Recent advances have highlighted the gut microbiota as a significant contributor to the development and progression of atherosclerosis, which is an inflammatory cardiovascular disease (CVD) characterized by plaque buildup within arterial walls. The gut microbiota, consisting of a diverse collection of microorganisms, impacts the host’s metabolism, immune responses, and lipid processing, all of which contribute to atherosclerosis. This review explores the complex mechanisms through which gut dysbiosis promotes atherogenesis. We emphasize the potential of integrating microbiota modulation with traditional cardiovascular care, offering a holistic approach to managing atherosclerosis. Important pathways involve the translocation of inflammatory microbial components, modulation of lipid metabolism through metabolites such as trimethylamine-N-oxide (TMAO), and the production of short-chain fatty acids (SCFAs) that influence vascular health. Studies reveal distinct microbial profiles in atherosclerosis patients, with increased pathogenic bacteria (Megamonas, Veillonella, Streptococcus) and reduced anti-inflammatory genera (Bifidobacterium, Roseburia), highlighting the potential of these profiles as biomarkers and therapeutic targets. Probiotics are live microorganisms that have health benefits on the host. Prebiotics are non-digestible dietary fibers that stimulate the growth and activity of beneficial gut bacteria. Interventions targeting microbiota, such as probiotics, prebiotics, dietary modifications, and faecal microbiota transplantation (FMT), present effective approaches for restoring microbial equilibrium and justifying cardiovascular risk. Future research should focus on longitudinal, multi-omics studies to clarify causal links and refine therapeutic applications.

Metabolomics, the research area studying chemical processes involving metabolites, finds its utility in inflammasome biomarker discovery, thus representing a novel approach for cardiometabolic syndrome pathogeny acknowledgements. Metabolite biomarkers discovery is expected to improve the disease evolution and outcome. The activation of abundantly expressed NLRP3 inflammasome represents the background process of the diabetes mellitus disturbances like hyperglycemia and insulin resistance, as well as for myocardial cell death and fibrosis, all of them being features characteristic for cardiometabolic syndrome. Many molecules like troponins, brain natriuretic protein (BNP), ST2/IL-33, C-reactive protein (CRP), TNF, IL-1β, and IL-18 cytokines have been already examined as molecular markers for diagnosing or predicting different cardiac disturbances like myocardial infarction, heart failure, or myocarditis. In addition, metabolomics research comes with new findings arguing that NLRP3 inflammasome becomes a promising molecular tool to use for clinical and therapeutical management providing new targets for therapies in cardiometabolic syndrome. Inflammasome markers analyses, along with other molecular or genetic biomarkers, will result in a better understanding of cardiometabolic syndrome pathogenesis and therapeutic targets. Screening, diagnostic, and prognostic biomarkers resulted from inflammasome biomarker research will become standard of care in cardiometabolic syndrome management, their utility becoming the first magnitude.

Direct oral anticoagulants (DOACs) such as apixaban or dabigatran are excellent options in preventing embolic cardiovascular events. Observational studies have shown that gastrointestinal bleeding risks produced by DOACs could be lowered when correcting some host co‑factors i.e. Helicobacter pylori (HP) infection. The upper digestive bleeding (UDB) rates in patients with DOAC indication and the usefulness of anti‑HP therapy addition were compared. An observational retrospective study was conducted of medical records of 260 patients treated with DOACs, 130 of whom were concomitantly treated for HP infection in accordance with Maastricht V/Florence consensus. The severity of bleeding, the complexity of endoscopic treatment required to stop the bleeding, the re‑bleeding rates, the surgical treatment indication and the overall mortality rates were compared between the groups. The risk of UDB was higher in HP‑untreated patients in both types of DOACs used (respectively 2.08, 2.02). HP‑untreated Forrest Ia/Ib/IIa and IIb DOACs patients had more severe bleedings compared with same class of HP‑treated patients (P=0.007/0.005; 0.009/0.006; 0.048/0.005, 0.044/0.049, respectively). Endoscopic treatments such as adrenaline injections combined with metallic clip attachments were more frequently mandatory in HP‑untreated DOACs patients for classes Ia/b and IIa (respectively, P=0.000/0.001, P=0.003/0.003). The re‑bleeding rates were higher in HP‑untreated patients with concomitant DOACs (OR 82.5; 95% CI 30.1‑121.7; P=0.005). A history of peptic ulcer or UDB was associated with a 2.9‑fold higher risk of UDB in HP‑untreated compared with HP‑treated patients, slightly increased for dabigatran compared with apixaban (RR 3.06, 2.72, P<0.5, respectively). Surgical intervention and the UDB‑related mortality rates were higher in HP‑untreated patients (P=0.041/0.044, P=0.007, respectively). HP‑eradication treatment and bacterial clearance improve the safety profile of DOACs treatment, especially in fragile patients, in whom the UDB rates can be lowered, and the overall outcome can be enhanced by this combined approach.

DLBCL is a testament to the complexity of nature. It is characterized by remarkable diversity in its molecular and pathological subtypes and clinical manifestations. Despite the strides made in DLBCL treatment and the introduction of innovative drugs, around one-third of patients face a relapse or develop refractory disease. Recent findings over the past ten years have highlighted the critical interplay between the evolution of DLBCL and various epigenetic mechanisms, including chromatin remodeling, DNA methylation, histone modifications, and the regulatory roles of non-coding RNAs. These epigenetic alterations are integral to the pathways of oncogenesis, tumor progression, and the development of therapeutic resistance. In the past decade, the identification of dysregulated epigenetic mechanisms in lymphomas has paved the way for an exciting field of epigenetic therapies. Crucially, these epigenetic transformations span beyond tumor cells to include the sophisticated network within the tumor microenvironment (TME). While the exploration of epigenetic dysregulation in lymphoma cells is thriving, the mechanisms affecting the functions of immune cells in the TME invite further investigation. This review is dedicated to weaving together the narrative of epigenetic alterations impacting both lymphoma cells with a focus on their infiltrating immune companions.

Tuberculosis (TB) is a highly contagious bacterial infection caused by Mycobacterium tuberculosis (MTB), affecting about 1/3rd of the world population and being responsible for lot of deaths worldwide, despite the progress achieved in the diagnosis and treatment fields. TB can affect the peritoneum, the TB ascites being a concern for physicians, especially when dealing with immunocompromised patients. The clinical presentation of TB ascites is challenging, due to nonspecific symptoms that make confusion with other diseases and the late results of cultures from ascites. The late diagnosis leads to a delayed treatment and high mortality. This manuscript describes recent tools used for early diagnosis in TB ascites. Molecular methods based on mycobacterial nucleic acid amplification tests (NAATs), polymerase chain reaction (PCR) detecting minimal amounts of bacterial DNA, or interferongamma release assays (IGRA) and biochemical methods such as the serum-ascites albumin gradient (SAAG) 40 UI/ml were recently considered more accurate diagnostic procedures. These methods allow a rapid and accurate differential diagnosis of ascites fluid, making possible the early treatment with appropriate drugs.