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BackgroundZika fever gained importance in Brazil in 2015 due to its association with congenital syndrome. Although Zika virus (ZIKV) crosses the placenta and infects the fetus, its pathogenesis remains incompletely understood. This study investigated the effects of ZIKV infection in HTR-8/SVneo trophoblast cells.MethodsCells were infected with ZIKV (MOI 0.1, 0.2, or 1) or Mock control for 24 or 48 hours. Infection rate and viability were assessed by immunofluorescence and flow cytometry. Ultrastructural changes were analyzed by transmission electron microscopy. Mitochondrial membrane potential was evaluated by flow cytometry. Gene expression related to mitochondrial dynamics, antioxidant response ( sod, cat, nrf2 ), was analyzed by RT-qPCR. Protein expression (SOD, CAT, NRF2), enzymatic activities (SOD, CAT), and oxidative damage markers (8-OHdG, MDA, NO) were assessed by immunofluorescence and/or colorimetric assays.ResultsMOI 1 for 24 hours produced the highest NS1 expression and infection rate (62.53%) and higher viability (89% vs. 28.1%), establishing this as the optimal condition. Infected cells exhibited mitochondrial damage, including ruptured membranes and loss of cristae, dilated endoplasmic reticulum, clusters of virus-like particles, and vesicle secretion. Mitochondrial membrane potential was reduced, along with decreased transcripts of genes involved in mitochondrial dynamics. Although sod, cat , and nrf2 transcripts were reduced, protein immunolabeling and SOD activity were increased, whereas CAT activity was decreased. Elevated levels of 8-OHdG, MDA, and NO confirmed oxidative stress.ConclusionZIKV infection induces mitochondrial dysfunction, oxidative stress, and impaired mitophagy in HTR-8/SVneo trophoblast cells, highlighting mitochondrial dysfunction as a major component of the cellular response to ZIKV infection in trophoblast cells.

Fibrosis is a common feature in most pathogenetic processes in the liver, and usually results from a chronic insult that depletes the regenerative capacity of hepatocytes and activates multiple inflammatory pathways, recruiting resident and circulating immune cells, endothelial cells, non-parenchymal hepatic stellate cells, and fibroblasts, which become activated and lead to excessive extracellular matrix accumulation. The ongoing development of liver fibrosis results in a clinically silent and progressive loss of hepatocyte function, demanding the constant need for liver transplantation in clinical practice, and motivating the search for other treatments as the chances of obtaining compatible viable livers become scarcer. Although initially cell therapy has emerged as a plausible alternative to organ transplantation, many factors still challenge the establishment of this technique as a main or even additional therapeutic tool. Herein, the authors discuss the most recent advances and point out the corners and some controversies over several protocols and models that have shown promising results as potential candidates for cell therapy for liver fibrosis, presenting the respective mechanisms proposed for liver regeneration in each case.

Bone marrow cells (BMC) migrate to the injured liver after transplantation, contributing to regeneration through multiple pathways, but mechanisms involved are unclear. This work aimed to study BMC migration, characterize cytokine profile, cell populations and proliferation in mice with liver fibrosis transplanted with GFP+ BMC. Confocal microscopy analysis showed GFP+ BMC near regions expressing HGF and SDF-1 in the fibrotic liver. Impaired liver cell proliferation in fibrotic groups was restored after BMC transplantation. Regarding total cell populations, there was a significant reduction in CD68+ cells and increased Ly6G+ cells in transplanted fibrotic group. BMC contributed to the total populations of CD144, CD11b and Ly6G cells in the fibrotic liver, related to an increment of anti-fibrotic cytokines (IL-10, IL-13, IFN-γ and HGF) and reduction of pro-inflammatory cytokines (IL-17A and IL-6). Therefore, HGF and SDF-1 may represent important chemoattractants for transplanted BMC in the injured liver, where these cells can give rise to populations of extrahepatic macrophages, neutrophils and endothelial progenitor cells that can interact synergistically with other liver cells towards the modulation of an anti-fibrotic cytokine profile promoting the onset of liver regeneration.

Purpose The association of targeted therapy with chemotherapy is encouraged to increase the treatment efficiency, especially in hypoxic triple-negative breast cancer. The APE1 redox activity has stood out as a potential tumor target. However, the effect of the association of the APE1 redox inhibitors with doxorubicin in hypoxia still needs to be evidenced. Therefore, our objective was to investigate the effect of the APX2009 (APE1 inhibitor) on the sensitization of breast cancer cells to doxorubicin in normoxia and hypoxia. Methods The WST-1 assay was used to evaluate cell viability after APX2009 and doxorubicin application under normoxia and hypoxia conditions in the MCF-7 and MDA-MB-231 cells. Apoptosis was analyzed by annexin assay and detection of caspases-3/7 activity by luminescence-based assay. The clinical association between APE1 inhibition signature and doxorubicin sensitivity was evaluated by bioinformatics analyses. Results MDA-MB-231 and MCF-7 cell lines were more sensitive to APX2009 in normoxia than in hypoxia. Co-treatment with APX2009 and doxorubicin in hypoxia further decreased the viability of triple-negative MDA-MB-231 cells than treatment alone, which was accompanied by doxorubicin intracellular accumulation, and increase of apoptotic cells percentage, and caspases-3/7 activity. Moderate association was found between APE1 inhibition signature and doxorubicin sensitivity in the hypoxic basal subtype. Conclusion The findings suggest that APX2009 sensitizes the MDA-MB-231 cells to doxorubicin in hypoxia by doxorubicin intracellular accumulation and caspases-3/7-mediated apoptosis.

In this article, we aim to evaluate the effects of photobiomodulation on mitochondria quantity, biogenesis, and mitophagy-associated genes in breast cancer (BC) cells. Both models were irradiated with a low-power infrared laser (880 nm, 150 mW) and amber LED (617 nm, 1500 mW), alone or simultaneously. We evaluated the mRNA expression of PINK1 and PGC-1α genes, and the mitochondrial number was assessed based on the ratio of mitochondrial DNA/genomic DNA (mtDNA/gDNA). No significant difference was observed in the mtDNA/gDNA ratio comparing the low-power infrared laser (LPIL) and LED-irradiated groups to their control counterparts. Similarly, no difference was observed in the mRNA levels of PINK1 and PGC-1α of the irradiated group with an LPIL and LED alone or in combination. In conclusion, PBM with LPIL and LED did not alter the mtDNA/gDNA ratio nor modulate the mRNA levels of the genes related to mitophagy and biogenesis in BC cells.

This study explores the digitalization of healthcare phenomenon in relation to patient empowerment. Because digital environments change the way individuals interact with healthcare providers, there are consequences for patients’ ability to act and determine their health outcomes in a digital health ecosystem.An assessment of the mediatization of healthcare was therefore conducted through a critical phenomenological analysis of patients’ lived experiences. This methodology facilitated an investigation of their descriptive and subjective reflections on health structures and the means of entering into capabilities that can, but not necessarily do, emerge from specific technical artifacts. Through in-depth interviews, I accessed patients’ perspectives and narratives to phenomenologically enter into their consciousness intentionalities. These revealed that mediatized healthcare certainly affects, possibly enables, and risks constraining health agency.In theoretical terms, this study was based on structural dimensions within the theories of mediatization (Couldry & Hepp, 2017) and health lifestyles (Cookerham, 2005), combined with the individual dimensions of patients’ capabilities (Oosterlaken, 2015) represented by empowerment constructs (Palumbo, 2017), where it elaborates on matters of structure and agency as interrelated and negotiated concepts.The thesis concludes with a critical discussion of the avoidance of technological determinism of the phenomenon: digital tools were incorporated in some of the capabilities of participants, and indeed sometimes contribute to their empowerment, but not always and not for everything. Empowerment must be seen as a process rather than an outcome and, concerning digitalization processes, must be investigated by scrutinizing individual initiatives embedded in a long chain of interconnectedness.

Karst water systems are highly vulnerable to land use pressures, requiring integrated assessments to support conservation and management. This study evaluated the physicochemical, microbiological, and pesticide-related water quality in the Environmental Protection Area Nascentes do Rio Vermelho (APANRV), a karst conservation unit in the Brazilian Cerrado. Sixteen sampling sites (rivers, springs, and cave waters) were monitored during the dry (May 2024) and rainy (October 2024) seasons. Analyses included nutrients, major ions, Escherichia coli, and a broad spectrum of pesticides. The results showed marked spatial and seasonal variability, with elevated hardness and conductivity in karst areas due to carbonate dissolution. Nitrate and total phosphorus reached peak values of 13.59 and 0.132 mg L−1, respectively, indicating localized nutrient enrichment. E. coli concentrations reached ≥2419.6 MPN 100 mL−1, exceeding regulatory limits, particularly during the rainy season at recreational cave sites. Pesticides were detected in both seasons, with 11 compounds in the dry season and 8 in the rainy season, including atrazine degradation products, and maximum quantified concentrations up to 1.8 µg L−1 (acephate). These findings highlight the combined influence of geology, seasonality, and land use on karst water quality and reinforce the need for continuous monitoring and targeted management strategies.

Woody canopies regulate exchanges of energy, water and carbon, and their three-dimensional (3D) structure supports much of terrestrial biodiversity. Remote sensing technologies such as airborne laser scanning (ALS) now enable the 3D mapping of entire landscapes. However, we lack the large, harmonized and geographically representative ALS collections needed to build a global picture of woody ecosystem structure. To address this challenge, we developed the Global Canopy Atlas (GCA): 3,458 ALS acquisitions transformed into standardized and analysis-ready maps of canopy height and elevation at 1 m2 resolution. The GCA covers 56,554 km2 across all major biomes. 19% of this area has been scanned multiple times, and 87% of all GCA products are openly available, covering 95% of the total area. To showcase its wide range of applications, we applied the GCA in three case studies. First, we validated three global satellite-derived canopy height maps, finding poor performance at native resolution (1-30 m, R2 < 0.38) and moderate performance at 250 m resolution (R2 < 0.65). Second, analyzing global patterns in canopy gap size frequency we discovered an unexpectedly large variation of power law exponents from branch to stand level (α = 1.52 to 2.38), pointing to a fundamental scale-dependence of forest structure. Third, we developed a framework to standardize forest turnover quantification from multi-source, multi-temporal ALS. In a temperate forest in North America it revealed that 21% of canopy gaps closed within 12 years of opening and would thus be missed by infrequent monitoring. As demonstrated by these case studies, the GCA provides a novel data source for ecologists, foresters, remote sensing scientists and the ecosystem modelling community that substantially advances our ability to understand the structure and dynamics of woody ecosystems at global scales.