995 resultados para METABOLIC COMPLICATIONS
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BACKGROUND: Metabolic syndrome (MetS) associated with psychiatric disorders and psychotropic treatments represents a major health issue. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) is an enzyme that catalyzes tissue regeneration of active cortisol from cortisone. Elevated enzymatic activity of 11β-HSD1 may lead to the development of MetS. METHODS: We investigated the association between seven HSD11B1 gene (encoding 11β-HSD1) polymorphisms and BMI and MetS components in a psychiatric sample treated with potential weight gain-inducing psychotropic drugs (n=478). The polymorphisms that survived Bonferroni correction were analyzed in two independent psychiatric samples (nR1=168, nR2=188) and in several large population-based samples (n1=5338; n2=123 865; n3>100 000). RESULTS: HSD11B1 rs846910-A, rs375319-A, and rs4844488-G allele carriers were found to be associated with lower BMI, waist circumference, and diastolic blood pressure compared with the reference genotype (Pcorrected<0.05). These associations were exclusively detected in women (n=257) with more than 3.1 kg/m, 7.5 cm, and 4.2 mmHg lower BMI, waist circumference, and diastolic blood pressure, respectively, in rs846910-A, rs375319-A, and rs4844488-G allele carriers compared with noncarriers (Pcorrected<0.05). Conversely, carriers of the rs846906-T allele had significantly higher waist circumference and triglycerides and lower high-density lipoprotein-cholesterol exclusively in men (Pcorrected=0.028). The rs846906-T allele was also associated with a higher risk of MetS at 3 months of follow-up (odds ratio: 3.31, 95% confidence interval: 1.53-7.17, Pcorrected=0.014). No association was observed between HSD11B1 polymorphisms and BMI and MetS components in the population-based samples. CONCLUSIONS: Our results indicate that HSD11B1 polymorphisms may contribute toward the development of MetS in psychiatric patients treated with potential weight gain-inducing psychotropic drugs, but do not play a significant role in the general population.
MetaNetX.org: a website and repository for accessing, analysing and manipulating metabolic networks.
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SUMMARY: MetaNetX.org is a website for accessing, analysing and manipulating genome-scale metabolic networks (GSMs) as well as biochemical pathways. It consistently integrates data from various public resources and makes the data accessible in a standardized format using a common namespace. Currently, it provides access to hundreds of GSMs and pathways that can be interactively compared (two or more), analysed (e.g. detection of dead-end metabolites and reactions, flux balance analysis or simulation of reaction and gene knockouts), manipulated and exported. Users can also upload their own metabolic models, choose to automatically map them into the common namespace and subsequently make use of the website's functionality. Availability and implementation: MetaNetX.org is available at http://metanetx.org. CONTACT: help@metanetx.org.
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Objective:We investigated to what extent changes in metabolic rate and composition of weight loss explained the less-than-expected weight loss in obese men and women during a diet-plus-exercise intervention.Design:In all, 16 obese men and women (41±9 years; body mass index (BMI) 39±6 kg m(-2)) were investigated in energy balance before, after and twice during a 12-week very-low-energy diet(565-650 kcal per day) plus exercise (aerobic plus resistance training) intervention. The relative energy deficit (EDef) from baseline requirements was severe (74%-87%). Body composition was measured by deuterium dilution and dual energy X-ray absorptiometry, and resting metabolic rate (RMR) was measured by indirect calorimetry. Fat mass (FM) and fat-free mass (FFM) were converted into energy equivalents using constants 9.45 kcal per g FM and 1.13 kcal per g FFM. Predicted weight loss was calculated from the EDef using the '7700 kcal kg(-1) rule'.Results:Changes in weight (-18.6±5.0 kg), FM (-15.5±4.3 kg) and FFM (-3.1±1.9 kg) did not differ between genders. Measured weight loss was on average 67% of the predicted value, but ranged from 39% to 94%. Relative EDef was correlated with the decrease in RMR (R=0.70, P<0.01), and the decrease in RMR correlated with the difference between actual and expected weight loss (R=0.51, P<0.01). Changes in metabolic rate explained on average 67% of the less-than-expected weight loss, and variability in the proportion of weight lost as FM accounted for a further 5%. On average, after adjustment for changes in metabolic rate and body composition of weight lost, actual weight loss reached 90% of the predicted values.Conclusion:Although weight loss was 33% lower than predicted at baseline from standard energy equivalents, the majority of this differential was explained by physiological variables. Although lower-than-expected weight loss is often attributed to incomplete adherence to prescribed interventions, the influence of baseline calculation errors and metabolic downregulation should not be discounted.
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Abstract : Fructose is a simple sugar, whose consumption has increased over the past decades. In rodents, a high-fructose diet (HFrD) induces several features of the metabolic syndrome. The aim of the studies included in this thesis was to investigate the metabolic effects of a HFrD in humans, with a focus on insulin sensitivity and ectopic fat deposition. Moreover, we addressed the question whether these effects may differ between individuals according to gender and the genetic background. The first study was designed to evaluate the impact of a 4-week HFrD on insulin sensitivity and lipid metabolism in 7 healthy men. Insulin sensitivity, intrahepatocellular lipids (IHCL) and intramyocellular lipids (IMCL) contents were measured before and after 1 and 4 weeks of HFrD (1.5 g fructose/kg body weight/day). Insulin sensitivity was assessed by a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H-magnetic resonance spectroscopy (MRS). Fructose caused significant (P<0.05) increases in fasting plasma concentrations of triacylglycerol (TG) (+36%), VLDL-TG (+72%) and glucose (+6%) without any change in body weight, IHCL, IMCL, and insulin sensitivity. In the second study, muscle biopsies were taken from five of these healthy male subjects before and after 4 weeks of HFrD. mRNA concentrations of 18 genes involved in lipid and carbohydrate metabolism were quantified by real-time quantitative PCR. We found that a 4-week HFrD increased the expression of genes involved in lipid synthesis, while it decreased those involved in insulin sensitivity and lipid oxidation; these molecular changes maybe early markers of insulin resistance and altered lipid metabolism. The third study aimed at delineating whether male and females equally respond to a HFrD. For this purpose, higher doses of fructose (twice the dose of the previous study) were provided to 8 healthy young males and 8 healthy young females over 6 days. HFrD significantly increased fasting TG in males (+71 %), whereas this increase was markedly blunted in females (+16%). Males also developed hepatic insulin resistance, characterized by increased hepatic glucose output (+12%), and showed higher alanine aminotransferase concentration (+38%), but none of these effect was observed in females. This study suggests that short-term HFrD leads to hypertriglyceridemia and hepatic insulin resistance in men, but premenopausal women seem protected against these effects. Finally, the fourth study investigated whether healthy offspring of type 2 diabetic patients (OffT2D), a subgroup of individuals prone to metabolic disorders due to their genetic background, may have exacerbated response to HFrD. Eight healthy males (Ctrl) and 16 OffT2D received a HFrD and isocaloric diet in a randomized order. In both groups, HFrD significantly increased IHCL (Ctrl: +76%; OffT2D: +79%) and fasting plasma VLDL-TG (Ctrl: +51 %; OffT2D: +110%). In absolute values, these increments were significantly higher in OffT2D, suggesting that these individuals may be more prone to developing metabolic disorders when challenged by high fructose intake. In order to better delineate the specific effects of fructose vs the hypercaloric energy content, we repeated the complete metabolic investigations after an isocaloric high glucose diet in four of the eight Ctrl volunteers. After a high glucose diet, TG and IHCL concentrations remained similar to the control values, in contrast to the marked increases observed after the HFrD. In conclusion, the studies included in this thesis provided novel insights into the metabolic effects of fructose in humans. They showed that fructose may rapidly increase fasting VLDL-TG, IHCL and lead to hepatic insulin resistance; these effects seem specific to fructose, and potential mechanisms may involve both stimulation of hepatic de novo lipogenesis and decreased lipid oxidation. Moreover, the results suggest that women seem protected against such deleterious effects, while OffT2D displayed exacerbated response. Résumé : Le fructose est un sucre simple, dont la consommation a augmenté durant les dernières décennies. Dans les modèles animaux, un régime riche en fructose (RRFru) peut induire plusieurs composantes du syndrome métabolique. Le but de cette thèse était d'étudier les effets d'un régime riche en fructose sur la sensibilité à l'insuline et la déposition de lipides ectopiques chez l'humain, et si ces effets variaient selon le genre ou le background génétique. La première étude avait pour but d'évaluer l'effet d'un RRFru d'une durée de 4 semaines sur la sensibilité à l'insuline et le métabolisme des lipides chez des hommes sains. La sensibilité à l'insuline, les lipides intrahépatiques (IHCL) et intramusculaires (IMCL) ont été mesurés avant, et après 1 et 4 semaines du RRFru (1.5 g fructose/kg/jour). La sensibilité à l'insuline a été déterminée par un clamp hyperinsulinémique euglycémique, et les IHCL/IMCL par spectroscopie à résonnance magnétique. Le fructose a augmenté les concentrations plasmatiques à jeun des VLDL- triglycérides (TG) (+72%) et de glucose (+6%), sans induire de changement au niveau de la sensibilité à l'insuline, IHCL ou IMCL. Dans la deuxième étude, des biopsies de muscle squelettique ont été prélevées chez cinq de ces volontaires avant et après les 4 semaines de RRFru. Les concentrations de mRNA de 18 gènes impliqués dans le métabolisme des lipides et des hydrates de carbone ont été mesurées par RT-PCR quantitative. Le RRFru a augmenté l'expression de gènes impliqués dans la synthèse de lipides, et diminué celles de gènes impliqués dans la sensibilité à l'insuline et l'oxydation de lipides. Ces changements pourraient constituer des altérations précoces de la sensibilité à l'insuline et du métabolisme lipidique en réponse au fructose. La troisième étude avait pour but de définir si les réponses au RRFru étaient semblables entre les hommes et les femmes. Pour ceci, des doses plus élevées de fructose ont été administrées à 8 jeunes hommes et 8 jeunes femmes durant 6 jours. Le RRFru a augmenté les TG chez les hommes (+71 %), et de manière nettement plus modeste chez les femmes (+16%). Les hommes ont développé une résistance hépatique à l'insuline, ainsi qu'une augmentation des concentrations d'alanine aminotransférase (+38%), mais aucun de ces effets n'a été observé chez les femmes. Cette étude suggère qu'à court terme, un RRFru mène à une hypertriglycéridémie et résistance hépatique à l'insuline chez l'homme, tandis que les femmes semblent en être protégées. Finalement, la 4ème étude a investigué si des personnes apparentées à des patients diabétiques de type 2 (AppDT2), qui constituent un groupe d'individus à risque de développer des maladies métaboliques en raison de leur background génétique, avaient des réponses plus marquées au RRFru. Huit hommes sains (Ctrl) et 16 AppDT2 on reçu dans un ordre randomisé un RRFru et une diète isocalorique durant 6 jours. Dans les deux groupes, le RRFru a augmenté significativement les IHCL (Ctrl: +76%; AppDT2: +79%) et les VLDL-TG plasmatiques à jeun (Ctrl: +51%; AppDT2: +110%). En valeurs absolues, ces deux augmentations étaient plus importantes dans le groupe des AppDT2, suggérant que ces individus sont plus à risque de développer des problèmes métaboliques suite à un apport de fructose. Afin de définir les effets spécifiques du fructose, quatre des huit sujets Ctrl ont été soumis à un régime riche en glucose. Après le régime riche en glucose, les concentrations de TG et d'IHCL étaient semblables aux valeurs obtenues après une diète isocalorique, contrairement aux nombreux effets observés après le RRFru. En conclusion, ces différentes études ont démontré que chez l'humain, le fructose peut rapidement induire une augmentation des VLDL-TG à jeun, des IHCL et une résistance hépatique à l'insuline ; ces effets semblent être spécifiques au fructose. De plus, les différents résultats obtenus montrent que les femmes développent des effets moindres en réponse au fructose, contrairement aux AppDT2, chez qui les effets du fructose semblent plus marqués. Résumé grand public : Le fructose est un sucre simple, présent naturellement et en faibles quantités dans les fruits, mais également constituant du sucrose - appelé aussi sucre de table. Depuis les années 1970, la consommation de fructose a augmenté dans les pays industrialisés et émergents, principalement par le biais d'une hausse de consommation de boissons sucrées de type soda. Dans des modèles animaux tels que les rongeurs, un régime riche en fructose mène au développement de plusieurs facteurs de risques étroitement liés aux maladies cardiovasculaires, à l'obésité et au diabète de type 2; ceux-ci sont caractérisés par une augmentation des concentrations de glucose et de lipides sanguins, ainsi qu'une accumulation de lipides dits « ectopiques », à savoir dans le foie et les muscles. Le but de cette thèse était de définir les effets d'un régime riche en fructose chez l'être humain. De plus, nous nous sommes intéressés à savoir si ces effets étaient semblables entre différents groupes d'individus, à savoir des personnes de sexe masculin / féminin, ou des personnes dont au moins un des parents est diabétique de type 2. Pour ceci, différents groupes de volontaires (hommes, femmes, avec histoire familiale de diabète de type 2) âgés de 18-30 ans se sont soumis à une alimentation enrichie en fructose, d'une durée allant de 6 à 28 jours, suivant l'étude à laquelle ils participaient. La quantité de fructose consommée en plus de l'alimentation normale durant ces périodes équivalait au contenu en fructose de 2-4 litres de boissons sucrées par jour. Des prises de sang ont été effectuées au terme de chacun de ces différents régimes, ainsi que des mesures de sensibilité à l'insuline et de concentrations de lipides dans le foie et le muscle par résonnance magnétique nucléaire, en collaboration avec l'Hôpital de l'Ile de Berne. Les résultats montrent qu'après 6 jours de régime riche en fructose, les volontaires sains de sexe masculin ont presque doublé leurs concentrations de lipides sanguins et hépatiques. De plus, le foie de ces volontaires réagissait moins bien à l'insuline, ce qui pourrait mener à long terme à des maladies métaboliques comme le diabète de type 2. Un des mécanismes postulés est que le fructose pourrait stimuler la formation de lipides dans le foie, contribuant ainsi à un dysfonctionnement de cet organe. De manière surprenante, des femmes d'âge et d'IMC (Indice de Masse Corporelle) comparables aux hommes étudiés n'ont pas développé ces différents effets en réponse au régime riche en fructose. Il semblerait donc qu'elles possèdent certaines propriétés pouvant les «protéger », du moins à court terme, des problèmes métaboliques induits par le fructose. De tels mécanismes sont pour l'heure inconnus, mais il est possible que des différences hormonales, ou de répartition de la masse graisseuse dans le corps, puissent jouer un rôle. Enfin, nous avons également démontré que chez certaines personnes ayant au moins un parent (père ou mère) diabétique de type 2, les augmentations de lipides sanguins et hépatiques induits par le fructose étaient plus marquées que chez des volontaires sans parents diabétiques. Ceci est néanmoins à tempérer par le fait que nous avons observé une grande hétérogénéité des réponses parmi ces individus, découlant certainement d'interactions complexes entre différents facteurs tels que la génétique, le mode de vie, l'alimentation et l'activité physique. Ces différents résultats donnent lieu à une meilleure compréhension du rôle de facteurs alimentaires dans le développement de problèmes métaboliques tels que le diabète de type 2. Ils vont également permettre de tester différentes approches thérapeutiques. Bien qu'ayant été obtenus avec des doses de fructose importantes, ces études soulignent l'effet potentiellement dangereux pour la santé d'une alimentation riche en sucres.
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The scientific evidence, demonstrates that the obesity reduces the possibility that a woman, conceive naturally and diminishes the success of the treatment for the fertility. Nurses of the Unit of Attended Reproduction and of the Units of Nutrition and Dietary, they consider necessary to design an educational program of Formation and Information, to change attitudes related with the overweight and the obesity, in even not fertile. The strategy of this Program is based in the control and reduction of the weight, assuring the adhesion to the treatment of fertility, with interactive works shops for the change of alimentary habits, giving emotional support and indications to practice adapted physical exercise. This Nursing Intervention is applied like one tool that develops abilities for the learning and training; never using diets or products of the denominated miracle. The narrow collaboration and investigating participation among the nurses of these Units, bear the design of a methodology channeled to the obtaining of some prospective results that can be evaluated regarding the obtained results.
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Background: We aim to investigate the possibility of using 18F-positron emission tomography/computer tomography (PET-CT) to predict the histopathologic response in locally advanced rectal cancer (LARC) treated with preoperative chemoradiation (CRT). Methods: The study included 50 patients with LARC treated with preoperative CRT. All patients were evaluated by PET-CT before and after CRT, and results were compared to histopathologic response quantified by tumour regression grade (patients with TRG 1-2 being defined as responders and patients with grade 3-5 as non-responders). Furthermore, the predictive value of metabolic imaging for pathologic complete response (ypCR) was investigated. Results: Responders and non-responders showed statistically significant differences according to Mandard's criteria for maximum standardized uptake value (SUVmax) before and after CRT with a specificity of 76,6% and a positive predictive value of 66,7%. Furthermore, SUVmax values after CRT were able to differentiate patients with ypCR with a sensitivity of 63% and a specificity of 74,4% (positive predictive value 41,2% and negative predictive value 87,9%); This rather low sensitivity and specificity determined that PET-CT was only able to distinguish 7 cases of ypCR from a total of 11 patients. Conclusions: We conclude that 18-F PET-CT performed five to seven weeks after the end of CRT can visualise functional tumour response in LARC. In contrast, metabolic imaging with 18-F PET-CT is not able to predict patients with ypCR accurately
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The current drug options for the treatment of chronic Chagas disease have not been sufficient and high hopes have been placed on the use of genomic data from the human parasite Trypanosoma cruzi to identify new drug targets and develop appropriate treatments for both acute and chronic Chagas disease. However, the lack of a complete assembly of the genomic sequence and the presence of many predicted proteins with unknown or unsure functions has hampered our complete view of the parasite's metabolic pathways. Moreover, pinpointing new drug targets has proven to be more complex than anticipated and has revealed large holes in our understanding of metabolic pathways and their integrated regulation, not only for this parasite, but for many other similar pathogens. Using an in silicocomparative study on pathway annotation and searching for analogous and specific enzymes, we have been able to predict a considerable number of additional enzymatic functions in T. cruzi. Here we focus on the energetic pathways, such as glycolysis, the pentose phosphate shunt, the Krebs cycle and lipid metabolism. We point out many enzymes that are analogous to those of the human host, which could be potential new therapeutic targets.
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This document summarizes the issues raised in a think-tank meeting held by professionals with expertise in pediatric Home Parenteral Nutrition. This nutritional technology enables patients to return home to their family and social environment, improves their quality of life and decreases health-care costs; however, it is complex and requires an experienced nutritional support team. Patient selection is normally made according to their underlying disease, the estimated duration of support and family and social characteristics. The patient''s family must agree to take on caregiver's responsibilities and should be able to perform treatment safely and effectively after receiving proper training from the nutritional support team. Close monitoring must be carried out to ensure tolerance and effectiveness of nutritional support, thereby avoiding complications. This nutritional treatment achieves, in most cases, recovery and intestinal adaptation in varying periods of time. In certain diseases, and when home parenteral nutrition becomes complicated, intestinal transplant may be recommendable, so referral to rehabilitation units and Intestinal Transplantation should be made early on.
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Home enteral nutrition (HEN) is a type of enteral nutrition (EN) which is becoming progressively more widespread in pediatrics due to the benefits it affords to patients, their families and to reducing hospital costs. However, the true extent of its use is unknown in Spain as the data-base set up for this purpose is still underused (Registro de Nutrición Enteral Pediátrica Ambulatoria y Domiciliaria -NEPAD-). More thorough registration of patients in the NEPAD online register will provide information about the characteristics of HEN in Spain: prevalence, diagnosis, the population sector being administered HEN, complications and developments. Likewise, forecast and planning of the necessary resources could be made while those in use could be analysed.
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Trypanosoma cruzi infection of the adipose tissue of mice triggers the local expression of inflammatory mediators and a reduction in the expression of the adipokine adiponectin. T. cruzi can be detected in adipose tissue by PCR 300 days post-infection. Infection of cultured adipocytes results in increased expression of cytokines and chemokines and a reduction in the expression of adiponectin and the peroxisome proliferator-activated receptor ³, both of which are negative regulators of inflammation. Infection also results in the upregulation of cyclin D1, the Notch pathway, and extracellular signal-regulated kinase and a reduction in the expression of caveolin-1. Thus, T. cruzi infection of cultured adipocytes leads to an upregulation of the inflammatory process. Since adiponectin null mice have a cardiomyopathic phenotype, it is possible that the reduction in adiponectin contributes to the pathogenesis of chagasic cardiomyopathy. Adipose tissue may serve as a reservoir for T. cruzi from which parasites can become reactivated during periods of immunosuppression. T. cruzi infection of mice often results in hypoglycemia. In contrast, hyperglycemia as observed in diabetes results in increased parasitemia and mortality. Adipose tissue is an important target tissue of T. cruzi and the infection of this tissue is associated with a profound impact on systemic metabolism, increasing the risk of metabolic syndrome.
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Current applications of cardiac magnetic resonance (CMR) imaging offer a wide spectrum of indications in the setting of acute cardiac care. In particular, CMR is helpful for the differential diagnosis of chest pain by detection of myocarditis and pericarditis. Also, takotsubo cardiomyopathy and acute aortic diseases can be evaluated by CMR and are important differential diagnoses in patients with acute chest pain. In patients with restricted windows for echocardiography, CMR is the method of choice to evaluate complications of acute myocardial infarction (AMI). In AMI, CMR allows for a unique characterization of myocardial damage by quantifying necrosis, microvascular obstruction, oedema (=area at risk), and haemorrhage. These capabilities will help us to understand better the pathophysiological events during infarction and will also allow to assess new treatment strategies in AMI. To what extent the information on tissue damage will guide patient management is not yet clear and further research in this field is warranted. In the near future, CMR will certainly become more routine in acute cardiac care units, as manufacturers are now focusing strongly on this aspect of user-friendliness. Finally, in the next decade or so, MRI of other nuclei such as fluorine and carbon might become a clinical reality, which would allow for metabolic and targeted molecular imaging with excellent sensitivity and specificity
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BACKGROUND Obesity is the most frequent metabolic disease in the World, and is associated with several comorbidities. Bariatric procedures arise as a promising treatment when classical approach is ineffective. Half of the operated patients are reproductive-aged women and there is evidence that obesity is related to worse maternal and fetal outcomes. Because nutritional status is affected by bariatric surgery and is a vital component during pregnancy, the aim of our study is to asses the impact of bariatric surgery on pregnancy in these patients. MATERIAL AND METHODS We studied 10 women and 15 pregnancies following bariatric surgery between 2003 and 2009. The visits took place every three months by an obstetrician and an endocrinologist with experience in nutrition, recording clinical features and lab work. RESULTS We found iron deficiency in 80% of the pregnancies, vitamin D in 46,7%, vitamin A in 20%, vitamin E in 13,3% and vitamin B12 in 26,7%. There were no complications during pregnancy, except one case of gravidic hiperemesis. There were nine deliveries without malformations, three of them were small for gestational age newborns and one suffered aspiration pneumonia. There were three stillbirths and one preterm delivery with fetal death. CONCLUSIONS our results show fewer complications during pregnancy in these women than obese women and similar to general population.
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Nutritional support in acute renal failure must take into account the patient's catabolism and the treatment of the renal failure. Hypermetabolic failure is common in these patients, requiring continuous renal replacement therapy or daily hemodialysis. In patients with normal catabolism (urea nitrogen below 10 g/day) and preserved diuresis, conservative treatment can be attempted. In these patients, relatively hypoproteic nutritional support is essential, using proteins with high biological value and limiting fluid and electrolyte intake according to the patient's individual requirements. Micronutrient intake should be adjusted, the only buffering agent used being bicarbonate. Limitations on fluid, electrolyte and nitrogen intake no longer apply when extrarenal clearance techniques are used but intake of these substances should be modified according to the type of clearance. Depending on their hemofiltration flow, continuous renal replacement systems require high daily nitrogen intake, which can sometimes reach 2.5 g protein/kg. The amount of volume replacement can induce energy overload and therefore the use of glucose-free replacement fluids and glucose-free dialysis or a glucose concentration of 1 g/L, with bicarbonate as a buffer, is recommended. Monitoring of electrolyte levels (especially those of phosphorus, potassium and magnesium) and of micronutrients is essential and administration of these substances should be individually-tailored.
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BACKGROUND: The Contegra® is a conduit made from the bovine jugular vein and then interposed between the right ventricle and the pulmonary artery. It is used for cardiac malformations in the reconstruction of right ventricular outflow tract. OBJECTIVE: To describe both normal and pathological appearances of the Contegra® in radiological imaging, to describe imaging of complications and to define the role of CT and MRI in postoperative follow-up. MATERIALS AND METHODS: Forty-three examinations of 24 patients (17 boys and 7 girls; mean age: 10.8 years old) with Contegra® conduits were reviewed. Anatomical description and measurements of the conduits were performed. Pathological items examined included stenosis, dilatation, plicature or twist, thrombus or vegetations, calcifications and valvular regurgitation. Findings were correlated to the echographic gradient through the conduit when available. RESULTS: CT and MR work-up showed Contegra® stenosis (n = 12), dilatation (n = 9) and plicature or twist (n = 7). CT displayed thrombus or vegetations in the Contegra® in three clinically infected patients. Calcifications of the conduit were present at CT in 12 patients and valvular regurgitation in three patients. The comparison between CT and/or MR results showed a good correlation between the echographic gradient and the presence of stenosis in the Contegra®. CONCLUSION: CT and MR bring additional information about permeability and postoperative anatomy especially when echocardiography is inconclusive. Both techniques depict the normal appearance of the conduit, and allow comparison and precise evaluation of changes in the postoperative follow-up.
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Several epidemiological studies have related an increase of lipids in the postprandial state to an individual risk for the development of CVD, possibly due to the increased plasma levels of TAG and fatty acids (FA) through enzymes of FA metabolism. The interaction between nutrition and the human genome determines gene expression and metabolic response. The aim of the present study was to evaluate the influence of a fat overload on the gene mRNA levels of lipogenic regulators in peripheral blood mononuclear cells (PBMC) from patients with the metabolic syndrome. The study included twenty-one patients with criteria for the metabolic syndrome who underwent a fat overload. Measurements were made before and after the fat overload of anthropometric and biochemical variables and also the gene mRNA levels of lipogenic factors. The main results were that the fat overload led to an increased mRNA levels of sterol regulatory element binding protein-1 (SREBP1), retinoid X receptor α (RXRα) and liver X receptor α (LXRα) in PBMC, and this increase was associated with the FA synthase (FASN) mRNA levels. We also found that TAG levels correlated with FASN mRNA levels. In addition, there was a positive correlation of SREBP1 with RXRα and of LXRα with the plasma lipoperoxide concentration. The fat overload led to an increase in regulators of lipogenesis in PBMC from patients with the metabolic syndrome.