Protein–phenolic interactions and inhibition of glycation – combining a systematic review and experimental models for enhanced physiological relevance

Background: While antiglycative capacity has been attributed to (poly)phenols, the exact mechanism of action remains unclear. Studies so far are often relying on supra-physiological concentrations and use of non-bioavailable compounds.<p></p> Methods: To inform the design of a physiologically relevant in-vitro study, we carried out a systematic literature review of dietary interventions reporting plasma concentrations polyphenol metabolites. Bovine Serum Albumin (BSA) was pre-treated prior to in vitro glycation: either no treatment (native), pre-oxidised (incubated with 10nM H2O2, for 8 hours) or incubated with a mixture of phenolic acids at physiologically relevant concentrations, for 8 hours). In-vitro glycation was carried out in presence of i) glucose only (0, 5 or 10mM), ii) glucose (0, 5 or 10mM) plus H2O2 (10nM), or iii) glucose (0, 5 or 10mM) plus phenolic acids (10-160nM). Fructosamine was measured using the nitroblue tetrazolium method.<p></p> Results: Following (high) dietary polyphenol intake, 3-hydroxyphenylacetic acid is the most abundant phenolic acid in peripheral blood (up to 338μM) with concentrations for other phenolic acids ranging from 13nM-200μM. Presence of six phenolic acids with BSA during in-vitro glycation did not lower fructosamine formation. However, when BSA was pre-incubated with phenolic acids, significantly lower concentration of fructosamine was detected under glycoxidative conditions (glucose 5 or 10mM plus H2O2 10nM) (p<0.001 vs. native BSA).<p></p> Conclusion: Protein pre-treatment, either with oxidants or phenolic acids, is an important regulator of subsequent glycation in a physiologically relevant system. High quality in-vitro studies under conditions closer to physiology are feasible and should be employed more frequently.<p></p&gt

Changing distributions of body size and adiposity with age

Background: Adiposity and health risks are better indicated by waist circumference than body mass index (BMI). Patterns of change with age are incompletely documented.<p></p> Methods: Adults aged 18–92 years in the Scottish and English Health Surveys of 1994–96 and 2008–10 were divided into fifteen 5-year age bands. Sex-specific prevalences of overweight/obesity and of increased/high waist circumference against age were compared using analysis of covariance. <p></p> Results: Data available for 7932 Scottish and 55 925 English subjects in 1994–96, and for 27 391 Scottish and 30 929 English in 2008–10, showed generally similar patterns of change in the two countries. Prevalences of both elevated BMI and waist circumference rose with age for longer in 2008–10 than in 1994–96, reaching higher peaks at greater ages, particularly among men. Between 1994–96 and 2008–10, maximum prevalences of BMI >30 increased from 25 to 38% (larger increases in men than women), reaching a peak at age 60–70 years in both sexes. This peak prevalence was 5–10 years later than in 1994–96 for men and remained unchanged for women. Between 1994–96 and 2008–10, maximum prevalences of high waist circumference (men>>102 cm, women>88 cm) increased from 30 to –70% in both sexes, peaking in 2008–10 at ages 80–85 years (men) and 65–70 years (women). In 2008–10, proportions of adults with ‘normal’ BMI (18.5–25) fell with age to 15–20% at age 60–70 years (men) and 75 years (women). Among all those with BMI=18.5–25, aged>65 years, the proportions with unhealthily elevated waist circumference were 30 (men>94 cm) and 55% (women>80 cm). <p></p> Conclusions: Almost 40% of men and women are now becoming obese. People are growing fatter later in life, with waist circumference rising more persistently than BMI, which may indicate increased loss of muscle mass and sarcopenia in old age. Among older people, few now have ‘normal’ BMI, and of these up to half have elevated waist circumference, raising questions for the suitability of BMI as a measure of adiposity in this age group. <p></p&gt

Diagnostics of accelerating plasma Semiannual progress report, 1 Sep. 1968 - 28 Feb. 1969

Accelerating plasma diagnostics - validity of local thermal equilibrium assumption in electromagnetic shock tubes, and current-sheet velocity in coaxial plasma accelerato

Effects of moderate weight loss on anginal symptoms and indices of coagulation and fibrinolysis in overweight patients with angina pectoris

Objective: To evaluate the effects of moderate weight loss, in overweight patients with angina, on plasma coagulation, fibrinolytic indicies and pain frequency. Design: Single- stranded 12-week dietary intervention, an individualised eating plan with quantitative advice delivered by a dietitian. Target weight loss of 0.5 kg per week. Setting: Outpatient research clinic. Subjects: Fifty-four volunteers with angina pectoris were recruited. Five subjects withdrew, so 27 males, 22 females, mean body mass index (BMI) 29.3 (s.d. 4.3) kg/m(2) and age 60.3 (s.d. 6.5) y completed the intervention. Measurements: Body weight and frequency of anginal pain. Plasma fibrinogen, red cell aggregation (RCA), viscosity, factor VII activity, plasminogen activator inhibitor (PAI) activity, tissue plasminogen activator antigen (t-PA), plasma cholesterol, triglyceride and insulin. Results: After the 12-week dietary intervention period, mean body weight fell by 3.5 (s.d. 2.6) kg or 4.3% (P = 0.0001), range -11.7 to +1.7 kg. Mean angina frequency fell by 1.8 (s.d. 3.6) from 3.2 to 1.4 episodes/week (P = 0.009) and plasma cholesterol by 0.4 (s.d. 0.7) from 6.3 to 5.9 mmol/1 (P = 0.0001). HDL cholesterol and triglyceride were unchanged. Of the coagulation and fibrinolytic factors, factor VII activity and RCA were significantly reduced by 5 (s.d. 20), IU/dl (P = 0.04) and 1.3 (s.d. 1.3) arbitrary units (P = 0.014), respectively. Conclusions: A conventional dietetic intervention, resulting in 4% weight loss, offers the potential to reduce atherosclerotic and thrombotic risk, and to reduce pain frequency, in angina patients. Given the importance of this result in a public health context, these results indicate that this may be a fruitful area for future nutrition research

Space requirements for pullets and layers on litter

UNEVEN growth, cannibalism, weakened resistance to disease, unsanitary conditions and poor production commonly arise from failure to provide sufficient floor, feed and watering space for pullets and layers

The Evolution of Failure: Explaining Cancer as an Evolutionary Process

One of the major developments in cancer research in recent years has been the construction of models that treat cancer as a cellular population subject to natural selection. We expand on this idea, drawing upon multilevel selection theory. Cancer is best understood in our view from a multilevel perspective, as both a by-product of selection at other levels of organization, and as subject to selection (and drift) at several levels of organization. Cancer is a by-product in two senses. First, cancer cells co-opt signaling pathways that are otherwise adaptive at the organismic level. Second, cancer is also a by-product of features distinctive to the metazoan lineage: cellular plasticity and modularity. Applying the multilevel perspective in this way permits one to explain transitions in complexity and individuality in cancer progression. Our argument is a reply to Germain’s (2012) scepticism towards the explanatory relevance of natural selection for cancer. The extent to which cancer fulfills the conditions for being a paradigmatic Darwinian population depends on the scale of analysis, and the details of the purported selective scenario. Taking a multilevel perspective clarifies some of the complexities surrounding how to best understand the relevance of evolutionary thinking in cancer progression

Diagnostics of accelerating plasma Semiannual progress report, 1 Mar. - 31 Aug. 1968

Plasma diagnostics in electromagnetically driven shock tubes using laser scattering methods as compared to spectroscopic technique

Seeing double: the low-carb diet

No abstract available

Role of oxidative stress in physiological albumin glycation: a neglected interaction

Protein glycation is a key mechanism involved in chronic disease development in both diabetic and nondiabetic individuals. About 12–18% of circulating proteins are glycated in vivo in normoglycemic blood, but in vitro studies have hitherto failed to demonstrate glucose-driven glycation below a concentration of 30 mM. Bovine serum albumin (BSA), reduced BSA (mercaptalbumin) (both 40 g/L), and human plasma were incubated with glucose concentrations of 0–30 mM for 4 weeks at 37 °C. All were tested preoxidized for 8 h before glycation with 10 nM H2O2 or continuously exposed to 10 nM H2O2 throughout the incubation period. Fructosamine was measured (nitroblue tetrazolium method) at 2 and 4 weeks. Oxidized BSA (both preoxidized and continuously exposed to H2O2) was more readily glycated than native BSA at all glucose concentrations (p = 0.03). Moreover, only oxidized BSA was glycated at physiological glucose concentration (5 mM) compared to glucose-free control (glycation increased by 35% compared to native albumin, p < 0.05). Both 5 and 10 mM glucose led to higher glycation when mercaptalbumin was oxidized than when unoxidized (p < 0.05). Fructosamine concentration in human plasma was also significantly higher when oxidized and exposed to 5 mM glucose, compared to unoxidized plasma (p = 0.03). The interaction between glucose concentration and oxidation was significant in all protein models (p < 0.05). This study has for the first time demonstrated albumin glycation in vitro, using physiological concentrations of albumin, glucose, and hydrogen peroxide, identifying low-grade oxidative stress as a key element early in the glycation process

Variations in caffeine and chlorogenic acid contents of coffees: what are we drinking?

The effect of roasting of coffee beans and the extraction of ground coffee with different volumes of hot pressurised water on the caffeine and the total caffeoylquinic acids (CQAs) content of the resultant beverages was investigated. While caffeine was stable higher roasting temperatures resulted in a loss of CQAs so that the caffeine/CQA ratio was a good marker of the degree of roasting. The caffeine and CQA content and volume was determined for 104 espresso coffees obtained from coffee shops in Scotland, Italy and Spain, limited numbers of cappuccino coffees from commercial outlets and several instant coffees. The caffeine content ranged from 48–317 mg per serving and CQAs from 6–188 mg. It is evident that the ingestion of 200 mg of caffeine per day can be readily and unwittingly exceeded by regular coffee drinkers. This is the upper limit of caffeine intake from all sources recommended by US and UK health agencies for pregnant women. In view of the variable volume of serving sizes, it is also clear that the term “one cup of coffee” is not a reproducible measurement for consumption, yet it is the prevailing unit used in epidemiology to assess coffee consumption and to link the potential effects of the beverage and its components on the outcome of diseases. More accurate measurement of the intake of coffee and its potentially bioactive components are required if epidemiological studies are to produce more reliable information