Mitochondria-related oxidative stress is a pathomechanism causally linked to coronary heart disease (CHD) and diabetes mellitus (DM). Recently, mitochondrial monoamine oxidases (MAOs) have emerged as novel sources of oxidative stress in the cardiovascular system and experimental diabetes. The present study was purported to assess the mitochondrial impairment and the contribution of MAOs-related oxidative stress to the cardiovascular dysfunction in coronary patients with/without DM. Right atrial appendages were obtained from 75 patients randomized into 3 groups: (1) Control (CTRL), valvular patients without CHD; (2) CHD, patients with confirmed CHD; and (3) CHD-DM, patients with CHD and DM. Mitochondrial respiration was measured by high-resolution respirometry and MAOs expression was evaluated by RT-PCR and immunohistochemistry. Hydrogen peroxide (H2O2) emission was assessed by confocal microscopy and spectrophotometrically. The impairment of mitochondrial respiration was substrate-independent in CHD-DM group. MAOs expression was comparable among the groups, with the predominance of MAO-B isoform but no significant differences regarding oxidative stress were detected by either method. Incubation of atrial samples with MAOs inhibitors significantly reduced the H2O2 in all groups. In conclusion, abnormal mitochondrial respiration occurs in CHD and is more severe in DM and MAOs contribute to oxidative stress in human diseased hearts with/without DM.

TCs (telocytes) are actually defined as stromal cells with specific long and thin prolongations, called Tp (telopodes). They have been positively identified in various tissues and we now report their presence in the esophagus. These cells were identified by TEM (transmission electron microscopy) in esophageal samples of Wistar rats (n = 5) occurring beneath the basal epithelial layer, in submucosa, closely related to smooth and striated muscular fibres, as also in the adventitia. They are closely related to mast cells, macrophages and microvessels. Hybrid morphologies of stromal cells processes were found: cytoplasmic processes continued distally in a telopodial fashion. Telopodes alone may not be sufficient, however, for a safe diagnosis of TCs in TEM. A larger set of specific standards (such as the telopodial emergence, and the size of the cell body and telopodes) should be considered to differentiate TCs from various species of fibroblasts. The morphological and ultrastructural features should distinguish between TCs and interstitial cells of Cajal in the digestive tract.

Monoamine oxidases (MAOs) are mitochondrial enzymes with 2 isoforms that have emerged as important contributors to cardiovascular oxidative stress via the constant generation of hydrogen peroxide. The present study was purported to assess whether MAO-derived H 2 O 2 contributes to the endothelial dysfunction in mammary arteries harvested from coronary heart disease patients with/without diabetes mellitus subjected to coronary artery bypass grafting.To this aim the effects of MAO inhibition on vascular contractility to phenylephrine and endothelial-dependent relaxation (EDR) in response to acetylcholine were studied in vascular segments. Clorgyline (irreversible MAO A inhibitor), selegiline (irreversible MAO B inhibitor), and moclobemide (reversible MAO A inhibitor) were applied in the organ bath (10µmol/L). MAO expression was assessed by immunohistochemistry. We found a constant impairment of EDR that has been significantly attenuated in the presence of the MAO A and B inhibitors in both groups of coronary heart disease patients. MAO B was the dominant isoform in all human diseased vessels. In conclusion, in vitro inhibition of MAO significantly improved endothelium-dependent relaxation in human mammary arteries, regardless the presence of diabetes. These data suggest that MAO inhibitors might be useful in restoring endothelial response in clinical conditions associated with increased oxidative stress, such as coronary artery disease and diabetes.Key words: monoamine oxidases, coronary artery disease, diabetes mellitus, endothelial dysfunction, MAO inhibitors IntroductionCoronary heart disease (CHD) is currently the leading cause of morbidity due to heart failure and its evolution is aggravated by the presence of diabetes mellitus (DM) whose prevalence is increasing at an alarming rate worldwide. Nowadays, it is widely accepted that A large body of experimental evidence showed that under physiological conditions the amount of H 2 O 2 generated via MAO is reduced but in cardiac pathologies (such as myocardial ischemia/reperfusion and heart failure) the increased activity of the MAO-A isoform becomed deleterious (Bianchi et al. 2005a; Kaludercic et al. 2011; Kaludercic et al. 2010).Accordingly, in the rodent heart, MAO-A activation contributes to the ischemia/reperfusion injury in the in vivo model of regional ischemia (Bianchi et al. 2005a,b; Carpi et al. 2009) and to the maladaptive ventricular remodeling in the transverse aortic constriction-induced model of heart failure, respectively (Kaludercic et al. 2010;Villeneuve et al. 2013).Furthermore, an elegant study has unequivocally proven the role of MAO-B activation in triggering mitochondrial dysfunction besides the cardiac structural and functional alterations in mice with experimentally induced heart failure (Kaludercic et al. 2014). Recently, we described the role of MAOs as mediators of endothelial dysfunction and the beneficial effect of MAO inhibition in murine diseased vessels (Sturza et al. 2013), and in experimental diabetes mellitus, respec...

Toxoplasma gondii is an obligate intracellular parasite that most commonly causes asymptomatic infection in immunocompetent hosts, but can have devastating consequences in congenitally infected infants and immunocompromised patients. We evaluated the seroprevalence of T. gondii in the general population in Western Romania. Sera from 304 individuals were analysed with the Pastorex Toxo test, which allows the simultaneous detection of T. gondii IgG and/or IgM antibodies. T. gondii antibodies were demonstrated in 197 individuals (64.8%) and the prevalence increased with age: 35.0% in those < 20 years versus 76.8% in those ≥ 70 years (p < 0.001). There was a higher prevalence of T. gondii antibodies in rural areas (76.9%) than in urban regions (55.3%) (p < 0.001). Our results suggest a high prevalence of T. gondii antibodies in Western Romania.

Phytocompounds and medicinal herbs were used in traditional ancient medicine and are nowadays increasingly screened in both experimental and clinical settings due to their beneficial effects in several major pathologies. Similar to the drug industry, phytotherapy is interested in using nanobased delivery systems to view the identification and characterization of the cellular and molecular therapeutic targets of plant components. Eugenol, the major phenolic constituent of clove essential oil, is a particularly versatile phytochemical with a vast range of therapeutic properties, among which the anti-inflammatory, antioxidant, and anticarcinogenic effects have been systematically addressed. In the past decade, with the emerging understanding of the role of mitochondria as critical organelles in the pathophysiology of noncommunicable diseases, research regarding the role of phytochemicals as modulators of bioenergetics and metabolism is on a rise. Here, we present a brief overview of the major pharmacological properties of eugenol, with special emphasis on its applications in dental medicine, and provide preliminary data regarding its effects, alone, and included in polyurethane nanostructures, on mitochondrial bioenergetics, and glycolysis in human HaCaT keratinocytes.

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Oxidative stress is a pathomechanism causally linked to the progression of chronic cardiovascular diseases and diabetes. Mitochondria have emerged as the most relevant source of reactive oxygen species, the major culprit being classically considered the respiratory chain at the inner mitochondrial membrane. In the past decade, several experimental studies unequivocally demonstrated the contribution of monoamine oxidases (MAOs) at the outer mitochondrial membrane to the maladaptative ventricular hypertrophy and endothelial dysfunction. This paper addresses the contribution of mitochondrial dysfunction to the pathogenesis of heart failure and diabetes together with the mounting evidence for an emerging role of MAO inhibition as putative cardioprotective strategy in both conditions.