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Purpose The purpose of this study was to investigate the influence of multiple demographic and radiographic findings on the size of labral tears identified at the time of hip arthroscopy. Methods Data were prospectively collected for patients treated with arthroscopic labral repair or debridement from February 2008 to August 2011. Preoperative radiographic and demographic data were collected for 392 patients during the study period. Exclusion criteria included revision surgery and previous hip conditions. An anteroposterior pelvic view, 45° Dunn view, and false‐profile view were used to measure Tönnis grade, neck‐shaft angle, alpha angle, lateral center edge angle (LCEA), anterior center edge angle (ACEA), acetabular inclination, and the extent of crossover sign when present. At the time of surgery, labral tear size and location were documented for all patients, using traditional acetabular clock face nomenclature for sizing. A multiple linear regression analysis was then performed to assess the correlation of radiographic and demographic findings with the size of the labral tear. Results Regression analysis displayed statistical significance for sex ( P < .0001), age ( P < .0001), and alpha angle ( P = .005) with labral tear size. For female patients, Tönnis grade ( P = .0004) and neck‐shaft angle ( P = .004) correlated with labral tear size. This model accounted for only 26% of variation in labral tear size. Conclusions Preoperative risk factors for the extent of labral tear size are male sex, increasing age, and increasing alpha angle. Labral tears were larger in female patients with higher Tönnis grades and lower neck‐shaft angles. Measurements of acetabular coverage and version showed no correlation with labral tear size. The majority of labral tear size variation was not accounted for in this model. Level of Evidence Level IV, therapeutic case series.

Background— Patients with severe tricuspid regurgitation (TR) frequently present with exertional fatigue and dyspnea, but the hemodynamic basis for exercise limitation in people with TR remains unclear. Methods and Results— Twelve subjects with normal left ventricular (LV) ejection fraction and grade ≥3 TR underwent high-fidelity invasive hemodynamic exercise testing with simultaneous expired gas analysis and were compared with 13 age- and sex-matched controls. At rest, TR subjects had lower pulmonary blood flow (3.6±0.4 versus 5.1±1.9 L/min; P =0.01), increased right atrial pressure (12±5 versus 4±1 mm Hg; P =0.0002), and higher pulmonary capillary wedge pressure (17±5 versus 9±3 mm Hg; P =0.0001). However, LV transmural pressure (pulmonary capillary wedge pressure−right atrial pressure), which reflects LV preload independent of right heart congestion and pericardial restraint, was similar in TR and controls (6±3 versus 4±2 mm Hg; P =0.3). With exercise, TR subjects displayed lower peak V O 2 (10.3±2.8 versus 13.8±4.2 mL/min per kg; P =0.02), lower pulmonary blood flow (6.4±1.3 versus 10.3±3.3 L/min; P =0.001), and less increase in pulmonary blood flow relative to V O 2 (+4.6±1.1vs +6.2±0.7; P =0.001). TR subjects displayed higher pulmonary capillary wedge pressure with exercise, but this was solely because of RA hypertension (27±9 versus 8±3 mm Hg; P <0.0001), because LV transmural pressure dropped with exercise in subjects with TR (−5±6 versus +3±3 mm Hg; P =0.0007), suggesting inadequate LV diastolic filling, despite high pulmonary capillary wedge pressure. Conclusions— Impaired exercise capacity in people with severe TR is related to low cardiac output reserve relative to metabolic needs, coupled with elevated systemic and pulmonary venous pressures. Left heart pressures are elevated with exercise in subjects with TR, despite low LV preload, secondary to enhanced ventricular interaction.

Heart failure with preserved ejection fraction (HFpEF) is a major cause of morbidity and mortality. Exercise training is an established adjuvant therapy in heart failure; however, the effects of high-intensity interval training (HIIT) in HFpEF are unknown. We compared the effects of HIIT vs. moderate-intensity aerobic continuous training (MI-ACT) on peak oxygen uptake (V̇o2peak), left ventricular diastolic dysfunction, and endothelial function in patients with HFpEF. Nineteen patients with HFpEF (age 70 ± 8.3 yr) were randomized to either HIIT (4 × 4 min at 85-90% peak heart rate, with 3 min active recovery) or MI-ACT (30 min at 70% peak heart rate). Fifteen patients completed exercise training (HIIT: n = 9; MI-ACT: n = 6). Patients trained 3 days/wk for 4 wk. Before and after training patients underwent a treadmill test for V̇o2peak determination, 2D-echocardiography for assessment of left ventricular diastolic dysfunction, and brachial artery flow-mediated dilation (FMD) for assessment of endothelial function. HIIT improved V̇o2peak (pre = 19.2 ± 5.2 ml·kg−1·min−1; post = 21.0 ± 5.2 ml·kg−1·min−1; P = 0.04) and left ventricular diastolic dysfunction grade (pre = 2.1 ± 0.3; post = 1.3 ± 0.7; P = 0.02), but FMD was unchanged (pre = 6.9 ± 3.7%; post = 7.0 ± 4.2%). No changes were observed following MI-ACT. A trend for reduced left atrial volume index was observed following HIIT compared with MI-ACT (−3.3 ± 6.6 vs. +5.8 ± 10.7 ml/m2; P = 0.06). In HFpEF patients 4 wk of HIIT significantly improved V̇o2peak and left ventricular diastolic dysfunction. HIIT may provide a more robust stimulus than MI-ACT for early exercise training adaptations in HFpEF.

During World War 2, Earl Wood was charged with elucidating the biomedical factors in acceleration-induced loss of consciousness experienced by pilots in high-performance aircraft. For this, he developed devices for measurement and recording of blood pressure and tissue blood content. Those data lead to the design and fabrication of successful countermeasures to acceleration-induced loss of consciousness with an inflatable “G-suit” and “M1” breath-holding maneuver. After World War 2, he utilized and modified these instruments and made use of indicator dilution techniques by continuous intracardiac blood sampling to greatly increase the specificity and sensitivity of diagnosis of intracardiac anatomic and functional abnormalities in patients with congenital heart disease. This contributed to the greatly increased success rate of open-heart surgery in the 1950s. In the 1960s, he built on the then recently available video-coupled electronic X-ray image intensifier to develop X-ray fluoroscopy-based recording of indicator dilution signals in all cardiac chambers and surrounding great vessels without the need for placing catheter tips at those locations for blood sampling. However, these blood flow-related data were of limited value, as they were not measured concurrent with myocardial functional demand for perfusion. In the 1970s, he overcame this limitation by developing a high-speed multislice X-ray imaging scanner to provide tomographic images of concurrent dynamic cardiac anatomy and the indicator dilution-based estimates of blood flow distributions. On his retirement at age 70 in 1982, he had accomplished his 2 decade-old goal of the ability to make accurate concurrent, minimally invasive, and indicator dilution-based measurement of cardiovascular structure to function relationships.

ABSTRACT A 65-year-old female with a history of multiple tick bites presented with fever and pancytopenia. Intracytoplasmic rickettsial morulae were detected on peripheral smear and bone marrow biopsy specimens, and PCR amplified Ehrlichia ewingii DNA from both specimens. To our knowledge, this is the first report of E. ewingii infection of human bone marrow.

The aim of this preliminary case study series was to investigate epidermal innervation in pediatric patients with significant neurological impairment and self‐injurious behavior. We enrolled four pediatric patients with self‐injury (two males, two females; mean age 12y, range 9–14y) and used archival specimens from healthy, age‐matched children with typical development for comparison purposes. Epidermal nerve fiber density, peptide content, and mast cell degranulation patterns from non‐damaged skin were tested between the patients and the comparison group. The male patients with self‐injury had significantly increased epidermal nerve fiber densities, increased substance P positive fiber count and extensive mast cell degranulation compared with sex‐ and age‐matched individuals with typical development. Our case series shows for the first time altered peripheral innervation from non‐damaged tissue in children with significant self‐injury and developmental disability compared with a healthy comparison group. Establishing the role of peripheral nociceptive and immune modulatory neural pathways may offer new treatment avenues for this devastating neurobehavioral disorder.

Biomedical scientists can exploit initiatives from U.S. federal regulatory and funding agencies aimed at accelerating clinical translation.

Objectives. To highlight the case of a patient with multiple transient ischemic attacks and visual disturbances diagnosed with carotid stump syndrome and managed with endovascular approach. Case Presentation. We present the case of a carotid stump syndrome in an elderly patient found to have moderate left internal carotid artery stenosis in response to an advertisement for carotid screening. After a medical therapeutic approach and a close follow-up, transient ischemic attacks recurred. Computed tomographic angiography showed an occlusion of the left internal carotid artery and the presence of moderate stenosis in the right internal carotid artery, which was treated by endovascular stenting and balloon insertion. One month later, the patient presented with visual disturbances due to the left carotid stump and severe stenosis of the left external carotid artery that was reapproached by endovascular stenting. Conclusion. Considerations should be given to the carotid stump syndrome as a source of emboli for ischemic strokes, and vascular assessment could be used to detect and treat this syndrome.

Polycystic kidney disease (PKD) is a life‐threatening genetic disorder characterized by the presence of fluid‐filled cysts primarily in the kidneys. PKD can be inherited as autosomal recessive (ARPKD) or autosomal dominant (ADPKD) traits. Mutations in either the PKD1 or PKD2 genes, which encode polycystin 1 and polycystin 2, are the underlying cause of ADPKD. Progressive cyst formation and renal enlargement lead to renal insufficiency in these patients, which need to be managed by lifelong dialysis or renal transplantation. While characteristic features of PKD are abnormalities in epithelial cell proliferation, fluid secretion, extracellular matrix and differentiation, the molecular mechanisms underlying these events are not understood. Here we review the progress that has been made in defining the function of the polycystins, and how disruption of these functions may be involved in cystogenesis. WIREs Dev Biol 2014, 3:465–487. doi: 10.1002/wdev.152This article is categorized under: Signaling Pathways > Global Signaling Mechanisms Birth Defects > Organ Anomalies