14 research outputs found

    The Italian Museo Nazionale dell’Antartide

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    These abstract proceedings were produced based on the program for the POLAR2018 SCAR/IASC Open Science Conference, updated until 25 May 2018

    Modulation of Mrp1 (ABCc1) and Pgp (ABCb1) by Bilirubin at the Blood-CSF and Blood-Brain Barriers in the Gunn Rat

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    Accumulation of unconjugated bilirubin (UCB) in the brain causes bilirubin encephalopathy. Pgp (ABCb1) and Mrp1 (ABCc1), highly expressed in the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) respectively, may modulate the accumulation of UCB in brain. We examined the effect of prolonged exposure to elevated concentrations of UCB on expression of the two transporters in homozygous, jaundiced (jj) Gunn rats compared to heterozygous, not jaundiced (Jj) littermates at different developmental stages (2, 9, 17 and 60 days after birth). BBB Pgp protein expression was low in both jj and Jj pups at 9 days (about 16–27% of adult values), despite the up-regulation in jj animals (2 and 1.3 fold higher than age matched Jj animals at P9 and P17–P60, respectively); Mrp1 protein expression was barely detectable. Conversely, at the BCSFB Mrp1 protein expression was rather high (60–70% of the adult values) in both jj and Jj at P2, but was markedly (50%) down-regulated in jj pups starting at P9, particularly in the 4th ventricle choroid plexuses: Pgp was almost undetectable. The Mrp1 protein down regulation was accompanied by a modest up-regulation of mRNA, suggesting a translational rather than a transcriptional inhibition. In vitro exposure of choroid plexus epithelial cells obtained from normal rats to UCB, also resulted in a down-regulation of Mrp1 protein. These data suggest that down-regulation of Mrp1 protein at the BSCFB, resulting from a direct effect of UCB on epithelial cells, may impact the Mrp1-mediated neuroprotective functions of the blood-cerebrospinal fluid barrier and actually potentiate UCB neurotoxicity

    Un approccio ecosostenibile alla progettazione edilizia. Il protocollo di valutazione energetico-ambientale (VEA) della regione Friuli Venezia Giulia

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    L'obiettivo di progettare e costruire organismi edilizi secondo criteri di ecosostenibilit\ue0 ha portato, nell'ultimo decennio, ad un'evoluzione delle forme architettoniche degli stessi organismi e delle soluzioni tecnologiche dei sistemi costruttivi. Tali sviluppi risultano dovuti anche all'emanazione di una specifica normativa in materia di contenimento dei consumi energetici e di miglioramento della qualit\ue0 ambientale degli organismi edilizi stessi. All'interno di tale ambito il volume, frutto di ricerche sviluppate presso il Dipartimento di ingegneria civile ed ambientale dell'Universit\ue0 di Trieste, si prefigge di individuare e relazionare vari aspetti architettonici, tecnici e funzionali che rientrano nella vasta tematica della progettazione sostenibile. Il presente volume si presta quindi ad un duplice livello di lettura. Il primo illustra le metodologie ed i criteri di certificazione contenuti nel Protocollo di Valutazione energetica ed ambientale (VEA) della Regione Friuli Venezia Giulia, definendo le modalit\ue0 di verifica dei temi trattati in tale documento; il secondo livello invece individua strumenti e strategie per un approccio ad una progettazione architettonica relazionata all'esigenza di salvaguardia ambientale

    Effects of maturation on RNA transcription and protein expression of 4 MRP genes in human placenta and in BeWo cells.

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    The placenta is a multifunctional organ that protects the fetus from toxic compounds and the MRPs contribute to this function. The expression of MRP1, MRP2, MRP3, and MRP5 was compared in human placental tissue and in BeWo cells by real-time RT-PCR analysis; protein expression was assessed by Western blot. MRP1 and MRP3 were the most abundantly expressed genes in placenta but only MRP1 was highly expressed in the BeWo cells. Expression of MRP1 increased 4-fold in the third as compared with first trimester placental samples, and increased 20-fold with polarization of BeWo cells. MRP2, MRP3, and MRP5 were weakly expressed both in placenta and BeWo cells. Protein expression followed mRNA quantification for MRP1 and MRP5 but not for MRP2 and MRP3. These data indicated that MRP1 and MRP5 increase with trophoblast maturation, suggesting a particular role for these proteins in the organ functional development

    Magnetic Resonance Contrast Agents: From the Bench to the Patient.

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    Magnetic Resonance Imaging is gaining a prominent role in the routine clinical investigation. To further improve this technique it is crucial that contrast agents are developed with more optimal organ specificity. This will not only result in a better diagnostic efficiency but also in a reduction of the amount of the agent administered. A combination of techniques has been employed to increase the target selectivity of the contrast agent and thereby the feasibility to visualize different organs. The organ targeting is based on the understanding of the mechanisms involved in the interaction of the agent with plasma proteins (albumin in particular) as well as the different membrane transporters involved in the uptake and in the excretion of the agent from the organ. The physicochemical properties of the contrast agents play a major role in the interaction with these various proteins. In this review we address the relationship between the structure of the contrast agents and their binding to different plasma proteins and membrane transporters in different organs, with special reference to the liver and kidney. The present and potentially future applications of these concepts in the clinical setting are also discussed

    Molecular determinants in the transport of a bile acid derived diagnostic agent in tumoral and non-tumoral cell lines of human liver.

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    Contrast-enhanced magnetic resonance imaging (CE-MRI) is a valuable technique for the diagnosis of liver diseases. As gadocoletic acid trisodium salt (B22956/1), a new contrast agent showing high biliary excretion, may be potentially advantageous in hepatobiliary imaging, the aim of the study was to investigate the molecular mechanisms of hepatic transport of the B22956 ion in a cellular model of hepatic tumor. B22956 ion uptake was measured in tumoral (HepG2) and nontumoral (Chang liver) hepatic cell lines. Absolute quantitative real-time reverse transcriptase (RT)-polymerase chain reaction (PCR) analyses, using cloned PCR products as standards, were performed on total RNA of both cell lines and normal liver to evaluate the transcription of 12 transport genes: SLCO1A2, SLCO2B1, SLCO1B1, SLCO3A1, SLCO4A1, SLCO1B3, SLC22A7, SLC22A8, SLC22A1, SLC10A1, SLC15A1, and SLC15A2. B22956 transport was more efficient in Chang liver than in HepG2 cells and was inhibited by cholecystokinin-8, a specific substrate of OATP1B3. Real-time RT-PCR analyses revealed different transcription profiles in the tumoral and nontumoral cell lines. Compared with normal liver, the expression of SLCO1B1, SLCO3A1, and SLCO1B3 was greatly repressed in HepG2 cells, whereas SLCO2B1, SLC22A7, and SLC22A8 expression was either maintained or increased. On the contrary, in Chang liver cells, SLC22A7 and SLC22A8 genes were undetectable, whereas the expression of SLCO3A1, SLCO4A1, and SLCO1B3 was similar to normal liver. Transport studies and gene expression analyses indicated that B22956 ion is a good substrate to the liver-specific OATP1B3, reported to be poorly expressed or absent in human liver tumors. Therefore, B22956 may be helpful in detecting hepatic neoplastic lesions by CE-MRI

    Propagación de pulsos transionosféricos de señales de satélites GPS

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    Es bien conocido que un perfil ionosférico determinístico y completamente estratificado puede distorsionar las señales GPS (Global Positioning System) poniendo límite a las mediciones geodésicas. En el estudio presente, nos referirnos a la propagación de pulsos o de paquetes de ondas a través de un medio horizontalmente estratificado, como el plasma ionosférico. Aquí obtenemos las ecuaciones de trazado de rayos, calculamos el camino de grupo Y el tiempo de retardo del pulso. Aplicamos en nuestros cálculos el modelo ionosférico Penn State MK3 despreciando los efectos de colisiones, la estratificación esférica y las irregularidades. El modelo escogido describe las partes de las capas ionosféricas en la región del máximo de la densidad electrónica, y mediante la integración numérica se determina el tiempo de retardo del pulso. doi: https://doi.org/10.22201/igeof.00167169p.1992.31.2.58
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