Weihua Zhang

This survey explores the transformative impact of foundation models (FMs) in artificial intelligence, focusing on their integration with federated learning (FL) in biomedical research. Foundation models such as ChatGPT, LLaMa, and CLIP, which are trained on vast datasets through methods including unsupervised pretraining, self-supervised learning, instructed fine-tuning, and reinforcement learning from human feedback, represent significant advancements in machine learning. These models, with their ability to generate coherent text and realistic images, are crucial for biomedical applications that require processing diverse data forms such as clinical reports, diagnostic images, and multimodal patient interactions. The incorporation of FL with these sophisticated models presents a promising strategy to harness their analytical power while safeguarding the privacy of sensitive medical data. This approach not only enhances the capabilities of FMs in medical diagnostics and personalized treatment but also addresses critical concerns about data privacy and security in healthcare. This survey reviews the current applications of FMs in federated settings, underscores the challenges, and identifies future research directions including scaling FMs, managing data diversity, and enhancing communication efficiency within FL frameworks. The objective is to encourage further research into the combined potential of FMs and FL, laying the groundwork for healthcare innovations.

1. Acute myocardial infarction (AMI) is strongly associated with atherosclerosis, and is responsible for significant morbidity and mortality worldwide. The pathogenic mechanisms that underlie atherosclerosis and AMI are undefined at present. The calcium-sensing receptor (CaSR) is a member of the superfamily of G-protein coupled receptors. It has been demonstrated previously that the expression of CaSR is increased in atherosclerotic cardiac tissue of rats. It has also been suggested that CaSR has a crucial role in cardiac ischaemia-reperfusion injury, apoptosis and hypertrophy. However, it remains to be determined whether an increase in the expression of CaSR influences the sensitivity of cardiomyocytes to AMI. 2. The present study used cultured ventricular cardiomyocytes from neonatal rats to investigate the effect of oxidized low-density lipoprotein (ox-LDL), ischaemia-reperfusion, GdCl(3) (an agonist of CaSR) and NPS-2390 (an antagonist of CaSR) on the expression of CaSR. The amount of apoptosis, alterations in the morphology of the cells, the intracellular calcium concentration ([Ca(2+)](i)) and components of critical mitochondrial pathways were also analysed. 3. Cardiomyocytes treated with ox-LDL showed upregulated expression of CaSR, cytochrome c (cyt-c), Bax and activated caspase 3 (17 kD) and downregulated expression of Bcl-2, as well as elevated [Ca(2+)](i) and apoptosis. Application of GdCl(3) augmented these effects, and NPS-2390 decreased the expression of CaSR and reduced apoptosis. 4. In conclusion, ox-LDL was found to increase the expression of CaSR in a manner that was dependent on time and dose. It also augmented apoptosis during simulated ischaemia-reperfusion in cultured ventricular cardiomyocytes from neonatal rats.

PURPOSE: Obesity is a worldwide metabolic disease and a critical risk factor for several chronic conditions. Obstructive sleep apnea (OSA) is an important complication of obesity. With the soaring morbidity of obesity, the prevalence of OSA has markedly increased. However, the underlying mechanism of the high relevance between obesity and OSA has not been elucidated. This study investigated the effects of obesity on the structure and function of the genioglossus to explore the possible mechanisms involved in OSA combined with obesity. METHODS: Six-week-old male C57BL/6J mice were fed high-fat diet (HFD, 60% energy) or normal diet (Control, 10% energy) for 16 weeks. The muscle fibre structure and electromyography (EMG) activity of genioglossus were measured. The ultrastructure and function of mitochondrial, oxidative damage and apoptosis in genioglossus were detected by transmission electron microscopy (TEM), qPCR, Western blotting, immunohistochemistry and TUNEL staining. We further studied the influence of palmitic acid (PA) on the proliferation and myogenic differentiation of C2C12 myoblasts, as well as mitochondrial function, oxidative stress, and apoptosis in C2C12 myotubes. RESULTS: Compared with the control, the number of muscle fibres was decreased, the fibre type was remarkably changed, and the EMG activity had declined in genioglossus. In addition, a HFD also reduced mitochondria quantity and function, induced excessive oxidative stress and increased apoptosis in genioglossus. In vitro, PA treatment significantly inhibited the proliferation and myogenic differentiation of C2C12 myoblasts. Moreover, PA decreased the mitochondrial membrane potential, upregulated mitochondrial reactive oxygen species (ROS) levels, and activated the mitochondrial-related apoptotic pathway in myotubes. CONCLUSION: Our findings suggest that a HFD caused genioglossus injury in obese mice. The mitochondrial dysfunction and the accompanying oxidative stress were involved in the genioglossus injury, which may provide potential therapeutic targets for OSA with obesity.