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Environmental pollution is a worldwide problem recognized by the World Health Organization as a major health risk factor that affects low-, middle- and high-income countries. Suspended particulate matter is among the most dangerous pollutants, since it contains toxicologically relevant agents, such as metals, including vanadium. Vanadium is a transition metal that is emitted into the atmosphere especially by the burning of fossil fuels to which dwellers are exposed. The objective of this literature review is to describe the toxic effects of vanadium and its compounds when they enter the body by inhalation, based especially on the results of a murine experimental model that elucidates the systemic effects that vanadium has on living organisms. To achieve this goal, we reviewed 85 articles on the relevance of vanadium as a component of particulate matter and its toxic effects. Throughout several years of research with the murine experimental model, we have shown that this element generates adverse effects in all the systems evaluated, because it causes immunotoxicity, hematotoxicity, neurotoxicity, nephrotoxicity and reprotoxicity, among other noxious effects. The results with this experimental model add evidence of the effects generated by environmental pollutants and increase the body of evidence that can lead us to make more intelligent environmental decisions for the welfare of all living beings.

Air pollution is a worldwide public health issue and it is associated with millions of premature deaths due to cancer, thrombosis, and pulmonary and cardiovascular diseases. Thrombosis is the excessive clotting that blocks a blood vessel, and its etiology is multifactorial. In recent years, growing evidence has linked air pollution, especially particulate matter (PM) and metals, to the development of thrombosis. PM and metals induce lung and systemic inflammation and oxidative stress that are frequent mechanisms in thrombosis. Platelets are important effectors of physiological hemostasis and pathological thrombosis. They are responsible for the formation of the initial plug and are important in the cellular model of coagulation. Therefore, any changes in their morphology or function or an increase in activation could be extremely relevant in thrombosis. Megakaryocytes (MKs) in the bone marrow and in the lungs are the precursor cells of platelets, and the latter is the first organ injured by air pollution. There is substantial evidence of the effect that PM and metals have on platelets, but there is almost no research about the effect of PM and metals on MKs. It is very likely that the alterations produced by air pollution originate in these cells. In this article, we review the biology of MKs and platelets and their role in particulate air pollution-related thrombosis to emphasize the need for further research in this field.

Carbon nanotubes (CNTs) have been a focus of attention due to their possible applications in medicine, by serving as scaffolds for cell growth and proliferation and improving mesenchymal cell transplantation and engraftment. The emphasis on the benefits of CNTs has been offset by the ample debate on the safety of nanotechnologies. In this study, we determine whether functionalized multiwalled CNTs (fMWCNTs) and functionalized oxygen-doped multiwalled CNTs (fCOxs) have toxic effects on rat mesenchymal stem cells (MSCs) in vitro by analyzing morphology and cell proliferation and, using in vivo models, whether they are able to transform MSCs in cancer cells or induce embryotoxicity. Our results demonstrate that there are statistically significant differences in cell proliferation and the cell cycle of MSCs in culture. We identified dramatic changes in cells that were treated with fMWCNTs. Our evaluation of the transformation to cancer cells and cytotoxicity process showed little effect. However, we found a severe embryotoxicity in chicken embryos that were treated with fMWCNTs, while fCOxs seem to exert cardioembryotoxicity and a discrete teratogenicity. Furthermore, it seems that the time of contact plays an important role during cell transformation and embryotoxicity. A single contact with fMWCNTs is not sufficient to transform cells in a short time; an exposure of fMWCNTs for 2 weeks led to cell transformation risk and cardioembryotoxicity effects., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Alzheimer's disease (AD) is a neurodegenerative process exacerbated by several risk factors including impaired glucose metabolism in the brain that could cause molecular and neurochemical alterations in cognitive regions such as the hippocampus (Hp). Consequently, this process could cause neuronal morphological changes; however, the mechanism remains elusive. We induced chronic hyperglycemia after streptozotocin (STZ) administration. Then, we examined spatial learning and memory using the Morris water maze test and evaluated neuronal morphological changes using the Golgi-Cox stain procedure in hyperglycemic rats that received a Aβ 25-35 unilateral injection into the Hp. Our results demonstrate that STZ combined with Aβ 25-35 induced significant deficits in the spatial memory. In addition, we observed a significant reduction in the number of dendritic spines of pyramidal neurons in the dorsal Hp of rats with STZ plus Aβ 25-35 . In conclusion, the reduced spine density of pyramidal neurons in the CA1 dorsal Hp could produce the spatial memory deficit observed in these animals. These results suggest that hyperglycemia can trigger Aβ-induced neurodegeneration and thus the appearance of AD symptoms would be accelerated. Synapse 68:585-594, 2014. © 2014 Wiley Periodicals, Inc., (© 2014 Wiley Periodicals, Inc.)

Unlabelled: Our objective was to determine the normal dimensions of the ventricular segment of the human fetal heart between 13 and 20 weeks' gestation., Study Design: 103 hearts obtained by necropsy were dissected and measurements of different portions of ventricles were determined under stereoscopic magnification. In each ventricle were measured anteroposterior and lateral diameters, inlet and outlet length, and thickness of walls at different levels. Our results showed the cardiac apex was constituted by the left ventricle in 68.9% of the hearts. Both ventricles showed linear growth during this period of fetal development. Ranges in median values of external and internal ventricular measurements were determined. The left ventricular wall was thicker than the right, and the right ventricular cavity was larger. This study provides morphometric reference information concerning the dimensions and growth of both ventricles of the fetal heart, which may be useful in pediatric cardiac surgery and echocardiography.

The role of the superior atrioventricular cushion in the normal development of the left ventricular infundibulum was experimentally studied in the chick embryo. 178 embryos at stages 19-24 of Hamburger and Hamilton were selectively labeled using gelatin-india ink; afterward embryos were reincubated until the mature heart stage, in which the final location of the labels was determined. In addition, anatomical microscopic studies were carried out on the chick embryo heart at different stages of the development. 91 embryos were obtained at the mature heart stage, 46 of which were normal. In 82,6% of these 46 embryos labels were found in the left ventricular infundibulum and were distributed in the following regions: (1) base of the free portion of the anteroseptal mitral leaflet (mitroaortic continuity); (2) the same region plus the left surface of the anterior basal portion of the ventricular septum, and (3) the left surface of the anterior basal portion of the ventricular septum. Anatomical microscopic studies showed that the superior atrioventricular cushion appears at stage 18, fusing with the inferior cushion at stage 28. Our results permit us to conclude that the superior atrioventricular cushion plays an important role in the normal development of the left ventricular infundibulum, and it contributes in the posterolateral and anteromedial wall formation.

Seventy-nine specimens with transposition of the great arteries were reviewed. Among them were 45 with ventricular septal defect, including 6 with so-called "posterior aorta transposition". The morphology of the mitral valve was carefully studied. Mitral valve anomalies were found in 24 cases (30%). The anomalies involving the mitral valve were classified into 4 groups according to the different components of the valve: A) specimens with anomalies of the leaflets--2 cases with mitral cleft; B) those with anomalies of the commissures--1 case with a mitral gap; C) those with abnormalities of the chordae tendinae--2 cases of malattachment of the chordae tendinae to the ventricular septum and 2 with bridging chordae between the papillary muscles; and D) those with abnormalities of the papillary muscles--5 cases with a parachute valve, 10 with a "form fruste" of the parachute mitral valve (hypoplasia of one papillary muscle and short chordae tendinae) and 2 with abnormally placed papillary muscles, which reached the pulmonary annulus. In 14 cases, abnormalities of the tricuspid valve were also encountered, including 8 cases with a tricuspid gap and 6 with a malattachment of tricuspid chordae on the border of a ventricular septal defect. It can be concluded that mitral valve anomalies are not uncommon in transposition of the great arteries. This pathology must be carefully evaluated at the time of surgery, particularly in those patients for whom an anatomic correction is considered, for in those cases the left ventricle will be supplying the systemic circulation and therefore, a completely normal mitral valve will be required.(ABSTRACT TRUNCATED AT 250 WORDS)