Background:The prevalence of hip fracture is increasing with the continued aging of the population. The aim of this study was to compare the results after implementing the project accelerated post-operative recovery after surgery femur in patients aged over 60 years.Methods:Patients were observed during two distinct periods: Before implantation and after the implementation of the project Acerto. Patients underwent spinal anesthesia with post-operative analgesia by lumbar plexus block. Data evaluation was carried out in four stages of the study in both groups: Before arrival to the operating room during surgery, post-anesthesia care unit and on the ward in the morning of day 1 post-operatively.Results:The project implementation significantly reduces the length of stay, the number of suspension of surgery, duration of fasting, the incidence of hunger and thirst and the reintroduction of oral feeding. Oral feeding 2-4 h before surgery with dextrinomaltose not attended with nausea and vomiting. All patients were able to discharge on day 1 post-operatively.Conclusions:The use of clinical measures of accelerating patient recovery decreased length of stay, the number of suspensions of surgery, the time of fasting, the time of oral food reintroduction, high earlier and faster return to family life, working as humanization of treatment to the elderly.

It is often assumed that the transfer of maternal glucocorticoids (GCs; e.g., corticosterone or cortisol) to offspring is an inevitable cost associated with adverse or stressful conditions experienced by mothers. However, recent evidence indicates that maternal GCs may adaptively programme particular physiological and molecular pathways during development to enhance offspring fitness. In this context, an important mechanism through which maternal GCs may lastingly affect offspring phenotypic quality and survival is via effects on embryo telomerase activity and so on offspring postnatal telomere length. Here, using a field experimental design for which we manipulated the corticosterone content in yellow‐legged gull (Larus michahellis) eggs, we show that embryos from corticosterone‐injected eggs not only had a higher telomerase activity but also longer telomeres just after hatching. A complementary analysis further revealed that gull hatchlings with longer telomeres had a higher survival probability during the period when most of the chick mortality occurs. Given the important role that telomere length and its restoring mechanisms have on ageing trajectories and disease risk, our findings provide a new mechanistic link by which mothers may presumably shape offspring life‐history trajectories and phenotype.

BackgroundConditions experienced by a female during early life may affect her reproductive strategies and maternal investment later in life. This effect of early environmental conditions is a potentially important mechanism by which animals can compensate for the negative impacts of climate change. In this study, we experimentally tested whether three-spined sticklebacks (Gasterosteus aculeatus) change their maternal strategy according to environmental temperatures experienced earlier in life. We studied maternal investment from a life-history perspective because females are expected to adjust their reproductive strategy in relation to their current and future reproductive returns as well as offspring fitness.ResultsF1 families were reared in control and elevated winter temperatures and their reproductive trajectories were studied when returned to common conditions. Females that had experienced the warm winter treatment (n = 141) had a lower fecundity and reduced breeding and total lifespan compared to the control individuals (n = 159). Whereas the control females tended to produce their heaviest and largest clutches in their first reproductive attempt, the warm-acclimated females invested less in their first clutch, but then produced increasingly heavy clutches over the course of the breeding season. Egg mass increased with clutch number at a similar rate in the two groups. The warm-acclimated females increased the investment of carotenoids in the first and last clutches of the season. Thus, any transgenerational effects of the maternal thermal environment on offspring phenotype may be mediated by the allocation of antioxidants into eggs but not by egg size.ConclusionsOur results indicate that conditions experienced by females during juvenile life have a profound effect on life-time maternal reproductive strategies. The temperature-induced changes in maternal strategy may be due to constraints imposed by the higher energetic costs of a warm environment, but it is possible that they allow the offspring to compensate for higher energetic costs and damage when they face the same thermal stress as did their mothers.Electronic supplementary materialThe online version of this article (10.1186/s12898-017-0144-x) contains supplementary material, which is available to authorized users.

It has been proposed that animals usually restrain their growth because fast growth leads to an increased production of mitochondrial reactive oxygen species (mtROS), which can damage mitochondrial DNA and promote mitochondrial dysfunction. Here, we explicitly test whether this occurs in a wild bird by supplementing chicks with a mitochondria-targeted ROS scavenger, mitoubiquinone (mitoQ), and examining growth rates and mtDNA damage. In the yellow-legged gull Larus michahellis, mitoQ supplementation increased the early growth rate of chicks but did not reduce mtDNA damage. The level of mtDNA damage was negatively correlated with chick mass, but this relationship was not affected by the mitoQ treatment. We also found that chick growth was positively correlated with both mtDNA copy number and the mitochondrial enzymatic activity of citrate synthase, suggesting a link between mitochondrial content and growth. Additionally, we found that MitoQ supplementation increased mitochondrial content (in males), altered the relationship between mtDNA copy number and damage, and downregulated some transcriptional pathways related to cell rejuvenation, suggesting that scavenging mtROS during development enhanced growth rates but at the expense of cellular turnover. Our study confirms the central role of mitochondria modulating life-history trade-offs during development by other mechanisms than mtROS-inflicted damage.

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