Citations

Background: Preventive medicine techniques have alleviated billions of dollars’ worth of the economic burden in the medical care system through the implementation of vaccinations and screenings before the onset of disease symptoms. Knowledge of biomechanical tendencies has progressed rapidly over the past 20 years such that clinicians can identify, in healthy athletes, the underlying mechanisms that lead to catastrophic injuries such as anterior cruciate ligament (ACL) ruptures. As such, preventive medicine concepts can be applied to noncontact musculoskeletal injuries to reduce the economic burden of sports medicine treatments and enhance the long-term health of athletes. Purpose: To illustrate the practical medical benefits that could be gained from preventive biomechanics applied to the ACL as well as the need and feasibility for the broad implementation of these principles. Study Design: Literature review. Methods: The recent literature pertinent to the screening and prevention of musculoskeletal injuries was reviewed and compiled into a clinical commentary on the current state and applicability of preventive biomechanics. Results: Investigators have identified neuromuscular training protocols that screen for and correct the underlying biomechanical deficits that lead to ACL injuries. The literature shows that when athletes comply with these prescribed training protocols, the incidence of injuries is significantly reduced within that population. Such preventive biomechanics practices employ basic training methods that would be familiar to athletic coaches and have the potential to save billions of dollars in cost in sports medicine. Conclusion: The widespread implementation of preventive biomechanics concepts could profoundly affect the field of sports medicine with a minimum of initial investment.

Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of familial Parkinson's disease (PD), resembling the sporadic disorder. Intensive effort has been directed toward LRRK2 mouse modeling and investigation, aimed at reproducing the human disease to inform mechanistic studies of pathogenesis and design of neuroprotective therapies. The physiological function of LRRK2 is still under exploration, but a clear role in striatal neurophysiology and animal behavior has emerged. Alterations in LRRK2 impair dopamine (DA) transmission, regulation and signaling, in addition to corticostriatal synaptic plasticity. Consistently, several subtle abnormalities in motor and nonmotor abilities have been demonstrated in LRRK2 genetic mouse models, generally paralleling preclinical symptoms of early DA dysfunction. However, the variability in model design and phenotypes observed requires a critical approach in interpreting the results, adapting the model used to the specific research question. Etiologically appropriate knockin mice might represent the ultimate animal model in which to study early disease mechanisms and therapies as well as to investigate drug effectiveness and off-target consequences.

ABSTRACTObjectives:Celiac disease (CD) is a common immune‐mediated disorder that affects up to 1% of the general population. Recent reports suggest that the incidence of CD has reached a plateau in many countries. We aim to study the incidence and altered presentation of childhood CD in a well‐defined population.Methods:Using the Rochester Epidemiology Project, we retrospectively reviewed Mayo Clinic and Olmsted Medical Center medical records from January 1994 to December 2014. We identified all CD cases of patients ages 18 years or younger at the time of diagnosis. Incidence rates were calculated by adjusting for age, sex, and calendar year and standardizing to the 2010 US white population.Results:We identified 100 patients with CD. Incidence of CD has increased from 8.1 per 100,000 person‐years (2000–2002) to 21.5 per 100,000 person‐years (2011–2014). There was an increase in CD prevalence in children from 2010 (0.10%) to 2014 (0.17%). Thirty‐four patients (34%) presented with classical CD symptoms, 43 (43%) had nonclassical CD, and 23 (23%) were diagnosed by screening asymptomatic high‐risk patients. Thirty‐six patients (36%) had complete villous atrophy, 51 (51%) had partial atrophy, and 11 (11%) had increased intraepithelial lymphocytes. Two patients were diagnosed without biopsy. Most patients (67%) had a normal body mass index, 17% were overweight/obese, and only 9% were underweight.Conclusions:Both incidence and prevalence of CD have continued to increase in children during the past 15 years in Olmsted County, Minnesota. Clinical and pathologic presentations of CD are changing over time (more nonclassical and asymptomatic cases are emerging).

Purpose of review Subarachnoid hemorrhage from a ruptured aneurysm (aSAH) is a complex disorder with the potential to have devastating effects on the brain as well as other organ systems. After more than 3 decades of research, the underlying pathophysiologic mechanisms remain incompletely understood and important questions remain regarding the evaluation and management of these patients. The purpose of this review is to analyze the recent literature and improve our understanding of certain key clinical aspects. Recent findings Growing body of evidence highlights the usefulness of CT perfusion scans in the diagnosis of vasospasm and delayed cerebral ischemia (DCI). Hypervolemia leads to worse cardiopulmonary outcomes and does not improve DCI. The traditional triple H therapy is falling out of favor with hemodynamic augmentation alone now considered the mainstay of medical management. Randomized controlled trials have shown that simvastatin and intravenous magnesium do not prevent DCI or improve functional outcomes after aneurysmal subarachnoid hemorrhage (aSAH). Emerging data using multimodality monitoring has further advanced our understanding of the pathophysiology of DCI in poor grade aSAH. Summary The brief review will focus on the postinterventional care of aSAH patients outlining the recent advances over the past few years.

Summary Objectives To evaluate obesity and overweight in children with congenital adrenal hyperplasia ( CAH ) and associations with glucocorticoids, fludrocortisone and disease control. Adjusting body mass index‐for‐height‐age ( BMI HA ) percentile is proposed to correct misclassification of obese/overweight status in CAH children with advanced bone age and tall‐for‐age stature. Design Longitudinal. Patients One hundred and ninety‐four children with CAH seen from 1970 to 2013: 124 salt wasting ( SW ); 70 simple virilizing ( SV ); 102 females. Measurements Body mass index (BMI) end‐points were overweight (85–94 percentile) and obese (≥95 percentile). Results Approximately 50% of the children had at least one BMI measurement ≥95 percentile and about 70% had at least one ≥85 percentile. Using BMI HA percentiles, obesity incidence decreased slightly in SW children (47–43%) and markedly in SV children (50–33%); however, overweight status was not reduced. Only 6% of SW and 1% of SV children were persistently obese (≥3 clinic visits) when BMI HA was applied, whereas overweight status persisted in 35% of SW and 33% of SV children. Most obesity or overweight when using BMI HA occurred before age 10 and there was no association with hydrocortisone (HC) or fludrocortisone dosing. Adiposity rebound for SW children occurred by 3·3 years and in SV females by age 3·8 years, over a year earlier than the adiposity rebound for healthy children. Conclusion Children with CAH are at higher risk for early onset obesity and overweight with or without using BMI HA but rates of persistent obesity were lower than previously reported. Careful HC dosing during early childhood is needed to prevent increased weight gain and an early adiposity rebound.