Explore the vast range of titles available.

The mandate of the Task Force Hemispheric Transport of Air Pollution (TF HTAP) under the Convention on Long-Range Transboundary Air Pollution (CLRTAP) is to improve the scientific understanding of the intercontinental air pollution transport, to quantify impacts on human health, vegetation and climate, to identify emission mitigation options across the regions of the Northern Hemisphere, and to guide future policies on these aspects. The harmonization and improvement of regional emission inventories is imperative to obtain consolidated estimates on the formation of global-scale air pollution. An emissions data set has been constructed using regional emission grid maps (annual and monthly) for SO2, NOx, CO, NMVOC, NH3, PM10, PM2.5, BC and OC for the years 2008 and 2010, with the purpose of providing consistent information to global and regional scale modelling efforts. This compilation of different regional gridded inventories – including that of the Environmental Protection Agency (EPA) for USA, the EPA and Environment Canada (for Canada), the European Monitoring and Evaluation Programme (EMEP) and Netherlands Organisation for Applied Scientific Research (TNO) for Europe, and the Model Inter-comparison Study for Asia (MICS-Asia III) for China, India and other Asian countries – was gap-filled with the emission grid maps of the Emissions Database for Global Atmospheric Research (EDGARv4.3) for the rest of the world (mainly South America, Africa, Russia and Oceania). Emissions from seven main categories of human activities (power, industry, residential, agriculture, ground transport, aviation and shipping) were estimated and spatially distributed on a common grid of 0.1° × 0.1° longitude-latitude, to yield monthly, global, sector-specific grid maps for each substance and year. The HTAP_v2.2 air pollutant grid maps are considered to combine latest available regional information within a complete global data set. The disaggregation by sectors, high spatial and temporal resolution and detailed information on the data sources and references used will provide the user the required transparency. Because HTAP_v2.2 contains primarily official and/or widely used regional emission grid maps, it can be recommended as a global baseline emission inventory, which is regionally accepted as a reference and from which different scenarios assessing emission reduction policies at a global scale could start. An analysis of country-specific implied emission factors shows a large difference between industrialised countries and developing countries for acidifying gaseous air pollutant emissions (SO2 and NOx) from the energy and industry sectors. This is not observed for the particulate matter emissions (PM10, PM2.5), which show large differences between countries in the residential sector instead. The per capita emissions of all world countries, classified from low to high income, reveal an increase in level and in variation for gaseous acidifying pollutants, but not for aerosols. For aerosols, an opposite trend is apparent with higher per capita emissions of particulate matter for low income countries.

Introduction Ischemia/reperfusion (I/R) injury, such as myocardial infarction, stroke, and peripheral vascular disease, has been recognized as the most frequent causes of devastating disorders and death currently. Protective effect of various preconditioning stimuli, including hyperbaric oxygen (HBO), has been proposed in the management of I/R. Methods In this study, we searched and reviewed up‐to‐date published papers to explore the pathophysiology of I/R injury and to understand the mechanisms underlying the protective effect of HBO as conditioning strategy. Results Animal study and clinic observation support the notion that HBO therapy and conditioning provide beneficial effect against the deleterious effects of postischemic reperfusion. Several explanations have been proposed. The first likely mechanism may be that HBO counteracts hypoxia and reduces I/R injury by improving oxygen delivery to an area with diminished blood flow. Secondly, by reducing hypoxia–ischemia, HBO reduces all the pathological events as a consequence of hypoxia, including tissue edema, increased affective area permeability, postischemia derangement of tissue metabolism, and inflammation. Thirdly, HBO may directly affect cell apoptosis, signal transduction, and gene expression in those that are sensitive to oxygen or hypoxia. HBO provides a reservoir of oxygen at cellular level not only carried by blood, but also by diffusion from the interstitial tissue where it reaches high concentration that may last for several hours, improves endothelial function and rheology, and decreases local inflammation and edema. Conclusion Evidence suggests the benefits of HBO when used as a preconditioning stimulus in the setting of I/R injury. Translating the beneficial effects of HBO into current practice requires, as for the “conditioning strategies”, a thorough consideration of risk factors, comorbidities, and comedications that could interfere with HBO‐related protection. Experimental evidence suggests the benefits of HBO used as a preconditioning stimulus in I/R injury. HBO seems to have certain advantages over the drugs, not only because it can act on different complementary levels, but it also offers a reservoir of oxygen that may last for a few hours and may be of great importance in case of sudden hypoxia or ischemia, improves endothelial function and rheology, and decreases local inflammation and edema. Last but not least, oxygen reaches to cellular level not only carried by blood, but also by diffusion from the interstitial tissue where it reaches high concentration during HBO treatment, thus providing increased availability as compared to any drug. Moreover, the low cost and insignificant adverse events make HBO preferable to other types of preconditioning.

This paper examines the system of conflict resolution maintained by a Roma group that has migrated from the Romanian regions of Transylvania and Banat to over 16 countries in Western Europe and North America. The analysis is based on a long-term collaborative ethnography that enabled the detailed reconstruction of 76 conflicts that occurred between 2001 and 2022. Of these conflicts, 56 were resolved through kris hearings conducted by a tribunal of selected judges or krisoniere. This paper provides an initial analysis of this database, addressing four key aspects of the kris procedures: (1) How does this system work today within diasporic networks that rely heavily on digital technologies for transnational communication? (2) What is the profile of the judges or krisoniere and how do they work within the kris assemblies? (3) What types of conflicts does the system address and how are they linked to the socio-political organization of this diaspora? (4) How are kris resolutions enforced in the absence of political leadership or the coercive power of state institutions? This autonomous justice system, epitomized by the kris hearings, represents a form of embedded legal pluralism and network governance. Consensus within this social field is fostered by the goal of minimizing threat and violence while maintaining connectedness in the face of exclusion and discrimination. This article was published open access under a CC BY-NC-ND licence: https://creativecommons.org/licences/by-nc-nd/4.0.

IntroductionParaphrenia is a chronic psychosis that has generally lost its status as an independent nosological entity, not being included in DSM-5. From the perspective of the particular psychopathological picture and the impact of the disease on the patient’s functioning in roles, paraphrenia remains a challenge for the clinician in terms of nosological classification and the correct therapeutic approach.ObjectivesWe take into account a patient who presents the classic diagnostic criteria of paraphrenia with a clinical and evolutionary picture followed for 15 years, with the aim of bringing the paraphrenic phenomenology back to the fore.MethodsThe case presentation will focus on the richness and absurdity of the delusional ideas that are in great contrast with the good insertion into reality of the subject and the preservation of the core of the personality. We will also describe the main landmarks of positive and differential diagnosis.ResultsWe believe that paraphrenia deserves to be differentiated from other psychotic disorders through the particular variant of insight that also explains the significant capacities of dissimulation and as a result of insertion into the roles of life. This attribute also explains the increased potential for danger and unpredictability of the paraphrenic patient.ConclusionsOur approach is an argument for the psychopathological understanding of paraphrenic psychotic phenomenology independent of different nosographic classification systems. We are trying to contribute to increasing the quality of differential diagnosis in psychoses.Keywordspsychosis, paraphrenia, differential diagnosisDisclosure of InterestNone Declared

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.

The increasing pollution of surface and groundwater bodies by pharmaceuticals is a general environmental problem requiring routine monitoring. Conventional analytical techniques used to quantify traces of pharmaceuticals are relatively expensive and generally demand long analysis times, associated with difficulties in performing field analyses. Propranolol, a widely used β-blocker, is representative of an emerging class of pharmaceutical pollutants with a noticeable presence in the aquatic environment. In this context, we focused on developing an innovative, highly accessible analytical platform based on self-assembled metal colloidal nanoparticle films for the fast and sensitive detection of propranolol based on Surface Enhanced Raman Spectroscopy (SERS). The ideal nature of the metal used as the active SERS substrate was investigated by comparing silver and gold self-assembled colloidal nanoparticle films, and the improved enhancement observed on the gold substrate was discussed and supported by Density Functional Theory calculations, optical spectra analyses, and Finite-Difference Time-Domain simulations. Next, direct detection of propranolol at low concentrations was demonstrated, reaching the ppb regime. Finally, we showed that the self-assembled gold nanoparticle films could be successfully used as working electrodes in electrochemical-SERS analyses, opening the possibility of implementing them in a wide array of analytical applications and fundamental studies. This study reports for the first time a direct comparison between gold and silver nanoparticle films and, thus, contributes to a more rational design of nanoparticle-based SERS substrates for sensing applications.

Chronic venous disease (CVD) and its major manifestation, varicose veins (VV) of the lower limbs, is a common, multifactorial disease that affects a significant percentage of adult and elderly people worldwide. Its prevalence has been constantly increasing with the aging of the population and, particularly, with the obesity pandemic (hence, the term ‘phlebesity’). The major pathophysiological mechanisms that are potentiating each other in a vicious cycle, leading to chronic venous hypertension, are represented by endothelial dysfunction, chronic inflammation, impaired hemodynamics, and venous wall remodeling. Oxidative stress is another pathomechanism responsible for CVD and its complications, with the increased generation of reactive oxygen species and decreased antioxidant defense being reported to contribute to VV formation. Herein, we present evidence for the role of impaired redox homeostasis as pathophysiological mechanism responsible for chronic local and systemic oxidative stress in patients with CVD.

There is a growing body of evidence pointing to the role of purinergic signaling in the development and progression of various conditions that have inflammation as a common pathogenetic denominator. The aim of the present study was to assess the involvement of P 2 Y 11 purinergic receptors in the regulation of vascular function in aortic segments obtained using an experimental model of acute inflammation, the lipopolysaccharide (LPS, 8 mg/kg, i.p)-treated rats. Twelve hours after LPS administration, thoracic aortas were isolated and used for studies of vascular reactivity in the organ bath and for the measurement of reactive oxygen species (ROS) generation, respectively. LPS treatment significantly increased contractility to phenylephrine and attenuated the endothelium-dependent relaxation of the vascular segments in response to acetylcholine; an increased production of hydrogen peroxide (H 2 O 2 ) was also recorded. The P 2 Y 11 activator, NF 546, decreased the LPS-induced aortic H 2 O 2 release and partially normalized the vasomotor function, namely reduced contractility and improved relaxation. The effect was abolished by co-treatment with the P 2 Y 11 inhibitor, NF 340, and also after endothelium denudation. Importantly, NF 546 did not elicit an antioxidant effect by acting as a H 2 O 2 scavenger, suggesting that the beneficial outcome of this treatment on the vasculature is the consequence of P 2 Y 11 stimulation. In conclusion, purinergic P 2 Y 11 receptors stimulation improves vascular function and mitigates oxidative stress in the setting of acute systemic inflammation, revealing salutary effects and therapeutic potential in pathologies associated with endothelial dysfunction.

Chronic kidney disease (CKD) has emerged as one of the most progressive diseases with increased mortality and morbidity. Metabolomics offers new insights into CKD pathogenesis and the discovery of new biomarkers for the early diagnosis of CKD. The aim of this cross-sectional study was to assess metabolomic profiling of serum and urine samples obtained from CKD patients. Untargeted metabolomics followed by multivariate and univariate analysis of blood and urine samples from 88 patients with CKD, staged by estimated glomerular filtration rate (eGFR), and 20 healthy control subjects was performed using ultra-high-performance liquid chromatography coupled with electrospray ionization-quadrupole-time of flight-mass spectrometry. Serum levels of Oleoyl glycine, alpha-lipoic acid, Propylthiouracil, and L-cysteine correlated directly with eGFR. Negative correlations were observed between serum 5-Hydroxyindoleacetic acid, Phenylalanine, Pyridoxamine, Cysteinyl glycine, Propenoylcarnitine, Uridine, and All-trans retinoic acid levels and eGFR. In urine samples, the majority of molecules were increased in patients with advanced CKD as compared with early CKD patients and controls. Amino acids, antioxidants, uremic toxins, acylcarnitines, and tryptophane metabolites were found in all CKD stages. Their dual variations in serum and urine may explain their impact on both glomerular and tubular structures, even in the early stages of CKD. Patients with CKD display a specific metabolomic profile. Since this paper represents a pilot study, future research is needed to confirm our findings that metabolites can serve as indicators of early CKD.

We have previous evidence that in anesthetized dogs the inorganic sodium nitrite protects against the severe ventricular arrhythmias, resulting from coronary artery occlusion and reperfusion, when administered 24 h before. The present study aimed to examine, whether in this effect changes in mitochondrial morphology and function would play a role. Thirty dogs were infused intravenously either with saline ( = 15) or sodium nitrite (0.2 μmol/kg/min; = 15) for 20 min, and 24 h later, 10 dogs from each group were subjected to a 25 min period of occlusion and then reperfusion of the left anterior descending coronary artery. The severity of ischaemia and ventricular arrhythmias were examined . Left ventricular tissue samples were collected either before the occlusion (5 saline and 5 nitrite treated dogs) or, in dogs subjected to occlusion, 2 min after reperfusion. Changes in mitochondrial morphology, in complex I and complex II-dependent oxidative phosphorylation (OXPHOS), in ATP, superoxide, and peroxynitrite productions were determined. The administration of sodium nitrite 24 h before ischemia/reperfusion significantly attenuated the severity of ischaemia, and markedly reduced the number and incidence of ventricular arrhythmias. Nitrite also attenuated the ischaemia and reperfusion (I/R)-induced structural alterations, such as reductions in mitochondrial area, perimeter, and Feret diameter, as well as the increase in mitochondrial roundness. The administration of nitrite, however, enhanced the I/R-induced reduction in the mitochondrial respiratory parameters; compared to the controls, 24 h after the infusion of nitrite, there were further significant decreases, e.g., in the complex I-dependent OXPHOS (by -20 vs. -53%), respiratory control ratio (by -14 vs. -61%) and in the P/E control coupling ratio (by 2 vs. -36%). Nitrite also significantly reduced the I/R-induced generation of superoxide, without substantially influencing the ATP production. The results suggest that sodium nitrite may have an effect on the mitochondria; it preserves the mitochondrial structure and modifies the mitochondrial function, when administered 24 h prior to I/R. We propose that nitrite affects primary the phosphorylation system (indicated by the decreased P/E ratio), and the reduction in superoxide production would result from the subsequent suppression of the ROS producing complexes; an effect which may certainly contribute to the antiarrhythmic effect of nitrite.