14 research outputs found

    In vivo 1 H MR spectroscopic imaging of aggressive prostate cancer: Can we detect lactate?

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    Contains fulltext : 138270.pdf (publisher's version ) (Closed access)PURPOSE: A semi-LASER sequence was optimized for in vivo lactate detection in the prostate. METHODS: The ethical committee waived the need for informed consent to measure 17 patients with high grade prostate cancer on a 3T system. A semi-LASER sequence was used with an echo time of 144 ms and optimized interpulse timing for a spectral citrate shape with high signal intensity. An LCModel basis set was developed for fitting choline, creatine, spermine, citrate, and lactate and was used to fit all spectra in tumor-containing voxels. For patients without detectable lactate, the minimal detectable lactate concentration was determined by adding in all spectra of tumor tissue a simulated lactate signal. The amplitude of the simulated lactate signal was iteratively decreased until its fit reached a Cramér Rao lower bound >20\%, which was then set as the patient-specific detection limit. RESULTS: In none of the patients a convincing lactate signal was found. We estimated that on average the lactate levels in high grade prostate cancer are below 1.5 mM (range 0.9-3.5 mM), Interestingly, in one patient with extensive necrosis in the tumor biopsy samples (Gleason score 5+5), large lipid resonances were observed, which originated from the tumor. CONCLUSION: The minimal detectable lactate concentration of 1.5 mM in high grade prostate cancer indicates that if lactate is increased it remains at low concentrations. Magn Reson Med, 2013. © 2013 Wiley Periodicals, Inc

    Changes in venous hemodynamics after renal transplantation.

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    Arcobacter spp. possess two very short flagellins of which FlaA is essential for motility

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    Like Campylobacter and Helicobacter spp., Arcobacter spp. possess two flagellin genes (flaA and flaB) located adjacent to each other. The aim of this study was to characterize the flagellin proteins of Arcobacter spp., because these proteins are known virulence factors in the Epsilonproteobacteria, to which these three species belong. With the exception of Arcobacter nitrofigilis, Arcobacter flagellins are almost half the size of those in other Epsilonproteobacteria. Arcobacter flagellin proteins lack a large part of the variable central region. The low homology observed among flagellins of different Arcobacter species indicates genetic heterology between the members of this genus. Unlike in other Epsilonproteobacteria, the transcription of flagellin genes is not regulated by sigma(28)- or sigma(54)-dependent promoters, which suggests that transcription must be regulated in a different way in Arcobacter spp. Mutational studies revealed that only FlaA is needed for the motility of Arcobacter spp. Quantitative PCR analysis showed that transcription of flaB is higher at 30 degrees C than at 37 degrees C. Mutation of flaB had no effect on motility or on flaA transcription while mutation of flaA abolished motility and increased the transcription of flaB. These results underline that the genus Arcobacter is an unusual taxon in the epsilon subdivision of the Proteobacteria

    Dietary lipids do not contribute to the higher hepatic triglyceride levels of fructose- compared to glucose-fed mice

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    Item does not contain fulltextFructose consumption has been associated with the surge in obesity and dyslipidemia. This may be mediated by the fructose effects on hepatic lipids and ATP levels. Fructose metabolism provides carbons for de novo lipogenesis (DNL) and stimulates enterocyte secretion of apoB48. Thus, fructose-induced hepatic triglyceride (HTG) accumulation can be attributed to both DNL stimulation and dietary lipid absorption. The aim of this study was to assess the effects of fructose diet on HTG and ATP content and the contributions of dietary lipids and DNL to HTG. Measurements were performed in vivo in mice by magnetic resonance imaging (MRI) and novel magnetic resonance spectroscopy (MRS) approaches. Abdominal adipose tissue volume and intramyocellular lipid levels were comparable between 8-wk fructose- and glucose-fed mice. HTG levels were ∼1.5-fold higher in fructose-fed than in glucose-fed mice (P<0.05). Metabolic flux analysis by (13)C and (2)H MRS showed that this was not due to dietary lipid absorption, but due to DNL stimulation. The contribution of oral lipids to HTG was, after 5 h, 1.60 ± 0.23\% for fructose and 2.16 ± 0.35\% for glucose diets (P=0.26), whereas that of DNL was higher in fructose than in glucose diets (2.55±0.51 vs.1.13±0.24\%, P=0.01). Hepatic energy status, assessed by (31)P MRS, was similar for fructose- and glucose-fed mice. Fructose-induced HTG accumulation is better explained by DNL and not by dietary lipid uptake, while not compromising ATP homeostasis.-Nunes, P. M., Wright, A. J., Veltien, A., van Asten, J. J. A., Tack, C. J., Jones, J. G., Heerschap, A. Dietary lipids do not contribute to the higher hepatic triglyceride levels of fructose- compared to glucose-fed mice
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