Publications by authors named "Juana Lopez"

Lipid nanoparticles (LNPs) are successfully used for RNA-based gene delivery. In the context of gene replacement therapies, however, delivery of DNA expression plasmids using LNPs as a non-viral vector could be a promising strategy for the induction of longer-lasting effects. Therefore, DNA expression plasmids (3 to 4 kbp) coding for fluorescent markers or luciferase were combined with LNPs.

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Article Synopsis
  • - Factor H-related proteins, especially FHR-1, play a role in complement activation and are linked to medical conditions like atypical hemolytic uremic syndrome (aHUS) by competing with Factor H for binding with C3b.
  • - Researchers studied FHR-1 mutants, finding that aHUS-associated variants can bind sialic acids, enhancing their ability to compete with Factor H, which leads to increased complement activation.
  • - The study highlights that higher FHR-1 activity compared to Factor H may lead to uncontrolled complement activation and potential diseases due to an imbalance in their activity ratios.
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The American mink, , is an invasive species in Chile. Its impact on native fauna and public health has not been studied in depth in the country. In this study, we searched for gastrointestinal parasites, including helminths and zoonotic sp.

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Lafora disease (LD) is a fatal progressive epilepsy essentially caused by loss-of-function mutations in the glycogen phosphatase laforin or the ubiquitin E3 ligase malin. Glycogen in LD is hyperphosphorylated and poorly hydrosoluble. It precipitates and accumulates into neurotoxic Lafora bodies (LBs).

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Background: Using their voices in inappropriate working conditions causes teachers to misuse their voices, because in order to be heard they need to force their voices.

Objective: This preliminary study examines the effects of a short-term voice training program aimed at teachers.

Methods: The pre- and posttraining evaluations consisted of acoustic, perceptual (GRBAS [grade, roughness, breathiness, asthenia, and strain]), aerodynamic, and subjective measurements (VHI-10).

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In order to provide tools for future health-based monitoring programs, we developed reference intervals for hematology and plasma biochemistry and partitioned data for sex and season (winter and autumn). Ninety-one physically healthy kelp gulls (Larus dominicanus) were sampled in the city of Talcahuano, Chile, during winter (July-September) of 2007, autumn (April-June) and winter of 2008, and autumn of 2009. After blood sampling, the kelp gulls were euthanized by cervical dislocation.

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Lafora progressive myoclonus epilepsy (Lafora disease) is a fatal autosomal recessive neurodegenerative disorder characterized by the presence of glycogen-like intracellular inclusions called Lafora bodies. The vast majority of patients carry mutations in either the EPM2A or EPM2B genes, encoding laforin, a glucan phosphatase, and malin, an E3 ubiquitin ligase, respectively. Although the precise physiological role of these proteins is not fully understood, work in past years has established a link between glycogen synthesis, Lafora bodies formation and Lafora disease development.

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The Gulf of California is one of the most fish diverse areas of the Tropical Eastern Pacific Ocean. In spite of its economic value, few works have considered fish community studies for optimum management. With the aim to determine the seasonal and spatial variation of fish communities in eight locations around the San José Island, some ecological research was conducted from March 2001 to February 2002.

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Lafora disease (LD), a fatal neurodegenerative disorder characterized by intracellular inclusions called Lafora bodies (LBs), is caused by recessive loss-of-function mutations in the genes encoding either laforin or malin. Previous studies suggested a role of these proteins in regulating glycogen biosynthesis, in glycogen dephosphorylation and in the modulation of intracellular proteolytic systems. However, the contribution of each of these processes to LD pathogenesis is unclear.

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Lafora disease (LD), a fatal neurodegenerative disorder characterized by the presence of intracellular inclusions called Lafora bodies (LBs), is caused by loss-of-function mutations in laforin or malin. Previous studies suggested a role of these proteins in the regulation of glycogen biosynthesis, in glycogen dephosphorylation and in the modulation of the intracellular proteolytic systems. However, the contribution of each of these processes to LD pathogenesis is unclear.

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The mechanics of hMSH2-hMSH6 ATP binding and hydrolysis are critical to several proposed mechanisms for mismatch repair (MMR), which in turn rely on the detailed coordination of ATP processing between the individual hMSH2 and hMSH6 subunits. Here we show that hMSH2-hMSH6 is strictly controlled by hMSH2 and magnesium in a complex with ADP (hMSH2(magnesium-ADP)-hMSH6). Destabilization of magnesium results in ADP release from hMSH2 that allows high affinity ATP binding by hMSH6, which then enhances ATP binding by hMSH2.

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A 32-year-old woman with no structural heart disease was referred for evaluation due to daily occasional palpitations and documented left bundle branch block (LBBB) on surface electrocardiogram (EKG). Continuous 24-hour Holter monitoring revealed a broad range of repetitive intermittent LBBB grades with a rate-dependent pattern that was also associated with circadian variations.

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A high prevalence of obstructive sleep apnea has been demonstrated in patients with atrial fibrillation. Our comments want to emphasize the importance of identifying and treating a large proportion of patients with atrial fibrillation who have undiagnosed obstructive sleep apnea as an additional preventive strategy for atrial fibrillation patients.

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