Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

The results obtained in our study of Hispanic school-age children show that adiposity is correlated with CRP concentrations and SBP values as has been earlier described in Caucasian populations. However, we failed to find a significant relationship between low-grade inflammation and SBP levels. Further studies are needed in order to explore alternative pathophysiological mechanisms linking obesity and high blood pressure in children and to define the impact of these associations on the cardiovascular risk of our pediatric population.

Enterobacterales represent the largest group of bacterial pathogens in humans and are responsible for severe, deep-seated infections, often resulting in sepsis or death. They are also a prominent cause of multidrug-resistant (MDR) infections, and some species are recognized as biothreat pathogens. Tools for noninvasive, whole-body analysis that can localize a pathogen with specificity are needed, but no such technology currently exists. We previously demonstrated that positron emission tomography (PET) with 2-deoxy-2-[18F]fluoro-d-sorbitol (18F-FDS) can selectively detect Enterobacterales infections in murine models. Here, we demonstrate that uptake of 18F-FDS by bacteria occurs via a metabolically conserved sorbitol-specific pathway with rapid in vitro 18F-FDS uptake noted in clinical strains, including MDR isolates. Whole-body 18F-FDS PET/computerized tomography (CT) in 26 prospectively enrolled patients with either microbiologically confirmed Enterobacterales infection or other pathologies demonstrated that 18F-FDS PET/CT was safe, could rapidly detect and localize Enterobacterales infections due to drug-susceptible or MDR strains, and differentiated them from sterile inflammation or cancerous lesions. Repeat imaging in the same patients monitored antibiotic efficacy with decreases in PET signal correlating with clinical improvement. To facilitate the use of 18F-FDS, we developed a self-contained, solid-phase cartridge to rapidly (<10 min) formulate ready-to-use 18F-FDS from commercially available 2-deoxy-2-[18F]fluoro-d-glucose (18F-FDG) at room temperature. In a hamster model, 18F-FDS PET/CT also differentiated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia from secondary Klebsiella pneumoniae pneumonia—a leading cause of complications in hospitalized patients with COVID-19. These data support 18F-FDS as an innovative and readily available, pathogen-specific PET technology with clinical applications.

The prevalence of cardiovascular diseases (CVD) and diabetes mellitus type 2 (DM 2) is decreasing in developed countries despite the increase in the percentage of subjects with obesity and other well-recognized cardiovascular risk factors. In contrast, the recent transition of the economic model experienced by developing countries, characterized by the adoption of a Western lifestyle, that we have named "socioeconomic pathology," has led to an increase in the burden of CVD. It has been demonstrated that conventional cardiovascular risk factors in developed and developing countries are the same. Why then does the population of developing countries currently have a higher incidence of CVD than that of developed countries if they share the same risk factors? We have proposed the existence of a higher susceptibility to the development of systemic inflammation at low levels of abdominal obesity in the population of developing countries and the consequent endothelial dysfunction, insulin resistance, DM 2, and CVD. In contrast, an important percentage of obese people living in developed countries have a healthy phenotype and low risk of developing CVD and DM 2. Human epidemiologic studies and experimental dietary interventions in animal models have provided considerable evidence to suggest that nutritional imbalance and metabolic disturbances early in life may later have a persistent effect on an adult's health that may even be transmitted to the next generations. Epigenetic changes dependent on nutrition could be key in this evolutionary health behavior, acting as a buffering system, permitting the adaptation to environmental conditions by silencing or increasing the expression of certain genes.

No abstract