S-adenosyl-l-methionine: (S) -7,8,13, 14-tetrahydroberberine--n-methyltransferase, a branch point enzyme in the biosynthesis of benzophenanthridine and protopine alkaloids.

The enzyme which transfers the CH3-group of S-adenosylmethionine to the nitrogen atom of (S)-tetrahydroberberine and (S)-stylopine is found to occur in a number of plant cell cultures originating from species containing alkaloids; it is located at an important branch point in isoquinoline alkaloid biosynthesis

Calculation of Cause-specific Mortality Impacts of Fine Particulate Matter in GAINS

In the early 2000s, the GAINS (Greenhouse gas - Air pollution Interactions and Synergies) model used emerging epidemiological evidence to estimate premature mortality of the European population that can be attributed to the exposure to fine particulate matter and to identify cost-effective emission control strategies that reduce health impacts at least cost (Amann et al., 2011, p.accepted for publication). Based on the review of available studies on the health effects of PM conducted by the UNECE Task Force on Health (UNECE/WHO, 2003), the GAINS impact assessment employed the associations between population exposure to PM2.5 and all-cause mortality of the American Cancer Society study (Pope et al., 2002). In the meantime, a wealth of new epidemiological studies have sharpened the evidence about health effects of particulate matter and revealed more specific associations between ambient concentrations of PM2.5 and health impacts (e.g., Pope et al., 2009). In particular, new studies establish robust relationships between exposure to fine particles and specific causes of deaths. These new insights should facilitate a more specific estimate of the role of particular death causes that are associated with bad air quality, and a more precise estimate of the total mortality impacts in different countries as baseline death rates from different diseases vary over countries. This background paper describes a revised approach of the health impact assessment in GAINS that employs cause-specific concentration-response relationships for lung cancer, cardio-vascular and respiratory diseases for the European countries. Data on cause-specific deaths in the European countries have been extracted from the 2010 version of the World Health Organization database on mortality indicators by 67 causes of death, age and sex (HFA-MDB) for the latest available year. As a result, the cause-specific approach results in higher impact estimates than the former calculation for all-cause mortality. The difference depends on the relative shares of death causes in the various countries; for the EU-27, cause-specific calculations for the year 2000 result in 16% higher health effects, keeping all other factors constant (i.e., PM exposure, population, etc.). In the non-EU countries, the difference amounts to 54%, essentially due to the higher share of cardio-vascular deaths

Cost Functions for Controlling SO2 Emissions in Europe

This paper marks an important step in the development of the Regional Acidification INformation and Simulation (RAINS) model. One of the major goals of the project since its beginning four years ago, has been to get RAINS used in policy analysis. To that end the model should include variables that are very crucial in the eyes of the decision makers. The cost of reducing air pollutant emissions certainly is such an important policy relevant variable. The authors have successfully developed a uniform approach for establishing cost-of-control functions for emissions of sulfur dioxide in virtually all European countries. This uniformity is particularly important for comparing the cost-effectiveness of various scenarios for controlling acid deposition in Europe. Currently the assumptions and the numbers in this paper are under review by experts in many of the European countries. The cost-of-control functions allow the evaluation of targeted deposition levels at a variety of locations in Europe. This will be the topic of a subsequent paper. In the near future we will also develop similar control function for the emissions of nitrogen oxides and will eventually combine the functions into one cost-of-control function for acidifying emissions

Decomposing Air Pollutant Emissions in Asia: Determinants and Projections

High levels of air pollution pose an urgent social and public health challenge in many Asian regions. This study evaluates the role of key factors that determined the changes in emission levels in China, India and Japan over the past 25 years. While emissions of air pollutants have been declining in Japan since the 1990s, China and India have experienced a rapid growth in pollution levels in recent years. Around 2005, control measures for sulfur emissions started to deliver expected reductions in China, followed by cuts in nitrogen oxides ten years later. Despite recent policy interventions, growing emission trends in India persist. A decomposition analysis of emission-driving factors indicates that emission levels would have been at least two-times higher without the improvements in energy intensity and efficiency, combined with end-of-pipe measures. Due to the continuous reliance on fossil fuels, the abatement effect of a cleaner fuel mix was in most cases significantly smaller than other factors. A reassessment of emission projections developed in the past suggests a decisive impact of energy and environmental policies. It is expected that targeted legislative instruments will play a dominant role in achieving future air-quality goals in Asia

Effect of acute severe hypoxia on peripheral fatigue and endurance capacity in healthy humans

Effect of acute severe hypoxia on peripheral fatigue and endurance capacity in healthy humans. Am J Physiol Regul Integr Comp Physiol 292: R598–R606, 2007. First published September 7, 2006; doi:10.1152/ajpregu.00269.2006.—We hypothesized that severe hypoxia limits exercise performance via decreased contractility of limb locomotor muscles. Nine male subjects [mean SE maximum O2 uptake (V˙ O2 max) 56.5 2.7 ml kg 1 min 1] cycled at 90% V˙ O2 max to exhaustion in normoxia [NORM-EXH; inspired O2 fraction (FIO2) 0.21, arterial O2 saturation (SpO2) 93 1%] and hypoxia (HYPOX-EXH; FIO2 0.13, SpO2 76 1%). The subjects also exercised in normoxia for a time equal to that achieved in hypoxia (NORM-CTRL; SpO2 96 1%). Quadriceps twitch force, in response to supramaximal single (nonpotentiated and potentiated 1 Hz) and paired magnetic stimuli of the femoral nerve (10–100 Hz), was assessed pre- and at 2.5, 35, and 70 min postexercise. Hypoxia exacerbated exercise-induced peripheral fatigue, as evidenced by a greater decrease in potentiated twitch force in HYPOX-EXH vs. NORM-CTRL ( 39 4 vs. 24 3%, P 0.01). Time to exhaustion was reduced by more than two-thirds in HYPOX-EXH vs. NORM-EXH (4.2 0.5 vs. 13.4 0.8 min, P 0.01); however, peripheral fatigue was not different in HYPOX-EXH vs. NORM-EXH ( 34 4 vs. 39 4%, P 0.05). Blood lactate concentration and perceptions of limb discomfort were higher throughout HYPOX-EXH vs. NORM-CTRL but were not different at end-exercise in HYPOX-EXH vs. NORM-EXH. We conclude that severe hypoxia exacerbates peripheral fatigue of limb locomotor muscles and that this effect may contribute, in part, to the early termination of exercise