Differential effects of nitrogen vs. phosphorus limitation on terrestrial carbon storage in two subtropical forests: A Bayesian approach.

Nitrogen (N) and phosphorus (P) have been demonstrated to limit terrestrial carbon (C) storage in terrestrial ecosystems. However, the reliable indicator to infer N and P limitation are still lacking, especially in subtropical forests. Here we used a terrestrial ecosystem (TECO) model framework in combination with a Bayesian approach to evaluate effects of nutrient limitation from added N/P processes and data sets on C storage capacities in two subtropical forests (Tiantong and Qianyanzhou [QYZ]). Three of the six simulation experiments were developed with assimilating data (TECO C model with C data [C-C], TECO C-N coupling model with C and N data [CN-CN], and TECO C-N-P model with C, N, and P data [CNP-CNP]), and the other three ones were simulated without assimilating data (C-only, CN-only, and CNP-only). We found that P dominantly constrained C storage capacities in Tiantong (42%) whereas N limitation decreased C storage projections in QYZ (44%). Our analysis indicated that the stoichiometry of wood biomass and soil microbe (e.g., N:P ratio) were more sensitive indicators of N or P limitation than that of other pools. Furthermore, effects of P-induced limitation were mainly on root biomass by additional P data and on both metabolic litter and soil organic carbon (SOC) by added P processes. N-induced effects were mainly from added N data that limited plant non-photosynthetic tissues (e.g., woody biomass and litter). The different effects of N and P modules on C storage projections reflected the diverse nutrient acquisition strategies associated with stand ages and plant species under nutrient stressed environment. These findings suggest that the interaction between plants and microorganisms regulate effects of nutrient availability on ecosystem C storage, and stoichiometric flexibility of N and P in plant and soil C pools could improve the representation of N and P limitation in terrestrial ecosystem models.

Vitamin B6 prevents excessive inflammation by reducing accumulation of sphingosine-1-phosphate in a sphingosine-1-phosphate lyase-dependent manner.

Vitamin B6 is necessary to maintain normal metabolism and immune response, especially the anti-inflammatory immune response. However, the exact mechanism by which vitamin B6 plays the anti-inflammatory role is still unclear. Here, we report a novel mechanism of preventing excessive inflammation by vitamin B6 via reduction in the accumulation of sphingosine-1-phosphate (S1P) in a S1P lyase (SPL)-dependent manner in macrophages. Vitamin B6 supplementation decreased the expression of pro-inflammatory cytokines by suppressing nuclear factor-κB and mitogen-activated protein kinases signalling pathways. Furthermore, vitamin B6-reduced accumulation of S1P by promoting SPL activity. The anti-inflammatory effects of vitamin B6 were inhibited by S1P supplementation or SPL deficiency. Importantly, vitamin B6 supplementation protected mice from lethal endotoxic shock and attenuated experimental autoimmune encephalomyelitis progression. Collectively, these findings revealed a novel anti-inflammatory mechanism of vitamin B6 and provided guidance on its clinical use.

Vitamin B1 Helps to Limit Mycobacterium tuberculosis Growth via Regulating Innate Immunity in a Peroxisome Proliferator-Activated Receptor-γ-Dependent Manner.

It is known that vitamin B1 (VB1) has a protective effect against oxidative retinal damage induced by anti-tuberculosis drugs. However, it remains unclear whether VB1 regulates immune responses during Mycobacterium tuberculosis (MTB) infection. We report here that VB1 promotes the protective immune response to limit the survival of MTB within macrophages and in vivo through regulation of peroxisome proliferator-activated receptor γ (PPAR-γ). VB1 promotes macrophage polarization into classically activated phenotypes with strong microbicidal activity and enhanced tumor necrosis factor-α and interleukin-6 expression at least in part by promoting nuclear factor-κB signaling. In addition, VB1 increases mitochondrial respiration and lipid metabolism and PPAR-γ integrates the metabolic and inflammatory signals regulated by VB1. Using both PPAR-γ agonists and deficient mice, we demonstrate that VB1 enhances anti-MTB activities in macrophages and in vivo by down-regulating PPAR-γ activity. Our data demonstrate important functions of VB1 in regulating innate immune responses against MTB and reveal novel mechanisms by which VB1 exerts its function in macrophages.

An imperative need for global change research in tropical forests.

Tropical forests play a crucial role in regulating regional and global climate dynamics, and model projections suggest that rapid climate change may result in forest dieback or savannization. However, these predictions are largely based on results from leaf-level studies. How tropical forests respond and feedback to climate change is largely unknown at the ecosystem level. Several complementary approaches have been used to evaluate the effects of climate change on tropical forests, but the results are conflicting, largely due to confounding effects of multiple factors. Although altered precipitation and nitrogen deposition experiments have been conducted in tropical forests, large-scale warming and elevated carbon dioxide (CO2) manipulations are completely lacking, leaving many hypotheses and model predictions untested. Ecosystem-scale experiments to manipulate temperature and CO2 concentration individually or in combination are thus urgently needed to examine their main and interactive effects on tropical forests. Such experiments will provide indispensable data and help gain essential knowledge on biogeochemical, hydrological and biophysical responses and feedbacks of tropical forests to climate change. These datasets can also inform regional and global models for predicting future states of tropical forests and climate systems. The success of such large-scale experiments in natural tropical forests will require an international framework to coordinate collaboration so as to meet the challenges in cost, technological infrastructure and scientific endeavor.

International differences in evolution of early discharge after acute myocardial infarction.

BACKGROUND: Early discharge of low-risk patients with acute myocardial infarction is feasible and can be achieved at no additional risk of adverse events. We aimed to identify the extent to which countries have taken advantage of the opportunity for early discharge. METHODS: The study population consisted of 54174 patients enrolled in GUSTO-I, GUSTO-III, and ASSENT-2 studies (enrollment period 1990-98) in the USA, Canada, Australia, New Zealand, Belgium, France, Germany, Spain, and Poland. We identified patients with uncomplicated acute myocardial infarction who were eligible for early discharge on the basis of previously established criteria, and assessed the extent to which these patients were discharged early--defined as discharged alive within 4 days of admission. The economic consequences (defined as potentially unnecessary hospital days consumed per 100 patients enrolled) were also investigated. FINDINGS: Patients in all European countries had significantly longer stays than did those from non-European countries. Over the study period, the number of eligible patients discharged on or before day 4 increased in the USA, Canada, Australia, and New Zealand. Despite this increase, no more than 40% of patients who were eligible for early discharge were actually discharged early. The rate of early discharge of eligible patients was consistently low (<2%) in Belgium, France, Germany, Spain, and Poland. In ASSENT-2, which is the most recent trial in this study, the number of potentially unnecessary hospital days (per 100 patients enrolled) ranged from 65 in New Zealand to 839 in Germany. INTERPRETATION: Despite more than a decade of research, there is still a lot of variation between countries in international length-of-stay patterns in acute myocardial infarction. The potential for more efficient discharge of low-risk patients exists in all countries investigated, but was especially evident in the European countries included in the study (Belgium, France, Germany, Spain, and Poland).

Troponin T and quantitative ST-segment depression offer complementary prognostic information in the risk stratification of acute coronary syndrome patients.

OBJECTIVES: Our primary objective was to examine the prognostic relationship between baseline quantitative ST-segment depression (ST) and cardiac troponin T (cTnT) elevation. The secondary objectives were to: 1) examine whether ST provided additional insight into therapeutic efficacy of glycoprotein IIb/IIIa therapy similar to that demonstrated by cTnT; and 2) explore whether the time to evaluation impacted on each marker's relative prognostic utility. BACKGROUND: The relationship between the baseline electrocardiogram (ECG) and cTnT measurements in risk-stratifying patients presenting with acute coronary syndromes (ACS) has not been evaluated comprehensively. METHODS: The study population consisted of 959 patients enrolled in the cTnT substudy of the Platelet IIb/IIIa Antagonism for the Reduction of Acute coronary syndrome events in a Global Organization Network (PARAGON)-B trial. Patients were classified as having no ST (n = 387), 1 mm ST (n = 433), and ST > or =2 mm (n = 139). Forty-percent (n = 381) were classified as cTnT-positive based on a definition of > or =0.1 ng/ml. RESULTS: Six-month death/(re)myocardial infarction rates were 8.4% among cTnT-negative patients with no ST and 26.8% among cTnT-positive patients with ST > or =2 mm. On ECGs done after 6 h of symptom onset, ST > or =2 mm was associated with higher risk compared to its presence on ECGs done earlier (odds ratio [OR] 7.3 vs. 2.1). In contrast, the presence of elevated cTnT within 6 h of symptom was associated with a higher risk of adverse events compared with elevations after 6 h (OR 2.4 vs. 1.5). CONCLUSIONS: Quantitative ST and cTnT status are complementary in assessing risk among ACS patients and both should be employed to determine prognosis and assist in medical decision making.