Significance: The expression of genes involved in hippocampal synaptic plasticity, learning, and memory requires that Ca²⁺signals generated in spines, dendrites, or the soma by neuronal stimulation reach the nucleus. Here, we report that stimulation of hippocampal neurons induces Ca²⁺release mediated by RyR2 channels, which contributes to nuclear Ca²⁺signal generation. Suppression of RyR-mediated Ca²⁺release inhibited the activity-induced phosphorylation of the nuclear transcriptional regulator CREB and the expression of the Npas4 transcription factor and RyR2, which play crucial roles in hippocampal memory processes. We propose that RyR-mediated Ca²⁺release induced by neuronal stimulation, by promoting the sequential generation of nuclear Ca²⁺signals, CREB phosphorylation, and Npas4/RyR2 up-regulation, plays a significant role in hippocampal synaptic plasticity and spatial memory processes.

Medical imaging is essential nowadays throughout medical education, research, and care. Accordingly, international efforts have been made to set large-scale image repositories for these purposes. Yet, to date, browsing of large-scale medical image repositories has been troublesome, time-consuming, and generally limited by text search engines. A paradigm shift, by means of a query-by-example search engine, would alleviate these constraints and beneficially impact several practical demands throughout the medical field. The current project aims to address this gap in medical imaging consumption by developing a content-based image retrieval (CBIR) system, which combines two image processing architectures based on deep learning. Furthermore, a first-of-its-kind intelligent visual browser was designed that interactively displays a set of imaging examinations with similar visual content on a similarity map, making it possible to search for and efficiently navigate through a large-scale medical imaging repository, even if it has been set with incomplete and curated metadata. Users may, likewise, provide text keywords, in which case the system performs a content- and metadata-based search. The system was fashioned with an anonymizer service and designed to be fully interoperable according to international standards, to stimulate its integration within electronic healthcare systems and its adoption for medical education, research and care. Professionals of the healthcare sector, by means of a self-administered questionnaire, underscored that this CBIR system and intelligent interactive visual browser would be highly useful for these purposes. Further studies are warranted to complete a comprehensive assessment of the performance of the system through case description and protocolized evaluations by medical imaging specialists.

Trypanosoma cruzi calreticulin (TcCRT), a 47-kDa chaperone, translocates from the endoplasmic reticulum to the area of flagellum emergence. There, it binds to complement components C1 and mannan-binding lectin (MBL), thus acting as a main virulence factor, and inhibits the classical and lectin pathways. The localization and functions of TcCRT, once the parasite is inside the host cell, are unknown. In parasites infecting murine macrophages, polyclonal anti-TcCRT antibodies detected TcCRT mainly in the parasite nucleus and kinetoplast. However, with a monoclonal antibody (E2G7), the resolution and specificity of the label markedly improved, and TcCRT was detected mainly in the parasite kinetoplast. Gold particles, bound to the respective antibodies, were used as probes in electron microscopy. This organelle may represent a stopover and accumulation site for TcCRT, previous its translocation to the area of flagellum emergence. Finally, early during T. cruzi infection and by unknown mechanisms, an important decrease in the number of MHC-I positive host cells was observed.

In response to brain insults, astrocytes become reactive, promoting protection and tissue repair. However, astroglial reactivity is typical of brain pathologies, including Alzheimer's disease (AD). Considering the heterogeneity of the reactive response, the role of astrocytes in the course of different forms of AD has been underestimated. Colombia has the largest human group known to have familial AD (FAD). This group carries the autosomal dominant and fully penetrant mutation E280A in PSEN1, which causes early‐onset AD. Recently, our group identified an E280A carrier who did not develop FAD. The individual was homozygous for the Christchurch mutation R136S in APOE3 (APOEch). Remarkably, APOE is the main genetic risk factor for developing sporadic AD (SAD) and most of cerebral ApoE is produced by astroglia. Here, we characterized astrocyte properties related to reactivity, glutamate homeostasis, and structural integrity of the gliovascular unit (GVU), as factors that could underlie the pathogenesis or protection of AD. Specifically, through histological and 3D microscopy analyses of postmortem samples, we briefly describe the histopathology and cytoarchitecture of the frontal cortex of SAD, FAD, and APOEch, and demonstrate that, while astrodegeneration and vascular deterioration are prominent in SAD, FAD is characterized by hyperreactive‐like glia, and APOEch displays the mildest astrocytic and vascular alterations despite having the highest burden of Aβ. Notably, astroglial, gliovascular, and vascular disturbances, as well as brain cell death, correlate with the specific astrocytic phenotypes identified in each condition. This study provides new insights into the potential relevance of the gliovasculature in the development and protection of AD. To our knowledge, this is the first study assessing the components of the GVU in human samples of SAD, FAD, and APOEch.