Academic literature on the topic 'Ascites'

Cirrhosis is characterized by the progressive development of portal hypertension. Portal hypertension, associated with sodium retention, leads to the formation of ascites. Ascites may be difficult to treat and, thereby, become "refractory". To date, the mortality of patients with refractory ascites remains high. In order to offer patients adequate treatment, it is important to identify complications that may develop and the factors of good and poor prognosis affecting their survival. One can retain five specific complications of cirrhosis with ascites: hepatorenal syndrome, spontaneous bacterial peritonitis, paracentesis induced circulatory dysfunction, hepatic hydrothorax and dilutional hyponatremia. This thesis reported an update of pathogenesis, complications and treatment of refractory ascites. Our original clinical research has, meanwhile, focused on the identification of different prognostic factors in refractory ascites in direct relation to these five complications. We have focused on the effect of the administration of beta blockers in patients with refractory ascites: this treatment is widely prescribed for prevention of gastrointestinal bleeding. It is associated in these patients with higher mortality and a high incidence of paracentesis induced circulatory dysfunction. We specified that the severe hyponatremia, leading to withhold diuretic therapy, is a more accurate prognostic factor than the MELDNa score in refractory ascites. With regard to the hepatorenal syndrome of slow onset (type 2), we emphasized the high frequency of this syndrome in refractory ascites. We showed that there was an association between the level of portal hypertension and the incidence of spontaneous bacterial peritonitis. Furthermore, we demonstrated that the presence of bacterial DNA in ascites of outpatients suffering from refractory ascites was particularly low. The detection of this DNA is not a precursor to infection of ascites. In conclusion, with a systematic analysis of various prognostic factors related to complications of ascites in cirrhotic patients, this work gives a better understanding of their chances of survival. This will allow a more adequate stratification in the decision trees for a cure of the disease such as liver transplantation.<br>Doctorat en Sciences médicales<br>info:eu-repo/semantics/nonPublished

Continuous genetic improvement of growth and conformation traits in broiler populations has coincided with an increase in defects in heart and lung function. These defects have led to an increased incidence of metabolic disorders such as ascites (AS) (or pulmonary hypertension), a functional hypoxia. The incidence of AS in well-managed flocks is low, but it nonetheless causes important economic losses to the breeding industry and is an important issue from a welfare standpoint. The aim of this thesis was to study the genetics of AS-related quantitative traits. A low blood oxygen saturation (SaO) value is a good indicator of AS susceptibility. The existence of substantial genetic (polygenic) variation for SaO was demonstrated for four meat-type chicken lines. Estimates of heritabilities for SaO ranged from 0.1 to 0.2 and additive genetic correlations with production traits were not different from zero. SaO data from one of these lines were analysed using a mixed inheritance model (i.e. including a major locus (MG) and polygenes) and the results suggested that a MG with two alleles at intermediate frequencies affected SaO. The putative MG accounted for a difference of 13% SaO between homozygotes and the decreasing allele was recessive. The MG was also estimated to have an overdominant effect on weight and fleshing score. The mode of action of the putative MG on SaO and production traits would hinder manipulation of its allele frequency without the use of molecular markers. A population was designed to map this putative MG. Power studies were performed to select a number of sires and their half-sib progeny. Sires were selected on the basis of their probability of being heterozygous at the putative MG as estimated by the segregation analysis. Regions around the three ryanodine receptor loci (RYR1, RYR2 and RYR3), which are candidate genes for AS, were chosen to perform a linkage study. No evidence of linkage of any of the regions studied with SaO, as a predictor of AS, was detected.

Le syndrome néphrotique (SN) est causé par une altération glomérulaire, responsable d’une excrétion urinaire anormale de protéines plasmatiques, compliquée d’hypoalbuminémie. Le SN est toujours associé à une rétention rénale de Na + qui conduit à la génération d'ascite et / ou d'œdèmes. La pathogénie de la rétention de Na + et de la constitution d’œdèmes n’est pas entièrement élucidée. Dans notre étude, nous avons évalué le rôle possible des espèces réactives de l'oxygène (ROS) dans cette pathogénie. Notre étude dans le modèle de rat aminonucléoside puromycine (PAN) de SN fournit des éléments de preuve d'un rôle critique des ROS dans les troubles hydro-électrolytiques associés au SN. Dans le rein, l'endocytose de l'albumine anormalement filtrée dans le néphron distal induit un stress oxydatif qui est responsable de l’augmentation de la Na, K-ATPase. Dans le péritoine, le SN est associé à une augmentation marquée de la perméabilité à l'eau et à une diminution du coefficient de réflexion des protéines de la barrière péritonéale. Ces modifications, déclenchées par le stress oxydatif et l'activation subséquente de NF-kB, comptent pour environ deux tiers du volume de l'ascite. Enfin, nous avons confirmé que le stress oxydatif participe à la sécrétion de l'angiotensine-aldostérone et est nécessaire à l’apparition de l'hyperaldostéronémie observée chez les rats PAN-néphrotiques<br>Nephrotic Syndrome (NS) is a nonspecific kidney disorder defined by abnormal urinary excretion of plasma proteins and hypoalbuminemia. NS is always associated with a renal retention of Na+ leading to the generation of ascites and/or edema. The pathogenesis of Na+ retention and edema is not fully elucidated. In our studies we evaluated the possible role of reactive oxygen species (ROS) in this pathogenesis. Our studies in the puromycin aminonucleoside (PAN) rat model of NS provided pieces of evidence for a critical role of ROS in the hydro-electrolytic disorders associated with NS. In the kidney, endocytosis of abnormally filtered albumin in the distal nephron induces an oxidative stress which is responsible for the up-regulation of Na,K-ATPase. In the peritoneum, NS is associated with a marked increase in water permeability and a decrease in the reflection coefficient to proteins of the peritoneal barrier. These changes, which are triggered by oxidative stress and subsequent activation of NF-kB, account for approximately two-third of the volume of ascites. Finally, we confirmed that oxidative stress participates in the angiotensin-stimulated secretion of aldosterone and is required for the hyperaldosteronemia observed in PAN-nephrotic rats

Ovarian cancers often develop resistance mechanisms against the standard platinum and taxane chemotherapy, which indicates the need for novel therapeutics to improve patient outcome. In vitro assays were performed to assess the effects and mechanism of action of a novel peptide, GAP-107B8, on ovarian cancer cell viability. Xenograft models were used to determine GAP-107B8’s effects on tumour burden in immune-incompetent mice. GAP-107B8 significantly reduced cell viability in ovarian cancer cell lines, although no synergistic effects with carboplatin were observed. This reduction in cell viability was due in part to apoptosis and may involve mechanisms leading to decreased pAKT, but without any change in pPKC levels. In vivo, GAP-107B8 had no effect on ovarian tumour burden, but significantly reduced ascites volume. The findings suggest that GAP-107B8 can reduce some malignant characteristics of cancer cells in vitro and in vivo and should be evaluated further as a potential therapeutic for ovarian cancer.