Frailty has a stronger association with inflammation than age in older veterans

Background

Upregulation of pro-inflammatory cytokines has not only been associated with increased morbidity and mortality in older adults but also has been linked to frailty. In the current study we aimed to compare the relative relationship of age and frailty on inflammation and thrombosis in older veterans.

Results

We analyzed 117 subjects (age range 62–95 years; median 81) divided into 3 cohorts: non-frail, pre-frail and frail based on the Fried phenotype of frailty. Serum inflammatory markers were determined using commercially available ELISA kits. Frail and pre-frail (PF) subjects had higher levels than non-frail (NF) subjects of IL-6 (NF vs. PF: p?=?0.002; NF vs. F: p?<?0.001), TNFR1 (NF vs. F: p?=?0.012), TNFRII (NF vs. F: 0.002; NF vs. PF: p?=?0.005) and inflammatory index: = 0.333*log(IL-6)?+?0.666*log(sTNFR1) (NF vs. F: p?=?0.009; NF vs. PF: p?<?0.001). Frailty status explained a greater percent of variability in markers of inflammation than age: IL-6 (12 % vs. 0.3 %), TNFR1 (5 % vs. 4 %), TNFR2 (11 % vs. 6 %), inflammatory index (16 % vs. 8 %). Aging was significantly associated with higher fibrinogen (p?=?0.04) and D-dimer levels (p?=?0.01) but only among NF subjects.

Conclusion

In conclusion, these data suggest that among older veterans, frailty status has a stronger association with inflammation and the inflammatory index than age does. Larger studies, in more diverse populations are needed to confirm these findings.

     

Feeding ecology has a stronger evolutionary influence on functional morphology than on body mass in mammals

Ecological specialization is a central driver of adaptive evolution. However, selective pressures may uniquely affect different ecomorphological traits (e.g., size and shape), complicating efforts to investigate the role of ecology in generating phenotypic diversity. Comparative studies can help remedy this issue by identifying specific relationships between ecologies and morphologies, thus elucidating functionally relevant traits. Jaw shape is a dietary correlate that offers considerable insight on mammalian evolution, but few studies have examined the influence of diet on jaw morphology across mammals. To this end, I apply phylogenetic comparative methods to mandibular measurements and dietary data for a diverse sample of mammals. Especially powerful predictors of diet are metrics that capture either the size of the angular process, which increases with greater herbivory, or the length of the posterior portion of the jaw, which decreases with greater herbivory. The size of the angular process likely reflects sizes of attached muscles that produce jaw movements needed to grind plant material. Further, I examine the impact of feeding ecology on body mass, an oft-used ecological surrogate in macroevolutionary studies. Although body mass commonly increases with evolutionary shifts to herbivory, it is outperformed by functional jaw morphology as a predictor of diet. Body mass is influenced by numerous factors beyond diet, and it may be evolutionarily labile relative to functional morphologies. This suggests that ecological diversification events may initially facilitate body mass diversification at smaller taxonomic and temporal scales, but sustained selective pressures will subsequently drive greater trait partitioning in functional morphologies.     

Land use change has stronger effects on functional diversity than taxonomic diversity in tropical Andean hummingbirds

Land use change modifies the environment at multiple spatial scales, and is a main driver of species declines and deterioration of ecosystem services. However, most of the research on the effects of land use change has focused on taxonomic diversity, while functional diversity, an important predictor of ecosystem services, is often neglected. We explored how local and landscape scale characteristics influence functional and taxonomic diversity of hummingbirds in the Andes Mountains in southern Ecuador. Data was collected in six landscapes along a land use gradient, from an almost intact landscape to one dominated by cattle pastures. We used point counts to sample hummingbirds from 2011 to 2012 to assessed how local factors (i.e., vegetation structure, flowering plants richness, nectar availability) and landscape factors (i.e., landscape heterogeneity, native vegetation cover) influenced taxonomic and functional diversity. Then, we analyzed environment – trait relationships (RLQ test) to explore how different hummingbird functional traits influenced species responses to these factors. Taxonomic and functional diversity of hummingbirds were positively associated with landscape heterogeneity but only functional diversity was positively related to native vegetation coverage. We found a weak response of taxonomic and functional diversity to land use change at the local scale. Environment‐trait associations showed that body mass of hummingbirds likely influenced species sensitivity to land use change. In conclusion, landscape heterogeneity created by land use change can positively influence hummingbird taxonomic and functional diversity; however, a reduction of native vegetation cover could decrease functional diversity. Given that functional diversity can mediate ecosystem services, the conservation of native vegetation cover could play a key role in the maintenance of hummingbird pollination services in the tropical Andes. Moreover, there are particular functional traits, such as body mass, that increase a species sensitivity to land use change.     

Carvedilol has stronger anti-inflammation and anti-virus effects than metoprolol in murine model with coxsackievirus B3-induced viral myocarditis

Aims

This study aims to compare the effects of carvedilol and metoprolol in alleviating viral myocarditis (VMC) induced by coxsackievirus B3 (CVB3) in mice.

Methods

A total of 116 Balb/c mice were included in this study. Ninety-six mice were inoculated intraperitoneally with CVB3 to induce VMC. The CVB3 inoculated mice were evenly divided into myocarditis group (n = 32), carvedilol group (n = 32) and metoprolol group (n = 32). Twenty mice (control group) were inoculated intraperitoneally with normal saline. Hematoxylin and eosin staining and histopathologic scoring were used to investigate the effects of carvedilol and metoprolol on myocardial histopathologic changes on days 3 and 5. In addition, serum cTn-I levels, cytokine levels and virus titers were determined using chemiluminescence immunoassay, enzyme-linked immunosorbent assay and plaque assay, respectively, on days 3 and 5. Finally, the levels of phosphorylated p38MAPK were studied using immunohistochemical staining and Western blotting on day 5.

Results

Carvedilol had a stronger effect than metoprolol in reducing the pathological scores of VMC induced by CVB3. Both carvedilol and metoprolol reduced the levels of cTn-I, but the effect of carvedilol was stronger. Carvedilol and metoprolol decreased the levels of myocardial pro-inflammatory cytokines and increased the expression of anti-inflammatory cytokine, with the effects of carvedilol being stronger than those of metoprolol. Carvedilol had a stronger effect in reducing myocardial virus concentration compared with metoprolol. Carvedilol was stronger than metoprolol in decreasing the levels of myocardial phosphorylated p38MAPK.

Conclusions

In conclusion, carvedilol was more potent than metoprolol in ameliorating myocardial lesions in VMC, probably due to its stronger modulation of the balance between pro- and anti-inflammatory cytokines by inhibiting the activation of p38MAPK pathway through β1- and β2-adrenoreceptors.     

Forest maturity has a stronger influence on the prevalence of spider monkeys than howler monkeys in an anthropogenically impacted rainforest landscape

Primates - The transformation and depletion of primary forest over the past few decades have placed almost half of the world’s primate species under the threat of extinction. Developing any...     

High midday temperature stress has stronger effects on biomass than on photosynthesis: A mesocosm experiment on four tropical seagrass species

The effect of repeated midday temperature stress on the photosynthetic performance and biomass production of seagrass was studied in a mesocosm setup with four common tropical species, including Thalassia hemprichii, Cymodocea serrulata, Enhalus acoroides, and Thalassodendron ciliatum. To mimic natural conditions during low tides, the plants were exposed to temperature spikes of different maximal temperatures, that is, ambient (29–33°C), 34, 36, 40, and 45°C, during three midday hours for seven consecutive days. At temperatures of up to 36°C, all species could maintain full photosynthetic rates (measured as the electron transport rate, ETR) throughout the experiment without displaying any obvious photosynthetic stress responses (measured as declining maximal quantum yield, Fv/Fm). All species except T. ciliatum could also withstand 40°C, and only at 45°C did all species display significantly lower photosynthetic rates and declining Fv/Fm. Biomass estimation, however, revealed a different pattern, where significant losses of both above‐ and belowground seagrass biomass occurred in all species at both 40 and 45°C (except for C. serrulata in the 40°C treatment). Biomass losses were clearly higher in the shoots than in the belowground root–rhizome complex. The findings indicate that, although tropical seagrasses presently can cope with high midday temperature stress, a few degrees increase in maximum daily temperature could cause significant losses in seagrass biomass and productivity.     

Adenoviruses C in non-hospitalized Mexican children older than five years of age with acute respiratory infection

Adenoviruses (AdV) are commonly involved in acute respiratory infections (ARI), which cause high morbidity and mortality in children. AdV are grouped in six species (A-F), which are associated with a wide range of diseases. The aim of this study was to identify the AdV species infecting non-hospitalized Mexican children with ARI symptoms, attending to the same school. For that, a PCR/RFLP assay was designed for a region of the hexon gene, which was chosen, based on the bioinformatical analysis of AdV genomes obtained from GenBank. A total of 100 children's nasopharyngeal samples were collected from January to June, 2005, and used for viral isolation in A549 cells and PCR/RFLP analysis. Only 15 samples produced cytopathic effect, and in all of them AdV C was identified. AdV C was also identified in eight additional nasopharyngeal samples which were negative for viral isolation. In summary, this outpatient population showed a rate of AdV infection of 23%, and only AdV C was detected.     

Floodplain ants show a stronger response to an extensive flood than to variations in fallen‐timber load

Understanding how species respond to differences in resource availability is critical to managing biodiversity under the increasing pressures associated with climate change and growing human populations. Over the last century, the floodplain forests of Australia's largest river system, the Murray‐Darling Basin, have been much affected by intensive harvesting of timber and firewood, and increasingly stressed by river regulation and, recently, an extended drought. Fallen timber – logs and shed branches – is known to play a key role in the ecology of several important species on these floodplains. Here, we monitored the response of the ant assemblages of a floodplain forest along the Murray River to a large‐scale (34 ha) experimental manipulation of fallen‐timber load (0 to 80 t ha^?1) over 4 years. The forest was subjected to an incidental, extensive flood that enabled us to examine how two important stressors (timber removal and river regulation) affect ant assemblages. Ants showed little response to the proximity of fallen timber within plots, prior to the flood, or to different loads among plots, unlike other floodplain biota. After the flood, both ant abundance and species richness increased and species composition changed. However, this increase in species richness after flooding was less pronounced in plots with higher amounts of fallen timber. Managing river red gum forest using a mosaic of flood regimes, more representative of historical conditions, is likely to be the most effective way to maintain and enhance the diversity of ants and other biota on these important floodplains.     

Guilt by association: What p120-catenin has to hide

Members of the p120-catenin family associate with cadherins and regulate their stability at the plasma membrane. How p120-catenin limits cadherin endocytosis has long remained a mystery. In this issue, Nanes et al. (2012. J. Cell Biol. doi:10.1083/jcb.201205029) identify a conserved acidic motif within cadherins that acts as a physical platform for p120-catenin binding. However, in the absence of p120-catenin, the motif acts as an endocytic signal. These results provide new insight into p120-catenin’s role as guardian of intercellular junction dynamics.Adhesion receptors of the classical cadherin family have a major role in establishing tissue organization and maintaining tissue homeostasis (Gumbiner, 1996). Classical cadherins are transmembrane glycoproteins that use their extracellular domains to establish calcium-dependent trans homophilic interactions with cadherins in neighboring cells. To enhance adhesive strength, cadherin ectodomains oligomerize through lateral (cis) interactions, whereas their cytoplasmic domains anchor to the actomyosin cytoskeleton. The cytoplasmic domain of cadherins is highly conserved and binds to proteins called catenins. p120-catenin (p120) associates with the transmembrane adjacent domain (juxtamembrane; JMD) of the cadherin cytoplasmic tail, whereas β-catenin interacts with the more distal portion of cadherin’s cytoplasmic domain. β-Catenin in turn, binds α-catenin, which, through multiple interactions, both indirect and direct, can associate with the actin cytoskeleton (Perez-Moreno and Fuchs, 2006).Cellular rearrangements are orchestrated by dynamic assembly/disassembly of cadherin complexes. The process is fueled by endocytosis of cadherin complexes (Le et al., 1999; de Beco et al., 2009). Endocytosis can be stimulated by proteins that associate with cadherin–catenin complexes, including proteases that shed the cadherin ectodomains, and the ubiquitin ligase Hakai (Fujita et al., 2002). Cadherin internalization can be regulated by different pathways depending on the cellular context, involving clathrin-dependent and clathrin-independent mechanisms. These endocytic processes must be carefully regulated, as an untimely destabilization of cadherin-mediated adhesion can lead to alterations in tissue architecture and growth, features of several diseases, including cancers (Mosesson et al., 2008).In the past decade, p120 catenins (p120, ARVCF, δ-catenin, and p0071) have emerged as critical regulators of cadherin-mediated adhesion (Reynolds, 2007). p120, the founding family member, is a component of cadherin complexes (Reynolds et al., 1994), and its association with the cadherin JMD is important for retaining cadherins at the membrane (Ireton et al., 2002). Moreover, p120 loss causes rapid internalization of cadherins, followed by proteasomal and/or lysosomal-mediated degradation (Davis et al., 2003; Xiao et al., 2003a,b, 2005; Miyashita and Ozawa, 2007).Although these studies expose p120 as a master regulator of cadherin levels at the membrane, exactly how p120 governs cadherin endocytosis rates has remained unclear. Based upon experiments in which endocytic machinery components (clathrin, dynamin, and AP2) have been impaired (Chiasson et al., 2009) or cadherin endocytic motifs have been mutated (Hong et al., 2010; Troyanovsky et al., 2007), researchers have posited that p120 binding to cadherins may in some way prevent junctional complex endocytosis. In this issue, Nanes et al. add new molecular insights into the mechanism. The authors show that the VE-cadherin JMD functions as a bimodal platform for either p120 binding or endocytic signaling. Moreover, they identify a key conserved amino acid residue within the JMD, which, when mutated, blocks endocytosis without the need for p120.Recently, the cocrystallization of p120 bound to E-cadherin’s JMD has yielded insights into the essential residues of this binding interface (Ishiyama et al., 2010). Previous studies had attributed the core function of p120-cadherin to its ability to bind and mask a dileucine endocytic motif present in the JMD (Miyashita and Ozawa, 2007; Hong et al., 2010). The crystal structure showed that interactions between p120 and the JMD domain might be sufficient to sterically prevent accessibility of the dileucine cadherin endocytic motif to endocytic adaptors such as the AP2-clathrin adaptor, thereby placing this motif at the crux of the bimodal switch controlling the mutually exclusive binding of either p120 or the endocytic machinery.The affinity of p120 and AP2 for the JMD dileucine motif is similar, pointing toward the existence of a balanced regulation of cadherin endocytic rates and cadherin retention at the membrane. However, evaluating this balance in cellular contexts has not been possible because of the inability to uncouple p120 binding to the JMD and endocytosis. Nanes et al. (2012) have now overcome this hurdle. They first used a simulated model of the p120–E-cadherin crystal structure, which highlighted a conserved p120-binding region that is present in the JMD of both VE- and E-cadherin. However, the VE-cadherin JMD lacked endocytic dileucine and tyrosine residues present in E-cadherin, which are involved in clathrin internalization and Hakai-dependent ubiquitination, respectively.Because both types of adherens junctions undergo dynamic endocytic-based remodeling, the authors astutely realized that they might be able to exploit VE- and E-cadherin differences to unearth novel endocytic signals within the sequence that might be conserved among cadherins. To this end, the author first used mutant VE-cadherin chimeric proteins, consisting of the cytoplasmic domain of VE-cadherin fused to the extracellular domain of the IL-2 receptor, and internalization assays. They discovered that the core p120-binding region on its own was endocytosed, in a fashion similar to the full VE-cadherin cytoplasmic tail. This occurred in a clathrin-dependent manner, as previously observed in Kowalzcyk’s laboratory (Chiasson et al., 2009). Point mutagenesis identified some mutants no longer able to bind p120, which is consistent with previous findings (Thoreson et al., 2000). But the authors made an interesting finding: mutations in a conserved acidic motif (DEE) within the p120-core binding region of the JMD displayed loss of p120 binding and also blocked cadherin internalization (Fig. 1). Moreover, DEE mutant VE-cadherins localized stably at the membrane even in the absence of p120, although with an increased diffusion within the membrane. This increase in mobility suggests a reduction in cadherin lateral clustering, a process modulated by the binding of p120 to the JMD (Yap et al., 1998). Interestingly, in crystal structures, the E-cadherin JMD binding to p120 induced oligomerization of the complex (Ishiyama et al., 2010).Open in a separate windowFigure 1.Model of VE-cadherin stabilization at the cell membrane. (A) VE-cadherin binds to p120 and β-catenin. p120 associates with the juxtamembrane (JMD) domain of the cadherin cytoplasmic tail, whereas β-catenin binds to the more distal portion (catenin binding domain, CBD). Cadherin internalization is triggered by p120 dissociation, exposing a conserved endocytic factor recognition motif (DEE; 646–648) within the JMD. (B) When this motif is mutated in VE-cadherin, adherens junctions are resistant to endocytosis independent of p120 binding.These new tools now allow uncoupling of p120 binding from cadherin endocytosis, which will be instrumental in unraveling new p120 cadherin roles in cell adhesion. The VE-cadherin mutant that fails to bind to p-120 still coimmunoprecipitates with β-catenin. These findings are intriguing, given that overexpression of p120 can rescue the otherwise poor adhesive properties of cadherins mutant for β-catenin binding (Ohkubo and Ozawa, 1999). In addition, interactions between p120 and α-catenin at adherens junctions seem to contribute in preventing cadherin endocytosis (Troyanovsky et al., 2011). Given these collective results, it will be interesting in the future to measure the binding affinities of endocytosis-uncoupled VE-cadherin mutants for its binding partners.Overall, these data provide strong evidence that the JMD landing pad provides the nuts and bolts of the decision of whether an adherens junction remains at the cell surface or whether it is internalized. But who makes the decision? Recent results from Gumbiner’s group provide a possible clue. They show that cadherin activation stimulates the dephosphorylation of specific Ser/Thr residues within the N-terminal domain of p120, and this in turn stabilizes intercellular adhesion (Petrova et al., 2012).The new tools developed by Kowalczyk’s group (Nanes et al., 2012) will pave the way for researchers to dig further into the mechanism. In the current study, the authors use their newfound tools to analyze the consequences to cell migration when p120-JMD binding is uncoupled from endocytosis. In scratched monolayers of endothelial cells, cell migration was decreased. Importantly, when they examined the VE-cadherin mutant in which p120 binding was blocked but cadherin internalization could proceed normally, cell migration was largely normal. These findings indicate that the migration defects seen in the cells expressing the E-cadherin mutant are rooted in inhibition of endocytosis, rather than lack of p120 recruitment to junctions. They further suggest that endocytic trafficking of cadherins is necessary to transiently destabilize cell–cell contacts that otherwise impede migration. This notion is particularly intriguing given that when E-cadherins are stabilized at intercellular junctions, they can sequester proteins that are required for integrin-based migration (Livshits et al., 2012). Kowalczyk’s findings (Nanes et al., 2012) now suggest a means by which dynamic changes in intercellular adhesion can be achieved to trigger such downstream events.Although less well characterized, there are other regulatory circuits that might also be affected by transiently liberating p120 from intercellular junctions. Thus, for example, p120 enhances cadherin stability through its ability to interact with afadin and Rap1, thereby bridging connections with nectin intercellular junctions (Hoshino et al., 2005). Other direct and indirect p120 associates that might affect cadherin internalization include the endocytic adaptor Numb (Sato et al., 2011) and the signaling enzyme γ-secretase (Kiss et al., 2008). Additionally, p120 can also regulate Rac1 activity, which influences cadherin endocytosis in a clathrin-independent way (Akhtar and Hotchin, 2001). Thus, removing p120 or devising additional mutations to uncouple these interactions may be needed to fully unravel all the mysteries underlying p120’s power in governing intercellular adhesion in tissue development and maintenance (Davis and Reynolds, 2006; Elia et al., 2006; Perez-Moreno et al., 2006; Smalley-Freed et al., 2010; Marciano et al., 2011; Stairs et al., 2011; Chacon-Heszele et al., 2012; Kurley et al., 2012). That said, by dissecting p120’s web at the crossroads between intercellular junction stabilization and endocytosis, Kowalczyk and coworkers (Nanes et al., 2012) now illustrate the power of their approach and provide new insights into how similar strategies might ultimately enable this molecular crossword puzzle to be solved.     

Competition and coexistence in plant communities: intraspecific competition is stronger than interspecific competition

Theory predicts that intraspecific competition should be stronger than interspecific competition for any pair of stably coexisting species, yet previous literature reviews found little support for this pattern. We screened over 5400 publications and identified 39 studies that quantified phenomenological intraspecific and interspecific interactions in terrestrial plant communities. Of the 67% of species pairs in which both intra‐ and interspecific effects were negative (competitive), intraspecific competition was, on average, four to five‐fold stronger than interspecific competition. Of the remaining pairs, 93% featured intraspecific competition and interspecific facilitation, a situation that stabilises coexistence. The difference between intra‐ and interspecific effects tended to be larger in observational than experimental data sets, in field than greenhouse studies, and in studies that quantified population growth over the full life cycle rather than single fitness components. Our results imply that processes promoting stable coexistence at local scales are common and consequential across terrestrial plant communities.     

Coordination of construction behavior in the termite Procornitermes araujoi: structure is a stronger stimulus than volatile marking

We studied the behavioral coordination mechanisms underlying morphogenesis in shelter construction by the termite Procornitermes araujoi. We detected positive feedback in both digging and pellet deposition behavior. The literature suggests two stimuli for these positive feedbacks: the emerging structure itself or volatile chemical marking added to the construction material. The experiments showed that the most important stimulus is the change in structure, but indirect evidence suggests that there is also some chemical marking involved. Beyond shedding light on the behavioral mechanisms of termite shelter construction, these results also stress the necessity of direct experimental approaches in order to identify and properly weight different coordination mechanisms underlying morphogenesis in biological systems.     

Staphylococcus aureus primase has higher initiation specificity, interacts with single-stranded DNA stronger, but is less stimulated by its helicase than Escherichia coli primase

The study of primases from model organisms such as Escherichia coli , phage T7 and phage T4 has demonstrated the essential nature of primase function, which is to generate de novo RNA polymers to prime DNA polymerase. However, little is known about the function of primases from other eubacteria. Their overall low primary sequence homology may result in functional differences. To help understand which primase functions were conserved, primase and its replication partner helicase from the pathogenic Gram-positive bacteria Staphylococcus aureus were compared in detail with that of E. coli primase and helicase. The conserved properties were to primer initiation and elongation and included slow kinetics, low fidelity and poor sugar specificity. The significant differences included S. aureus primase having sixfold higher kinetic affinity for its template than E. coli primase under equivalent conditions. This naturally higher activity was balanced by its fourfold lower stimulation by its replication fork helicase compared with E. coli primase. The most significant difference between the two primases was that S. aureus helicase stimulation did not broaden the S. aureus primase initiation specificity, which has important biological implications.     

Younger genes are less likely to be essential than older genes, and duplicates are less likely to be essential than singletons of the same age

Recently duplicated genes are believed to often overlap in function and expression. A priori, they are thus less likely to be essential. Although this was indeed observed in yeast, mouse singletons and duplicates were reported to be equally often essential. This contradiction can only partly be explained by experimental biases. We herein show that older genes (i.e., genes with earlier phyletic origin) are more likely to be essential, regardless of their duplication status. At a given phyletic gene age, duplicates are always less likely to be essential compared with singletons. The "paradoxical" high essentiality among mouse gene duplicates is then caused by different age profiles of singletons and duplicates, with the latter tending to be derived from older genes.     

Breeding phenological response to spring weather conditions in common Finnish birds: resident species respond stronger than migratory species

National bird‐nest record schemes provide a valuable data source to study large‐scale changes in basic breeding biology and effects of climate change on birds. Using nest‐record scheme data from 26 common Finnish breeding bird species from whole Finland, we estimated the laydate of the first egg for 129 063 nesting attempts. We then investigated the relationship of mean spring temperature and spring precipitation sum to changes in the onset of laying over the period 1961–2012. In addition, we examine differences in response to these climatic variables for species grouped for different life history strategies; migration, diet and habitat. Finally, we test whether body size is related to the strength of phenological response. We show that 26 common Finnish breeding bird species have advanced their laying dates over time and to an increase in the mean spring temperature over the study period. When species are grouped according life history strategies, we find that breeding phenological change is negatively associated with changes in the mean spring temperature where residents respond strongest to changes in mean spring temperature, but also short‐ and long‐distance migrants advance laydates with increasing spring temperatures. Breeding phenological change is also associated with spring precipitation, where resident species delay and short‐distance migrants advance the onset of breeding. In addition we find that omnivorous species respond stronger than insectivorous species to changes in spring temperature. In contrast to results from an earlier study, we do not find evidence that small‐sized species respond stronger to spring temperature than large‐sized species. As climate warming is predicted to continue in the future, long‐term citizen science schemes, such as the Finnish nest‐card scheme, prove to be a valuable cost‐effective way to monitor the environment and allow investigation into how species are responding to changes in their environment.