Existing vital sign monitoring systems in the neonatal intensive care unit (NICU) require multiple wires connected to rigid sensors with strongly adherent interfaces to the skin. We introduce a pair of ultrathin, soft, skin-like electronic devices whose coordinated, wireless operation reproduces the functionality of these traditional technologies but bypasses their intrinsic limitations. The enabling advances in engineering science include designs that support wireless, battery-free operation; real-time, in-sensor data analytics; time-synchronized, continuous data streaming; soft mechanics and gentle adhesive interfaces to the skin; and compatibility with visual inspection and with medical imaging techniques used in the NICU. Preliminary studies on neonates admitted to operating NICUs demonstrate performance comparable to the most advanced clinical-standard monitoring systems.

We provide a comprehensive description of the clinical spectrum of rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation in terms of timing and scope of symptoms, study of candidate genes, and screening for chromosomal deletions and duplications. Negative PHOX2B sequencing results demonstrate that this entity is distinct from congenital central hypoventilation syndrome.

Standard of care management in neonatal and pediatric intensive care units (NICUs and PICUs) involve continuous monitoring of vital signs with hard-wired devices that adhere to the skin and, in certain instances, include catheter-loaded pressure sensors that insert into the arteries. These protocols involve risks for complications and impediments to clinical care and skin-to-skin contact between parent and child. Here we present a wireless, non-invasive technology that not only offers measurement equivalency to these management standards but also supports a range of important additional features (without limitations or shortcomings of existing approaches), supported by data from pilot clinical studies in the neonatal intensive care unit (NICU) and pediatric ICU (PICU). The combined capabilities of these platforms extend beyond clinical quality measurements of vital signs (heart rate, respiration rate, temperature and blood oxygenation) to include novel modalities for (1) tracking movements and changes in body orientation, (2) quantifying the physiological benefits of skin-to-skin care (e.g. Kangaroo care) for neonates, (3) capturing acoustic signatures of cardiac activity by directly measuring mechanical vibrations generated through the skin on the chest, (4) recording vocal biomarkers associated with tonality and temporal characteristics of crying impervious to confounding ambient noise, and (5) monitoring a reliable surrogate for systolic blood pressure. The results have potential to significantly enhance the quality of neonatal and pediatric critical care.In the United States, over 480,000 critically-ill infants and children enter intensive care units (ICUs) each year. Those less than one year of age suffer from the highest morbidity and mortality rates and therefore require the most intensive care 1,2 . These fragile patients include

These data suggest that nonpolyalanine repeat mutations produce more severe disruption of PHOX2B function. Patients carrying these mutations should be evaluated for HSCR and neural crest tumors. Because incomplete penetrance can occur in families of CCHS probands with PHOX2B mutations, genetic screening of appropriate family members is indicated to evaluate reproductive risk and because asymptomatic mutation carriers may be at risk for developing alveolar hypoventilation.

Rapid-onset Obesity with Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation (ROHHAD) is a rare and complex pediatric disorder. Despite increased identification and advancing knowledge of the disease course, the variable onset and timing of phenotypic features in ROHHAD often result in delayed or missed diagnosis, potentially leading to fatal central hypoventilation, cardiorespiratory arrest, and impaired neurocognitive development. The 5-hydroxytryptamine receptor 1A (HTR 1A ), orthopedia (OTP), and pituitary adenylate cyclase activating polypeptide (PACAP) genes were targeted in the etiology of ROHHAD based on their roles in the embryologic development of the hypothalamus and autonomic nervous system. We hypothesized that variations of HTR 1A , OTP, and/or PACAP would be associated with ROHHAD. All coding regions and intron-exon boundaries of the HTR 1A , OTP, and PACAP genes, in addition to the promoter region of the HTR 1A gene, were analyzed by standard sequencing in 25 ROHHAD cases and 25 matched controls. Thirteen variations, including six protein-changing mutations, were identified. None of these variations were significantly correlated with ROHHAD. This report provides evidence that variation of the HTR 1A , OTP, and PACAP genes are not responsible for ROHHAD. These results represent a further step in the investigation of the genetic determinants of ROHHAD. (Pediatr Res 70: 375-378, 2011)