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

Comparative pathogenesis of type 1 (European genotype) and type 2 (North American genotype) porcine reproductive and respiratory syndrome virus in infected boar

Background : Porcine reproductive and respiratory syndrome virus (PRRSV) now has two main genotypes, genotype 1 (European) and genotype 2 (North American). There is a lack of data on the comparison of pathogenicity of the two genotypes in boars. The objectives of the present study were to evaluate the amount of PRRSV present in semen over time and compare the viral distribution and microscopic lesions of type 1 and type 2 PRRSV-infected boars. Methods : Twenty-four 8-month-old PRRSV-naïve Duroc boars were randomly allocated to 3 treatment groups. The boars in groups 1 (n = 9) and 2 (n = 9) were intranasally inoculated with type 1 or type 2 PRRSV, respectively. The boars in groups 1 (n = 6) served as negative controls. Semen and blood samples were collected up to 35 days post-inoculation (dpi), and necropsies were performed on 14, 21, and 35 dpi. Results : There were no significant differences in the genomic copy number of PRRSV, microscopic testicular lesion score, number of PRRSV-positive germ cells, or number of apoptotic cells between the type 1 and type 2 PRRSV-infected boars throughout the experiment. Histopathological changes were manifested by the desquamation of spermatocytes and the presence of multinucleated giant cells in seminiferous tubules of both type 1 and type 2 PRRSV-infected boars. The distribution of PRRSV-positive cells was focal; the virus was found in single germ cells or small clusters of germ cells, localized to the spermatogonia, spermatocytes, spermatids, and non-sperm cells in type 1 and type 2 PRRSV-infected boars. Conclusions : The results of this study demonstrated that two genotypes of PRRSV do not have significantly different virulence toward the male reproductive system of pigs.This research was supported by contract research funds of the Research Institute for Veterinary Science (RIVS) from the College of Veterinary Medicine and by Brain Korea 21 Program for Veterinary Science in the Republic of Korea.Peer Reviewe

Real-Time Detection of Nitric Oxide Release in Live Cells Utilizing Fluorinated Xerogel-Derived Nitric Oxide Sensor

Nitric oxide (NO) is an important signaling molecule that regulates a diverse range of physiological and cellular processes in many tissues. Therefore, the accurate detection of physiological NO concentration is crucial to the understanding of NO signaling and its biological role. There has been growing interest in the development of electrochemical sensors for direct and real-time monitoring of NO. As the direct electrooxidation of NO requires a relatively high working potential, further surface modification with permselective membranes is required to achieve the desired selectivity for NO via size exclusion or electrostatic repulsion. Here we reported a planar-type NO sensor with a fluorinated xerogel-derived gas permeable membrane for real-time detection of NO release in live cells. First, we evaluated the biocompatibility of xerogel-derived NO permeable membranes modified with fluorinated functional groups by growing RAW 264.7 macrophages on them. And we performed the AFM measurements to examine the morphology of RAW 264.7 macrophages on xerogel membrane. Finally, we successfully detected NO release in RAW 264.7 macrophages, using a planar-type xerogel-derived NO sensor. As a result, fluorinated xerogel-derived membrane could be utilized as both NO permeable and cell-adhesive membranes. Besides, planar-type xerogel-based NO sensors can be easily applied to the cellular sensing system, with a simple coating procedure

Anti-malarial activity of 6-(8'Z-pentadecenyl)-salicylic acid from Viola websteri in mice

<p>Abstract</p> <p>Background</p> <p>Petroleum ether extracts of <it>Viola websteri </it>Hemsl (Violaceae) were reported to have anti-plasmodial activity against <it>Plasmodium falciparum in vitro</it>, with this activity being largely attributable to 6-(8'Z-pentadecenyl)-salicylic acid (6-SA).</p> <p>Methods</p> <p>The schizontocidal activity of 6-SA on early <it>Plasmodium berghei </it>infections was evaluated in a four-day test. The possible 'repository' activity of 6-SA was assessed using the method described by Peters. The median lethal dose (LD₅₀) of 6-SA, when given intraperitoneally, was also determined using uninfected ICR mice and the method of Lorke.</p> <p>Results</p> <p>In the present study, 6-SA was found to have anti-malarial activity <it>in vivo</it>, when tested against <it>P. berghei </it>in mice. 6-SA at 5, 10 and 25 mg/kg·day exhibited a significant blood schizontocidal activity in four-day early infections, repository evaluations and established infections with a significant mean survival time comparable to that of the standard drug, chloroquine (5 mg/kg·day).</p> <p>Conclusion</p> <p>6-SA possesses a moderate anti-malarial activity that could be exploited for malaria therapy.</p

Dysfunction of 67-kDa Laminin Receptor Disrupts BBB Integrity via Impaired Dystrophin/AQP4 Complex and p38 MAPK/VEGF Activation Following Status Epilepticus

Status epilepticus (SE, a prolonged seizure activity) impairs brain-blood barrier (BBB) integrity, which results in secondary complications following SE. The non-integrin 67-kDa laminin receptor (67-kDa LR) plays a role in cell adherence to laminin (a major glycoprotein component in basement membrane), and participates laminin-mediated signaling pathways including p38 mitogen-activated protein kinase (p38 MAPK). Thus, we investigated the role of 67-kDa LR in SE-induced vasogenic edema formation in the rat piriform cortex (PC). SE diminished 67-kDa LR expression, but increased laminin expression, in endothelial cells accompanied by the reduced SMI-71 (a rat BBB barrier marker) expression. Astroglial 67-kDa LR expression was also reduced in the PC due to massive astroglial loss. 67-kDa LR neutralization led to serum extravasation in the PC concomitant with the reduced SMI-71 expression. 67-kDa LR neutralization also decreased expressions of dystrophin and aquaporin-4 (AQP4). In addition, it increased p38 MAPK phosphorylation and expressions of vascular endothelial growth factor (VEGF), laminin and endothelial nitric oxide synthase (eNOS), which were abrogated by SB202190, a p38 MAPK inhibitor. Therefore, our findings indicate that 67-kDa LR dysfunction may disrupt dystrophin-AQP4 complex, which would evoke vasogenic edema formation and subsequent laminin over-expression via activating p38 MAPK/VEGF axis