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Background: Post-stroke depression (PSD) has been proven to be associated with stroke severity. Thus, we hypothesized that the prevalence of PSD would be lower in patients with mild stroke. We aim to explore predictors of depression at 3 months after mild acute ischemic stroke (MAIS) onset and to develop a practical and convenient prediction model for the early identification of patients at high risk. Methods: A total of 519 patients with MAIS were consecutively recruited from three hospitals in Wuhan city, Hubei province. MAIS was defined as a National Institute of Health Stroke Scale (NIHSS) score of ≤5 at admission. Meeting the DSM-V diagnostic criteria and a 17-item Hamilton Rating Scale for Depression (HAMD-17) score of >7 at their 3-month follow-up were considered the primary outcomes. A multivariable logistic regression model was used to determine the factors adjusted for potential confounders, and all independent predictors were brought into the construction of a nomogram to predict PSD. Results: The prevalence of PSD is up to 32% at 3 months after MAIS onset. After adjusting for potential confounders, indirect bilirubin (p = 0.029), physical activity (p = 0.001), smoking (p = 0.025), hospitalization days (p = 0.014), neuroticism (p < 0.001), and MMSE (p < 0.001) remained independently and significantly related with PSD. The concordance index (C-index) of the nomogram jointly constructed by the aforementioned six factors was 0.723 (95% CI: 0.678-0.768). Conclusion: The prevalence of PSD seems equally high even if the ischemic stroke is mild, which calls for great concern from clinicians. In addition, our study found that a higher level of indirect bilirubin can lower the risk of PSD. This finding may provide a potential new approach to PSD treatment. Furthermore, the nomogram including bilirubin is convenient and practical to predict PSD after MAIS onset. [ABSTRACT FROM AUTHOR]

Neutrophil extracellular traps (NETs) are produced by neutrophil activation and usually have both anti-infective and pro-damage effects. Streptococcus uberis (S. uberis), one of the common causative organisms of mastitis, can lead to the production of NETs. Taurine, a free amino acid abundant in the organism, has been shown to have immunomodulatory effects. In this study, we investigated the molecular mechanisms of S. uberis-induced NETs formation and the regulatory role of taurine. The results showed that NETs had a disruptive effect on mammary epithelial cells and barriers, but do not significantly inhibit the proliferation of S. uberis. S. uberis induced NADPH oxidasedependent NETs. TLR2-mediated activation of the MAPK signaling pathway was involved in this process. Taurine could inhibit the activation of MAPK signaling pathway and NADPH oxidase by modulating the activity of TAK1, thereby inhibiting the production of ROS and NETs. The effects of taurine on NADPH oxidase and NETs in S. uberis infection were also demonstrated in vivo. These results suggest that taurine can protect mammary epithelial cells and barriers from damage by reducing S. uberis-induced NETs. These data provide new insights and strategies for the prevention and control of mastitis. [ABSTRACT FROM AUTHOR]

Background: Swine influenza is an economically important respiratory disease of swine resulting from infection with influenza A virus. Swine influenza virus (SIV) becomes the focus as pigs have been hypothesized to serve as an intermediate host for the adaptation of avian influenza viruses to humans or as mixing vessels for the generation of genetically reassortant viruses. The ability of the innate immune system to detect and respond to pathogens is important for survival. Therefore, there is a critical need to evaluate the immediate response to viral infection, especially the role of the toll-like receptors (TLRs) and RNA helicase RIG-I-like receptors (RLRs) innate immunity signaling pathways in H3N2 swine influenza virus infection. Method: In this study, porcine alveolar macrophages (PAMs) were obtained from porcine lungs and were infected with SIV at a multiplicity of infection (MOI) of 5 in vitro. The changes of the related receptors, signaling proteins and effector molecules of TLRs and RLRs signaling pathways post H3N2 virus infection of PAMs were quantified by Real-time quantitative RT-PCR and western blotting. Results: The results showed that H3N2 SIV infection significantly increased mRNA expression of TLR-3, TLR-7, RIG-I and MDA5 after 4 hpi (P < 0.05). Western blotting showed that the protein levels of TLR-3, TLR-7 and RIG-I also had a significantly increase after PAM exposed to virus. A significant change of MyD88, MAVS, IRF-3 and IRF-7 mRNA expression were present at 8 hpi. More than a 4-fold increase was induced for TNF-α and IL-1β mRNA expression. And the concentration of TNF-α and IL-1β peaked at 12 and 24 hpi, respectively. IFN-α, IFN-β mRNA and protein levels increased after SIV infection and significant differences was observed at 8, 12 and 24 hpi. Conclusion: These results indicate that H3N2 swine influenza virus infection significantly influences the expression of the receptors, adapter proteins and downstream effector molecules of RLRs and TLRs signaling pathways. This study enhances our understanding of innate immunity signaling pathways in PAM anti-infection of H3N2 SIV. [ABSTRACT FROM AUTHOR]

Objective: A lipopolysaccharide (LPS)-induced mastitis model in rats was used to study the protective effect of β-glucan. Materials and methods: On gestation day 10, β-glucan was administered to rats daily by gavage at either 0 (control), 0.1 mg/kg BW, 1 mg/kg BW and 10 mg/kg BW until parturition. LPS or pyrogen-free physiological saline was inoculated into the mammary gland 72 h after parturition and the rats were euthanized at 12 h post-infection. Results: LPS increased dectin1 and toll-like receptor 4 (TLR4) mRNA and protein expression significantly in mammary tissues. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, N-acetyl-β-D-glucosaminidase (NAGase), inducible nitric oxide synthase (iNOs) in mammary tissues and serum, and myeloperoxidase (MPO) in mammary tissues were significantly increased 12 h after LPS infusion. β-glucan administration could enhance dectin1 mRNA and protein expression while downregulating the expression of TLR4. Level of TNF-α, IL-1β in mammary tissues and serum, MPO, NAGase and iNOs activity in mammary tissues was decreased, but the level of IL-2 in serum was increased by α-glucan. Conclusion: The results indicate that β-glucan may protect mammary tissue against LPS-induced rat acute mastitis. [ABSTRACT FROM AUTHOR]