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Search Results: 1 - 10 of 401256 matches for " Zanlungo M "
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Medicina molecular: Presente y futuro
Zanlungo M,Silvana; Arrese J,Marco; Rigotti R,Attilio;
Revista médica de Chile , 1999, DOI: 10.4067/S0034-98871999000800014
Abstract: the genetic background of individuals is recognized as an important clue in the analysis of classical hereditary and multifactorial acquired diseases. this new concept derives from the development and increasing use of molecular genetics in clinical medicine. the application of molecular biology techniques in biomedical investigation has encompassed the identification of the pathogenesis and etiology of diseases, prenatal diagnosis the production of new therapeutic agents, gene therapy and the development of pharmacogenetics. the impact on the fundamentals and practice of clinical medicine that will have the use of molecular biology is analyzed in this review.
Medicina molecular: Presente y futuro Molecular medicine: Present and future
Silvana Zanlungo M,Marco Arrese J,Attilio Rigotti R
Revista médica de Chile , 1999,
Abstract: The genetic background of individuals is recognized as an important clue in the analysis of classical hereditary and multifactorial acquired diseases. This new concept derives from the development and increasing use of molecular genetics in clinical medicine. The application of molecular biology techniques in biomedical investigation has encompassed the identification of the pathogenesis and etiology of diseases, prenatal diagnosis the production of new therapeutic agents, gene therapy and the development of pharmacogenetics. The impact on the fundamentals and practice of clinical medicine that will have the use of molecular biology is analyzed in this review.
A Microscopic “Social Norm” Model to Obtain Realistic Macroscopic Velocity and Density Pedestrian Distributions
Francesco Zanlungo, Tetsushi Ikeda, Takayuki Kanda
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0050720
Abstract: We propose a way to introduce in microscopic pedestrian models a “social norm” in collision avoiding and overtaking, i.e. the tendency, shared by pedestrians belonging to the same culture, to avoid collisions and perform overtaking in a preferred direction. The “social norm” is implemented, regardless of the specific collision avoiding model, as a rotation in the perceived velocity vector of the opponent at the moment of computation of the collision avoiding strategy, and justified as an expectation that the opponent will follow the same “social norm” (for example a tendency to avoid on the left and overtake on the right, as proposed in this work for Japanese pedestrians). By comparing with real world data, we show that the introduction of this norm allows for a better reproduction of macroscopic pedestrian density and velocity patterns.
Cholinergic Abnormalities, Endosomal Alterations and Up-Regulation of Nerve Growth Factor Signaling in Niemann-Pick Type C Disease
Carolina Cabeza, Alicia Figueroa, Oscar M Lazo, Carolina Galleguillos, Claudia Pissani, Andrés Klein, Christian Gonzalez-Billault, Nibaldo C Inestrosa, Alejandra R Alvarez, Silvana Zanlungo, Francisca C Bronfman
Molecular Neurodegeneration , 2012, DOI: 10.1186/1750-1326-7-11
Abstract: NPC1-deficient cholinergic cells respond to NGF after axotomy and exhibit increased levels of choline acetyl transferase (ChAT), whose gene is under the control of NGF signaling, compared to wild type cholinergic neurons. This finding was correlated with increased ChAT and phosphorylated Akt in basal forebrain homogenates. In addition, we found that cholinergic neurons from NPC1-deficient mice had disrupted neuronal morphology, suggesting early signs of neurodegeneration. Consistently, PC12 cells treated with U18666A presented a clear NPC cellular phenotype with a prominent endocytic dysfunction that includes an increased size of TrkA-containing endosomes and reduced recycling of the receptor. This result correlates with increased sensitivity to NGF, and, in particular, with up-regulation of the Akt and PLC-γ signaling pathways, increased neurite extension, increased phosphorylation of tau protein and cell death when PC12 cells are differentiated and treated with U18666A.Our results suggest that the NPC cellular phenotype causes neuronal dysfunction through the abnormal up-regulation of survival pathways, which causes the perturbation of signaling cascades and anomalous phosphorylation of the cytoskeleton.Neurotrophins (NGF, BDNF, NT3 and NT4) regulate different aspects of the developing and mature nervous system, including neuronal survival and neuronal morphology. These small proteins exert these effects by binding to members of the Trk family of receptor tyrosine kinases (TrkA, TrkB and TrkC) or to the p75 neurotrophin receptor (p75). Whereas p75 binds all neurotrophins, in addition to other ligands (e.g., proneurotrophins and amyloid peptides), each Trk binds preferentially to its cognate neurotrophin. For example, TrkA, TrkB and TrkC bind NGF, BDNF and NT3, respectively [1-3].Several neurodegenerative diseases are produced by alterations in molecules related to endocytosis and vesicular trafficking, which are cellular processes that regulate neurotrophin signal
Molecular Mechanisms Underlying the Link between Nuclear Receptor Function and Cholesterol Gallstone Formation
Mary Carmen Vázquez,Attilio Rigotti,Silvana Zanlungo
Journal of Lipids , 2012, DOI: 10.1155/2012/547643
Abstract: Cholesterol gallstone disease is highly prevalent in western countries, particularly in women and some specific ethnic groups. The formation of water-insoluble cholesterol crystals is due to a misbalance between the three major lipids present in the bile: cholesterol, bile salts, and phospholipids. Many proteins implicated in biliary lipid secretion in the liver are regulated by several transcription factors, including nuclear receptors LXR and FXR. Human and murine genetic, physiological, pathophysiological, and pharmacological evidence is consistent with the relevance of these nuclear receptors in gallstone formation. In addition, there is emerging data that also suggests a role for estrogen receptor ESR1 in abnormal cholesterol metabolism leading to gallstone disease. A better comprehension of the role of nuclear receptor function in gallstone formation may help to design new and more effective therapeutic strategies for this highly prevalent disease condition. 1. Introduction Cholesterol gallstone disease (CGD) is one of the most common digestive disease conditions in both industrialized and developing western countries. Worldwide CGD prevalence ranges between 5% and 20% [1], being more common in women than men in every population that has been studied [2]. It is particularly prevalent in some specific ethnic groups including Mapuche and North American Indians as well as Chilean and Mexican Hispanics. Among these populations, CGD has an earlier onset and reaches prevalence rates over 50% and 70% in middle age male and women, respectively. CGD is also a key risk factor for gallbladder cancer. Therefore, CGD represents a serious burden for healthcare systems [3, 4]. Some of the pathogenic hallmarks of CGD are increased biliary cholesterol secretion, increased bile acid hydrophobicity, cholesterol microcrystal formation, growth, and aggregation with the formation of macroscopic stones in the gallbladder, and gallbladder inflammation [5–7]. The primary pathogenic mechanism associated with CGD is a disrupted balance between the three major lipids present in bile: cholesterol, bile salts, and phospholipids [8]. Under physiological conditions, bile cholesterol is kept in solution by its incorporation into mixed micelles together with phospholipids and bile salts. When either too much cholesterol or not enough solubilizing bile salt and phospholipid molecules are secreted, cholesterol comes out of solution and then crystallizes [9]. In addition, several biliary proteins have been described as nucleating factors that may promote cholesterol crystallization.
El síndrome metabólico: De factor agravante a principal factor de riesgo patogénico en diversas enfermedades crónicas The metabolic syndrome: From an aggravating condition to a pathogenic risk factor for chronic diseases
ROMMY VON BERNHARDI,SILVANA ZANLUNGO,MARCO ARRESE,ANTONIO ARTEAGA
Revista médica de Chile , 2010,
Abstract: In recent years, a rapidly increasing number of studies have focused on the association between metabolic syndrome and several chronic diseases. However, it is difficult to determine a well defined pathogenic relationship, due to the etiological heterogeneity and comorbidities of these diseases. Research efforts are aiming to identify the convergent biological mechanisms that mediate the effects of hyperinsulinemia, hyperglycemia, dyslipidemia, and hypertension. All these conditions define the metabolic syndrome, that increases the risk for several diseases. The knowledge of these biological mechanisms associated with this syndrome will elucidate the pathogenic association between a variety of chronic diseases, including its pathogenic link with cardiovascular diseases and the most common forms of dementia. The development of new therapeutic and preventive strategies for these diseases will be a corollary of this research.
Oxidative Stress: A Pathogenic Mechanism for Niemann-Pick Type C Disease
Mary Carmen Vázquez,Elisa Balboa,Alejandra R. Alvarez,Silvana Zanlungo
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/205713
Abstract: Niemann-Pick type C (NPC) disease is a neurovisceral atypical lipid storage disorder involving the accumulation of cholesterol and other lipids in the late endocytic pathway. The pathogenic mechanism that links the accumulation of intracellular cholesterol with cell death in NPC disease in both the CNS and the liver is currently unknown. Oxidative stress has been observed in the livers and brains of NPC mice and in different NPC cellular models. Moreover, there is evidence of an elevation of oxidative stress markers in the serumof NPC patients. Recent evidence strongly suggests that mitochondrial dysfunction plays an important role in NPC pathogenesis and that mitochondria could be a significant source of oxidative stress in this disease. In this context, the accumulation of vitamin E in the late endosomal/lysosomal compartments in NPC could lead to a potential decrease of its bioavailability and could be another possible cause of oxidative damage. Another possible source of reactive species in NPC is the diminished activity of different antioxidant enzymes. Moreover, because NPC is mainly caused by the accumulation of free cholesterol, oxidized cholesterol derivatives produced by oxidative stress may contribute to the pathogenesis of the disease.
El síndrome metabólico: De factor agravante a principal factor de riesgo patogénico en diversas enfermedades crónicas
VON BERNHARDI,ROMMY; ZANLUNGO,SILVANA; ARRESE,MARCO; ARTEAGA,ANTONIO; RIGOTTI,ATTILIO;
Revista médica de Chile , 2010, DOI: 10.4067/S0034-98872010000800012
Abstract: in recent years, a rapidly increasing number of studies have focused on the association between metabolic syndrome and several chronic diseases. however, it is difficult to determine a well defined pathogenic relationship, due to the etiological heterogeneity and comorbidities of these diseases. research efforts are aiming to identify the convergent biological mechanisms that mediate the effects of hyperinsulinemia, hyperglycemia, dyslipidemia, and hypertension. all these conditions define the metabolic syndrome, that increases the risk for several diseases. the knowledge of these biological mechanisms associated with this syndrome will elucidate the pathogenic association between a variety of chronic diseases, including its pathogenic link with cardiovascular diseases and the most common forms of dementia. the development of new therapeutic and preventive strategies for these diseases will be a corollary of this research.
Deciphering the Crowd: Modeling and Identification of Pedestrian Group Motion
Zeynep Yücel,Francesco Zanlungo,Tetsushi Ikeda,Takahiro Miyashita,Norihiro Hagita
Sensors , 2013, DOI: 10.3390/s130100875
Abstract: Associating attributes to pedestrians in a crowd is relevant for various areas like surveillance, customer profiling and service providing. The attributes of interest greatly depend on the application domain and might involve such social relations as friends or family as well as the hierarchy of the group including the leader or subordinates. Nevertheless, the complex social setting inherently complicates this task. We attack this problem by exploiting the small group structures in the crowd. The relations among individuals and their peers within a social group are reliable indicators of social attributes. To that end, this paper identifies social groups based on explicit motion models integrated through a hypothesis testing scheme. We develop two models relating positional and directional relations. A pair of pedestrians is identified as belonging to the same group or not by utilizing the two models in parallel, which defines a compound hypothesis testing scheme. By testing the proposed approach on three datasets with different environmental properties and group characteristics, it is demonstrated that we achieve an identification accuracy of 87% to 99%. The contribution of this study lies in its definition of positional and directional relation models, its description of compound evaluations, and the resolution of ambiguities with our proposed uncertainty measure based on the local and global indicators of group relation.
Fecal bile acid excretion and messenger RNA expression levels of ileal transporters in high risk gallstone patients
Jorge Herrera, Ludwig Amigo, Constanze Husche, Carlos Benítez, Silvana Zanlungo, Dieter Lütjohann, Juan Miquel, Flavio Nervi
Lipids in Health and Disease , 2009, DOI: 10.1186/1476-511x-8-53
Abstract: Excretion of fecal BA was measured in seven GS females and in ten GS-free individuals, all with a body mass index < 29. Participants ingested the stool marker Cr2O3 (300 mg/day) for 10 days, and fecal specimens were collected on the last 3 days. Chromium was measured by a colorimetric method, and BA was quantitated by gas chromatography/mass spectroscopy. Intake of calories, nutrients, fiber and cholesterol were similar in the GS and GS-free subjects. Mean BA excretion levels were 520 ± 80 mg/day for the GS-free group, and 461 ± 105 mg/day for the GS group. Messenger RNA expression levels were determined by RT-PCR on biopsy samples obtained from ileum during diagnostic colonoscopy (14 GS-free controls and 16 GS patients) and from liver during surgery performed at 8 and 10 AM (12 GS and 10 GS-free patients operated on for gastrointestinal malignancies), all with a body mass index < 29. Messenger RNA level of the BA transporter genes for ileal lipid binding protein, multidrug resistance-associated protein 3, organic solute transporter alpha, and organic solute transporter beta were similar in GS and GS-free subjects. Messenger RNA level of Cyp27A1, encoding the enzyme 27α-hydroxylase, the short heterodimer partner and farnesoid X receptor remained unchanged, whereas the mRNA level of Cyp7A1, the rate limiting step of BA synthesis, was increased more than 400% (p < 0.01) in the liver of GS compared to GS-free subjects.Hispanics with GS have fecal BA excretion rates and mRNA levels of genes for ileal BA transporters that are similar to GS-free subjects. However, mRNA expression levels of Cyp7A1 are increased in GS, indicating that regulation of BA synthesis is abnormal in Hispanics with GS.Cholesterol gallstone disease (GS) is prevalent worldwide, and is endemic among American Indians and Hispanics [1,2]. In GS, the primary abnormality is secretion by the liver into the gallbladder of bile that is supersaturated with cholesterol. This leads to precipitation of cholester
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