Adolescent athletes return to sports rapidly after posterior spine fusion for idiopathic scoliosis: a prospective cohort study.

PURPOSE: No consensus exists regarding the timing for return to sports after PSF for patients with AIS. Return-to-play protocols are based on expert opinion and vary widely. The purpose of this study was to determine how rapidly athletes return to baseline sports activity following posterior spinal fusion for adolescent idiopathic scoliosis. METHODS: Athletes were consecutively enrolled. Inclusion criteria included competition at a junior varsity level or greater for ≥ 3 months yearly, major Cobb angle of 40-75°, age 10-18 years, and one year of follow-up. Athletes completed preoperative sports performance and Patient Reported Outcomes Measurement Information System (PROMIS) physical activity, pain interference, and depressive symptoms questionnaires. Self-assessments were repeated monthly until one year after PSF. RESULTS: Twenty-six athletes were enrolled. The median time to return to sport was 2.7 months [range: 0.6-13 months]. At twelve months, 24 of 26 [90.1%; 95% CI 36.9-74.9%] athletes reported they had returned to the sport at their presurgical level of play. Participation in contact sports was associated with a longer return to sport relative to participation in non-contact/limited contact sports [Hazard Ratio: 0.37, 95% 95% CI 0.14-0.97, p = 0.0427]. Conditioning and flexibility were the most common barriers to return to sport. CONCLUSIONS: When released to unrestricted activity at 4-8 weeks, athletes rapidly return to baseline levels of sports performance, with over half achieving this metric by 3 months.

A 9-Month-Old with Skeletal Abnormalities and a Consanguineous Sibling with Mucopolysaccharidosis IVA: The Role of Urinary Glycosaminoglycan Testing in Disease Diagnosis and Treatment Monitoring.

Mucopolysaccharidosis IVA (MPS IVA) is a rare autosomal recessive lysosomal storage disorder resulting from N-acetylgalactosamine-6-sulfatase (GALNS) deficiency that occurs in approximately 1 in 76 000 to 1 in 640 000 live births. Given that the diagnosis of MPS IVA relies heavily on the results of initial urine glycosaminoglycan (GAG) screening, cases that present with falsely normal urine GAG concentrations can delay the diagnosis and follow-up care for patients. This case study follows a patient diagnosed with MPS IVA at 9 months of age based on relation to a consanguineous 3-year-old sibling with MPS IVA and the use of direct enzyme activity analysis. Details regarding skeletal presentation and identification of genetic variants are presented along with data on follow-up urinary GAG monitoring during treatment with enzyme replacement therapy and treatment for a growth hormone disorder.

ß-Arrestin2 Improves Post-Myocardial Infarction Heart Failure via Sarco(endo)plasmic Reticulum Ca2+-ATPase-Dependent Positive Inotropy in Cardiomyocytes.

Heart failure is the leading cause of death in the Western world, and new and innovative treatments are needed. The GPCR (G protein-coupled receptor) adapter proteins ßarr (ß-arrestin)-1 and ßarr-2 are functionally distinct in the heart. ßarr1 is cardiotoxic, decreasing contractility by opposing ß1AR (adrenergic receptor) signaling and promoting apoptosis/inflammation post-myocardial infarction (MI). Conversely, ßarr2 inhibits apoptosis/inflammation post-MI but its effects on cardiac function are not well understood. Herein, we sought to investigate whether ßarr2 actually increases cardiac contractility. Via proteomic investigations in transgenic mouse hearts and in H9c2 rat cardiomyocytes, we have uncovered that ßarr2 directly interacts with SERCA2a (sarco[endo]plasmic reticulum Ca2+-ATPase) in vivo and in vitro in a ß1AR-dependent manner. This interaction causes acute SERCA2a SUMO (small ubiquitin-like modifier)-ylation, increasing SERCA2a activity and thus, cardiac contractility. ßarr1 lacks this effect. Moreover, ßarr2 does not desensitize ß1AR cAMP-dependent procontractile signaling in cardiomyocytes, again contrary to ßarr1. In vivo, post-MI heart failure mice overexpressing cardiac ßarr2 have markedly improved cardiac function, apoptosis, inflammation, and adverse remodeling markers, as well as increased SERCA2a SUMOylation, levels, and activity, compared with control animals. Notably, ßarr2 is capable of ameliorating cardiac function and remodeling post-MI despite not increasing cardiac ßAR number or cAMP levels in vivo. In conclusion, enhancement of cardiac ßarr2 levels/signaling via cardiac-specific gene transfer augments cardiac function safely, that is, while attenuating post-MI remodeling. Thus, cardiac ßarr2 gene transfer might be a novel, safe positive inotropic therapy for both acute and chronic post-MI heart failure.