Recommendations for the diagnosis of pediatric tuberculosis

Tuberculosis (TB) is still the world's second most frequent cause of death due to infectious diseases after HIV infection, and this has aroused greater interest in identifying and managing exposed subjects, whether they are simply infected or have developed one of the clinical variants of the disease. Unfortunately, not even the latest laboratory techniques are always successful in identifying affected children because they are more likely to have negative cultures and tuberculin skin test results, equivocal chest X-ray findings, and atypical clinical manifestations than adults. Furthermore, they are at greater risk of progressing from infection to active disease, particularly if they are very young. Consequently, pediatricians have to use different diagnostic strategies that specifically address the needs of children. This document describes the recommendations of a group of scientific societies concerning the signs and symptoms suggesting pediatric TB, and the diagnostic approach towards children with suspected disease

Modulation of Vascular Reactivity by Novel Synthetic Benzopyran Analogues in Rat Aortas

A substantial body of research described ATP-dependent potassium (K ATP ) channels, sarcolemmal and mitochondrial, with different physiological functions and pharmacological behaviour in various tissues (pancreatic â-cells, brain, skeletal muscle and vascular smooth muscle). The present study was purported to assess the effects of three novel benzopyran derivatives, KL-1487, KL-1492 and KL-1507, analogues of BMS191095 (a selective opener of mitoK ATP channels) on vascular function and reactive oxygen species (ROS) production. To this aim, we performed organ bath experiments on rat aortic rings in the presence vs. absence of each of the mentioned compounds (10 µmol/L). Incubation of vascular rings with each benzopyran analogue elicited a significant decrease of the contractile response to phenylephrine vs. control, thus suggesting a vasodilator action. However, only two of the benzopyran derivatives, KL-1492 and KL-1507, significantly improved the endothelial-dependent relaxation. Interestingly, these effects were present also in endothelium denuded vessels. None of these compounds modified vascular ROS production. In conclusion, in murine aortic segments, KL-1492 and KL-1507, two novel benzopyran analogues elicited an endothelial- independent modulation of vascular reactivity. Further studies will elucidate whether these compounds may be useful in restoring the vascular response in pathological conditions associated with endothelial dysfunction. Keywords: benzopyran derivatives, endothelial function, organ bath, vascular murine ring

Assessment of Mitochondrial Dysfunction and Monoamine Oxidase Contribution to Oxidative Stress in Human Diabetic Hearts

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