Early and accurate diagnoses of pathogenic microorganisms is essential to correctly identify diseases, treating infections, and tracking disease outbreaks associated with microbial infections, to develop precautionary measures that allow a fast and effective response in epidemics and pandemics, thus improving public health. Aptamers are a class of synthetic nucleic acid molecules with the potential to be used for medical purposes, since they can be directed towards any target molecule. Currently, the use of aptamers has increased because they are a useful tool in the detection of specific targets. We present a brief review of the use of aptamers to detect and identify bacteria or even some toxins with clinical importance. This work describes the advances in the technology of aptamers, with the purpose of providing knowledge to develop new aptamers for diagnoses and treatment of different diseases caused by infectious microorganisms.

The post-COVID condition (PCC) is a pathology stemming from COVID-19, and studying its pathophysiology, diagnosis, and treatment is crucial. Neuroinflammation causes the most common manifestations of this disease including headaches, fatigue, insomnia, depression, anxiety, among others. Currently, there are no specific management proposals; however, given that the inflammatory component involves cytokines and free radicals, these conditions must be treated to reduce the current symptoms and provide neuroprotection to reduce the risk of a long-term neurodegenerative disease. It has been shown that cannabis has compounds with immunomodulatory and antioxidant functions in other pathologies. Therefore, exploring this approach could provide a viable therapeutic option for PCC, which is the purpose of this review. This review involved an exhaustive search in specialized databases including PubMed, PubChem, ProQuest, EBSCO, Scopus, Science Direct, Web of Science, and Clinical Trials. Phytocannabinoids, including cannabidiol (CBD), cannabigerol (CBG), and Delta-9-tetrahydrocannabinol (THC), exhibit significant antioxidative and anti-inflammatory properties and have been shown to be an effective treatment for neuroinflammatory conditions. These compounds could be promising adjuvants for PCC alone or in combination with other antioxidants or therapies. PCC presents significant challenges to neurological health, and neuroinflammation and oxidative stress play central roles in its pathogenesis. Antioxidant therapy and cannabinoid-based approaches represent promising areas of research and treatment for mitigating adverse effects, but further studies are needed.

Post-COVID condition (PCC) is a complex syndrome characterized by the persistence of diverse symptoms—including respiratory, neurological, and psychiatric manifestations—that last for weeks or months after acute Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection. Epidemiological data indicate a higher prevalence among women and older adults, with significant impacts on daily functioning. The pathophysiology of PCC is multifactorial, involving immune dysregulation, viral persistence, mitochondrial dysfunction, and oxidative stress, all of which contribute to sustained neuroinflammation. This narrative review examines the clinical features, risk factors, and current evidence on antioxidant-based interventions as potential therapeutic strategies for PCC. A wide range of compounds—including vitamins, polyphenols, and endogenous antioxidants—have shown promise in mitigating neuroinflammation and oxidative damage in both clinical and experimental settings. Antioxidants may help restore redox balance and improve neurological outcomes in affected patients. However, further clinical research is essential to determine their efficacy, safety, and optimal therapeutic protocols.

Fungi use oxylipins (oxidized lipids) as signaling molecules to induce asexual development. These molecules play an essential role in the response to wounding, exerting a protective effect against plant pathogens, and are part of the inflammatory process in animals. However, the physiological and molecular mechanisms triggered by oxylipins that lead to asexual development in fungi are not well understood. Using a genetic approach, mass spectrometry, and phenotypic analysis, we describe the functional role of a patatin-like phospholipase ( plp1 ) and a unique lipoxygenase ( lox1 ) in the response to injury in the model fungus Trichoderma atroviride. lox1 and plp1 are co-expressed and regulated by damage signaling and sensing components. Phenotypic analysis revealed an essential defect in the emergence of aerial hyphae in the lox1 and plp1 null mutant strains, blocking injury-induced conidiation. In addition, functional loss analysis demonstrated that both genes are essential for wound-associated linoleic acid-derived oxylipin 13-hydroxy-9Z,11E-octadecadienoic acid (13-HODE) production and the transcriptional reprogramming required for conidiation. T. atroviride requires LOX1 and PLP1 to induce transcription factors involved in asexual development such as brlA , hox2 , and azf1 homologs at the early stages of the response and at a later stage to activate lipid metabolism and the structural proteins involved in aerial mycelium emergence. Our study shows how the cooperative function of lox1 and plp1 , during the response to wounding, regulates the molecular and physiological processes of damaged-sensitized cells that lead to reproductive aerial mycelium development and consequently, ensure survival through asexual reproduction. IMPORTANCE: In addition to being considered a biocontrol agent, the fungus Trichoderma atroviride is a relevant model for studying mechanisms of response to injury conserved in plants and animals that opens a new landscape in relation to regeneration and cell differentiation mechanisms. Here, we reveal the co-functionality of a lipoxygenase and a patatin-like phospholipase co-expressed in response to wounding in fungi. This pair of enzymes produces oxidized lipids that can function as signaling molecules or oxidative stress signals that, in ascomycetes, induce asexual development. Furthermore, we determined that both genes participate in the regulation of the synthesis of 13-HODE and the establishment of the physiological responses necessary for the formation of reproductive aerial mycelium ultimately leading to asexual development. Our results suggest an injury-induced pathway to produce oxylipins and uncovered physiological mechanisms regulated by LOX1 and PLP1 to induce conidiation, opening new hypotheses for the novo regeneration mechanisms of filamentous fungi.

Tumor innervation is a complex interaction between nerves and cancer cells that consists of axons invading tumors, and its complexity remains largely unknown in humans. Although some retrospective studies have provided important insights into the relationship between nerves and tumors, further knowledge is required about this biological process. Animal experiments have elucidated several molecular and cellular mechanisms of tumor innervation; however, no experimental models currently exist to study interactions between human cancer and nerve cells. Human pluripotent stem cells can differentiate into neurons for research purposes; however, the use of these neurons to study interactions with cancer cells remains largely unexplored. Hence, here we analyze the potential of human pluripotent stem cells to study the interaction of cancer cells and neurons derived from human pluripotent stem cells to unravel the poorly understood mechanisms of human tumor innervation.

Background: Glucagon-like peptide-1 receptor (GLP-1R) agonists are increasingly prescribed for type 2 diabetes mellitus and obesity treatment. Preclinical evidence in glioblastoma cell lines suggests antitumour activity through ferroptosis induction; however, the transcriptomic and prognostic contexts of GLP1R expression in human IDH-wildtype glioblastoma are poorly characterised. Methods: We analysed GLP1R mRNA expression and its survival, immune, and ferroptosis correlates in IDH-wildtype primary glioblastoma across three cohorts: TCGA-GBM (discovery, n=245), CGGA_mRNAseq_693 (n=105), and CGGA_mRNAseq_325 (n=74) as pre-specified validation. Continuous-variable multivariable Cox regression was adjusted for age, KPS, MGMT methylation, and treatment. Pre-ranked GSEA, ssGSEA immune deconvolution, and ferroptosis-axis correlations were pre-specified, and replication was scored against a 13-criterion scorecard. Reporting followed the REMARK guidelines. Findings: Across 424 patients, GLP1R expression showed a protective hazard direction in all three cohorts (adjusted HR 0·81, 0·393, and 0·094 in TCGA, CGGA_693, and CGGA_325, respectively), without reaching statistical significance in any individual dataset. GLP1R-high tumours showed reproducible depletion of TNFα/NF-κB signalling, interferon-γ response, glycolysis, and oxidative phosphorylation across all three cohorts, an immune-cold microenvironment (eight Bindea signatures directionally negative in CGGA_693), and a discovery-cohort association with reduced NRF2/redox transcriptional tone (NFE2L2, HMOX1) that did not replicate in external validation. Interpretation: GLP1R expression delineates a transcriptomically coherent, immune-cold subgroup of IDH-wildtype glioblastoma. These findings provide a clinical context for the experimental GLP-1R–ferroptosis axis, although the axis itself did not replicate across cohorts, and a biological rationale for biomarker-stratified evaluation of GLP-1R agonists, ferroptosis inducers, and immune-priming combinations in this uniformly lethal disease.