| 1. |
- Ekstrand, Jan, et al.
(författare)
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Upper extremity injuries in male elite football players
- 2013
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Ingår i: Knee Surgery, Sports Traumatology, Arthroscopy. - : Springer Verlag (Germany). - 0942-2056 .- 1433-7347. ; 21:7, s. 1626-1632
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Tidskriftsartikel (refereegranskat)abstract
- To investigate the epidemiology of upper extremity injuries in male elite football players and to describe their characteristics, incidence and lay-off times. less thanbrgreater than less thanbrgreater thanBetween 2001 and 2011, 57 male European elite football teams (2,914 players and 6,215 player seasons) were followed prospectively. Time-loss injuries and exposure to training and matches were recorded on individual basis. less thanbrgreater than less thanbrgreater thanIn total, 11,750 injuries were recorded, 355 (3 %) of those affected the upper extremities giving an incidence of 0.23 injuries/1,000 h of football. The incidence in match play was almost 7 times higher than in training (0.83 vs. 0.12 injuries/1,000 h, rate ratio 6.7, 95 % confidence interval 5.5-8.3). As much as 32 % of traumatic match injuries occurred as a result of foul play situations. Goalkeepers had a significantly higher incidence of upper extremity injuries compared to outfield players (0.80 vs. 0.16 injuries/1,000 h, rate ratio 5.0, 95 % confidence interval 4.0-6.2). The average absence due to an upper extremity injury was 23 +/- A 34 days. less thanbrgreater than less thanbrgreater thanUpper extremity injuries are uncommon among male elite football players. Goalkeepers, however, are prone to upper extremity injury, with a five times higher incidence compared to outfield players. less thanbrgreater than less thanbrgreater thanII.
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| 2. |
- Pannee, Josef, 1979, et al.
(författare)
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The amyloid-beta degradation pattern in plasma A possible tool for clinical trials in Alzheimer's disease
- 2014
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940 .- 1872-7972. ; 573, s. 7-12
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Tidskriftsartikel (refereegranskat)abstract
- Amyloid beta (A beta) is the main component of plaques, the central neuropathological hallmark in Alzheimer's disease (AD). A beta is derived from the amyloid precursor protein (APP) by beta- and gamma-secretase-mediated cleavages. A large number of A beta peptides are found in cerebrospinal fluid and these peptides are produced in specific metabolic pathways, which are important for diagnosis, in drug development and to explore disease pathogenesis. To investigate whether a similar pattern could be found also in blood samples, an immunoprecipitation (IP) based method for enrichment of A beta peptides from human plasma was developed. The peptides were analyzed using matrix-assisted-laser-desorption/ionization time-of-flight/time-of-flight mass spectrometry for A beta profiling and selected reaction monitoring (SRM) for MS quantification of A beta 1-38, A beta 1-40 and A beta 1-42 using tripe quadrupole MS. Sixteen N- or C-terminally truncated A beta peptides were reproducibly detected in human plasma, of which 11 were verified by tandem MS. In a pilot study including 9 AD patients and 10 controls, where A beta 1-38, A beta 1-40 and A beta 1-42 were quantified using SRM, no AD-associated change in plasma levels of the peptides were observed. Using MS-based measurement techniques, we show that several A beta peptides can be monitored in a single analysis and the developed methods have the potential to be used as a read out in clinical trials of drugs affecting APP processing or A beta homeostasis.
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