Pulmão “Encarcerado” por um Fibrotórax Calcificado

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Lesão de Dieulafoy: Papel do Mapeamento por Ecoendoscopia

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Resolving the Sources of Plasma Glucose Excursions following a Glucose Tolerance Test in the Rat with Deuterated Water and [U-13C]Glucose

Sources of plasma glucose excursions (PGE) following a glucose tolerance test enriched with [U-13C]glucose and deuterated water were directly resolved by 13C and 2H Nuclear Magnetic Resonance spectroscopy analysis of plasma glucose and water enrichments in rat. Plasma water 2H-enrichment attained isotopic steady-state within 2–4 minutes following the load. The fraction of PGE derived from endogenous sources was determined from the ratio of plasma glucose position 2 and plasma water 2H-enrichments. The fractional gluconeogenic contributions to PGE were obtained from plasma glucose positions 2 and 5 2H-positional enrichment ratios and load contributions were estimated from plasma [U-13C]glucose enrichments. At 15 minutes, the load contributed 26±5% of PGE while 14±2% originated from gluconeogenesis in healthy control rats. Between 15 and 120 minutes, the load contribution fell whereas the gluconeogenic contribution remained constant. High-fat fed animals had significant higher 120-minute blood glucose (173±6 mg/dL vs. 139±10 mg/dL, p<0.05) and gluconeogenic contributions to PGE (59±5 mg/dL vs. 38±3 mg/dL, p<0.01) relative to standard chow-fed controls. In summary, the endogenous and load components of PGE can be resolved during a glucose tolerance test and these measurements revealed that plasma glucose synthesis via gluconeogenesis remained active during the period immediately following a glucose load. In rats that were placed on high-fat diet, the development of glucose intolerance was associated with a significantly higher gluconeogenic contribution to plasma glucose levels after the load

FOAM Is the Concept: Medicine in the 21st Century?

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Clinical and microbiological characteristics associated with mortality in spontaneous bacterial peritonitis: a multicenter cohort study.

OBJECTIVES: Spontaneous bacterial peritonitis (SBP) is a prevalent and high mortality complication of cirrhosis. We aimed to describe these patients' clinical and microbiological characteristics and evaluate their impact on outcomes. METHODS: This was a retrospective cohort study including 139 consecutive patients with positive culture SBP from three Portuguese centers diagnosed between 2009 and 2014. Multivariate logistic regression was used to study associations with 30-day mortality. RESULTS: The mean age of the patients was 62 years and 81% of patients were men. The mean model for end-stage liver disease score was 19. Hepatic encephalopathy, hepatorenal syndrome, and variceal bleeding developed in 47, 30, and 21% of patients, respectively. Gram-positive bacteria were isolated in the ascitic fluid of 42% of patients. Resistance to quinolones and multiresistance were found in 33 and 17% of patients, respectively. C-reactive protein level (adjusted odds ratio, 1.16 per 1 mg/l increment) and development of hepatorenal syndrome (adjusted odds ratio, 2.86) were associated independently with 30-day mortality (model's area under the curve, 0.78). CONCLUSION: In this cohort, SBP portended high early mortality. Gram-positive bacteria, bacteria resistant to quinolones, and multiresistant bacteria were identified in considerable proportions of patients. In the setting of the high early mortality and changing microbiological profile, SBP management strategies need to be improved.info:eu-repo/semantics/publishedVersio

Insulin Pulse Characteristics and Insulin Action in Non-diabetic Humans

OBJECTIVE: Pulsatile insulin secretion is impaired in diseases such as type 2 diabetes that are characterized by insulin resistance. This has led to the suggestion that changes in insulin pulsatility directly impair insulin signaling. We sought to examine the effects of pulse characteristics on insulin action in humans, hypothesizing that a decrease in pulse amplitude or frequency is associated with impaired hepatic insulin action. METHODS: We studied 29 nondiabetic subjects on two occasions. On 1 occasion, hepatic and peripheral insulin action was measured using a euglycemic clamp. The deuterated water method was used to estimate the contribution of gluconeogenesis to endogenous glucose production. On a separate study day, we utilized nonparametric stochastic deconvolution of frequently sampled peripheral C-peptide concentrations during fasting to reconstruct portal insulin secretion. In addition to measuring basal and pulsatile insulin secretion, we used approximate entropy to measure orderliness and Fourier transform to measure the average, and the dispersion of, insulin pulse frequencies. RESULTS: In univariate analysis, basal insulin secretion (R(2) = 0.16) and insulin pulse amplitude (R(2) = 0.09) correlated weakly with insulin-induced suppression of gluconeogenesis. However, after adjustment for age, sex, and weight, these associations were no longer significant. The other pulse characteristics also did not correlate with the ability of insulin to suppress endogenous glucose production (and gluconeogenesis) or to stimulate glucose disappearance. CONCLUSIONS: Overall, our data demonstrate that insulin pulse characteristics, considered independently of other factors, do not correlate with measures of hepatic and peripheral insulin sensitivity in nondiabetic humans