Browsing by Author "Moreno, M."

Now showing 1 - 3 of 3
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    Biglycan Is a New Extracellular Component of the Chordin-Bmp4 Signaling Pathway
    (2005) Moreno, M.; Brandan, Enrique; Larraín Correa, Juan Agustín
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    Decoupled PI Controllers Based on Pulse-Frequency Modulation for Current Sharing in Multi-Phase LLC Resonant Converters
    (2021) Moreno, M.; Pereda Torres, Javier Eduardo; Rojas, F.; Dominguez-Lopez, I.
    The LLC series resonant converter has emerged as a solution to applications requiring power conversion with isolation, reduced volume and high efficiency, such as PV systems and EV chargers. However, the LLC resonant converter is limited in power, so it requires a multi-phase configuration in order to provide higher currents. This configuration connects the outputs of two or more LLC converters in parallel, increasing the output current but introducing imbalance and circulating currents due to the mismatch and tolerance values of components in each resonant tank. This paper proposes a simple PI control scheme to compensate the current imbalance and eliminate circulating currents generated when several LLC resonant converters are connected in parallel. Unlike reported current sharing methods, the proposed control scheme is based on multiple current control loops operating independently, using the switching frequency of each parallel-connected unit as a degree of freedom of the overall converter. The proposed control scheme has been successfully validated under simulations and experimental assessment, implementing two resonant tanks with ±5% tolerance of parameters, providing excellent steady-state and transient performance.
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    Tp53 Abnormalities Are Frequent and Early Events in the Sequential Pathogenesis of Gallbladder Carcinoma
    (2005) Moreno, M.; Pimentel González, Eduardo Fernando; Gazdar, Adi F.; Wistuba Oyarzun, Ignacio; Miquel Poblete Juan Francisco
    Background: Gallbladder carcinoma (GBC) is a frequent neoplasm in Hispanic and native American populations. GBC is preceded by gallstones, chronic cholecystitis and dysplastic changes of the gallbladder epithelium. The knowledge of the molecular events involved in its pathogenesis is scarce. Aims: We investigated the role of TP53 inactivation in the sequential pathogenesis of GBC. Methods: Invasive tumor-, dysplastic- and histologically normal GB ep ithelial-cells were obtained from archival formalin fixed tissues from GBC and GB from gallstone pa tients without GBC. Normal GB epithelia from 5 non-gallstone specimens were also studied. DNA extracted was examined for loss of heterozygosity (LOH) using 2 microsatellite markers and for TP53 mutations at exons 5 to 8. Results: GBCs demonstrated a high frequency of LOH (81%) and mutation (67%), and both abnormalities indicating gene inactivation were detected in 52%. Similar frequency of TP53 Abnormalities are frequent and early events in the sequential pathogenesis of gallbladder carcinomaivation (38%) were detected in their accompanying normal and dysplastic epithelia. Noteworthy, one third of normal and dysplastic epithelia obtained from GBs of gallstone patients without GBC demonstrated either TP53 allele loss or mutation, but gene inactivation was less frequent (11%). Most mutations affected exons 5 and 7, and they were more frequently missense point mutations. The same TP53 mutation was de tected in only a subset (27%) of comparisons between non-malignant epithelia adjacent to GBCs, indicating that TP53 mutation occurs independently at several epithelial foci. Conclusions: These findings indicate that TP53 abnormalities are early and frequent events in the pathogenesis of GBC, starting from chronic cholecystitis.