Presence of the deleted hobo element Th in Eurasian populations of Drosophila melanogaster

International audienc

Hobo elements and their deletion-derivative sequences in Drosophila melanogaster and its sibling species D simulans, D mauritiana and D sechellia

International audienc

Séquences homologues à l'élément P chez des espèces de Drosophila du groupe obscura et chez Scaptomyza pallida (Drosophilidae)

International audienc

Mise en évidence de mâles hétérozygotes chez l'hyménoptère Diadromus pulchellus (Ichneumonide)

International audienc

Absence of single-locus complementary sex determination in the braconid wasps Asobara tabida and Alysia manducator

In species with single-locus complementary sex determination (sl-CSD), sex is determined by multiple alleles at a single locus. In the haplodiploid Hymenoptera, sl-CSD results in females, if individuals are heterozygous at the sex locus, and in males, if individuals are hemizygous (haploid males) or homozygous (diploid males). Several hymenopteran species have been shown to have sl-CSD, but in several others sl-CSD is absent and the phylogenetic distribution remains unclear. In the family Braconidae, all four species tested so far were shown to possess sl-CSD. In this study, inbreeding experiments were used to test for the presence of sl-CSD in two species belonging to a subfamily of the Braconidae, Asobara tabida and Alysia manducator (Alysiinae). In both species inbreeding experiments showed no difference in brood size or sex ratio compared to the (outbred) control group. Furthermore, the sex ratios found in the inbreeding treatment differed significantly from the sex ratios expected under sl-CSD. Therefore, we conclude that sl-CSD is absent in these species. This study is the first to show the lack of sl-CSD in species of the Braconidae family and that hymenopteran sex-determining mechanisms can vary, even within a family.

The diagnostic criteria for small fibre neuropathy: from symptoms to neuropathology

Small fibre neuropathy (SFN), a condition dominated by neuropathic pain, is frequently encountered in clinical practise either as prevalent manifestation of more diffuse neuropathy or distinct nosologic entity. Aetiology of SFN includes pre-diabetes status and immune-mediated diseases, though it remains frequently unknown. Due to their physiologic characteristics, small nerve fibres cannot be investigated by routine electrophysiological tests, making the diagnosis particularly difficult. Quantitative sensory testing (QST) to assess the psychophysical thresholds for cold and warm sensations and skin biopsy with quantification of somatic intraepidermal nerve fibres (IENF) have been used to determine the damage to small nerve fibres. Nevertheless, the diagnostic criteria for SFN have not been defined yet and a ‘gold standard’ for clinical practise and research is not available. We screened 486 patients referred to our institutions and collected 124 patients with sensory neuropathy. Among them, we identified 67 patients with pure SFN using a new diagnostic ‘gold standard’, based on the presence of at least two abnormal results at clinical, QST and skin biopsy examination. The diagnosis of SFN was achieved by abnormal clinical and skin biopsy findings in 43.3% of patients, abnormal skin biopsy and QST findings in 37.3% of patients, abnormal clinical and QST findings in 11.9% of patients, whereas 7.5% patients had abnormal results at all the examinations. Skin biopsy showed a diagnostic efficiency of 88.4%, clinical examination of 54.6% and QST of 46.9%. Receiver operating characteristic curve analysis confirmed the significantly higher performance of skin biopsy comparing with QST. However, we found a significant inverse correlation between IENF density and both cold and warm thresholds at the leg. Clinical examination revealed pinprick and thermal hypoesthesia in about 50% patients, and signs of peripheral vascular autonomic dysfunction in about 70% of patients. Spontaneous pain dominated the clinical picture in most SFN patients. Neuropathic pain intensity was more severe in patients with SFN than in patients with large or mixed fibre neuropathy, but there was no significant correlation with IENF density. The aetiology of SFN was initially unknown in 41.8% of patients and at 2-year follow-up a potential cause could be determined in 25% of them. Over the same period, 13% of SFN patients showed the involvement of large nerve fibres, whereas in 45.6% of them the clinical picture did not change. Spontaneous remission of neuropathic pain occurred in 10.9% of SFN patients, while it worsened in 30.4% of them