Epigenetic MicroRNAs as Prognostic Markers of Postoperative Atrial Fibrillation: A Systematic Review.

Postoperative atrial fibrillation (POAF) is a common complication after cardiac surgery, increasing the risk for adverse outcomes such as perioperative and long-term mortality, stroke, myocardial infarction, and other thromboembolic events. Epigenetic biomarkers show promise as prognostic tools for POAF. Epigenetic changes, such as DNA methylation, histone modification, and microRNAs (miRNA), can result in altered gene expression and the development of various pathological conditions. This systematic review aims to present the current literature on the association between various epigenetic markers and the development of POAF following cardiac surgery. Here, an electronic literature search was performed using MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, ClinicalTrials.gov, and Google Scholar to identify studies that reported the role of epigenetic markers in the development of POAF. Five of the 6 studies focused on miRNAs and their association with POAF. In POAF patients, the expression of miR-1 and miR-483-5p were upregulated in the right atrial appendage (RAA), while the levels of miR-133A, miR-208a, miR-23a, miR-26a, miR-29a, miR-29b, and miR-29c were decreased in the RAA and venous blood. One study examined cytosines followed by guanines (CpGs) as DNA methylation markers. Across all studies, 488 human subjects who had undergone cardiac surgery were investigated, and 195 subjects (39.9%) developed new-onset POAF. The current literature suggests that miRNAs may play a role in predicting the development of atrial fibrillation after cardiac surgery. However, more robust clinical data are required to justify their role in routine clinical practice.

Contemporaneous Perioperative Inflammatory and Angiogenic Cytokine Profiles of Surgical Breast, Colorectal, and Prostate Cancer Patients: Clinical Implications.

Surgery-induced tumor growth acceleration and synchronous metastatic growth promotion have been observed for decades. Surgery-induced wound healing, orchestrated through growth factors, chemokines, and cytokines, can negatively impact patients harboring residual or metastatic disease. We provide detailed clinical evidence of this process in surgical breast, prostate, and colorectal cancer patients. Plasma samples were analyzed from 68 cancer patients who had not received treatment before surgery or adjuvant therapy until at least four weeks post-surgery. The levels of plasma cytokines, chemokines, and growth factors were simultaneously quantified and profiled using multiplexed immunoassays for eight time points sampled per patient. The immunologic processes are induced immediately after surgery in patients, characterized by a drastic short-term shift in the expression levels of pro-inflammatory and angiogenic molecules and cytokines. A rapid and significant spike in circulating plasma levels of hepatocyte growth factor (HGF), interleukin-6 (IL-6), placental growth factor (PLGF), and matrix metalloproteinase-9 (MMP-9) after surgery was noted. The rise in these molecules was concomitant with a significant drop in transforming growth factor-ß1 (TGF-ß1), platelet-derived growth factor (PDGF-AB/BB), insulin-like growth factor-1 (IGF-1), and monocyte chemoattractant protein-2 (MCP-2). If not earlier, each plasma analyte was normalized to baseline levels within 1-2 weeks after surgery, suggesting that surgical intervention alone was responsible for these effects. The effects of surgical tumor removal on disrupting the pro-inflammatory and angiogenic plasma profiles of cancer patients provide evidence for potentiating malignant progression. Our findings indicate a narrow therapeutic window of opportunity after surgery to prevent disease recurrence.

Contemporaneous SARS-CoV-2-Neutralizing Antibodies Mediated by N-glycan Shields.

Mutations and the glycosylation of epitopes can convert immunogenic epitopes into non-immunogenic ones via natural selection or evolutionary pressure, thereby decreasing their sensitivity to neutralizing antibodies. Based on Thomas Francis's theory, memory B and T cells induced during primary infections or vaccination will freeze the new mutated epitopes specific to naïve B and T cells from the repertoire. On this basis, some researchers argue that the current vaccines derived from the previous strains of the SARS-CoV-2 virus do not increase immunity and may also prevent the immune response against new epitopes. However, evidence shows that even if the binding affinity is reduced, the previous antibodies or T cell receptors (TCRs) can still bind to this new epitope of the Beta, Gamma, and Delta variant if their concentration is high enough (from a booster injection) and neutralize the virus. This paper presents some convincing immunological reasons that may challenge this theory and argue for the continuation of universal vaccination to prevent further mutations of the SARS-CoV-2 virus. Simultaneously, the information presented can be used to develop vaccines that target novel epitopes or create new recombinant drugs that do not lose their effectiveness when the virus mutates.

Metamorphic Effect of Angiogenic Switch in Tumor Development: Conundrum of Tumor Angiogenesis Toward Progression and Metastatic Potential.

Our understanding of angiogenesis has significantly expanded over the past five decades. More recently, research has focused on this process at a more molecular level, looking at it through the signaling pathways that activate it and its non-direct downstream effects. This review discusses current findings in molecular angiogenesis, focusing on its impact on the immune system. Moreover, the impairment of this process in cancer progression and metastasis is highlighted, and current anti-angiogenic treatments and their effects on tumor growth are discussed.