Heat Loss May Explain Bill Size Differences between Birds Occupying Different Habitats

Background

Research on variation in bill morphology has focused on the role of diet. Bills have other functions, however, including a role in heat and water balance. The role of the bill in heat loss may be particularly important in birds where water is limiting. Song sparrows localized in coastal dunes and salt marsh edge (Melospiza melodia atlantica) are similar in size to, but have bills with a 17% greater surface area than, those that live in mesic habitats (M. m. melodia), a pattern shared with other coastal sparrows. We tested the hypotheses that sparrows can use their bills to dissipate “dry” heat, and that heat loss from the bill is higher in M. m. atlantica than M. m. melodia, which would indicate a role of heat loss and water conservation in selection for bill size.

Methodology/Principal Findings

Bill, tarsus, and body surface temperatures were measured using thermal imaging of sparrows exposed to temperatures from 15–37°C and combined with surface area and physical modeling to estimate the contribution of each body part to total heat loss. Song sparrow bills averaged 5–10°C hotter than ambient. The bill of M. m atlantica dissipated up to 33% more heat and 38% greater proportion of total heat than that of M. m. melodia. This could potentially reduce water loss requirements by approximately 7.7%.

Conclusions/Significance

This >30% higher heat loss in the bill of M. m. atlantica is independent of evaporative water loss and thus could play an important role in the water balance of sparrows occupying the hot and exposed dune/salt marsh environments during the summer. Heat loss capacity and water conservation could play an important role in the selection for bill size differences between bird populations and should be considered along with trophic adaptations when studying variation in bill size.     

Circulating Levels of Dimethylarginines,Chronic Kidney Disease and Long-Term Clinical Outcome in Non-ST-Elevation Myocardial Infarction

Background

Mechanisms linking chronic kidney disease (CKD) and adverse outcomes in acute coronary syndromes (ACS) are not fully understood. Among potential key players, reduced nitric oxide (NO) synthesis due to its endogenous inhibitors, asymmetric (ADMA) and symmetric (SDMA) dimethylarginine could be involved. We measured plasma concentration of arginine, ADMA and SDMA and investigated their relationship with CKD and long-term outcome in non-ST-elevation myocardial infarction (NSTEMI).

Methodology/Principal Findings

We prospectively measured arginine, ADMA, and SDMA at hospital admission in 104 NSTEMI patients. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m². We considered a primary end point of combined cardiac death and re-infarction at a median follow-up of 21 months. In CKD (n = 33) and no-CKD (n = 71) patients, arginine and ADMA were similar, whereas SDMA was significantly higher in CKD patients (0.65±0.23 vs. 0.42±0.12 µmol/L; P<0.0001). Twenty-four (23%) patients had an adverse cardiac event during follow-up: 12 (36%) were CKD and 12 (17%) no-CKD patients (P = 0.02). When study population was stratified according to arginine, ADMA and SDMA median values, only SDMA (median 0.46 µmol/L) was associated with the primary end-point (P = 0.0016). In models adjusted for age, hemoglobin and left ventricular ejection fraction, the hazard ratio (HR) for CKD and SDMA were high (HR 2.93, interquartile range [IQR] 1.15–7.53; P = 0.02 and HR 6.80, IQR 2.09–22.2; P = 0.001, respectively) but, after mutual adjustment, only SDMA remained significantly associated with the primary end point (HR 5.73, IQR 1.55–21.2; P = 0.009).

Conclusions/Significance

In NSTEMI patients, elevated SDMA plasma levels are associated with CKD and worse long-term prognosis.     

Translational fusion and redirection to thylakoid lumen as strategies to improve the accumulation of a camelid antibody fragment in transplastomic tobacco

Fragments from camelid single-chain antibodies known as VHHs or nanobodies represent a valuable tool in diagnostics, investigation and passive immunity therapy. Here, we explored different strategies to improve the accumulation of a neutralizing VHH antibody against rotavirus in tobacco transplastomic plants. First, we attempted to express the VHH in the chloroplast stroma and then two alternative strategies were carried out to improve the expression levels: expression as a translational fusion to the β-glucuronidase enzyme (GUS-E-VHH), and redirection of the VHH into the thylakoid lumen (pep-VHH). Every attempt to produce transplastomic plants expressing the VHH in the stroma was futile. The transgene turned out to be unstable and the presence of the VHH protein was almost undetectable. Although pep-VHH plants also presented some of the aforementioned problems, higher accumulation of the nanobody was observed (2-3% of the total soluble proteins). The use of β-glucuronidase as a partner protein turned out to be a successful strategy and expression levels reached 3% of the total soluble proteins. The functionality of the VHHs produced by pep-VHH and GUS-E-VHH plants was studied and compared with that of the antibody produced in Escherichia coli. This work contributes to optimizing the expression of VHH in transplastomic plants. Recombinant proteins could be obtained either by accumulation in the thylakoid lumen or as a fusion protein with β-glucuronidase, and both strategies allow for further optimization.     

Control of cardiovascular variability during undisturbed wake-sleep behavior in hypocretin-deficient mice

The central neural mechanisms underlying differences in cardiovascular variability between wakefulness, non-rapid-eye-movement sleep (NREMS), and rapid-eye-movement sleep (REMS) remain poorly understood. These mechanisms may involve hypocretin (HCRT)/orexin signaling. HCRT signaling is linked to wake-sleep states, involved in central autonomic control, and impaired in narcoleptic patients. Thus, we investigated whether HCRT signaling plays a role in controlling cardiovascular variability during spontaneous behavior in HCRT-deficient mice. HCRT-ataxin3 transgenic mice lacking HCRT neurons (TG), knockout mice lacking HCRT peptides (KO), and wild-type controls (WT) were instrumented with electrodes for sleep recordings and a telemetric blood pressure transducer. Fluctuations of systolic blood pressure (SBP) and heart period (HP) during undisturbed wake-sleep behavior were analyzed with the sequence technique, cross-correlation functions, and coherent averaging of SBP surges. During NREMS, all mice had lower SBP variability, greater baroreflex contribution to HP control at low frequencies, and greater amplitude of the central autonomic and baroreflex changes in HP associated with SBP surges than during wakefulness. During REMS, all mice had higher SBP variability and depressed central autonomic and baroreflex HP controls relative to NREMS. HP variability during REMS was higher than during NREMS in WT only. TG and KO also had lower amplitude of the cardiac baroreflex response to SBP surges during REMS than WT. These results indicate that chronic lack of HCRT signaling may cause subtle alterations in the control of HP during spontaneous behavior. Conversely, the integrity of HCRT signaling is not necessary for the occurrence of physiological sleep-dependent changes in SBP variability.     

Photosynthetic characteristics and growth performance of closely related aspen taxa: On the systematic relatedness of the Eurasian Populus tremula and the North American P. tremuloides

The European and American aspen species Populus tremula and P. tremuloides are closely related taxa with very large distribution ranges and high economic importance. Genetic and morphological data are not fully congruent with respect to the question of the systematic relatedness of these sister taxa, pointing either at separate species on the two continents or a single aggregate species with circumarctic distribution. In a replicated growth trial with 1-year-old saplings, we compared about 30 morphological (leaf size, leaf area, leaf numbers, leaf growth, leaf phenology and the ratio of leaves lost to leaves produced) and physiological traits (A_max, quantum yield, carboxylation efficiency, maximum rates of carboxylation and electron transport, leaf dark respiration, leaf conductance, leaf water potential and WUE) with the aim to obtain evidence in support of or against the one-species hypothesis and to identify key determinants of growth in the two aspen taxa.     

Dual effect of Mesorhizobium loti T3SS functionality on the symbiotic process

Mesorhizobium loti MAFF303099 has a functional type III secretory system (T3SS) involved in the nodulation process on Lotus tenuis and Lotus japonicus. Four putative M.?loti T3SS effectors (Mlr6358, Mlr6331, Mlr6361, and Mlr6316) have been previously described, and it has been demonstrated that the N-terminal regions of Mlr6361 and Mlr6358 mediate the secretion via a T3SS. Here, we demonstrate the capacity of Mlr6316 and Mlr6331 N-terminal regions to direct the secretion of a translational fusion to a reporter peptide through T3SS. By using single, double, and triple mutants, we demonstrated the positive and negative participation of some of these proteins in the determination of competitiveness on Lotus spp. Low competitiveness values correlated with low nodulation efficiency for a mutant deficient in three of the putative M.?loti effectors. Our data suggest that the net effect of M.?loti T3SS function on symbiotic process with Lotus results from a balance between positive and negative effects.     

Cytoskeletal architecture regulates cyclooxygenase-2 in human endothelial cells: Autocrine modulation by prostacyclin

Endothelium is a highly dynamic tissue that controls vascular homeostasis. This requires constant rearrangements of the shape or function of endothelial cells that cannot set aside the role of the cytoskeleton. The aim of this study was to determine the mechanisms by means of which cytoskeletal alterations induce cyclooxygenase‐2 (Cox‐2) expression in human endothelial cells using compounds that interfere with microtubule or actin architecture. Microtubule disruption by nocodazole markedly increased Cox‐2 expression and activity, and provoked paracellular gap formation, a cardinal feature of endothelial barrier dysfunction. The Cox‐2 metabolite prostacyclin down‐regulated Cox‐2 through an autocrine receptor‐mediated mechanism, and partially prevented the disassembly of endothelial monolayers. There was also an interaction between microtubules and actin filaments in nocodazole‐induced Cox‐2 expression. Nocodazole provoked the dissolution of the F‐actin cortical ring and stress fiber formation, increased actin glutathionylation, and concomitantly lowered intracellular levels of reduced glutathione. The restoration of glutathione levels by N‐acetylcysteine opposed Cox‐2 expression and preserved the integrity of endothelial monolayers. Among the signaling pathways connecting microtubule disruption with Cox‐2 up‐regulation, crucial roles are played by Src family kinase activation, serine/threonine phosphatase 2A inhibition, and the phosphorylation of mitogen activated protein kinase p38. Our findings provide a mechanistic insight into the observation that Cox‐2 is induced in endothelial cells under cytoskeleton‐perturbing conditions such as those occurring in the presence of atherogenic/inflammatory stimuli and oxidative stress. In this scenario, Cox‐2 up‐regulation by endothelia exposed to noxious conditions can be considered protective of the vasodilatory and anti‐thrombotic properties of the vessel wall. J. Cell. Physiol. 227: 3847–3856, 2012. © 2012 Wiley Periodicals, Inc.     

The critical role of complement alternative pathway regulator factor H in allergen-induced airway hyperresponsiveness and inflammation

Activation of the alternative pathway of complement plays a critical role in the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation in mice. Endogenous factor H, a potent inhibitor of the alternative pathway, is increased in the airways of sensitized and challenged mice, but its role in regulating inflammation or AHR has been unknown. We found that blocking the tissue-binding function of factor H with a competitive antagonist increased complement activation and tissue inflammation after allergen challenge of sensitized mice. Conversely, administration of a fusion protein that contains the iC3b/C3d binding region of complement receptor 2 linked to the inhibitory region of factor H, a molecule directly targeting complement-activating surfaces, protected mice in both primary and secondary challenge models of AHR and lung inflammation. Thus, although endogenous factor H does play a role in limiting the development of AHR, strategies to deliver the complement-regulatory region of factor H specifically to the site of inflammation provide greater protection than that afforded by endogenous regulators. Such an agent may be an effective therapy for the treatment of asthma.     

Anion inhibition studies of the fastest carbonic anhydrase (CA) known,the extremo-CA from the bacterium Sulfurihydrogenibium azorense

The α-carbonic anhydrase (CA, EC 4.2.1.1) from the extremophilic bacterium Sulfurihydrogenibium azorense, SazCA, is the fastest CA known to date as a catalyst for CO₂ hydration to bicarbonate and protons. We report an inhibition study of this enzyme with inorganic anions and several other small molecules known to interact with these metalloenzymes. Bicarbonate, carbonate and sulfate were ineffective SazCA inhibitors whereas most other inorganic anions were submillimolar inhibitors. The best inhibition was observed with trithiocarbonate, diethyldithiocarbamate, sulfamide, sulfamate, phenylboronic, and phenylarsonic acid, which showed inhibition constants in the range of 3–39 μM. As SazCA is very stable at high temperatures (being an ‘extremo-CA’) and very effective as a catalyst, the inhibition studies reported here may be crucial for designing biotechnological applications for this enzyme, for example for CO₂ capture processes.     

A new approach to improve acoustic trapping effectiveness for Aedes aegypti (Diptera: Culicidae)

Monitoring mosquito populations is essential to designing and implementing control strategies. Recent strategies based on releasing biologically modified mosquitoes have increased the need to effectively monitor mosquito abundance. Unfortunately, existing surveillance traps are of limited value due to their high cost and low capture rates. Here, we report the results of experiments designed to evaluate the effectiveness of an acoustic trap prototype. Stimuli synthesized from recordings of Ae. aegypti wingbeat signals and pure tones were evaluated as attractants to males in indoor and semi‐field conditions. Overall, the acoustic trap´s efficacy differed significantly between indoor and semi‐field conditions. After two hours of indoor recapture, ～69% of males were collected from acoustic traps broadcasting pure tones while ～78% of males were collected using synthesized wingbeat signals. Under semi‐field conditions, however, acoustic traps collected less than ～1.7% of the males released. Increasing the intensity of the signals up to 90 dB (SPL re. 20 uPa at 1 m from the trap) did not improve the capture rate under semi‐field conditions. Overall, our results indicate that acoustic signals synthesized from recordings of wingbeats can be used to enhance capture of male Ae. aegypti.