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Objectives To evaluate the incidence of snow-sports-related head injuries among children and adolescents reported to emergency departments (EDs), and to examine the trend from 1996 to 2010 in ED visits for snow-sports-related traumatic brain injury (TBI) among children and adolescents. Methods A retrospective, population-based cohort study was conducted using data from the National Electronic Injury Surveillance System for patients (aged ≤17 years) treated in EDs in the USA from 1996 to 2010, for TBIs associated with snow sports (defined as skiing or snowboarding). National estimates of snow sports participation were obtained from the National Ski Area Association and utilised to calculate incidence rates. Analyses were conducted separately for children (aged 4–12 years) and adolescents (aged 13–17 years). Results An estimated number of 78 538 (95% CI 66 350 to 90 727) snow sports-related head injuries among children and adolescents were treated in EDs during the 14-year study period. Among these, 77.2% were TBIs (intracranial injury, concussion or fracture). The annual average incidence rate of TBI was 2.24 per 10 000 resort visits for children compared with 3.13 per 10 000 visits for adolescents. The incidence of TBI increased from 1996 to 2010 among adolescents (p<0.003). Conclusions Given the increasing incidence of TBI among adolescents and the increased recognition of the importance of concussions, greater awareness efforts may be needed to ensure safety, especially helmet use, as youth engage in snow sports.

Fresh isolates of the oral bacterial pathogen Actinobacillus actinomycetemcomitans exhibit a fimbriated, rough colony phenotype. Evidence suggests that the fimbrial subunit gene flp is part of a cluster of 14 genes (flp to tadG) thought to encode proteins involved in the synthesis, assembly and export of these fimbriae. To determine the transcriptional organization of the 59 terminus of this gene cluster, total RNA from rough and smooth phenotype variants of A. actinomycetemcomitans strain 283 were analysed by RT-PCR. Primers designed to amplify regions spanning gene junctions or multiple genes yielded amplicons at each individual gene junction from flp to tadD for both the rough and smooth variants. Semi-quantitative RT-PCR of the rcpA to tadZ amplicon revealed that significantly more mRNA was transcribed from the rough than the smooth variant. Longer amplicons encompassing flp to tadZ (3?9 kb) and tadA to tadD (2?1 kb) were also detected, but only from the rough variant. Rapid amplification of cDNA ends (RACE) was used to identify the 59 end of the mRNA containing flp. Antisense primers located within rcpC, orfB and flp-2 enabled amplification of a RACE product that was subsequently isolated and subcloned into pGEM-T. DNA sequencing indicated that the 59 end of the mRNA was located at a G or T nucleotide 2102 to 2101 nt upstream of flp. Corresponding s 70 consensus sequences were located at 210 (TATAAT) and 235 (TTGCAT) relative to the transcription start site. These data confirm that the flp gene cluster is an operon transcribed as a polycistronic message commencing from a G or T nucleotide located in the intergenic region upstream of flp. Promoter function of the flp upstream region was confirmed using a lacZ reporter gene construct transformed into Escherichia coli. RT-PCR analysis further suggests that although transcription does occur in both the rough and smooth variants, full-length transcripts are rapidly degraded or are significantly downregulated in the smooth variant. INTRODUCTIONThe oral bacterium Actinobacillus actinomycetemcomitans is a Gram-negative coccobacillus most notably associated with localized juvenile periodontitis, an aggressive form of early onset periodontitis affecting children 10 to 17 years old, and some cases of refractory adult periodontitis (Haraszthy et al., 2000;Slots & Dahlen, 1985; Tanner et al., 1979;Zambon, 1985). It is a member of the HACEK (Haemophilus aphrophilus, Haemophilus parainfluenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens and Kingella kingae) group of human pathogens responsible for approximately 3 % of endocarditis (el Khizzi et al., 1997;Serra & Tonato, 1969; Steckelberg et al., 1990;Vandepitte et al., 1977) and other extra-oral infections (Burgher et al., 1973;Martin et al., 1967;Muhle et al., 1979;Overholt, 1966;Page & King, 1966). It has also been associated with atheromatous plaques and may play a role in their formation (Haraszthy et al., 2000). Newer niches are being discovered for A. actinomycetemcomitans, ...

Large numbers of people travel to high altitudes, entering an environment of hypobaric hypoxia. Exposure to low oxygen tension leads to a series of important physiologic responses that allow individuals to tolerate these hypoxic conditions. However, in some cases hypoxia triggers maladaptive responses that lead to various forms of acute and chronic high altitude illness, such as high-altitude pulmonary edema or chronic mountain sickness. Because the respiratory system plays a critical role in these adaptive and maladaptive responses, patients with underlying lung disease may be at increased risk for complications in this environment and warrant careful evaluation before any planned sojourn to higher altitudes. In this review, we describe respiratory disorders that occur with both acute and chronic exposures to high altitudes. These disorders may occur in any individual who ascends to high altitude, regardless of his/her baseline pulmonary status. We then consider the safety of high-altitude travel in patients with various forms of underlying lung disease. The available data regarding how these patients fare in hypoxic conditions are reviewed, and recommendations are provided for management prior to and during the planned sojourn.