A systematic study of in-reactor granule yield data was set up in the laboratory. Methanogenic granular sludge growth in fed batch shake flasks for different substrates appeared to decrease with the energy content of the substrate and required the presence of a mixing force. In UASB reactors, granular cell yields were found to be quite variable suggesting the involvement of complex microbiological interactions. The factor foremost in influencing the build-up in the reactor of granular sludge was the presence of high-energy carbohydrates; pre-acidified influents affected in-reactor granular sludge yield very negatively. The influence of sulphate reduction and sulphide concentrations was found not to be of primary importance. The ionic strength of the medium also had no strong influence. Granule formation proceeded somewhat better at low than at nigh strength buffer capacity. High levels of protein, however, reduced the in-reactor granular sludge build-up strongly. Measurement of the acid production by granular and fluffy sludges revealed that the former rapidly produce volatile acids, particularly propionate, while the latter do not. Measurement of the pH in the granule indicated that the outside layer of the granule is rich in acidogens. Calculations of proton and hydrogen fluxes in the granule support the concept that acidogens, able to ferment high energy carbohydrates efficiently to cells and exo-cellular binding materials, might be of primary importance for in-reactor granular growth.
The intricate (micro)vascular architecture of the liver has not yet been fully unravelled. Although current models are often idealized simplifications of the complex anatomical reality, correct morphological information is instrumental for scientific and clinical purposes. Previously, both vascular corrosion casting (VCC) and immunohistochemistry (IHC) have been separately used to study the hepatic vasculature. Nevertheless, these techniques still face a number of challenges such as dual casting in VCC and limited imaging depths for IHC. We have optimized both techniques and combined their complementary strengths to develop a framework for multilevel reconstruction of the hepatic circulation in the rat. The VCC and micro-CT scanning protocol was improved by enabling dual casting, optimizing the contrast agent concentration, and adjusting the viscosity of the resin (PU4ii). IHC was improved with an optimized clearing technique (CUBIC) that extended the imaging depth for confocal microscopy more than five-fold. Using in-house developed software (DeLiver), the vascular network - in both VCC and IHC datasets - was automatically segmented and/or morphologically analysed. Our methodological framework allows 3D reconstruction and quantification of the hepatic circulation, ranging from the major blood vessels down to the intertwined and interconnected sinusoids. We believe that the presented framework will have value beyond studies of the liver, and will facilitate a better understanding of various parenchymal organs in general, in physiological and pathological circumstances.
Cirrhosis represents the end-stage of any persistent chronically active liver disease. It is characterized by the complete replacement of normal liver tissue by fibrosis, regenerative nodules, and complete fibrotic vascularized septa. The resulting angioarchitectural distortion contributes to an increasing intrahepatic vascular resistance, impeding liver perfusion and leading to portal hypertension. To date, knowledge on the dynamically evolving pathological changes of the hepatic vasculature during cirrhogenesis remains limited. More specifically, detailed anatomical data on the vascular adaptations during disease development is lacking. To address this need, we studied the 3D architecture of the hepatic vasculature during induction of cirrhogenesis in a rat model. Cirrhosis was chemically induced with thioacetamide (TAA). At predefined time points, the hepatic vasculature was fixed and visualized using a combination of vascular corrosion casting and deep tissue microscopy. Three-dimensional reconstruction and data-fitting enabled cirrhogenic features to extracted at multiple scales, portraying the impact of cirrhosis on the hepatic vasculature. At the macrolevel, we noticed that regenerative nodules severely compressed pliant venous vessels from 12 weeks of TAA intoxication onwards. Especially hepatic veins were highly affected by this compression, with collapsed vessel segments severely reducing perfusion capabilities. At the microlevel, we discovered zone-specific sinusoidal degeneration, with sinusoids located near the surface being more affected than those in the middle of a liver lobe. Our data shed light on and quantify the evolving angioarchitecture during cirrhogenesis. These findings may prove helpful for future targeted invasive interventions.
Background and Aims The impact of long-term endurance sport participation (on top of a healthy lifestyle) on coronary atherosclerosis and acute cardiac events remains controversial. Methods The Master@Heart study is a well-balanced prospective observational cohort study. Overall, 191 lifelong master endurance athletes, 191 late-onset athletes (endurance sports initiation after 30 years of age), and 176 healthy non-athletes, all male with a low cardiovascular risk profile, were included. Peak oxygen uptake (VO2peak) quantified fitness. The primary endpoint was the prevalence of coronary plaques (calcified, mixed, and non-calcified) on computed tomography coronary angiography. Analyses were corrected for multiple cardiovascular risk factors. Results The median age was 55 (50–60) years in all groups. Lifelong and late-onset athletes had higher VO2peak than non-athletes (159 [143-177] vs 155 [138-169] vs 122 [108-138] % predicted). Lifelong endurance sports was associated with having ≥1 coronary plaque (odds ratio [OR] 1.86, 95% confidence interval [CI] 1.17–2.94), ≥1 proximal plaque (OR 1.96, 95% CI 1.24–3.11), ≥1 calcified plaques (OR 1.58, 95% CI 1.01–2.49), ≥1 calcified proximal plaque (OR 2.07, 95% CI 1.28–3.35), ≥1 non-calcified plaque (OR 1.95, 95% CI 1.12–3.40), ≥1 non-calcified proximal plaque (OR 2.80, 95% CI 1.39–5.65) and ≥1 mixed plaque (OR 1.78, 95% CI 1.06–2.99) as compared to a healthy non-athletic lifestyle. Conclusion Lifelong endurance sport participation is not associated with a more favorable coronary plaque composition compared to a healthy lifestyle. Lifelong endurance athletes had more coronary plaques, including more non-calcified plaques in proximal segments, than fit and healthy individuals with a similarly low cardiovascular risk profile. Longitudinal research is needed to reconcile these findings with the risk of cardiovascular events at the higher end of the endurance exercise spectrum.
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