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.

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: Hospital malnutrition remains a significant global issue. Accurate screening and diagnosis within 24 to 48 hours of admission are crucial for reducing morbidity and mortality. The global leadership initiative on malnutrition (GLIM) criteria provide a standardized framework for diagnosing malnutrition, but their validation in military hospitals has been limited. Objectives: To validate the GLIM criteria for diagnosing malnutrition in hospitalized patients at a third-level military hospital. Methods: A cross-sectional study was conducted involving hospitalized patients at Mexico City’s Central Military Hospital. The GLIM criteria were compared to the subjective global assessment (SGA). Sensitivity, specificity, predictive values, and concordance were assessed. Results: Nutritional screening indicated that 19.5% of patients were malnourished according to the GLIM criteria, while 19.8% were identified as malnourished by the SGA. Regarding severity, 18.3% had moderate malnutrition and 1.2% had severe malnutrition according to the GLIM criteria; for the SGA, the corresponding prevalences were 18.2% and 1.5%. In terms of validation, compared to the SGA, the GLIM criteria demonstrated a sensitivity of 81.25% and a specificity of 95.37%, with moderate agreement (Kappa = 0.755). Conclusions: The GLIM criteria are a reliable diagnostic tool for hospital-acquired malnutrition and should be implemented in accordance with global standardization.

Over time, our understanding of the central nervous system (CNS) as an immunologically privileged site where immune-cell infiltration takes place has changed; research has transformed the dominant view, showing that the CNS is an immunologically specialized tissue featuring complex interactions between the immune system and CNS processes, where the choroid plexus (CP) has an essential role in regulating neuronal tissue homeostasis and immune-cell trafficking. Although immune-cell entry into the CNS is tightly controlled, small numbers of antigen-experienced lymphocytes can access cerebrospinal fluid (CSF) compartments for immune surveillance under normal conditions. During an injury, such as cerebral ischemia or spinal cord damage, dendritic cell precursors infiltrate the CNS, suggesting their involvement in modulating lymphocyte activity. However, the immunoregulatory function of the CP alone is insufficient to prevent damage. Injury can trigger a cascade of events including activation of microglia toward a pro-inflammatory M1 phenotype, infiltration of peripheral immune cells across the blood–brain barrier (BBB), and uncontrolled neuroinflammation. T cells play a critical role in this process. Th1 cells exacerbate inflammation upon recognizing neural antigens, whereas Th2 cells promote recovery by releasing neurotrophic factors. This highlights the dual role of inflammation in CNS injury and repair.