This study demonstrates that clinical MRI can provide accurate measurements of cartilage topography, thickness, contact areas and surface curvatures of the knee.

AimsAnecdotal observations suggest that sub-clinical electrophysiological manifestations of arrhythmogenic right ventricular cardiomyopathy (ARVC) develop before detectable structural changes ensue on cardiac imaging. To test this hypothesis, we investigated a murine model with conditional cardiac genetic deletion of one desmoplakin allele (DSP ±) and compared the findings to patients with non-diagnostic features of ARVC who carried mutations in desmoplakin.Methods and resultsMurine: the DSP (±) mice underwent electrophysiological, echocardiographic, and immunohistochemical studies. They had normal echocardiograms but delayed conduction and inducible ventricular tachycardia associated with mislocalization and reduced intercalated disc expression of Cx43. Sodium current density and myocardial histology were normal at 2 months of age. Human: ten patients with heterozygous mutations in DSP without overt structural heart disease (DSP+) and 12 controls with supraventricular tachycardia were studied by high-density electrophysiological mapping of the right ventricle. Using a standard S1–S2 protocol, restitution curves of local conduction and repolarization parameters were constructed. Significantly greater mean increases in delay were identified particularly in the outflow tract vs. controls (P< 0.01) coupled with more uniform wavefront progression. The odds of a segment with a maximal activation–repolarization interval restitution slope >1 was 99% higher (95% CI: 13%; 351%, P= 0.017) in DSP+ vs. controls. Immunostaining revealed Cx43 mislocalization and variable Na channel distribution.ConclusionDesmoplakin disease causes connexin mislocalization in the mouse and man preceding any overt histological abnormalities resulting in significant alterations in conduction–repolarization kinetics prior to morphological changes detectable on conventional cardiac imaging. Haploinsufficiency of desmoplakin is sufficient to cause significant Cx43 mislocalization. Changes in sodium current density and histological abnormalities may contribute to a worsening phenotype or disease but are not necessary to generate an arrhythmogenic substrate. This has important implications for the earlier diagnosis of ARVC and risk stratification.

A computerized detection system for the diagnosis of Schizophrenia (SZ) using a convolutional neural system is described in this study. Schizophrenia is an anomaly in the brain characterized by behavioral symptoms such as hallucinations and disorganized speech. Electroencephalograms (EEG) indicate brain disorders and are prominently used to study brain diseases. We collected EEG signals from 14 healthy subjects and 14 SZ patients and developed an eleven-layered convolutional neural network (CNN) model to analyze the signals. Conventional machine learning techniques are often laborious and subject to intra-observer variability. Deep learning algorithms that have the ability to automatically extract significant features and classify them are thus employed in this study. Features are extracted automatically at the convolution stage, with the most significant features extracted at the max-pooling stage, and the fully connected layer is utilized to classify the signals. The proposed model generated classification accuracies of 98.07% and 81.26% for non-subject based testing and subject based testing, respectively. The developed model can likely aid clinicians as a diagnostic tool to detect early stages of SZ.

Gap junction conductance and distribution is heterogeneous in different regions of reentrant circuits. Lateralization of Cx43 gap junctions in CCP of reentrant circuits is associated with normal transverse conductance between cell pairs. In contrast, absence of lateralization in OP is associated with reduced transverse conductance. Despite normal anisotropic ratio, conduction velocity in CCP region remains slower than normal. This suggests that the effects of Cx43 remodeling in the infarcted heart should be interpreted in conjunction with other types of remodeling occurring in the EBZ (i.e. sarcolemmal ion channels).

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