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Search Results: 1 - 10 of 3361 matches for " Jesus Egido "
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Preliminary study of community-acquired Staphylococcus aureus infection in Manaus Hospital, Amazonia Region, Brazil
Egido, Jesus M.;Barros, Marcus L.;
Revista da Sociedade Brasileira de Medicina Tropical , 2003, DOI: 10.1590/S0037-86822003000600011
Abstract: methicillin resistant staphylococcus aureus is considered a public health problem with a strong potential for dissemination and high rates of morbidity and mortality. in this study we describe bacteriological and epidemiological characteristics of staphylococcus aureus in manaus (amazon region). during the one-year study period (2000-2001), sixteen cases of acute pyogenic multiple abscess were evaluated. community-acquired s. aureus was identified as causative agent in 10 (62.5%) patients. the strains tested with antimicrobials by discs diffusion method, exhibited a high rate of sensitivity to cephalexin (100%), erythromycin (90%). oxacillin-susceptible staphylococcus aureus was 90%. no isolate was resistant to vancomycin. to our knowledge, no series of community-acquired staphylococcus aureus in manaus hospital has been published. our partial results showed a high rate of antimicrobial sensitivity among community-acquired staphylococcus aureus in the hospital of tropical medicine institute of manaus, amazon region.
Preliminary study of community-acquired Staphylococcus aureus infection in Manaus Hospital, Amazonia Region, Brazil
Egido Jesus M.,Barros Marcus L.
Revista da Sociedade Brasileira de Medicina Tropical , 2003,
Abstract: Methicillin resistant Staphylococcus aureus is considered a public health problem with a strong potential for dissemination and high rates of morbidity and mortality. In this study we describe bacteriological and epidemiological characteristics of Staphylococcus aureus in Manaus (Amazon region). During the one-year study period (2000-2001), sixteen cases of acute pyogenic multiple abscess were evaluated. Community-acquired S. aureus was identified as causative agent in 10 (62.5%) patients. The strains tested with antimicrobials by discs diffusion method, exhibited a high rate of sensitivity to cephalexin (100%), erythromycin (90%). Oxacillin-susceptible Staphylococcus aureus was 90%. No isolate was resistant to Vancomycin. To our knowledge, no series of community-acquired Staphylococcus aureus in Manaus hospital has been published. Our partial results showed a high rate of antimicrobial sensitivity among community-acquired Staphylococcus aureus in the hospital of Tropical Medicine Institute of Manaus, Amazon Region.
Antioxidants in Kidney Diseases: The Impact of Bardoxolone Methyl
Jorge Rojas-Rivera,Alberto Ortiz,Jesus Egido
International Journal of Nephrology , 2012, DOI: 10.1155/2012/321714
Abstract: Drugs targeting the renin-angiotensin-aldosterone system (RAAS) are the mainstay of therapy to retard the progression of proteinuric chronic kidney disease (CKD) such as diabetic nephropathy. However, diabetic nephropathy is still the first cause of end-stage renal disease. New drugs targeted to the pathogenesis and mechanisms of progression of these diseases beyond RAAS inhibition are needed. There is solid experimental evidence of a key role of oxidative stress and its interrelation with inflammation on renal damage. However, randomized and well-powered trials on these agents in CKD are scarce. We now review the biological bases of oxidative stress and its role in kidney diseases, with focus on diabetic nephropathy, as well as the role of the Keap1-Nrf2 pathway and recent clinical trials targeting this pathway with bardoxolone methyl. 1. Background Chronic kidney disease (CKD) is a serious public health problem, which carries a high morbidity and mortality [1]. CKD is characterized by a progressive loss of renal function, chronic inflammation, oxidative stress, vascular remodeling, and glomerular and tubulointerstitial scarring. CKD treatment still represents a clinical challenge. Diabetic nephropathy (DN) is the leading cause of CKD and end-stage renal disease (ESRD) [2]. The renin-angiotensin-aldosterone system (RAAS) is a major pathway involved in the pathogenesis and progression of DN [3, 4], and RAAS blockade is an effective therapeutic strategy to reduce proteinuria and slow progression of diabetic and nondiabetic CKD. However targeting the system sets off compensatory mechanisms that may increase angiotensin II, aldosterone, or renin, and partial RAAS blockade does not prevent progression in all CKD patients. Angiotensin II (AT II) is the key mediator of the RAAS [5–7]. Animal models of experimental diabetes, clinical trials, and metanalysis have clearly demonstrated the effectiveness of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) therapy to improve glomerular/tubulointerstitial damage, reduce proteinuria, and decrease CKD progression, independently of blood pressure (BP) control [8–13]. Dual RAAS blockade with ACEI plus ARB inhibits compensatory AT II activity resulting from ACE-independent pathways and limits compensatory AT production induced by AT1 receptor blockade. This combination reduced proteinuria by 25–45% in DN [14–16]. Results are worse for DN with diminished kidney function or nonproteinuric CKD with ischemic renal injury, probably due to advanced structural renal changes [13, 17, 18]
Juxtaglomerular apparatus hyperplasia under dual angiotensin blockade. A footprint of adequate RAS inhibition or a concern for renal fibrosis?
Beatriz Fernandez-Fernandez, Alberto Ortiz, Carmen Gomez-Guerrero, Antonio Barat, Catalina Martin-Cleary, Jesus Egido
BMC Nephrology , 2012, DOI: 10.1186/1471-2369-13-21
Abstract: We present a patient with corticoid resistant nephrotic syndrome who developed marked juxtaglomerular apparatus hyperplasia and renin expression in the context of dual angiotensin system blockade.Although renin may have profibrotic effects mediated by (pro)renin receptor activation, this report raises questions on the potential consequences of local renin activation on chronic kidney disease in patients with dual angiotensin blockade.
Bisphenol A in Chronic Kidney Disease
Emilio González-Parra,Jose Antonio Herrero,Usama Elewa,Ricardo J. Bosch,Alberto Ortiz Arduán,Jesus Egido
International Journal of Nephrology , 2013, DOI: 10.1155/2013/437857
Abstract: Phenols are uremic toxins of intestinal origin formed by bacteria during protein metabolism. Of these molecules, p-cresol is the most studied and has been associated with renal function impairment and vascular damage. Bisphenol A (BPA) is a molecule with structural similarity with phenols found in plastic food and beverage containers as well as in some dialyzers. BPA is considered an environmental toxicant based on animal and cell culture studies. Japanese authorities recently banned BPA use in baby bottles based on observational association studies in newborns. BPA is excreted in urine and uremic patients present higher serum levels, but there is insufficient evidence to set cut-off levels or to link BPA to any harmful effect in CKD. However, the renal elimination and potential exposure during dialysis warrant the monitoring of BPA exposure and the design of observational studies in which the potential health risks of BPA for end-stage renal disease patients are evaluated. 1. Uremic Toxins Multiple molecules accumulate in chronic kidney disease (CKD), are responsible for uremic symptoms, and contribute to increased mortality (uremic toxins). Removal of uremic toxins therefore is accompanied by an improvement in the clinical situation. The term of uremic toxin was created by Piorry in 1847 to indicate the “blood contamination with urine” to refer to the signs and symptoms resulting from kidney disease that increase mortality. Bergstrom [1] proposed that a uremic toxin should be defined as one molecule that meets the following premises:(1)the chemical identity and concentration in biological fluids should be known,(2)the concentration in uremic individuals should be higher than in nonuremic subjects,(3)the concentration should correlate with uremic symptoms, and symptoms should disappear by decreasing the concentration. Uremic toxins have been classified according to size [2]. Over 350 small uremic toxins have been described with a molecular weight below 500?Da [3]. Medium-sized molecules have a molecular weight between 500 and 5000?Da. Many uremic toxins are bound to proteins which hamper their clearance. Uremic toxins are responsible for uremic disease. Among the changes that have been directly related to uremic toxins we find progressive loss of renal function, cardiovascular morbidity, and uremic symptoms such as anorexia, vomiting, weakness, sleep disturbances, and neuropathy. The origin of uremic toxins is multiple. Most uremic toxins originate from the endogenous cellular metabolism. However, there is a growing list of uremic toxins originated in
"La piel tiene una característica simbólica porque es donde el cuerpo y el espíritu se unen" "The skin has a symbolic feature because is the place where body and spirit join"
Antonio Egido
Gerokomos , 2011,
Zarzuelas y óperas a lo divino y a lo humano de Calderón de la Barca
Aurora Egido
Castilla : Estudios de Literatura , 2009,
Animal Models of Cardiovascular Diseases
Carlos Zaragoza,Carmen Gomez-Guerrero,Jose Luis Martin-Ventura,Luis Blanco-Colio,Bego a Lavin,Be at Mallavia,Carlos Tarin,Sebastian Mas,Alberto Ortiz,Jesus Egido
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/497841
Abstract: Cardiovascular diseases are the first leading cause of death and morbidity in developed countries. The use of animal models have contributed to increase our knowledge, providing new approaches focused to improve the diagnostic and the treatment of these pathologies. Several models have been developed to address cardiovascular complications, including atherothrombotic and cardiac diseases, and the same pathology have been successfully recreated in different species, including small and big animal models of disease. However, genetic and environmental factors play a significant role in cardiovascular pathophysiology, making difficult to match a particular disease, with a single experimental model. Therefore, no exclusive method perfectly recreates the human complication, and depending on the model, additional considerations of cost, infrastructure, and the requirement for specialized personnel, should also have in mind. Considering all these facts, and depending on the budgets available, models should be selected that best reproduce the disease being investigated. Here we will describe models of atherothrombotic diseases, including expanding and occlusive animal models, as well as models of heart failure. Given the wide range of models available, today it is possible to devise the best strategy, which may help us to find more efficient and reliable solutions against human cardiovascular diseases.
Gene Deficiency in Activating Fcγ Receptors Influences the Macrophage Phenotypic Balance and Reduces Atherosclerosis in Mice
Be?at Mallavia, Ainhoa Oguiza, Oscar Lopez-Franco, Carlota Recio, Guadalupe Ortiz-Mu?oz, Iolanda Lazaro, Virginia Lopez-Parra, Jesus Egido, Carmen Gomez-Guerrero
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066754
Abstract: Immunity contributes to arterial inflammation during atherosclerosis. Oxidized low-density lipoproteins induce an autoimmune response characterized by specific antibodies and immune complexes in atherosclerotic patients. We hypothesize that specific Fcγ receptors for IgG constant region participate in atherogenesis by regulating the inflammatory state of lesional macrophages. In vivo we examined the role of activating Fcγ receptors in atherosclerosis progression using bone marrow transplantation from mice deficient in γ-chain (the common signaling subunit of activating Fcγ receptors) to hyperlipidemic mice. Hematopoietic deficiency of Fcγ receptors significantly reduced atherosclerotic lesion size, which was associated with decreased number of macrophages and T lymphocytes, and increased T regulatory cell function. Lesions of Fcγ receptor deficient mice exhibited increased plaque stability, as evidenced by higher collagen and smooth muscle cell content and decreased apoptosis. These effects were independent of changes in serum lipids and antibody response to oxidized low-density lipoproteins. Activating Fcγ receptor deficiency reduced pro-inflammatory gene expression, nuclear factor-κB activity, and M1 macrophages at the lesion site, while increasing anti-inflammatory genes and M2 macrophages. The decreased inflammation in the lesions was mirrored by a reduced number of classical inflammatory monocytes in blood. In vitro, lack of activating Fcγ receptors attenuated foam cell formation, oxidative stress and pro-inflammatory gene expression, and increased M2-associated genes in murine macrophages. Our study demonstrates that activating Fcγ receptors influence the macrophage phenotypic balance in the artery wall of atherosclerotic mice and suggests that modulation of Fcγ receptor-mediated inflammatory responses could effectively suppress atherosclerosis.
L’educació com a exposició
Miriam Prieto Egido
Temps d'Educació , 2009,
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