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The active forms of Au and Pt in CeO2-based catalysts for the water-gas shift (WGS) reaction are an issue that remains unclear, although it has been widely studied. On one hand, ionic species might be responsible for weakening the Ce-O bonds, thus increasing the oxygen mobility and WGS activity. On the other hand, the close contact of Au or Pt atoms with CeO2 oxygen vacancies at the metal-CeO2 interface might provide the active sites for an efficient reaction. In this work, using in situ X-ray absorption spectroscopy, we demonstrate that both Au and Pt remain unoxidized during the reaction. Remarkable differences involving the dynamics established by both species under WGS atmospheres were recognized. For the prereduced Pt catalyst, the increase of the conversion coincided with a restructuration of the Pt atoms into cuboctahedrical metallic particles without significant variations on the overall particle size. Contrary to the relatively static behavior of Pt0, Au0 nanoparticles exhibited a sequence of particle splitting and agglomeration while maintaining a zero oxidation state despite not being located in a metallic environment during the process. High WGS activity was obtained when Au atoms were surrounded by oxygen. The fact that Au preserves its unoxidized state indicates that the chemical interaction between Au and oxygen must be necessarily electrostatic and that such an electrostatic interaction is fundamental for a top performance in the WGS process.

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We determined the effect of conjugated equine estrogen plus medroxyprogesterone acetate on calcium content of aortic atherosclerotic lesions in oophorectomized adult New Zealand rabbits submitted to a cholesterol rich diet. Five groups of 10 animals each were studied: G1 = control, G2 = cholesterol diet only, G3 = diet plus conjugated equine estrogen (0.625 mg/day); G4 and G5 = diet, conjugated equine estrogen (0.625 mg/day) plus medroxyprogesterone acetate (5 and 10 mg/day, respectively). Mean weight varied from 2.7 +/- 0.27 to 3.1 +/- 0.20 kg (P = 0.38) between groups at the beginning and 3.1 +/- 0.27 to 3.5 +/- 0.20 kg (P = 0.35) at the end of the experiment. Cholesterol and triglyceride levels were determined at the time of oophorectomy, 21 days after surgery (time 0), and at the end of follow-up of 90 days. The planimetric method was used to measure plaque and caryometric method for histopathologic examination of the aorta. Calcium content was determined by the method of von Kossa. A similar increase in cholesterol occurred in all treated groups without differences between them at the end of the study. Groups G4 and G5 had smaller areas of atherosclerotic lesions (2.33 +/- 2.8 and 2.45 +/- 2.1 cm(2), respectively) than the groups receiving no progestogens (G2: 5.6 +/- 4 and G3: 4.6 +/- 2.8 cm(2); P = 0.02). The relation between lesion area and total aorta area was smaller in groups treated with combined drugs compared to the groups receiving no progesterone (G4: 14.9 +/- 13 and G5: 14.2 +/- 13.4 vs G2: 35.8 +/- 26 and G3: 25 +/- 8 cm(2), respectively; P = 0.017). Oral conjugated equine estrogen (0.625 mg/day) plus medroxyprogesterone acetate (5 or 10 mg/day) provoked a greater reduction in atherosclerotic plaque area and calcium content in treated groups, suggesting a dose-dependent effect.

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We determined the effect of conjugated equine estrogen plus medroxyprogesterone acetate on calcium content of aortic atherosclerotic lesions in oophorectomized adult New Zealand rabbits submitted to a cholesterol rich diet. Five groups of 10 animals each were studied: G1 = control, G2 = cholesterol diet only, G3 = diet plus conjugated equine estrogen (0.625 mg/day); G4 and G5 = diet, conjugated equine estrogen (0.625 mg/day) plus medroxyprogesterone acetate (5 and 10 mg/day, respectively). Mean weight varied from 2.7 ± 0.27 to 3.1 ± 0.20 kg (P = 0.38) between groups at the beginning and 3.1 ± 0.27 to 3.5 ± 0.20 kg (P = 0.35) at the end of the experiment. Cholesterol and triglyceride levels were determined at the time of oophorectomy, 21 days after surgery (time 0), and at the end of follow-up of 90 days. The planimetric method was used to measure plaque and caryometric method for histopathologic examination of the aorta. Calcium content was determined by the method of von Kossa. A similar increase in cholesterol occurred in all treated groups without differences between them at the end of the study. Groups G4 and G5 had smaller areas of atherosclerotic lesions (2.33 ± 2.8 and 2.45 ± 2.1 cm², respectively) than the groups receiving no progestogens (G2: 5.6 ± 4 and G3: 4.6 ± 2.8 cm²; P = 0.02). The relation between lesion area and total aorta area was smaller in groups treated with combined drugs compared to the groups receiving no progesterone (G4: 14.9 ± 13 and G5: 14.2 ± 13.4 vs G2: 35.8 ± 26 and G3: 25 ± 8 cm², respectively; P = 0.017). Oral conjugated equine estrogen (0.625 mg/day) plus medroxyprogesterone acetate (5 or 10 mg/day) provoked a greater reduction in atherosclerotic plaque area and calcium content in treated groups, suggesting a dose-dependent effect.

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OBJECTIVE: To report about a group of physicians' understanding of the recommendations of the II Brazilian Guidelines Conference on Dyslipidemias, and about the state of the art of primary and secondary prevention of atherosclerosis. METHODS: Through the use of a questionnaire on dyslipidemia, atherosclerosis prevention, and recommendations for lipid targets established by the II Brazilian Guidelines Conference on Dyslipidemias, 746 physicians, 98% cardiologists, were evaluated. RESULTS: Eighty-seven percent of the respondents stated that the treatment of dyslipidemia changes the natural history of coronary disease. Although most of the participants followed the total cholesterol recommendations (<200mg/dL for atherosclerosis prevention), only 55.8% would adopt the target of LDL-C <100 mg/dL for secondary prevention. Between 30.5 and 36.7% answered, in different questions, that the recommended level for HDL-C should be <35mg/dL. Only 32.7% would treat their patients indefinitely with lipid- lowering drugs. If the drug treatment did not reach the proposed target, only 35.5% would increase the dosage, and 29.4% would change the medication. Participants did not know the targets proposed for diabetics. CONCLUSION: Although the participating physicians valued the role played by lipids in the prevention of atherosclerosis, serious deficiencies exist in their knowledge of the recommendations given during the II Brazilian Guidelines Conference on Dyslipidemias.

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OBJECTIVE: To characterize the risk profile for atherosclerosis (AS) in adolescents and young adults of a private university in São Paulo. METHODS: Clinical, nutritional, and laboratory parameters were evaluated in 209 students of both genders aged 17 to 25 years. In addition to determination of the lipid profile, the association of its abnormal values with other risk factors for AS was also investigated. RESULTS: Increased levels of total cholesterol, LDL-C and triglycerides (TG) were observed in 9.1%, 7.6% and 16.3% of the students, respectively, and decreased levels of HDL-C in 8.6% of them. Prevalence of the remaining risk factors analyzed was elevated: sedentary life style (78.9%); high intake of total fat (77.5%); high cholesterol intake (35.9%); smoking, hypertension (15.8%) and obesity (7.2%). There was an association between elevated LDL-C and TG levels and sedentary life style and body mass index. CONCLUSION: The high prevalence of risk factors for AS in young individuals draws attention to the need for adopting preventive plans.

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The purpose of the present study was to examine the importance of magnesium in endothelial function after arterial balloon injury. Male Wistar rats were fed normal, high or low concentrations of magnesium. Three weeks later the animals underwent endothelial injury of the thoracic aorta by a balloon catheter or a sham operation. Biochemical, histological and endothelial function analysis were performed 15 days after the surgical treatment. The animals fed a low magnesium diet presented the lowest level of serum magnesium and the highest ionized blood calcium levels. Histomorphometric analysis revealed no differences among groups neither regarding the magnitude of intimal thickening nor the recovery of endothelial coverage. However, when vasoreactivity responses were compared in the balloon-injured group, those animals fed a high magnesium diet had the better endothelium-dependent vascular relaxation. In conclusion, a higher magnesium level in the diet was beneficial to vessels that underwent endothelial injury by balloon catheter.

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PURPOSE: To evaluate lipid profile changes associated with cholestyramine addition in hypercholesterolemic patients with established coronary heart disease under treatment with HMG-CoA reductase inhibitors that had not achieved the ideal value of LDL-cholesterol. METHODS: Twenty patients with coronary heart disease, (12 submitted to coronary artery bypass grafts, 3 to coronary angioplasty and 5 maintained under clinical management) with mean age of 60.78 years old, who were under hypolipemic diet and were medicated with lovastatin 20 mg/d or simvastatin 10 mg/d, received cholestyramine, doses ranging from 8 to 16 g/day during 8 weeks, aiming to reduce LDL-cholesterol to values less than 100 mg/dL. RESULTS: There was a significant reduction of total cholesterol, from initial mean value of 239.52 mg/dL to final mean value of 199.00 mg/dL, with a mean reduction of 16.92%. The mean value of LDL-cholesterol was also reduced significantly from 172.73 mg/dL to 118.26 mg/dL, with a mean reduction of 31.53%. Mean triglyceridemia increased, still within the normal reference values, from 145.05 mg/dL to 162.00 mg/dL, and the mean difference was 11.69%. There was a significant increase of HDL-cholesterol fraction from an initial mean value of 38.00 mg/dL to a final mean value of 48.21 mg/dL, mean difference of 26.87%. Side effects were not frequent, and did not interfere in the duration of the study. CONCLUSION: The association of cholestyramine to HMG-CoA reductase inhibitors, both in low doses, in patients with primary hypercholesterolemia and high coronary risk is a good therapeutic option that can reach benefits on the lipid profile similar to those obtained when these drugs are used in association or separately in higher doses.

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We have studied fibrinogen levels (Clauss technique) in atherothrombotic ischemic stroke patients, in order to determine its role as a thrombogenic risk factor. Twenty nine patients (20 men and 9 women) between 25 and 79 years old were studied; they all have had a atherothrombotic stroke. They were classified into two groups according to the result of their carotid doppler ultrasonography: gl-without carotid flow reduction (n = 19) and g2-with carotid flow reduction (n = 10). The fibrinogen mean value was 269 mg/dl in gl and 353 mg/dl in g2. There were 47% of patients in gl and 80% of patients in g2 who presented levels > 300 mg/dl. The proportions of the groups were significantly different (p < 0.05). Considering the epidemiological value of 300 mg/dl, we conclude that the fibrinogen can be an independent risk factor for ischemic atherothrombotic stroke, specially in those whose carotid flow is reduced.

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PURPOSE: To evaluate the clinical efficacy of etofibrate in primary hyperlipidemia in patients from clinical centers representative of all main Brazilian cities. METHODS: One thousand, nine hundred and fourty three hyperlipidemic patients were submitted to diet and drug treatment with etofibrate (500 mg/day) for eight weeks. The data b WAS analyzed as to changes in the lipoprotein profile, as well as the side effects. RESULTS: There was an important reduction in total cholesterol (19.88%), triglycerides (29.59%), LDL-c (14.89%) and VLDL-c (14.54%) concentration. There was a significant increase in HDL-c (18.14%). Adverse effects were observed in 8.5% of the patients, without major clinical relevance, however, in 1.44% the treatment had to be interrupted. CONCLUSION: Administration of etofibrate promoted positive changes in all parameters of the lipid and lipoprotein profile, thus reducing the risk of atherosclerotic disease, without significant side effects in the great majority of sample studied.

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PURPOSE: To evaluate modifications on lipid profile, fibrinogen and platelet aggregation induced by etofibrate. METHODS: Twenty-one adult patients were studied. They all had primary hyperlipidemia and had already been on the AHA step I diet and placebo. Etofibrate (500mg/day) was administered for 60 days in the active phase, when lipid parameters, fibrinogen and platelet aggregation were measured. RESULTS: The % significant reductions were: total cholesterol (-9.50%), LDL-cholesterol (-7.88%), triglycerides (-19.07%), total cholesterol/HDL-cholesterol(-11.90%), LDL-cholesterol/HDL-cholesterol (-10.20%), fibrinogen (-12.79%), platelet aggregation with adrenaline (-24.02%), with ADP 1 mumol (-30.13%), and ADP 3 mumol (-24.51%). CONCLUSION: The beneficial effects of etofibrate were observed not only on the lipid profile but also on the thrombogenic parameters measured by fibrinogen and platelet aggregation.

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Objetivo - avaliar os efeitos do etofibrato sobre variáveis lipídicas, fibrinogênio e agregaçäo plaquetária. Métodos - foram selecionados 21 portadores de hiperlipidemia primária, associada a fatores de risco para doença coronária, após introduçäo de dieta (AHA fase I) e dias, analisando-se as modificaçöes lipídicas induzidas (colesterol total e fraçöes, triglicérides) e efeitos sobre o fibrinogênio e agregaçäo plaquetária. Resultados - foram observadas reduçöes percentuais significantes das variávs: colesterol total (9,50 por cento), LDL-colesterol (-7,88 por cento), triglicérides (19,07 por cento), colesterol total/HDL-colesterol (-11,90 por cento), LDL-colesterol/HDL-colesterol (-19,20 por cento), fibrinogênio (-12, 79 por cento) agregaçäo plaquetária com adrenalina (-24,02 por cento), com ADP 1 ymol (-30,13 por cento), com ADP 3 ymol (-24,51 por cento). Conclusäo - efietos benéficos do etofibrato foram observados näo somente sobre o perfil lipídico mas, também sobre variáveis de trobogenicidae como o fibrinogênio e a agregaçäo plaquetária.

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PURPOSE: To evaluate the effects of pravastatin on lipoproteins, Lp (a), apo B and apo A-I and its tolerability in primary hypercholesterolemic patients in our outpatient lipid clinic. METHODS: Twenty-two primary hypercholesterolemic patients were evaluated. They had all been treated previously with other hypocholesterolemic drugs, including the statins, forming a specific and homogeneous group with hypercholesterolemia and definite coronary risk. After 7 weeks with American Heart Association phase I diet and placebo drug, pravastatin was administered during 12 weeks. All patients received an initial daily dose of 10 mg for six weeks. After this period, this dose was increased to 20 mg. The levels of cholesterol, triglycerides, high-density lipoprotein, lipoprotein (a) and apolipoproteins A-1 and B were determined. RESULTS: No changes occurred with diet and placebo, but pravastatin at a daily dose of 10 mg, reduced significantly cholesterol level (7.22%), LDL-cholesterol (13.08%) and increased HDL-cholesterol (7.81%). The results were better with 20 mg, achieving a reduction of (28.21%) in cholesterol, (36.88%) in LDL-cholesterol, (17.06%) in apo B level and an increase of (10.06%) in HDL-cholesterol. The smaller effect observed with the more commonly used dosage (10 mg/day) was most probably due to the characteristics of the sample with already established hypercholesterolemia, being thus dependent of higher concentrations of medications, as observed in previous treatments in our outpatient clinic. Side affects with this drug were rare. No biochemical changes were observed that would interrupt the continuation of therapy. CONCLUSION: Pravastatin was well tolerated and promoted favorable changes in the total cholesterol, LDL, apo B and cholesterol/HDL and LDL/HDL ratios of primary hypercholesterolemic patients.

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PURPOSE: To compare the effects of lovastatin and gemfibrozil in patients with primary hyperlipidemias. PATIENTS AND METHODS: Forty patients with cholesterolemia over 200 mg/dl and triglyceridemia not higher than 350 mg/dl, excluded secondary causes, were selected. Twenty patients received lovastatin and 20 gemfibrozil. In order to establish the lipid profile, blood samples were taken after 2 months without medication, after 4 weeks of diet and placebo and after 6 and 12 weeks of active treatment. Biochemical profile was determined before and after the treatment with active drug. RESULTS: Thirty nine patients completed the study. Total and LDL-cholesterol were significantly reduced (p less than 0.05) by both drugs but lovastatin had greater effect. Only gemfibrozil reduced triglycerides significantly. Neither drug had significant effects on HDL-cholesterol. The tolerance was satisfactory; only one patient (using gemfibrozil) needed to stop the treatment due to gastrointestinal side effects. The biochemical profile did not present any significant alteration. CONCLUSION: Both drugs produced useful effects on the lipid profile. Lovastatin produced greater reductions of total and LDL-cholesterol, while gemfibrozil was more active reducing triglycerides. Neither drug changed significantly the HDL-cholesterol.

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