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Even though essential oils (EOs) have been used for therapeutic purposes, there is now a renewed interest in the antimicrobial properties of phytochemicals and EOs in particular. Their demonstrated low levels of induction of antimicrobial resistance make them interesting for bactericidal applications, though their complex composition makes it necessary to focus on the study of their main components to identify the most effective ones. Herein, the evaluation of the antimicrobial action of different molecules present in EOs against planktonic and biofilm-forming Gram-positive (Staphylococcus aureus) and Gram-negative (Escherichia coli) bacteria was assessed. The bactericidal mechanisms of the different molecules, as well as their cytocompatibility, were also studied. Carvacrol, cinnamaldehyde, and thymol exhibit the highest in vitro antimicrobial activities against E. coli and S. aureus, with membrane disruption the bactericidal mechanism identified. The addition of those compounds (≥0.5 mg/mL) hampers S. aureus biofilm formation and partially eliminates preformed biofilms. The subcytotoxic values of the tested EO molecules (0.015–0.090 mg/mL) are lower than the minimum inhibitory and bactericidal concentrations obtained for bacteria (0.2–0.5 mg/mL) but are higher than that obtained for chlorhexidine (0.004 mg/mL), indicating the reduced cytotoxicity of EOs. Therefore, carvacrol, cinnamaldehyde, and thymol are molecules contained in EOs that could be used against E. coli– and S. aureus–mediated infections without a potential induction of bactericidal resistance and with lower cell toxicity than the conventional widely used chlorhexidine.

Hereditary spastic paraplegia (HSP) describes a heterogeneous group of genetic neurodegenerative disorders in which the most severely affected neurons are those of the spinal cord. These disorders are characterised clinically by progressive spasticity and weakness of the lower limbs, and pathologically by retrograde axonal degeneration of the corticospinal tracts and posterior columns. In recent years, genetic studies have identified key cellular functions that are vital for the maintenance of axonal homoeostasis in HSP. Here, we describe the clinical and diagnostic features of the various forms of HSP. We also discuss the genes that have been identified and the emerging pathogenic mechanisms.

Among emerging arthropod-borne viruses (arbovirus), West Nile virus (WNV) is a flavivirus that can be associated with severe neuroinvasive infections in humans. In 2018, the European WNV epidemic resulted in over 2000 cases, representing the most important arboviral epidemic in the European continent. Characterization of inflammation and neuronal biomarkers released during WNV infection, especially in the context of neuronal impairments, could provide insight into the development of predictive tools that could be beneficial for patient outcomes. We first analyzed the inflammatory signature in the serum of WNV-infected mice and found increased concentrations of several inflammatory cytokines. We next analyzed serum and cerebrospinal-fluid (CSF) samples from a cohort of patients infected by WNV between 2018 and 2019 in Hungary to quantify a large panel of inflammatory cytokines and neurological factors. We found higher levels of inflammatory cytokines (e.g., IL4, IL6, and IL10) and neuronal factors (e.g., BDNF, GFAP, MIF, TDP-43) in the sera of WNV-infected patients with neuroinvasive disease. Furthermore, the serum inflammatory profile of these patients persisted for several weeks after initial infection, potentially leading to long-term sequelae and having a deleterious effect on brain neurovasculature. This work suggests that early signs of increased serum concentrations of inflammatory cytokines and neuronal factors could be a signature underlying the development of severe neurological impairments. Biomarkers could play an important role in patient monitoring to improve care and prevent undesirable outcomes.

Phylogenetic analyses show that ZIKV can be classified into 2 main lineages: the African lineage and the Asian lineage, the latter of which is responsible for the recent epidemics. Because recent ZIKV infections were associated with the development of congenital and neurological disorders, a key question was raised as to whether Asian-lineage ZIKV strains were phenotypically different from the African lineage strains. Importantly, infections with African strains resulted in more weight loss, mortality, and severe prolonged neurological symptoms compared to Asian strains. [...]induction of type 1 and 2 interferon (IFN) were higher following infection with African strains associated with enhanced levels of inflammatory cytokines such as interleukin 6 (IL6) or tumor necrosis factor (TNF). [...]these systems have limitations, in particular, studying viral pathogenesis using animals lacking a key component of antiviral immunity, which makes it still difficult to derive definitive conclusions regarding ZIKV virulence in humans. [...]many unanswered questions remain, in particular, regarding the mechanisms of host restriction, immune evasion, and inflammatory response as well as the long-term neurodevelopmental implications of congenital infection in humans. [...]the data reviewed here indicate that there are intrinsic differences in the pathogenicity/virulence of African- and Asian-lineage ZIKV strains.

Arthropod-borne viruses or arbovirus, are most commonly associated with acute infections, resulting on various symptoms ranging from mild fever to more severe disorders such as hemorrhagic fever. Moreover, some arboviral infections can be associated with important neuroinflammation that can trigger neurological disorders including encephalitis, paralysis, ophthalmological impairments, or developmental defects, which in some cases, can lead to long-term defects of the central nervous system (CNS). This is well illustrated in Zika virus-associated congenital brain malformations but also in West Nile virus-induced synaptic dysfunctions that can last well beyond infection and lead to cognitive deficits. Here, we summarize clinical and mechanistic data reporting on cognitive disturbances triggered by arboviral infections, which may highlight growing public health issues spanning the five continents.

Zika virus (ZIKV) is a neurotropic Orthoflavivirus transmitted by mosquito vectors, which has evolved into two lineages, namely African and Asian. ZIKV from the Asian lineage has been responsible for epidemics in the Pacific and the Americas, the largest of which occurred in Brazil in 2015 and was associated with severe neurological disorders, including cases of microcephaly and other congenital fetal malformations. Although never implicated in human epidemics, African strains exhibit faster replication, higher virus production, and greater virulence in animal models compared to their Asian counterparts. A key feature that may account for the better fitness of African ZIKV strains compared to Asian ones is the fact that they are more resistant to interferon (IFN). IFN response is a major host defense mechanism against viral infections, which culminates in the induction of hundreds of IFN-induced genes (ISGs) whose products inhibit viral replication. By screening an array of ISGs known for their antiviral activity, we show that African ZIKV strains are globally more resistant than their Asian counterparts to ISG-mediated restriction. In particular, SHFL, RTP4 and IFI6, which were the three most active ISGs against Asian viruses, had little or no effect on the replication of African ZIKV strains. These observations therefore suggest that if African strains are more resistant to the antiviral effect of IFN than Asian strains, this is not because they have greater capacity to inhibit IFN signaling, but rather because they are able to escape ISG-mediated restriction. Our results provide an explanation as to why viruses of African origin spread more rapidly and efficiently in vitro than their Asian counterparts as repeatedly demonstrated. However, it remains unclear why, despite their greater virulence and resistance to cellular antiviral defenses, ZIKV strains of the African lineage have never been identified in large-scale epidemics.

Background Medical Humanities (MH) integrate the human sciences, arts and social sciences into medical education to foster empathy, ethical reflection and critical thinking. This article presents the MH programme at Universidad Francisco de Vitoria (UFV), framed within the InspirE5 model—an internationally informed framework for designing and evaluating health humanities curricula. Methods We conducted a qualitative descriptive-interpretive study using document analysis and triangulated phenomenological interpretation. A multidisciplinary team analysed the programme according to the five domains of the InspirE5 model: Environment, Expectations, Experiences, Evidence, and Enhancement. Results The UFV MH programme aligns closely with the InspirE5 capabilities, integrating them into a longitudinal, compulsory curriculum. It includes diverse pedagogical methods—such as mentoring, experiential learning, reflective writing, and interdisciplinary seminars—fostering person-centredness, ambiguity tolerance, and ethical imagination. Conclusions The programme demonstrates a coherent integration of MH across six academic years and provides a model of transformative, transdisciplinary education. Its alignment with the InspirE5 framework strengthens its value as a paradigm for medical humanities development, assessment and international comparison.

For the effective management of infected chronic wounds, the incorporation of antimicrobial drugs into wound dressings can increase their local availability at the infection site. Mesoporous silicon dioxide SBA-15 is an excellent drug carrier with tunable drug release kinetics. In this work, synthesized SBA-15 loaded with the natural antimicrobial compound thymol (THY) was incorporated into polycaprolactone (PCL) electrospun nanofibers to obtain an advanced wound dressing. Rod-shaped particles with internal parallel channels oriented along the longitudinal axis (diameter: 138 ± 30 nm, length: 563 ± 100 nm) were loaded with 70.8 wt.% of THY. Fiber mats were prepared using these particles as nanofillers within polycaprolactone (PCL) electrospun fibers. The resulting mats contained 5.6 wt.% of THY and more than half of this loading was released in the first 7 h. This release would prevent an initial bacterial colonization and also inhibit or eliminate bacterial growth as in vitro shown against Staphylococcus aureus ATCC 25923. Minimal inhibitory concentration (MIC: 0.07 mg/mL) and minimal bactericidal concentration (MBC: 0.11 mg/mL) of released THY were lower than the amount of free THY required, demonstrating the benefit of drug encapsulation for a more efficient bactericidal capacity due to the direct contact between mats and bacteria.

To gain access to the brain, a so-called immune-privileged organ due to its physical separation from the blood stream, pathogens and particularly viruses have been selected throughout evolution for their use of specific mechanisms. They can enter the central nervous system through direct infection of nerves or cerebral barriers or through cell-mediated transport. Indeed, peripheral lymphoid and myeloid immune cells can interact with the blood–brain and the blood–cerebrospinal fluid barriers and allow viral brain access using the “Trojan horse” mechanism. Among immune cells, at the frontier between innate and adaptive immune responses, dendritic cells (DCs) can be pathogen carriers, regulate or exacerbate antiviral responses and neuroinflammation, and therefore be involved in viral transmission and spread. In this review, we highlight an important contribution of DCs in the development and the consequences of viral brain infections.