Sympatric divergence and clinal variation in multiple coloration traits of Ficedula flycatchers.

Geographic variation in phenotypes plays a key role in fundamental evolutionary processes such as local adaptation, population differentiation and speciation, but the selective forces behind it are rarely known. We found support for the hypothesis that geographic variation in plumage traits of the pied flycatcher Ficedula hypoleuca is explained by character displacement with the collared flycatcher Ficedula albicollis in the contact zone. The plumage traits of the pied flycatcher differed strongly from the more conspicuous collared flycatcher in a sympatric area but increased in conspicuousness with increasing distance to there. Phenotypic differentiation (PST ) was higher than that in neutral genetic markers (FST ), and the effect of geographic distance remained when statistically controlling for neutral genetic differentiation. This suggests that a cline created by character displacement and gene flow explains phenotypic variation across the distribution of this species. The different plumage traits of the pied flycatcher are strongly to moderately correlated, indicating that they evolve non-independently from each other. The flycatchers provide an example of plumage patterns diverging in two species that differ in several aspects of appearance. The divergence in sympatry and convergence in allopatry in these birds provide a possibility to study the evolutionary mechanisms behind the highly divergent avian plumage patterns.

Candidate genes for colour and vision exhibit signals of selection across the pied flycatcher (Ficedula hypoleuca) breeding range.

The role of natural selection in shaping adaptive trait differentiation in natural populations has long been recognized. Determining its molecular basis, however, remains a challenge. Here, we search for signals of selection in candidate genes for colour and its perception in a passerine bird. Pied flycatcher plumage varies geographically in both its structural and pigment-based properties. Both characteristics appear to be shaped by selection. A single-locus outlier test revealed 2 of 14 loci to show significantly elevated signals of divergence. The first of these, the follistatin gene, is expressed in the developing feather bud and is found in pathways with genes that determine the structure of feathers and may thus be important in generating variation in structural colouration. The second is a gene potentially underlying the ability to detect this variation: SWS1 opsin. These two loci were most differentiated in two Spanish pied flycatcher populations, which are also among the populations that have the highest UV reflectance. The follistatin and SWS1 opsin genes thus provide strong candidates for future investigations on the molecular basis of adaptively significant traits and their co-evolution.

[Newer inhalation anaesthetics and neuro-anaesthesia: what is the place for sevoflurane or desflurane?]. / Les nouveaux agents volatils halogénés en neuro-anesthésie: quelle place pour le sévoflurane ou le desflurane?

The effects on cerebral circulation and metabolism of sevoflurane and desflurane are largely comparable to isoflurane. Both induce a direct vasodilation of the cerebral vessels, resulting in a less pronounced decrease in cerebral blood flow compared to the decrease in cerebral metabolism. This direct vasodilation seems to be dose-dependent and more pronounced for desflurane > isoflurane > sevoflurane. Many reports suggest luxury perfusion at high concentrations of desflurane. Sevoflurane maintains intact cerebral autoregulation up to 1.5 MAC. Desflurane induces a significant impairment in autoregulation, with a completely abolished autoregulation at 1.5 MAC. Both sevoflurane and desflurane (up to 1.5 MAC) maintain normal CO(2) regulation. As to their effect on final intracranial pressure (ICP), both sevoflurane and desflurane revealed no increases in ICP. However, compared to intravenous hypnotics, subdural ICP is higher with volatiles because of their tendency to increase cerebral swelling after dura opening (isoflurane > sevoflurane). Several case reports have noted seizure-like movements, as well as EEG recorded seizures during induction of sevoflurane anesthesia. Especially, in children during inhalational induction with hyperventilation at a high sevoflurane concentration, severe epileptiform EEG with a hyperdynamic response were observed, which urges for caution using inhalational sevoflurane induction in children for neurosurgical procedures. Neuroprotective properties (reduced neuronal death either by necrosis or apoptosis) have been attributed to all volatile agents. However, these neuroprotective effects have been described in experimental or animal models, so their possible effect on humans remains to be proven.

[Management of neurosurgical patient operated upon for intracranial tumour]. / Prise en charge du patient neurochirurgical avec tumeur intracrânienne.

UNLABELLED: 1. Neurological state of patient. PROCEDURES: (low risk of ICP problems or ischemia, little need for brain relaxation). - Volatile-based technique; "high-risk" procedures (anticipated ICP problems, significant risk of intraoperative cerebral ischemia, need for excellent brain relaxation): use total intravenous anaesthesia. EXTRACRANIAL MONITORING: For example, cardiovascular or renal, venous air embolism. Intracranial monitoring. - General environment vs. specific functions-metabolic (jugular venous bulb), neurophysiological (EEG/EP), functional (transcranial Doppler). 4. Induction of anaesthesia. GOALS: Ventilatory control (early mild hyperventilation; avoid hypercapnia, hypoxemia); blood pressure control (avoid CNS arousal: adequate antinociception, anaesthesia); optimal position on ICP-volume curve. PATIENT POSITIONING: Pin holder application --> maximal nociceptive stimulus, block by deeper anaesthesia or analgesia and local anesthetic pin site infiltration. Alternative: antihypertensives. 5. Maintenance of anaesthesia. GOALS: Controlling brain tension via control of CMR and CBF: preventing CNS arousal (depth of anaesthesia, antinociception); treating consequences of CNS arousal (sympatholysis, antihypertensives); the "chemical brain retractor concept". NEUROPROTECTION: Maintenance of an optimal intracranial environment (matching cerebral substrate demand and supply). 6. Emergence from anaesthesia. GOALS: Maintain intra/extracranial homeostasis. Avoid factors --> intracranial bleeding and/or increasing CBF/ICP. The patient should be calm, co-operative and responsive to verbal commands soon after emergence. EARLY VS. LATE EMERGENCE: Ideal: rapid emergence to permit early assessment of surgical results and postoperative neurological follow-up, but there are still some categories of patients where early emergence is not appropriate.