OBJECTIVES Data on the elemental status, redistribution of the elements, role of occupational exposure and dietary assessment in preeclampsia (PE) are scarce. There are many disparities in the findings of essential and non-essential elements' role in PE. In this article we overview the changes in the content of selected elements in pregnancy complicated with the disorder of complex and not fully understood etiology. We have focused on important limitations and highlighted shortcomings in research from the last ten years period. METHODS The Scopus and PubMed electronic databases have been searched for English-language articles published within the time interval 2008-2018, with full text available and with the key words "preeclampsia" and "chemical element" (i.e. separately Cd, Pb, As, Ni, Mo, Co, Cr, Mn, Se, I, Fe, Sr, Cu, Zn, Mg, K and Na) appearing in the title, abstract or keywords. RESULTS A total of 48 publications were eligible for this overview. Surprisingly only 4% of papers considered environmental exr possible in the periconceptional period as well. It still needs to be established whether the deficiency of certain elements or their excess may be an etiopathogenic factor and a developmental cause of PE, and if it may serve as a target of actions in the causal treatment or even prevention of the occurrence of this disease. BACKGROUND The safety and efficacy of angiotensin converting enzyme inhibition (ACEI) after heart transplantation (HT) is unknown. This study examined long-term clinical outcomes after ACEI in HT recipients. METHODS The ACEI after HT study was a prospective, randomized trial that tested the efficacy of ACEI with ramipril after HT.  https://www.selleckchem.com/products/dbet6.html  In this study, long-term clinical outcomes were assessed in 91 patients randomized to either ramipril or placebo (median, 5.8 years). The primary endpoint was a composite of death, retransplantation, hospitalization for rejection or heart failure, and coronary revascularization. RESULTS The primary endpoint occurred in 10 of 45 patients (22.2%) in the ramipril group and in 14 of 46 patients (30.4%) in the placebo group (Hazard ratio (HR), 0.68; 95% CI, 0.29-1.51; P = .34). When the analysis was restricted to comparing patients who remained on a renin-angiotensin system inhibitor beyond 1 year with those who did not, there was a trend to improved outcomes (HR, 0.54; 95% CI, 0.22-1.28, P = .16). There was no significant difference in creatinine, blood urea nitrogen, and potassium at 3 years after randomization. The cumulative incidence of the primary endpoint was significantly higher in patients in whom the index of microcirculatory resistance increased from baseline to 1 year compared with those in whom it did not (39.1 vs 17.4%, HR 3.36; 95% CI, 1.07-12.7; P = .037). CONCLUSION The use of ramipril after HT safely lowers blood pressure and is associated with favorable long-term clinical outcomes. Clinical Trial Registration-URL https//www.clinicaltrials.gov. Unique identifier NCT01078363. The existing treatments for nonalcoholic steatohepatitis (NASH) are not completely effective. The need for new alternatives without adverse effects and low cost, such as the flavonoid (-)-epicatechin (EC), which has beneficial effects on lipid metabolism and cardiovascular diseases, arises. The objective of this work was to analyze EC effects in the NASH induced by a Paigen-type diet (PD). Mice were administered with (1) normal chow and water, (2) PD + fructose 30% and (3) PD + fructose 30% + EC (1 mg/kg) per gavage during 9 weeks. At the end of each treatment, serum was collected for analysis of the biochemical profile and liver enzymes. The liver was collected for microscopic analysis and for the evaluation of the relative expression of Plin2, Plin3, CD36, adiponectin and UCP2. Results showed that EC reduced weight gain and decreased triglyceride (TG), low-density lipoprotein cholesterol, TG/high-density lipoprotein and the activity of liver enzymes (alanine aminotransferase and alkaline phosphatase), suggesting lower liver damage. The microscopic analysis showed less "balloonization" of the hepatocyte, small drops of lipids, less accumulation of collagen and infiltration of inflammatory cells as compared to nontreated group. Finally, a decrease in the expression of Plin 2 was observed. While CD36 decreased, adiponectin and UCP2 increased. In conclusion, EC improves the biochemical profile, the microscopic characteristics and protein expression. Therefore, it may be a possible therapeutic approach for NASH since it prevents the progression of the hepatic and metabolic damage induced by high-fat diets. Elevated blood uric acid (UA) levels have been positively associated with the severity of periodontitis. It thus brings out a hypothesis that hyperuricemia, a pathological elevation of blood UA, might be a risk factor for periodontitis. Namely, periodontitis individuals with Hu might acquire more severe periodontal destruction compared to those without Hu. To support the hypothesis, four aspects of evidences are proposed. First, hyperuricemia and periodontitis share many metabolic and inflammatory comorbidities such as metabolic syndrome, diabetes and cardiovascular diseases which are commonly related to elevated UA levels and gout. Second, observational and interventional studies have found altered UA levels in blood and saliva in periodontitis patients or after periodontal treatment, suggesting an epidemiological connection between hyperuricemia and periodontitis. Third, plausible immuno-metabolic mechanisms by which hyperuricemia might promote the progression of periodontitis are suggested, such as impaired immune response, oxidative stress, pathological bone remodeling and dysbiosis. The last, our empirical data exhibited elevated UA levels in gingival tissue in periodontitis mice compared to controls. If the hypothesis is true, given the high prevalence of the two conditions, hyperuricemia would be a significant risk factor increasing the global burden of periodontal diseases. Evidences on a directional correlation between hyperuricemia and periodontitis are sparse. Longitudinal and experimental studies would be necessary to determine the magnitude of periodontal risk, if any, exacerbated by hyperuricemia and the underlying mechanisms.