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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 alfaRESUMO
Advances in the deposition process have led to dramatic improvements in the electronic properties of polycrystalline diamond films produced by chemical vapor deposition (CVD). It is now possible to produce CVD diamond with properties approaching those of IIa natural diamonds. The combined electron-hole mobility, as measured by transient photoconductivity at low carrier density, is 4000 square centimeters per volt per second at an electric field of 200 volts per centimeter and is comparable to that of the best single-crystal IIa natural diamonds. Carrier lifetimes measured under the same conditions are 150 picoseconds for the CVD diamond and 300 picoseconds for single-crystal diamond. The collection distance at a field of 10 kilovolts per centimeter is 15 micrometers for the CVD diamond as compared to 30 micrometers for natural diamonds. The electrical qualities appear to correlate with the width of the diamond Raman peak. Also, although the collection distance at the highest fields in the films nearly equals the average grain size, there is no evidence of deleterious grain boundary effects.
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Polycrystalline diamond films synthesized by microwave-assisted chemical vapor deposition (MACVD) were examined with transient photoconductivity, and two fundamental electrical transport properties, the carrier mobility and lifetime, were measured. The highest mobility measured is 50 centimeters squared per volt per second at low initial carrier densities (<10(15) per cubic centimeter). Electron-hole scattering causes the carrier mobility to decrease at higher carrier densities. Although not measured directly, the carrier lifetime was inferred to be 40 picoseconds. The average drift length of the carriers is smaller than the average grain size and appears to be limited by defects within the grains. The carrier mobility in the MACVD films is higher than values measured in lower quality dc-plasma films but is much smaller than that of single-crystal natural diamond.
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The present study investigated the effect of systemic administration of the GABA(B) receptor agonist, baclofen, on the development and expression of d-methamphetamine (d-MA)-induced place preference in male Wistar rats. Using a biased and 8-day schedule of conditioning, it was found that administration of d-MA (0.5 mg/kg, i.p.) produced significant place preference. The administration of baclofen (2.5 and 5.0 mg/kg, i.p.) 30 min prior to the exposure to d-MA attenuated the development of d-MA-induced place preference (p<0.05). In addition, when it was acutely administered 30 min prior to the testing session of an already established d-MA place preference, baclofen (1.25-5.0 mg/kg, i.p.) attenuated the expression of this conditioned response in a dose-dependent manner. These results showed that baclofen suppressed the rewarding effect produced by d-MA and may be potentially effective in the treatment of methamphetamine dependence and craving.
Assuntos
Baclofeno/farmacologia , Condicionamento Psicológico/efeitos dos fármacos , Dextroanfetamina/farmacologia , Agonistas dos Receptores de GABA-B , Reforço Psicológico , Animais , Relação Dose-Resposta a Droga , Masculino , Ratos , Ratos WistarRESUMO
In many applications, multilayer mirrors are exposed to damaging fluences of x rays. In x-ray laser cavities intense optical and broad-band x radiation, from the x-ray laser plasma amplifier, can damage multilayer mirrors on time scales of hundreds of picoseconds. We describe experiments using short duration (500 ps) bursts of soft x rays from a laser produced gold plasma to damage multilayer mirrors designed to reflect wavelengths close to 45 Å at normal incidence. The effect of the damaging x-ray flux on normal incidence reflectivity was time resolved for W/C, WRe/C, WC/C, 303-stainless-steel/C, and Cr3C2/C multilayers. The damage thresholds of the different mirrors were compared, and the Cr3C2/C mirrors were found to be the most resilient. The outer layers of the multilayers were observed to expand slowly as x rays were absorbed, and a more rapid expansion then preceded the total loss of reflectivity, at temperatures well below the melting temperature of the mirror components. It is believed that the dominant expansion mechanism is a change in the amorphous carbon layers to a more graphitic structure. The data are fit quite well by a model that assumes expansion of up to 25% in the thickness of the outermost carbon layers, followed by intermixing of the hotter layers. The rapid expansion has been observed to occur in times from 40 to 150 ps and may be the fastest resolution to date of the phenomenon of graphitization. The integrated reflectivity of the mirrors was observed to increase by up to a factor of 2.5 as they damaged; this reflectivity increase may be consistent with a reduction in the layer roughness.