Sexual activity and substance use among adolescents by category of physical activity plus team sports participation

OBJECTIVE: To determine whether being both vigorously active and a team sports participant or being vigorously physically active but not a team member is associated with substance use and sexual risk behaviors. DESIGN: Cross-sectional, using data from the 1999 national Youth Risk Behavior Survey. PARTICIPANTS: A nationally representative sample of 15 349 US high school students. MAIN OUTCOME MEASURES: Sexual risk behaviors and substance use among those who were both physically active and team sports participants, physically active but not on a sports team, physically nonactive but on a sports team, and physically nonactive and not on a sports team by sex and race/ethnicity. RESULTS: Nationwide, 41.9% of the students were both physically active and participants on a sports team, 22.1% were physically active but not sports team members, 12.6% were physically nonactive sports team members, and 22.3% were physically nonactive and not sports team members. More female (mean [SD], 29.3% [2.2%]) than male students (15.3% [1.9%]) were nonactive, and more male students were both physically active and participants in team sports (48.9% [3.4%]) than were female students (34.8% [3.2%]). Black students were more likely to be physically nonactive in both the team and nonteam categories than were students overall. Relative to nonactive nonteam female students, physically active female students on sports teams were less likely to be substance users or engage in sexual risk behaviors than were active nonteam and nonactive team female students. Other associations were specific to racial/ethnic subgroups. CONCLUSION: Overall, being both physically active and a team sports participant was associated with a lower prevalence of several health risk behaviors.     

The epsilon-sarcoglycan gene (SGCE), mutated in myoclonus-dystonia syndrome,is maternally imprinted

Myoclonus-dystonia syndrome (MDS) is a non-degenerative neurological disorder that has been described to be inherited in an autosomal dominant mode with incomplete penetrance. MDS is caused by loss of function mutations in the epsilon-sarcoglycan gene. Reinvestigation of MDS pedigrees provided evidence for a maternal imprinting mechanism. As differential methylated regions (DMRs) are a characteristic feature of imprinted genes, we studied the methylation pattern of CpG dinucleotides within the CpG island containing the promoter region and the first exon of the SGCE gene by bisulphite genomic sequencing. Our findings revealed that in peripheral blood leukocytes the maternal allele is methylated, while the paternal allele is unmethylated. We also showed that most likely the maternal allele is completely methylated in brain tissue. Furthermore, CpG dinucleotides in maternal and paternal uniparental disomy 7 (UPD7) lymphoblastoid cell lines show a corresponding parent-of-origin specific methylation pattern. The effect of differential methylation on the expression of the SGCE gene was tested in UPD7 cell lines with only a weak RT-PCR signal observed in matUPD7 and a strong signal in patUPD7. These results provide strong evidence for a maternal imprinting of the SGCE gene. The inheritance pattern in MDS families is in agreement with such an imprinting mechanism with the exception of a few cases. We investigated one affected female that inherited the mutated allele from her mother. Surprisingly, we found the paternal wild type allele expressed whereas the mutated maternal allele was not detectable in peripheral blood cDNA.     

The clinical evaluation of HER‐2 status: which test to use?

Accurate determination of the status of the type I receptor tyrosine kinase HER-2 in breast carcinomas provides significant insight into patient prognosis and may also inform selection of chemotherapeutic and hormonal treatments. At present, however, the single most important application of HER-2 testing is in the selection of patients for treatment with targeted therapies such as Herceptin. Although, based on current literature, fluorescence in situ hybridization (FISH) detection of HER-2 gene amplification may provide more accurate information in this context, this method is not yet widely available. Therefore, screening by immunohistochemistry (IHC) for HER-2 protein, backed by rigorous quality controls and FISH testing of equivocal cases with intermediate staining intensity, remains the current practice. In laboratories with highly standardized testing and quality assurance procedures, this protocol appears highly effective. Improvements in fixation procedures, standardization of antibodies, and use of automated image analysis may all increase the precision of IHC testing. However, on the basis of current data, there is a case to be made for the wider implementation of FISH testing to determine HER-2 status in breast cancer.     

Conditioning deficits of CaM-kinase transgenic Drosophila melanogaster in a new excitatory courtship assay

Courtship suppression is an associative conditioning procedure in Drosophila melanogaster that is ethologically based and capable of being tested on individual flies. We have expanded the range of the courtship conditioning by developing an excitatory procedure in which male flies learn to associate a novel odor with the courtship stimulating cues of virgin females. Wild-type males normally court other mature males very little, but following training, the odor alone is able to elicit increased levels of courtship towards an object male. Flies expressing an inhibitor of calcium/calmodulin-dependent protein kinase II (CaMKII) were previously shown to have no retention one hour after training in the courtship suppression task, as manifested in their persistent courting of a virgin female. A possible trivial explanation for this response is that the CaMKII-inhibited fly strains (ala1 and ala2) were merely hyperactive courters. The poor performance of these mutants in the new excitatory conditioning procedure confirms that their conditioning deficit results from a disruption of an associative mechanism per se.     

Speaking with a mirror: engagement of mirror neurons via choral speech and its derivatives induces stuttering inhibition

'Choral speech', 'unison speech', or 'imitation speech' has long been known to immediately induce reflexive, spontaneous, and natural sounding fluency, even the most severe cases of stuttering. Unlike typical post-therapeutic speech, a hallmark characteristic of choral speech is the sense of 'invulnerability' to stuttering, regardless of phonetic context, situational environment, or audience size. We suggest that choral speech immediately inhibits stuttering by engaging mirror systems of neurons, innate primitive neuronal substrates that dominate the initial phases of language development due to their predisposition to reflexively imitate gestural action sequences in a fluent manner. Since mirror systems are primordial in nature, they take precedence over the much later developing stuttering pathology. We suggest that stuttering may best be ameliorated by reengaging mirror neurons via choral speech or one of its derivatives (using digital signal processing technology) to provide gestural mirrors, that are nature's way of immediately overriding the central stuttering block.