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1.
Zhonghua Gan Zang Bing Za Zhi ; 29(6): 545-550, 2021 Jun 20.
Article in Chinese | MEDLINE | ID: mdl-34225429

ABSTRACT

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.


Subject(s)
Chemical and Drug Induced Liver Injury , Liver Failure, Acute , Vitamin D/therapeutic use , Alanine Transaminase , Animals , Aspartate Aminotransferases , Chemical and Drug Induced Liver Injury/prevention & control , Galactosamine , Interleukin-1beta , Lipopolysaccharides , Liver , Liver Failure, Acute/drug therapy , Liver Failure, Acute/prevention & control , Mice , NLR Family, Pyrin Domain-Containing 3 Protein , Tumor Necrosis Factor-alpha
2.
AJNR Am J Neuroradiol ; 34(1): 115-20, 2013 Jan.
Article in English | MEDLINE | ID: mdl-22723060

ABSTRACT

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.


Subject(s)
Blood-Brain Barrier/anatomy & histology , Blood-Brain Barrier/surgery , High-Intensity Focused Ultrasound Ablation/methods , Magnetic Resonance Imaging/methods , Neuronavigation/methods , Animals , Blood-Brain Barrier/radiation effects , Feasibility Studies , Pilot Projects , Swine
3.
Appl Opt ; 38(25): 5452-7, 1999 Sep 01.
Article in English | MEDLINE | ID: mdl-18324053

ABSTRACT

The influence of the TiO(2) concentration (

4.
Appl Opt ; 35(25): 5073-9, 1996 Sep 01.
Article in English | MEDLINE | ID: mdl-21102938

ABSTRACT

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.

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