Patient Understanding of Provider Credentials and Selection of Plastic Surgery Providers.

BACKGROUND: Many physicians who are not board-certified plastic surgeons have started performing aesthetic procedures, leading to unsafe practices that jeopardize patients' health. METHODS: Patients of a cosmetic and reconstructive private plastic surgery practice were asked to complete a survey that assessed their understanding of plastic surgeon credentials and advertising practices, and what influences their choice of a plastic surgeon. RESULTS: Eighty-five patients completed the survey, with 37.2% reporting prior aesthetic surgery; 84.9% were unaware of the lack of legal regulations governing the advertising practices of physicians. When asked if a doctor can perform surgery to improve their appearance without being a board-certified plastic surgeon, 22.1% responded "yes," 50% responded "no," and 27.9% responded "I don't know;" 98.8% reported a sense of comfort knowing their provider is board-certified in plastic surgery. When asked what factors help them decide if a surgeon is knowledgeable and trustworthy, the overwhelming majority reported referral from patients and providers as the most important factor, followed by online ratings and reviews. When deciding whether to recommend a plastic surgeon, personal experience was the most important factor. When deciding who should perform their cosmetic procedure, the most important factor was experience, followed by plastic surgery board certification. DISCUSSION: Current physician advertising practices lack strict guidelines and are often misleading. Patients would benefit from more thorough education on these practices. Of the various plastic surgeon assessment factors, most patients rely heavily on feedback obtained from patients and providers.

Glucocorticoids improve calcium cycling in cardiac myocytes after cardiopulmonary bypass.

BACKGROUND: Glucocorticoids can reduce myocardial dysfunction associated with ischemia and reperfusion injury following cardiopulmonary bypass (CPB) and circulatory arrest. The hypothesis was that maintenance of cardiac function after CPB with methylprednisolone therapy results, in part, from preservation of myocyte calcium cycling. METHODS: Piglets (5-7 kg) underwent CPB and 120 min of hypothermic circulatory arrest with (CPB-GC) or without (CPB) methylprednisolone (30 mgkg(-1)) administered 6h before and at CPB. Controls (No-CPB) did not undergo CPB or receive glucocorticoids (n=6 per treatment). Myocardial function was monitored in vivo for 120 min after CPB. Calcium cycling was analyzed using rapid line-scan confocal microscopy in isolated, fluo-3-AM-loaded cardiac myocytes. Phospholamban phosphorylation and sarco(endo)plasmic reticulum calcium-ATPase (SERCA2a) protein levels were determined by immunoblotting of myocardium collected 120 min after CPB. Calpain activation in myocardium was measured by fluorometric assay. RESULTS: Preload recruitable stroke work in vivo 120 min after reperfusion decreased from baseline in CPB (47.4±12 versus 26.4±8.3 slope of the regression line, P<0.05), but was not different in CPB-GC (41±8.1 versus 37.6±2.2, P=0.7). In myocytes isolated from piglets, total calcium transient time remained unaltered in CPB-GC (368±52.5 ms) compared with controls (434.5±35.3 ms; P=0.07), but was prolonged in CPB myocytes (632±83.4 ms; P<0.01). Calcium transient amplitude was blunted in myocytes from CPB (757±168 nM) compared with controls (1127±126 nM, P<0.05) but was maintained in CPB-GC (1021±155 nM, P>0.05). Activation of calpain after CPB was reduced with glucocorticoids. Phospholamban phosphorylation and SERCA2a protein levels in myocardium were decreased in CPB compared with No-CPB and CPB-GC (P<0.05). CONCLUSIONS: The glucocorticoid-mediated improvement in myocardial function after CPB might be due, in part, to prevention of calpain activation and maintenance of cardiac myocyte calcium cycling.

Large nipple areolar complex angiofibroma treated with combined surgical debulking and carbon dioxide laser therapy - a case report.

Here, we describe single case review of a 14-year-old female who presented with an angiofibroma on the right nipple areolar complex, which was treated successfully with debulking and CO2 laser. After 8 months of follow up, there has still been no recurrence of disease.

Calcineurin/NFAT coupling participates in pathological, but not physiological, cardiac hypertrophy.

Calcineurin (PP2B) is a calcium/calmodulin-activated, serine-threonine phosphatase that transmits signals to the nucleus through the dephosphorylation and translocation of nuclear factor of activated T cell (NFAT) transcription factors. Whereas calcineurin-NFAT signaling has been implicated in regulating the hypertrophic growth of the myocardium, considerable controversy persists as to its role in maintaining versus initiating hypertrophy, its role in pathological versus physiological hypertrophy, and its role in heart failure. To address these issues, NFAT-luciferase reporter transgenic mice were generated and characterized. These mice showed robust and calcineurin-specific activation in the heart that was inhibited with cyclosporin A. In the adult heart, NFAT-luciferase activity was upregulated in a delayed, but sustained manner throughout eight weeks of pathological cardiac hypertrophy induced by pressure-overload, or more dramatically following myocardial infarction-induced heart failure. In contrast, physiological hypertrophy as produced in two separate models of exercise training failed to show significant calcineurin-NFAT coupling in the heart at multiple time points, despite measurable increases in heart to body weight ratios. Moreover, stimulation of hypertrophy with growth hormone-insulin-like growth factor-1 (GH-IGF-1) failed to activate calcineurin-NFAT signaling in the heart or in culture, despite hypertrophy, activation of Akt, and activation of p70 S6K. Calcineurin Abeta gene-targeted mice also showed a normal hypertrophic response after GH-IGF-1 infusion. Lastly, exercise- or GH-IGF-1-induced cardiac growth failed to show induction of hypertrophic marker gene expression compared with pressure-overloaded animals. Although a direct cause-and-effect relationship between NFAT-luciferase activity and pathological hypertrophy was not proven here, our results support the hypothesis that separable signaling pathways regulate pathological versus physiological hypertrophic growth of the myocardium, with calcineurin-NFAT potentially serving a regulatory role that is more specialized for maladaptive hypertrophy and heart failure.

Impaired intracellular Ca2+ dynamics in live cardiomyocytes revealed by rapid line scan confocal microscopy.

Altered intracellular Ca2+ dynamics are characteristically observed in cardiomyocytes from failing hearts. Studies of Ca2+ handling in myocytes predominantly use Fluo-3 AM, a visible light excitable Ca2+ chelating fluorescent dye in conjunction with rapid line-scanning confocal microscopy. However, Fluo-3 AM does not allow for traditional ratiometric determination of intracellular Ca2+ concentration and has required the use of mathematic correction factors with values obtained from separate procedures to convert Fluo-3 AM fluorescence to appropriate Ca2+ concentrations. This study describes methodology to directly measure intracellular Ca2+ levels using inactivated, Fluo-3-AM-loaded cardiomyocytes equilibrated with Ca2+ concentration standards. Titration of Ca2+ concentration exhibits a linear relationship to increasing Fluo-3 AM fluorescence intensity. Images obtained from individual myocyte confocal scans were recorded, average pixel intensity values were calculated, and a plot is generated relating the average pixel intensity to known Ca2+ concentrations. These standard plots can be used to convert transient Ca2+ fluorescence obtained with experimental cells to Ca2+ concentrations by linear regression analysis. Standards are determined on the same microscope used for acquisition of unknown Ca2+ concentrations, simplifying data interpretation and assuring accuracy of conversion values. This procedure eliminates additional equipment, ratiometric imaging, and mathematic correction factors and should be useful to investigators requiring a straightforward method for measuring Ca2+ concentrations in live cells using Ca2+-chelating dyes exhibiting variable fluorescence intensity.

Aerobic exercise adaptations in trained adolescent runners following a season of cross-country training.

Adaptations in aerobic exercise responses as well as the relationship between aerobic exercise responses and running performance were examined in a group of previously trained adolescent runners (n = 9; 15.9 +/- 1.0 years) over the course of a competitive cross-country season. Running economy (RE), submaximal blood lactate concentration [BLa] and VO2max were assessed before and immediately after the season. Five-km race time improved (P < 0.05) from 18.68 +/- 1.10 min at the beginning of the season to 18.16 +/- 1.11 min at the end of the season. Significant increases were observed in peak VO2 (61.6 +/- 3.5 to 65.3 +/- 2.9 mL x kg(-1) x min(-1)) and graded exercise test time (11.32 +/- 1.56 to 12.22 +/- 0.79 min). There was a tendency for RE (P = 0.051) to worsen slightly and for [BLa] (P = 0. 057) to decline as a result of training. At the beginning of the season submaximal [BLa] at 14 km x hr(-1) (r = 0.86) and graded exercise test time (r = -0.87) were significantly related to 5-km time. At the end of the season, RE (r = 0.78) and [BLa] (r = 0.77) at 14 km x hr(-1) and graded exercise test time (r = -0.69) were significantly related to race time. In this well-trained group of runners, further training during the cross-country season increased peak VO2 and improved race time. Submaximal [BLa] and graded exercise test time appear to be the most robust predictors of performance, while RE became a significant predictor of race time at the end of the season.

Intracellular Ca2+ measurements in live cells by rapid line scan confocal microscopy: simplified calibration methodology.

Altered intracellular Ca2+ dynamics are characteristically observed in cardiomyocytes from failing hearts. Studies of Ca2+ handling in myocytes predominantly use Fluo-3 AM, a visible light excitable Ca2+ chelating fluorescent dye in conjunction with rapid line-scanning confocal microscopy. However, Fluo-3 AM does not allow for traditional ratiometric determination of intracellular Ca2+ concentration and has required use of mathematic correction factors with values obtained from separate procedures to convert Fluo-3 AM fluorescence to appropriate CA2+ concentrations. This study describes methodology to directly measure intracellular Ca2+ levels using inactivated, Fluo-3 AM loaded cardiomyocytes equilibrated with Ca2+ concentration standards. Titration of Ca2+ concentration exhibits a linear relationship to increasing Fluo-3 AM fluorescence intensity. Images obtained from individual myocyte confocal scans were recorded, average pixel intensity values were calculated, and a plot is generated relating the average pixel intensity to known Ca2+ concentrations. These standard plots can be used to convert transient Ca2+ fluorescence obtained with experimental cells to Ca2+ concentrations by linear regression analysis. Standards are determined on the same microscope used for acquisition of unknown Ca2+ concentrations, simplifying data interpretaton and assuring accuracy of conversion values. This procedure eliminates additional equipment, ratiometric imaging, and mathematic correction factors and should be used to investigators requiring a straightforward method for measuring Ca2+ concentrations in live cells using Ca2+-chelating dyes exhibiting variable fluorescence intensity.

The influence of exercise test protocol on perceived exertion at submaximal exercise intensities in children.

This study examined ratings of perceived exertion (RPE) using Borg's 6-20 scale at 50 W, 80 W, and ventilatory threshold (VT) in 10-year-old children (n = 15) during two different graded exercise tests. Power output was increased by 10 W.min(-1) in one protocol and by 30 W.3 min(-1) in the other. The cardiorespiratory responses at VT and peak exercise were similar between protocols. At 50 W and 80 W the cardiorespiratory responses were generally lower (P < 0.05) in the 10W trial. However, RPE was 11.5 +/- 2.9 and 12.1 +/- 3.2 at 50 W and 15.1 +/- 2.7 and 15.3 +/- 2.8 at 80 W in the 10-W and 30-W trials, respectively (P > 0.05). The RPE at VT was 13.9 +/- 2.4 in the 10-W trial and 12.4 +/- 2.4 in the 30-W trial (P < 0.05). In that variations in submaximal RPE did not coincide with variations in central mediators of exertion, locals cues of exertion may have provided the dominate sensory signal.

Calcium dynamics in the failing heart: restoration by beta-adrenergic receptor blockade.

Changes in calcium (Ca2+) regulation contribute to loss of contractile function in dilated cardiomyopathy. Clinical treatment using beta-adrenergic receptor antagonists (beta-blockers) slows deterioration of cardiac function in end-stage heart failure patients; however, the effects of beta-blocker treatment on Ca2+ dynamics in the failing heart are unknown. To address this issue, tropomodulin-overexpressing transgenic (TOT) mice, which suffer from dilated cardiomyopathy, were treated with a nonselective beta-receptor blocker (5 mg. kg-1. day-1 propranolol) for 2 wk. Ca2+ dynamics in isolated cardiomyocytes of TOT mice significantly improved after treatment compared with untreated TOT mice. Frequency-dependent diastolic and Ca2+ transient amplitudes were returned to normal in propranolol-treated TOT mice and but not in untreated TOT mice. Ca2+ kinetic measurements of time to peak and time decay of the caffeine-induced Ca2+ transient to 50% relaxation were also normalized. Immunoblot analysis of untreated TOT heart samples showed a 3.6-fold reduction of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), whereas Na+/Ca2+ exchanger (NCX) concentrations were increased 2.6-fold relative to nontransgenic samples. Propranolol treatment of TOT mice reversed the alterations in SERCA and NCX protein levels but not potassium channels. Although restoration of Ca2+ dynamics occurred within 2 wk of beta-blockade treatment, evidence of functional improvement in cardiac contractility assessed by echocardiography took 10 wk to materialize. These results demonstrate that beta-adrenergic blockade restores Ca2+ dynamics and normalizes expression of Ca2+-handling proteins, eventually leading to improved hemodynamic function in cardiomyopathic hearts.