Metabolic syndrome (MetS) is a group of physiological abnormalities characterized by obesity, insulin resistance (IR), and hypertriglyceridemia, which carry the risk of developing cardiovascular disease (CVD) and type 2 diabetes (T2D). Immune and metabolic alterations have been observed in MetS and are associated with autoimmune development. Systemic lupus erythematosus (SLE) is an autoimmune disease caused by a complex interaction of environmental, hormonal, and genetic factors and hyperactivation of immune cells. Patients with SLE have a high prevalence of MetS, in which elevated CVD is observed. Among the efforts of multidisciplinary healthcare teams to make an early diagnosis, a wide variety of factors have been considered and associated with the generation of biomarkers. This review aimed to elucidate some primary biomarkers and propose a set of assessments to improve the projection of the diagnosis and evolution of patients. These biomarkers include metabolic profiles, cytokines, cardiovascular tests, and microRNAs (miRs), which have been observed to be dysregulated in these patients and associated with outcomes.

Background. Leprosy is a debilitating infectious disease of human skin and nerves. Genetics factors of the host play an important role in the disease susceptibility. Toll-interacting protein (TOLLIP) is an inhibitory adaptor protein within the toll-like receptor (TLR) pathway, which recognizes structurally conserved molecular patterns of microbial pathogens, initiating immune responses. The objective of this study was to investigate the association of variants in theTOLLIPgene with susceptibility to leprosy in Mexican patients.Methods.TOLLIPpolymorphisms were studied using a case-control design of Mexican patients with lepromatous leprosy (LL). The polymorphisms ofTOLLIPat loci −526 C>G (rs5743854), 1309956C>T (rs3750920), 1298430C>A (rs5744015), and 1292831 G>A (rs3750919) were analyzed by PCR, with sequence-specific primers in LL patients and healthy subjects (HS) as controls.Results. Genotype distributions were in Hardy Weinberg equilibrium for all sites except for rs3750920. Neither genotype nor allele frequencies were statistically different between LL patients and controls (P>0.05). The maximum pairwise D’ coefficient reached was 0.44 of linkage (P=0.01) for all the polymorphisms except for rs5743854. The three loci haplotype comparison yielded no significant differences between groups.Conclusions. Just the individuals with genotype C/C of rs3750920 have a trend of protective effect to developing LL.

Chronic migraines have been described chiefly only from a clinical perspective. However, searching for reliable molecular markers has allowed for the discovery of the expression of different genes mainly associated with inflammation, neuro-vascularization, and pain-related pathways. The interest in microRNAs (miRs) that can regulate the expression of these genes has gained significant relevance since multiple miRs could play a key role in regulating these events. In this study, miRs were searched in samples from patients with chronic migraine, and the inclusion criteria were carefully reviewed. Different bioinformatic tools, such as miRbase, targetscan, miRPath, tissue atlas, and miR2Disease, were used to analyze the samples. Our findings revealed that some of the miRs were expressed more (miR-197, miR-101, miR-92a, miR-375, and miR-146b) and less (miR-133a/b, miR-134, miR-195, and miR-340) than others. We concluded that, during chronic migraine, common pathways, such as inflammation, vascularization, neurodevelopment, nociceptive pain, and pharmacological resistance, were associated with this disease.

Background: Migraine is a disabling neurological disorder where the release of neuropeptides and a local and systemic proinflammatory state prevail. MicroRNAs (miRs) are epigenetic regulators that control the expression of genes involved in inflammation, neovascularization, and pain-related processes. Cytokines mediate the inflammatory state, while miRs can modulate their expression. Methods: This is an analytical and observational study in which subjects with a diagnosis of chronic and episodic migraine and healthy controls were recruited, and the migraine patients were classified by episodic or chronic migraine, as well as with or without aura. Cytokines were measured using the ELISA technique, and the microRNAs hsa-miR-197-3p, hsa-miR-101-3p, and hsa-miR-143-3p were evaluated using qPCR methodology. We also utilized bioinformatic tools, such as miRBase, TargetScan, miRNet, and miRPath, to analyze the interactions and pathways involved. Results: Our findings revealed that hsa-miR-197-3p is elevated in patients without aura (29.91 ± 11.14 with aura vs. 81.10 ± 53.85 without aura, RU; p = 0.021), whereas hsa-miR-143-3p is elevated in episodic migraine (0.0639 ± 0.0227 in EM vs. 0.0308 ± 0.0174, RU p = 0.011). Furthermore, we found higher levels of IL-17 (9.46 ± 1.06 in CM vs. 7.61 ± 2.12 in EM, p = 0.030), IL-6 (4.95 ± 2.84 in CM vs. 1.52 ± 0.98 non-migraine subjects, p = 0.016), and TNFα in chronic migraine patients (0.46 ± 0.24 in CM vs. 0.20 ± 0.05 in non-migraine, p = 0.011 and vs. 0.20 ± 0.13 in EM, p = 0.016). Conclusions: Inflammation is present in migraine regardless of the clinical characteristics of the patients, although it may be accentuated in chronic migraine. Our preliminary findings suggest a potential role for peripheral inflammatory markers, including specific microRNAs (miR-197, miR-101, and miR-143) and cytokines (TNF-α, IL-6, and IL-17A), in the pathophysiology of migraine. These results, although limited by sample size and cross-sectional design, highlight molecular pathways that warrant further investigation.

MicroRNAs (miR) have emerged as key regulatory molecules in immune response and inflammation. This study investigated the association between the plasma expression levels of miR-146a-5p, miR-143-3p, miR-145-5p and rheumatoid arthritis (RA) clinical activity measured by standard tools such as the Simplified Disease Activity Index (SDAI). Forty-eight RA patients fulfilling the EULAR/ACR 2010 criteria and 39 clinical apparently healthy subjects (HS) were included. Patients were categorized based on disease clinical activity using standard scores. Expression levels of miR were determined by RT-qPCR to be analyzed in the context of disease clinical activity, serum inflammation markers and autoantibodies such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP). Bioinformatic analysis was performed to assess gene interactions and signaling pathways. The expression of miR-146a-5p showed higher expression in patients with low or moderate clinical disease activity. In addition, miR-145-5p was negatively correlated with both RF and anti-CCP antibodies. Bioinformatic analysis revealed that the miRs could simultaneously regulate myosin VI (MYO6) and connective tissue growth factor (CTGF) genes. Our findings suggest that the plasma levels of the analyzed miR are associated with key serological markers and low to moderate disease clinical activity in RA patients according to SDAI score. The bioinformatics data supports the potential for these miRs to regulate genes involved in RA pathology.

Equisetum hyemale extract promotes wound healing in diabetic rats, but its cytotoxicity limits its use. This study aimed to encapsulate the extract in collagen–polyurethane–dextran semi-interpenetrating network hydrogels containing 20–30 wt% dextran and 20–40 wt% extract. The physicochemical properties, in vitro biological responses, and wound-healing performance of the hydrogels were subsequently evaluated. The hydrogels exhibited crosslinking degrees of 65–80%, swelling capacities of 2800–3100%, predominantly elastic behavior, and structural integrity for up to 30 days under hydrolytic and proteolytic conditions. The D20C20 formulation (20% dextran and 20% extract) showed the greatest polyphenol permeation (940 µg/mL after 120 h) and permeability coefficient (Kp = 9.9 × 10⁻³ cm/h). Cell viability varied depending on the formulation, cell type, and exposure time. Macrophages and mononuclear cells exhibited transient increases in the MTT-derived viability signal after 24 h, followed by decreases after 72 h. However, fibroblast viability remained consistent across formulations. Most formulations increased IL-10 and reduced MCP-1 in lipopolysaccharide-stimulated macrophages after 72 h. No hemolysis or dermal irritation occurred under the tested conditions. In diabetic rats, D20C20 achieved complete wound closure by day 17. The regenerated tissue exhibited a more organized collagen arrangement. These findings support further investigation of D20C20 as a potential wound-healing material.