5-fluorouracil (5-FU) remains the gold standard of treatment for colorectal cancer, but its poor bioavailability and high systemic toxicity highlight the urgent need for the development of novel delivery strategies to increase the efficacy of 5-FU treatment. The present study is aimed to design and validate a PEGylated Silk Fibroin Nanocarrier (SF/PEG nanoparticles (NPs)) as an efficient 5-FU delivery system for potential intravenous administration. Using the human adenocarcinoma HT–29 cell line as an in vitro model for colorectal cancer, the cytotoxicity screening of the SF/PEG NPs showed that pristine nanocarriers were highly biocompatible, while the addition of 5-FU triggers a dramatic reduction in tumor cell viability, proliferation potential and mitochondrial integrity as well as a significant increase in nitric oxide production. Despite their high in vitro cytotoxicity, the 5-FU SF/PEG NPs were found hemocompatible as no impact on red blood cells hemolysis or the phagocytic activity of the granulocytes was observed. Exposure of HT–29 tumor cells and blood samples to 5-FU SF/PEG NPs augmented the tumor necrosis factor-α levels. Moreover, 5-FU SF/PEG NPs showed an impact on tumor cell migration and invasive potential as both of these processes were inhibited by the NP treatment.

We present the case of a patient with a giant paraesophageal hernia associated with paroxysmal postprandial atrial fibrillation that was suppressed after surgery. The imaging investigations showed the intrathoracic displacement of a large part of the stomach, which pushed the left atrial wall causing atrial fibrillation. The laparoscopic surgical repair acted as sole treatment for this condition.

Colorectal cancer (CRC) remains a major global challenge, with growing attention to its pathogenesis as mediated by the gut microbiome and epigenetic regulation. Despite therapeutic progress, clinical management remains difficult. CRC accounts for ~10% of cancers and is the second leading cause of cancer death worldwide. Romania bears a substantial burden, with many diagnoses at advanced stages. Etiology—Integrated Genetic, Environmental, and Microbial Determinants. Hereditary syndromes explain 10–15% of cases; most are sporadic, with hypermutated MSI/POLE (~15%), non-hypermutated chromosomal instability (~85%), and a CpG island methylator phenotype (~20%). GWAS implicate loci near SMAD7, TCF7L2, and CDH1; in Romania, SMAD7 rs4939827 associates with risk. Lifestyle exposures—high red/processed meat, low fiber, adiposity, alcohol, and smoking—shape susceptibility. Microbiome–Epigenome Interactions. Dysbiosis promotes carcinogenesis via genotoxins (e.g., colibactin), hydrogen sulfide, activation of NF-κB/STAT3, barrier disruption, and epigenetic remodeling of DNA methylation and microRNAs. Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, and pks⁺ Escherichia coli exemplifies these links. Population-Specific Risk—Romania within Lifestyle–Microbiome Evidence. Incidence is rising, including early-onset disease. Romania lacks CRC-specific microbiome datasets. However, metabolic cohorts show loss of butyrate producers, enrichment of pathobionts, and SCFA imbalance—patterns that mirror European CRC cohorts—and exhibit regional heterogeneity. Beyond Fusobacterium nucleatum. Additional oncobacteria shape tumor biology. Peptostreptococcus stomatis activates integrin α6/β4→ERBB2–MAPK and can bypass targeted inhibitors, while Parvimonas micra enhances WNT/β-catenin programs and Th17-skewed immunity. Together, these data support a systems view in which microbial cues and host epigenetic control jointly drive CRC initiation, progression, metastasis, and treatment response.

Nowadays, using polymers with specific characteristics to coat the surface of a device to prevent undesired biological responses can represent an optimal strategy for developing new and more efficient implants for biomedical applications. Among them, zwitterionic phosphorylcholine-based polymers are of interest due to their properties to resist cell and bacterial adhesion. In this work, the Matrix-Assisted Laser Evaporation (MAPLE) technique was investigated as a new approach for functionalising Polydimethylsiloxane (PDMS) surfaces with zwitterionic poly(2-Methacryloyloxyethyl-Phosphorylcholine) (pMPC) polymer. Evaluation of the physical–chemical properties of the new coatings revealed that the technique proposed has the advantage of achieving uniform and homogeneous stable moderate hydrophilic pMPC thin layers onto hydrophobic PDMS without any pre-treatment, therefore avoiding the major disadvantage of hydrophobicity recovery. The capacity of modified PDMS surfaces to reduce bacterial adhesion and biofilm formation was tested for Gram-positive bacteria, Staphylococcus aureus (S. aureus), and Gram-negative bacteria, Escherichia coli (E. coli). Cell adhesion, proliferation and morphology of human THP-1 differentiated macrophages and human normal CCD-1070Sk fibroblasts on the different surfaces were also assessed. Biological in vitro investigation revealed a significantly reduced adherence on PDMS–pMPC of both E. coli (from 29 × 10 ⁶ to 3 × 10² CFU/mL) and S. aureus (from 29 × 10⁶ to 3 × 10² CFU/mL) bacterial strains. Additionally, coated surfaces induced a significant inhibition of biofilm formation, an effect observed mainly for E. coli. Moreover, the pMPC coatings improved the capacity of PDMS to reduce the adhesion and proliferation of human macrophages by 50% and of human fibroblast by 40% compared to unmodified scaffold, circumventing undesired cell responses such as inflammation and fibrosis. All these highlighted the potential for the new PDMS–pMPC interfaces obtained by MAPLE to be used in the biomedical field to design new PDMS-based implants exhibiting long-term hydrophilic profile stability and better mitigating foreign body response and microbial infection.

Background: Systemic inflammatory indices are increasingly used to predict prognosis in colorectal cancer (CRC), yet direct comparisons between colon cancer (CC) and rectal cancer (RC) remain limited. Methods: We conducted a retrospective matched-cohort study including 296 patients (148 with CC and 148 with RC) surgically treated between January 2018 and December 2024. Patients were matched by tumor stage, sex, and age (±3 years). Preoperative blood samples were used to calculate several inflammatory markers, including Neutrophil-to-Lymphocyte Ratio (NLR), Platelet-to-Lymphocyte Ratio (PLR), Monocyte-to-Lymphocyte Ratio (MLR), Systemic Inflammation Response Index (SIRI), Systemic Immune-Inflammation Index (SII), and Aggregate Index of Systemic Inflammation (AISI). Subgroup analyses were performed based on the Charlson Comorbidity Index (>3 vs. ≤3), surgical context (elective vs. emergency), and tumor stage (T1–T2 vs. T3–T4). Results: Colon cancer patients exhibited significantly higher levels of systemic inflammation compared to those with rectal cancer, with notable differences in NLR (3.99 vs. 2.84, p < 0.001), PLR (219.8 vs. 163.3, p < 0.001), SIRI (3.7 vs. 1.91, p = 0.004), SII (1533.8 vs. 847.8, p < 0.001), and AISI (1714.7 vs. 593.6, p = 0.009). These differences remained statistically significant in key subgroups. In elective surgeries, CC patients had elevated PLR (p < 0.001), SIRI (p = 0.003), SII (p < 0.001), and AISI (p = 0.013). Among patients with advanced tumors (T3–T4), CC was associated with higher SII (p < 0.001), AISI (p = 0.008), PLR (p < 0.001), and SIRI (p = 0.004). For those with a Charlson index > 3, CC patients showed significantly higher PLR (p < 0.001), NLR (p < 0.001) and SIRI (p = 0.001). Conclusions: colon cancer presents with a markedly stronger systemic inflammatory response than rectal cancer, particularly in patients with advanced disease, elective surgical treatment, and higher comorbidity burden. These findings suggest that indices such as SIRI, SII, and PLR may serve as valuable stratification tools beyond tumor location in CRC.