2 , and more than 1772 h at 4 mA cm-2 , 1 mAh cm-2 ). Moreover, the cell shows a high average coulombic efficiency of ≈99.6% for ≈600 cycles at 1 mA cm-2 with a cycling capacity of 1 mAh cm-2 . This work provides a facile yet effective method for developing reversible aqueous zinc metal batteries.
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Alzheimer's disease (AD), a common neurodegenerative disease, is characterised by the deposition of amyloid-ß (Aß) plaques and neurofibrillary tangles. An increasing number of studies have demonstrated that Aß causes neuronal damage and mitochondrial dysfunction. Herein, we evaluated the neuroprotective effect of sodium butyrate (NaB) against Aß induced neurotoxicity in PC12 cells. The results revealed that 3 mM of NaB promoted the expression of angiotensin-converting enzyme and brain-derived neurotrophic factor, which exert a neuroprotective effect by activating G protein-coupled receptors. Moreover, NaB could significantly improve mitochondrial dysfunction caused by Aß. In conclusion, NaB protected PC12 cells from Aß-induced cell damage, highlighting the potential of NaB in AD treatment.
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Enfermedad de Alzheimer , Enfermedades Neurodegenerativas , Fármacos Neuroprotectores , Animales , Ratas , Enfermedad de Alzheimer/tratamiento farmacológico , Enfermedad de Alzheimer/metabolismo , Péptidos beta-Amiloides/toxicidad , Péptidos beta-Amiloides/metabolismo , Antioxidantes/metabolismo , Apoptosis , Ácido Butírico/farmacología , Supervivencia Celular , Potencial de la Membrana Mitocondrial , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Células PC12 , Fragmentos de Péptidos/toxicidad , Fragmentos de Péptidos/metabolismoRESUMEN
Accumulation of amyloid ß (Aß) peptide, inflammation, and oxidative stress contribute to Alzheimer's disease (AD) and trigger complex pathogenesis. The ketone body ß-hydroxybutyrate (BHBA) is an endogenous metabolic intermediate that protects against stroke and neurodegenerative diseases, but the underlying mechanisms are unclear. The present study aims to elucidate the protective effects of BHBA in the early stage of AD model and investigate the underlying molecular mechanisms. Three-and-half-month-old double-transgenic mice (5XFAD) overexpressing ß-amyloid precursor protein (APP) and presenilin-1 (PS1) were used as the AD model. The 5XFAD mice received 1.5 mmol/kg/d BHBA subcutaneously for 28 days. Morris water maze test, nest construction, and passive avoidance experiments were performed to assess the therapeutic effects on AD prevention in vivo, and brain pathology of 5XFAD mice including amyloid plaque deposition and microglia activation were assessed. Gene expression profiles in the cortexes of 5XFAD- and BHBA-treated 5XFAD mice were performed with high-throughput sequencing and bioinformatic analysis. Mouse HT22 cells were treated with 2 mM BHBA to explore its in vitro protective effects of BHBA on hippocampal neurons against Aß oligomer toxicity, ATP production, ROS generation, and mitochondrial aerobic respiratory function. APP, BACE1, and neprilysin (NEP) expression levels were evaluated in HT22 cells following treatment with BHBA by measuring the presence or absence of G protein-coupled receptor 109A (GPR109A). BHBA improved cognitive function of 5XFAD mice in Morris water maze test, nesting construction and passive avoidance experiments, and attenuated Aß accumulation and microglia overactivation in the brain. BHBA also enhanced mitochondrial respiratory function of hippocampal neurons and protected it from Aß toxicity. The enzymes, APP and NEP were regulated by BHBA via G-protein-coupled receptor 109A (GPR109A). Furthermore, RNA sequencing revealed that BHBA-regulated genes mainly annotated in aging, immune system, nervous system, and neurodegenerative diseases. Our data suggested that BHBA confers protection against the AD-like pathological events in the AD mouse model by targeting multiple aspects of AD and it may become a promising candidate for the prevention and treatment of AD.
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Ácido 3-Hidroxibutírico/farmacología , Enfermedad de Alzheimer/tratamiento farmacológico , Cognición/efectos de los fármacos , Hipocampo/metabolismo , Neuronas/metabolismo , Enfermedad de Alzheimer/genética , Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/patología , Precursor de Proteína beta-Amiloide/genética , Precursor de Proteína beta-Amiloide/metabolismo , Animales , Línea Celular , Modelos Animales de Enfermedad , Regulación de la Expresión Génica , Hipocampo/patología , Ratones , Ratones Transgénicos , Neuronas/patologíaRESUMEN
Alzheimer's disease (AD) is a common neurodegenerative disease. Aß plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central nervous system diseases. The aim of this study is to research the protective effects of NaB on neurons against Aß toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on Aß-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury. In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF. Therefore, NaB protects N2a cells from Aß-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.
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Péptidos beta-Amiloides/toxicidad , Ácido Butírico/farmacología , Fármacos Neuroprotectores/farmacología , Animales , Factor Neurotrófico Derivado del Encéfalo/análisis , Supervivencia Celular/efectos de los fármacos , Transporte de Electrón/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Ratones , Receptores Acoplados a Proteínas G/fisiología , Células Tumorales CultivadasRESUMEN
Zinc ion batteries are considered as potential energy storage devices due to their advantages of low-cost, high-safety, and high theoretical capacity. However, dendrite growth and chemical corrosion occurring on Zn anode limit their commercialization. These problems can be tackled through the optimization of the electrolyte. However, the screening of electrolyte additives using normal electrochemical methods is time-consuming and labor-intensive. Herein, a fast and simple method based on the digital holography is developed. It can realize the in situ monitoring of electrode/electrolyte interface and provide direct information concerning ion concentration evolution of the diffusion layer. It is effective and time-saving in estimating the homogeneity of the deposition layer and predicting the tendency of dendrite growth, thus able to value the applicability of electrolyte additives. The feasibility of this method is further validated by the forecast and evaluation of thioacetamide additive. Based on systematic characterization, it is proved that the introduction of thioacetamide can not only regulate the interficial ion flux to induce dendrite-free Zn deposition, but also construct adsorption molecule layers to inhibit side reactions of Zn anode. Being easy to operate, capable of in situ observation, and able to endure harsh conditions, digital holography method will be a promising approach for the interfacial investigation of other battery systems.
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Digital holography has been employed for in situ observation of dynamic processes occurring at the electrode|electrolyte interface during the anodic dissolution of Alloy 690 in solutions containing SO4 2- + SCN- with or without magnetic field (MF). It was found that MF increased the anodic current of Alloy 690 in 0.5 M Na2SO4 + 5 mM KSCN solution but showed a decreased value when evaluated in 0.5 M H2SO4 + 5 mM KSCN solution. For each solution, as a result of the stirring effect due to Lorentz force, MF showed a decreased localized damage further preventing pitting corrosion. The content of nickel and iron at grain boundaries is higher than that on the grain body, in accordance with the Cr-depletion theory. MF increased the anodic dissolution of nickel and iron, which in turn increased the anodic dissolution at grain boundaries. In situ inline digital holography revealed that IGC begins at one grain boundary and progresses to adjacent grain boundaries with or without MF.
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Gut microbes control host immunity and homeostasis, and their abnormal changes are associated with the occurrence and development of diseases. GPR109A is an essential receptor on intestinal epithelial cells and interacts with gut microbes. Moreover, increased Enterotoxigenic Escherichia coli K88 strain colonization promotes GPR109A expression in vivo. This study evaluated the detailed mechanism of pathogenic bacteria promoting GPR109A expression. The results revealed that ETEC K88 indirectly fosters GPR109A expression in intestinal epithelial cells by stimulating the production of IL-1ß and TNF-α through macrophages which are mediated by ERK1/2 pathway. The study explains the molecular mechanisms by which the bacteria regulate the homeostasis of the host intestinal gene expression during ETEC infection.
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Escherichia coli Enterotoxigénica , Infecciones por Escherichia coli , Animales , Escherichia coli Enterotoxigénica/fisiología , Infecciones por Escherichia coli/veterinaria , Infecciones por Escherichia coli/microbiología , Células Epiteliales/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Macrófagos/metabolismo , Mucosa Intestinal/metabolismoRESUMEN
A Mach-Zehnder interferometer is employed to detect localized corrosion at the metal/solution interface in the potentiodynamic sweep of the iron electrode in solutions. During the electrochemical reactions, local variations of the electrolyte's refractive index, which correlate with the concentration of dissolved species, change the optical path length (OPL) of the object beam when the beam passes through the electrolyte. The distribution of the OPL difference was obtained to present the concentration change of the metal ions visually, which enable direct evidence of corrosion processes. The OPL difference distribution shows localized and general corrosion during the anodic dissolution of the iron electrode in solutions with and without chloride ions, respectively. This method provides an approach for dynamic detection of localized corrosion at the metal/solution interface.
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The morbidity associated with neurodegenerative diseases (NDs) is increasing, posing a threat to the mental and physical quality of life of humans. The crucial effect of microbiota on brain physiological processes is mediated through a bidirectional interaction, termed as the gut-brain axis (GBA), which is being investigated in studies. Many clinical and laboratory trials have indicated the importance of microbiota in the development of NDs via various microbial molecules that transmit from the gut to the brain across the GBA or nervous system. In this review, we summarize the implications of gut microbiota in ND, which will be beneficial for understanding the etiology and progression of NDs that may in turn help in developing ND interventions and clinical treatments for these diseases.
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Microbioma Gastrointestinal , Enfermedades Neurodegenerativas , Encéfalo/fisiología , Eje Cerebro-Intestino , Microbioma Gastrointestinal/fisiología , Humanos , Calidad de VidaRESUMEN
A high-quality protein substitute, Hermetia illucens (black soldier fly) larvae powder, is rich in protein and often used in animal feed. This study aimed to investigate the feasibility and optimal ratio of replacing fish meal with H. illucens larvae in weaned piglets and to demonstrate the effects on piglets' growth performance, intestinal microflora and immune performance. Forty-eight female weaned piglets were randomly classified into three groups. Each group consisted of eight pens (replicates), with two piglets per pen. Three groups containing different proportions of H. illucens larvae (0, 4, and 8%) were referred to as C, HI4, and HI8. We first designed a 28-day feeding experiment to detect growth performance; after that, the piglets were induced with oral gavage of enterotoxigenic Escherichia coli K88 (ETEC K88) and recording diarrhea on day 29 of the experiment. Samples were taken on the 32nd day to detect the effect of H. illucens larvae on the immune performance of the weaned piglets. H. illucens larvae replacement did not cause any obvious change in the growth performance nether in HI4 nor in HI8 of weaned piglets with 28 d feeding stage. H. illucens larvae could improve the intestinal health of weaned piglets by increasing the content of Lactobacillus and reducing the content of Streptococcus. Compared with C+K88 group, the diarrhea rate was attenuated for the H. illucens supplemented group. The integrity of ileum villi in HI4+K88 and HI8+K88 groups was better than that in C+K88 group, and the villi in C+K88 group were severely damaged. The expression of IL-10, Occludin and Claudin-3 in the intestinal mucosa of the HI4+K88 group and HI8+K88 group were significantly increased (P < 0.05), and the expression of TNF-α was significantly decreased (P < 0.05) compared with the C+K88 group. The results of immunoblotting also validated that the same ETEC K88 treatment of weaned piglets enhanced the expression of tight junction protein in the intestinal mucosa of the H. illucens addition group. ETEC-induced diarrhea will be reduced by the diet of weaned piglets containing H. illucens larvae, ameliorating the immune performance of piglets. Our results indicates that the optimal dosage of H. illucens replacement in weaned piglets is 4%.
RESUMEN
Newborn piglets are prone to diarrhea after weaning as a result of changes in their environment and feed. Enterotoxigenic Escherichia coli (ETEC) K88 strain is a typical pathogen that causes diarrhea in such stage of piglets. Hermetia illucens larvae are widely used in livestock and poultry production because of their high nutritional value and immunoregulatory effects. This study aimed to evaluate the protective effects of H. illucens feed in protecting against ETEC induced diarrhea in piglets and to unravel the mechanisms of immune modulation and intestinal barrier maintenance. The results showed that after ETEC infection, citric acid in the serum of the groups fed on H. illucens larvae increased significantly, which stimulated macrophages to secrete cytokines that promote B lymphocyte differentiation, ultimately increasing the production of IgA and IgG in serum. Concomitantly, citric acid also had a positive effect on the intestinal barrier damaged due to ETEC infection by inhibiting the production of inflammatory cytokines, reducing the Bcl-2/Bax ratio, and promoting the expression of tight junction proteins. Correlation analysis showed that the increase of citric acid levels might be related to Massilia. Thus, citric acid derived from H. illucens larvae can improve the immune performance of weaned piglets and reduce ETEC-induced damage to the intestinal barrier in weaned piglets.
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Several studies have reported an intricate link between the G protein-coupled receptor 109A (GPR109A) and intestinal health. Upon activation, induced by butyric acid and ß-hydroxybutyric acid, GPR109A regulates the expression of tight junction proteins, exerts anti-inflammatory effects, and maintains the integrity of the intestinal barrier. However, its function and the mechanism of action in combating the infection caused by exogenous pathogenic microorganisms remain unclear. This study established an animal model of infection by oral enterotoxigenic Escherichia coli (ETEC) gavage to examine the underlying mechanism(s) and protective effects of GPR109A on the intestinal tract. Experimental GPR109A-/-and GPR109A+/+ mice were orally administered with 1 × 109 colony-forming units (CFUs) of ETEC, and changes in body weight were then observed. The colonization and translocation of ETEC in the intestine were detected by the plate counting method. The expression of tight junction proteins and the levels of inflammatory factors and secretory IgA (SIgA) in the intestine were detected by quantitative real-time polymerase chain reaction (q-PCR), western blotting, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. The results demonstrated that GPR109A-/-mice were more susceptible to ETEC infection, showing more severe inflammatory reactions and intestinal damage. Moreover, the secretion of IgA in the intestinal tract of GPR109A+/+ mice was significantly increased after ETEC infection, whereas the IgA levels in GPR109A-/-mice did not change significantly. We added 5 g/L sodium butyrate to the drinking water of all mice. The GPR109A+/+ mice were protected against ETEC infection and no effect was observed in GPR109A-/-mice. Similarly, sodium butyrate increased the SIgA content in the gut of the GPR109A+/+ mice and no effect was observed in GPR109A-/-mice. In conclusion, activated GPR109A is effective against the colonization and translocation of ETEC in the gut and maintains the integrity of the intestinal barrier, possibly by promoting the secretion of intestinal IgA.