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Introduction: The effect of the treating surgeon's subspecialty training on the outcomes of managing displaced supracondylar humerus fractures in the pediatric cohort remains under debate. The objective of this study was to examine patient outcomes and treatment variables for these injuries based on the surgeon subspecialty training. Methods: A retrospective study of children who had undergone primary closed reduction and percutaneous fixation for displaced supracondylar humerus fractures was done from January 2012 through May 2019. The following four groups with differing orthopaedic subspecialty training were evaluated: (1) pediatric fellowship trained (2) trauma fellowship trained, (3) sports medicine fellowship trained, and (4) all others. Outcomes examined included time to surgery, surgical time, fluoroscopy usage, postoperative follow-up protocols, radiographic measurements of alignment, and complications between surgeon groups. Results: Two hundred thirty-one cases were included (mean age 6 ± 2 years). Pediatric fellowship-trained surgeons took patients to surgery in a more delayed fashion (>12 hours, P = 0.02). Surgical time and fluoroscopy usage were significantly shorter for pediatric fellowship-trained surgeons (P < 0.001). No statistical difference was noted in pin configuration constructs between the groups. Pediatric fellowship-trained surgeons, on average, saw patients two times postoperatively within a year with most patients being within 30 days. Complications were not statistically different between the groups. Conclusions: Pediatric fellowship-trained orthopaedic surgeons provide more efficient care on a more delayed basis for displaced supracondylar humerus fractures than other subspecialty-trained orthopaedic surgeons. However, if barriers exist that limit the practicality or availability of these specialists, nonpediatric fellowship-trained surgeons achieve similar and satisfactory outcomes. Level of Evidence: Level III retrospective cohort study

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Women with preeclampsia (PE) have a greater risk of developing hypertension, cardiovascular disease (CVD), and renal disease later in life. Angiotensin II type I receptor agonistic autoantibodies (AT1-AAs) are elevated in women with PE during pregnancy and up to 2-year postpartum (PP), and in the reduced uterine perfusion pressure (RUPP) rat model of PE. Blockade of AT1-AA with a specific 7 amino acid peptide binding sequence (‘n7AAc’) improves pathophysiology observed in RUPP rats; however, the long-term effects of AT1-AA inhibition in PP is unknown. Pregnant Sprague Dawley rats were divided into three groups: normal pregnant (NP) (n = 16), RUPP (n = 15), and RUPP + ‘n7AAc’ (n = 16). Gestational day 14, RUPP surgery was performed and ‘n7AAc’ (144 μg/day) administered via osmotic minipump. At 10-week PP, mean arterial pressure (MAP), renal glomerular filtration rate (GFR) and cardiac functions, and cardiac mitochondria function were assessed. MAP was elevated PP in RUPP vs. NP (126 ± 4 vs. 116 ± 3 mmHg, p < 0.05), but was normalized in in RUPP + ‘n7AAc’ (109 ± 3 mmHg) vs. RUPP (p < 0.05). PP heart size was reduced by RUPP + ’n7AAc’ vs. RUPP rats (p < 0.05). Complex IV protein abundance and enzymatic activity, along with glutamate/malate-driven respiration (complexes I, III, and IV), were reduced in the heart of RUPP vs. NP rats which was prevented with ‘n7AAc’. AT1-AA inhibition during pregnancy not only improves blood pressure and pathophysiology of PE in rats during pregnancy, but also long-term changes in blood pressure, cardiac hypertrophy, and cardiac mitochondrial function PP.

Background There is a lack of valid and reliable tests that assess upper extremity strength and function for rehabilitation and injury prevention purposes in throwing athletes. The Athletic Shoulder (ASH) test has been proposed as a reliable measure of shoulder strength, but has not yet been studied in baseball pitchers. Hypothesis/Purpose The purpose of this study was to establish values for healthy baseball pitchers performing the ASH test, compare those values with other common tests of shoulder strength and function, and compare ASH test performance bilaterally. It was hypothesized that the dominant arm would perform significantly better on the ASH test compared to the non-dominant arm. A secondary purpose of the study was to evaluate if ASH test performance was related to fastball velocity in baseball pitchers. It was hypothesized that ASH test performance would positively correlate with fastball velocity. Study Design Cross-Sectional Study Methods College and high school baseball pitchers were recruited to complete shoulder range of motion (ROM), isokinetic shoulder strength, and isometric shoulder strength testing using the ASH test. The ASH test was used to assess force production as a proxy for strength bilaterally at four levels of shoulder abduction (0°, 90°, 135°, and 180°), using a force plate. Approximately one-week later subjects returned for a bullpen session where fastball velocity was recorded with a radar gun. Bilateral differences in passive ROM, isokinetic, and isometric shoulder strength were examined using paired t-tests while linear relationships between isometric shoulder strength and fastball velocity were assessed using Pearson correlations. Results Thirty-five healthy pitchers participated in the study (19.7 ± 1.8 years). Pitchers demonstrated significantly greater isometric shoulder strength at the 90° and 135° abduction positions with the throwing arm compared to the non-throwing arm. Pitchers also demonstrated commonly observed musculoskeletal adaptations in the throwing arm such as increased passive external rotation, decreased passive internal rotation, and greater internal and external rotator strength during isokinetic testing. Peak force production during the ASH test was not related to fastball velocity. Conclusion The ASH test is capable of detecting bilateral shoulder strength adaptations commonly observed in other clinical tests in healthy pitchers. Pitchers demonstrated greater isometric peak force during the ASH test at levels of shoulder abduction similar to those observed in pitching. While these results may be intriguing for clinical use, peak force from the ASH test was not correlated to fastball velocity in pitchers, and therefore should be used with caution for predictions in this realm. Level of Evidence 2 Clinical Relevance A need exists for objective measures of shoulder strength for rehabilitation and injury risk monitoring in throwing athletes that are easy to administer, have high reliability and validity, and provide minimal re-injury risk to athletes recovering from injury. What is known about the subject Data from the ASH test has been published previously in non-throwing athletes and was shown to be valid and reliable in that group. However, the test has not been explored widely in throwing athletes who are known to have significant musculoskeletal adaptations to the throwing shoulder. What this study adds to existing knowledge The results from this study confirm that the ASH test is sensitive enough to detect the adaptations that are present in the healthy throwing athlete’s shoulder. Due to the prior proven validity and reliability and these results, the test can be used to monitor throwing arm strength and function during rehabilitation or as a pre/intra-season screening tool to help describe arm health.

Women with preeclampsia (PE) have a greater risk of developing hypertension, cardiovascular disease (CVD), and renal disease later in life. Angiotensin II type I receptor agonistic autoantibodies (AT1-AAs) are elevated in women with PE during pregnancy and up to 2 years postpartum (PP), and in the reduced uterine perfusion pressure (RUPP) rat model of PE. Blockade of AT1-AA with a specific 7 amino acid peptide binding sequence (‘n7AAc’) improves pathophysiology observed in RUPP rats; however, the long-term effects of AT1-AA inhibition in PP is unknown. Pregnant Sprague Dawley rats were divided into 3 groups: normal pregnant (NP) (n = 16), RUPP (n = 15), and RUPP+‘n7AAc’ (n = 16). Gestational day 14, RUPP surgery was performed and ‘n7AAc’ (144 µg/day) administered via osmotic minipump. At 10 weeks PP, mean arterial pressure (MAP), renal glomerular filtration rate (GFR) and cardiac functions, and cardiac mitochondria function were assessed. MAP was elevated PP in RUPP vs NP (126 ± 4 vs. 116 ± 3 mmHg, p < 0.05), but was normalized in in RUPP+‘n7AAc’ (109 ± 3 mmHg) vs. RUPP (p < 0.05). PP heart size was reduced by RUPP+’n7AAc’ vs. RUPP rats (p < 0.05). Complex IV protein abundance and enzymatic activity, along with glutamate/malate-driven respiration (complexes I, III, and IV), were reduced in the heart of RUPP vs NP rats which was prevented with ‘n7AAc’. AT1-AA inhibition during pregnancy not only improves blood pressure and pathophysiology of PE in rats during pregnancy, but also long-term changes in blood pressure, cardiac hypertrophy, and cardiac mitochondrial function PP.

The intra- and extracerebral Doppler artery blood velocity responses to a 10-mmHg abrupt blood pressure (BP) decrease in ten healthy men were studied. This decrease was obtained using two cuffs placed over both thighs. First, cuffs were inflated to pressures greater than the arterial BP for 5 min. Next, they were deflated to 60 mmHg in order to prevent venous return from the legs. We obtained a decrease in mean arterial BP of from 101 (10) to 90 (10) mmHg [mean (SD), P < 0.01] without modifications in the heart rate [HR, 88 (14) beats min-1]. Middle cerebral artery mean blood velocity (MCAmv) decreased immediately from 50 (10) to 42 (12) cm s-1 (P < 0.05). Simultaneously, temporal superficial artery mean blood velocity (TSAmv) decreased from 11 (3) to 7 (2) cm s-1 (P < 0.05) and common carotid artery blood flow (CCAbf) decreased from 305 (23) to 233 (33) ml min-1 (P < 0.05). After 5 s, MCAmv and CCAbf returned to baseline values, whereas TSAmv [8 (2) cm s-1], mean arterial BP [86 (10) mmHg] remained low and HR increased [92 (12) beats min-1]. TSAmv, BP and HR returned to baseline values in 1 min. These data confirm that cerebral blood flow (CBF) is very rapidly regulated but that blood flow in extracranial territories is not and that it follows the arterial BP changes.

Women with preeclampsia (PE) have a risk of developing cardiovascular diseases (CVD) later in life. The angiotensin II type I receptor agonistic autoantibodies (AT1-AAs) are elevated in women with PE, PE women 2 years post-partum (PP), and the reduced uterine perfusion pressure (RUPP) rat model of PE. Blockade of the AT1-AA by using a specific binding seven amino acid peptide sequence (7AA) improves the pathology of PE in RUPP rats. The long-term effects of AT1-AA inhibition on blood pressure, NK cell activation, heart mitochondria (mt) proteins, and CVD in the RUPP model PP is unknown. Therefore, we hypothesized that PP RUPP rats have elevated blood pressure, NK cell activation, and changes in heart mt proteins, which will be prevented in RUPP rats administered the 7AA during pregnancy. Methods: Pregnant Sprague Dawley rats were divided into groups; normal pregnant (NP) (n=7), RUPP (n=10), and RUPP+7AA (n=9). Gestational day 14, RUPP surgery was performed and 7AA (2 μg/ml) administered via minipump. Results: At 8 and 10 weeks (wks) PP, blood pressure (MAP), blood, and hearts were collected. NK cells were quantified by flow cytometry. At 8 wks PP, MAP was elevated in RUPP vs. NP (130±2 vs. 123±4 mmHg, ns), and RUPP+7AA (124±4 mmHg) treatment prevented this increase. At 10 wks, MAP was elevated in RUPP vs NP (133±5 vs. 120±5 mmHg, p=0.08), with a significant decrease in MAP in RUPP+7AA (107±6 mmHg) vs. RUPP (p<0.05). Total circulating NK cells were increased in RUPP vs NP (45±9. vs. 29± 8% gated cells, ns), which was prevented in RUPP+7AA (19±16 % gated cells) at 8 wks PP. Hearts were enlarged with RUPP vs NP (0.41±0.04 vs. 0.36±0.02g/100gBW, ns), which was normalized in RUPP+7AA (0.34±0.02g/100gBW). Previous studies show that during pregnancy complex IV is significantly lower along with a decrease mt function in RUPP vs NP. Complex IV mt proteins in the heart were elevated in RUPP+7AA vs. RUPP (5.5±1.7 vs. 3.0±0.2 AU, ns). Conclusion: In summary, PP PE rats have an increase in MAP, NK cells, and larger hearts. AT1-AA inhibition restores complex IV mt levels and improves HTN, immune activation, and cardiac hypertrophy PP. This study highlights the importance of AT1-AA inhibition during PE to prevent CVD later in life. Supported: AHA18CDA34110264