Sports helmets now and in the future

The paper reports on a symposium on sports helmets and presents a synthesis of information and opinion from a range of presenters and disciplines. A review of the literature shows that helmets play an important role in head injury prevention and control. Helmets have been shown to be very efficacious and effective in a range of sports and in preventing specific head injury risks, especially moderate to severe head injury. The symposium emphasised the importance of helmet standards and the need for further development. There are calls for helmets that address the needs of competitive (elite) athletes separate to helmets for recreational athletes. Deficiencies in the evidence base for head injury risks and helmet efficacy and effectiveness were identified in some sports. Issues in designing helmets that are suitable to prevent severe head injuries and concussion were discussed and explained from biomechanical and engineering perspectives. The need to evaluate helmet performance in oblique impacts and incorporate this into standards was covered in a number of presentations. There are emerging opportunities with in-helmet technology to improve impact performance or to measure impact exposure. In-helmet technology as it matures may provide critical information on the severity of the impact, the location of the injured athlete, for example, snowboarder, and assist in the retrieval and immediate, as well as the long-term medical management of the athlete. It was identified that athletes, families and sports organisations can benefit from access to information on helmet performance. The importance of selecting the appropriate-sized helmet and ensuring that the helmet and visor were adjusted and restrained optimally was emphasised. The translation pathway from the science to new and better helmets is the development of appropriate helmet standards and the requirement for only helmets to be used that are certified to those standards.     

Molecular analysis of microdeletions of the Y chromosome in Venezuelan males with idiopathic infertility

Today infertility is a major health problem affecting about 10-20% of couples. A male factor is assumed to be responsible in about 50% of the infertile couples. The origin of reduced testicular sperm function is unknown in about 60-70% of cases. There are several causes of male infertility such as varicocele, spermatic duct obstruction, and endocrine disorders. Micro-deletions in the Yq are known to represent the pathogenic mechanisms for infertile males. Three different non-overlapping regions designated as AZFa, AZFb, and AZFc are located in interval 5-6 of Yq, and are associated with impaired spermatogenesis in humans. To determine the prevalence of Y chromosomal microdeletions in Venezuelan males with idiopathic infertility, chromosomal, seminal, histological and molecular analyses were carried out in 29 Venezuelan males with idiopathic azoospermia or oligoospermia. Y-microdeletions analyses were performed using a multiplex polymerase chain reaction (PCR)-based technique with 22 sequences-tagged-sites (STSs). One of 29 patients (3.4%) had Yq microdeletions on AZFc. The frequency of AZF microdeletions in Venezuelan patients was similar to other populations with different ethnical or geographical origin.     

Chronic pain and sensory changes after augmentation mammoplasty: long term effects of preincisional administration of methylprednisolone

We studied the prevalence of chronic pain and long term sensory changes after cosmetic augmentation mammoplasty and the effects of a single i.v. preoperative dose of methylprednisolone 125 mg (n=74), parecoxib 40 mg (n=71), or placebo (n=74). A questionnaire was mailed 6 weeks and 1 year after surgery. Response rate after 1 year was 80%. At 1 year non-evoked pain was present in 13%, and evoked pain was present in 20% with no statistically significant differences between the groups. Methylprednisolone was associated with reduced odds for hyperesthesia at 1 year (OR 0.3, 95% CI 0.1-0.6), and significantly reduced the prevalence of hyperesthesia (30%) compared with placebo (56%, P<0.01) and parecoxib (51%, P<0.04). Factors associated with increased odds for pain at 1 year were intensity of pain during the first 6 days after surgery (OR 1.3, 95% CI 1.1-1.6), pain at 6 weeks (OR 18.4, 95% CI 6.9-49.3), hyperesthesia at 6 weeks (OR 2.3, 95% CI 1.1-5.1) and present hyperesthesia (OR 3.1, 95% CI 1.4-6.7). We conclude that persistent pain and sensory changes are common after augmentation mammoplasty, and that patients having pain at 6 weeks most likely will have pain also at 1 year. Acute postoperative pain, hyperesthesia at 6 weeks, and the presence of hyperesthesia increased the odds for pain at 1 year. Preoperative methylprednisolone resulted in significantly less hyperesthesia compared with both parecoxib and placebo, but did not significantly reduce the prevalence of persistent spontaneous or evoked pain.     

Is it safe to use TNF-α blockers for systemic inflammatory disease in patients with heart failure? Importance of dosage and receptor specificity

Tumor necrosis factor-alpha (TNF-α) blockers are widely used in the treatment of chronic inflammatory diseases, especially chronic arthritis. Current guidelines advise against the use of such agents in patients who have a concomitant heart failure. Consequently, a group of patients with a devastating inflammatory disease cannot benefit from an excellent treatment option. After a critical review of the current literature, we conclude that there is not sufficient evidence to warn against such a regimen if recommended standard doses are used. A negative effect on the heart function seems to occur if unconventional high doses of TNF-α blockers are given. The theoretical background for this is discussed.     

Inhalation of nitric oxide inhibits ADP-induced platelet aggregation and alpha-granule release

To gather further information about the effects on blood platelet activation of in vivo exposure to nitric oxide (NO), platelet reactivity was studied in blood from healthy, non-smoking male volunteers before and after 30 min inhalation of 40ppm NO. Whole blood was stimulated in vitro with adenosine diphosphate or thrombin receptor activation peptide (TRAP-6). In an ex vivo perfusion model, non-anticoagulated blood was exposed to immobilised collagen at arterial blood flow conditions (2600 s -1 ). Blood samples from both the in vitro and ex vivo experiments were stained with fluorochrome-labelled Annexin-V and antibodies against CD42a, CD45, CD49b, CD61, CD62P and fibrinogen, and analysed with a three-colour flow cytometry technique. NO inhalation reduced the platelet activation response to adenosine diphosphate (ADP) stimulation by decreasing platelet-platelet aggregation, alpha-granule release and platelet-leukocyte conjugate formation. TRAP-stimulated platelet activation, collagen-induced platelet activation and thrombus growth was unaffected by NO inhalation. We therefore suggest an ADP receptor inhibitor mode of action of inhaled NO, selective on the newly suggested G protein- and phospholipase C-coupled P2Y1 receptor. Our results demonstrate that blood platelet activation in healthy subjects is modulated by inhalation of NO in therapeutically relevant doses, although the clinical impact of our findings remains unclear.     

Intracellular rescuing of a B. melitensis 16M virB mutant by co-infection with a wild type strain

Brucella is a broad-range, facultative intracellular pathogen that can survive and replicate in an endoplasmic reticulum (ER)-derived replication niche by preventing fusion of its membrane-bound compartment with late endosomes and lysosomes. This vacuolar hijacking was demonstrated to be dependent on the type IV secretion system VirB but no secreted effectors have been identified yet. A virB mutant is unable to reach its ER-derived replicative niche and does not multiply intracellularly. In this paper, we showed that, by co-infecting bovine macrophages or HeLa cells with the wild type (WT) strain of Brucella melitensis 16M and a deletion mutant of the complete virB operon, the replication of DeltavirB is rescued in almost 20% of the co-infected cells. Furthermore, we demonstrated that co-infections with the WT strains of Brucella abortus or Brucella suis were equally able to rescue the replication of the B. melitensis DeltavirB mutant. By contrast, no rescue was observed when the WT strain was given 1h before or after the infection with the DeltavirB mutant. Finally, vacuoles containing the rescued DeltavirB mutant were shown to exclude the LAMP-1 marker in a way similar to the WT containing vacuoles.     

Viral infection in placenta relevant cells – a morphological and immunohistochemical cell culture study

Viral infections in pregnancy are known to cause fetal malformation, growth restriction, and even fetal death. Macroscopic placental examination usually shows slight and unspecific changes. Histology may show secondary, non‐specific tissue reaction, i.e. villitis with lymphocytic invasion. Primary specific morphology characteristics are known for some virus, like cytomegalovirus, parvovirus, and herpes simplex, however many viral infections show non‐specific changes. Placenta relevant cells as human first trimester trophoblasts HTR8/SVneo, primary human umbilical vein endothelial cells (HUVEC), and primary human embryonic fibroblasts were examined following infection with commonly occurring virus like adenovirus and enterovirus. Morphology in routine stained sections and virus‐specific immunostains were studied 4, 8, 24, 48, 72 h after infection. Nuclear enlargement was seen in the infected cells. A specific diagnosis of adenovirus or enterovirus infection, however, was not possible without specific immunostains.