PINNsFormer: A Transformer-Based Framework For Physics-Informed Neural Networks

Physics-Informed Neural Networks (PINNs) have emerged as a promising deep learning framework for approximating numerical solutions for partial differential equations (PDEs). While conventional PINNs and most related studies adopt fully-connected multilayer perceptrons (MLP) as the backbone structure, they have neglected the temporal relations in PDEs and failed to approximate the true solution. In this paper, we propose a novel Transformer-based framework, namely PINNsFormer, that accurately approximates PDEs' solutions by capturing the temporal dependencies with multi-head attention mechanisms in Transformer-based models. Instead of approximating point predictions, PINNsFormer adapts input vectors to pseudo sequences and point-wise PINNs loss to a sequential PINNs loss. In addition, PINNsFormer is equipped with a novel activation function, namely Wavelet, which anticipates the Fourier decomposition through deep neural networks. We empirically demonstrate PINNsFormer's ability to capture the PDE solutions for various scenarios, in which conventional PINNs have failed to learn. We also show that PINNsFormer achieves superior approximation accuracy on such problems than conventional PINNs with non-sensitive hyperparameters, in trade of marginal computational and memory costs, with extensive experiments.Comment: 15 pages (including 9 pages of main text, 3 pages of references, and 3 pages of appendix), 4 figures, 5 table

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field