RESUMO
OBJECTIVE: To investigate the clinical significance of antiplatelet aggregation therapy for patients diagnosed with acute cerebral infarction (ACI) complicated with the cerebral microbleeds (CMBs). METHODS: Thirty patients with ACI and 36 patients with intracerebral hemorrhage (ICH) were included in this research. Two groups, studied by susceptibility-weighted imaging (SWI), were compared in terms of the number, location, and severity of CMBs. Then, 30 cases of ACI patients were divided into CMBs sub-group and non-CMBs sub-group. Univariate analysis between these two sub-groups was performed to determine the risk factors regarding the incidence of CMBs. For ACI patients, the number of CMBs before and after applying anti-platelet treatment were compared to examine the impacts of anti-platelet treatment on hemorrhagic transformation. RESULTS: CMBs were found to be more prevalent and severe in ICH patients than in ACI patients. CMBs in patients with ICH were more severe than in patients with ischemic stroke (IS), which indicates that CMBs closely relate to ICH. Hypertension and leukoaraiosis were found to have significant effects on the incidence of CMBs. After anti-platelet treatment, patients with CMBs (≥5) increased the number of CMB, whereas there was no obvious effect on patients with the CMBs less than 5 or no CMBs. CONCLUSIONS: The number of CMBs increased significantly among ACI patients with 5 or more CMBs before the anti-platelet treatment. CMBs are more frequently found in patients with hemorrhagic stroke than in patients with ischemic stroke, and more severe than the latter, which suggests that the clinical impact of higher association between the increase of the number of the CMBs and the hemorrhagic stroke.
Assuntos
Hemorragia Cerebral , Infarto Cerebral , Interpretação de Imagem Assistida por Computador/métodos , Imageamento por Ressonância Magnética/métodos , Inibidores da Agregação Plaquetária , Adulto , Idoso , Idoso de 80 Anos ou mais , Encéfalo/diagnóstico por imagem , Hemorragia Cerebral/diagnóstico por imagem , Hemorragia Cerebral/tratamento farmacológico , Hemorragia Cerebral/prevenção & controle , Infarto Cerebral/diagnóstico por imagem , Infarto Cerebral/tratamento farmacológico , Infarto Cerebral/prevenção & controle , Monitoramento de Medicamentos , Humanos , Pessoa de Meia-Idade , Inibidores da Agregação Plaquetária/efeitos adversos , Inibidores da Agregação Plaquetária/uso terapêuticoRESUMO
The past decades have witnessed great advances in nanotechnology since tremendous efforts have been devoted for the design, synthesis, and application of nanoparticles. However, for most mineral materials such as calcium sulfate, it is still a challenge to prepare their nanoparticles, especially with uniform size and high monodispersity. In this work, we report a route to regulate the morphology and structure of α-calcium sulfate hemihydrate (α-HH) and successfully synthesize and stabilize its mesocrystals for the first time. The ellipsoidal mesocrystals in length of 300-500 nm are composed by α-HH nanoparticles arranged in the same crystallographic fashion and interspaced with EDTA. The time-dependent experiments indicate the α-HH aggregates evolve from irregular structure to mesocrystal structure with the subsequent growth of subunits and then partially fuse into single crystals. Disorganizing the mesocrystal structure before the emergence of fusion reaps α-HH nanorods in a length of 30-80 nm and a width of 10-20 nm with high monodispersion. This ingenious concept paves an alternative way for nanoparticle preparation and is readily extended to other inorganic systems.
RESUMO
We report a facile and green chemical solution approach to synthesize monodisperse α-calcium sulfate hemihydrate (α-HH) nanoellipsoids with a length of 600 nm and a width of 300 nm by simply mixing Ca(2+) and SO4(2-) glycerol-water precursor solutions in the presence of Na2EDTA. The α-HH nanoellipsoid is formed through a Na2EDTA-mediated self-assembly of small primary building blocks (α-HH domains: â¼14 nm). The study on the morphological evolution of α-HH reveals that the controlled synergy of supersaturation (precursor concentration) and Na2EDTA is crucial for the development of α-HH into nanoellipsoids. Further thermal annealing of the nanoellipsoid could make the α-HH domains transit into calcium sulfate anhydrites and grow up, generating the gaps between them and resulting in a porous structure. This work paves a new way for preparing high-quality α-HH nanoellipsoids with a monodisperse nanosize and a porous structure, promising their future application in many fields such as biomedicine.
Assuntos
Sulfato de Cálcio/síntese química , Nanopartículas/química , Sulfato de Cálcio/química , Tamanho da Partícula , Porosidade , Propriedades de SuperfícieRESUMO
BACKGROUND: HF is a common complication of MI. The underlying mechanisms of myocardial fibrosis in HF after MI are incompletely defined. Here, this study aims to investigate the role of PTX3 KD in HF after MI. METHODS: Bioinformatics analysis based on GSE86569 dataset was performed to explore the potential role of PTX3 in HF. Male C57/BL6J mice were administered with lentiviral vector encoding PTX3 KD or empty vector, and then underwent either coronary ligation or sham surgery. Echocardiography, Masson staining, and immunofluorescence counterstaining were conducted to evaluate the cardiac function and fibrosis. Cardiac fibroblasts were isolated and transfected with lentiviral vector encoding PTX3 KD in vitro to verify the in vivo findings. RESULTS: Bioinformatics analysis based on GSE86569 revealed the aberrant expression of PTX3 in HF patients. Echocardiography showed that PTX3 KD reversed the HF-induced cardiac dysfunction with better cardiac function parameters. Masson staining demonstrated that the obvious infarct and high fibrosis ratio in HF mice were remarkably improved after PTX3 KD. Immunofluorescence staining indicated that the HF-induced increase expression of α-SMA was significantly suppressed by PTX3 KD. Additionally, both in vivo and in vitro results confirmed that PTX3 KD decreased the fibrosis-related up-regulation of collagen I, collagen III, and p-STAT3. However, the result was opposite after IL-6 treatment. CONCLUSIONS: PTX3 KD protects the cardiac function and counteracts the myocardial fibrosis by down-regulating IL-6/STAT3 pathway in HF.
Assuntos
Insuficiência Cardíaca , Infarto do Miocárdio , Animais , Proteína C-Reativa , Colágeno Tipo I/metabolismo , Fibrose , Insuficiência Cardíaca/metabolismo , Humanos , Interleucina-6/metabolismo , Masculino , Camundongos , Infarto do Miocárdio/complicações , Infarto do Miocárdio/genética , Infarto do Miocárdio/metabolismo , Miocárdio/patologia , Componente Amiloide P SéricoRESUMO
Transforming gypsum into α-calcium sulfate hemihydrate (α-HH) provides a promising utilization pathway for the abundant amount of chemical gypsum. The transformation follows the route of "dissolution-recrystallization", during which the arsenic pollutant in gypsum is released into the solution, and hence raises the possibility of being distributed into the product of α-HH, a potential harm that has always been neglected. Investigation of the transformation process at neutral pH revealed that the arsenate ions in solution were distributed into α-HH and generated an enrichment of arsenic by 4-6 times. Arsenate ions distributed into α-HH by substitution for lattice sulfate, adsorption on α-HH facets and occupation for surface sulfate sites. While at higher concentrations, calcium arsenate coprecipitated with α-HH or even crystallized independently. Increasing temperature accelerated the phase transformation and restrained arsenate migration into α-HH due to the lag of distribution balance. The pH of solution modulated the dominant arsenate species and decreasing pH weakened arsenate substitution capacity for sulfate in α-HH. This work uncovers arsenate distribution mechanism during the transformation of gypsum into α-HH and provides a feasible method to restrain arsenate distribution into product, which helps to understand arsenate behavior in hydrothermal solution with high concentration of sulfate minerals and provides a guidance for controlling pollutants distribution into product.
Assuntos
Sulfato de Cálcio/química , Modelos Químicos , Adsorção , Arseniatos/química , Arsênio , Compostos de Cálcio/química , Concentração de Íons de Hidrogênio , SulfatosRESUMO
Lung cancer, especially lung adenocarcinoma, is one of the most common neoplasms worldwide. However, the mechanisms underlying its initiation, development, and metastasis are still poorly understood. Destrin (DSTN) is a member of ADF/cofilin family. Its detailed biological function remains unknown, although it is reported that DSTN is involved in cytoskeleton remodeling and regulation of actin filament turnover. Recent evidence has shown that high expression of cofilin-1 is associated with invasion and poor prognosis of several types of human tumors, but the detailed mechanism is still entirely unclear, particularly in lung cancer tumorigenesis and malignancy. Here, we report that DSTN was highly expressed in a mouse lung cancer model induced by urethane and in clinical lung adenocarcinoma tissue samples. Its expression level was positively correlated with cancer development, as well as metastasis to the liver and lymph nodes. Consistently, it was directly associated with the poor prognosis of lung adenocarcinoma patients. Furthermore, we also found that DSTN promotes cell proliferation, invasion, and migration in vitro, and facilitates subcutaneous tumor formation and lung metastasis via intravenous injection in vivo. Mechanically, DSTN associates with and facilitates nuclear translocation of ß-catenin, which promotes epithelial-to-mesenchymal transition (EMT). Taken together, our results indicated that DSTN enhances lung cancer malignancy through facilitating ß-catenin nuclear translocation and inducing EMT. Combined with multivariate analyses, DSTN might potentially serve as a therapeutic target and an independent prognostic marker of lung adenocarcinoma. IMPLICATIONS: This finding indicates that DSTN facilitates ß-catenin nuclear translocation and promotes malignancy in lung adenocarcinoma.