Flaxseed Ingestion Alters Ratio of Enterolactone Enantiomers in Human Serum

Enterolactone (EL) is an enterolignan found in human subjects. In this pilot study, the enantiomeric ratios of serum EL were determined in serum from healthy adults during consumption of habitual diet, and after an 8-day supplementation with flaxseed (25 g/day). (−)EL dominated in all serum samples collected during habitual diet consumption. However, the ratio of (−)EL and (+)EL enantiomers differed markedly between individuals. Flaxseed ingestion increased significantly the proportion of (+)EL in all subjects. Moreover, a small but significant increase in serum (−)EL concentration was measured. After flaxseed ingestion, (−)EL concentrations correlated with those of (+)EL suggesting that the stereochemistry of the parent plant lignan in flaxseed is not a major determinant of EL formation in human subjects. Comparison of EL concentrations obtained with the validated chromatographic methods (HPLC-MS/MS, HPLC-CEAD, and GC-MS) and the time-resolved fluoroimmunoassay (TR-FIA) revealed that the immunoassay method underestimates human serum EL concentrations after the flaxseed ingestion

Lifestyle Behaviours and Plasma Vitamin C and β-Carotene Levels from the ELAN Population (Liège, Belgium)

Several factors, including fruit and vegetables intakes, have been shown to significantly influence the plasma concentrations of the two antioxidants vitamin C and β-carotene. Deficiency levels of 6 mg/L (34.2 μM) for vitamin C and of 0.22 mg/L (0.4 μM) for β-carotene have been suggested below which cardiovascular risk might be increased. The present study performed on 897 presumably healthy subjects aged 40–60 years aimed to examine how modifiable lifestyle factors may be related to vitamin C and/or β-carotene deficiency. Gender, smoking, lack of regular physical activity and of daily fruit consumption (≥2/day), and social status (in particular, unemployment) were found to be significant risk factors for vitamin C deficiency. For β-carotene deficiency, the same factors were identified except social status; moreover, overweight and OC use in women were also found to have a deleterious effect. For non exposed subjects, the probability of developing vitamin C deficiency was 4% in men and 2.4% in women. This probability increased to 66.3% for men and to 44.3% for women (and even to 50.4% under OC use), when all risk factors were present. For β-carotene deficiency, the corresponding probabilities were equal to 29.7% in men and 13.7% in women (no risk factor present), and to 86.1% for men and 69.9% (91.6% for OC use) for women (all factors present), respectively

Socioeconomic position, John Henryism, and incidence of acute myocardial infarction in Finnish men

Previous cross-sectional studies examining whether John Henryism (JH), or high-effort coping with socioeconomic adversity, potentiates the inverse association between socioeconomic position (SEP) and cardiovascular health have focused mainly on hypertension in African Americans. We conducted the first longitudinal test of this hypothesis on incident acute myocardial infarction (AMI) using data from the Kuopio Ischemic Heart Disease Risk Factor Study in Finland (N = 1405 men, 42-60 years). We hypothesized that the expected inverse gradient between SEP and AMI risk would be stronger for men scoring high on JH than for those scoring low. John Henryism was measured by a Finnish version of the JH Scale for Active Coping. Four different measures of SEP were used: childhood SEP, education, income, and occupation. AMI hazard ratios (HR) by SEP and JH were estimated using COX proportional hazard models, before and after adjustment for study covariates. 205 cases of AMI occurred over a median of 14.9 years. Men employed in lower rank (farmer, blue-collar) occupations who scored high on JH had significantly higher age-adjusted risks of AMI than men in higher rank (white-collar) occupations (HR = 3.14, 95% CI: 1.65-5.98 for blue collar; HR = 2.33, 95% Cl: 1.04-5.22 for farmers) who also scored high on JH. No socioeconomic differences in AMI were observed for men who scored low on JH (HR = 136, 95% CI: 0.74 2.47 for blue collar; HR = 0.93, 95% CI: 0.59-1.48 for farmers; p = 0.002 for the SEP x JH interaction). These findings persisted after adjustment for sociodemographic, behavioral, and biological factors. Results for other SEP measures were in the same direction, but did not reach statistical significance. Repetitive high-effort coping with adversity (John Henryism) was independently associated with increased risk for AMI in Finnish men, underscoring the potential relevance of the John Henryism hypothesis to CVD outcomes other than hypertension and to populations other than African Americans. (C) 2016 Published by Elsevier Ltd.Peer reviewe

Nature of gene action for fruit quality characters of tomato (Solanum lycopersicum)

Nature of gene action for three important fruit quality characters of tomato viz., total soluble solids (TSS), β-carotene and lycopene contents were determined by analyzing one 7 x 7 half diallel population and six genetic populations (P1, P2, F1, F2 , BC1 and BC2) of two cross combinations. The nature of gene action determined from two biometrical methods matched well and it appeared that the fruit quality characters were under the control of both fixable and non-fixable gene effects, with the non-fixable gene effects with gene interactions being more important. Diallel analysis revealed moderate narrow sense heritability estimates and 6-parameter model suggested duplicate epistasis as well as significant additive x additive type non-allelic interaction with negative sign for the characters, which will hinder the pace of progress through simple selection. Single seed descent method with progeny row testing and deferred selection will be the best breeding method to develop line bred varieties with good fruit quality character.Keywords: Gene action, diallel, generation mean, fruit quality, tomatoAfrican Journal of Biotechnology Vol. 12(20), pp. 2869-287

Urinary Bisphenol A and Hypertension in a Multiethnic Sample of US Adults

Background. Bisphenol A (BPA) is a common chemical used in the manufacture of polycarbonate plastics and epoxy resins, with >93% of US adults having detectable BPA levels in urine. Recent animal studies have suggested that BPA exposure may have a role in several mechanisms involved in the development of hypertension, including weight gain, insulin resistance, thyroid dysfunction, endothelial dysfunction, and oxidative stress. However, no previous human study has examined the association between markers of BPA exposure and hypertension. Methods. We examined urinary BPA levels in 1380 subjects from the National Health and Nutritional Examination Survey 2003-2004. Main outcome-of-interest was hypertension, defined as blood pressure-reducing medication use and/or blood pressures >140/90 mm of Hg (n = 580). Results. We observed a positive association between increasing levels of urinary BPA and hypertension independent of confounding factors such as age, gender, race/ethnicity, smoking, body mass index (BMI), diabetes mellitus and total serum cholesterol levels. Compared to tertile 1 (referent), the multivariate-adjusted odds ratio (95% confidence interval) of hypertension associated with tertile 3 was 1.50 (1.12−2.00); P-trend = 0.007. The association was consistently present in subgroup analyses by race/ethnicity, smoking status, BMI, and diabetes mellitus. Conclusions. Urinary BPA levels are associated with hypertension, independent of traditional risk factors

Features of liver tissue remodeling in intestinal failure during and after weaning off parenteral nutrition

Background. Intestinal failure is associated frequently with liver injury, which persists after weaning off parenteral nutrition. We compared features of liver remodeling in intestinal failure during and after weaning off parenteral nutrition. Methods. Liver biopsies and serum samples were obtained from 25 intestinal failure patients at a median age of 9.7 years (interquartile range: 4.6-18) and from age-matched control patients. Seven patients had been receiving parenteral nutrition for 53 months (22-160), and 18 patients had been weaned off parenteral nutrition 6.3 years (2.4-17) earlier, after having received parenteral nutrition for 10 months (3.3-34). Expression of alpha smooth muscle actin, collagen 1, proinflammatory cytokines, growth factors, and matrix metalloproteinases (MMPs) was measured. Results. Significant increases in immunohistochemical expression of alpha-smooth muscle actin and collagen 1 were observed predominantly in portal areas and were similar to increases seen in patients currently receiving parenteral nutrition and in patients weaned off parenteral nutrition. Gene and protein expressions of alpha-smooth muscle actin and collagen were interrelated. Gene expression of ACTA2, encoding alpha-smooth muscle actin, was increased only in patients who were receiving parenteral nutrition currently. Comparable upregulation of interleukin-1 (alpha and beta), epidermal growth factor, integrin-beta 6, and MMP9 gene expression was observed in both patient groups, irrespective of whether they were receiving parenteral nutrition currently. Liver expression and serum levels of TIMP1 and MMP7 were increased only in the patients on parenteral nutrition currently but were not increased after weaning off parenteral nutrition. Conclusion. Intestinal failure is characterized by abnormal activation of hepatic myofibroblast and accumulation of collagen both during and after weaning off parenteral nutrition. Persistent transcriptional upregulation of proinflammatory and fibrogenic cytokines after weaning off parenteral nutrition suggests that factors other than parenteral nutrition may contribute to intestinal failure associated liver disease.Peer reviewe

Immunologic burden links periodontitis to acute coronary syndrome

Peer reviewe

Oxidative Stress and Inflammation in Heart Disease: Do Antioxidants Have a Role in Treatment and/or Prevention?

Inflammation triggered by oxidative stress is the cause of much, perhaps even most, chronic human disease including human aging. The oxidative stress originates mainly in mitochondria from reactive oxygen and reactive nitrogen species (ROS/RNS) and can be identified in most of the key steps in the pathophysiology of atherosclerosis and the consequential clinical manifestations of cardiovascular disease. In addition to the formation of atherosclerosis, it involves lipid metabolism, plaque rupture, thrombosis, myocardial injury, apoptosis, fibrosis and failure. The recognition of the critical importance of oxidative stress has led to the enthusiastic use of antioxidants in the treatment and prevention of heart disease, but the results of prospective, randomized clinical trials have been overall disappointing. Can this contradiction be explained and what are its implications for the discovery/development of future antioxidant therapeutics

Determinants of HDL Cholesterol Efflux Capacity after Virgin Olive Oil Ingestion: Interrelationships with Fluidity of HDL Monolayer

Scope: Cholesterol efflux capacity of HDL (CEC) is inversely associated with cardiovascular risk. HDL composition, fluidity, oxidation, and size are related with CEC. We aimed to assess which HDL parameters were CEC determinants after virgin olive oil (VOO) ingestion. Methods and results: Post‐hoc analyses from the VOHF study, a crossover intervention with three types of VOO. We assessed the relationship of 3‐week changes in HDL‐related variables after intervention periods with independence of the type of VOO. After univariate analyses, mixed linear models were fitted with variables related with CEC and fluidity. Fluidity and Apolipoprotein (Apo)A‐I content in HDL was directly associated, and HDL oxidative status inversely, with CEC. A reduction in free cholesterol, an increase in triglycerides in HDL, and a decrease in small HDL particle number or an increase in HDL mean size, were associated to HDL fluidity. Conclusions: HDL fluidity, ApoA‐I concentration, and oxidative status are major determinants for CEC after VOO. The impact on CEC of changes in free cholesterol and triglycerides in HDL, and those of small HDL or HDL mean size, could be mechanistically linked through HDL fluidity. Our work points out novel therapeutic targets to improve HDL functionality in humans through nutritional or pharmacological interventions.Fil: Fernández Castillejo, Sara. Universitat Rovira I Virgili; EspañaFil: Rubió, Laura. Universitat Rovira I Virgili; España. Universidad de Lleida; EspañaFil: Hernáez, Álvaro. Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición; EspañaFil: Catalán, Úrsula. Universitat Rovira I Virgili; EspañaFil: Pedret, Anna. Universitat Rovira I Virgili; EspañaFil: Valls, Rosa M.. Universitat Rovira I Virgili; EspañaFil: Mosse, Juana Inés. Universidad de Lleida; España. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Covas, Maria Isabel. Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición; EspañaFil: Remaley, Alan T.. National Institutes of Health; Estados UnidosFil: Castañer, Olga. Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición; EspañaFil: Motilva, Maria José. Universidad de Lleida; EspañaFil: Solá, Rosa. Universitat Rovira I Virgili; Españ

Ferritin in Adult-Onset Still's Disease: Just a Useful Innocent Bystander?

Background. Adult-Onset Still's Disease (AOSD) is an immune-mediated systemic disease with quotidian-spiking fever, rash, and inflammatory arthritis. Hyperferritinemia is a prominent feature, often used for screening. Methods. The key terms “ferritin” and “hyperferritinemia” were used to search PubMed and Medline and were cross-referenced with “Still's Disease.” Results. Hyperferritinemia, although nonspecific, is particularly prevalent in AOSD. While most clinicians associate ferritin with iron metabolism, this is mostly true for the H isoform and not for the L isoform that tends to increase dramatically in hyperferritenemia. In these situations, hyperferritinemia is not associated with iron metabolism and may even mask an underlying iron deficiency. We review, in systematic fashion, the current basic science and clinical literature regarding the regulation of ferritin and its use in the diagnosis and management of AOSD. Conclusion. Serum hyperferritinemia in AOSD has been described for 2 decades, although its mechanism has not yet been completely elucidated. Regulation by proinflammatory cytokines such as interleukin (IL)-1b, IL-6, IL-18, MCSF, and INF-α provides a link to the disease pathogenesis and may explain rapid resolution of hyperferritinemia after targeted treatment and inhibition of key cytokines