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Buenos Aires, Argentina

The Pontifical Catholic University of Argentina, whose full name in Spanish is Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires", also known as Universidad Católica Argentina , is a university in Argentina with campuses in the cities of Buenos Aires, Santa Fe, Rosario, Paraná, Mendoza and Pergamino. The main campus is located in Puerto Madero, one of the most modern neighborhoods of Buenos Aires.It is considered, according to a 2011 study by the Spanish Ministry of Education as one of the best private universities in Latin America. It is the second university preferred by Argentine employers and the sixth in all Latin America.Its predecessor, the Catholic University of Buenos Aires was founded by the Argentine episcopate in 1910, but their degrees, in law, were not recognized by the Argentine government, and the institution was closed in 1922.In 1955, Decree 6403 concerning the freedom of education enabled the creation of private universities with the authority to deliver academic qualifications. In 1956 the bishops decided to create the Catholic University of Argentina, formally founded on March 7, 1958.Cardinal Jorge Mario Bergoglio was UCA's Grand Chancellor, by virtue of his office as Primate of Argentina and Metropolitan Archbishop of the Roman Catholic Archdiocese of Buenos Aires, the capital of Argentina, until his election in 2013 as Pope Francis to succeed Pope Emeritus Benedict XVI. When Mario Aurelio Poli was named Archbishop of Buenos Aires by Pope Francis later in 2013, he became Grand Chancellor of the University. In May 2013 Pope Francis named Victor Manuel Fernández, the University's President , as titular archbishop of Tiburnia. Wikipedia.

Garcia-Burgos D.,University of Granada | Zamora M.C.,CONICET | Zamora M.C.,Pontifical Catholic University of Argentina
Food Quality and Preference | Year: 2015

Preferences for and consumption of bitter foods such as vegetables and fruit are important in addressing the epidemic of obesity as healthy dietary patterns contribute to its prevention. However, few studies have been undertaken to understand the preference for bitter-tasting foods. A generally accepted but not proven explanation is that these acquired preferences involve changes in affective and motivational processes in order to overcome the innate rejection of bitter tastes. To examine this issue we compared the hedonic and incentive responses to bitter substances among bitter likers and dislikers. In addition, the effects of hunger, stress and weight concern on bitter preferences were also explored. Fifty-nine healthy adults (age. = 24.8. ±. 6.3; body mass index. = 22.0. ±. 2.8) were divided into bitter likers and bitter dislikers according to their food preferences. Both groups sampled the unreinforced flavours of coffee, beer, chocolate and grapefruit under four motivational states induced by static pictures (neutral, food, stressor and obesity) at the time of testing. The results showed that the bitter solutions elicited less aversive responses (higher hedonic ratings and less intense disgust reactions) and fewer avoidance behaviours (slower response time and lower amount of water for rinsing) in bitter likers after viewing neutral images. On the other hand, likers exhibited a further reduction in disgust to coffee after viewing stressor pictures, and also drank more water after tasting chocolate following the obesity pictures, compared with the dislikers. The expression of disgust increased in bitter likers, as well as the amount of water used to rinse the mouth, after tasting chocolate following pictures showing obesity compared with pictures showing food. These results show, for the first time, not only the implication of affective and incentive components in reversal of the predisposition to reject bitterness but also the motivational modulation of the expression of rejection of bitter tastes in humans. © 2014 Elsevier Ltd. Source

Garcia-Burgos D.,University of Granada | Zamora M.C.,Pontifical Catholic University of Argentina
Appetite | Year: 2013

Differences in food consumption among body-weight statuses (e.g., higher fruit intake linked with lower body mass index (BMI) and energy-dense products with higher BMI) has raised the question of why people who are overweight or are at risk of becoming overweight eat differently from thinner peopl>e. One explanation, in terms of sensitivity to affective properties of food, suggests that palatability-driven consumption is likely to be an important contributor to food intake, and therefore body weight. Extending this approach to unpalatable tastes, we examined the relationship between aversive reactions to foods and BMI. We hypothesized that people who have a high BMI will show more negative affective reactions to bitter-tasting stimuli, even after controlling for sensory perception differences. Given that hedonic reactions may influence consumption even without conscious feelings of pleasure/displeasure, the facial expressions were included in order to provide more direct access to affective systems than subjective reports. Forty adults (28 females, 12 males) participated voluntarily. Their ages ranged from 18 to 46. years (M=24.2, SD=5.8). On the basis of BMI, participants were classified as low BMI (BMI. <. 20; n=20) and high BMI (BMI. >. 23; n=20). The mean BMI was 19.1 for low BMI (SD=0.7) and 25.2 for high BMI participants (SD=1.8). Each subject tasted 5. mL of a grapefruit juice drink and a bitter chocolate drink. Subjects rated the drinks' hedonic and incentive value, familiarity and bitter intensity immediately after each stimulus presentation. The results indicated that high BMI participants reacted to bitter stimuli showing more profound changes from baseline in neutral and disgust facial expressions compared with low BMI. No differences between groups were detected for the subjective pleasantness and familiarity. The research here is the first to examine how affective facial reactions to bitter food, apart from taste responsiveness, can predict differences in BMI. © 2013 Elsevier Ltd. Source

Dubocovich M.L.,State University of New York at Buffalo | Dubocovich M.L.,Northwestern University | Delagrange P.,Institute Of Recherches Servier | Krause D.N.,University of California at Irvine | And 3 more authors.
Pharmacological Reviews | Year: 2010

The hormone melatonin (5-methoxy-N-acetyltryptamine) is synthesized primarily in the pineal gland and retina, and in several peripheral tissues and organs. In the circulation, the concentration of melatonin follows a circadian rhythm, with high levels at night providing timing cues to target tissues endowed with melatonin receptors. Melatonin receptors receive and translate melatonin's message to influence daily and seasonal rhythms of physiology and behavior. The melatonin message is translated through activation of two G protein-coupled receptors, MT1 and MT2, that are potential therapeutic targets in disorders ranging from insomnia and circadian sleep disorders to depression, cardiovascular diseases, and cancer. This review summarizes the steps taken since melatonin's discovery by Aaron Lerner in 1958 to functionally characterize, clone, and localize receptors in mammalian tissues. The pharmacological and molecular properties of the receptors are described as well as current efforts to discover and develop ligands for treatment of a number of illnesses, including sleep disorders, depression, and cancer. Copyright © 2010 by The American Society for Pharmacology and Experimental Therapeutics. Source

Hardeland R.,University of Gottingen | Cardinali D.P.,Pontifical Catholic University of Argentina | Brown G.M.,University of Toronto | Pandi-Perumal S.R.,New York University
Progress in Neurobiology | Year: 2015

Melatonin is known to possess several properties of value for healthy aging, as a direct and indirect antioxidant, protectant and modulator of mitochondrial function, antiexcitotoxic agent, enhancer of circadian amplitudes, immune modulator and neuroprotectant. It is levels tend to decrease in the course of senescence and are more strongly reduced in several neurodegenerative disorders, especially Alzheimer's disease, and in diseases related to insulin resistance such as diabetes type 2. Although the role of melatonin in aging and age-related diseases has been repeatedly discussed, the newly emerged concept of inflammaging, that is, the contribution of low-grade inflammation to senescence progression has not yet been the focus of melatonin research. This review addresses the multiple protective actions of melatonin and its kynuramine metabolites that are relevant to the attenuation of inflammatory responses and progression of inflammaging in the brain, i.e. avoidance of excitotoxicity, reduction of free radical formation by support of mitochondrial electron flux, prevention of NADPH oxidase activation and suppression of inducible nitric oxide synthase, as well as downregulation of proinflammatory cytokines. The experimental evidence is primarily discussed on the basis of aging and senescence-accelerated animals, actions in the immune system, and the relationship between melatonin and sirtuins, having properties of aging suppressors. Sirtuins act either as accessory components or downstream factors of circadian oscillators, which are also under control by melatonin. Inflammaging is assumed to strongly contribute to neurodegeneration of the circadian master clock observed in advanced senescence and, even more, in Alzheimer's disease, a change that affects countless physiological functions. © 2015 Elsevier Ltd. Source

Valdivieso A.G.,Pontifical Catholic University of Argentina
Analytical biochemistry | Year: 2011

Cystic fibrosis (CF) is a frequent autosomal recessive disease caused by mutations that impair the CF transmembrane conductance regulator (CFTR) protein function. CFTR is a chloride channel activated by cyclic AMP (cAMP) via protein kinase A (PKA) and ATP hydrolysis. We describe here a method to measure CFTR activity in a monolayer of cultured cells using a fluorescence spectrophotometer and the chloride-sensitive probe 6-methoxy-N-(3-sulfopropyl)quinolinium (SPQ). Modifying a slice holder, the spectrophotometer quartz cuvette was converted in a perfusion chamber, allowing measurement of CFTR activity in real time, in a monolayer of T84 colon carcinoma cells. The SPQ Stern-Volmer constant (K(Cl(-))) for chloride in water solution was 115.0 ± 2.8M(-1), whereas the intracellular (K(Cl(-))) was 17.8 ± 0.8 M(-1), for T84 cells. A functional analysis was performed by measuring CFTR activity in T84 cells. The CFTR transport inhibitors CFTR(inh)-172 (5 μM) and glibenclamide (100 μM) showed a significant reduction (P<0.05) in CFTR activity. This simple method allows measuring CFTR activity in a very simple, reproducible, and sensitive way. Copyright © 2011 Elsevier Inc. All rights reserved. Source

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