The use of derivatives of natural and synthetic origin has gained attention because of their therapeutic effects against human diseases. Coumarins are one of the most common organic molecules and are used in medicine for their pharmacological and biological effects, such as anti-inflammatory, anticoagulant, antihypertensive, anticonvulsant, antioxidant, antimicrobial, and neuroprotective, among others. In addition, coumarin derivates can modulate signaling pathways that impact several cell processes. The objective of this review is to provide a narrative overview of the use of coumarin-derived compounds as potential therapeutic agents, as it has been shown that substituents on the basic core of coumarin have therapeutic effects against several human diseases and types of cancer, including breast, lung, colorectal, liver, and kidney cancer. In published studies, molecular docking has represented a powerful tool to evaluate and explain how these compounds selectively bind to proteins involved in various cellular processes, leading to specific interactions with a beneficial impact on human health. We also included studies that evaluated molecular interactions to identify potential biological targets with beneficial effects against human diseases.

Inflammatory Bowel Disease (IBD) is a chronic gastrointestinal disorder characterized by periods of activity and remission. IBD includes Crohn’s disease (CD) and ulcerative colitis (UC), and even though IBD has not been considered as a heritable disease, there are genetic variants associated with increased risk for the disease. 5-Hydroxytriptamine (5-HT), or serotonin, exerts a wide range of gastrointestinal effects under both normal and pathological conditions. Furthermore, Serotonin Transporter (SERT) coded by Solute Carrier Family 6 Member 4 (SLC6A4) gene (located in the 17q11.1-q12 chromosome), possesses genetic variants, such as Serotonin Transporter Gene Variable Number Tandem Repeat in Intron 2 (STin2-VNTR) and Serotonin-Transporter-linked promoter region (5-HTTLPR), which have an influence over the functionality of SERT in the re-uptake and bioavailability of serotonin. The intestinal microbiota is a crucial actor in normal human gut physiology, exerting effects on serotonin, SERT function, and inflammatory processes. As a consequence of abnormal serotonin signaling and SERT function under these inflammatory processes, the use of selective serotonin re-uptake inhibitors (SSRIs) has been seen to improve disease activity and extraintestinal manifestations, such as depression and anxiety. The aim of this study is to integrate scientific data linking the intestinal microbiota as a regulator of gut serotonin signaling and re-uptake, as well as its role in the pathogenesis of IBD. We performed a narrative review, including a literature search in the PubMed database of both review and original articles (no date restriction), as well as information about the SLC6A4 gene and its genetic variants obtained from the Ensembl website. Scientific evidence from in vitro, in vivo, and clinical trials regarding the use of selective serotonin reuptake inhibitors as an adjuvant therapy in patients with IBD is also discussed. A total of 194 articles were used between reviews, in vivo, in vitro studies, and clinical trials.

SARS-CoV-2 is the etiological agent of COVID-19 and may evolve from asymptomatic disease to fatal outcomes. Real-time reverse-transcription polymerase chain reaction (RT-PCR) screening is the gold standard to diagnose severe accurate respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but this test is not 100% accurate, as false negatives can occur. We aimed to evaluate the potential false-negative results in hospitalized patients suspected of viral respiratory disease but with a negative previous SARS-CoV-2 RT-PCR and analyze variables that may increase the success of COVID-19 diagnosis in this group of patients. A total of 55 hospitalized patients suspected of viral respiratory disease but with a previous negative RT-PCR result for SARS-CoV-2 were included. All the participants had clinical findings related to COVID-19 and underwent a second SARS-CoV-2 RT-PCR. Chest-computed axial tomography (CT) was used as an auxiliary tool for COVID-19 diagnosis. After the second test, 36 patients (65.5%) were positive for SARS-CoV-2 (COVID-19 group), and 19 patients (34.5%) were negative (controls). There were differences between the groups in the platelet count and the levels of D-dimer, procalcitonin, and glucose (p < 0.05). Chest CT scans categorized as COVID-19 Reporting and Data System 5 (CO-RADS 5) were more frequent in the COVID-19 group than in the control group (91.7% vs. 52.6%; p = 0.003). CO-RADS 5 remained an independent predictor of COVID-19 diagnosis in a second SARS-CoV-2 screening (p = 0.013; odds ratio = 7.0, 95% confidence interval 1.5–32.7). In conclusion, chest CT classified as CO-RADS 5 was an independent predictor of a positive second SARS-CoV-2 RT-PCR, increasing the odds of COVID-19 diagnosis by seven times. Based on our results, in hospitalized patients with a chest CT classified as CO-RADS 5, a second SARS-CoV-2 RT-PCR test should be mandatory when the first one is negative. This approach could increase SARS-CoV-2 detection up to 65% and could allow for isolation and treatment, thus improving the patient outcome and avoiding further contagion.

Hemophagocytic syndrome (HPS) is a common complication in pediatric populations but a rare disease in adults. Also known as hemophagocytic lymphohistiocytosis (HLH), the few cases reported in adults have been primarily caused by severe infections and hematologic malignancies. We highlight the importance of considering HPS as a differential diagnosis in patients with persistent inflammatory conditions. This report describes the aggressive clinical course of a 58-year-old female patient. Prompt recognition of HPS may improve outcomes in such cases.

Post-COVID-19 condition can include persistent cognitive symptoms, commonly described as impaired attention, memory difficulties, slowed processing, and “brain fog.” Clinical and translational evidence implicates systemic inflammation, neurovascular dysfunction, blood–brain barrier disruption, glial inflammatory responses, oxidative stress, and altered synaptic or network function; their relative contributions remain uncertain and may differ across patient subgroups. Resveratrol is a polyphenolic compound that modifies inflammatory, redox, metabolic, endothelial, and antiviral pathways in experimental systems. This focused narrative review examines whether those actions provide a mechanistic basis for the use of resveratrol in post-COVID-19 cognitive dysfunction. Evidence was considered according to biological proximity to the intended indication, distinguishing human post-acute sequelae of SARS-CoV-2 infection (PASC) studies from acute-COVID-19, non-COVID-19 clinical, animal, organoid, and cell-based evidence. The review identifies candidate neurovascular, immune, and metabolic processes, evaluates where resveratrol evidence intersects with those processes, and distinguishes molecular observations from clinical questions that remain to be tested for to define the therapeutic potential of using resveratrol to treat post-COVID-19 cognitive impairment.