Sexual History Documentation in Pediatric Patients with Technology Dependence.

Adolescent sexual health documentation reflects the depth of discussion physicians conduct with their patients. Limited studies exist on rates of sexual history documentation in technology-dependent patients. We sought to identify whether treatment gaps exist in a technology-dependent adolescent population. Well-child visits for patients with enterotomy or tracheostomy dependence, 12 to 19 years age, and seen in our urban clinic over a 3-year period (n = 14) were compared with a randomly selected peer group without technology dependence. Documentation of sexual activity, sexual orientation, safe sex and sexually transmitted infection (STI) guidance, and contraception or condom use were noted. Results demonstrate lower rates of documentation in sexual orientation, safe sex and STI guidance, and contraception or condom use in patients with technology dependence when compared with patients without technology dependence. Similar differences were noted in the 16- to 19-year group between the experimental and control groups. No differences were noted between gender and age groups.

Activation of neuronal adenosine A1 receptors causes hypothermia through central and peripheral mechanisms.

Extracellular adenosine, a danger signal, can cause hypothermia. We generated mice lacking neuronal adenosine A1 receptors (A1AR, encoded by the Adora1 gene) to examine the contribution of these receptors to hypothermia. Intracerebroventricular injection of the selective A1AR agonist (Cl-ENBA, 5'-chloro-5'-deoxy-N6-endo-norbornyladenosine) produced hypothermia, which was reduced in mice with deletion of A1AR in neurons. A non-brain penetrant A1AR agonist [SPA, N6-(p-sulfophenyl) adenosine] also caused hypothermia, in wild type but not mice lacking neuronal A1AR, suggesting that peripheral neuronal A1AR can also cause hypothermia. Mice expressing Cre recombinase from the Adora1 locus were generated to investigate the role of specific cell populations in body temperature regulation. Chemogenetic activation of Adora1-Cre-expressing cells in the preoptic area did not change body temperature. In contrast, activation of Adora1-Cre-expressing dorsomedial hypothalamus cells increased core body temperature, concordant with agonism at the endogenous inhibitory A1AR causing hypothermia. These results suggest that A1AR agonism causes hypothermia via two distinct mechanisms: brain neuronal A1AR and A1AR on neurons outside the blood-brain barrier. The variety of mechanisms that adenosine can use to induce hypothermia underscores the importance of hypothermia in the mouse response to major metabolic stress or injury.