EfficientViT: Lightweight Multi-Scale Attention for On-Device Semantic Segmentation

Semantic segmentation enables many appealing real-world applications, such as computational photography, autonomous driving, etc. However, the vast computational cost makes deploying state-of-the-art semantic segmentation models on edge devices with limited hardware resources difficult. This work presents EfficientViT, a new family of semantic segmentation models with a novel lightweight multi-scale attention for on-device semantic segmentation. Unlike prior semantic segmentation models that rely on heavy self-attention, hardware-inefficient large-kernel convolution, or complicated topology structure to obtain good performances, our lightweight multi-scale attention achieves a global receptive field and multi-scale learning (two critical features for semantic segmentation models) with only lightweight and hardware-efficient operations. As such, EfficientViT delivers remarkable performance gains over previous state-of-the-art semantic segmentation models across popular benchmark datasets with significant speedup on the mobile platform. Without performance loss on Cityscapes, our EfficientViT provides up to 15x and 9.3x mobile latency reduction over SegFormer and SegNeXt, respectively. Maintaining the same mobile latency, EfficientViT provides +7.4 mIoU gain on ADE20K over SegNeXt. Code: https://github.com/mit-han-lab/efficientvit.Comment: Tech repor

A tale of two estrogen receptors (ERs): how differential ER-estrogen responsive element interactions contribute to subtype-specific transcriptional responses

The interaction of ERα and ERβ with ERE constitutes the initial step in the canonical nuclear E2 signaling in which E2-ERβ is a weaker transactivator than E2-ERα. This perspective summarizes recent findings to discuss potential mechanisms that contribute to ER subtype-specific transcriptional responses

The potential contribution of miRNA-200-3p to the fatty acid metabolism by regulating AjEHHADH during aestivation in sea cucumber

The sea cucumber (Apostichopus japonicus) has become a good model organism for studying environmentally-induced aestivation by a marine invertebrate more recently. In the present study, we hypothesized that miRNA-200-3p may contribute to establish rapid biological control to regulate fatty acid meta

Metabolic response of longitudinal muscles to acute hypoxia in sea cucumber Apostichopus japonicus (Selenka): A metabolome integrated analysis

Hypoxia is a severe problem in aquatic environments worldwide and has caused mass mortality of sea cucumbers (& other species) for decades, seriously affecting the sustainable development of aquaculture. Investigations of the metabolic disruptions and biochemical responses associated with acute hypoxia stress in sea cucumbers can provide a theoretical basis and guidance for improving aquaculture. A metabolomics approach to characterize changes in the profiles of endogenous small molecules in response to acute hypoxia can help to identify the main underlying causes of metabolic damage and potentially suggest solutions to alleviate to improve viability. The current study uses liquid chromatography-mass spectrometry (LC-MS) and multivariate analysis methods to evaluate the metabolic profile of longitudinal muscles from A. japonicus exposed to acute hypoxia stress (by bubbling the aquaria water with nitrogen aeration to decrease dissolved oxygen to 2 mg/L in 2 min) for 6 or 24 h (experimental groups EG6 or EG24) and control group (CG, n = 10, respectively). The results showed that 29 and 62 metabolites were influenced significantly in EG6 and EG24, respectively, mainly including lipids, glycosides and their derivatives. Levels of most lipids (fatty acids, glycerolipids, glycerophospholipids, sphingolipids and sterols) were elevated in both experimental groups, and increased with elongation of hypoxia, implying that the homeostasis of synthesis and degradation of lipids and their derivatives was strongly affected by hypoxia stress. Pathway enrichment analysis was performed to further assess the importance of differential metabolite expression to the development of the A. japoni

Immunosuppressive Tumor Microenvironment and Immunotherapy of Epstein–Barr Virus-Associated Malignancies

The Epstein–Barr virus (EBV) can cause different types of cancer in human beings when the virus infects different cell types with various latent patterns. EBV shapes a distinct and immunosuppressive tumor microenvironment (TME) to its benefit by influencing and interacting with different components in the TME. Different EBV-associated malignancies adopt similar but slightly specific immunosuppressive mechanisms by encoding different EBV products to escape both innate and adaptive immune responses. Strategies reversing the immunosuppressive TME of EBV-associated malignancies have been under evaluation in clinical practice. As the interactions among EBV, tumor cells, and TME are intricate, in this review, we mainly discuss the epidemiology of EBV, the life cycle of EBV, the cellular and molecular composition of TME, and a landscape of different EBV-associated malignancies and immunotherapy by targeting the TME

Chromosome-level genome assembly of the northern Pacific seastar Asterias amurensis

Abstract Asterias amurensis has attracted widespread concern because of its population outbreaks, which has impacted fisheries and aquaculture, as well as disrupting local ecosystems. A high-quality reference genome is necessary to better investigate mechanisms of outbreak and adaptive changes. Combining PacBio HiFi and Hi-C sequencing data, we generated a chromosome-level A. amurensis genome with a size of 491.53 Mb. The contig N50 and scaffold N50 were 8.05 and 23.75 Mb, respectively. The result of BUSCO analysis revealed a completeness score of 98.85%. A total of 16,531 protein-coding genes were predicted in the genome, of which 94.63% were functionally annotated. The high-quality genome assembly resulting from this study will provide a valuable genetic resource for future research on the mechanism of population outbreaks and invasion ecology

Fractional amplitude of low-frequency fluctuations and functional connectivity in comatose patients subjected to resting-state functional magnetic resonance imaging

Objective: The objective of the study is to investigate the changes of fractional amplitude of low-frequency fluctuations (fALFFs) and functional connectivity (FC) in the brain function of comatose patients with resting-state blood-oxygenation-level-dependent functional magnetic resonance imaging (BOLD-fMRI) and to discuss the underlying neurophysiological mechanism of disease. Materials and Methods: Resting-state BOLD-fMRI scans were conducted on 20 comatose patients and 20 age-matched and gender-matched controls. The differences of fALFF between two groups were analyzed with two-sample t-test; significant differences of connectivity between groups were acquired to calculate the FC of the precuneus with other brain regions. Results: Compared to the control group, the comatose patients exhibited a significant reduction in fALFF in various areas, including the right cingulate gyrus, left precuneus, right inferior parietal lobule, right superior parietal lobule, bilateral anterior/posterior central gyrus, middle frontal gyrus, right superior frontal gyrus, right superior temporal gyrus, and the bilateral cerebellar hemispheres (P < 0.05, Alphasim correction). Compared with controls, the brain region FC correlated with the precuneus reduced mainly located in the bilateral inferior parietal lobule, posterior central gyrus, lenticular nucleus, left anterior central gyrus, left medial frontal gyrus, left anterior lobe of the cerebellum, right insula, right transverse temporal gyri, and right thalamus. Regions whose FC increased include the left superior frontal gyrus, left side of the callosum, left superior parietal lobule, and both sides of the cingulate (P < 0.05, Alphasim correction). Conclusion: Measurements of fALFF and FC obtained by resting-state BOLD-fMRI could provide considerable information for the analysis and evaluation of the brain function of comatose patients from the perspective of local function and global functional network and provide the theoretical basis for the study of coma nerve physiological mechanism

Single-Chain Estrogen Receptors (ERs) Reveal that the ERα/β Heterodimer Emulates Functions of the ERα Dimer in Genomic Estrogen Signaling Pathways

The effects of estrogens, particularly 17β-estradiol (E2), are mediated by estrogen receptor α (ERα) and ERβ. Upon binding to E2, ERs homo- and heterodimerize when coexpressed. The ER dimer then regulates the transcription of target genes through estrogen responsive element (ERE)-dependent and -independent pathways that constitute genomic estrogen signaling. Although ERα and ERβ have similar ERE and E2 binding properties, they display different transregulatory capacities in both ERE-dependent and -independent signaling pathways. It is therefore likely that the heterodimerization provides novel functions to ERs by combining distinct properties of the contributing partners. The elucidation of the role of the ER heterodimer is critical for the understanding of physiology and pathophysiology of E2 signaling. However, differentially determining target gene responses during cosynthesis of ER subtypes is difficult, since dimers formed are a heterogeneous population of homo- and heterodimers. To circumvent the pivotal dimerization step in ER action and hence produce a homogeneous ER heterodimer population, we utilized a genetic fusion strategy. We joined the cDNAs of ERα and/or ERβ to produce single-chain ERs to simulate the ER homo- and heterodimers. The fusion ERs interacted with ERE and E2 in a manner similar to that observed with the ER dimers. The homofusion receptors mimicked the functions of the parent ER dimers in the ERE-dependent and -independent pathways in transfected mammalian cells, whereas heterofusion receptors emulated the transregulatory properties of the ERα dimer. These results suggest that ERα is the functionally dominant partner in the ERα/β heterodimer

Preventing graft restenosis after coronary artery bypass grafting with tissue-type plasminogen activator

Abstract Objective To explore the feasibility and safety of using tissue-type plasminogen activator (t-PA) to prevent graft restenosis after coronary artery bypass grafting (CABG). Methods In this prospective observational study, 37 patients underwent CABG between June 2009 and May 2013. These patients were grouped according to the anti-coagulation strategy after surgery: t-PA (n = 12) and conventional treatments (n = 25). In the t-PA group, the patients received acetylsalicylic acid (ASA) and clopidogrel plus intravenous infusion of t-PA (0.25 mg/kg/day) starting at 24 h after surgery and that lasted for 3 days. In the conventional group, the patients received only ASA and clopidogrel. 64-row spiral computed tomographic coronary angiography was performed at 1 week, 1, and 3 months after surgery to evaluate the patency of the graft vessel. Results The mean stenosis severity of the saphenous vein grafts was lower in the t-PA group compared with the conventional group at 3 months after surgery (p  0.05). The patency rate of the grafts was not significantly different between the two groups at 1 week, 1, and 3 months after surgery (p > 0.05). Conclusion Early application of t-PA after CABG was feasible and safe, and might help prevent early restenosis of SV grafts. Additional clinical randomized trials are necessary to address this issue