FAIR: Frequency-aware Image Restoration for Industrial Visual Anomaly Detection

Image reconstruction-based anomaly detection models are widely explored in industrial visual inspection. However, existing models usually suffer from the trade-off between normal reconstruction fidelity and abnormal reconstruction distinguishability, which damages the performance. In this paper, we find that the above trade-off can be better mitigated by leveraging the distinct frequency biases between normal and abnormal reconstruction errors. To this end, we propose Frequency-aware Image Restoration (FAIR), a novel self-supervised image restoration task that restores images from their high-frequency components. It enables precise reconstruction of normal patterns while mitigating unfavorable generalization to anomalies. Using only a simple vanilla UNet, FAIR achieves state-of-the-art performance with higher efficiency on various defect detection datasets. Code: https://github.com/liutongkun/FAIR.Comment: 12 pages, 10 figure

Tropical Cyclone Temperature Profiles and Cloud Macro-/Micro-Physical Properties Based on AIRS Data

We used the observations from Atmospheric Infrared Sounder (AIRS) onboard Aqua over the northwest Pacific Ocean from 2006–2015 to study the relationships between (i) tropical cyclone (TC) temperature structure and intensity and (ii) cloud macro-/micro-physical properties and TC intensity. TC intensity had a positive correlation with warm-core strength (correlation coefficient of 0.8556). The warm-core strength increased gradually from 1 K for tropical depression (TD) to >15 K for super typhoon (Super TY). The vertical areas affected by the warm core expanded as TC intensity increased. The positive correlation between TC intensity and warm-core height was slightly weaker. The warm-core heights for TD, tropical storm (TS), and severe tropical storm (STS) were concentrated between 300 and 500 hPa, while those for typhoon (TY), severe typhoon (STY), and Super TY varied from 200 to 350 hPa. Analyses of the cloud macro-/micro-physical properties showed that the top of TC cloud systems mainly consisted of ice clouds. For TCs of all intensities, areas near the TC center showed lower cloud-top pressures and lower cloud-top temperatures, more cloud fractions, and larger ice-cloud effective diameters. With the increase in TC intensity, the levels of ice clouds around the TC center became higher and the spiral cloud-rain bands became larger. When a TC developed into a TY, STY, or Super TY, the convection in the clouds was stronger, releasing more heat, thus forming a much warmer warm core

Can sulforaphane alter growth performance, innate immunity and antioxidant capability of common carp (Cyprinus carpio Huanghe var)?

Sulforaphane (SFN) is a plant extract with demonstrated immunity, anti-inflammatory and antioxidant properties. However, its research on aquatic animals is still lacking. Herein, this study aimed to investigate the effects of SFN on growth performance, innate immunity and antioxidant capability of common carp (Cyprinus carpio Huanghe var). Fish (76.17 ± 0.23 g) were fed diets supplemented with five levels (0, 5 mg kg−1, 10 mg kg−1,15 mg kg−1 and 20 mg kg−1) of SFN for 8 weeks. The results indicated that fish fed 10 mg kg−1 SFN showed higher weight gain rate (P < 0.05) than the control group and the group of 15 mg kg−1 SFN. Feed conversion ratio was significantly lower (P < 0.05) in fish fed 10 mg kg−1 SFN than the group of 15 mg kg−1 SFN. Plasma complement component 4 and interleukin-10 (IL-10) contents, acid phosphatase activity, and liver superoxide dismutase, glutathione peroxidase and catalase activities, glutathione content, and interleukin-1β, IL-10, tumor necrosis factor-α (TNF-α) and toll-like receptor 2 mRNA expressions all increased (P < 0.05) in response to dietary SFN levels from 0 to 10 mg kg−1, then decreased with further increasing SFN levels. Plasma TNF-α content increased (P < 0.05) in response to dietary SFN levels from 0 to 15 mg kg−1, then decreased with further increasing SFN levels. Plasma lysozyme and myeloperoxidase activities both increased (P < 0.05) in response to dietary SFN levels from 0 to 5 mg kg−1, then decreased with further increasing SFN levels. Liver malonaldehyde content was significantly lower (P < 0.05) in fish fed 10 mg kg−1 SFN than other groups except for the 5 mg kg−1 SFN. Overall, these findings suggested that dietary SFN could promote growth, enhance immunity and antioxidant capacity, and the best benefit was obtained in fish fed 10 mg kg−1. These results encouraged further research of SFN as feed additive in aquaculture and provided basic data for the future application of SFN in aquatic animals

Activated microglia induce bone marrow mesenchymal stem cells to produce glial cell-derived neurotrophic factor and protect neurons against oxygen-glucose deprivation injury

In this study, we investigated interactions among microglia (MG), bone marrow mesenchymal stem cells (BMSCs) and neurons in cerebral ischemia and the potential mechanisms using an in vitro oxygen-glucose deprivation (OGD) model. Rat BMSCs were incubated with conditioned medium (CM) from in vitro cultures of OGD-activated rat MG and murine BV2 MG cells. Effects of glial cell-derived neurotrophic factor (GDNF) on rat neuron viability, apoptosis, lactate dehydrogenase (LDH) leakage and mitochondrial membrane potential (MMP) were analyzed in this model. OGD-activated MG promoted GDNF production by BMSCs (P < 0.01). TNFα, but not IL6 or IL1β, promoted GDNF production by BMSCs (P < 0.001). GDNF or CM pre-treated BMSCs elevated neuronal viability and suppressed apoptosis (P < 0.05 or P < 0.01); these effects were inhibited by the RET antibody. GDNF activated MEK/ERK and PI3K/AKT signaling but not JNK/c-JUN. Furthermore, GDNF upregulated B cell lymphoma 2 (BCL2) and heat shock 60 kDa protein 1 (HSP60) levels, suppressed LDH leakage, and promoted MMP. Thus, activated MG produce TNFα to stimulate GDNF production by BMSCs, which prevents and repairs OGD-induced neuronal injury, possibly via regulating MEK/ERK and PI3K/AKT signaling. These findings will facilitate the prevention and treatment of neuronal injury by cerebral ischemia

responses of BV2 microglial cells through TSG-6

Mesenchymal stem cells inhibit lipopolysaccharide-induced inflammator

Bone Marrow-Derived Mesenchymal Stem Cells Maintain the Resting Phenotype of Microglia and Inhibit Microglial Activation

<div><p>Many studies have shown that microglia in the activated state may be neurotoxic. It has been proven that uncontrolled or over-activated microglia play an important role in many neurodegenerative disorders. Bone marrow-derived mesenchymal stem cells (BMSCs) have been shown in many animal models to have a therapeutic effect on neural damage. Such a therapeutic effect is attributed to the fact that BMSCs have the ability to differentiate into neurons and to produce trophic factors, but there is little information available in the literature concerning whether BMSCs play a therapeutic role by affecting microglial activity. In this study, we triggered an inflammatory response situation <i>in vitro</i> by stimulating microglia with the bacterial endotoxin lipopolysaccharide (LPS), and then culturing these microglia with BMSC-conditioned medium (BMSC-CM). We found that BMSC-CM significantly inhibited proliferation and secretion of pro-inflammatory factors by activated microglia. Furthermore, we found that the phagocytic capacity of microglia was also inhibited by BMSC-CM. Finally, we investigated whether the induction of apoptosis and the production of nitric oxide (NO) were involved in the inhibition of microglial activation. We found that BMSC-CM significantly induced apoptosis of microglia, while no apoptosis was apparent in the LPS-stimulated microglia. Our study also provides evidence that NO participates in the inhibitory effect of BMSCs. Our experimental results provide evidence that BMSCs have the ability to maintain the resting phenotype of microglia or to control microglial activation through their production of several factors, indicating that BMSCs could be a promising therapeutic tool for treatment of diseases associated with microglial activation.</p></div