Beyond illness: Variation in haemosporidian load explains differences in vocal performance in a songbird

In animal communication, signals are expected to evolve to be honest, so that receivers avoid being manipulated by signalers. One way that signals can evolve to be honest is for them to be costly, with only high‐quality individuals being able to bear the costs of signal expression. It has been proposed that parasites can introduce costs that affect the expression of sexually selected traits, and there is evidence to support the role of parasitism in modulating animal behavior. If host infection status or intensity is found to relate to differences in signal expression, it may indicate a fitness cost that mediates honesty of signals. Birdsong is a good model for testing this, and physically challenging songs representing complex motor patterns provide a good example of sexually selected traits indicating individual condition. We performed a field study to evaluate the relationship between song performance and avian malaria infection in a common songbird. Previous work on this subject has almost always evaluated avian malaria in terms of binary infection status; however, parasitemia—infection intensity—is rarely assessed, even though differences in parasite load may have profound physiological consequences. We estimated parasitemia levels by using real‐time PCR. We found that birds with higher parasitemia displayed lower vocal performance, providing evidence that this song trait is an honest signal of parasitic load of haemosporidian parasites. To our knowledge, this study links parasite load and the expression of a sexually selected trait in a way that has not been addressed in the past. Studies using song performance traits and parasitemia offer an important perspective for understanding evolution of characters via sexual selection.     

Length–weight relationships of 20 fish species from Bahía de Matanchen,in the southeast Gulf of California,Mexico

Length–weight relationship (LWR) parameters were determined for 20 fish species belonging to 14 genera and seven families. The fishes were collected monthly (May 2013 to February 2014) by soft‐bottom trawls in Bahía de Matanchén, southeast of the Gulf of California. Sizes ranged between 5.5 and 36.0 cm total length (TL) and weighed between 1 and 901 g. The allometric coefficient (b) of the LWR varied from 2.638 for Chloroscombrus orqueta to 3.668 for Neopisthopterus tropicus. This is the first report of LWR estimations for 15 of the species.     

Zinc hyperaccumulation substitutes for defense failures beyond salicylate and jasmonate signaling pathways of Alternaria brassicicola attack in Noccaea caerulescens

The hypothesis of metal defense as a substitute for a defective biotic stress signaling system in metal hyperaccumulators was tested using the pathosystem Alternaria brassicicola–Noccaea caerulescens under low (2 µM), medium (12 µM) and high (102 µM) Zn supply. Regardless the Zn supply, N. caerulescens responded to fungal attack with the activation of both HMA4 coding for a Zn transporter, and biotic stress signaling pathways. Salicylate, jasmonate, abscisic acid and indoleacetic acid concentrations, as well as biotic stress marker genes (PDF1.2, CHIB, LOX2, PR1 and BGL2) were activated 24 h upon inoculation. Based on the activation of defense genes 24 h after the inoculation an incompatible fungal–plant interaction could be predicted. Nonetheless, in the longer term (7 days) no effective protection against A. brassicicola was achieved in plants exposed to low and medium Zn supply. After 1 week the biotic stress markers were even further increased in these plants, and this compatible interaction was apparently not caused by a failure in the signaling of the fungal attack, but due to the lack of specificity in the type of the activated defense mechanisms. Only plants receiving high Zn exhibited an incompatible fungal interaction. High Zn accumulation in these plants, possibly in cooperation with high glucosinolate concentrations, substituted for the ineffective defense system and the interaction turned into incompatible. In a threshold‐type response, these joint effects efficiently hampered fungal spread and, consequently decreased the biotic stress signaling.     

Spectral attenuation of brain and retina tissues in the near‐infrared range measured using a fiber‐based supercontinuum device

A novel setup for the efficient constant optical measurements of biological tissues in the near infrared is presented. The system combines the use of a fiber‐based supercontinuum source with a simple optics fiber collimator. This configuration allows a wide spectral range of measurement and, at the same time, can efficiently filter the straightforward transmitted light while avoiding scattered light. As a performance example, the optical characterization of rat brain and retina tissues are shown. The attenuation coefficient for both tissues in the near infrared region is also obtained. This technique could be applied in clinical research as a noninvasive method with several potential practical applications.     

Design of a bivalent peptide with two independent elements of secondary structure able to fold autonomously.

This article describes a strategy to develop, starting from a de novo design, bivalent peptides containing two different (alpha-helix and beta-hairpin) and independent secondary-structure elements. The design was based on the use of conformationally restricted peptide libraries. Structural characterization by NMR revealed that the peptides were stable and did not show any long-range NOE interactions between the N-terminal beta-hairpin and the C-terminal alpha-helix. These results suggest that the two elements of secondary structure are stable and well folded.     

Minimum information specification for in situ hybridization and immunohistochemistry experiments (MISFISHIE)

One purpose of the biomedical literature is to report results in sufficient detail that the methods of data collection and analysis can be independently replicated and verified. Here we present reporting guidelines for gene expression localization experiments: the minimum information specification for in situ hybridization and immunohistochemistry experiments (MISFISHIE). MISFISHIE is modeled after the Minimum Information About a Microarray Experiment (MIAME) specification for microarray experiments. Both guidelines define what information should be reported without dictating a format for encoding that information. MISFISHIE describes six types of information to be provided for each experiment: experimental design, biomaterials and treatments, reporters, staining, imaging data and image characterizations. This specification has benefited the consortium within which it was developed and is expected to benefit the wider research community. We welcome feedback from the scientific community to help improve our proposal.     

G protein-coupled receptor kinase 2 (GRK2) in migration and inflammation

G protein-coupled receptor kinase 2 (GRK2) is a key modulator of G protein-coupled receptors and other plasma membrane receptors stimulated by chemotactic messengers. On top of that, GRK2 has been reported to interact with a variety of signal transduction proteins related to cell migration such as MEK, Akt, PI3Kgamma or GIT. Interestingly, the levels of expression and activity of this kinase are altered in a number of inflammatory disorders (as rheumatoid arthritis or multiple sclerosis), thus suggesting that it may play an important role in the onset or development of these pathologies. This review summarizes the mechanisms involved in the control of GRK2 expression and function and highlights novel functional interactions of this protein that might help to explain how altered GRK2 levels affects cell migration in different cell types and pathological settings.     

Cu(I)-glutathione complex: a potential source of superoxide radicals generation

Cu(2+) ions and GSH molecules interact swiftly to form the complex Cu(I)-glutathione. We investigated the potential capacity of such complex to reduce molecular oxygen. The addition of SOD to a solution containing Cu(I)-glutathione led to a sustained decline of the basal oxygen level. Such effect was partially reverted by the addition of catalase. The complex was able to induce the reduction of cytochrome c and the oxidation of dyhydroethidium into 2-hydroxyethidium. Both effects were totally blocked by SOD. The ability of the complex to generate superoxide radicals was confirmed by EPR spin-trapping. Cu(I)-glutathione induces no oxidation of fluorescein, a hydroxyl radical-sensitive probe. We conclude that in solutions containing the complex, oxygen is continually reduced into superoxide, and that-in absence of interceptors-the latter radicals are quantitatively re-oxidized into molecular oxygen. We suggest that, by functioning as a continuous source of superoxide, the complex could potentially affect a broad range of susceptible biological targets.     

Causal role of oxidative stress in liver preconditioning by thyroid hormone in rats

Hepatic ischemia-reperfusion (IR) injury, a major clinical drawback during surgery, is abolished by L-3,3',5-triiodothyronine (T(3)) administration. Considering that the triggering mechanisms are unknown, the aim of this study is to assess the role of oxidative stress in T(3) preconditioning using N-acetylcysteine (NAC) before T(3) administration. Male Sprague-Dawley rats given a single dose of 0.1 mg of T(3)/kg were subjected to 1 h ischemia followed by 20 h reperfusion, in groups of animals pretreated with 0.5 g of NAC/kg 0.5 h before T(3) or with the respective control vehicles. At the end of the reperfusion period, blood and liver samples were taken for analysis of serum aspartate aminotransferase (AST) and hepatic histology, glutathione (GSH) and protein carbonyl contents, and nuclear factor-kappaB (NF-kappaB) and activating protein 1 (AP-1) DNA binding. The IR protocol used led to a 4.5-fold increase in serum AST levels and drastic changes in liver histology, with significant GSH depletion and enhancement of protein carbonyl levels and of the protein carbonyl/GSH content ratio, whereas NF-kappaB and AP-1 DNA binding was decreased and enhanced, respectively. In a time window of 48 h, T(3) exerted protection against hepatic IR injury, with 88% reduction in the protein carbonyl/GSH ratio and normalization of NF-kappaB and AP-1 DNA binding, changes that were suppressed by NAC administration before T(3). Data presented suggest that a transient increase in the oxidative stress status of the liver is an important trigger for T(3) preconditioning, evidenced in a warm IR injury model through antioxidant intervention.