Bone Age Assessment in Young Children Using Automatic Carpal Bone Feature Extraction and Support Vector Regression

Boundary extraction of carpal bone images is a critical operation of the automatic bone age assessment system, since the contrast between the bony structure and soft tissue are very poor. In this paper, we present an edge following technique for boundary extraction in carpal bone images and apply it to assess bone age in young children. Our proposed technique can detect the boundaries of carpal bones in X-ray images by using the information from the vector image model and the edge map. Feature analysis of the carpal bones can reveal the important information for bone age assessment. Five features for bone age assessment are calculated from the boundary extraction result of each carpal bone. All features are taken as input into the support vector regression (SVR) that assesses the bone age. We compare the SVR with the neural network regression (NNR). We use 180 images of carpal bone from a digital hand atlas to assess the bone age of young children from 0 to 6 years old. Leave-one-out cross validation is used for testing the efficiency of the techniques. The opinions of the skilled radiologists provided in the atlas are used as the ground truth in bone age assessment. The SVR is able to provide more accurate bone age assessment results than the NNR. The experimental results from SVR are very close to the bone age assessment by skilled radiologists.     

T-type calcium channel as a portal of iron uptake into cardiomyocytes of beta-thalassemic mice

Objectives: Iron‐overload condition can be found in β‐thalassemic patients with regular blood transfusion, leading to iron deposition in various organs including the heart. Elevated cardiac iron causes iron‐overload cardiomyopathy, a condition that provokes mortality because of heart failure in patients with thalassemia. Previous studies demonstrated that myocardial iron uptake may occur via L‐type calcium channels (LTCCs). However, direct evidence regarding the claimed pathway in thalassemic cardiomyocytes has never been investigated. Methods: Hearts from genetic‐altered β‐thalassemic mice and adult wild‐type mice were used for cultured ventricular cardiomyocytes. Blockers for LTCC, T‐type calcium channel (TTCC), transferrin receptor1 (TfR1), and divalent metal transporter1 (DMT1) were used, and quantification of cellular iron uptake under various iron loading conditions was performed by Calcein‐AM fluorescence assay. Microarray analysis was performed to investigate gene expressions in the hearts of these mice. Results: This study demonstrated that iron uptake under iron‐overload conditions in the cultured ventricular myocytes of thalassemic mice was greater than that of wild‐type cells (P < 0.01). TTCC blocker, efonidipine, and an iron chelator, deferoxamine, could prevent iron uptake into cultured cardiomyocytes, whereas blockers of TfR1, DMT1, and LTCC could not. Microarray analysis from thalassemic hearts demonstrated highly up‐regulated genes of TTCC, zinc transporter, and transferrin receptor2. Conclusions: Our findings indicated that iron uptake mechanisms in cultured thalassemic cardiomyocytes are mainly mediated by TTCC, suggesting that TTCC is the important pathway for iron uptake in this cultured thalassemic cardiomyocyte model.     

Delayed afterdepolarization inhibitor: a potential pharmacologic intervention to improve defibrillation efficacy

INTRODUCTION: Electrical and optical mapping studies of defibrillation have demonstrated that following shocks of strength near the defibrillation threshold (DFT), the first several postshock cycles always arise focally. No immediate postshock reentry was observed. Delayed afterdepolarizations (DADs) have been suggested as a possible cause of this rapid repetitive postshock activity. The aim of this study was to test the hypothesis that DFT is decreased by application of a DAD inhibitor. METHODS AND RESULTS: Six pigs (30-35 kg) were studied. First, control DFT was determined using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic, 6/4 msec) was delivered after 10 seconds of ventricular fibrillation (VF). Then, flunarizine (a DAD inhibitor) was injected intravenously (2 mg/kg bolus and 4 mg/kg/hour maintenance) and the DFT was again determined. A third DFT was determined 50 minutes after drug infusion was terminated to allow the drug to wash out. DFT after flunarizine application (520 +/- 90 V, 14 +/- 3 J) was significantly lower than control DFT (663 +/- 133 V, 23 +/- 4 J). After the drug washed out, DFT (653 +/- 107 V, 22 +/- 4 J) returned to the control DFT value (P = 0.6). Flunarizine reduced the DFT approximately 22% by leading-edge voltage and approximately 40% by energy. CONCLUSION: Flunarizine, a DAD inhibitor, significantly improved defibrillation efficacy. This finding suggests that DADs could be the source of the rapid repetitive focal activation cycles arising after failed near-DFT shocks before degeneration back into VF. Future studies are needed to investigate the cause of the earliest postshock activation and to determine if the DADs are responsible.     

Cardiac mortality is associated with low levels of omega-3 and omega-6 fatty acids in the heart of cadavers with a history of coronary heart disease

The benefits of omega-3 (ie, eicosapentaenoic acid and docosahexaenoic acid [DHA]) and omega-6 (ie, linoleic acid and arachidonic acid [AA]) fatty acids on reducing cardiac mortality are still debated. In this study, we tested the hypothesis that high levels of omega-3 and omega-6 fatty acids in heart tissues are associated with low cardiac mortality in Thai cadavers. One hundred fresh cadavers were examined in this study. The cause of death, history of coronary heart disease (CHD), and fish consumption habits were obtained from death certificates, cadaver medical record profiles, and a questionnaire to a person who lived with the subject before death. In each cadaver, biopsies of cardiac tissues were taken from the interventricular septum for measurement of fatty acid. Of the 100 cadavers (average age, 69 ± 13 years), 60 were men. The frequency of fish consumption was directly associated with omega-3 and omega-6 fatty acids in heart tissues (P < .01). History of CHD and cause of death (cardiac vs noncardiac) were not significantly associated with levels of omega-3 or omega-6 fatty acids. However, in cadavers with a history of CHD, high levels of omega-3 and omega-6, particularly DHA and AA, were associated with low cardiac mortality (P < .05). Fish consumption is associated with levels of omega-3 and omega-6 fatty acids in heart tissues. Although omega-3 and omega-6 fatty acids are not associated with cardiac mortality in the overall studied population, their low levels (especially DHA and AA) in heart tissues are associated with high cardiac mortality in cadavers with a history of CHD.     

Phosphodiesterase-3 inhibitor （cilostazol） attenuates oxidative stress-induced mitochondrial dysfunction in the heart

Background Cilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this beneficial effect is still unclear. Since cardiac mito-chondria have been shown to play a crucial role in fatal cardiac arrhythmias and that oxidative stress is one of the main contributors to arr-hythmia generation, we tested the effects of cilostazol on cardiac mitochondria under severe oxidative stress. Methods Mitochondria were isolated from rat hearts and treated with H2O2 to induce oxidative stress. Cilostazol, at various concentrations, was used to study its protective effects. Pharmacological interventions, including a mitochondrial permeability transition pore （mPTP） blocker, cyclosporine A （CsA）, and an inner membrane anion channel （IMAC） blocker, 4＇-chlorodiazepam （CDP）, were used to investigate the mechanistic role of cilostazol on cardiac mitochondria. Cardiac mitochondrial reactive oxygen species （ROS） production, mitochondrial membrane potential change and mi-tochondrial swelling were determined as indicators of cardiac mitochondrial function. Results Cilostazol preserved cardiac mitochondrial function when exposed to oxidative stress by preventing mitochondrial depolarization, mitochondrial swelling, and decreasing ROS produc-tion. Conclusions Our findings suggest that cardioprotective effects of cilostazol reported previously could be due to its prevention of car-diac mitochondrial dysfunction caused by severe oxidative stress.