33 research outputs found

    Metabolic effects of the dietary monosaccharides fructose, fructose-glucose, or glucose in mice fed a starch-containing moderate high-fat diet

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    Fructose consumption has been linked to obesity and increased hepatic de novo lipogenesis (DNL). Excessive caloric intake often confounds the results of fructose studies, and experimental diets are generally low-fat diets, not representative for westernized diets. Here, we compared the effects of dietary fructose with those of dietary glucose, in adult male and female mice on a starch-containing moderate high-fat (HF) diet. After 5 weeks fattening on a HF high-glucose (HF-G) diet, mice were stratified per sex and assigned to one of the three intervention diets for 6 weeks: HF high fructose (HF-F), HF with equimolar glucose and fructose (HF-GF), or HF-G. Bodyweight (BW) and food intake were measured weekly. Indirect calorimetry was performed on week 5; animals were sacrificed in food-deprived state on week 6. Data were analyzed within sex. BW gain was similar among animals on the HF-G, HF-GF, and HF-F diets. Cumulative food intake was slightly lower in HF-F animals (both sexes). However, energy expenditure was not affected, or were circulating insulin and glucose concentrations, and hepatic triglyceride levels at endpoint. Hepatic gene expression analysis showed only minor alterations in hexokinase and glycolysis-related expression in males, and no alterations in sugar transporters, or DNL-related enzymes. In females, no consistent alterations in hepatic or small intestine gene expression were seen. Concluding, partial or complete replacement of dietary glucose with fructose does not increase caloric intake, and does not affect BW, hepatic triglyceride levels, or insulin concentrations in male and female mice on a moderate high-fat diet.</p

    In Vitro Evaluation of Enterococcus faecalis Adhesion on Various Endodontic Medicaments

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    E. faecalis in endodontic infection represents a biofilm type of disease, which explains the bacteria’s resistance to various antimicrobial compounds and the subsequent failure after endodontic treatment. The purpose of this study was to compare antimicrobial activities and bacteria kinetic adhesion in vitro for three endodontic medicaments with a clinical isolate of E. faecalis. We devised a shake culture which contained the following intracanalar preparations: CPD, Endoidrox (EIX), PulpCanalSealer (PCS); these were immersed in a liquid culture medium inoculated with the microorganism. The shake system velocity was able to prevent non-specific bacteria adhesion and simulated the salivary flow. Specimens were collected daily (from both the medium and medicaments) for 10 days; the viable cells were counted by plate count, while the adhesion index AI° [E. faecalis fg DNA] /mm2 was evaluated in the pastes after DNA extraction, by quantitative real time PCR for the 16S rRNA gene. A partial growth inhibition, during the first 24 hours, was observed in the liquid medium and on the medicaments for EIX and subsequently for CPD (six logs). EIX showed the lowest adhesion coefficient (5*102 [fg DNA]/mm2) for nine days and was similar to the control. PCS showed no antimicrobial/antibiofilm properties. This showed that “calcium oxide” base compounds could be active against biofilm progression and at least in the short term (2-4 days) on E. faecalis cells growing in planktonic cultures

    Carbohydrates Regulate Virulence Gene Expression in Streptococcus suis

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    Streptococcus suis is a major pig pathogen as well as an emerging zoonotic pathogen. Previous work has demonstrated that the S. suis extracellular amylopullulanase enzyme (ApuA) that degrades {alpha}-glucans also functions as an adhesin for porcine epithelial cells. To identify the mechanisms linking carbohydrate metabolism and virulence, we first compared the transcriptome of S. suis in minimal medium supplemented with glucose to minimal medium containing a complex carbohydrate pullulan as a carbon source. The relative expression of eighteen virulence genes including suilysin and apuA was increased during growth in presence of pullulan, compared to growth in glucose. Increased virulence potential of S. suis grown in pullulan was demonstrated using hemolytic assays and increased adhesion and invasion of porcine epithelial cells in vitro. A metabolic map of S. suis was generated and combined with transcriptome data to visualize the metabolic adaption of S. suis during adhesion and invasion of the porcine epithelial cells representing an in vitro model of infection. The role of carbon catabolite control in virulence gene regulation was investigated and the molecular mechanism of transcriptional regulation was elucidated for apuA. We demonstrate that relief of CcpA repression is a crucial transcriptional control mechanism linking carbohydrate mechanism and virulence. The model for the transcriptional regulation of two important virulence factors apuA and suilysin was verified by qPCR analysis of gene expression in S. suis recovered from the organs and blood of infected pigs

    LA DISCIPLINA OSTETRICA

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    Le premesse di base di questo testo si fondano sui principi fondamentali della disciplina ostetrica: porre l’attenzione sulla salute e il benessere della persona, considerata nella sua globalità. Specificità dell’intervento assistenziale dell’ostetrica/o è di rispondere con autonomia e responsabilità ai bisogni di salute che interessano le manifestazioni/eventi naturali del ciclo della vita: il periodo preconcezionale, la nascita, l’infanzia, l’adolescenza, l’età fertile, la gravidanza, il parto, il puerperio, la menopausa/il climaterio. La pratica ostetrica si basa sulle evidenze scientifiche, che devono essere costantemente aggiornate, e si integra anche con quella di altre figure professionali. Nel volume si evidenziano le teorie, i concetti, i modelli, i progressi assistenziali che rappresentano il sapere guida teorico-pratico dell’esercizio professionale dell’ostetrica/o in ambito ostetrico, neonatale e ginecologico, sia in regime di libera professione o di dipendenza presso le strutture socio-sanitarie pubbliche o private

    LA DISCIPLINA OSTETRICA

    No full text
    Nel volume si evidenziano le teorie, i concetti, i modelli, i progressi assistenziali che rappresentano il sapere guida teorico-pratico dell’esercizio professionale dell’ostetrica/o in ambito ostetrico, neonatale e ginecologic

    Metabolic effects of the dietary monosaccharides fructose, fructose-glucose, or glucose in mice fed a starch-containing moderate high-fat diet

    No full text
    Fructose consumption has been linked to obesity and increased hepatic de novo lipogenesis (DNL). Excessive caloric intake often confounds the results of fructose studies, and experimental diets are generally low-fat diets, not representative for westernized diets. Here, we compared the effects of dietary fructose with those of dietary glucose, in adult male and female mice on a starch-containing moderate high-fat (HF) diet. After 5 weeks fattening on a HF high-glucose (HF-G) diet, mice were stratified per sex and assigned to one of the three intervention diets for 6 weeks: HF high fructose (HF-F), HF with equimolar glucose and fructose (HF-GF), or HF-G. Bodyweight (BW) and food intake were measured weekly. Indirect calorimetry was performed on week 5; animals were sacrificed in food-deprived state on week 6. Data were analyzed within sex. BW gain was similar among animals on the HF-G, HF-GF, and HF-F diets. Cumulative food intake was slightly lower in HF-F animals (both sexes). However, energy expenditure was not affected, or were circulating insulin and glucose concentrations, and hepatic triglyceride levels at endpoint. Hepatic gene expression analysis showed only minor alterations in hexokinase and glycolysis-related expression in males, and no alterations in sugar transporters, or DNL-related enzymes. In females, no consistent alterations in hepatic or small intestine gene expression were seen. Concluding, partial or complete replacement of dietary glucose with fructose does not increase caloric intake, and does not affect BW, hepatic triglyceride levels, or insulin concentrations in male and female mice on a moderate high-fat diet

    Increased expression of c-fos, c-jun and LRF-1 is not required for in vivo priming of hepatocytes by the mitogen TCPOBOP

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    The notion that an increased expression of immediate early genes such as c-fos and c-jun is an absolute requirement for the G(0)-G(1) transition of the hepatocytes has recently been challenged by the finding that rat liver cell proliferation induced by primary mitogens may occur in the absence of such changes (Columbano and Shinozuka, 1996). To further investigate the relationship between immediate early genes and hepatocyte proliferation, we have compared the hepatic levels of c-fos, c-jun and LRF-1 transcripts during mouse liver cell proliferation in two conditions: (i) direct hyperplasia induced by the non-genotoxic hepatocarcinogen 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, and (ii) compensatory regeneration caused by a necrogenic dose of carbon tetrachloride. The results show striking differences in the activation of early genes. In spite of a rapid stimulation of S phase by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (approximately 8% of hepatocytes were BrdU-positive as early as 24 h after mitogen treatment versus 1% of labelled hepatocytes after 2/3 partial hepatectomy), no changes in the expression of c-fos, c-jun and LRF-1 could be observed. Moreover, no change in steady state mRNA hepatic levels of IGFBP-1 (a gene highly expressed in rat liver following partial hepatectomy), and only a slight increase in c-myc and PRL-1, was found after mitogen administration. On the contrary, a rapid, massive and transient increase in the hepatic mRNA levels of all these genes was observed during carbon tetrachloride induced regeneration. The results indicate that increased expression of immediate early genes may be dependent upon the nature of the proliferative stimulus, and it may not be a prerequisite in certain in vivo conditions such as proliferation induced in the absence of liver tissue damage
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