LFS-GAN: Lifelong Few-Shot Image Generation

We address a challenging lifelong few-shot image generation task for the first time. In this situation, a generative model learns a sequence of tasks using only a few samples per task. Consequently, the learned model encounters both catastrophic forgetting and overfitting problems at a time. Existing studies on lifelong GANs have proposed modulation-based methods to prevent catastrophic forgetting. However, they require considerable additional parameters and cannot generate high-fidelity and diverse images from limited data. On the other hand, the existing few-shot GANs suffer from severe catastrophic forgetting when learning multiple tasks. To alleviate these issues, we propose a framework called Lifelong Few-Shot GAN (LFS-GAN) that can generate high-quality and diverse images in lifelong few-shot image generation task. Our proposed framework learns each task using an efficient task-specific modulator - Learnable Factorized Tensor (LeFT). LeFT is rank-constrained and has a rich representation ability due to its unique reconstruction technique. Furthermore, we propose a novel mode seeking loss to improve the diversity of our model in low-data circumstances. Extensive experiments demonstrate that the proposed LFS-GAN can generate high-fidelity and diverse images without any forgetting and mode collapse in various domains, achieving state-of-the-art in lifelong few-shot image generation task. Surprisingly, we find that our LFS-GAN even outperforms the existing few-shot GANs in the few-shot image generation task. The code is available at Github.Comment: 20 pages, 19 figures, 14 tables, ICCV 2023 Poste

Reliable Multivalued Conductance States in TaOx, Memristors through Oxygen Plasma-Assisted Electrode Deposition with in Situ-Biased Conductance State Transmission Electron Microscopy Analysis

Transition metal oxide-based memristors have widely been proposed for applications toward artificial synapses. In general, memristors have two or more electrically switchable stable resistance states that device researchers see as an analogue to the ion channels found in biological synapses. The mechanism behind resistive switching in metal oxides has been divided into electrochemical metallization models and valence change models. The stability of the resistance states in the memristor vary widely depending on: oxide material, electrode material, deposition conditions, film thickness, and programming conditions. So far, it has been extremely challenging to obtain reliable memristors with more than two stable multivalued states along with endurances greater than similar to 1000 cycles for each of those states. Using an oxygen plasma-assisted sputter deposition method of noble metal electrodes, we found that the metal-oxide interface could be deposited with substantially lower interface roughness observable at the nanometer scale. This markedly improved device reliability and function, allowing for a demonstration of memristors with four completely distinct levels from similar to 6 x 10(-6) to similar to 4 x 10(-8) S that were tested up to 10(4) cycles per level. Furthermore through a unique in situ transmission electron microscopy study, we were able to verify a redox reaction-type model to be dominant in our samples, leading to the higher degree of electrical state controllability. For solid-state synapse applications, the improvements to electrical properties will lead to simple device structures, with an overall power and area reduction of at least 1000 times when compared to SRAM.11Ysciescopu

Homeobox gene Dlx-2 is implicated in metabolic stress-induced necrosis

<p>Abstract</p> <p>Background</p> <p>In contrast to tumor-suppressive apoptosis and autophagic cell death, necrosis promotes tumor progression by releasing the pro-inflammatory and tumor-promoting cytokine high mobility group box 1 (HMGB1), and its presence in tumor patients is associated with poor prognosis. Thus, necrosis has important clinical implications in tumor development; however, its molecular mechanism remains poorly understood.</p> <p>Results</p> <p>In the present study, we show that Distal-less 2 (Dlx-2), a homeobox gene of the Dlx family that is involved in embryonic development, is induced in cancer cell lines dependently of reactive oxygen species (ROS) in response to glucose deprivation (GD), one of the metabolic stresses occurring in solid tumors. Increased Dlx-2 expression was also detected in the inner regions, which experience metabolic stress, of human tumors and of a multicellular tumor spheroid, an <it>in vitro </it>model of solid tumors. Dlx-2 short hairpin RNA (shRNA) inhibited metabolic stress-induced increase in propidium iodide-positive cell population and HMGB1 and lactate dehydrogenase (LDH) release, indicating the important role(s) of Dlx-2 in metabolic stress-induced necrosis. Dlx-2 shRNA appeared to exert its anti-necrotic effects by preventing metabolic stress-induced increases in mitochondrial ROS, which are responsible for triggering necrosis.</p> <p>Conclusions</p> <p>These results suggest that Dlx-2 may be involved in tumor progression via the regulation of metabolic stress-induced necrosis.</p

Controllable synthesis of molybdenum tungsten disulfide alloy for vertically composition-controlled multilayer

The effective synthesis of two-dimensional transition metal dichalcogenides alloy is essential for successful application in electronic and optical devices based on a tunable band gap. Here we show a synthesis process for Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;S&lt;inf&gt;2&lt;/inf&gt; alloy using sulfurization of super-cycle atomic layer deposition Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;O&lt;inf&gt;y&lt;/inf&gt;. Various spectroscopic and microscopic results indicate that the synthesized Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;S&lt;inf&gt;2&lt;/inf&gt; alloys have complete mixing of Mo and Watoms and tunable band gap by systematically controlled composition and layer number. Based on this, we synthesize a vertically composition-controlled (VCC) Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;S&lt;inf&gt;2&lt;/inf&gt; multilayer using five continuous super-cycles with different cycle ratios for each super-cycle. Angle-resolved X-ray photoemission spectroscopy, Raman and ultraviolet-visible spectrophotometer results reveal that a VCC Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;S&lt;inf&gt;2&lt;/inf&gt; multilayer has different vertical composition and broadband light absorption with strong interlayer coupling within a VCC Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;S&lt;inf&gt;2&lt;/inf&gt; multilayer. Further, we demonstrate that a VCC Mo&lt;inf&gt;1-x&lt;/inf&gt;W&lt;inf&gt;x&lt;/inf&gt;S&lt;inf&gt;2&lt;/inf&gt; multilayer photodetector generates three to four times greater photocurrent than MoS&lt;inf&gt;2&lt;/inf&gt;-and WS&lt;inf&gt;2&lt;/inf&gt;-based devices, owing to the broadband light absorption. &amp;#169; 2015 Macmillan Publishers Limitedopen1

Phase-dependent electrocatalytic nitrate reduction to ammonia on Janus Cu@Ni tandem catalyst

Electrosynthesis of NH3 from nitrate anion (NO3–) reduction (NO3–RR) is a cascade reaction, which is considered a great potential alternative to the Haber–Bosch route to reduce CO2 emissions and alleviate the adverse effects of excessive NO3– contamination in the environment. Frequently, solid solution alloys (SSAs) with a single-phase active site may struggle to fully utilize their benefits during the entire process of nitrate (NO3–) reduction, which involves multiple intermediate reactions. In this study, we showed that by separating Cu and Ni in a Janus Cu@Ni catalyst structure, we can achieve high performance in NO3–RR, yielding a high Faradaic efficiency (92.5%) and a production rate of NH3 (1127 mmol h–1 g–1) at −0.2 V versus RHE, compared to CuNi SSA (82.6%, 264 mmol h–1 g–1). Here, we demonstrate that a Janus Cu@Ni catalyst with short-range ordered catalytic sites favors the adsorption of NO through a bridge-bond mode. Simultaneously, a hydrogen spillover process was observed, in which Ni dissociates H2O to generate *H which spontaneously migrates to adjacent catalytic sites to hydrogenate the *NOx intermediates. This facilitates N–O bond cleavage, resulting in the NH3 production rate nearly 5 times higher than that of CuNi SSA, where NO was linearly bonded on its surface. The study of this catalytic effect, a cooperative tandem enhancement, provides insights into the design of multifunctional heterogeneous catalysts for electrochemical NH3 synthesis

Evaluation of the Chemical Characteristics and Predictive Model of Water-Soluble Inorganic Ions for Fine Particulate Matter Generated in Pohang

Objectives This study aims to contribute to establishing the regional effective management of fine particulate matter by evaluating the chemical characteristics and contribution of fine particulate matter, and the accuracy of predictive model of fine particulate matter through the measurement of water-soluble inorganic ions (WSIIs) and electrical conductivity for fine particulate matter generated in Pohang. Methods PM10 and PM2.5 samples were simultaneously collected using a low volume air sampler from April to November 2022. For sample analysis, cations of Ca2+, Mg2+, K+, NH4+, Na+ and anions of Cl-, NO3-, SO42-, and electrical conductivity were measured after pretreatment by ultrasonic extraction. Results and Discussion The average concentrations of WSIIs for PM10 and PM2.5 in Pohang were 12.1μg/m3 and 8.5μg/m3, respectively, accounting for 35.5% and 50.0% of each fine particulate matter. The sum of NH4+, NO3-, SO42- concentration was found to account for the majority of 71% and 78% of WSIIs in PM10 and PM2.5, respectively. The PM2.5/PM10 ratios for NH4+, K+, and SO42- were 95%, 89%, and 81%, respectively, mostly present in PM2.5. The average ratio of PM2.5/PM10 for NO3- was 54%, but it rose sharply to 79% in November when the temperature was low, indicating an increase in contribution to the generation of PM2.5 in winter. During the sampling period excluding April and July, the ion balance for cations and anions was relatively good at a 1:1 ratio and showed chemical properties of fine particulate matter close to neutral. A regression model was evaluated for the measured electrical conductivity of WSIIs and the concentration of fine particulate matter. The MAE and RMSE values for PM2.5 were 1.8μg/m3 and 2.4μg/m3, respectively, which were lower than PM10 (MAE 7.5 μg/m3, RMSE 10.3μg/m3), indicating high precision and accuracy. Conclusion This study confirmed the origin of fine particulate matter generated in Pohang through WSIIs analysis, and suggested that the measured electrical conductivity of WSIIs could be used as a key parameter for measuring the concentration of fine particulate matter

Regulation of Tumor Progression by Programmed Necrosis

Rapidly growing malignant tumors frequently encounter hypoxia and nutrient (e.g., glucose) deprivation, which occurs because of insufficient blood supply. This results in necrotic cell death in the core region of solid tumors. Necrotic cells release their cellular cytoplasmic contents into the extracellular space, such as high mobility group box 1 (HMGB1), which is a nonhistone nuclear protein, but acts as a proinflammatory and tumor-promoting cytokine when released by necrotic cells. These released molecules recruit immune and inflammatory cells, which exert tumor-promoting activity by inducing angiogenesis, proliferation, and invasion. Development of a necrotic core in cancer patients is also associated with poor prognosis. Conventionally, necrosis has been thought of as an unregulated process, unlike programmed cell death processes like apoptosis and autophagy. Recently, necrosis has been recognized as a programmed cell death, encompassing processes such as oncosis, necroptosis, and others. Metabolic stress-induced necrosis and its regulatory mechanisms have been poorly investigated until recently. Snail and Dlx-2, EMT-inducing transcription factors, are responsible for metabolic stress-induced necrosis in tumors. Snail and Dlx-2 contribute to tumor progression by promoting necrosis and inducing EMT and oncogenic metabolism. Oncogenic metabolism has been shown to play a role(s) in initiating necrosis. Here, we discuss the molecular mechanisms underlying metabolic stress-induced programmed necrosis that promote tumor progression and aggressiveness

Mesenchymal Stem Cells Transfer Mitochondria to the Cells with Virtually No Mitochondrial Function but Not with Pathogenic mtDNA Mutations

It has been reported that human mesenchymal stem cells (MSCs) can transfer mitochondria to the cells with severely compromised mitochondrial function. We tested whether the reported intercellular mitochondrial transfer could be replicated in different types of cells or under different experimental conditions, and tried to elucidate possible mechanism. Using biochemical selection methods, we found exponentially growing cells in restrictive media (uridine− and bromodeoxyuridine [BrdU]+) during the coculture of MSCs (uridine-independent and BrdU-sensitive) and 143B-derived cells with severe mitochondrial dysfunction induced by either long-term ethidium bromide treatment or short-term rhodamine 6G (R6G) treatment (uridine-dependent but BrdU-resistant). The exponentially growing cells had nuclear DNA fingerprint patterns identical to 143B, and a sequence of mitochondrial DNA (mtDNA) identical to the MSCs. Since R6G causes rapid and irreversible damage to mitochondria without the removal of mtDNA, the mitochondrial function appears to be restored through a direct transfer of mitochondria rather than mtDNA alone. Conditioned media, which were prepared by treating mtDNA-less 143B ρ0 cells under uridine-free condition, induced increased chemotaxis in MSC, which was also supported by transcriptome analysis. Cytochalasin B, an inhibitor of chemotaxis and cytoskeletal assembly, blocked mitochondrial transfer phenomenon in the above condition. However, we could not find any evidence of mitochondrial transfer to the cells harboring human pathogenic mtDNA mutations (A3243G mutation or 4,977 bp deletion). Thus, the mitochondrial transfer is limited to the condition of a near total absence of mitochondrial function. Elucidation of the mechanism of mitochondrial transfer will help us create a potential cell therapy-based mitochondrial restoration or mitochondrial gene therapy for human diseases caused by mitochondrial dysfunction

Combined inhibition of Bcl-2 family members and YAP induces synthetic lethality in metastatic gastric cancer with RASA1 and NF2 deficiency

Background Targetable molecular drivers of gastric cancer (GC) metastasis remain largely unidentified, leading to limited targeted therapy options for advanced GC. We aimed to identify molecular drivers for metastasis and devise corresponding therapeutic strategies. Methods We performed an unbiased in vivo genome-wide CRISPR/Cas9 knockout (KO) screening in peritoneal dissemination using genetically engineered GC mouse models. Candidate genes were validated through in vivo transplantation assays using KO cells. We analyzed target expression patterns in GC clinical samples using immunohistochemistry. The functional contributions of target genes were studied through knockdown, KO, and overexpression approaches in tumorsphere and organoid assays. Small chemical inhibitors against Bcl-2 members and YAP were tested in vitro and in vivo. Results We identified Nf2 and Rasa1 as metastasis-suppressing genes through the screening. Clinically, RASA1 mutations along with low NF2 expression define a distinct molecular subtype of metastatic GC exhibiting aggressive traits. NF2 and RASA1 deficiency increased in vivo metastasis and in vitro tumorsphere formation by synergistically amplifying Wnt and YAP signaling in cancer stem cells (CSCs). NF2 deficiency enhanced Bcl-2-mediated Wnt signaling, conferring resistance to YAP inhibition in CSCs. This resistance was counteracted via synthetic lethality achieved by simultaneous inhibition of YAP and Bcl-2. RASA1 deficiency amplified the Wnt pathway via Bcl-xL, contributing to cancer stemness. RASA1 mutation created vulnerability to Bcl-xL inhibition, but the additional NF2 deletion conferred resistance to Bcl-xL inhibition due to YAP activation. The combined inhibition of Bcl-xL and YAP synergistically suppressed cancer stemness and in vivo metastasis in RASA1 and NF2 co-deficiency. Conclusion Our research unveils the intricate interplay between YAP and Bcl-2 family members, which can lead to synthetic lethality, offering a potential strategy to overcome drug resistance. Importantly, our findings support a personalized medicine approach where combined therapy targeting YAP and Bcl-2, tailored to NF2 and RASA1 status, could effectively manage metastatic GC.This research was supported by grants of the National Research Foundation (NRF) funded by the Korean government (NRF-RS-2023–00208984, NRF-2021M3H9A1030260, NRF-2021R1F1A1051220, NRF-2016M3A9D5A01952416)