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Biology subjects

Lachowski, D.

Publications and source records attributed to Lachowski, D..

2 recordsLinked to original sources

High-fidelity bioimage restoration via adversarial learning

Live-cell microscopy restoration is constrained by a trade-off between inference latency and texture preservation. While diffusion models provide high textural fidelity, the computational cost of iterative sampling currently limits their use in low-latency instrument feedback loops. Here, we present NAFNet GAN, a restoration framework that couples an activation-free backbone with a perceptual adversarial objective to enable high-throughput analysis. Unlike diffusion architectures, NAFNet GAN achieves an inference latency of[~] 110 ms for 1024 x 1024 inputs, potentially suitable for real-time instrument feedback loops. Across eight datasets ranging from STED nanoscopy to histopathology, the method achieves the lowest Learned Perceptual Image Patch Similarity (LPIPS) scores in 7 of 8 benchmarks while preserving structural coherence (e.g., MS-SSIM > 0.968 in Cryo-EM), which facilitates reliable downstream analysis. Supported by performance benchmarks in the AI4Life Denoising Challenge, NAFNet GAN restores structural features from low-photon-budget acquisitions, maintaining the temporal resolution required for dynamic live-cell workflows.

bioengineering↗

Retinoid acid receptor β mechanically regulates the activity of pancreatic cancer cells

Pancreatic ductal adenocarcinoma (PDAC) is the most common and lethal form of pancreatic cancer, characterised by stromal remodelling, elevated matrix stiffness and high metastatic rate. Retinoids, compounds derived from vitamin A, have a history of clinical use in cancer for their anti-proliferative and differentiation effects, and more recently have been explored as anti-stromal therapies in PDAC for their ability to induce mechanical quiescence in cancer associated fibroblasts. Here we demonstrate that retinoic acid receptor {beta} (RAR-{beta}) transcriptionally represses myosin light chain 2 (MLC-2) expression, a key regulatory component of the contractile actomyosin machinery. In turn, MLC-2 downregulation results in decreased cytoskeletal stiffness and traction force generation, impaired response to mechanical stimuli via mechanosensing and reduced ability to invade through the basement membrane.

bioengineering↗