Objectives: The pathogenesis of oral cavity cancers is complex. We tested the hypothesis that oral microbiota dysbiosis is associated with oral cavity cancer. Materials and methods: Patients with primary oral cavity cancer who met the inclusion and exclusion criteria were included in the study. Matching healthy individuals were recruited as controls. Data on socio-demographic and behavioral factors, self-reported periodontal measures and habits, and current dental status were collected using a structured questionnaire and periodontal chartings. In addition to self-reported oral health measures, each participant received a standard and detailed clinical examination. DNA was extracted from saliva samples from patients and healthy controls. Next-generation sequencing was performed by targeting V3-V4 gene regions of the 16 S rRNA with subsequent bioinformatic analyses. Results: Patients with oral cavity cancers had a lower quality of oral health than healthy controls. Proteobacteria, Aggregatibacter, Haemophilus, and Neisseria decreased, while Firmicutes, Bacteroidetes, Actinobacteria, Lactobacillus, Gemella, and Fusobacteria increased in oral cancer patients. At the species level, C. durum, L. umeaens, N. subflava, A. massiliensis, and V. dispar were significantly lower, while G. haemolysans was significantly increased (p < 0.05). Major periodontopathogens associated with periodontal disease (P. gingivalis and F.nucleatum) increased 6.5- and 2.8-fold, respectively. Conclusion: These data suggested that patients with oral cancer had worse oral health conditions and a distinct oral microbiome composition that is affected by personal daily habits and may be associated with the pathogenicity of the disease and interspecies interactions. Clinical relevance: This paper demonstrates the link between oral bacteria and oral cancers, identifying mechanistic interactions between species of oral microbiome.

Hepatitis E virus (HEV) is one of the major foodborne viral pathogens transmitted through the fecal-oral route. Four genotypes of HEV are known to infect humans and it is reported that different types of HEV are active in zoonotic transitions. It is known that the HEV genotype 1 and HEV genotype 2 infections are generally acute and the HEV genotype 3 infections are chronic. Therefore, in the studies related to HEV infections, it is important to determine the genotypes to monitortreatment regimens. Although raw milk is often used in communities due to its low cost, there are limited data on the rates and the genotypes of HEV in our country and in the world. In light of this information, we aimed to investigate epidemiologically the quantity and genotypes of HEV RNA in 231 raw milk (48 cow milk, 65 goat milk, 65 sheep milk, and 53 donkey milk) samples. Viral RNAs were isolated from raw milk samples and the ORF2 region of HEV was investigated by the qRt-PCR method to determine quantitatively the presence of HEV RNA. In addition, among HEV RNA positive samples, the ORF2 region of HEV was amplified by nested PCR and the amplicons were sequenced. HEV RNA was detected in 47 (20.34%) raw milk samples, Positivity was detected in 14 (29.16%) of cow milk, 12 (18.46%) of goat milk, 8 of sheep milk (12.3) and 13 of donkey milk (24.5%). The amount of HEV RNA in cow milk found as the highest in both proportion and quantity. When the distribution of the HEV genotypes in the 47 positive samples was examined, 27 (57.44%) HEV genotype 1a, 10 (21.27%) HEV genotype 1b, 4 (8.5%) HEV genotype 4c, 2 (4.2%) HEV genotype 3a, (2.13) HEV genotype 1c, 1 (2.13%) HEV genotype 3e, 1 (2.13%) HEV genotype 3f and 1 (2.13%) HEV genotype 3g were determined. Although genotype 1a is more frequent, it has been revealed that different genotypes encountered in our country. In conclusion, it has been determined that HEV, one of the major foodborne viral agents, may be encountered in raw milk, and the genotypes that can cause infections in human are found especially in raw milk from animal sources. For the prevention of foodborne outbreaks, the presence of HEV in raw milk should not be ignored.

Escherichia coli sequence type 131 is an important multidrug resistant clone responsible from more than half of ESBL-producing E.coli isolates. Aim of this study was to investigate the presence of O25b-ST131 clone, CTX-M-15 and CTX-M-1 genes in the E. coli strains isolated from both hospital and community acquired UTIs by real-time PCR and to reveal molecular epidemiological data. Non-duplicate E. coli (n = 101) strains isolated from UTI patients were included. Bacterial identifications were performed with VITEK Compact. Antimicrobial susceptibility tests, phenotypic ESBL and E-tests were performed conventionally. Real-time PCR was utilized to detect presence of O25b-ST131 clone, blaCTX-M-15 and blaCTX-M-1. O25b-ST131 clone, CTX-M-1 and CTX-M-15 were detected in 22%, 73%, 37% in UTIs, respectively. Presence of O25b-ST131 clones and CTX-M-1 genes among E. coli strains isolated from inpatients were found statistically higher than outpatients. The most effective choice was found to be fosfomycin and nitrofurantoin in outpatients and inpatients, respectively. The MIC90 values of Amikacin, Cefotaxime, Cefepime and Ciprofloxacin were higher in inpatients than in oupatients, whereas Cefotaxime and Ciprofloxacin MIC50 values were found to be higher in inpatients than in outpatients. The highest increase of MIC90 values was observed in O25b-ST131, CTX-M-1 and CTX-M-15 coexistence. The presence of O25b-ST131 clone, CTX-M-1 and CTX-M-15 genes in E. coli strains in patients with UTI has been revealed. In the presence of the O25b-ST131 clone, a significant increase was observed in the ciprofloxacin MIC values indicating the importance of monitorization of the clone using molecular epidemiology.

Fusobacterium nucleatum, a pathobiont in periodontal disease, contributes to alveolar bone destruction. We assessed the efficacy of a new targeted antimicrobial, FP-100, in eradicating F. nucleatum from the oral microbial community in vitro and in vivo and evaluated its effectiveness in reducing bone loss in a mouse periodontitis model. A multispecies bacterial community was cultured and treated with two concentrations of FP-100 over two days. Microbial profiles were examined at 24-h intervals using 16S rRNA sequencing. A ligature-induced periodontitis mouse model was employed to test FP-100 in vivo. FP-100 significantly reduced Fusobacterium spp. within the in vitro community (p < 0.05) without altering microbial diversity at a 2 μM concentration. In mice, cultivable F. nucleatum was undetectable in FP-100-treated ligatures but persistent in controls. Beta diversity plots showed distinct microbial structures between treated and control mice. Alveolar bone loss was significantly reduced in the FP-100 group (p = 0.018), with concurrent decreases in gingival IL-1β and TNF-α expression (p = 0.052 and 0.018, respectively). FP-100 effectively eliminates F. nucleatum from oral microbiota and significantly reduces bone loss in a mouse periodontitis model, demonstrating its potential as a targeted therapeutic agent for periodontal disease.

NAFLD is the most common cause of chronic liver disease worldwide. The miRNAs and lncRNAs are important endogenous ncRNAs families that can regulate molecular mechanisms. The aim of this study was to analyze the miRNA and lncRNA expression profiles in serum samples of NAFLD patients with different types of hepatosteatosis compared to healthy controls by the qPCR method. A total of180 NAFLD patients and 60 healthy controls were included. miRCURY LNA miRNA miRNome PCR human panel I + II kit and LncProfiler qPCR Array Kit were used to detect miRNA and lncRNA expression, respectively. DIANA miRPath and DIANA-lncBase web servers were used for interaction analysis. As a result, 75 miRNA and 24 lncRNA expression changes were determined. For miRNAs and lncRNAs, 30 and 5 were downregulated and 45 and 19 were upregulated, respectively. hsa-miR-21 was upregulated 2-fold whereas miR-197 was downregulated 0.25-fold. Among lncRNAs, NEAT1 was upregulated 2.9-fold while lncRNA MEG3 was downregulated 0.41-fold. A weak correlation was found between hsa-miR-122 and lncRNA MALAT1. As a conclusion, it is clear that lncRNA–miRNA interaction is involved in the molecular mechanisms of the emergence of NAFLD. The lncRNAs MEG3 and PTENP1 interacted with hsa-miR-21. It was thought that this interaction should be investigated as a biomarker for the development of NAFLD.