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1.
Opt Lett ; 38(21): 4312-5, 2013 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-24177081

RESUMO

We demonstrate an optical coherence tomography device that simultaneously combines different novel ultrabroad bandwidth light sources centered in the 800 and 1060 nm regions, operating at 66 kHz depth scan rate, and a confocal laser scanning ophthalmoscope-based eye tracker to permit motion-artifact-free, ultrahigh resolution and high contrast retinal and choroidal imaging. The two wavelengths of the device provide the complementary information needed for diagnosis of subtle retinal changes, while also increasing visibility of deeper-lying layers to image pathologies that include opaque media in the anterior eye segment or eyes with increased choroidal thickness.


Assuntos
Corioide/fisiologia , Movimentos Oculares , Retina/fisiologia , Tomografia de Coerência Óptica/métodos , Humanos , Processamento de Imagem Assistida por Computador , Fatores de Tempo
2.
Nephron ; 51(1): 67-72, 1989.
Artigo em Inglês | MEDLINE | ID: mdl-2915757

RESUMO

Both ethanol consumption and uremia are considered to be associated with wasting, malnutrition and debilitation. The present study was designed to investigate as to whether ethanol exerts a stimulatory effect on the catabolic state of renal failure. Rats underwent 5/6-nephrectomy and were fed either with or without ethanol. The degree of uremia was comparable in both groups. Ethanol-fed uremic rats, however, displayed higher serum levels of urea (+ 103%) and glucose (+29%), as compared to uremic animals without alcohol. Subsequently, the urea N appearance was enhanced (+60%) in uremic rats with alcohol as compared to uremic animals without alcohol. In sham rats urea N appearance was also increased (+39%) following ethanol administration in comparison to sham-operated rats without alcohol, albeit to a lesser degree. Urinary Nt-methylhistidine excretion, an indicator of myofibrillar protein breakdown, was enhanced throughout the experiment in uremic rats receiving ethanol. Finally, ethanol caused higher urinary excretion rates of corticosterone in uremic animals as compared to uremic rats without ethanol. There was a significant correlation between urinary corticosterone excretion and both urea N appearance and urinary Nt-methylhistidine excretion. We conclude that ethanol consumption further aggravates the catabolic state of uremia and that this is mediated by an increment in glucocorticoid production.


Assuntos
Etanol/farmacologia , Uremia/metabolismo , Consumo de Bebidas Alcoólicas , Animais , Análise Química do Sangue , Doença Crônica , Masculino , Metilistidinas/urina , Nitrogênio/análise , Ratos , Ratos Endogâmicos , Ureia/análise , Uremia/sangue
3.
Nephron ; 50(4): 338-44, 1988.
Artigo em Inglês | MEDLINE | ID: mdl-3070415

RESUMO

Skeletal muscle wasting in men as well as enhanced urea production in animals due to ethanol consumption has been demonstrated by numerous authors. Furthermore, the outcome of acute renal failure is closely related to the extent of catabolism. The present study was performed to investigate whether chronic ethanol exposition prior to binephrectomy (BN) may represent a predisposing factor for enhanced protein breakdown. Rats underwent BN after exposure to ethanol or isocaloric substrate for 4 weeks. Blood chemistries and muscle samples were obtained 48 h after BN. Animals fed with ethanol revealed significantly higher levels of serum urea nitrogen (SUN) and urea nitrogen appearance (UNA) in comparison to controls. Preconditioning on ethanol-derived calories induced an accelerated fractional degradation rate of myofibrillar protein as demonstrated by a significantly enhanced serum Nt-methylhistidine/creatinine ratio. The increase in serum indicators of enhanced myofibrillar breakdown correlated with the stimulated activities of alkaline myofibrillar protease and cathepsin B. Finally, serum corticosterone levels were enhanced in the experimental group in comparison to controls, indicating an ethanol-related adrenocortical stimulation to be a possible mediating factor of enhanced catabolism in ARF. Thus, chronic ethanol intake prior to the onset of ARF seems to be a risk factor for enhanced catabolism in the course of acute uremia.


Assuntos
Injúria Renal Aguda/enzimologia , Alcoolismo/enzimologia , Etanol/farmacologia , Músculos/enzimologia , Peptídeo Hidrolases/metabolismo , Injúria Renal Aguda/sangue , Injúria Renal Aguda/complicações , Alcoolismo/sangue , Alcoolismo/complicações , Animais , Nitrogênio da Ureia Sanguínea , Catepsina B/metabolismo , Corticosterona/sangue , Modelos Animais de Doenças , Eletrólitos/sangue , Masculino , Músculos/efeitos dos fármacos , Nefrectomia , Ratos , Ratos Endogâmicos
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