Different outcomes of a cardiac rehabilitation programme in functional parameters among myocardial infarction survivors according to ejection fraction

Introduction

Exercise-based cardiac rehabilitation (EBCR) is part of the management of patients who have suffered an acute myocardial infarction (AMI). Patients with a reduced ejection fraction (EF) comprise a higher-risk subgroup and are referred less often for these programmes. This study aimed at assessing the impact of the baseline EF on the functional benefits, as assessed by peak oxygen uptake (pVO₂) and exercise duration, of an EBCR programme in AMI survivors.

Methods

Observational, retrospective cohort study including all patients admitted to a tertiary centre due to an AMI who completed a phase II EBCR programme after discharge, between November 2012 and April 2017. Functional parameters were assessed by a symptom-limited cardiopulmonary exercise test.

Results

A total of 379 patients were included [40.9% with reduced EF (<50%) at discharge]. After the programme, pVO₂ and exercise duration increased significantly (p < 0.001). Patients with a reduced EF had a lower pVO₂ and completed a shorter duration of exercise at the beginning and end of the programme. This group presented a higher increase in pVO₂ (p = 0.001) and exercise duration (p = 0.007). This was maintained after adjusting for age, gender, history of coronary artery disease, number of sessions, Killip classification, arterial hypertension, dyslipidaemia, diabetes mellitus, smoking status and baseline pVO₂.

Conclusion

A phase II EBCR programme was associated with significant improvements in pVO₂ and exercise duration among AMI survivors, irrespective of baseline EF classification. Those with a reduced baseline EF derived an even greater improvement, highlighting the importance of EBCR in this subgroup of patients.

     

Regime shifts of Mediterranean forest carbon uptake and reduced resilience driven by multidecadal ocean surface temperatures

The mechanisms translating global circulation changes into rapid abrupt shifts in forest carbon capture in semi‐arid biomes remain poorly understood. Here, we report unprecedented multidecadal shifts in forest carbon uptake in semi‐arid Mediterranean pine forests in Spain over 1950–2012. The averaged carbon sink reduction varies between 31% and 37%, and reaches values in the range of 50% in the most affected forest stands. Regime shifts in forest carbon uptake are associated with climatic early warning signals, decreased forest regional synchrony and reduced long‐term carbon sink resilience. We identify the mechanisms linked to ocean multidecadal variability that shape regime shifts in carbon capture. First, we show that low‐frequency variations of the surface temperature of the Atlantic Ocean induce shifts in the non‐stationary effects of El Niño Southern Oscillation (ENSO) on regional forest carbon capture. Modelling evidence supports that the non‐stationary effects of ENSO can be propagated from tropical areas to semi‐arid Mediterranean biomes through atmospheric wave trains. Second, decadal changes in the Atlantic Multidecadal Oscillation (AMO) significantly alter sea–air heat exchanges, modifying in turn ocean vapour transport over land and land surface temperatures, and promoting sustained drought conditions in spring and summer that reduce forest carbon uptake. Third, we show that lagged effects of AMO on the winter North Atlantic Oscillation also contribute to the maintenance of long‐term droughts. Finally, we show that the reported strong, negative effects of ocean surface temperature (AMO) on forest carbon uptake in the last decades are unprecedented over the last 150 years. Our results provide new, unreported explanations for carbon uptake shifts in these drought‐prone forests and review the expected impacts of global warming on the profiled mechanisms.     

Comparative life cycle assessment of first- and second-generation ethanol from sugarcane in Brazil

The International Journal of Life Cycle Assessment - The use of bagasse and trash from sugarcane fields in ethanol production is supposed to increase the ethanol yield per hectare, to reduce the...     

31° South: The physiology of adaptation to arid conditions in a passerine bird

Arid environments provide ideal ground for investigating the mechanisms of adaptive evolution. High temperatures and low water availability are relentless stressors for many endotherms, including birds; yet birds persist in deserts. While physiological adaptation probably involves metabolic phenotypes, the underlying mechanisms (plasticity, genetics) are largely uncharacterized. To explore this, we took an intraspecific approach that focused on a species that is resident over a mesic to arid gradient, the Karoo scrub‐robin (Cercotrichas coryphaeus). Specifically, we integrated environmental (climatic and primary productivity), physiological (metabolic rates: a measure of energy expenditure), genotypic (genetic variation underlying the machinery of energy production) and microbiome (involved in processing food from where energy is retrieved) data, to infer the mechanism of physiological adaptation. We that found the variation in energetic physiology phenotypes and gut microbiome composition are associated with environmental features as well as with variation in genes underlying energy metabolic pathways. Specifically, we identified a small list of candidate adaptive genes, some of them with known ties to relevant physiology phenotypes. Together our results suggest that selective pressures on energetic physiology mediated by genes related to energy homeostasis and possibly microbiota composition may facilitate adaptation to local conditions and provide an explanation to the high avian intraspecific divergence observed in harsh environments.     

Modulation of immune response to induced‐arthritis by low‐level laser therapy

As low‐level laser therapy immune cells responses are not always clarified, this study aimed to evaluate cytokines and immune cells profile after low‐level laser therapy (LLLT) on arthritis‐induced model. Arthritis was induced in C57BL/6 mice divided into five groups: euthanized 5 hours after inflammation induction; untreated; dexamethasone treated; LLLT at 3 Jcm^?2; LLLT at 30 Jcm^?2. Cytokine measurements by enzyme‐linked immunosorbent assay and mRNA cytokine relative levels by real‐time quantitative polymerase chain reaction were performed with arthritic ankle (IL‐1β, IL‐6, TNF‐α, IL‐10 and TGF‐β). Macrophages, dendritic cells, natural killer cells, lymphocytes CD4⁺, CD8⁺, Treg and costimulatory proteins were quantified in proximal lymph node by flow cytometry. Data showed decrease in all cytokine levels after LLLT and alteration in mRNA relative levels, depending on the energy density used. LLLT was able to increase of immune cell populations analyzed in the lymph node as well as costimulatory proteins expression on macrophages and dendritic cells. Treg TCD4⁺ and TCD8⁺ population enrichment were observed in LLLT at 3 and 30 Jcm^?2 groups, respectively. Furthermore, Treg TCD8⁺ cells expressing higher levels of CD25 were observed at LLLT at 30 Jcm^?2 group. Our results indicate that LLLT could change the inflammatory course of arthritis, tending to accelerate its resolution through immune cells photobiostimulation.      

Urbanization and Mismatch with Protected Areas Place the Conservation of a Threatened Species at Risk

In this work, we report the predicted distribution of the threatened fluminense swallowtail butterfly, Parides ascanius (Cramer 1775), and correlate it to the presence of urban and protected areas within its range. The distribution was modeled using a genetic algorithm. The predicted distribution of the fluminense swallowtail shows high agreement within Rio de Janeiro state, in a near-continuous strip of 2,038,253 ha along the coastal lowlands, 17.8 percent of which is within urban areas. Only 8.7 percent (178,187 ha) of the remaining (nonurban) predicted model overlapped at least partially with protected areas (19 in all). Almost half of these protected areas also overlapped with urban areas, resulting in an additional loss of 58,751 ha. In seven of 19 protected areas, the distribution of P. ascanius was predicted by less than 50 percent of the models; five of the remaining protected areas are less restrictive reserves. Despite the wide distribution predicted by the models, only two of the observed occurrence points matched the predicted distribution within protected areas. Modeling threatened species distribution is a useful tool for highlighting gaps in networks of protected areas and should aid in planning to fill these gaps. However, in several developing countries with high biodiversity, there is insufficient basic biological information for many threatened species. In these cases, prospecting field studies are urgently needed.     

Trypanosoma brucei brucei: biochemical characterization of ecto-nucleoside triphosphate diphosphohydrolase activities

In this work we describe the ability of living cells of Trypanosoma brucei brucei to hydrolyze extracellular ATP. In these intact parasites there was a low level of ATP hydrolysis in the absence of any divalent metal (4.72+/-0.51 nmol Pi x 10(-7) cells x h(-1)). The ATP hydrolysis was stimulated by MgCl(2) and the Mg-dependent ecto-ATPase activity was 27.15+/-2.91 nmol Pi x 10(-7) cells x h(-1). This stimulatory activity was also observed when MgCl(2) was replaced by MnCl(2). CaCl(2) and ZnCl(2) were also able to stimulate the ATPase activity, although less than MgCl(2). The apparent K(m) for ATP was 0.61 mM. This ecto-ATPase activity was insensitive to inhibitors of other ATPase and phosphatase activities. To confirm that this Mg-dependent ATPase activity is an ecto-ATPase activity, we used an impermeable inhibitor, DIDS (4, 4'-diisothiocyanostylbene 2'-2'-disulfonic acid), as well as suramin, an antagonist of P(2) purinoreceptors and inhibitor of some ecto-ATPases. These two reagents inhibited the Mg(2+)-dependent ATPase activity in a dose-dependent manner. Living cells sequentially hydrolyzed the ATP molecule generating ADP, AMP and adenosine, and supplementation of the culture medium with ATP was able to sustain the proliferation of T. brucei brucei as well as adenosine supplementation. Furthermore, the E-NTPDase activity of T. brucei brucei is modulated by the availability of purines in the medium. These results indicate that this surface enzyme may play a role in the salvage of purines from the extracellular medium in T. brucei brucei.     

PRAS40 is a target for mammalian target of rapamycin complex 1 and is required for signaling downstream of this complex

Signaling through the mammalian target of rapamycin complex 1 (mTORC1) is positively regulated by amino acids and insulin. PRAS40 associates with mTORC1 (which contains raptor) but not mTORC2. PRAS40 interacts with raptor, and this requires an intact TOR-signaling (TOS) motif in PRAS40. Like TOS motif-containing proteins such as eIF4E-binding protein 1 (4E-BP1), PRAS40 is a substrate for phosphorylation by mTORC1. Consistent with this, starvation of cells of amino acids or treatment with rapamycin alters the phosphorylation of PRAS40. PRAS40 binds 14-3-3 proteins, and this requires both amino acids and insulin. Binding of PRAS40 to 14-3-3 proteins is inhibited by TSC1/2 (negative regulators of mTORC1) and stimulated by Rheb in a rapamycin-sensitive manner. This confirms that PRAS40 is a target for regulation by mTORC1. Small interfering RNA-mediated knockdown of PRAS40 impairs both the amino acid- and insulin-stimulated phosphorylation of 4E-BP1 and the phosphorylation of S6. However, this has no effect on the phosphorylation of Akt or TSC2 (an Akt substrate). These data place PRAS40 downstream of mTORC1 but upstream of its effectors, such as S6K1 and 4E-BP1.