Applied physiology of female soccer: an update.

The popularity and professionalism of female soccer has increased markedly in recent years, with elite players now employed on either a professional or semi-professional basis. The previous review of the physiological demands of female soccer was undertaken two decades ago when the sport was in its relative infancy. Increased research coupled with greater training and competition demands warrants an updated review to consider the effect on physical performance and injury patterns. The physical demands of match-play along with the influence of factors such as the standard of competition, playing position and fatigue have been explored. Total distance covered for elite female players is approximately 10 km, with 1.7 km completed at high speed (>15 kmh(-1)) [corrected].Elite players complete 28% more high-speed running and 24 % more sprinting than moderate-level players. Decrements in high-speed running distance have been reported between and within halves, which may indicate an inability to maintain high-intensity activity. Although the physical capacity of female players is the most thoroughly researched area, comparisons are difficult due to differing protocols. Elite players exhibit maximal oxygen uptake (VO2max) values of 49.4-57.6 mL·kg(-1)·min(-1), Yo Yo Intermittent Endurance test level 2 (YYIE2) scores of 1,774 ± 532 m [mean ± standard deviation (SD)] and 20 m sprint times of 3.17 ± 0.03 s (mean ± SD). Reasons for the increased prevalence of anterior cruciate ligament injuries in females (2-6 times greater than males) are discussed, with anatomical, biomechanical loading and neuromuscular activation differences being cited in the literature. This review presents an in-depth contemporary examination of the applied physiology of the female soccer player.

Copy number variation and incomplete linkage disequilibrium interfere with the HCP5 genotyping assay for abacavir hypersensitivity.

Carriers of HLA-B*57:01 are at risk for Abacavir hypersensitivity reaction (ABC-HSR). In Caucasians, a SNP (rs2395029) in the HCP5 gene is reported to be in linkage disequilibrium (LD) with HLA-B*57:01. Genotyping the HCP5 SNP has increasingly been adopted as a simple method to screen for susceptibility to ABC-HSR. We genotyped both the HCP5 SNP and HLA-B*57:01 in a set of 1888 samples and found a good correlation; significantly, however, one HLA-B*57:01-positive sample tested negative for the HCP5 SNP. In addition, HCP5 could not be amplified in two samples, both negative for HLA-B*57:01. Further investigation demonstrated both samples were homozygous for deletion of the HCP5 gene. The fact HCP5 occurs within a region of copy number variation and the fact LD is incomplete and may vary between ethnicities should be considered when using the HCP5 SNP as a surrogate marker for HLA-B*57:01.

Does generic entry always increase consumer welfare?

This article examines how the nature of competition between brands in a therapeutic category changes after generic entry and provide a framework for analyzing the effect of generic entry on consumer welfare that takes into account the generic free riding problem. It demonstrates that changes in competition along dimensions other than retail price--such as competition in research and development efforts and in promotional activities--may, in certain situations, result in generic entry having an overall negative impact on consumer welfare.

Infection with transmissible strains of Pseudomonas aeruginosa and clinical outcomes in adults with cystic fibrosis.

CONTEXT: Studies from Australia and the United Kingdom have shown that some patients with cystic fibrosis are infected with common transmissible strains of Pseudomonas aeruginosa. OBJECTIVES: To determine the prevalence and incidence of infection with transmissible strains of P. aeruginosa and whether presence of the organism was associated with adverse clinical outcomes in Canada. DESIGN, SETTING, AND PARTICIPANTS: Prospective observational cohort study of adult patients cared for at cystic fibrosis clinics in Ontario, Canada, with enrollment from September 2005 to September 2008. Sputum was collected at baseline, 3 months, and yearly thereafter for 3 years; and retrieved P. aeruginosa isolates were genotyped. Vital status (death or lung transplant) was assessed for all enrolled patients until December 31, 2009. MAIN OUTCOME MEASURES: Incidence and prevalence of P. aeruginosa isolation, rates of decline in lung function, and time to death or lung transplantation. RESULTS: Of the 446 patients with cystic fibrosis studied, 102 were discovered to be infected with 1 of 2 common transmissible strains of P. aeruginosa at study entry. Sixty-seven patients were infected with strain A (15%), 32 were infected with strain B (7%), and 3 were simultaneously infected with both strains (0.6%). Strain A was found to be genetically identical to the Liverpool epidemic strain but strain B has not been previously described as an epidemic strain. The incidence rate of new infections with these 2 transmissible strains was relatively low (7.0 per 1000 person-years; 95% confidence interval [CI], 1.8-12.2 per 1000 person-years). Compared with patients infected with unique strains of P. aeruginosa, patients infected with the Liverpool epidemic strain (strain A) and strain B had similar declines in lung function (difference in decline in percent predicted forced expiratory volume in the first second of expiration of 0.64% per year [95% CI, -1.52% to 2.80% per year] and 1.66% per year [95% CI, -1.00% to 4.30%], respectively). However, the 3-year rate of death or lung transplantation was greater in those infected with the Liverpool epidemic strain (18.6%) compared with those infected with unique strains (8.7%) (adjusted hazard ratio, 3.26 [95% CI, 1.41 to 7.54]; P = .01). CONCLUSIONS: A common strain of P. aeruginosa (Liverpool epidemic strain/strain A) infects patients with cystic fibrosis in Canada and the United Kingdom. Infection with this strain in adult Canadian patients with cystic fibrosis was associated with a greater risk of death or lung transplantation.

Characterization of clonal strains of Pseudomonas aeruginosa isolated from cystic fibrosis patients in Ontario, Canada.

Pseudomonas aeruginosa is an opportunistic pathogen that can form biofilms in the lungs and airways of cystic fibrosis (CF) patients, resulting in chronic endobronchial infection. Two clonal strains of P. aeruginosa, named type A and type B, have recently been identified and have been found to infect more than 20% of CF patients in Ontario, Canada. In this study, 4 type A and 4 type B isolates retrieved from 8 CF patients in Ontario, Canada, were characterized. All 8 isolates grew well in rich medium and formed biofilms in vitro. Antibiotic resistance profiles of bacteria grown in biofilms and planktonic culture were studied via minimal bactericidal concentration assays for tobramycin, gentamicin, and ciprofloxacin. Compared to laboratory strains of P. aeruginosa, all 8 isolates showed increased resistance to all antibiotics studied in both biofilm and planktonic assays. Gene expression analysis of mexX, representing the MexXY-OprM efflux pump, and mexA, representing MexAB-OprM, revealed that these genes were up-regulated in the 8 clinical isolates. These results suggest clonal type A and type B isolates of P. aeruginosa isolated from CF patients in Ontario, Canada, show a multidrug resistance pattern that can be partially explained as being due to the increased expression of common antibiotic efflux systems.