Intelligent medicine is eager to automatically generate radiology reports to ease the tedious work of radiologists. Previous researches mainly focused on the text generation with encoder-decoder structure, while CNN networks for visual features ignored the long-range dependencies correlated with textual information. Besides, few studies exploit cross-modal mappings to promote radiology report generation. To alleviate the above problems, we propose a novel end-to-end radiology report generation model dubbed Self-Supervised dual-Stream Network (S3-Net). Specifically, a Dual-Stream Visual Feature Extractor (DSVFE) composed of ResNet and SwinTransformer is proposed to capture more abundant and effective visual features, where the former focuses on local response and the latter explores long-range dependencies. Then, we introduced the Fusion Alignment Module (FAM) to fuse the dual-stream visual features and facilitate alignment between visual features and text features. Furthermore, the Self-Supervised Learning with Mask(SSLM) is introduced to further enhance the visual feature representation ability. Experimental results on two mainstream radiology reporting datasets (IU X-ray and MIMIC-CXR) show that our proposed approach outperforms previous models in terms of language generation metrics.

The heterogeneity of functional cardiomyocytes arises during heart development, which is essential to the complex and highly coordinated cardiac physiological function. Yet the biological and physiological identities and the origin of the specialized cardiomyocyte populations have not been fully comprehended. Here we report a previously unrecognised population of cardiomyocytes expressing Dbhgene encoding dopamine beta-hydroxylase in murine heart. We determined how these myocytes are distributed across the heart by utilising advanced single-cell and spatial transcriptomic analyses, genetic fate mapping and molecular imaging with computational reconstruction. We demonstrated that they form the key functional components of the cardiac conduction system by using optogenetic electrophysiology and conditional cardiomyocyte Dbh gene deletion models. We revealed their close relationship with sympathetic innervation during cardiac conduction system formation. Our study thus provides new insights into the development and heterogeneity of the mammalian cardiac conduction system by revealing a new cardiomyocyte population with potential catecholaminergic endocrine function.

Recently some researches have focused on the Domain-Generalization (DG) Re-ID problem that training and testing are not in the same domain distribution. To fit the unseen complex scenes, recently deep feature matching-based methods for DG Re-ID have been developed and achieved the state-of-the-arts. However, they ignored some cases in which the accuracy of key region matching is unstable at a single scale, and the bad impact of style variations for feature representations. To address the issues, we propose a novel deep image matching model named Multi-scale Transformer-based Matching Network (MTMN) for DG Re-ID problem. MTMN matches two images with multi-scale local respondence instead of fixed representations. Specifically, the Transformer is carefully modified to formulate efficient local interactions between query and gallery images in multiple scales. Moreover, the style normalization is introduced to filter out identity-irrelated features to promote the matching results. Comprehensive experiments on several DG Re-ID tasks demonstrate the superiority of the proposed method compared with the state-of-the-arts, e.g., 5.4% and 2.6% gains in Rank-1 and mAP on Market-1501 $\rightarrow$ MSMT17(V1) task.

Robust, spontaneous pacemaker activity originating in the sinoatrial node (SAN) of the heart is essential for cardiovascular function. Anatomical, electrophysiological, and molecular methods as well as mathematical modeling approaches have quite thoroughly characterized the transmembrane fluxes of Na⁺, K⁺ and Ca²⁺ that produce SAN action potentials (AP) and ‘pacemaker depolarizations’ in a number of different in vitro adult mammalian heart preparations. Possible ionic mechanisms that are responsible for SAN primary pacemaker activity are described in terms of: (i) a Ca²⁺-regulated mechanism based on a requirement for phasic release of Ca²⁺ from intracellular stores and activation of an inward current-mediated by Na⁺/Ca²⁺ exchange; (ii) time- and voltage-dependent activation of Na⁺ or Ca²⁺ currents, as well as a cyclic nucleotide-activated current, I_f; and/or (iii) a combination of (i) and (ii). Electrophysiological studies of single spontaneously active SAN myocytes in both adult mouse and rabbit hearts consistently reveal significant expression of a rapidly activating time- and voltage-dependent K⁺ current, often denoted I_Kr, that is selectively expressed in the leading or primary pacemaker region of the adult mouse SAN. The main goal of the present study was to examine by combined experimental and simulation approaches the functional or physiological roles of this K⁺ current in the pacemaker activity. Our patch clamp data of mouse SAN myocytes on the effects of a pharmacological blocker, E4031, revealed that a rapidly activating K⁺ current is essential for action potential (AP) repolarization, and its deactivation during the pacemaker potential contributes a small but significant component to the pacemaker depolarization. Mathematical simulations using a murine SAN AP model confirm that well known biophysical properties of a delayed rectifier K⁺ current can contribute to its role in generating spontaneous myogenic activity.

A number of distinct electrophysiological mechanisms that modulate the myogenic spontaneous pacemaker activity in the sinoatrial node (SAN) of the mammalian heart have been investigated extensively. There is agreement that several (3 or 4) different transmembrane ionic current changes (referred to as the voltage clock) are involved; and that the resulting net current interacts with direct and indirect effects of changes in intracellular Ca²⁺ (the calcium clock). However, significant uncertainties, and important knowledge gaps, remain concerning the functional roles in SAN spontaneous pacing of many of the individual ion channel- or exchanger-mediated transmembrane current changes. We report results from patch clamp studies and mathematical modeling of the hyperpolarization-activated current, I_f, in the generation/modulation of the diastolic depolarization, or pacemaker potential, produced by individual myocytes that were enzymatically isolated from the adult mouse sinoatrial node (SAN). Amphotericin-mediated patch microelectrode recordings at 35 °C were made under control conditions and in the presence of 5 or 10 nM isoproterenol (ISO). These sets of results were complemented and integrated with mathematical modeling of the current changes that take place in the range of membrane potentials (−70 to −50 mV), which corresponds to the ‘pacemaker depolarization’ in the adult mouse SAN. Our results reveal a very small, but functionally important, approximately steady-state or time-independent current generated by residual activation of I_f channels that are expressed in these pacemaker myocytes. Recordings of the pacemaker depolarization and action potential, combined with measurements of changes in I_f, and the well-known increases in the L-type Ca²⁺ current, I_CaL, demonstrated that I_CaL activation, is essential for myogenic pacing. Moreover, after being enhanced (approximately 3-fold) by 5 or 10 nM ISO, I_CaL contributes significantly to the positive chronotropic effect. Our mathematical model has been developed in an attempt to better understand the underlying mechanisms for the pacemaker depolarization and action potential in adult mouse SAN myocytes. After being updated with our new experimental data describing I_f, our simulations reveal a novel functional component of I_f in adult mouse SAN. Computational work carried out with this model also confirms that in the presence of ISO the residual activation of I_f and opening of I_CaL channels combine to generate a net current change during the slow diastolic depolarization phase that is essential for the observed accelerated pacemaking rate of these SAN myocytes.