Hazelnuts are rich in monounsaturated fatty acids and antioxidant bioactive substances: their consumption has been associated with a decreased risk of cardiovascular disease events. A systematic review and a meta-analysis was performed to combine the results from several trials and to estimate the pooled (overall) effect of hazelnuts on blood lipids and body weight outcomes. Specifically, a Bayesian random effect meta-analysis of mean differences of Δ-changes from baseline across treatment (MDΔ) (i.e., hazelnut-enriched diet vs. control diet) has been conducted. Nine studies representing 425 participants were included in the analysis. The intervention diet lasted 28–84 days with a dosage of hazelnuts ranging from 29 to 69 g/day. Out of nine studies, three randomized studies have been meta-analyzed showing a significant reduction in low-density lipoprotein (LDL) cholesterol (pooled MDΔ = −0.150 mmol/L; 95% highest posterior density interval (95%HPD) = −0.308; −0.003) in favor of a hazelnut-enriched diet. Total cholesterol showed a marked trend toward a decrease (pooled MDΔ = −0.127 mmol/L; 95%HPD = −0.284; 0.014) and high-density lipoprotein (HDL) cholesterol remained substantially stable (pooled MDΔ = 0.002 mmol/L; 95%HPD = −0.140; 0.147). No effects on triglycerides (pooled MDΔ = 0.045 mmol/L; 95%HPD = −0.195; 0.269) and body mass index (BMI) (pooled MDΔ = 0.062 kg/m²; 95%HPD = −0.293; 0.469) were found. Hazelnut-enriched diet is associated with a decrease of LDL and total cholesterol, while HDL cholesterol, triglycerides and BMI remain substantially unchanged.

Background: The classic ketogenic diet (cKD) has been used worldwide as an effective therapy for children with drug-resistant epilepsy. However, there have been no studies performed in Middle Eastern countries in order to assess the efficacy, side effects, predictors of cKD response and factors mostly associated with diet adherence. This study aims to assess the efficacy of cKD ratios of 4:1 and 3:1 and their influence on growth and biochemical parameters, particularly lipid profile and liver function tests (LFTs), and the factors most associated with diet adherence in a cohort of children with drug-resistant epilepsy in Bahrain. Methods: Baseline and follow-up data related to patients’ demographic and biochemical variables, epilepsy episodes, diet history and anthropometric measurements were retrieved for a total of 24 children treated with cKD in Bahrain. Results: After 6 months cKD initiation, 58.3% were positive responders with >50% seizure rate reduction, and 33.3% became seizure-free at 12 months. After 6 months of intervention with cKD, the level of triglycerides and albumin had a significant (p < 0.05) average increase over time of +1.47 mmol/L and 4.3 g/L, respectively. Although the median values of total cholesterol and alanine transaminase increased, respectively, following cKD initiation, the difference over time was not statistically significant. The mean z-scores for weight, height, and body mass index (or weight-for-length) did not change significantly at 12 months follow-up. cKD duration was the highest correlated variable with cKD efficacy (r = 0.76), which was followed by age at cKD initiation (r = 0.47). The cKD was discontinued by 14 patients (58.3%) during the first follow-up period (6 months), which was mainly due to inefficacy (n = 8), poor compliance (n = 3), food refusal (n = 1), achieved required efficacy (n = 1) and death (n = 1). Conclusions: cKD is an effective treatment for patients with drug-resistant epilepsy, and positive response to cKD was the main factor that increased adherence to the diet. Although long-term cKD could increase the risk of dyslipidemia and hepatic problems, it appears safe for children. Consequently, close monitoring and emphasis on healthy fats is of high priority.

In January 2022, our institution launched a comprehensive cancer genome profiling program on 10 cancer types using a non-IVD solution named the TruSight Oncology 500 Assay provided by Illumina^®. The assay analyzes both DNA and RNA, identifying Single-Nucleotide Variants (SNV)s and Insertion–Deletion (InDel) in 523 genes, as well as known and unknown fusions and splicing variants in 55 genes and Copy Number Alterations (CNVs), Mutational Tumor Burden (MTB) and Microsatellite Instability (MSI). According to the current European IVD Directive 98/79/EC, an internal validation was performed before running the test. A dedicated open-source bioinformatics pipeline was developed for data postprocessing, panel assessment and embedding in high-performance computing framework using the container technology to ensure scalability and reproducibility. Our protocols, applied to 71 DNA and 64 RNA samples, showed full agreement between the TruSight Oncology 500 assay and standard approaches, with only minor limitations, allowing to routinely perform our protocol in patient screening.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most recent definition for steatotic liver disease associated with metabolic syndrome. The results of recent metabolic and observational studies suggest a potential beneficial effect of food-derived flavonoids in some chronic diseases, including MASLD. The study aims to evaluate the protective role of diet flavonoids in subjects with and without MASLD belonging to a cohort living in the South of Italy. Methods: The study cohort comprised 1297 participants assessed in the NUTRIHEP cohort (2015–2018), divided into two groups, based on presence or absence of MASLD. Results: The results indicated statistically significant flavonoid consumption, showing a protective role against MASLD, at an optimal concentration of 165 mg/day, with an OR value of 0.63, (p = 0.001, 95% C.I.: 0.47; 0.83 t). The OR remained almost unchanged when the intake increased from 165 mg per day to 185 mg per day. Conclusions: In conclusion, our study results show a protective role of flavonoids against MASLD. Consuming only 165 mg of flavonoids daily can activate this protective function, reducing the risk of MASLD.

The progression of colorectal cancer (CRC) is driven by dynamic interactions between tumor cells and their microenvironment, particularly the extracellular matrix (ECM). Ion channels, critical regulators of cellular signaling, have emerged as mediators of ECM remodeling and tumor aggressiveness. In this study, we integrate transcriptomic data from 185 CRC tumors and 157 adjacent normal tissues with network modeling to dissect the interplay between ion channels and the ECM. We identified 4036 differentially expressed genes (DEGs), including 188 ion channel-associated DEGs (IC-DEGs) enriched in ECM-related pathways, such as collagen assembly, matrix metalloproteinase regulation, and mechanotransduction. Structural equation modeling revealed an active CRC−ion channel module (CRC-IC) comprising 482 nodes and 422 edges, highlighting dysregulated interactions between ECM components (e.g., COL1A1, COL5A2, VCAN, LAMA4, LA-MA5, LAMC1), ion channels (e.g., TRPM5 and SLC16A1), and cytoskeletal regulators. Key nodes, including CHST11 and VCAN, were associated with ECM sulfation, tumor invasiveness, and immune evasion. Notably, survival was associated with MAPK1, SLC16A1, and ABCB4 in relation to patient prognosis. Our findings underscore the pivotal role of ion channels as co-factors in ECM dynamics in CRC, offering mechanistic insights into tumor-stroma crosstalk and identifying potential therapeutic targets to disrupt microenvironment-driven progression.