Abstract
Oxysterols are oxidized species of cholesterol coming from exogenous (e.g. dietary) and endogenous (in vivo) sources. They play critical roles in normal physiologic functions such as ...regulation of cellular cholesterol homeostasis. Most of biological effects are mediated by interaction with nuclear receptor LXRα, highly expressed in the liver as well as in many other tissues. Such interaction participates in the regulation of whole-body cholesterol metabolism, by acting as "lipid sensors". Moreover, it seems that oxysterols are also suspected to play key roles in several pathologies, including cardiovascular and inflammatory disease, cancer, and neurodegeneration. Growing evidence suggests that oxysterols may contribute to liver injury in non-alcoholic fatty liver disease. The present review focuses on the current status of knowledge on oxysterols' biological role, with an emphasis on LXR signaling and oxysterols' physiopathological relevance in NAFLD, suggesting new pharmacological development that needs to be addressed in the near future.
An increased mitochondrial proton leak occurs in aging, but the origin of such modification remains unclear. This study defined the cause of mitochondrial uncoupling in mitotic (liver) and ...postmitotic (heart) rat tissues during aging and its effects on energy homeostasis and free radical production. Proton leak in old heart mitochondria was dependent on uncoupling proteins' upregulation, whereas it was caused by alterations in the mitochondrial membrane composition in old liver. ATP homeostasis was impaired in both tissues from old animals and was associated to disrupted F0F1-ATPase activity. H2O2 production rate and 4-hydroxy-2-nonenalprotein adducts were higher in old liver mitochondria compared with young liver mitochondria, but they were similar in heart mitochondria from both groups. Moreover, key mitochondrial biogenesis regulators were upregulated in old liver but downregulated in old heart. In conclusion, uncoupling proteins mediate proton leak and avoid oxidative damage in heart, acting as a protective mechanism. This does not occur in liver, where ATP depletion and oxidative stress may stimulate mitochondrial biogenesis and eliminate damaged cells.
The Italian law about waste, has recently introduced (L. 28/2012) a new way to classify the waste, taking into account its Ecotoxicity (assignment of hazardous characteristic H14 according to ADR ...criteria). Pending EU guidelines, different procedures have been followed leading to distinct results in the hazardous characterization. The problem is particularly complex in the cases of bottom ashes because of the content of heavy metals potentially hazardous for environment. Due to the nature of bottom ash, it is very difficult to define the exact chemical species of an heavy metal. In order to classify the waste, this aspect is very important since different chemical species of the same metal present different concentration limits to assess the environmental hazard using additive methods. In this study, a comparison between available classification methods is performed, showing their applicability to bottom ashes. It is also shown how the results may change using CLP and ADR criteria.
Non-alcoholic fatty liver disease (NAFLD), a condition that leads to fibrosis, is caused by intake of very high-fat diets (HFDs). However, while the negative impact on the liver of these diets has ...been an issue of interest, systematic research on the effect of HFDs are lacking.
To characterize the overall impact of HFDs on both molecular and morphological signs of liver remodeling.
A study was conducted on male C57BL/6J mice to assess the effect of 4- and 8-week HFDs (60% kcal from fat) on (i) liver steatosis and fibrosis, and (ii) expression of factors involved in inflammation and angiogenesis.
After an 8-week HFD, vascular endothelial growth factor type-2 receptor (VEGF-R2) and fatty acid translocase/trombospondin-1 receptor (CD36) were overexpressed in liver tissue of mice given HFDs. These changes suggest impaired liver angiogenesis and occurred together with (i) increased GPR78-BiP and EIF2α phosphorylation, suggesting endoplasmic reticulum stress, (ii) induction of Col1a1 gene expression, a marker of fibrosis, and (iii) increased CD31 immunolabeling, consistent with active angiogenesis and fibrosis.
Our data show that very HFDs promote a rapid inflammatory response, as well as deregulation of angiogenesis, both consistent with development of liver fibrosis.
This work reports the main results of a bench scale membrane bioreactor operated for more than 100 days without sludge withdrawal and fed on real municipal wastewater. The experiments were oriented ...towards three main objectives. Firstly, the performance of the system was evaluated under two different volumetric loading rates (0.8 and 1.7
g
COD
L
react.
−1
d
−1). Secondly, biomass growth and accumulation of solids were assessed and a relationship between sludge concentration and volumetric loading rates was proposed. Thirdly, biomass activity was evaluated through respirometric tests, and endogenous and maximum respiration rates of heterotrophic and nitrifying bacteria were determined. The experimental campaign showed that these systems are easy to manage and very rapid to start-up. The SS concentrations under equilibrium conditions for both experimental periods were slightly lower than 10 times the volumetric loading rates, and the organic loading rates reached the same equilibrium value of 0.12
g
COD
g
TSS
−1
d
−1. Furthermore, under equilibrium conditions the system showed very limited sludge production (0.12
g
VSS
g
COD
rem
−1) and low biomass activity, although it readily responded to load variations. Further work is being carried out to evaluate the performance over the long term.
The removal of odours from wastewater treatment plants through diffusion of odour-containing air volumes into the aerated basins was investigated in a bench scale experimental campaign which lasted ...more than 200 days. Hydrogen sulphide was selected as a model odorous compound and its removal efficiencies were experimentally evaluated along with its effects on the biomass and on the main biochemical processes. Two bench scale sequencing batch reactors were fed in parallel on real primary sewage and monitored for chemical oxygen demand removal, nitrification and denitrification. The balance of H
2
S was also monitored after adding to one of them a Na
2
S liquid solution of 17 mgS l
reactor
−1
d
−1
, corresponding to a gas-phase concentration of 240 mgS (Nm
3
)
−1
. Results showed an average sulphide removal of 94% in the reactor supplied with Na
2
S. Moreover, microbial composition did not show relevant variations after the addition of sulphide, and the good features of activated sludge flocs were maintained also in terms of sludge settleability. No relevant effects of sulphide were detected on carbon and nitrogen metabolism and chemical oxygen demand removal, nitrification and denitrification efficiencies were always above 75%, 95%, and 50% respectively, and comparable across the two reactors.
Non-alcoholic fatty liver disease (NAFLD), a condition that leads to fibrosis, is caused by intake of very high-fat diets (HFDs). However, while the negative impact on the liver of these diets has ...been an issue of interest, systematic research on the effect of HFDs are lacking.
To characterize the overall impact of HFDs on both molecular and morphological signs of liver remodeling.
A study was conducted on male C57BL/6J mice to assess the effect of 4- and 8-week HFDs (60% kcal from fat) on (i) liver steatosis and fibrosis, and (ii) expression of factors involved in inflammation and angiogenesis.
After an 8-week HFD, vascular endothelial growth factor type-2 receptor (VEGF-R2) and fatty acid translocase/trombospondin-1 receptor (CD36) were overexpressed in liver tissue of mice given HFDs. These changes suggest impaired liver angiogenesis and occurred together with (i) increased GPR78-BiP and EIF2α phosphorylation, suggesting endoplasmic reticulum stress, (ii) induction of Col1a1 gene expression, a marker of fibrosis, and (iii) increased CD31 immunolabeling, consistent with active angiogenesis and fibrosis.
Our data show that very HFDs promote a rapid inflammatory response, as well as deregulation of angiogenesis, both consistent with development of liver fibrosis.
El hígado graso no alcohólico (HGNA) es una enfermedad hepática que ocasiona fibrosis y se genera por la ingesta de dietas ricas en grasa. Aunque los efectos nocivos de este tipo de dietas son de gran interés, no son muy abundantes los estudios sistemáticos sobre las consecuencias que su consumo puede tener en el hígado.
Evaluar los efectos de una dieta rica en grasa sobre el remodelado hepático, tanto a nivel morfológico como molecular.
Se utilizaron ratones macho C57BL/6J tratados durante 4/8 semanas con una dieta que contenía un 60% de las kilocalorías procedentes de grasa sobre: 1) la aparición de esteatosis y/o fibrosis hepática y 2) la expresión de factores implicados en procesos de inflamación y angiogénesis.
Tras 8 semanas de dieta se observó un incremento en el receptor del factor de crecimiento vascular endotelial tipo 2 (R2-FCVE) y en la translocasa de ácidos grasos (CD36). Estos cambios, que sugieren que los procesos angiogénicos del hígado están alterados, fueron simultáneos a: 1) un aumento del GPR78-BiP y de la fosforilación de EIF2α, marcadores de estrés del retículo endoplásmico, 2) la inducción en la expresión del gen de colágeno Col1a1, indicador de fibrosis y 3) un incremento de células inmunofluorescentes para CD31 compatible con procesos de angiogénesis y de fibrosis.
Nuestros resultados muestran que las dietas con alto contenido en grasa inducen la rápida activación de respuestas inflamatorias, así como alteraciones en la angiogénesis, siendo ambos procesos compatibles con el desarrollo de fibrosis hepática.
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