Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Zhonghua Gan Zang Bing Za Zhi ; 29(6): 545-550, 2021 Jun 20.
Artigo em Chinês | MEDLINE | ID: mdl-34225429

RESUMO

Objective: To explore the protective effect of vitamin D in acute liver failure through a mouse model. Methods: Acute liver failure was induced by combining D-galactosamine (D-GalN) lipopolysaccharide (LPS) to observe the effect of long-term vitamin D deficiency on liver injury and inflammatory signals in a mouse model. Acute liver failure was induced by thioacetamide (TAA) to observe the effect of vitamin D deficiency on the survival rate, and further high-dose of vitamin D supplementation protective effect was determined in a mouse model. Liver function was evaluated by measuring serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and liver inflammation by hematoxylin-eosin staining. The expressions of tumor necrosis factor (TNF-α), interleukin (IL) -1ß, NOD-like receptor family, pyrin domain containing 3 (NLRP-3), chemokines (CCL2, CXCL1 and CXCL2), etc. in liver tissues were detected by RT-qPCR. The quantitation of macrophages in liver tissue was detected by immunohistochemistry. The comparison between groups were performed by t-test. The survival curve was analyzed by log-rank (Mantel-Cox) test. Results: Long-term vitamin D deficiency had increased acute liver failure sensitivity in mice, which was manifested by increased blood cell extravasation, massive necrosis of parenchymal cells, up-regulation of TNF-α, IL-1ß, and NLRP-3 mRNA expression (P < 0.05), and increased macrophages quantitation (P < 0.05) in liver tissues. At the same time, vitamin D deficiency had increased the mice mortality rate because of liver injury (P < 0.01). On the contrary, pre-administration of high dose of vitamin D (100 IU/g) had significantly reduced liver injury, inhibited ALT and AST rise (P < 0.01), alleviated liver necrosis, and down-regulated the mRNA expression of inflammatory factors in liver tissues (P < 0.05). Conclusion: Mouse model shows that long-term vitamin D deficiency can aggravate drug-induced acute liver failure and reduce survival rates. Furthermore, high-dose of vitamin D has a certain hepatoprotective effect, which can significantly improve liver necrosis condition and inhibit inflammation. Therefore, adequate vitamin D can retain liver physiological balance to resist liver injury.


Assuntos
Doença Hepática Induzida por Substâncias e Drogas , Falência Hepática Aguda , Vitamina D/uso terapêutico , Alanina Transaminase , Animais , Aspartato Aminotransferases , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Galactosamina , Interleucina-1beta , Lipopolissacarídeos , Fígado , Falência Hepática Aguda/tratamento farmacológico , Falência Hepática Aguda/prevenção & controle , Camundongos , Proteína 3 que Contém Domínio de Pirina da Família NLR , Fator de Necrose Tumoral alfa
2.
AJNR Am J Neuroradiol ; 34(1): 115-20, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22723060

RESUMO

BACKGROUND AND PURPOSE: FUS-induced BBB opening is a promising technique for noninvasive and local delivery of drugs into the brain. Here we propose the novel use of a neuronavigation system to guide the FUS-induced BBB opening procedure and investigate its feasibility in vivo in large animals. MATERIALS AND METHODS: We developed an interface between the neuronavigator and FUS to allow guidance of the focal energy produced by the FUS transducer. The system was tested in 29 swine by more than 40 sonication procedures and evaluated by MR imaging. Gd-DTPA concentration was quantitated in vivo by MR imaging R1 relaxometry and compared with ICP-OES assay. Brain histology after FUS exposure was investigated using H&E and TUNEL staining. RESULTS: Neuronavigation could successfully guide the focal beam, with precision comparable to neurosurgical stereotactic procedures (2.3 ± 0.9 mm). A FUS pressure of 0.43 MPa resulted in consistent BBB opening. Neuronavigation-guided BBB opening increased Gd-DTPA deposition by up to 1.83 mmol/L (a 140% increase). MR relaxometry demonstrated high correlation with ICP-OES measurements (r(2) = 0.822), suggesting that Gd-DTPA deposition can be directly measured by imaging. CONCLUSIONS: Neuronavigation provides sufficient precision for guiding FUS to temporally and locally open the BBB. Gd-DTPA deposition in the brain can be quantified by MR relaxometry, providing a potential tool for the in vivo quantification of therapeutic agents in CNS disease treatment.


Assuntos
Barreira Hematoencefálica/anatomia & histologia , Barreira Hematoencefálica/cirurgia , Ablação por Ultrassom Focalizado de Alta Intensidade/métodos , Imageamento por Ressonância Magnética/métodos , Neuronavegação/métodos , Animais , Barreira Hematoencefálica/efeitos da radiação , Estudos de Viabilidade , Projetos Piloto , Suínos
3.
Appl Opt ; 38(25): 5452-7, 1999 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-18324053

RESUMO

The influence of the TiO(2) concentration (

4.
Appl Opt ; 35(25): 5073-9, 1996 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-21102938

RESUMO

The composition-dependent structural, microstructural, optical, and mechanical properties of TiO(2)-MgF(2) composite films prepared by reactive electron-beam coevaporation at a substrate temperature of 280 °C are systematically investigated with an x-ray diffractometer, transmission electron microscope, spectrophotometer and varied angle of incidence spectroscopic ellipsometry, and microhardness tester, respectively. A comparison of the films prepared by reactive ion-assisted coevaporation shows that the films prepared by reactive electron-beam coevaporation have lower refractive indices and hardnesses. However, TiO(2)-MgF(2) composite films prepared by both techniques exhibit similar softening and hardening phenomena and similar microstructures.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA