Great tits (Parus major) reduce body mass in response to wing area reduction: a field experiment

Flight performance is crucial in determining whether a smallbird will survive an attack by a predator. Given the importanceof body mass in determining flight performance, it has beensuggested that birds should strategically regulate body massas a response to predation risk. However, all experiments upto now have been carried out with captive birds, comparing experimental to control birds. Here we present data from thefirst experiment in the field using a within-individuals experimentaldesign. The wing area of wild great tits, Parus major, wasreduced by reversibly taping primaries five to seven. Thisallowed for the same individual to alternatively act as controlor experimental bird. Great tits reduced body mass (but not pectoral muscle width) during episodes of wing area reduction,lending support to the view that the reduction in body massexperienced by birds during molt is a strategy rather thanthe result of energetic stress. Theoretical models establishingthe different trade-offs that determine optimal body mass should therefore take into account this important life-history episode.     

Arterial vascularization of the sinuatrial node in the embryonic rat heart.

We studied the embryological development of the extracoronary cardiac vessels, determining their origins, courses and terminations in embryonic rat hearts. The sinuatrial node is supplied by an extracoronary artery, which can originate from (a) the right internal mammary artery, as a nodal artery, based on its origin; (b) the internal mammary artery, or (c) the right subclavian artery as a collateral artery of the cardiac branch of the cardiomediastinal trunk. The intimate relations of the nodal artery with the sinus node make it possible to study, at the same time, the development of the sinuatrial node in the rat embryo. The sinuatrial node always develops before the nodal artery, which does not appear until 16 or 16.5 days of development.     

Interactions of oritavancin, a new semi-synthetic lipoglycopeptide, with lipids extracted from Staphylococcus aureus

Oritavancin, a lipoglycopeptide with marked bactericidal activity against vancomycin-resistant Staphylococcus aureus and enterococci, induces calcein release from CL:POPE and POPG:POPE liposomes, an effect enhanced by an increase in POPG:POPE ratio, and decreased when replacing POPG by DPPG (Domenech et al., Biochim Biophys Acta 2009; 1788:1832-40). Using vesicles prepared from lipids extracted from S. aureus, we showed that oritavancin induces holes, erosion of the edges, and decrease of the thickness of the supported lipid bilayers (atomic force microscopy; AFM). Oritavancin also induced an increase of membrane permeability (calcein release) on a time- and dose-dependent manner. These effects were probably related to the ability of the drug to bind to lipid bilayers as shown by 8-anilino-1- naphthalene sulfonic acid (ANS) assay. Interaction of oritavancin with phospholipids at the level of their glycerol backbone and hydrophobic domain was studied by monitoring changes of Laurdan excitation generalized polarization (GP_ex) and 1,6-diphenyl-1,3,5-hexatriene (DPH) fluorescence anisotropy upon temperature increase. Oritavancin increased GP_ex values and the transition temperature, indicating a more ordered structure at the level of the glycerol backbone. Oritavancin slightly decreased DPH fluorescence depolarization intensities, suggesting an increase in fluidity at the level of acyl chains. Together, our data confirm the interaction of oritavancin with lipids and the potential role of a rigidifying effect at the level of glycerol backbone for membrane permeabilization. This work shows how AFM and biophysical methods may help in characterizing drug-membrane interactions, and sheds further light on the mode of action of oritavancin.     

Cholinesterase,acid phosphatase,and phospholipase C ofPseudomonas aeruginosa under hyperosmotic conditions in a high-phosphate medium

The presence of low choline or betaine concentrations in a culture medium containing succinate, NH₄Cl, and inorganic phosphate (Pi) as the carbon, nitrogen, and phosphate sources, respectively, permits the growth ofPseudomonas aeruginosa in a hyperosmolar medium. Dimethylglycine, acetylcholine, and phosphorylcholine were less effective as osmoprotectants than choline or betaine. Other alkylammonium compounds tested were virtually ineffective in this capacity. Bacterial growth was also observed in a hyperosmolar medium when choline was the sole carbon and nitrogen source. Choline could act as an osmoprotectant under all the conditions tested. However, the production of cholinesterase (ChE), acid phosphatase (Ac. Pase) and phospholipase C (PLC) took place only when choline was the carbon and nitrogen source. This fact confirms that the synthesis of PLC may occur even in the presence of a high Pi concentration in the medium. Inasmuch as in a high-P_i medium the synthesis of PLC and Ac. Pase (phosphorylcholine phosphatase) is dependent only on choline metabolism, it is postulated that both enzymes are involved in a set of reactions coordinated to produce the breakdown of the membrane phospholipids of the host cell in a hyperosmotic medium.     

Preconditioning tachycardia decreases the activity of the mitochondrial permeability transition pore in the dog heart

Cardioprotection by preconditioning is a central issue of current research on heart function. Several reports indicate that preventing the assembly and opening of the mitochondrial permeability transition pore (mPTP) protects the heart against ischemia–reperfusion injury. We have previously reported that brief episodes of tachycardia decrease the infarct size produced by subsequent prolonged occlusion of a coronary artery, indicating that controlled tachycardia is an effective preconditioning manoeuvre. The effects of preconditioning tachycardia on mPTP activity have not been reported. Therefore, in this work we investigated if preconditioning tachycardia protects against calcium-induced mitochondrial swelling, a measure of mPTP activity. We found that tachycardia decreased by 2.5-fold the rate of mitochondrial calcium-induced swelling, a factor that presumably contributes to the cardioprotective effects of tachycardia. The oxidative status of the cell increased after tachycardia, as evidenced by the decrease in the cellular and mitochondrial GSH/GSSG ratio. We also observed increased S-glutathionylation of cyclophilin-D, an essential mPTP component, after tachycardia. This reversible redox modification of cyclophilin-D may account, al least in part, for the decreased mPTP activity produced by preconditioning tachycardia.     

Site-directed mutations and kinetic studies show key residues involved in alkylammonium interactions and reveal two sites for phosphorylcholine in Pseudomonas aeruginosa phosphorylcholine phosphatase

Pseudomonas aeruginosa phosphorylcholine phosphatase (PchP) catalyzes the hydrolysis of phosphorylcholine (Pcho) to produce choline and inorganic phosphate. PchP belongs to the haloacid dehalogenase superfamily (HAD) and possesses the three characteristic motifs of this family: motif I ((31)D and (33)D), motif II ((166)S), and motif III ((242)K, (261)G, (262)D and (267)D), which fold to form the catalytic site that binds the metal ion and the phosphate moiety of Pcho. Based on comparisons to the PHOSPHO1 and PHOSPHO2 human enzymes and the choline-binding proteins of Gram-(+) bacteria, we selected residues (42)E and (43)E and the aromatic triplet (82)YYY(84) for site-directed mutagenesis to study the interactions with Pcho and p-nitrophenylphosphate as substrates of PchP. Because mutations in (42)E, (43)E and the three tyrosine residues affect both the substrate affinity and the inhibitory effect produced by high Pcho concentrations, we postulate that two sites, one catalytic and one inhibitory, are present in PchP and that they are adjacent and share residues.