Eustachian tube lumen opening into an abnormally pneumatized sphenoid bone.

Morphological abnormalities of left temporal and sphenoid bone were discovered in a 17-year-old boy during a post-traumatic cranial CT scan examination. The patient had not suffered from audiological disorders previously. He did not complain of hearing loss, vertigo or autophony. Further clinical investigations were normal including micro-otoscopy and nasopharyngeal endoscopy. The Valsalva maneuver was correctly performed. Audiometry and tympanometry were without any particularity

Prediction of charm-production fractions in neutrino interactions

The way a charm-quark fragments into a charmed hadron is a challenging problem both for the theoretical and the experimental particle physics. Moreover, in neutrino induced charm-production, peculiar processes occur such as quasi-elastic and diffractive charm-production which make the results from other experiments not directly comparable. We present here a method to extract the charmed fractions in neutrino induced events by using results from $e^+e^-$, $\pi N$, $\gamma N$ experiments while taking into account the peculiarities of charm-production in neutrino interactions. As results, we predict the fragmentation functions as a function of the neutrino energy and the semi-muonic branching ratio, $B_\mu$, and compare them with the available data

Glial β-Oxidation regulates drosophila energy metabolism

The brain's impotence to utilize long-chain fatty acids as fuel, one of the dogmas in neuroscience, is surprising, since the nervous system is the tissue most energy consuming and most vulnerable to a lack of energy. Challenging this view, we here show in vivo that loss of the Drosophila carnitine palmitoyltransferase 2 (CPT2), an enzyme required for mitochondrial β-oxidation of long-chain fatty acids as substrates for energy production, results in the accumulation of triacylglyceride-filled lipid droplets in adult Drosophila brain but not in obesity. CPT2 rescue in glial cells alone is sufficient to restore triacylglyceride homeostasis, and we suggest that this is mediated by the release of ketone bodies from the rescued glial cells. These results demonstrate that the adult brain is able to catabolize fatty acids for cellular energy production.This work was partially supported by the Flanders Fund for Scientific Research (FWO G 0.666.10N), NEUROBRAINNET IAP 7/16, Flemish Government Methusalem Grant, Spanish Ministry of Science (SAF2010-14906) and Innovation Ingenio-Consolider (CSD2010-00045) and Spanish Ministry of Economy and Competitiveness (SAF2013-45392).Peer Reviewe

Glial β-Oxidation regulates drosophila energy metabolism

The brain's impotence to utilize long-chain fatty acids as fuel, one of the dogmas in neuroscience, is surprising, since the nervous system is the tissue most energy consuming and most vulnerable to a lack of energy. Challenging this view, we here show in vivo that loss of the Drosophila carnitine palmitoyltransferase 2 (CPT2), an enzyme required for mitochondrial β-oxidation of long-chain fatty acids as substrates for energy production, results in the accumulation of triacylglyceride-filled lipid droplets in adult Drosophila brain but not in obesity. CPT2 rescue in glial cells alone is sufficient to restore triacylglyceride homeostasis, and we suggest that this is mediated by the release of ketone bodies from the rescued glial cells. These results demonstrate that the adult brain is able to catabolize fatty acids for cellular energy production.This work was partially supported by the Flanders Fund for Scientific Research (FWO G 0.666.10N), NEUROBRAINNET IAP 7/16, Flemish Government Methusalem Grant, Spanish Ministry of Science (SAF2010-14906) and Innovation Ingenio-Consolider (CSD2010-00045) and Spanish Ministry of Economy and Competitiveness (SAF2013-45392).Peer Reviewe

The Yeast Complex I Equivalent NADH Dehydrogenase Rescues pink1 Mutants

Pink1 is a mitochondrial kinase involved in Parkinson's disease, and loss of Pink1 function affects mitochondrial morphology via a pathway involving Parkin and components of the mitochondrial remodeling machinery. Pink1 loss also affects the enzymatic activity of isolated Complex I of the electron transport chain (ETC); however, the primary defect in pink1 mutants is unclear. We tested the hypothesis that ETC deficiency is upstream of other pink1-associated phenotypes. We expressed Saccaromyces cerevisiae Ndi1p, an enzyme that bypasses ETC Complex I, or sea squirt Ciona intestinalis AOX, an enzyme that bypasses ETC Complex III and IV, in pink1 mutant Drosophila and find that expression of Ndi1p, but not of AOX, rescues pink1-associated defects. Likewise, loss of function of subunits that encode for Complex I–associated proteins displays many of the pink1-associated phenotypes, and these defects are rescued by Ndi1p expression. Conversely, expression of Ndi1p fails to rescue any of the parkin mutant phenotypes. Additionally, unlike pink1 mutants, fly parkin mutants do not show reduced enzymatic activity of Complex I, indicating that Ndi1p acts downstream or parallel to Pink1, but upstream or independent of Parkin. Furthermore, while increasing mitochondrial fission or decreasing mitochondrial fusion rescues mitochondrial morphological defects in pink1 mutants, these manipulations fail to significantly rescue the reduced enzymatic activity of Complex I, indicating that functional defects observed at the level of Complex I enzymatic activity in pink1 mutant mitochondria do not arise from morphological defects. Our data indicate a central role for Complex I dysfunction in pink1-associated defects, and our genetic analyses with heterologous ETC enzymes suggest that Ndi1p-dependent NADH dehydrogenase activity largely acts downstream of, or in parallel to, Pink1 but upstream of Parkin and mitochondrial remodeling