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Background: Recent advances in deep learning have sparked new research interests in dynamic magnetic resonance imaging (MRI) reconstruction. However, existing deep learning‐based approaches suffer from insufficient reconstruction efficiency and accuracy due to the lack of time correlation modeling during the reconstruction procedure. Purpose: Inappropriate tensor processing steps and deep learning models may lead to not only a lack of modeling in the time dimension but also an increase in the overall size of the network. Therefore, this study aims to find suitable tensor processing methods and deep learning models to achieve better reconstruction results and a smaller network size. Methods: We propose a novel unrolling network method that enhances the reconstruction quality and reduces the parameter redundancy by introducing time correlation modeling into MRI reconstruction with low‐rank core matrix and convolutional long short‐term memory (ConvLSTM) unit. Results: We conduct extensive experiments on AMRG Cardiac MRI dataset to evaluate our proposed approach. The results demonstrate that compared to other state‐of‐the‐art approaches, our approach achieves higher peak signal‐to‐noise ratios and structural similarity indices at different accelerator factors with significantly fewer parameters. Conclusions: The improved reconstruction performance demonstrates that our proposed time correlation modeling is simple and effective for accelerating MRI reconstruction. We hope our approach can serve as a reference for future research in dynamic MRI reconstruction. [ABSTRACT FROM AUTHOR]

Objective: The objective of this study was to investigate the cumulative fraction of response of various dosage regimens of tedizolid phosphate against Staphylococcus aureus and Streptococcus pneumoniae in children, adolescents, and adults. Methods: Monte Carlo simulations were performed using previously published pharmacokinetic parameters and pharmacodynamic data to evaluate the efficacy of the simulated dosage strategies in terms of area under the concentration-time curve/minimum inhibitory concentration targets of tedizolid. Results: According to the results of the Monte Carlo simulations, currently approved dosage regimens of tedizolid phosphate were effective in the treatment of acute bacterial skin and skin structure infections (ABSSSIs) caused by methicillin-susceptible S. aureus and methicillin-resistant S. aureus (MRSA) including vancomycin-intermediate, heterogeneous vancomycin-intermediate, and daptomycin-non-susceptible MRSA in adult and paediatric patients aged 12 y and older. High-dose regimens of tedizolid phosphate should be the preferred option to optimize efficacy against ABSSSIs caused by linezolid-resistant MRSA, particularly chloramphenicol-florfenicol resistance-mediated isolates. The dosage regimens of 3 and 4 mg/kg/d of tedizolid phosphate were appropriate to treat ABSSSIs caused by methicillin-susceptible S. aureus and MRSA in children aged 2–6 and 6–12 y, respectively. Approved dosage regimens of tedizolid phosphate for patients older than 12 y may be sufficient against S. pneumoniae pneumonia but insufficient for S. aureus pneumonia. For neutropenic patients, almost all the simulated regimens of tedizolid phosphate were ineffective against S. aureus and S. pneumoniae. Conclusions: These pharmacokinetics/pharmacodynamics-based simulations rationalize and optimize the dosage regimens of tedizolid phosphate against S. aureus and S. pneumoniae in children, adolescents, and adults.

Cell death under stress conditions like hypoxia, involves multiple interconnected pathways. In this study, a stable dihydroorotate dehydrogenase (DHODH) knockdown human corneal epithelial cell line was established to explore the regulation of hypoxic cell death, which was mitigated by various cell death inhibitors, particularly by a lipid peroxyl radical scavenger liproxstatin-1 (Lip-1), suggesting that hypoxic cell death involves crosstalk of ferroptosis and PANoptosis. We discovered that both DHODH and Glutathione peroxidase 4 (GPX4) protected cells from hypoxic death by inhibiting lipid peroxidation, mitochondrial reactive oxygen species (ROS) and maintaining mitochondrial membrane potential. However, upregulation of DHODH suppressed GPX4 upstream, exhibiting a trade-off in the expression levels between DHODH and GPX4 under hypoxia, with DHODH exerting a more decisive impact on cell survival. DHODH knockdown under hypoxia did not significantly alter lipid peroxidation levels, demonstrating the balance between DHODH and GPX4 expression finely regulated cellular ferroptosis homeostasis. This study highlights the complex interplay between ferroptosis and PANoptosis in hypoxic cell death, particularly the dual role of DHODH in regulating both pathways. DHODH is not merely maintaining the quantity of mitochondria but is promoting the selection of mitochondria favorable to cell survival. These findings not only deepen our understanding of cell death but also suggest potential therapeutic strategies for diseases involving oxidative stress and mitochondrial dysfunction., Competing Interests: Declaration of interest This research was funded by the National Natural Science Foundation of China (No. 82171025, HTX; No. 82070934, MCZ). Selected artwork (mitochondria, proteins and arrows) shown in the graphical abstract were used from or adapted from pictures provided by Servier Medical Art (Servier; https://smart.servier.com/), licensed under a Creative Commons Attribution 4.0 Unported License., (Copyright © 2025 Elsevier Inc. All rights reserved.)