Being a multidrug-resistant and an invasive pathogen, Acinetobacter baumannii is one of the major causes of nosocomial infections in the current healthcare system. It has been recognized as an agent of pneumonia, septicemia, meningitis, urinary tract and wound infections, and is associated with high mortality. Pathogenesis in A. baumannii infections is an outcome of multiple virulence factors, including porins, capsules, and cell wall lipopolysaccharide, enzymes, biofilm production, motility, and iron-acquisition systems, among others. Such virulence factors help the organism to resist stressful environmental conditions and enable development of severe infections. Parallel to increased prevalence of infections caused by A. baumannii, challenging and diverse resistance mechanisms in this pathogen are well recognized, with major classes of antibiotics becoming minimally effective. Through a wide array of antibiotic-hydrolyzing enzymes, efflux pump changes, impermeability, and antibiotic target mutations, A. baumannii models a unique ability to maintain a multidrug-resistant phenotype, further complicating treatment. Understanding mechanisms behind diseases, virulence, and resistance acquisition are central to infectious disease knowledge about A. baumannii. The aims of this review are to highlight infections and disease-producing factors in A. baumannii and to touch base on mechanisms of resistance to various antibiotic classes.Forebrain neurons have relatively weak intrinsic antioxidant defenses compared to astrocytes, in part due to hypo-expression of Nrf2, an oxidative stress-induced master regulator of antioxidant and detoxification genes. Nevertheless, neurons do possess the capacity to auto-regulate their antioxidant defenses in response to electrical activity. Activity-dependent Ca2+ signals control the expression of several antioxidant genes, boosting redox buffering capacity, thus meeting the elevated antioxidant requirements associated with metabolically expensive electrical activity. These genes include examples which are reported Nrf2 target genes and yet are induced in a Nrf2-independent manner. Here we discuss the implications for Nrf2 hypofunction in neurons and the mechanisms underlying the Nrf2-independent induction of antioxidant genes by electrical activity. A significant proportion of Nrf2 target genes, defined as those genes controlled by Nrf2 in astrocytes, are regulated by activity-dependent Ca2+ signals in human stem cell-derived neurons. We propose that neurons interpret Ca2+ signals in a similar way to other cell types sense redox imbalance, to broadly induce antioxidant and detoxification genes.Reducing the 2015 level of malaria mortality by 90% by 2030 is a goal set by the World Health Organization (WHO). learn more In Burkina Faso, several malaria control programs proven to be effective were implemented over the last decade. In parallel, the progressive strengthening of the health surveillance system is generating valuable data, which represents a great opportunity for analyzing the trends in malaria burden and assessing the effect of these control programs. Complementary programs were rolled out at different time points and paces, and the present work aims at investigating both the spatial and temporal pattern of malaria case fatality rate (mCFR) by considering the effect of combining specific and unspecific malaria control programs. To this end, data on severe malaria cases and malaria deaths, aggregated at health district level between January 2013 and December 2018, were extracted from the national health data repository (ENDOS-BF). A Bayesian spatiotemporal zero-inflated Poisson model was fitted to quantify the strength of the association of malaria control programs with monthly mCFR trends at health district level. The model was adjusted for contextual variables. We found that monthly mCFR decreased from 2.0 (95% IC 1.9-2.1%) to 0.9 (95% IC 0.8-1.0%) deaths for 100 severe malaria cases in 2013 and 2018, respectively. Health districts with high mCFR were identified in the northern, northwestern and southwestern parts of the country. The availability of malaria rapid diagnosis tests (IRR 0.54; CrI 0.47, 0.62) and treatment (IRR 0.50; CrI 0.41, 0.61) were significantly associated with a reduction in the mCFR. The risk of dying from malaria was lower in the period after the free healthcare policy compared with the period before (IRR 0.47; CrI 0.38, 0.58). Our findings highlighted locations that are most in need of targeted interventions and the necessity to sustain and strengthen the launched health programs to further reduce the malaria deaths in Burkina Faso.MDA5 belongs to the RIG-I-like receptor family, which is involved in innate immunity. During viral infection, MDA5 generates an antiviral response by recognizing the ligand to activate interferon. However, the role and mechanism of MDA5 in canine influenza virus (CIV) infection are unclear. To understand the mechanism of canine MDA5-mediated innate immunity during CIV infection, we detected the distribution of MDA5 in beagles, and the structural prediction showed that MDA5 was mainly composed of a CARD domain, RD domain, and DExD/H helix structure. Moreover, we found that MDA5 inhibits CIV replication. Furthermore, in the dual luciferase assay, we revealed that the CARD region of MDA5 strongly activated the IFN-β promoter and mainly transmitted signals through the CARD region. Overexpression of the CARD region of MDA5 revealed that the MDA5-mediated signaling pathway could transmit signals by activating the IRF3/NF-κB and IRF3 promoters, promoting the expression of antiviral proteins and cytokine release, thereby inhibiting CIV replication. Upon silencing of MDA5, cytokine production decreased, while the replication ability of CIV was increased. Thus, this study revealed a novel mechanism by which MDA5 mediated CIV infection and provided new avenues for the development of antiviral strategies.Based on an 33Cr23Ni8Mn3N thermal simulation experiment, the application of an artificial neural network (ANN) in thermomechanical processing was studied. Based on the experimental data, a microstructure evolution model and constitutive equation of 33Cr23Ni8Mn3N heat-resistant steel were established. Stress, dynamic recrystallization (DRX) fraction, and DRX grain size were predicted. These models were evaluated by a variety of statistical indicators to determine that these models would work well if applied in predicting microstructure evolution and that they have high precision. Then, based on the weight of the ANN model, the sensitivity of the input parameters was analyzed to achieve an optimized ANN model. Based on the most widely used sensitivity analysis (SA) method (the Garson method), the input parameters were analyzed. The results show that the most important factor for the microstructure of 33Cr23Ni8Mn3N is the strain rate ( ε ˙ ). For the control of the microstructure, the control of the ε ˙ is preferred.