HISTAMINE IN THE BRAIN: BEYOND SLEEP AND MEMORY

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Posterior Semicircular Canal Benign Paroxysmal Positional Vertigo Presenting with Torsional Downbeating Nystagmus: An Apogeotropic Variant

The aim of this study is to verify the hypothesis that free-floating particles could sometimes localize into the distal portion of the non ampullary arm of the posterior semicircular canal (PSC) so that assuming the Dix-Hallpike’s positions, the clot could move towards the ampulla eliciting a inhibitory torsional-down beating paroxysmal positional nystagmus (PPNy), instead of typical excitatory torsional-up beating PPNy. Among 45 patients with vestibular signs suggesting anterior semicircular canal paroxysmal positional vertigo (PPV), collected from February 2003 to August 2006, we detected a group of 6 subjects whose clinical findings showed a singular behaviour during follow-up. At the first check-up, all patients were submitted to different types of physical manoeuvres for ASC canalolithiasis. Patients were controlled during the same session and after one week. When we found that nystagmus was qualitatively changed we adopted the appropriate physical therapies for that sign. At a next check-up, after having performed some physical therapies, all patients had a typical PSC PPNy of the opposite side, with respect to that of the ASC initially diagnosed. Basing on these observations we conclude that PSC PPV, similarly to lateral semicircular canal PPV, could manifests in a apogeotropic variant

Apogeotropic posterior semicircular canal benign paroxysmal positional vertigo: some clinical and therapeutic considerations

We lately reported the cases of patients complaining positional vertigo whose nystagmic pattern was that of a peripheral torsional vertical positional down beating nystagmus originating from a lithiasis of the non-ampullary arm of the posterior semicircular canal (PSC). We considered this particular pathological picture the apogeotropic variant of PSC benign paroxysmal positional vertigo (BPPV). Since the description of the pilot cases we observed more than 150 patients showing the same clinical sign and course of symptoms. In this paper we describe, in detail, both nystagmus of apogeotropic PSC BPPV (A-PSC BPPV) and symptoms reported by patients trying to give a reasonable explanation for these clinical features. Moreover we developed two specific physical therapies directed to cure A-PSC BPPV. Preliminary results of these techniques are related

Phylogeny and regulation of four lipocalin genes clustered in the chicken genome: evidence of a functional diversification after gene duplication

Producción CientíficaA novel lipocalin gene is here reported that represents the fourth member of a cluster we have identified in the chicken genome. This cluster also includes Chondrogenesis-Associated Lipocalins h and g (CALh, CALg) and Extracellular Fatty Acid Binding Protein (Ex- FABP). The new gene codes for a 22-kDa secreted protein with three cysteine residues and a series of sequence features well conserved in the lipocalin family. All the genes in the cluster are structurally similar presenting comparable exon/intron boundary positions and exon sizes. A phylogenetic analysis indicates the monophyletic grouping of these genes, and their relationship with the lipocalins a-1-microglobulin (A1mg), complement factor 8g chain (C8GC), prostaglandin D synthase (PGDS), and neutrophil-gelatinase-associated lipocalin (NGAL). The new cluster gene appears to be the ortholog of the mammalian C8GC and was thus named Ggal-C8GC. This orthology also suggests that this lipocalin was present in the ancestor common to reptiles and mammals. In addition to other expressing tissues, Ex-FABP, CALh and CALg genes are highly transcribed in chondrocytes at late stages of chondrogenesis during endochondral bone formation and/or upon inflammatory stimulation. Here, we show that they are also transcriptionally induced when chondrocytes are subjected to various biological events as cell quiescence, cell shape transition, and hormonal stimulation. By contrast, Ggal-C8GC transcripts are only barely detectable in chondrocytes, but are more abundant in liver, kidney, brain, heart, skeletal muscle and particularly in skin. Moreover, no expression induction was observed neither during chondrocyte differentiation, nor upon any of the stimulations mentioned above. This indicates that the Ggal-C8GC gene was co-opted for a novel function after the duplication events that gave rise to the cluster. The peculiar coordinated regulation of Ex-FABP, CALh and CALg, and the apparent divergent role of Ggal-C8GC suggest that these gene duplications may have been maintained during evolution by a sub-functionalization mechanism where some common function(s) are shared by several members of the cluster and some other specialized function(s) are unique to other members