Institution
University of Córdoba (Spain)
Education•Cordova, Spain•
About: University of Córdoba (Spain) is a education organization based out in Cordova, Spain. It is known for research contribution in the topics: Population & Catalysis. The organization has 12006 authors who have published 22998 publications receiving 537842 citations. The organization is also known as: University of Córdoba (Spain) & Universidad de Córdoba.
Topics: Population, Catalysis, Lithium, Extraction (chemistry), Detection limit
Papers published on a yearly basis
Papers
More filters
••
Carlos III Health Institute1, Rovira i Virgili University2, University of Navarra3, University of Valencia4, University of Las Palmas de Gran Canaria5, RMIT University6, University of Barcelona7, IMDEA8, University of Córdoba (Spain)9, University of Granada10, University of the Balearic Islands11, University of Málaga12, University of León13, Epigenomics AG14, University of Jaén15, Complutense University of Madrid16, Harvard University17
TL;DR: PREDIMED-Plus intensive lifestyle intervention for 12 months was effective in decreasing adiposity and improving cardiovascular risk factors in overweight/obese older adults with metabolic syndrome, as well as in individuals with or at risk for diabetes.
Abstract: OBJECTIVE The long-term impact of intentional weight loss on cardiovascular events remains unknown. We describe 12-month changes in body weight and cardiovascular risk factors in PREvencion con DIeta MEDiterranea (PREDIMED)-Plus, a trial designed to evaluate the long-term effectiveness of an intensive weight-loss lifestyle intervention on primary cardiovascular prevention. RESEARCH DESIGN AND METHODS Overweight/obese adults with metabolic syndrome aged 55–75 years ( n = 626) were randomized to an intensive weight-loss lifestyle intervention based on an energy-restricted Mediterranean diet, physical activity promotion, and behavioral support (IG) or a control group (CG). The primary and secondary outcomes were changes in weight and cardiovascular risk markers, respectively. RESULTS Diet and physical activity changes were in the expected direction, with significant improvements in IG versus CG. After 12 months, IG participants lost an average of 3.2 kg vs. 0.7 kg in the CG ( P P P 1c , and circulating levels of leptin, interleukin-18, and MCP-1 were greater in IG than CG participants ( P CONCLUSIONS PREDIMED-Plus intensive lifestyle intervention for 12 months was effective in decreasing adiposity and improving cardiovascular risk factors in overweight/obese older adults with metabolic syndrome, as well as in individuals with or at risk for diabetes.
201 citations
••
TL;DR: Results provide unequivocal evidence that kisspeptins exert direct pituitary effects in peripubertal male and female rats and suggest a possible autocrine/paracrine mode of action.
Abstract: Recent, compelling evidence indicates that kisspeptins, the products of KiSS-1 gene, and their receptor GPR54, represent key elements in the neuroendocrine control of reproduction, and that they act primarily by regulating gonadotrophin-releasing hormone (GnRH) secretion at the hypothalamus. Conversely, and despite earlier reports showing GPR54 expression in the pituitary, the potential physiological roles of kisspeptins at this gland have remained elusive. To clarify this issue, cultures of rat pituitary cells were used to evaluate expression of KiSS-1 and GPR54, and to monitor the ability of kisspeptin-10 to stimulate Ca(2+) responses in gonadotrophs and to elicit luteinising hormone (LH) secretion in vitro. The results obtained show that both GPR54 and KiSS-1 are expressed in the pituitary of peripubertal male and female rats. Moreover, kisspeptin-10 induced a rise in free cytosolic Ca(2+) concentration ([Ca(2+)](i)) in approximately 10% of male rat pituitary cells. Intriguingly, kisspeptin-responsive cells included not only gonadotrophs, in which a 62.8 +/- 16.0%[Ca(2+)](i) rise was observed, but also somatotrophs, wherein kisspeptin induced a 60.3 +/- 5.5%[Ca(2+)](i) increase. Accordingly, challenge of dispersed pituitary cells with increasing kisspeptin-10 concentrations induced dose-related LH and growth hormone (GH) secretory responses, which were nevertheless of lower magnitude than those evoked by the primary regulators GnRH and GH-releasing hormone, respectively. In particular, 10(-8) M kisspeptin caused maximal increases in LH release (218.7 +/- 23.6% and 180.4 +/- 7.2% in male and female rat pituitary cells, respectively), and also stimulated maximally GH secretion (181.9 +/- 14.9% and 260.2 +/- 15.9% in male and female rat pituitary cells, respectively). Additionally, moderate summation of kisspeptin- and GnRH-induced LH responses was observed after short-term incubation of male rat pituitary cells. In conclusion, our results provide unequivocal evidence that kisspeptins exert direct pituitary effects in peripubertal male and female rats and suggest a possible autocrine/paracrine mode of action. The precise relevance and underlying mechanisms of this potential new actions of kisspeptins (i.e. the direct modulation of gonadotrophic and somatotrophic axis at the pituitary) deserve further analysis.
201 citations
••
TL;DR: Plants represent a valuable model system for the study of DNA oxidative repair processes in eukaryotic cells and use mechanisms similar to those present in other eukARYotes to remove and/or tolerate oxidized bases and other oxidative DNA lesions.
Abstract: DNA damage caused by exposure to reactive oxygen species is one of the primary causes of DNA decay in most organisms. In plants, endogenous reactive oxygen species (ROS) are generated not only by respiration and photosynthesis, but also by active responses to certain environmental challenges, such as pathogen attack. Significant extracellular sources of activated oxygen include air pollutants such as ozone and oxidative effects of UV light and low-level ionizing radiation. Plants are well equipped to cope with oxidative damage to cellular macromolecules, including DNA. Oxidative attack on DNA generates both altered bases and damaged sugar residues that undergo fragmentation and lead to strand breaks. Recent advances in the study of DNA repair in higher plants show that they use mechanisms similar to those present in other eukaryotes to remove and/or tolerate oxidized bases and other oxidative DNA lesions. Therefore, plants represent a valuable model system for the study of DNA oxidative repair processes in eukaryotic cells.
200 citations
••
TL;DR: In this article, the anion exchange method was used to obtain a hydrotalcite-like compound [Zn2Al(OH)6]2edta·nH2O(ZnAl-edta) with the aim of uptake Cu2+, Cd2+ and Pb2+ from the aqueous solutions by chelating process between edta and metal cations.
200 citations
••
TL;DR: The role of central mTOR signaling is unveiled in the control of puberty onset and gonadotropin secretion, a phenomenon that involves the regulation of Kiss1 and may contribute to the functional coupling between energy balance and gonadal activation and function.
Abstract: The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that operates as sensor of cellular energy status and effector for its coupling to cell growth and proliferation. At the hypothalamic arcuate nucleus, mTOR signaling has been recently proposed as transducer for leptin effects on energy homeostasis and food intake. However, whether central mTOR also participates in metabolic regulation of fertility remains unexplored. We provide herein evidence for the involvement of mTOR in the control of puberty onset and LH secretion, likely via modulation of hypothalamic expression of Kiss1. Acute activation of mTOR by l-leucine stimulated LH secretion in pubertal female rats, whereas chronic l-leucine infusion partially rescued the state of hypogonadotropism induced by food restriction. Conversely, blockade of central mTOR signaling by rapamycin caused inhibition of the gonadotropic axis at puberty, with significantly delayed vaginal opening, decreased LH and estradiol levels, and ovarian and uterine atrophy. Inactivation of mTOR also blunted the positive effects of leptin on puberty onset in food-restricted females. Yet the GnRH/LH system retained their ability to respond to ovariectomy and kisspeptin-10 after sustained blockade of mTOR, ruling out the possibility of unspecific disruption of GnRH function by rapamycin. Finally, mTOR inactivation evoked a significant decrease of Kiss1 expression at the hypothalamus, with dramatic suppression of Kiss1 mRNA levels at the arcuate nucleus. Altogether our results unveil the role of central mTOR signaling in the control of puberty onset and gonadotropin secretion, a phenomenon that involves the regulation of Kiss1 and may contribute to the functional coupling between energy balance and gonadal activation and function.
199 citations
Authors
Showing all 12089 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jose M. Ordovas | 123 | 1024 | 70978 |
Liang Cheng | 116 | 1779 | 65520 |
Pedro W. Crous | 115 | 809 | 51925 |
Munther A. Khamashta | 109 | 623 | 50205 |
Luis Serrano | 105 | 452 | 42515 |
Raymond Vanholder | 103 | 841 | 40861 |
Carlos Dieguez | 101 | 545 | 36404 |
David G. Bostwick | 99 | 403 | 31638 |
Leon V. Kochian | 95 | 266 | 31301 |
Abhay Ashtekar | 94 | 366 | 37508 |
Néstor Armesto | 93 | 369 | 26848 |
Manuel Hidalgo | 92 | 538 | 41330 |
Rafael de Cabo | 91 | 317 | 35020 |
Harald Mischak | 90 | 445 | 27472 |
Manuel Tena-Sempere | 87 | 351 | 23100 |