Measured and predicted resting energy expenditure in wheelchair rugby athletes

Objective: Report measured resting energy expenditure (REE) in wheelchair rugby athletes and evaluate agreement between REE and the prediction models of Chun, Cunningham, Harris-Benedict, Mifflin, Nightingale and Gorgey, and Owen.

Design: Cohort-based validation study.

Setting. Paralympic team training camp.

Participants: Fourteen internationally competitive athletes who play wheelchair rugby, 13 of whom had cervical spinal cord injuries (SCI).

Outcome Measures: A portable metabolic analyzer was used to measure REE following an overnight fast and dual-energy X-ray absorptiometry (DXA) was used to assess lean body mass for the prediction equations.

Results: REE in the current sample was 1735?±?257?kcal?×?day^?1 ranging from 1324 to 2068?kcal?×?day^{?1 Bhambhani Y. Physiology of wheelchair racing in athletes with spinal cord injury. Sports Med 2002;32(1):23–51.[Crossref], [PubMed], [Web of Science ®] , [Google Scholar]}. Bland–Altman analyses revealed negative mean bias but similar limits of agreement between measured REE and scores predicted by Chun, Cunningham, Mifflin, Nightingale and Gorgey, and Owen models in elite athletes who play wheelchair rugby.

Conclusion: Prediction models regressed on persons with and without SCI under-predicted REE of competitive wheelchair rugby athletes. This outcome may be explained by the higher REE/fat-free mass (FFM) ratio of current athletes compared to less active samples. Findings from the current study will help practitioners to determine nutrient intake needs on training days of varied intensity.     

Effects of common pharmaceutical drugs (paracetamol and acetylsalicylic acid) short term exposure on biomarkers of the mussel Mytilus spp

Pharmaceutical drugs in the wild may pose significant risks to non-target exposed organisms. This situation is even more troublesome for coastal marine or estuarine environments, located in the vicinity of large human conglomerates, for which the putative number of pollutants is extremely high, and the regime by which wild organisms are exposed is continuous. In addition, the number of studies addressing this issue is still scarce, despite evidences that show the potential contamination profiles and adverse biological effects in organisms from such areas. In this study, the ecotoxicity of common pharmaceutical drugs (namely paracetamol and acetylsalicylic acid) was assessed, by studying the susceptibility of the mussel species Mytilus spp to oxidative stress after being exposed for 96 h to increasing but ecologically relevant concentrations of the two mentioned pharmaceuticals (paracetamol: 0, 0.5, 5, 50, and 500 μg/L; acetylsalicylic acid: 0, 0.1, 1, 10, and 100 μg/L). The oxidative status in exposed organisms was analyzed by measuring oxidative stress biomarkers, namely catalase (CAT), glutathione-S-transferases (GSTs), and lipoperoxidation (LPO) levels, whose alteration was indicative of chemical exposure, in both digestive gland and gills of the organisms. In addition, the food uptake and the nutritional reserve status of exposed organisms were also assessed, by measuring the consumption of ingested food, and levels of tissue reserves of glycogen in gills and digestive gland. No significant alterations were observed in the assessed oxidative stress parameters so it was possible to hypothesize that the studied drugs may have probably exerted a limited alteration of antioxidant defenses and damage, which was reverted by the activation of defensive adaptive mechanisms. This set of data evidenced that the pro-oxidative metabolism that was already described for both drugs in other animal models, was not fully established in the exposed mussels. On the contrary, glycogen reserves were substantially changed after exposure to both toxicants, being possible to observe opposite responses caused by both drugs. Food uptake was not altered following exposure to the drugs. Further evaluations are thus required to conclude about both drugs ecotoxicity and other parameters, namely seasonality, which should be considered when performing ecotoxicology tests, especially with the selected species.     

同型半胱氨酸体内代谢及调节的研究进展

同型半胱氨酸（Hcy）是体内一碳单位代谢的一个正常中间产物，Hcy的重要代谢途径就是转甲基反应，体内Hcy浓度的调节受到多种因素的影响，高Hcy浓度会导致多种疾病的发生，近年来Hcy与临床多种疾病相关性的研究更加受到重视，因此，对于Hcy体内代谢及调节因素的研究显得非常关键，本文就此进行综述。     

Extrapolation for a pharmacokinetic model for acetaminophen from adults to neonates: A Latin Hypercube Sampling analysis

Physiological and drug-specific parameters need to be adjusted when extrapolating a pharmacokinetic (PK) model from adults to neonates, so as to reproduce the time profiles of the studied drug(s) consistent with clinical, in vivo data or in vitro cell line measurements. In this paper we present a parameter analysis method, i.e. the Latin Hypercube Sampling (LHS) method for an acetaminophen (APAP) PK model. The original model consists of two compartments (the blood and the urine) with Michaelis-Menten kinetic parameters determined for APAP and its metabolites. The physiological parameters are scaled through allometric laws from adults to neonates, and APAP-specific parameters are adjusted for enzymatic maturational changes. The LHS method is used to statistically investigate the interplay between these parameters. The results for the extrapolated APAP model are consistent with published APAP PK data in neonates. We found the sulphation clearance parameter played a crucial role in the neonatal PK model, but its influence was weakened if the volume of distribution parameters were included. We suggest that this kind of in silico experiment could be valuable as the first step in PK model extrapolation between different ages.     

硫氧还蛋白相互作用蛋白在多囊卵巢综合征中作用的研究进展

多囊卵巢综合征（polycystic ovary syndrome，PCOS）是一种常见于育龄妇女的内分泌代谢性疾病，以月经不规则、高雄激素血症和卵巢多囊样改变为特征，常表现为肥胖、不孕和胰岛素抵抗。硫氧还蛋白相互作用蛋白（thioredoxin-interacting protein，TXNIP）是一种多功能调节剂，不仅参与胰岛素分泌和葡萄糖代谢的调节，还与氧化应激、炎症因子和情绪障碍密切相关。PCOS患者体内的TXNIP水平较健康人群明显增加，表明TXNIP可能参与PCOS及其并发症的发生、发展。近年体内外研究尝试应用中药提取物和西医药物抑制TXNIP的表达，TXNIP特异性抑制剂的发现使TXNIP有望成为抑制PCOS进程的有效靶点。综述TXNIP在PCOS中的作用进展，以期为PCOS发病机制的深入研究及临床诊疗提供新的思路和方向。     

Early effector maturation of naïve human CD8+ T cells requires mitochondrial biogenesis

The role of mitochondrial biogenesis during naïve to effector differentiation of CD8⁺ T cells remains ill explored. In this study, we describe a critical role for early mitochondrial biogenesis in supporting cytokine production of nascent activated human naïve CD8⁺ T cells. Specifically, we found that prior to the first round of cell division activated naïve CD8⁺ T cells rapidly increase mitochondrial mass, mitochondrial respiration, and mitochondrial reactive oxygen species (mROS) generation, which were all inter‐linked and important for CD8⁺ T cell effector maturation. Inhibition of early mitochondrial biogenesis diminished mROS dependent IL‐2 production – as well as subsequent IL‐2 dependent TNF, IFN‐γ, perforin, and granzyme B production. Together, these findings point to the importance of mitochondrial biogenesis during early effector maturation of CD8⁺ T cells.