The existence of genetic traits might explain the susceptibility to develop hypercholesterolemia and the inter-individual differences in statin response. This study was performed to evaluate whether individuals’ polymorphisms in HMG-CoA and KIF6 genes are independently associated with hypercholesterolemia, other lipid-associated traits, and statin response in unselected individuals enrolled in the Brisighella heart study (Survey 2012). A total of 1622 individuals, of which 183 under statin medication, were genotyped for a total of five polymorphisms (KIF6 rs20455, rs9471077, rs9462535; HMG-CoA rs3761740, rs3846662). The relationships between the five loci and clinical characteristics were analyzed. The principal basic parameters calculated on 12 h fasting blood included total cholesterol (TC), High Density Lipoprotein Cholesterol (HDL-C), Low-Density Lipoprotein Cholesterol (LDL-C), and triglycerides (TG). Hypercholesterolemia was defined as a TC >200 mg/dL or use of lipid-lowering medication. 965 individuals were characterized by hypercholesterolemia; these subjects were significantly older (p < 0.001), with body mass index (BMI) and waist circumference significantly higher (p < 0.001) compared to the others. HMG-CoA rs3846662 GG genotype was significantly over-represented in the hypercholesterolemic group (p = 0.030). HMG-CoA rs3846662 genotype was associated with the level of TC and LDL-C. Furthermore, in the same subset of untreated subjects, we observed a significant correlation between the KIF6 rs20455 and HDL-C. KIF6 variants were associated with a significantly lower (rs20455) or higher (rs9471077 and rs9462535) risk of obesity, in males only. No association between responsiveness to statins and the polymorphisms under investigation were observed. Our results showed associations between HMG-CoA rs3846662 and KIF6 rs20455 and lipid phenotypes, which may have an influence on dyslipidemia-related events. Moreover, this represents the first study implicating KIF6 variants with obesity in men, and point to the possible involvement of this genetic locus in the known gender-related differences in coronary artery disease.

Historically, the Kazakhs formed through an amalgam of nomadic tribes that previously belonged to the Golden Horde. The Kazakh tribes were geographically divided into three tribal...

Dark fermentation of organic waste offers a means of coupling molecular hydrogen (H₂) production with the bioconversion of wet organic feedstocks. However, its practical performance remains limited by unstable carbon and electron-flow distribution, substrate heterogeneity, and dynamic shifts in microbial community structure. This review critically evaluates microbial consortium engineering as a strategy to improve the selectivity, stability, and controllability of dark-fermentative H₂ production. Available experimental evidence indicates that H₂ productivity is determined not by a single high-performing strain but by the coordinated activity of microorganisms responsible for hydrolysis, fermentation of soluble compounds, and conversion through H₂-producing pathways. Disruption of this coordination redirects carbon and electrons toward lactate, alcohols, methane, and homoacetogenic pathways. Synthetic microbial consortia enable more targeted control over community composition and the allocation of metabolic functions; nevertheless, their operational performance and reproducibility may decline substantially when defined model substrates are replaced by chemically heterogeneous, non-sterile waste-derived substrates. The most reproducible performance is achieved when community composition is matched to feedstock chemistry and reactor operating conditions. Further progress will require a transition from empirical culture selection to substrate-specific engineering of microbial functions supported by metabolite profiling, molecular analyses, and mass- and electron-balance data.

Fusarium oxysporum-associated disease symptoms in rice (Oryza sativa L.) seedlings represent an experimentally tractable model for evaluating microbiome-mediated disease suppression under controlled conditions. Biological control of Fusarium-associated disease development in rice provides a promising ecological alternative to chemical fungicides. However, the mechanisms underlying the spatial reconfiguration of the host plant multicompartment microbiome in response to complex inoculants remain insufficiently understood. In this study, we investigated the ability of the monoculture Bacillus amyloliquefaciens Bn1 (B. amyloliquefaciens Bn) and phototrophic–heterotrophic consortia composed of Nostoc sp. J-1 and B. amyloliquefaciens Bn1 to suppress Fusarium oxysporum infection, with parallel profiling of bacterial and fungal communities in rhizosphere soil, the root endosphere, and the phyllosphere using 16S rRNA and ITS amplicon sequencing. Phenotypic screening showed that microbial inoculant application significantly reduced the disease index by up to 55% while maintaining plant dry weight. The protective phenotype was not primarily associated with shifts in alpha diversity, but rather with compartment-specific reorganization of microbial communities. These findings suggest that biological control efficacy was associated less with the overall taxonomic scale of microbiome disturbance than with the formation of a functionally balanced, compartment-specific holobiont architecture but by the formation of a functionally balanced, compartment-specific holobiont architecture, providing a conceptual basis for the targeted design of next-generation phototrophic–heterotrophic biopreparations.

Individuals chronically exposed to low-level ionising radiation (IR) run the risk of harmful and long-term adverse health effects, including gene mutations and cancer development. The search for reliable biomarkers of IR exposure in human population is still of great interest, as they may have a great implementation potential for the surveillance of occupationally exposed individuals. In this context, and considering previous literature, this study aimed to identify mutations in the human interferon alpha-2b (hIFNα-2b) as a potential biomarker of occupational chronic low-dose IR exposure linking low-IR exposure to the effects on haematopoiesis and reduced immunity. The analysis was performed in the genomic DNA of 51 uranium miners and 38 controls from Kazakhstan, and in 21 medical radiology workers and 21 controls from Italy. hIFNα-2b gene mutations were analysed with the real-time polymerase chain reaction (PCR) or Sanger sequencing. However, none of the investigated workers had the hIFNα-2b mutation. This finding highlights the need for further research to identify biomarkers for early detection of health effects associated with chronic low-dose IR exposure.

Background: Interindividual radiosensitivity is largely driven by genetic regulation of DNA damage recognition, repair, and cell-cycle control. TP53 and CDKN1A (p21) are key genomic markers associated with differential responses to ionizing radiation. Methods: This study investigated eight functional SNP markers across several key genes involved in DNA damage responses and cellular stress regulation, including TP53, CDKN1A/p21, APC, VEGF, XPD, and RAD51, in occupational groups exposed to chronic low-dose ionizing radiation at the Stepnogorsk Mining Chemical Combine and the Balkashinskoye uranium deposit. Genotyping was performed using PCR-based assays followed by restriction fragment length polymorphism (RFLP) analysis. Allele and genotype frequencies were compared between radiation-exposed workers and matched controls within Kazakh and Russian ethnic subgroups. Statistical differences were assessed using χ² tests, and associations with radioresistance were interpreted based on established functional characteristics of each polymorphism. Results: Four SNPs showed significant allele and genotype frequency shifts in radiation-exposed populations. The TP53 intron 3 insertion allele, TP53 intron 6 A allele, TP53 Pro72 (C) allele, and p21 codon 31 A allele were consistently enriched among exposed individuals. The strongest deviations were observed in Russian workers from Stepnogorsk (p < 0.01). These alleles are functionally associated with enhanced DNA repair efficiency, modified apoptotic responses, and strengthened cell-cycle checkpoint regulation. Conclusions: Significant enrichment of radioresistance-associated TP53 and CDKN1A (p21) variants was observed in uranium industry workers chronically exposed to low-to-moderate ionizing radiation. The observed patterns support a polygenic model of adaptive responses and emphasize the importance of genetic background in determining individual radiosensitivity under occupational exposure conditions.