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Acute lung injury (ALI) is a devastating clinical syndrome caused by different factors, with high morbidity and mortality. Lung injury and inflammation caused by lipopolysaccharide (LPS) can be modulated by NLRP3 inflammasome activation, yet its exact function within the airway epithelium is still unknown. Meanwhile, glucose transporter protein 1 (GLUT1) contributes to a number of inflammatory illnesses, including ALI. The present study aimed to assess GLUT1's function in NLRP3 inflammasome activation of airway epithelium in LPS-induced acute lung injury. BALB/c mice and BEAS-2B cells were exposed to LPS (5 mg/kg and 200 µg/mL, respectively), with or without GLUT1 antagonists (WZB117 or BAY876). LPS up-regulated pulmonary expression of NLRP3 and GLUT1 in mice, which could be blocked by WZB117 or BAY876. Pharmacological inhibition of GLUT1 in vivo significantly attenuated lung tissue damage, neutrophil accumulation, and proinflammatory factors release (TNF-α, IL-6, and IL-1ß) in LPS-exposed mice. Meanwhile, the activation markers of NLRP3 inflammasome (ASC, caspase-1, IL-1ß, and IL-18) induced by LPS were also suppressed. In cultured BEAS-2B cells, LPS induced an increase in GLUT1 expression and triggered activation of the NLRP3 inflammasome, both of which were inhibited by GLUT1 antagonists. These results illustrate that GLUT1 participates in LPS-induced ALI and promotes the activation of the NLRP3 inflammasome in airway epithelial cells.
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Lesão Pulmonar Aguda , Transportador de Glucose Tipo 1 , Inflamassomos , Lipopolissacarídeos , Camundongos Endogâmicos BALB C , Proteína 3 que Contém Domínio de Pirina da Família NLR , Animais , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Lesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/patologia , Lesão Pulmonar Aguda/induzido quimicamente , Inflamassomos/metabolismo , Camundongos , Transportador de Glucose Tipo 1/metabolismo , Humanos , Masculino , Mucosa Respiratória/metabolismo , Mucosa Respiratória/patologiaRESUMO
Aberrant expression of airway epithelial E-cadherin is a key feature of asthma, yet the underlying mechanisms are largely unknown. Ferroptosis is a novel form of regulated cell death involved in asthma pathogenesis. This study was aimed to evaluate the role of ferroptosis and to investigate whether ferroptosis mediates E-cadherin disruption in mixed granulocyte asthma (MGA). Two murine models of MGA were established using toluene diisocyanate (TDI) or ovalbumin with Complete Freund's Adjuvant (OVA/CFA). Specific antagonists of ferroptosis, including Liproxstatin-1 (Lip-1) and Ferrostatin-1 (Fer-1) were given to the mice. The allergen-exposed mice displayed markedly shrunk mitochondria in the airway epithelia, with decreased volume and denser staining accompanied by down-regulated GPX4 as well as up-regulated FTH1 and malondialdehyde, which are markers of ferroptosis. Decreased pulmonary expression of E-cadherin was also observed, with profound loss of membrane E-cadherin in the airway epithelia, as well as increased secretion of sE-cadherin. Treatment with Lip-1 not only showed potent protective effects against the allergen-induced airway hyperresponsiveness and inflammatory responses, but also rescued airway epithelial E-cadherin expression and inhibited the release of sE-cadherin. Taken together, our data demonstrated that ferroptosis mediates airway epithelial E-cadherin dysfunction in MGA.
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Asma , Caderinas , Modelos Animais de Doenças , Ferroptose , Granulócitos , Animais , Feminino , Camundongos , Asma/metabolismo , Asma/patologia , Asma/induzido quimicamente , Caderinas/metabolismo , Cicloexilaminas/farmacologia , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Células Epiteliais/efeitos dos fármacos , Ferroptose/efeitos dos fármacos , Granulócitos/metabolismo , Granulócitos/patologia , Camundongos Endogâmicos BALB C , Ovalbumina , Fenilenodiaminas/farmacologia , Quinoxalinas , Compostos de EspiroRESUMO
Impaired airway epithelial barrier and decreased expression of E-cadherin are key features of severe asthma. As a gatekeeper of the mucosa, E-cadherin can be cleaved from the cell surface and released into the apical lumen as a soluble form (sE-cadherin).This study was aimed to investigate the role of sE-cadherin in severe asthma.Induced sputum was obtained from healthy subjects and patients with asthma. Two murine models of severe asthma were established using either TDI (toluene diisocyanate) or OVA (ovalbumin)/CFA (complete Freund's adjuvants). The role of sE-cadherin in severe asthma was evaluated by intraperitoneal injection of DECMA-1, a neutralizing antibody against sE-cadherin. Mice or THP-1-derived macrophages were treated with recombinant sE-cadherin to explore the pro-inflammatory mechanism of sE-cadherin.Severe asthma patients had a significantly higher sputum sE-cadherin level than the health subjects with mild to moderate asthma, which were positively correlated with sputum HMGB1 level and glucocorticoid dosage required for daily control. Allergen exposure markedly increased sE-cadherin level in the bronchoalveolar lavage fluid in mice. Treatment of DECMA-1 significantly attenuated allergen-induced airway inflammation and hyperresponsivenes in both models of severe asthma. While exposure to recombinant sE-cadherin dramatically up-regulated VEGF expression in THP-1-derived macrophages, and increased neutophlil and eosinophil infiltration into the airway as well as the release of VEGF and IL-6 in mice, both of which can be suppressed by pharmacological inhibition of ERK signaling.Taken together, our data indicated that sE-cadherin contributed to the airway inflammation of severe asthma in an ERK-depedent pathway.
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BACKGROUND: Loss of E-cadherin in the airway epithelial cells is a critical contributor to the development of ALI/ARDS. Yet the underlying mechanisms are largely unknown. Increasing evidences have revealed the significance of ferroptosis in the pathophysiological process of ALI/ARDS. The aim of this study was to investigate the role of ferroptosis in dysregulation of airway epithelial E-cadherin in ALI/ARDS. METHODS: BALB/c mice were subjected to intratracheal instillation of lipopolysaccharide (LPS) to establish an ALI model. Two inhibitors of ferroptosis, liproxstatin-1 (Lip-1, at the dose of 10 mg/kg and 30 mg/kg) and ferrostatin-1 (Fer-1, at the dose of 1 mg/kg and 5 mg/kg), were respectively given to the mice through intraperitoneal injection after LPS challenge. The expression of ferroptotic markers, full-length E-cadherin and soluble E-cadherin (sE-cadherin) were both detected. RESULTS: LPS exposure dramatically down-regulated pulmonary expression of E-cadherin in mice, with profound loss of membrane E-cadherin in the airway epithelial cells and increased secretion of sE-cadherin in the airway lumen. At the same time, we found that the mitochondrial of airway epithelial cells in LPS-exposed mice exhibited significant morphological alterations that are hallmark features of ferroptosis, with smaller volume and increased membrane density. Other makers of ferroptosis were also detected, including increased cytoplasmic levels of iron and lipid peroxidates (MDA), as well as decreased GPX4 expression. 30 mg/kg of Lip-1 not only showed potent protective effects against the LPS-induced injury, inflammation, edema of the lung in those mice, but also rescued airway epithelial E-cadherin expression and decreased the release of sE-cadherin through inhibiting ferroptosis. While no noticeable changes induced by LPS were observed in mice treated with Lip-1 at 10 mg/kg nor Fer-1 at 1 mg/kg or 5 mg/kg. CONCLUSIONS: Taken together, these data demonstrated that ferroptosis mediates airway epithelial E-cadherin dysfunction in LPS-induced ALI.
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Lesão Pulmonar Aguda , Ferroptose , Síndrome do Desconforto Respiratório , Animais , Camundongos , Lesão Pulmonar Aguda/induzido quimicamente , Caderinas , Lipopolissacarídeos/toxicidade , Camundongos Endogâmicos BALB CRESUMO
Acute lung injury (ALI) is a severe disease with high mortality and poor prognosis, characterized by excessive and uncontrolled inflammatory response. Vascular endothelial growth factor A (VEGF-A) contributes to the development and progression of ALI. The aim of this study was to evaluate the role of glucose transporter 1 (GLUT1) in alveolar epithelial VEGF-A production in lipopolysaccharide (LPS)-induced ALI. An ALI mouse model was induced by LPS oropharyngeal instillation. Mice were challenged with LPS and then treated with WZB117, a specific antagonist of GLUT1. For the vitro experiments, cultured A549 cells (airway epithelial cell line) were exposed to LPS, with or without the GLUT1 inhibitors WZB117 or BAY876. LPS significantly upregulated of GLUT1 and VEGF-A both in the lung from ALI mice and in cultured A549. In vivo, treatment with WZB117 not only markedly decreased LPS-induced pulmonary edema, injury, neutrophilia, as well as levels of interleukin (IL)-1ß, IL-6 and tumor necrosis factor-α in bronchoalveolar lavage fluid (BALF), but also reduced VEGF-A production. Yet, the maximum tolerated concentration of WZB117 failed to suppress LPS-induced VEGF-A overexpression in vitro. While administration of BAY876 inhibited gene and protein expression as well as secretion of VEGF-A in response to LPS in A549. These results illustrated that GLUT1 upregulates VEGF-A production in alveolar epithelia from LPS-induced ALI, and inhibition of GLUT1 alleviates ALI.
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Lesão Pulmonar Aguda , Hidroxibenzoatos , Lipopolissacarídeos , Camundongos , Animais , Lipopolissacarídeos/toxicidade , Fator A de Crescimento do Endotélio Vascular/metabolismo , Transportador de Glucose Tipo 1 , Lesão Pulmonar Aguda/metabolismo , Pulmão/metabolismo , Epitélio/metabolismoRESUMO
OBJECTIVE: Down-regulation of bronchial epithelial E-cadherin is an important of feature of severe asthma, including steroid-insensitive asthma. Yet, the mechanisms involved in E-cadherin disruption are not fully understood. This study was aimed to investigate the role of glucose transporter 1 (GLUT1) in dysregulation of E-cadherin in toluene diisocyanate (TDI)-induced steroid-insensitive asthma. METHODS: A murine model of steroid-insensitive asthma was established by TDI sensitization and aerosol inhalation. Selective GLUT1 antagonists WZB117 and BAY876 were given to BALB/c mice after airway challenge. In vitro, primary human bronchial epithelial cells (HBECs) cultured in an airway-liquid interface (ALI) were exposed to TDI. RESULTS: TDI exposure markedly up-regulated GLUT1 in murine lungs and HBECs. Pharmacological inhibition of GLUT1 with BAY876 decreased airway hyperresponsiveness, neutrophil and eosinophil accumulation, as well as type 2 inflammation in vivo. Besides, the TDI-induced down-regulated expression of full-length E-cadherin was also partly recovered, accompanied by inhibited secretion of soluble E-cadherin (sE-cadherin). WZB117 also exhibited mild therapeutic effects, though not significant. In vitro, treatment with GLUT1 inhibitor relieved the TDI-induced disruption of E-cadherin in HBECs. CONCLUSIONS: Taken together, our data demonstrated that GLUT1 modulates bronchial epithelial E-cadherin dysfunction production in TDI-induced steroid-insensitive asthma.
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OBJECTIVES: T1 mapping can noninvasively quantify the native longitudinal relaxation time (T1 value) of myocardium and provide more information on myocardial fibrosis based on late gadolinium enhancement (LGE). However, the traditional approach of measuring T1 value limits the popularization and application of this technology in clinic because the whole short axis (SAX) of myocardium is required in the regions of interest (ROI). This study aims to evaluate the diagnostic ability of native T1 value obtained by comparison between the midventricular septum (ConSept) and SAX approaches in diffuse myocardial lesions. METHODS: Retrospective analysis was performed on 38 patients with non-ischemic dilated cardiomyopathy (NIDCM) and 27 healthy controls who underwent T1 mapping and gadolinium delayed enhancement (LGE) scanning on a 3.0T cardiac magnetic resonance (CMR) in Xiangya Hospital of Central South University. Patients with NIDCM were divided into a LGE positive group and a LGE negative group according to the presence or absence of LGE. The native T1 value was measured by the ROI placed in the ConSept and SAX, respectively. The ability to distinguish the impaired myocardium from the healthy myocardium and the native T1 values of the myocardium measured by the 2 approaches were compared between the NIDCM group and the control group. RESULTS: The native T1 values of NIDCM group using ConSept or SAX approach were significantly higher than those in the control group (all P<0.001), and the native T1 values in the LGE positive group were greater than those in the LGE negative group (all P<0.05). There was no significant difference in T1 value of middle, basal, and apical layer between the ConSept approach and SAX approach (all P>0.05). ConSept and SAX approaches had a good consistency [concordance correlation coefficient (CCC)=0.954]. CONCLUSIONS: Comparing to the SAX approach, ConSept approach is a simple and equivalent method to measure the native T1 value of myocardium and is suitable for clinical application.
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Cardiomiopatia Dilatada , Cardiomiopatia Dilatada/diagnóstico por imagem , Meios de Contraste , Gadolínio , Humanos , Imagem Cinética por Ressonância Magnética , Miocárdio , Valor Preditivo dos Testes , Estudos RetrospectivosRESUMO
OBJECTIVES: To design a standardized imaging diagnostic reporting mode for screening coronavirus disease 2019 (COVID-19), and to prospectively verify its effectiveness in clinical practice. METHODS: A new classification and standardized imaging diagnosis report mode of viral pneumonia was established by studying and summarizing the imaging findings of various kinds of viral pneumonia, combining with lesion density, interstitial changes, pleural effusion, lymph nodes, and some special signs. After systematic training, the radiologist experienced clinical practice for screening CT features. COVID-19 cases were screened retrospectively in the single-center. The confirmed cases were verified, and the diagnostic efficacy of the standardized imaging reporting system in screening COVID-19 was tested. RESULTS: There were 912 patients in this stage receiving the screening imaging examination. Of them, 190 patients were screened in the report mode and 30 patients were diagnosed as COVID-19. The CT manifestation of COVID-19 was characterized by pure ground glass lesions or with a few solid components, predominant subpleural distribution, no lymph node enlargement and pleural effusion, and often with paving-way sign and air bronchus sign. In combination with the above signs, the diagnostic efficacy of COVID-19 was 0.942. CONCLUSIONS: The standardized imaging diagnosis report mode based on COVID-19 chest image features is effective and practical, which should be popularized.
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Betacoronavirus , COVID-19 , Infecções por Coronavirus/diagnóstico , Humanos , Pandemias , Pneumonia Viral/diagnóstico , Estudos Retrospectivos , SARS-CoV-2 , Tomografia Computadorizada por Raios XRESUMO
Although continuous outbreak of coronavirus disease 2019, it has been widely reported, there were few reports regarding family cases. We reported a group of family cluster outbreak cases confirmed in Xiangya Hospital, Central South University, China, and their clinical and image characteristics have been analyzed in order to provide reference for the prevention and early diagnosis of this disease. A total of 5 patients from one family, including 4 adults and 1 child, had a history of human contact in Wuhan, Hubei. Four adult patients showed different symptoms, including cough, fever, pharyngeal pain, and dyspnea, while the child patient had no symptoms. Laboratory examination showed no abnormality in all the patients except for slight increase in CRP in 2 patients and mild abnormal liver function index in 1 patient. The chest CT showed that all patients had abnormal images, with different degrees of manifestations.All patients were finally diagnosed by the nucleic acid test.
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Betacoronavirus , Infecções por Coronavirus , Pandemias , Pneumonia Viral , Adulto , COVID-19 , Criança , China , Infecções por Coronavirus/epidemiologia , Surtos de Doenças , Humanos , Pneumonia Viral/epidemiologia , SARS-CoV-2RESUMO
OBJECTIVES: To investigate the role of chest CT for the diagnostic work-up for patients with suspected infection of coronavirus disease 2019 (COVID-19). METHODS: The clinical data and imaging findings of the first nucleic acid-negative COVID-19 patients were analyzed and compared with the first nucleic acid-positive patients. RESULTS: Compared with the first nucleic acid-positive patients, the onset time of the first nucleic acid-negative patients was shorter [(3.58±2.94) d], but the diagnosis was longer [(3.92±3.66) d]. There were no significant differences in the characteristics of the clinical data and radiological findings between the 2 groups (P>0.05). CONCLUSION: Chest CT examination is important to avoid COVID-19 missed diagnosis due to false negative nucleic acid.
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Betacoronavirus , Infecções por Coronavirus/diagnóstico por imagem , Pneumonia Viral/diagnóstico por imagem , COVID-19 , Humanos , Pandemias , SARS-CoV-2 , Tomografia Computadorizada por Raios XRESUMO
Steroid insensitivity constitutes a major problem for asthma management. Toluene diisocyanate (TDI) is one of the leading allergens of asthma that induces both T-helper Th2 and Th17 responses, and is often associated with poor responsiveness to steroid treatment in the clinic.We sought to evaluate the effects of inhaled and systemic steroids on a TDI-induced asthma model and to find how interleukin (IL)-17A and IL-17F function in this model. BALB/c mice were exposed to TDI for generating an asthma model and were treated with inhaled fluticasone propionate, systemic prednisone, anti-IL-17A, anti-IL-17F, recombinant IL-17A or IL-17F.Both fluticasone propionate and prednisone showed no effects on TDI-induced airway hyperresponsiveness (AHR), bronchial neutrophilia and eosinophilia, and epithelial goblet cell metaplasia. TDI-induced Th2 and Th17 signatures were not suppressed by fluticasone propionate or prednisone. Treatment with anti-IL-17A after TDI exposure led to increased AHR, aggravated mucus production and airway eosinophil recruitment, accompanied by amplified Th2 responses, whereas anti-IL-17F ameliorated TDI-induced AHR and airway neutrophilia, with decreased Th17 responses. Recombinant IL-17A and IL-17F showed opposite effects to the monoclonal antibodies.IL-17A and IL-17F exert distinct biological effects during airway inflammation of a TDI-induced asthma model, which is unresponsive to both inhaled and systemic steroids.
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Asma/tratamento farmacológico , Asma/imunologia , Interleucina-17/fisiologia , Animais , Broncodilatadores/uso terapêutico , Modelos Animais de Doenças , Resistência a Medicamentos , Fluticasona/uso terapêutico , Glucocorticoides/uso terapêutico , Camundongos , Camundongos Endogâmicos BALB C , Prednisona/uso terapêutico , Tolueno 2,4-Di-Isocianato/administração & dosagemRESUMO
Perovskite structure (ABO(3)) thin films have wide applications in electronic devices due to their unique properties, including high dielectric permittivity, ferroelectricity and piezoelectric coupling. Here, we report an approach to grow highly textured thick lead titanate (PbTiO(3)) filmson conductive substrates by a two-step hydrothermal reaction. Initially, vertically aligned TiO(2) nanowire arrays are grown on fluorine-doped tin oxide (FTO) coated glass, which act as template crystals for conversion to the perovskite structure. The PbTiO(3) films are then converted from TiO(2) NW arrays by diffusing Pb(2+) ions into the template through a second hydrothermal reaction. The dielectric permittivity and piezoelectric coupling coefficient (d(33)) of the PbTiO(3) films are as high as 795 at 1 kHz and 52 pm V−1, respectively. The reported process can also potentially be expanded for the assembly of other complex perovskite ATiO(3) (A = Ba, Ca, Cd,etc) films by using the highly aligned TiO(2) NW arrays as templates. Therefore, the approach introduced here opens up a new door to synthesize ferroelectric thin films on conductivesubstrates for application in sensors, actuators, and ultrasonic transducers that are important in various industrial and scientific areas.
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A novel approach for the synthesis of ultra-long (up to â¼45 µm) vertically aligned barium titanate (BaTiO3) nanowire (NW) arrays on an oxidized Ti substrate is developed. The fabrication method uses a two-step hydrothermal reaction that firstly, involves the growth of ultra-long aligned sodium titanate NW arrays and secondly, involves the transfer of these precursor sodium titanate NW arrays to BaTiO3 NW arrays while retaining the shape of the template nanowires. The ion-exchange during the second hydrothermal reaction in barium hydroxide solution results in the structural transformation from single-crystal sodium titanate NW arrays to BaTiO3 NW arrays. This synthesis approach is low-cost, scalable, and enables control over the morphology and aspect ratio of the resulting BaTiO3 NW arrays by tuning the hydrothermal reaction parameters. In addition to the synthesis methods reported here, the energy harvesting behavior of the BaTiO3 NW arrays is evaluated as a function of their aspect ratio and demonstrated to produce significant impact on the energy produced. The newly developed hydrothermal synthesis process for controlled growth of ultra-long, vertically aligned BaTiO3 NW arrays provides a promising method for their efficient utilization in nano-electromechanical system-based sensors, energy harvesters, and nano-scale electronic devices.
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Nanocomposites combining a high breakdown strength polymer and high dielectric permittivity ceramic filler have shown great potential for pulsed power applications. However, while current nanocomposites improve the dielectric permittivity of the capacitor, the gains come at the expense of the breakdown strength, which limits the ultimate performance of the capacitor. Here, we develop a new synthesis method for the growth of barium strontium titanate nanowires and demonstrate their use in ultra high energy density nanocomposites. This new synthesis process provides a facile approach to the growth of high aspect ratio nanowires with high yield and control over the stoichiometry of the solid solution. The nanowires are grown in the cubic phase with a Ba0.2Sr0.8TiO3 composition and have not been demonstrated prior to this report. The poly(vinylidene fluoride) nanocomposites resulting from this approach have high breakdown strength and high dielectric permittivity which results from the use of high aspect ratio fillers rather than equiaxial particles. The nanocomposites are shown to have an ultra high energy density of 14.86 J/cc at 450 MV/m and provide microsecond discharge time quicker than commercial biaxial oriented polypropylene capacitors. The energy density of our nanocomposites exceeds those reported in the literature for ceramic/polymer composites and is 1138% greater than the reported commercial capacitor with energy density of 1.2 J/cc at 640 MV/m for the current state of the art biaxial oriented polypropylene.
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Fontes de Energia Elétrica , Nanocompostos/química , Nanofios/química , Óxidos/química , Estrôncio/química , Titânio/química , Compostos de Bário/química , Cerâmica/química , Polímeros/química , Polipropilenos/químicaRESUMO
Asthma is quite heterogenous and can be categorized as eosinophilic, mixed granulocytic (presence of both eosinophils and neutrophils in the airways) and neutrophilic. Clinically, mixed granulocytic asthma (MGA) often tends to be severe and requires large doses of corticosteroids. High mobility group box 1 (HMGB1) is one of the epithelium-derived alarmins that contributes to type 2 inflammation and asthma. This study was aimed to investigate the role of glucose transporter 1 (GLUT1) in modulation of airway epithelial HMGB1 production in MGA. Induced sputum and bronchial biopsy specimens were obtained from healthy subjects and asthma patients. BALB/c mice, the airway epithelial cell line BEAS-2B, or primary human bronchial epithelial cells (HBECs) were immunized with allergens. Intracellular and extracellular HMGB1 were both detected. The role of GLUT1 was assessed by using a pharmacological antagonist BAY876. MGA patients have a significant higher sputum HMGB1 level than the health and subjects with other inflammatory phenotypes. Nuclear-to-cytoplasmic translocation of HMGB1 was also observed in the bronchial epithelia. Allergen exposure markedly induced GLUT1 expression in murine lungs and cultured epithelial cells. Pharmacological antagonism of GLUT1 with BAY876 dramatically decreased airway hyperresponsiveness, neutrophil and eosinophil accumulation, as well as type 2 inflammation in murine models of MGA. Besides, the allergen-induced up-regulation of HMGB1 was also partly recovered by BAY876, accompanied by inhibited secretion into the airway lumen. In vitro, treatment with BAY876 relieved the allergen-induced over-expression and secretion of HMGB1 in airway epithelia. Taken together, our data indicated that GLUT1 mediates bronchial epithelial HMGB1 release in MGA.
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Asma , Proteína HMGB1 , Humanos , Animais , Camundongos , Transportador de Glucose Tipo 1/genética , Proteína HMGB1/metabolismo , Asma/metabolismo , Células Epiteliais/metabolismo , Inflamação , AlérgenosRESUMO
Textured barium titanate (BaTiO(3)) films are attracting immense research interest due to their lead-free composition and excellent piezoelectric and dielectric properties. Most synthesis methods for these films require a high temperature, leading to the formation of a secondary phase and an overall decrease in the electrical properties of the ceramic. In order to alleviate these issues, a novel fabrication method is introduced by transferring oriented rutile TiO(2) nanowires to a textured BaTiO(3) film at temperatures below 160 °C. The microstructure and thickness of the fabricated BaTiO(3) films were characterized by scanning electron microscopy, and the crystal structure and degree of orientation were evaluated by x-ray diffraction patterns using the Lotgering method. It is shown that the thickness of the BaTiO(3) film can be controlled by the length of TiO(2) nanowire array template, and the degree of orientation of the textured BaTiO(3) films is highly dependent on the film thickness; the crystallographic orientation has been measured to reach up to 87%. The relative dielectric constant (ε(r) = 1300) and ferroelectric properties (P(r) = 2.7 µC cm(-2), E(c) = 4.0 kV mm(-1)) of the textured BaTiO(3) films were also characterized to demonstrate their potential application in sensors, random access memory, and micro-electromechanical systems.
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Graphene consists of a monolayer of sp(2) bonded carbon atoms and has attracted considerable interest over recent years due to its extreme mechanical, electrical, and thermal properties. Graphene nanocomposites have naturally begun to be studied to capitalize upon these properties. A range of complex chemical and physical processing methods have been devised that achieve isolated graphene sheets that attempt to prevent aggregation. Here we demonstrate that the simple casting of a polymer solution containing dispersed graphene oxide, followed by thermal reduction, can produce well-isolated monolayer reduced-graphene oxide. The presence of single layer reduced-graphene oxide is quantitatively demonstrated through transmission electron microscopy and selected area electron diffraction studies and the reduction is verified by thermogravimetric, X-ray photoelectron spectroscopy, infrared spectrum, and electrical conductivity studies. These findings provide a simple, environmentally benign and commercially viable process to produce reduced-graphene oxide reinforced polymers without complex manufacturing, dispersion or reduction processes.
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Cristalização/métodos , Grafite/química , Nanoestruturas/química , Nanoestruturas/ultraestrutura , Temperatura Alta , Substâncias Macromoleculares/química , Teste de Materiais , Conformação Molecular , Tamanho da Partícula , Propriedades de SuperfícieRESUMO
Dysfunction of epithelial barrier is crucial for the development of acute lung injury (ALI). This study was aimed to evaluate the role of glucose transporter 1 (GLUT1) in dysregulation of epithelial tight junction in ALI. GLUT1 was inhibited with specific antagonists WZB117 or BAY876 to see the effects on epithelial tight junction in a well-established LPS-induced mouse ALI model as well as in vitro cultured epithelial cells. Pharmacological inhibition of GLUT1 with WZB117 at either a low or high dose had no effects on lung injury and inflammation 24 h after LPS challenge, but significantly decreased the pulmonary inflammatory responses induced by LPS at 72 h with a high dose, which was verified by treatment with BAY876. WZB117 or BAY876 also recovered the expression of epithelial tight junction proteins ZO-1 and occludin. In cultured BEAS-2B and A549 cells, LPS induced increased GLUT1 expression, accompanied by decreased expression of tight junction protein ZO-1 and occludin. Blockade of GLUT1 restored LPS-induced disruption of ZO-1 and occludin in BEAS-2B rather than A549. Taken together, our results showed that GLUT1 is responsible for dysfunction of epithelial tight junctions in the late phase of LPS-induced ALI.
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Lesão Pulmonar Aguda , Junções Íntimas , Camundongos , Animais , Ocludina/metabolismo , Transportador de Glucose Tipo 1/metabolismo , Lipopolissacarídeos/farmacologia , Lipopolissacarídeos/metabolismo , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/metabolismo , Proteína da Zônula de Oclusão-1/metabolismo , Proteínas de Junções Íntimas/metabolismoRESUMO
Background: Nature therapy can significantly benefit the physiology and psychology of middle-aged and older people, but previous studies have focused on forest environments. The restoration potential of rural environments in urban fringe areas, which are more accessible to older people on a daily basis, has not been fully studied. This study assessed the effects of nature therapy on the physical and mental health of older women in a rural setting (locally known as Linpan) in the urban fringe area of Chengdu, China. Methods: We recruited a total of 60 older women (65.3 ± 5.5 years old) living in cities for 3 days of nature therapy in the winter (30 subjects) and spring (30 subjects), including 20 hypertensive patients. Results: The results showed that the overall blood pressure, pulse and sleep dysfunction rating scores of the participants were significantly lower than the pretest levels, and the finger blood oxygen saturation, mid-day salivary alpha-amylase and cortisol were increased post-treatment. Increases in these biomarker indicates and increase in stress. There were significant differences in the changes in systolic blood pressure between the hypertension group (HTN) and the normal group (normal) (HTN decreased by 8.8%, normal decreased by 5.4%), salivary alpha-amylase content (HTN decreased by 0.3%, normal increased by 16.9%), and sleep dysfunction rating scores (HTN decreased by 59.6%, normal decreased by 54%). The decreases in systolic blood pressure and pulse in the winter group were higher than those in the spring group by 1.8 and 4.4%, respectively, while the increases in salivary alpha-amylase content and salivary cortisol content were lower than those in the spring group by 11.7 and 11.2%, respectively, and the decrease in sleep dysfunction rating scores was lower than that in the spring group by 7.1%. Conclusion: Our study concluded that nature therapy based on various health activities in the Linpan has significant health effects on older women. It can regulate blood pressure and pulse in older women, relieve cardiovascular disease, improve sleep quality. Meanwhile, older women with high blood pressure experienced a more significant effect than the healthy group.
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Hipertensão , alfa-Amilases Salivares , Pessoa de Meia-Idade , Humanos , Feminino , Idoso , Hidrocortisona , Terapia de Relaxamento , Hipertensão/terapia , Pressão SanguíneaRESUMO
Background: Because eosinophilic granulomatosis with polyangiitis (EGPA) is so rare and the symptoms so varied, it can be a challenge to get a correct diagnosis in clinical practice. Cardiovascular involvement is the main cause of death of EGPA. We are the first to report of cardiac magnetic resonance (CMR) findings about right-sided heart involvement in EGPA. Patient Findings: The initial abnormalities detected by CMR were Löffler endocarditis with extensive thrombosis and left ventricular (LV) dysfunction. After active treatment, LV systolic function recovered and endocarditis with thrombosis significantly improved, but there was rapidly progressive pulmonary hypertension, enlargement of right atrium and right ventricle and persistent right-sided heart failure. The patient eventually died of sudden cardiac death 6 months after hospital discharge. Conclusions: Löffler endocarditis and right-sided heart involvement are both rare presentations in patients with EGPA. CMR is a reliable non-invasive tool to precisely and comprehensively assess cardiovascular involvement in EGPA.