A review of spine injuries and return to play.

OBJECTIVE: To review the literature for evidence that pertains to return to play and spine injuries, including cervical spinal stenosis, congenital and developmental abnormalities of the cervical spine, stingers, herniated nucleus pulposus, and spondylolysis/spondylolisthesis. DATA SOURCES: Electronic databases, Pubmed (1966-2005) and Sport Discus (1975-2005), were searched for pertinent literature. Also, additional articles were reviewed from bibliographies. DATA SYNTHESIS/METHODS: Summation of literature is given. No formal statistical analysis is presented. RESULTS: Even though the problems addressed in this paper can be serious, the literature is lacking evidence for guidance in return to play. The majority of the literature presented is expert opinion. CONCLUSIONS: Cervical spinal stenosis continues to be controversial, with different experts giving different definitions and return to play recommendations. Authors discuss functional cervical spinal stenosis seen on MRI and how this can lead to permanent sequelae. In regard to stingers, herniated nucleus pulposus, and spondylolysis/spondylolisthesis, there are differing opinions on evaluation and treatment. These conditions have less disagreement with regard to return to play. Most experts agree that with these problems or any other problem in sports medicine, an athlete needs to be symptom-free and have full active range of motion with near to full strength, even though there is a lack of research evidence in the literature.

Common athletic injuries in adolescent girls.

Teenaged girls constitute the fastest growing segment of children and adolescents participating in organized athletics. Adolescent girls appear to have similar injury rates as boys in comparable activities but different injury patterns. To properly diagnose and manage athletic injuries in adolescent girls, pediatric health care providers must be aware of these differences, especially as the literature and their knowledge base may be skewed to the traditional predominance of males in sport. This review identifies athletic injuries that are unique to or especially common in adolescent girls, including apophyseal injuries; breast and pelvic injuries; scoliosis and spondylolysis; multidirectional shoulder instability and "gymnast's wrist"; anterior cruciate ligament injuries and patellofemoral pain syndrome; chronic exertional lower-leg compartment syndrome, ankle sprains, and reflex sympathetic dystrophy; and stress fractures. It also briefly discusses possible risk factors for these injuries, emphasizing the female athlete triad.

Familial cryptic translocation resulting in Angelman syndrome:implications for imprinting or location of the Angelman gene?

Angelman syndrome (AS) is associated with a loss of maternal genetic information, which typically occurs as a result of a deletion at 15q11-q13 or paternal uniparental disomy of chromosome 15. We report a patient with AS as a result of an unbalanced cryptic translocation whose breakpoint, at 15q11.2, falls within this region. The proband was diagnosed clinically as having Angelman syndrome, but without a detectable cytogenetic deletion, by using high-resolution G-banding. FISH detected a deletion of D15S11 (IR4-3R), with an intact GABRB3 locus. Subsequent studies of the proband's mother and sister detected a cryptic reciprocal translocation between chromosomes 14 and 15 with the breakpoint being between SNRPN and D15S10 (3- 21). The proband was found to have inherited an unbalanced form, being monosomic from 15pter through SNRPN and trisomic for 14pter to 14q11.2. DNA methylation studies showed that the proband had a paternal-only DNA methylation pattern at SNRPN, D15S63 (PW71), and ZNF127. The mother and unaffected sister, both having the balanced translocation, demonstrated normal DNA methylation patterns at all three loci. These data suggest that the gene for AS most likely lies proximal to D15S10, in contrast to the previously published position, although a less likely possibility is that the maternally inherited imprinting center acts in trans in the unaffected balanced translocation carrier sister.

Inhalable particles and pulmonary host defense: in vivo and in vitro effects of ambient air and combustion particles.

The ability of particulate air pollutants (and possible constituents) to alter pulmonary host defenses was examined using an in vitro alveolar macrophage cytotoxicity assay and an in vivo bacterial infectivity screening test which employed intratracheal injection of the particles. A wide range of response between particles was seen at the 1.0-mg/ml level in vitro and the 0.1-mg/mouse level in vivo. A sample of fluidized-bed coal fly ash, bentonite, asbestos, some ambient air particles, and heavy metal oxides greatly increased susceptibility to pulmonary bacterial infection. Most coal fly ash samples and some air particles caused moderate increases in infectivity, while diesel particulates, volcanic ash, and crystalline silica caused only small increases. Cytotoxic effects on macrophages in vitro were observed with most of the particles. The in vivo and in vitro assays produced a similar ranking of toxicity; however, not all particles that were highly cytotoxic were potent in increasing bacterial infectivity. Increased toxicity measurable by either assay often appeared to be associated with small size or with the presence of metal in the particles.

Evaluation of the release of mutagens and 1-nitropyrene from diesel particles in the presence of lung macrophages in culture.

The release and recovery of mutagenic activity and 1-nitropyrene from diesel particles phagocytized and cultured with lung macrophages were studied. The Ames Salmonella typhimurium plate incorporation assay was used to measure mutagenic activity. Quantitative analysis of 1-nitropyrene was performed with liquid chromatography/fluorescence analysis. The cytotoxicity and phagocytosis of diesel particles with and without fetal calf serum were evaluated to select exposure concentrations that resulted in minimal toxicity and maximal engulfment of particles by the macrophages. The diesel-particle exposure concentrations for the mutagenicity studies were 200 micrograms/ml in the absence of serum and 375 micrograms/ml in the presence of serum. Engulfment and incubation of diesel particles with lung macrophages resulted in the loss of considerable mutagenic activity (97-98%) and significantly less 1-nitropyrene (10-25%). These studies suggest that lung macrophages have the capability to metabolize mutagenic nitroaromatics found in diesel particles.