Leonelo E Bautista
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Research Interests
Leonelo E Bautista has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
Anderson Peñuela
Fundación Cardiovascular del Oriente Colombiano, Calle 155A No. 23-58, Urbanización El Bosque, Sector E-1, Floridablanca, Santander, Colombia
1 shared publicationC Serrano
Fundación Cardiovascular del Oriente Colombiano, Bucanamanga, Columbia
1 shared publicationIván A Arenas
Faculty of Graduate Studies and Research, University of Alberta, 232 HMRC, Department of Medicine, Edmonton, Alberta, Canada T6G 2S2
1 shared publicationLuz X Martı́nez
Fundación Cardiovascular del Oriente Colombiano, Calle 155A No. 23-58, Urbanización El Bosque, Sector E-1, Floridablanca, Santander, Colombia
1 shared publicationOf Herrán
Instituto Colombiano de Investigación Biomédica, Universidad Industrial de Santander, Bucanamanga, Columbia
1 shared publication
Latest Publications
- 1 April 2003
- Published by Springer Nature in Journal of Human Hypertension
- Vol. 17 (4) , 223-230
Inflammation, endothelial dysfunction, and the risk of high blood pressure: epidemiologic and biological evidence
In spite of its high impact on cardiovascular and renal disease, knowledge on risk factors for the development of high blood pressure (HBP) is limited. Mild chronic inflammation may play a significant role in the incidence of HBP. A persistent low-grade inflammation state could be associated with high but within the 'normal range' cytokine plasma concentration. By impairing the capacity of the endothelium to generate vasodilating factors, particularly nitric oxide (NO), elevated cytokines may lead to the development of endothelial dysfunction, chronic impaired vasodilation, and HBP. These alterations in the L-arginine : NO pathway may play a major role in the development of HBP in young subjects, with inflammation-related alterations in the production of cyclo-oxygenase-derived vasoconstrictors becoming more prominent with advanced age. Cross-sectional independent associations between HBP and plasma levels of C-reactive protein, interleukin-6, and tissue necrosis factor alpha have been reported, but no prospective evidence of these associations is currently available.
- 1 April 2003
- Published by Springer Nature in Journal of Human Hypertension
- Vol. 17 (4) , 223-230
Inflammation, endothelial dysfunction, and the risk of high blood pressure: epidemiologic and biological evidence
In spite of its high impact on cardiovascular and renal disease, knowledge on risk factors for the development of high blood pressure (HBP) is limited. Mild chronic inflammation may play a significant role in the incidence of HBP. A persistent low-grade inflammation state could be associated with high but within the 'normal range' cytokine plasma concentration. By impairing the capacity of the endothelium to generate vasodilating factors, particularly nitric oxide (NO), elevated cytokines may lead to the development of endothelial dysfunction, chronic impaired vasodilation, and HBP. These alterations in the L-arginine : NO pathway may play a major role in the development of HBP in young subjects, with inflammation-related alterations in the production of cyclo-oxygenase-derived vasoconstrictors becoming more prominent with advanced age. Cross-sectional independent associations between HBP and plasma levels of C-reactive protein, interleukin-6, and tissue necrosis factor alpha have been reported, but no prospective evidence of these associations is currently available.
- 1 September 2002
- Published by Elsevier in Journal of Clinical Epidemiology
- Vol. 55 (9) , 882-887
Total plasma homocysteine level and risk of cardiovascular disease
- 1 September 2002
- Published by Elsevier in Journal of Clinical Epidemiology
- Vol. 55 (9) , 882-887
Total plasma homocysteine level and risk of cardiovascular disease
- 30 August 2001
- Published by Springer Nature in European Journal of Clinical Nutrition
- Vol. 55 (9) , 748-754
Effects of palm oil and dietary cholesterol on plasma lipoproteins: results from a dietary crossover trial in free-living subjects
Objective: To study the effects of palm oil (PO) and egg consumption (E) on plasma lipoproteins. Design: Randomized crossover trial. Setting: Free-living subjects. Subjects: Twenty-eight healthy male students aged 20–34 y. Interventions: Four typical Colombian diets (10 878 kJ/day; 57% energy in carbohydrates, 12% energy in proteins and 31% energy in fats) were consumed for 4 weeks. The HPOLC diet was high in PO (8.8% energy as palmitic acid, PA) and low in eggs (181.2 mg/kJ of dietary cholesterol, DC); the HPOHC diet was high in PO and high in eggs (866.1 mg/kJ of DC); the MPOMC diet was moderate in PO (6.3% energy as PA) and moderate in eggs (581.6 mg/kJ of DC); and the LOPOMC diet had no PO and was moderate in eggs (543.9 mg/kJ of DC). Main outcome: Total (TC), low density (LDL-c), and high density lipoprotein cholesterol (HDL-c), and triacylglycerols (TAG) were measured on a pool of three fasting blood samples collected in consecutive days the last week of each diet. Results: Comparison of the HPOHC and HPOLC diets showed increases in TC and LDL-c of 0.21 (P=0.01), and 0.16 mmol/l (P=0.05). Comparison of LOPOMC and MPOMC diets showed increases in TC and LDL-c of 0.39 (PPEuropean Journal of Clinical Nutrition (2001) 55, 748–754
- 30 August 2001
- Published by Springer Nature in European Journal of Clinical Nutrition
- Vol. 55 (9) , 748-754
Effects of palm oil and dietary cholesterol on plasma lipoproteins: results from a dietary crossover trial in free-living subjects
Objective: To study the effects of palm oil (PO) and egg consumption (E) on plasma lipoproteins. Design: Randomized crossover trial. Setting: Free-living subjects. Subjects: Twenty-eight healthy male students aged 20–34 y. Interventions: Four typical Colombian diets (10 878 kJ/day; 57% energy in carbohydrates, 12% energy in proteins and 31% energy in fats) were consumed for 4 weeks. The HPOLC diet was high in PO (8.8% energy as palmitic acid, PA) and low in eggs (181.2 mg/kJ of dietary cholesterol, DC); the HPOHC diet was high in PO and high in eggs (866.1 mg/kJ of DC); the MPOMC diet was moderate in PO (6.3% energy as PA) and moderate in eggs (581.6 mg/kJ of DC); and the LOPOMC diet had no PO and was moderate in eggs (543.9 mg/kJ of DC). Main outcome: Total (TC), low density (LDL-c), and high density lipoprotein cholesterol (HDL-c), and triacylglycerols (TAG) were measured on a pool of three fasting blood samples collected in consecutive days the last week of each diet. Results: Comparison of the HPOHC and HPOLC diets showed increases in TC and LDL-c of 0.21 (P=0.01), and 0.16 mmol/l (P=0.05). Comparison of LOPOMC and MPOMC diets showed increases in TC and LDL-c of 0.39 (PPEuropean Journal of Clinical Nutrition (2001) 55, 748–754