Citations

Abstract The purpose of this investigation was to examine the components of intimidation in ice hockey and to determine their effects on players, coaches, and referees. In a pilot test, hockey coaches (N = 17) from three levels of participation were invited to an informal, exploratory symposium to assess their opinions on the role of intimidation in ice hockey. The following themes emerged: a) coaches' behavior and expectations, b) observable behavior, c) player's perceived role, and d) sociological factors. A preliminary intimidation model was developed. A survey including 80 open-ended questionnaires designed to stimulate discussion on the definition of intimidation, methods used to intimidate, and factors perceived as intimidating, was distributed to players (N = 66), coaches (N = 8), and referees (N = 6). The data were analyzed using qualitative methods [1,2] and intimidation was defined. Results support a theoretical model, which serves as a point of departure for future research and visually depicts the components of intimidation and their interactions.

Abstract A modified approach to endoscopic carpal tunnel release has been developed and tested in 60 cadaveric specimens by three surgeons using the Agee endoscopic carpal tunnel release system. The modified approach, which includes specific localization of the hook of the hamate, flexor retinaculum, and the superficial palmar arch utilizing topographical landmarks, avoids entry into Guyon's canal and injury to the ulnar artery and nerve, median nerve, and common digital nerves. Use of the anatomic approach resulted in significantly superior results. There were fewer incomplete releases, and fewer surgical passes were required, for the inexperienced surgeons. When these anatomic considerations were not included, the learning curve was much steeper. For surgeons planning endoscopie surgical release of the transverse carpal ligament, the described topographical approach improves the technical competence with the procedure and reduces the number of complications and learning curve associated with new procedures. We recommend the use of topographical landmarks and other anatomic considerations during endoscopic carpal tunnel release.

53BP1 participates early in the DNA damage response and is involved in cell cycle checkpoint control. Moreover, the phenotype of mice and cells deficient in 53BP1 suggests a defect in DNA repair (Ward et al., 2003b). Therefore, we asked whether or not 53BP1 would be required for the efficient repair of DNA double strand breaks. Our data indicate that homologous recombination by gene conversion does not depend on 53BP1. Moreover, 53BP1-deficient mice support normal V(D)J recombination, indicating that 53BP1 is not required for “classic” nonhomologous end joining. However, class switch recombination is severely impaired in the absence of 53BP1, suggesting that 53BP1 facilitates DNA end joining in a way that is not required or redundant for the efficient closing of RAG-induced strand breaks. These findings are similar to those observed in mice or cells deficient in the tumor suppressors ATM and H2AX, further suggesting that the functions of ATM, H2AX, and 53BP1 are closely linked.

Triptans are the treatment of choice for acute migraine. While seemingly a homogenous group of drugs, results from a meta-analysis reveal significant differences in efficacy and tolerability among oral triptans. The incidence of drug-related central nervous system (CNS) side-effects with some triptans is as high as 15% and may be associated with functional impairment and reduced productivity. The occurrence of adverse events associated with triptans in general, and CNS side-effects in particular, may lead to a delay in initiating or even avoidance of an otherwise effective treatment. Potential explanations for differences among triptans in the incidence of CNS side-effects may relate to pharmacological and pharmacokinetic differences, including receptor binding, lipophilicity, and the presence of active metabolites. Of the triptans reviewed, at clinically relevant doses, almotriptan 12.5 mg, naratriptan 2.5 mg and sumatriptan 50 mg had the lowest incidence of CNS side-effects, while eletriptan 40 and 80 mg, rizatriptan 10 mg and zolmitriptan 2.5 and 5 mg had the highest incidence. The most likely explanations for the differences in CNS side-effects among triptans are the presence of active metabolites and high lipophilicity of the parent compound and active metabolites. Eletriptan, rizatriptan and zolmitriptan have active metabolites, while lipophilicity is lowest for almotriptan and sumatriptan. If CNS sideeffects are a clinically relevant concern in the individual patient, use of a triptan with a low incidence of CNS side-effects may offer the potential for earlier initiation of treatment and more effective outcomes.

The patho logical hallmark of chronic multiple sclerosis includes focal demyelination, gliosis, inflammation and axonal injury. There is limited information on whether these pathological features differ across the clinical pheno types of the disease (relapsing-remitting, secondary progressive, and primary progressive). This review will focus on the patho logical aspects of PPMS and pathogenic implications. A better understanding of the differences in PPMS pathology and patho genesis will lead to more effective treatment strategies.

Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular disease, endothelial dysfunction, and oxidative stress, generated by repetitive nocturnal hypoxemia and reperfusion. Circulating free nitrotyrosine has been reported as a novel biomarker of nitric oxide (NO)-induced oxidative/nitrosative stress. Nitrosative stress has been implicated as a possible mechanism for development of cardiovascular diseases. We tested the hypothesis that repetitive severe hypoxemia resulting from OSA would increase NO-mediated oxidative stress. We studied 10 men with newly diagnosed moderate to severe OSA who were free of other diseases, had never been treated for OSA, and were taking no medications. Nitrotyrosine measurements, performed by liquid chromatography-tandem mass spectrometry, were made before and after untreated apneic sleep. We compared free nitrotyrosine levels in these patients with those obtained at similar times in 10 healthy male control subjects without OSA, with similar age and body mass index. Evening baseline nitrotyrosine levels were similar before sleep in the control and OSA groups [0.16 ± 0.01 and 0.15 ± 0.01 ng/ml, respectively, P = not significant (NS)]. Neither normal nor disturbed apneic sleep led to significant changes of plasma nitrotyrosine (morning levels: control group 0.14 ± 0.01 ng/ml; OSA group 0.15 ± 0.01 ng/ml, P = NS). OSA was not accompanied by increased circulating free nitrotyrosine either at baseline or after sleep. This observation suggests that repetitive hypoxemia during OSA does not result in increased NO-mediated oxidative/nitrosative stress in otherwise healthy subjects with OSA.