8-Prenylkaempferol Suppresses Influenza A Virus-Induced RANTES Production in A549 Cells via Blocking PI3K-Mediated Transcriptional Activation of NF-κB and IRF3

8-Prenylkaempferol (8-PK) is a prenylflavonoid isolated from Sophora flavescens, a Chinese herb with antiviral and anti-inflammatory properties. In this study, we investigated its effect on regulated activation, normal T cell expressed and secreted (RANTES) secretion by influenza A virus (H1N1)-infected A549 alveolar epithelial cells. Cell inoculation with H1N1 evoked a significant induction in RANTES accumulation accompanied with time-related increase in nuclear translocation of nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF-3), but showed no effect on c-Jun phosphorylation. 8-PK could significantly inhibit not only RANTES production but also NF-κB and IRF-3 nuclear translocation. We had proved that both NF-κB and IRF-3 participated in H1N1-induced RANTES production since NF-κB inhibitor pyrrolidinedithio carbamate (PDTC) and IRF-3 siRNA attenuated significantly RANTES accumulation. H1N1 inoculation also increased PI3K activity as well as Akt phosphorylation and such responsiveness were attenuated by 8-PK. In the presence of wortmannin, nuclear translocation of NF-κB and IRF3 as well as RANTES production by H1N1 infection were all reversed, demonstrating that PI3K-Akt pathway is essential for NF-κB- and IRF-3-mediated RANTES production in A549 cells. Furthermore, 8-PK but not wortmannin, prevented effectively H1N1-evoked IκB degradation. In conclusion, 8-PK might be an anti-inflammatory agent for suppressing influenza A virus-induced RANTES production acts by blocking PI3K-mediated transcriptional activation of NF-κB and IRF-3 and in part by interfering with IκB degradation which subsequently decreases NF-κB translocation

Effect of Age on Allergen Responses of Allergic Patients in Southern Taiwan

To survey airborne and food allergen patterns in southern Taiwan and to analyze the effect of age on response to different allergens, we tested samples from 4,411 allergic patients at Kaohsiung Medical University Hospital using the MAST-CLA test (new Taiwan panel). A total of 2,212 (50.1%) samples showed a positive response. We grouped allergic patients into five age groups. Milk and egg white were the main food allergens in the younger groups (< 3 years old and 3-6 years old). Shrimp, crab, and shellfish were the main allergens in the groups aged 7-12, 13-18, and more than 18 years. Among airborne allergens, house dust and mites Dermatophagoides farinae and D. pteronyssinus were the main allergens in all age groups, whereas the frequency of response to cockroach allergen was low in the group aged less than 3 years, but increased in the other age groups. There was a sharp increase in the frequency of response to airborne allergens after 3 years old and a sharp decrease in response to food allergens. Among subjects allergic to both airborne and food allergens, there was a positive MAST-CLA rate of 19.9% to 26% (all five age groups, no significant difference). When we compared our results with those from Taipei Veterans General Hospital in northern Taiwan, there were significant differences for yeast, peanut, feather mix, dog dander, cockroach, D. farinae and D. pteronyssinus allergens (p < 0.01). These differences were probably caused by differences in patient location, patient age, disease patterns and allergen panels

Towards Adversarially Robust Continual Learning

Recent studies show that models trained by continual learning can achieve the comparable performances as the standard supervised learning and the learning flexibility of continual learning models enables their wide applications in the real world. Deep learning models, however, are shown to be vulnerable to adversarial attacks. Though there are many studies on the model robustness in the context of standard supervised learning, protecting continual learning from adversarial attacks has not yet been investigated. To fill in this research gap, we are the first to study adversarial robustness in continual learning and propose a novel method called \textbf{T}ask-\textbf{A}ware \textbf{B}oundary \textbf{A}ugmentation (TABA) to boost the robustness of continual learning models. With extensive experiments on CIFAR-10 and CIFAR-100, we show the efficacy of adversarial training and TABA in defending adversarial attacks.Comment: ICASSP 202

Toward the nonequilibrium thermodynamic analog of complexity and the Jarzynski identity

The Jarzynski identity can describe small-scale nonequilibrium systems through stochastic thermodynamics. The identity considers fluctuating trajectories in a phase space. The complexity geometry frames the discussions on quantum computational complexity using the method of Riemannian geometry, which builds a bridge between optimal quantum circuits and classical geodesics in the space of unitary operators. Complexity geometry enables the application of the methods of classical physics to deal with pure quantum problems. By combining the two frameworks, i.e., the Jarzynski identity and complexity geometry, we derived a complexity analog of the Jarzynski identity using the complexity geometry. We considered a set of geodesics in the space of unitary operators instead of the trajectories in a phase space. The obtained complexity version of the Jarzynski identity strengthened the evidence for the existence of a well-defined resource theory of uncomplexity and presented an extensive discussion on the second law of complexity. Furthermore, analogous to the thermodynamic fluctuation-dissipation theorem, we proposed a version of the fluctuation-dissipation theorem for the complexity. Although this study does not focus on holographic fluctuations, we found that the results are surprisingly suitable for capturing their information. The results obtained using nonequilibrium methods may contribute to understand the nature of the complexity and study the features of the holographic fluctuations.Comment: 47 pages, 7 figures, to appear in JHE

Integrable Open Spin Chains from Flavored ABJM Theory

We compute the two-loop anomalous dimension matrix in the scalar sector of planar ${\cal N}=3$ flavored ABJM theory. Using coordinate Bethe ansatz, we obtain the reflection matrix and confirm that the boundary Yang-Baxter equations are satisfied. This establishes the integrability of this theory in the scalar sector at the two-loop order.Comment: v2, 25 pages, 2 figures, minor corrections, references adde

3,4-Di-O-Caffeoylquinic Acid Inhibits Angiotensin-II-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating the JNK and PI3K/Akt Signaling Pathways

We previously reported 3,4-di-O-caffeoylquinic acid (CQC) protected vascular endothelial cells against oxidative stress and restored impaired endothelium-dependent vasodilatation. Here, we further investigated its anti-atherosclerotic effect against angiotensin II (Ang II) evoked proliferation and migration of cultured rat vascular smooth muscle cells (rVSMC). The results showed CQC (1–20 μM) clearly inhibited Ang-II-stimulated BrdU incorporation and cell migration of rVSMC in a concentration-dependent manner but without significant cytotoxicity. Western blot analysis revealed Ang II increased the phosphorylation levels of Akt and mitogen-activated protein kinases (MAPKs;p38, ERK1/2 and JNK) in rVSMC. In the presence of phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin and three individual MAPK inhibitors SB203580, PD98059 and SP600125, both Ang-II-induced cell proliferation and migration were significantly attenuated, although to differing extents, suggesting the PI3K and MAPK signal pathways all participated in regulating rVSMC proliferation and migration. Also, the CQC pretreatment markedly suppressed Ang-II-induced phosphorylation of Akt and JNK rather than ERK1/2, although it failed to affect p38 phosphorylation. In conclusion, our data demonstrate CQC may act by down-regulating Akt, JNK and part of the ERK1/2 pathways to inhibit Ang-II-induced rVSMC proliferation and migration. The anti-atherosclerotic effect of CQC is achieved either by endothelial cells protection or by VSMC proliferation/migration inhibition, suggesting this compound may be useful in preventing vascular diseases

Neuroprotective effects of lomerizine on retinal ganglion cells in the diet-induced obese C57BL/6J mice

AIM: To research the neuroprotective effects of lomerizine(LOM)on retinal ganglion cells(RGCs)in the diet-induced obese C57BL/6J mice. <p>METHODS: Fifty-four mice were randomly divided into two groups which were fed a high-fat diet for 19wk. One group mice were lavaged LOM by the dosage of 80mg/kg daily at the same time. The obese mice were selected and divided into diet-induced obesity(DIO)group, diet-induced obesity and lomerizine(DIO+LOM)group. The mice in the control(CON)group were fed a basal diet. The ultrastructural changes of RGCs were detected by transmission electron microscope. The cellular apoptosis was detected by TUNEL. The laser scanning confocal microscope was used to measure intracellular calcium ion concentration. <p>RESULTS: Compared with the CON group, the RGCs in DIO group showed smaller and condensation of nuclear chromatin and increased electron density of the cytoplasm, whereas the changes in DIO+LOM mice were obviously diminished. TUNEL staining showed that the number of apoptosis cells in the ganglion cell layer(GCL)increased in DIO group and the percentage of apoptotic cells was much higher than that in the CON groups(<i>P</i><0.01). The DIO+LOM group mice showed fewer apoptosis cells and the percentage of apoptotic cells in this group were significantly decreased than the DIO mice(<i>P</i><0.05). The Laser scanning confocal microscope detection showed Ca²⁺ staining intensity of RGCs in DIO group increased and its staining intensity ratio was significantly higher than in CON group(<i>P</i><0.01), the Ca²⁺ staining intensity and its staining intensity ratio in DIO+LOM group were significantly decreased than the DIO group(<i>P</i><0.01). <p>CONCLUSION: Lomerizine has neuroprotective effects on damage of retinal ganglion cells in diet-induced obesity mice, which may be related to the attenuation of intracellular Ca²⁺ overload