196 research outputs found

    Shining the light on public attitudes toward laser attacks on aircraft

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    With increasing incidents being reported, laser attacks present a significant threat to aircraft safety. Although no aircraft accidents have yet been directly attributed to laser attacks to date, experts agree that it is a legitimate threat to safety. To better understand this phenomenon, and ways in which it can be addressed, an important area to understand is the public perception of the severity of such incidents. This would include examining the attitudes the general public hold toward laser attacks, and what views they may hold towards regulation and punishment for these offences. Members of the general public (N=208) completed an online survey that examined their views towards the perceived occurrences and severity of laser attacks, whilst also examining their expectation of criminality and punishment of using a laser against an aircraft. Responses were analysed and presented, with discussion around the nature of public perception and expectation to laser attacks. Mitigations and interventions are explored, focussing on targeted educational/awareness programs that can be used to increase the awareness amongst the general public on the consequences of laser attacks on aircraft

    Galanin and galanin receptor expression in neuroblastic tumours: correlation with their differentiation status

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    Neuroblastoma and its benign differentiated counterpart, ganglioneuroma, are paediatric neuroblastic tumours arising in the sympathetic nervous system. Their broad spectrum of clinical virulence is mainly related to heterogeneous biologic background and tumour differentiation. Neuroblastic tumours synthesize various neuropeptides acting as neuromodulators. Previous studies suggested that galanin plays a role in sympathetic tissue where it could be involved in differentiation and development. We investigated the expression and distribution of galanin and its three known receptors (Gal-R1, Gal-R2, Gal-R3) in 19 samples of neuroblastic tumours tissue by immunohistochemistry, in situ hybridization and fluorescent-ligand binding. This study provides clear evidence for galanin and galanin receptor expression in human neuroblastic tumours. The messengers coding for galanin, Gal-R1 and -R3 were highly expressed in neuroblastoma and their amount dramatically decreased in ganglioneuroma. In contrast, Gal-R2 levels remained unchanged. Double labelling studies showed that galanin was mainly co-expressed with its receptors whatever the differentiation stage. In neuroblastic tumours, galanin might promote cell-survival or counteract neuronal differentiation through the different signalling pathways mediated by galanin receptors. Finally, our results suggest that galanin influences neuroblastoma growth and development as an autocrine/paracrine modulator. These findings suggest potential critical implications for galanin in neuroblastic tumours development

    Embryonal neural tumours and cell death

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    Mutations in the TRKA/NGF receptor gene in patients with congenital insensitivity to pain with anhidrosis

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    Congenital insensitivity to pain with anhidrosis (CIPA; MIM 256800) is an autosomal-recessive disorder characterized by recurrent episodes of unexplained fever, anhidrosis (absence of sweating) and absence of reaction to noxious stimuli, self-mutilating behaviour and mental retardation1−3. The genetic basis for CIPA is unknown. Nerve growth factor (NGF) induces neurite outgrowth and promotes survival of embryonic sensory and sympathetic neurons4. Mice lacking the gene for TrkA, a receptor tyrosine kinase for NGF5,6, share dramatic phenotypic features of CIPA, including loss of responses to painful stimuli, although anhidrosis is not apparent in these animals7. We therefore considered the human TRKA homologue as a candidate for the CIPA gene. The mRNA and genomic DNA encoding TRKA were analysed in three unrelated CIPA patients who had consanguineous parents. We detected a deletion-, splice- and missense-muta-tion in the tyrosine kinase domain in these three patients. Our findings strongly suggest that defects in TRKA cause CIPA and that the NGF−TRKA system has a crucial role in the development and function of the nociceptive reception as well as establishment of thermoregulation via sweating in humans. These results also implicate genes encoding other TRK and neurotrophin family members as candidates for developmental defect(s) of the nervous system
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