2,203 research outputs found
Estudio para la mejora de la calidad del grado en Trabajo Social en atenciĂłn a las necesidades de nuestros egresados y sus empleadores
Mediante este proyecto la Facultad de Trabajo Social de la UCM pretende conocer cuĂĄles son las necesidades formativas de nuestros alumnos con el principal objetivo de hacer una modificaciĂłn en la titulaciĂłn que pueda dar respuesta a las necesidades de conocimiento de nuestros profesionales asĂ como conocer las condiciones esenciales en las que nuestros egresado acceden al mercado laboral
A DNA intercalating dye-based RT-qPCR alternative to diagnose SARS-CoV-2
Early detection of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been proven crucial during the efforts to mitigate the effects of the COVID-19 pandemic. Several diagnostic methods have emerged in the past few months, each with different shortcomings and limitations. The current gold standard, RT-qPCR using fluorescent probes, relies on demanding equipment requirements plus the high costs of the probes and specific reaction mixes. To broaden the possibilities of reagents and thermocyclers that could be allocated towards this task, we have optimized an alternative strategy for RT-qPCR diagnosis. This is based on a widely used DNA-intercalating dye and can be implemented with several different qPCR reagents and instruments. Remarkably, the proposed qPCR method performs similarly to the broadly used TaqMan-based detection, in terms of specificity and sensitivity, thus representing a reliable tool. We think that, through enabling the use of vast range of thermocycler models and laboratory facilities for SARS-CoV-2 diagnosis, the alternative proposed here can increase dramatically the testing capability, especially in countries with limited access to costly technology and reagents.Fil: Fuchs Wightman, Federico. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Godoy Herz, Micaela Amalia. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Muñoz, Juan CristĂłbal. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Stigliano, Jose Nicolas. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Bragado, Laureano Fabian Tomas. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Nieto Moreno, NicolĂĄs. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Palavecino Ruiz, Marcos Daniel. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Servi, Lucas. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Cabrerizo, Gonzalo. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de Investigaciones BiomĂ©dicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones BiomĂ©dicas en Retrovirus y Sida; ArgentinaFil: Clemente, Jose Antonio. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Avaro, MartĂn. DirecciĂłn Nacional de Institutos de InvestigaciĂłn. AdministraciĂłn Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; ArgentinaFil: Pontoriero, Andrea. DirecciĂłn Nacional de Institutos de InvestigaciĂłn. AdministraciĂłn Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; ArgentinaFil: Benedetti, EstefanĂa. DirecciĂłn Nacional de Institutos de InvestigaciĂłn. AdministraciĂłn Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; ArgentinaFil: Baumeister, Elsa. DirecciĂłn Nacional de Institutos de InvestigaciĂłn. AdministraciĂłn Nacional de Laboratorios e Institutos de Salud. Instituto Nacional de Enfermedades Infecciosas; ArgentinaFil: Rudolf, Fabian. Eidgenössische Technische Hochschule ZĂŒrich; SuizaFil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de Investigaciones BiomĂ©dicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones BiomĂ©dicas en Retrovirus y Sida; ArgentinaFil: Garcia, Cybele. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de QuĂmica BiolĂłgica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de QuĂmica BiolĂłgica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Buggiano, Valeria Carmen. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Kornblihtt, Alberto Rodolfo. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Srebrow, Anabella. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: de la Mata, Manuel. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Muñoz, Manuel Javier. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Schor, Ignacio Esteban. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; ArgentinaFil: Petrillo, Ezequiel. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de FisiologĂa, BiologĂa Molecular y Neurociencias; Argentin
GlicĂŽmica da resposta imune: o universo de glicanos e lectinas em microambientes inflamatĂłrios e neoplĂĄsicos
Las galectinas, una familia de lectinas que reconocen glico-conjugados especĂficos en la superficie celular y la matriz, participan en diversos procesos biolĂłgicos como reguladores de la ho-meostasis de la respuesta inmune y de la progresiĂłn tumoral. Considerando el papel inmunomodulador de Galectina-1 (Gal-1) en modelos de inflamaciĂłn crĂłnica y su contribuciĂłn a la creaciĂłn de microambientes tolerogĂ©nicos, durante los Ășltimos años exploramos el impacto de esta proteĂna sobre el balance de cĂ©lulas T y la funcionalidad de cĂ©lulas dendrĂticas (CDs). Mientras las cĂ©lulas Th1 y Th17 poseen el repertorio de glicanos necesarios para la uniĂłn de Gal-1, los linfocitos Th2 son resistentes a la uniĂłn de esta proteĂna, lo cual explicarĂa el incremento en la susceptibilidad de los linfocitos Th1 y Th17 a la apoptosis inducida por Gal-1 y la consecuente desviaciĂłn en el balance de la respuesta inmune hacia un perfil Th2. AdemĂĄs, identificamos un circuito tolerogĂ©nico en el que Galâ1 induce la diferenciaciĂłn de CDs tolerogĂ©nicas productoras de ILâ27, la consecuente expansiĂłn de cĂ©lulas T regulatorias productoras de ILâ10 y la supresiĂłn de la inflamaciĂłn mediada por cĂ©lulas Th1 y Th17. Postulamos un nuevo mecanismo de regulaciĂłn homeostĂĄtica de la respuesta inmune basado en la interacciĂłn entre Galâ1 y sus gli-canos especĂficos, el cual permite anticipar nuevos horizontes terapĂ©uticos, en los que la modulaciĂłn de la expresiĂłn de Galâ1 o sus glicanos nos permitirĂa regular la respuesta inmune.Galectins, a family of endogenous glycan-binding proteins able to recognize specific glycoconjugates on cell surface and extracellular matrix, control critical immunological processes involved in immune homeostasis and tumor progression. Given the immunosuppressive role of Galectin-1 (Gal-1) in different models of chronic inflammation and its contribution to the creation of tolerogenic microenvironments in cancer and pregnancy models, the impact of this protein on T helper cell balance and dendritic cells (DCs) functionality was explored. A novel mechanism, based on the differential glycosylation of T helper cell subsets, by which Gal-1 preferentially eliminates antigen-specific Th1 and Th17 cells, leading to a shift toward a Th2 profile was identified. While Th1- and Th-17-differentiated cells expressed the repertoire of cell surface glycans that are critical for Gal-1-induced cell death, Th2 cells are protected from Gal-1 through differential sialylation of cell surface glycoproteins. More recently, the ability of Gal-1 to trigger the differentiation of tolerogenic dendritic cells (DCs), which promote resolution of autoimmune inflammation, was demonstrated. A tolerogenic circuit linking Gal-1 signaling, IL-27-producing DCs and IL-10-secreting T cells was identified. It can be postulated that molecular interactions between endogenous galectins and specific glycans constitute a novel mechanism of homeostatic regulation of immune responses. Understanding the role of protein-glycan interactions in the establishment of tolerogenic or inflammatory programs will enable the design of more rational immunotherapeutic strategies with broad biomedical implications.As galectinas, uma famĂlia de lectinas que reconhecem gli-coconjugados especĂficos na superfĂcie celular e a matriz, participam em diversos processos biolĂłgicos como reguladores da homeostase da resposta imune e da progressĂŁo tu-moral. Considerando o papel imunomodulador de Galec-tina-1 (Gal-1) em modelos de inflamação crĂŽnica e sua contribuição Ă criação de microambientes tolerogĂȘnicos, durante os Ășltimos anos exploramos o impacto desta proteĂna sobre o balanço de cĂ©lulas T e a funcionalidade de cĂ©lulas dendrĂticas (CDs). Enquanto as cĂ©lulas Th1 e Th17 possuem o repertĂłrio de glicanos necessĂĄrios para a uniĂŁo de Gal-1, os linfĂłcitos Th2 sĂŁo resistentes Ă uniĂŁo desta proteĂna, o qual explicaria o incremento na suscetibilidade dos linfĂłci-tos Th1 e Th17 Ă apoptose induzida por Gal-1 e o conse-guinte desvio no balanço da resposta imune para um perfil Th2. AlĂ©m disso, identificamos um circuito tolerogĂȘnico no qual Galâ1 induz a diferenciação de CDs tolerogĂȘnicas pro-dutoras de ILâ27, a conseguinte expansĂŁo de cĂ©lulas T re-gulatĂłrias produtoras de ILâ10 e a supressĂŁo da inflamação mediada por cĂ©lulas Th1 e Th17. Postulamos um novo mecanismo de regulação homeostĂĄtica da resposta imune ba-seado na interação entre Galâ1 e seus glicanos especĂficos, que permite antecipar novos horizontes terapĂȘuticos, nos quais a modulação da expressĂŁo de Galâ1 ou seus glicanos nos permitiria regular a resposta imune.Fil: Sundblad, Victoria. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Compagno, Daniel Georges. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de QuĂmica BiolĂłgica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Croci Russo, Diego Omar. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: D'alotto Moreno, Tomas. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Dergan Dylon, Leonardo Sebastian. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Di Lella, Santiago. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Gatto, Claudia. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de Investigaciones en IngenierĂa GenĂ©tica y BiologĂa Molecular; ArgentinaFil: Gentilini, Lucas Daniel. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Giribaldi, MarĂa Laura. Universidad de Buenos Aires. Facultad de Cs.exactas y Naturales. Departamento de Quimica Biologica. Laboratorio de Analisis Biologicos E Inmunoquimica; ArgentinaFil: Guardia, Carlos Manuel Alberto. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Ilarregui, Juan Martin. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Laderach, Diego Jose. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Ciudad Universitaria. Instituto de QuĂmica BiolĂłgica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: MartĂnez Allo, VerĂłnica Candela. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Mascanfroni, Ivan DarĂo. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Mendez Huergo, Santiago Patricio. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Salatino, Mariana. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Toscano, Marta Alicia. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; ArgentinaFil: Rabinovich, Gabriel Adrian. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de BiologĂa y Medicina Experimental (i); Argentina; Argentin
Neutrophils play a key role in the initiation of glomerular hematuria in a postinfectious igan experimental model
2 p.BACKGROUND AND AIMS: Hematuria is a common finding in patients with IgA nephropathy (IgAN), occurring mainly after upper respiratory tract infections.Hematuria can lead to acute kidney injury and chronic loss of renal function in IgAN.However, the mechanisms involved in egression of erythrocytes from the glomerular
capillaries into the urinary space are unknown. To answer this question, we developed an infection with Streptococcus pneumoniae (SP) in a humanized experimental IgAN model (a1KICD89tg mice) that resembles the pathological and clinical findings of disease (IgA1 and soluble CD89 mesangial deposits, complement activation,proteinuria and hematuria).METHOD: a1KICD89tg mice (12 weeks old) received an intranasal instillation of SP(107 bacteria). Blood, urine and renal samples were obtained during 1 month after induction of respiratory infection. The presence of SP in lungs from these mice was confirmed by microbiological analysis. Hematuria was quantified in the urinary
sediment and renal function was determined by biochemical analysis. Renal histological characteristics were evaluated by hematoxylin/eosin, massonâs trichrome and PAS staining. IgA glomerular deposits, activation of complement system and infiltration of proinflammatory cells was examined by immunohistochemistry or
immunofluorescence. Circulating leukocyte populations were studied on a hemocytometer. Renal inflammatory cytokines, metalloproteases, as well as markers of tubular and glomerular damage were determined in kidneys by RT-PCR and western-blot. To further validate the role of neutrophils in this pathological setting, we selective
depleted these cells through a single injection of anti-Ly6G mAb (200 mg/kg i.p).RESULTS: SP-intranasal instillation in a1KICD89tg mice increased hematuria,microalbuminuria and proteinuria, peaking at 48h after induction of the respiratory infection. SP instillation caused disruption of the glomerular basement membrane,with decreased expression of the slit diaphragm proteins nephrin and synaptopodin, as well as higher glomerular accumulation of IgA and proteins of complement system
(C3, MBL). Hematuria intensity was positively correlated with the presence of interstitial F4/80ĂŸ macrophages, matrix metalloproteinase 9 (MMP-9), inflammatory cytokines and chemokines (IL-1b, IL-6, TNF-a, CCL-2, CCL5 and CX3CL1/CX3CR1) as well as p65 NF-jB activation. Hematuria was negatively correlated with anti inflammatory IL-10 mRNA expression, Factor H levels and collagen IV content. Notably, SP infection induced expression of the tubular injury markers N-GAL andKIM-1. Increased peripheral neutrophils levels were observed in the SP-infected a1KICD89tg mice. Mechanistically, anti-Ly6G-mediated neutrophil depletion reduced SP-mediated hematuria, proteinuria and albuminuria, prevented loss of synaptopodin
and nephrin, decreased renal inflammation and MMP-9 expression in a1KICD89tg mice.CONCLUSION: In a humanized mouse model of IgAN, hematuria bouts following respiratory tract infections are caused by a neutrophil-mediated alteration of the glomerular filtration barrier (podocyte damage, complement deposits and loss of Collagen IV). These findings may help to unveil novel potential therapeutic approaches to combat one of the key elements in the progression of IgAN and related conditions.Peer reviewe
Circulating carotenoids are associated with favorable lipid and fatty acid profiles in an older population at high cardiovascular risk
Carotenoid intake has been reported to be associated with improved cardiovascular health, but there is little information on actual plasma concentrations of these compounds as biomarkers of cardiometabolic risk. The objective was to investigate the association between circulating plasma carotenoids and different cardiometabolic risk factors and the plasma fatty acid profile. This is a cross-sectional evaluation of baseline data conducted in a subcohort (106 women and 124 men) of an ongoing multi-factorial lifestyle trial for primary cardiovascular prevention. Plasma concentrations of carotenoids were quantified by liquid chromatography coupled to mass spectrometry. The associations between carotenoid concentrations and cardiometabolic risk factors were assessed using regression models adapted for interval-censored variables. Carotenoid concentrations were cross-sectionally inversely associated with serum triglyceride concentrations [-2.79 mg/dl (95% CI: -4.25, -1.34) and -5.15 mg/dl (95% CI: -7.38, -2.93), p-values = 0.0002 and <0.00001 in women and men, respectively], lower levels of plasma saturated fatty acids [-0.09% (95% CI: -0.14, -0.03) and -0.15 % (95% CI: -0.23, -0.08), p-values = 0.001 and 0.0001 in women and men, respectively], and higher levels of plasma polyunsaturated fatty acids [(0.12 % (95% CI: -0.01, 0.25) and 0.39 % (95% CI: 0.19, 0.59), p-values = 0.065 and 0.0001 in women and men, respectively] in the whole population. Plasma carotenoid concentrations were also associated with higher plasma HDL-cholesterol in women [0.47 mg/dl (95% CI: 0.23, 0.72), p-value: 0.0002], and lower fasting plasma glucose in men [-1.35 mg/dl (95% CI: -2.12, -0.59), p-value: 0.001]. Keywords: Mediterranean diet; PREDIMED-plus study; cardiovascular health; liquid chromatography; mass spectrometry; plasma carotenoids
RICORS2040 : The need for collaborative research in chronic kidney disease
Chronic kidney disease (CKD) is a silent and poorly known killer. The current concept of CKD is relatively young and uptake by the public, physicians and health authorities is not widespread. Physicians still confuse CKD with chronic kidney insufficiency or failure. For the wider public and health authorities, CKD evokes kidney replacement therapy (KRT). In Spain, the prevalence of KRT is 0.13%. Thus health authorities may consider CKD a non-issue: very few persons eventually need KRT and, for those in whom kidneys fail, the problem is 'solved' by dialysis or kidney transplantation. However, KRT is the tip of the iceberg in the burden of CKD. The main burden of CKD is accelerated ageing and premature death. The cut-off points for kidney function and kidney damage indexes that define CKD also mark an increased risk for all-cause premature death. CKD is the most prevalent risk factor for lethal coronavirus disease 2019 (COVID-19) and the factor that most increases the risk of death in COVID-19, after old age. Men and women undergoing KRT still have an annual mortality that is 10- to 100-fold higher than similar-age peers, and life expectancy is shortened by ~40 years for young persons on dialysis and by 15 years for young persons with a functioning kidney graft. CKD is expected to become the fifth greatest global cause of death by 2040 and the second greatest cause of death in Spain before the end of the century, a time when one in four Spaniards will have CKD. However, by 2022, CKD will become the only top-15 global predicted cause of death that is not supported by a dedicated well-funded Centres for Biomedical Research (CIBER) network structure in Spain. Realizing the underestimation of the CKD burden of disease by health authorities, the Decade of the Kidney initiative for 2020-2030 was launched by the American Association of Kidney Patients and the European Kidney Health Alliance. Leading Spanish kidney researchers grouped in the kidney collaborative research network Red de Investigación Renal have now applied for the Redes de Investigación Cooperativa Orientadas a Resultados en Salud (RICORS) call for collaborative research in Spain with the support of the Spanish Society of Nephrology, Federación Nacional de Asociaciones para la Lucha Contra las Enfermedades del Riñón and ONT: RICORS2040 aims to prevent the dire predictions for the global 2040 burden of CKD from becoming true
Canagliflozin and renal outcomes in type 2 diabetes and nephropathy
BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodiumâglucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with reninâangiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years
Impact of COVID-19 on cardiovascular testing in the United States versus the rest of the world
Objectives: This study sought to quantify and compare the decline in volumes of cardiovascular procedures between the United States and non-US institutions during the early phase of the coronavirus disease-2019 (COVID-19) pandemic.
Background: The COVID-19 pandemic has disrupted the care of many non-COVID-19 illnesses. Reductions in diagnostic cardiovascular testing around the world have led to concerns over the implications of reduced testing for cardiovascular disease (CVD) morbidity and mortality.
Methods: Data were submitted to the INCAPS-COVID (International Atomic Energy Agency Non-Invasive Cardiology Protocols Study of COVID-19), a multinational registry comprising 909 institutions in 108 countries (including 155 facilities in 40 U.S. states), assessing the impact of the COVID-19 pandemic on volumes of diagnostic cardiovascular procedures. Data were obtained for April 2020 and compared with volumes of baseline procedures from March 2019. We compared laboratory characteristics, practices, and procedure volumes between U.S. and non-U.S. facilities and between U.S. geographic regions and identified factors associated with volume reduction in the United States.
Results: Reductions in the volumes of procedures in the United States were similar to those in non-U.S. facilities (68% vs. 63%, respectively; p = 0.237), although U.S. facilities reported greater reductions in invasive coronary angiography (69% vs. 53%, respectively; p < 0.001). Significantly more U.S. facilities reported increased use of telehealth and patient screening measures than non-U.S. facilities, such as temperature checks, symptom screenings, and COVID-19 testing. Reductions in volumes of procedures differed between U.S. regions, with larger declines observed in the Northeast (76%) and Midwest (74%) than in the South (62%) and West (44%). Prevalence of COVID-19, staff redeployments, outpatient centers, and urban centers were associated with greater reductions in volume in U.S. facilities in a multivariable analysis.
Conclusions: We observed marked reductions in U.S. cardiovascular testing in the early phase of the pandemic and significant variability between U.S. regions. The association between reductions of volumes and COVID-19 prevalence in the United States highlighted the need for proactive efforts to maintain access to cardiovascular testing in areas most affected by outbreaks of COVID-19 infection
Penilaian Kinerja Keuangan Koperasi di Kabupaten Pelalawan
This paper describe development and financial performance of cooperative in District Pelalawan among 2007 - 2008. Studies on primary and secondary cooperative in 12 sub-districts. Method in this stady use performance measuring of productivity, efficiency, growth, liquidity, and solvability of cooperative. Productivity of cooperative in Pelalawan was highly but efficiency still low. Profit and income were highly, even liquidity of cooperative very high, and solvability was good
Infected pancreatic necrosis: outcomes and clinical predictors of mortality. A post hoc analysis of the MANCTRA-1 international study
: The identification of high-risk patients in the early stages of infected pancreatic necrosis (IPN) is critical, because it could help the clinicians to adopt more effective management strategies. We conducted a post hoc analysis of the MANCTRA-1 international study to assess the association between clinical risk factors and mortality among adult patients with IPN. Univariable and multivariable logistic regression models were used to identify prognostic factors of mortality. We identified 247 consecutive patients with IPN hospitalised between January 2019 and December 2020. History of uncontrolled arterial hypertension (pâ=â0.032; 95% CI 1.135-15.882; aOR 4.245), qSOFA (pâ=â0.005; 95% CI 1.359-5.879; aOR 2.828), renal failure (pâ=â0.022; 95% CI 1.138-5.442; aOR 2.489), and haemodynamic failure (pâ=â0.018; 95% CI 1.184-5.978; aOR 2.661), were identified as independent predictors of mortality in IPN patients. Cholangitis (pâ=â0.003; 95% CI 1.598-9.930; aOR 3.983), abdominal compartment syndrome (pâ=â0.032; 95% CI 1.090-6.967; aOR 2.735), and gastrointestinal/intra-abdominal bleeding (pâ=â0.009; 95% CI 1.286-5.712; aOR 2.710) were independently associated with the risk of mortality. Upfront open surgical necrosectomy was strongly associated with the risk of mortality (pâ<â0.001; 95% CI 1.912-7.442; aOR 3.772), whereas endoscopic drainage of pancreatic necrosis (pâ=â0.018; 95% CI 0.138-0.834; aOR 0.339) and enteral nutrition (pâ=â0.003; 95% CI 0.143-0.716; aOR 0.320) were found as protective factors. Organ failure, acute cholangitis, and upfront open surgical necrosectomy were the most significant predictors of mortality. Our study confirmed that, even in a subgroup of particularly ill patients such as those with IPN, upfront open surgery should be avoided as much as possible. Study protocol registered in ClinicalTrials.Gov (I.D. Number NCT04747990)
- âŠ