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Abstract Background Ticagrelor is a reversibly binding, direct-acting, oral, P2Y12 antagonist used for the prevention of atherothrombotic events in patients with coronary artery disease (CAD). Ticagrelor blocks adenosine reuptake through the inhibition of equilibrative nucleoside transporter 1 (ENT-1) on erythrocytes and platelets, thereby facilitating adenosine-induced physiological responses such as an increase in coronary blood flow velocity. Meanwhile, adenosine plays an important role in triggering ischemic preconditioning through the activation of the A1 receptor. Therefore, an increase in ticagrelor-enhanced adenosine bioavailability may confer beneficial effects through mechanisms related to preconditioning activation and improvement of coronary microvascular dysfunction. Methods To determine whether ticagrelor can trigger ischemic preconditioning and influence microvascular function, we designed this prospective, open-label, pilot study that enrolled patients with stable multivessel CAD requiring staged, fractional flow reserve (FFR)-guided percutaneous coronary intervention (PCI). Participants will be randomized in 1:1 ratios either to ticagrelor (loading dose (LD) 180 mg, maintenance dose (MD) 90 mg bid) or to clopidogrel (LD 600 mg, MD 75 mg) from 3 to 1 days before the scheduled PCI. The PCI operators will be blinded to the randomization arm. The primary endpoint is the delta (difference) between ST segment elevations (in millimeters, mm) as assessed by intracoronary electrocardiogram (ECG) during the two-step sequential coronary balloon inflation in the culprit vessel. Secondary endpoints are 1) changes in coronary flow reserve (CFR), index of microvascular resistance (IMR), and FFR measured in the culprit vessel and reference vessel at the end of PCI, and 2) angina score during inflations. This study started in 2018 with the aim of enrolling 100 patients. Based on the rate of negative FFR up to 30% and a drop-out rate up to 10%, we expect to detect an absolute difference of 4 mm among the study arms in the mean change of ST elevation following repeated balloon inflations. All study procedures were reviewed and approved by the Ethical Committee of the Catholic University of Sacred Heart. Discussion Ticagrelor might improve ischemia tolerance and microvascular function compared to clopidogrel, and these effects might translate to better long-term clinical outcomes. Trial registration EudraCT No. 2016–004746-28. No. NCT02701140. Trial status Information provided in this manuscript refers to the definitive version (n. 3.0) of the study protocol, dated 31 October 2017, and includes all protocol amendments. Recruitment started on 18 September 2018 and is currently ongoing. The enrollment is expected to be completed by the end of 2019. Trial sponsor Fondazione Policlinico Universitario A. Gemelli – Roma, Polo di Scienze Cardiovascolari e Toraciche, Largo Agostino Gemelli 8, 00168 Rome, Italy.

The 11th International meeting Probiotics Prebiotics & New Foods was held in Rome, at Università Urbaniana, from September 12th to 14th 2021. The congress has been attended by 570 people from 36 countries (Algiers, Argentina, Australia, Austria, Belgium, Bosnia – Herzegovina, Brazil, Canada, Denmark, Estonia, Finland, France, Germany, Greece, Ireland, Israel, Italy, Japan, Lithuania, Morocco, Netherlands, Poland, Portugal, UK, Romania, Russia, Saudi Arabia, Serbia, Singapore, Slovakia, Slovenia, Spain, Sweden, Swiss, Ukraine, USA).

The effort of the Humane Microbiome Project has led to the awareness that many districts of the human organism, like the skin, gastrointestinal tract, and genitals harbor their normal resident microbes. For this reason, the scientific community overcame the dogma that urines are sterile. Instead, the urinary tract hosts many bacteria, the so-called urobiome, that contribute to its homeostasis and pathology. Urobiome seems to be involved in the pathogenesis of the urinary tract infections (UTIs) and its relationship with the gut microbiome is still far from being understood. We describe a case of an emergent urinary condition, the “purple urine bag syndrome” (PUBS) that displayed with a peculiar combination of pathogens: Corynebacterium urealitycum and Enterococcus faecium. Both bacteria have been described as components of the urobiome and the latter is a well-known member of the gut microbiome but also a possible uropathogen. This case report is the starting point to analyze what we know about urobiome, its role in UTIs, and its interactions with the gut microbiome in the socalled “gut-UTIs axis”.

Objective: Recent randomized control trials (RCTs), have demonstrated the beneficial therapeutic effects of rifaximin for the treatment of the irritable bowel syndrome (IBS). However, in these studies different drug doses have been used and still the optimal therapeutic dose is missing. We aimed to determine rifaximin therapeutic benefit and optimal dose for IBS as evidenced by the results of a network meta-analysis (NWM) of published randomized controlled trials (RCTs). Materials and Methods: PubMed/MEDLINE, EMBASE, and Cochrane Library databases were searched for RCTs investigating the therapeutic effects of rifaximin on IBS through December 2019. Data from each selected RCT were evaluated individually based on an intention-to-treat analysis. A Bayesian NWM was performed to investigate the efficacy rank order of rifaximin therapeutic interventions in IBS. Results: Four eligible studies, including 5 sets of data, were included in this NWM. They included 1,803 IBS patients, randomized to placebo (908 patients), and rifaximin (895 patients). In patients who received rifaximin, four regimens were examined, i.e., (A) = 400 mg tds for 10 days, (B) = 400 mg bid for 10 days, (C) = 550 mg bid for 2 weeks and (D) = 550 mg tds for 2 weeks. The results showed that in IBS rifaximin 400 mg tid for 10 days showed the highest efficacy [SUCRA (surface under cumulative ranking) value 89.5%], in comparison to other rifaximin regimens used and placebo. Conclusions: This NWM showed that the therapeutic efficacy of rifaximin 400 mg tid in IBS patients was greater than that of placebo and the other rifaximin doses studied.

Microbiota is the set of microorganisms that compose our microbial community. The human microbiota comprises a vast collection of bacteria, viruses, fungi and protozoa that co-exist with us and establish physio-metabolic interactions with our cellular pathways. Qualitative and/or quantitative alterations of the microbiota, termed dysbiosis, has already been associated with a wide range of diseases and conditions, including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), diverticular disease (DD), colorectal cancer (CRC), asthma, obesity, diabetes mellitus, hypertension, and cardiovascular disease. Microbiota changes in the intestinal lumen stimulate chronic inflammation possibly triggering disease in genetically predisposed individuals. In this review we examined all studies published in the last year in order to provide the newest correlation between specific microbiota alterations and colonic disease, with a focus on future perspectives and strategies based on microbiota modulations.

In recent years we have seen an exponential growth in scientific research aimed at characterising the structure and composition of the microbiota, which colonises various organs and systems. These investigations were supported by the development of very recent microbiological analysis techniques, most of which include molecular methods. In more recent times, however, scientific research has focused more on the study and characterization of relationships between the microbiota and systemic diseases. The purpose of this review is to present the scientific evidence, published from April 2019 to March 2020, on the relationships between oral microbiota and systemic pathologies.

While it is increasingly outlined the link between gut microbiota and several systemic and gastrointestinal diseases, to date the role of the oral microbiota is not well clarified. Different factors like diet, smoke, alcohol, and use of probiotics have an active role in the development and modification of the oral microbiota. The relation between oral microbiota and oral diseases was better studied in the past, but during the last years, a deeper link between systemic disease and oral microbiota was discovered. This review aims to summarize the results of the most relevant studies published on this topic between April 2018 and March 2019.

Neoplasms are one of the main causes of mortality worldwide. Hepatocellular carcinoma (HCC), oesophageal, gastric, and colorectal cancer represent malignancies with major incidence and impact of the gastrointestinal tract. Unfortunately, patients are often diagnosed with advanced stage disease and this is why our aim should be to implement screening and prevention strategies in order to reduce global cancer-related mortality. Human microbiota is defined as a mix of bacteria, eukaryotes, viruses, and archaea that live in our body; these microorganisms interact with immunological, metabolic, endocrinological, and neurological networks contributing to their modulation, through the production of active metabolites. Several studies have shown a correlation between human gastrointestinal (GI) cancers and dysbiosis defined by the qualitative/quantitative alterations of microbiota, but the exact mechanism through which microbiota is able to interfere with our networks and promotes carcinogenesis has not yet been well defined. Nevertheless, we know that H. pylori acts as a risk factor for gastric cancer, while hepatitis viruses C and B represent a trigger for HCC. Following these examples, many researchers hypothesized that gut microbiota may promote GI cancers, through different mechanisms, such as chronic inflammation, promotion of oxidative stress, alterations of immune response and disruption of body homeostasis then pushing cells towards a path of degeneration. In this review, we analysed studies published in 2019 exploring the role that the human microbiota plays in the genesis and progression of GI tract neoplasms. We also explore if and how microbiota interacts with anti-cancer drugs pharmacodynamic and pharmacokinetics during the drug resistance process.