Federated Pseudo Modality Generation for Incomplete Multi-Modal MRI Reconstruction

While multi-modal learning has been widely used for MRI reconstruction, it relies on paired multi-modal data which is difficult to acquire in real clinical scenarios. Especially in the federated setting, the common situation is that several medical institutions only have single-modal data, termed the modality missing issue. Therefore, it is infeasible to deploy a standard federated learning framework in such conditions. In this paper, we propose a novel communication-efficient federated learning framework, namely Fed-PMG, to address the missing modality challenge in federated multi-modal MRI reconstruction. Specifically, we utilize a pseudo modality generation mechanism to recover the missing modality for each single-modal client by sharing the distribution information of the amplitude spectrum in frequency space. However, the step of sharing the original amplitude spectrum leads to heavy communication costs. To reduce the communication cost, we introduce a clustering scheme to project the set of amplitude spectrum into finite cluster centroids, and share them among the clients. With such an elaborate design, our approach can effectively complete the missing modality within an acceptable communication cost. Extensive experiments demonstrate that our proposed method can attain similar performance with the ideal scenario, i.e., all clients have the full set of modalities. The source code will be released.Comment: 10 pages, 5 figures

Medical treatment and long-term outcome of chronic atrial fibrillation in the aged with chest distress: a retrospective analysis versus sinus rhythm

Although “chest distress” is the most frequent complication in the aged with chronic atrial frbrillation (AF) in clinical practice, there are few data on the association between chronic AF and coronary artery disease (CAD) in the aged in terms of medical treatment and long-term outcome. We assessed coronary artery lesions in such patients and evaluated the efficacy of medical treatment in long-term follow-ups. Of 315 elderly patients (mean age: 77.39 ± 6.33 years) who had undergone coronary angiography for chest distress, 297 exhibited sinus rhythm (SR), whereas 18 patients exhibited chronic AF. Patients with AF were followed for 4.22 ± 2.21 years. Average diastolic blood pressure (DBP) of AF patients was observed to be markedly less than that of patients with SR (57.33 ± 6.87 mmHg vs 71.08 ± 10.54 mmHg, t-test: P < 0.01). Compared with SR patients, severe stenosis of the coronary artery in AF patients was reduced (73.06% vs 44.44%, Chi-square test: P < 0.01). AF patients with chest distress had high CHADS2 score (3.72 ± 1.27), but only 33.3% patients received oral anticoagulants, and such patients had a significantly lower rate of revascularization (21.43% vs 55.63%, Chi-square test: P < 0.01), and higher rate of all-cause death (22.22% vs 4.38%, Chi-square test: P < 0.01) and thromboembolism (16.67% vs 1.68%, Chi-square test: P < 0.01) in the long-term follow-ups compared with SR patients. Chest distress in the aged with AF was related to insufficient coronary blood supply that was primarily due to a reduced DBP rather than to occult CAD. Adequate and safe medical therapy was difficult to achieve in these patients. Such patients typically have a poor prognosis, and optimal therapeutic strategies to treat them are urgently needed

Dystrophin Is a Tumor Suppressor in Human Cancers with Myogenic Programs

Many common human mesenchymal tumors, including gastrointestinal stromal tumor (GIST), rhabdomyosarcoma (RMS), and leiomyosarcoma (LMS), feature myogenic differentiation1–3. Here we report that intragenic deletion of the dystrophin-encoding and muscular dystrophy-associated DMD gene is a frequent mechanism by which myogenic tumors progress to high-grade, lethal sarcomas. Dystrophin is expressed in nonneoplastic and benign counterparts for GIST, RMS and LMS, and the DMD deletions inactivate larger dystrophin isoforms, including 427kDa dystrophin, while preserving expression of an essential 71kDa isoform. Dystrophin inhibits myogenic sarcoma cell migration, invasion, anchorage independence, and invadopodia formation, and dystrophin inactivation was found in 96%, 100%, and 62% of metastatic GIST, embryonal RMS, and LMS, respectively. These findings validate dystrophin as a tumor suppressor and likely anti-metastatic factor, suggesting that therapies in development for muscular dystrophies may also have relevance in treatment of cancer

Carbon Emission Reduction Effect of China’s Financial Decentralization

Due to a lack of focus on China’s financial decentralization system, the existing research does not pay attention to the beneficial contribution of Chinese local governments to carbon emission reduction through their actions in the financial field. In this study, we collected 16 years of data from 30 provinces in China and utilized a two-way fixed-effects model to empirically test the impact of China’s financial decentralization on carbon emission reduction. The regression results show that China’s financial decentralization system has a significant carbon-emission reduction effect. A heterogeneity analysis shows that this effect is common in different regions of China and that fiscal decentralization will negatively moderate it. A mechanism analysis shows that under China’s financial decentralization system, the active intervention of local governments in local finance will significantly upgrade the energy consumption structure and ease the financing constraints of enterprises. The regression results of the spatial econometric model show that the carbon emission reduction effect of China’s financial decentralization still has a spatial spillover effect. Finally, we put forward corresponding policy recommendations