Several machine-learning algorithms have been proposed for remote sensing image classification during the past two decades. Among these machine learning algorithms, Random Forest (RF) and Support Vector Machines (SVM) have drawn attention to image classification in several remote sensing applications. This paper reviews RF and SVM concepts relevant to remote sensing image classification and applies a meta-analysis of 251 peer-reviewed journal papers. A database with more than 40 quantitative and qualitative fields was constructed from these reviewed papers. The meta-analysis mainly focuses on: (1) the analysis regarding the general characteristics of the studies, such as geographical distribution, frequency of the papers considering time, journals, application domains, and remote sensing software packages used in the case studies, and (2) a comparative analysis regarding the performances of RF and SVM classification against various parameters, such as data type, RS applications, spatial resolution, and the number of extracted features in the feature engineering step. The challenges, recommendations, and potential directions for future research are also discussed in detail. Moreover, a summary of the results is provided to aid researchers to customize their efforts in order to achieve the most accurate results based on their thematic applications.

Objectives To determine whether Gal-3 mediates sustained atrial fibrillation (AF)-induced atrial structural and electrical remodeling and contributes to AF perpetuation. Background Galectin-3 (Gal-3) mediates extracellular matrix remodeling in heart failure, but its role in AF progression remains unexplored. Methods We examined intracardiac blood samples from patients with AF (N=55) to identify potential biomarkers of AF recurrence. In a sheep model of tachypacing-induced AF (N=20), we tested the effects of Gal-3 inhibition during AF progression. Results In patients, intracardiac serum Gal-3 levels were greater in persistent than paroxysmal AF and independently predicted atrial tachyarrhythmia recurrences after a single ablation procedure. In the sheep model, both Gal-3 and TGF-β1 were elevated in the atria of persistent AF animals. The Gal-3 inhibitor GM-CT-01 (GMCT) reduced both Gal-3 and TGF-β1-induced sheep atrial fibroblast migration and proliferation in vitro. GMCT (12 mg/kg twice/week) prevented the increase in serum procollagen type III N-terminal peptide seen during progression to persistent AF, and also mitigated atrial dilatation, myocyte hypertrophy, fibrosis, and the expected increase in dominant frequency of excitation. Atria of GMCT-treated animals had significantly less TGF-β1-Smad2/3 signaling pathway activation and expression of α-smooth muscle actin and collagen than saline-treated animals. Ex-vivo hearts from GMCT-treated animals had significantly longer action potential durations and fewer rotors and wavebreaks during AF, and myocytes had lower functional expression of inward rectifier K+ channel (Kir2.3) than saline-treated animals. Importantly, GMCT increased the probability of spontaneous AF termination, decreased AF inducibility and reduced overall AF burden. Conclusions Inhibiting Gal-3 during AF progression might be useful as an adjuvant treatment to improve outcomes of catheter ablation for persistent AF. Gal-3 inhibition may be a potential new upstream therapy for prevention of AF progression.

Implantable cardioverter-defibrillator therapy for the primary prevention of sudden cardiac death in women does not reduce all-cause mortality. Further studies are needed to investigate the reasons for this ob servation and to define the population of women who may benefit most from implantable cardioverter-defibrillator therapy.

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The mechanism by which the healthy heart and brain die rapidly in the absence of oxygen is not well understood. We performed continuous electrocardiography and electroencephalography in rats undergoing experimental asphyxia and analyzed cortical release of core neurotransmitters, changes in brain and heart electrical activity, and brain-heart connectivity. Asphyxia stimulates a robust and sustained increase of functional and effective cortical connectivity, an immediate increase in cortical release of a large set of neurotransmitters, and a delayed activation of corticocardiac functional and effective connectivity that persists until the onset of ventricular fibrillation. Blocking the brain's autonomic outflow significantly delayed terminal ventricular fibrillation and lengthened the duration of detectable cortical activities despite the continued absence of oxygen. These results demonstrate that asphyxia activates a brainstorm, which accelerates premature death of the heart and the brain.asphyxic cardiac arrest | autonomic nervous system | coherence | directed connectivity | near-death experience

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