Institution
Federal University of São Paulo
Education•São Paulo, Brazil•
About: Federal University of São Paulo is a education organization based out in São Paulo, Brazil. It is known for research contribution in the topics: Population & Transplantation. The organization has 27971 authors who have published 49365 publications receiving 935536 citations. The organization is also known as: Universidade Federal de São Paulo & Universidade Federal de Sao Paulo.
Papers published on a yearly basis
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TL;DR: Atypical EPEC is more closely related to Shiga toxin–producing E. coli (STEC), and like STEC these strains appear to be emerging pathogens.
Abstract: Typical and atypical enteropathogenic Escherichia coli (EPEC) strains differ in several characteristics. Typical EPEC, a leading cause of infantile diarrhea in developing countries, is rare in industrialized countries, where atypical EPEC seems to be a more important cause of diarrhea. For typical EPEC, the only reservoir is humans; for atypical EPEC, both animals and humans can be reservoirs. Typical and atypical EPEC also differ in genetic characteristics, serotypes, and virulence properties. Atypical EPEC is more closely related to Shiga toxin–producing E. coli (STEC), and like STEC these strains appear to be emerging pathogens.
624 citations
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University of Glasgow1, University of Oxford2, University of Texas Health Science Center at San Antonio3, Novartis4, Moscow State University5, University of North Carolina at Chapel Hill6, University College Cork7, Federal University of São Paulo8, National Taiwan University9, Centre Hospitalier Universitaire de Nantes10, The Chinese University of Hong Kong11, University of Leicester12, University of California, Berkeley13, University of Bern14, Tulane University15, Royal North Shore Hospital16, Medical University of Warsaw17, Harvard University18, Istanbul University19, University of Tromsø20, University of Washington21, Alfred Hospital22, University of Toronto23, University of Cape Town24, Cordoba University25, University of Illinois at Chicago26, Lahey Hospital & Medical Center27, University Medical Center Utrecht28, Umeå University29, Dresden University of Technology30, University of Liège31, Aarhus University32, Cardiovascular Institute of the South33, University of Copenhagen34, Semmelweis University35, University of Helsinki36, Duke University37
TL;DR: Among patients with impaired glucose tolerance and cardiovascular disease or risk factors, the use of valsartan for 5 years, along with lifestyle modification, led to a relative reduction of 14% in the incidence of diabetes but did not reduce the rate of cardiovascular events.
Abstract: BACKGROUND: It is not known whether drugs that block the renin-angiotensin system reduce the risk of diabetes and cardiovascular events in patients with impaired glucose tolerance. METHODS: In this double-blind, randomized clinical trial with a 2-by-2 factorial design, we assigned 9306 patients with impaired glucose tolerance and established cardiovascular disease or cardiovascular risk factors to receive valsartan (up to 160 mg daily) or placebo (and nateglinide or placebo) in addition to lifestyle modification. We then followed the patients for a median of 5.0 years for the development of diabetes (6.5 years for vital status). We studied the effects of valsartan on the occurrence of three coprimary outcomes: the development of diabetes; an extended composite outcome of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, hospitalization for heart failure, arterial revascularization, or hospitalization for unstable angina; and a core composite outcome that excluded unstable angina and revascularization. RESULTS: The cumulative incidence of diabetes was 33.1% in the valsartan group, as compared with 36.8% in the placebo group (hazard ratio in the valsartan group, 0.86; 95% confidence interval [CI], 0.80 to 0.92; P<0.001). Valsartan, as compared with placebo, did not significantly reduce the incidence of either the extended cardiovascular outcome (14.5% vs. 14.8%; hazard ratio, 0.96; 95% CI, 0.86 to 1.07; P=0.43) or the core cardiovascular outcome (8.1% vs. 8.1%; hazard ratio, 0.99; 95% CI, 0.86 to 1.14; P=0.85). CONCLUSIONS: Among patients with impaired glucose tolerance and cardiovascular disease or risk factors, the use of valsartan for 5 years, along with lifestyle modification, led to a relative reduction of 14% in the incidence of diabetes but did not reduce the rate of cardiovascular events. (ClinicalTrials.gov number, NCT00097786.)
620 citations
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TL;DR: Cystatin C may represent a more adequate alternative to assess renal function in individuals with higher muscle mass when mild kidney impairment is suspected and was significantly related to serum and urinary creatinine but not with cystatin, even after adjustment for protein/meat intake and physical activity.
Abstract: Background and objectives: For addressing the influence of muscle mass on serum and urinary creatinine and serum cystatin C, body composition was assessed by skinfold thickness measurement and bioelectrical impedance analyses.
Design, setting, participants, & measurements: A total of 170 healthy individuals (92 women, 78 men) were classified as sedentary or with mild or moderate/intense physical activity. Blood, 24-h urine samples, and 24-h food recall were obtained from all individuals.
Results: Serum and urinary creatinine correlated significantly with body weight, but the level of correlation with lean mass was even greater. There was no significant correlation between body weight and lean mass with cystatin C. Individuals with moderate/intense physical activity presented significantly lower mean body mass index (23.1 ± 2.5 versus 25.7 ± 3.9 kg/m2) and higher lean mass (55.3 ± 10.0 versus 48.5 ± 10.4%), serum creatinine (1.04 ± 0.12 versus 0.95 ± 0.17 mg/dl), urinary creatinine (1437 ± 471 versus 1231 ± 430 mg/24 h), protein intake (1.4 ± 0.6 versus 1.1 ± 0.6 g/kg per d), and meat intake (0.7 ± 0.3 versus 0.5 ± 0.4 g/kg per d) than the sedentary individuals. Conversely, mean serum cystatin did not differ between these two groups. A multivariate analysis of covariance showed that lean mass was significantly related to serum and urinary creatinine but not with cystatin, even after adjustment for protein/meat intake and physical activity.
Conclusions: Cystatin C may represent a more adequate alternative to assess renal function in individuals with higher muscle mass when mild kidney impairment is suspected.
580 citations
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TL;DR: Evidence is presented that Trypanosoma cruzi-derived GPI anchors and GIPLs trigger CD25 expression on Chinese hamster ovary-K1 cells transfected with CD14 and Toll-like receptor-2 (TLR-2), but not wild-type (TLr-2-deficient) Chinese hamsters ovary cells, which may initiate host innate defense mechanisms and inflammatory response during protozoan infection.
Abstract: Glycosylphosphatidylinositol (GPI) anchors and glycoinositolphospholipids (GIPLs) from parasitic protozoa have been shown to exert a wide variety of effects on cells of the host innate immune system. However, the receptor(s) that are triggered by these protozoan glycolipids has not been identified. Here we present evidence that Trypanosoma cruzi-derived GPI anchors and GIPLs trigger CD25 expression on Chinese hamster ovary-K1 cells transfected with CD14 and Toll-like receptor-2 (TLR-2), but not wild-type (TLR-2-deficient) Chinese hamster ovary cells. The protozoan-derived GPI anchors and GIPLs containing alkylacylglycerol and saturated fatty acid chains or ceramide were found to be active in a concentration range of 100 nM to 1 microM. More importantly, the GPI anchors purified from T. cruzi trypomastigotes, which contain a longer glycan core and unsaturated fatty acids in the sn-2 position of the alkylacylglycerolipid component, triggered TLR-2 at subnanomolar concentrations. We performed experiments with macrophages from TLR-2 knockout and TLR-4 knockout mice, and found that TLR-2 expression appears to be essential for induction of IL-12, TNF-alpha, and NO by GPI anchors derived from T. cruzi trypomastigotes. Thus, highly purified GPI anchors from T. cruzi parasites are potent activators of TLR-2 from both mouse and human origin. The activation of TLR-2 may initiate host innate defense mechanisms and inflammatory response during protozoan infection, and may provide new strategies for immune intervention during protozoan infections.
579 citations
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TL;DR: It is shown that parasites induce the death and the detachment of their host hepatocytes, followed by the budding of parasite-filled vesicles (merosomes) into the sinusoid lumen, which ensures both the migration of parasites into the bloodstream and their protection from host immunity.
Abstract: The merozoite stage of the malaria parasite that infects erythrocytes and causes the symptoms of the disease is initially formed inside host hepatocytes. However, the mechanism by which hepatic merozoites reach blood vessels (sinusoids) in the liver and escape the host immune system before invading erythrocytes remains unknown. Here, we show that parasites induce the death and the detachment of their host hepatocytes, followed by the budding of parasite-filled vesicles (merosomes) into the sinusoid lumen. Parasites simultaneously inhibit the exposure of phosphatidylserine on the outer leaflet of host plasma membranes, which act as "eat me" signals to phagocytes. Thus, the hepatocyte-derived merosomes appear to ensure both the migration of parasites into the bloodstream and their protection from host immunity.
576 citations
Authors
Showing all 28240 results
Name | H-index | Papers | Citations |
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Majid Ezzati | 133 | 443 | 137171 |
Christian Guilleminault | 133 | 897 | 68844 |
Jean Rivier | 133 | 769 | 73919 |
Myron M. Levine | 123 | 789 | 60865 |
Werner Seeger | 114 | 1113 | 57464 |
Katherine L. Tucker | 106 | 683 | 39404 |
Michael Bader | 103 | 735 | 37525 |
Paulo A. Lotufo | 89 | 622 | 100527 |
Fernando Q. Cunha | 88 | 682 | 31501 |
Paul R. Sanberg | 87 | 635 | 29745 |
Harold A. Chapman | 87 | 191 | 26617 |
Ricardo T. Gazzinelli | 86 | 340 | 28233 |
Carlito B. Lebrilla | 86 | 495 | 25415 |
Roger S. McIntyre | 85 | 807 | 32040 |
Sergio Tufik | 85 | 1424 | 35174 |