Disjunct populations of European vascular plant species keep the same climatic niches

Aim Previous research on how climatic niches vary across species ranges has focused on a limited number of species, mostly invasive, and has not, to date, been very conclusive. Here we assess the degree of niche conservatism between distant populations of native alpine plant species that have been separated for thousands of years. Location European Alps and Fennoscandia. Methods Of the studied pool of 888 terrestrial vascular plant species occurring in both the Alps and Fennoscandia, we used two complementary approaches to test and quantify climatic-niche shifts for 31 species having strictly disjunct populations and 358 species having either a contiguous or a patchy distribution with distant populations. First, we used species distribution modelling to test for a region effect on each species' climatic niche. Second, we quantified niche overlap and shifts in niche width (i.e. ecological amplitude) and position (i.e. ecological optimum) within a bi-dimensional climatic space. Results Only one species (3%) of the 31 species with strictly disjunct populations and 58 species (16%) of the 358 species with distant populations showed a region effect on their climatic niche. Niche overlap was higher for species with strictly disjunct populations than for species with distant populations and highest for arctic-alpine species. Climatic niches were, on average, wider and located towards warmer and wetter conditions in the Alps. Main conclusion Climatic niches seem to be generally conserved between populations that are separated between the Alps and Fennoscandia and have probably been so for 10,000-15,000 years. Therefore, the basic assumption of species distribution models that a species' climatic niche is constant in space and time - at least on time scales 104 years or less - seems to be largely valid for arctic-alpine plants.

Prevention of vascular dysfunction and arterial hypertension in mice generated by assisted reproductive technologies by addition of melatonin to culture media.

Assisted reproductive technologies (ART) induce vascular dysfunction in humans and mice. In mice, ART-induced vascular dysfunction is related to epigenetic alteration of the endothelial nitric oxide synthase (eNOS) gene, resulting in decreased vascular eNOS expression and nitrite/nitrate synthesis. Melatonin is involved in epigenetic regulation, and its administration to sterile women improves the success rate of ART. We hypothesized that addition of melatonin to culture media may prevent ART-induced epigenetic and cardiovascular alterations in mice. We, therefore, assessed mesenteric-artery responses to acetylcholine and arterial blood pressure, together with DNA methylation of the eNOS gene promoter in vascular tissue and nitric oxide plasma concentration in 12-wk-old ART mice generated with and without addition of melatonin to culture media and in control mice. As expected, acetylcholine-induced mesenteric-artery dilation was impaired (P = 0.008 vs. control) and mean arterial blood pressure increased (109.5 ± 3.8 vs. 104.0 ± 4.7 mmHg, P = 0.002, ART vs. control) in ART compared with control mice. These alterations were associated with altered DNA methylation of the eNOS gene promoter (P < 0.001 vs. control) and decreased plasma nitric oxide concentration (10.1 ± 11.1 vs. 29.5 ± 8.0 μM) (P < 0.001 ART vs. control). Addition of melatonin (10(-6) M) to culture media prevented eNOS dysmethylation (P = 0.005, vs. ART + vehicle), normalized nitric oxide plasma concentration (23.1 ± 14.6 μM, P = 0.002 vs. ART + vehicle) and mesentery-artery responsiveness to acetylcholine (P < 0.008 vs. ART + vehicle), and prevented arterial hypertension (104.6 ± 3.4 mmHg, P < 0.003 vs. ART + vehicle). These findings provide proof of principle that modification of culture media prevents ART-induced vascular dysfunction. We speculate that this approach will also allow preventing ART-induced premature atherosclerosis in humans.

Utilização do índice de resistência vascular na diferenciação entre nódulos mamários benignos e malignos

OBJETIVO: O objetivo deste estudo foi avaliar o significado do Doppler espectral por meio da obtenção do índice de resistência vascular na diferenciação entre lesões mamárias benignas e malignas. MATERIAIS E MÉTODOS: Dezenove lesões malignas e 18 benignas, diagnosticadas por estudo histológico, foram submetidas previamente a análise de sua vascularização por meio do Doppler espectral para se obter o índice de resistência vascular. RESULTADOS: Observou-se diferença estatisticamente significante (p < 0,001) entre os valores médios do índice de resistência para os resultados benigno e maligno (0,62x 0,80, respectivamente), em nódulos maiores que 1 cm. Um índice de resistência 0,69 foi altamente associado a lesões malignas, com sensibilidade de 84,2%, especificidade de 88,9%, taxa de falso-positivo de 11,1% e taxa de falso-negativo de 15,8%. CONCLUSÃO: A análise do índice de resistência vascular pode fornecer grande auxílio na avaliação das lesões nodulares da mama maiores que 1 cm, em conjunto com as informações obtidas por meio da escala de cinzas, com elevada sensibilidade e especificidade.

Pathologies vasculaires lymphatiques: apport de la lympho-fluoroscopie [Lymphatic vascular pathologies: contribution of lympho-fluoroscopy].

Si l'examen clinique revêt une importance essentielle en lymphologie et exige des praticiens expérimentés, la lymphoscintigraphie et plus récemment la lympho-fluoroscopie au vert d'indocyanine constituent des moyens d'investigation précieux dans la prévention, le diagnostic et le traitement des pathologies vasculaires lymphatiques. L'intérêt de la lymphoscintigraphie réside dans l'analyse qualitative et quantitative de la migration des macromolécules par les vaisseaux lymphatiques et l'évaluation du secteur lymphatique profond. La lympho-fluoroscopie se distingue de la lymphoscintigraphie par l'obtention d'une cartographie détaillée des vaisseaux lymphatiques superficiels et d'images dynamiques en temps réel. Elle apporte à l'angiologue et au physiothérapeute des informations irremplaçables sur leur contractilité et la présence de dérivations compensatoires à privilégier lors du drainage lymphatique manuel. If clinical examination has an essential importance in lymphology disorders and requires experimented practitioners, lymphoscintigraphy and more recently green indocyanine lympho-fluoroscopy constitute precious complementary investigations in prevention, diagnosis, and treatment of lymphatic vascular pathologies. The lymphoscintigraphy interest lies in qualitative and quantitative analysis of macromolecules migration within lymphatic vessels and the deep lymphatic network. The lympho-fluoroscopy distinguishes itself from lymphoscintigraphy allowing real time superficial lymphatic vessels detailed mapping, gathering important information on their contractility, and the presence of compensatory derivations to be favored during manual lymphatic drainage to angiologist and physiotherapist.

Secondary growth of the Arabidopsis hypocotyl-vascular development in dimensions.

The secondary thickening of plant organs in extant dicotyledons is a massive growth process that constitutes the major carbon sink in perennial, woody plants. Yet, our understanding of its molecular genetic control has been mostly obtained by its analysis in an herbaceous annual model, Arabidopsis. Recent years have seen increased interest in this somewhat under-researched topic, and various (non-)cell autonomous factors that guide the extent and vascular patterning of secondary growth have been identified. Concomitantly, a more detailed understanding of vascular differentiation processes has been obtained through analyses of primary growth, mostly in the root meristem. A future challenge will be the integration of these patterning and differentiation modules together with cambial activity into the 4-dimensional frame of secondary thickening.

The promoter activity of human Mfn2 depends on Sp1 in vascular smooth muscle cells

AIMS: Mitofusin-2 (Mfn2) expression is dysregulated in vascular proliferative disorders and its overexpression attenuates the proliferation of vascular smooth muscle cells (VSMCs) and neointimal lesion development after balloon angioplasty. We sought to gain insight into the mechanisms that control Mfn2 expression in VSMCs. METHODS AND RESULTS: We cloned and characterized 2 kb of the 5'-flanking region of the human Mfn2 gene. Its TATA-less promoter contains a CpG island. In keeping with this, 5'-rapid amplification of cDNA ends revealed six transcriptional start sites (TSSs), of which TSS2 and TSS5 were the most frequently used. The strong CpG island was found to be non-methylated under conditions characterized by large differences in Mfn2 gene expression. The proximal Mfn2 promoter contains six putative Sp1 motifs. Sp1 binds to the Mfn2 promoter and its overexpression activates the Mfn2 promoter in VSMCs. Chemical inhibition of Sp1 reduced Mfn2 expression, and Sp1 silencing reduced transcriptional activity of the Mfn2 promoter. In keeping with this view, Sp1 and Mfn2 mRNA levels were down-regulated in the aorta early after an atherogenic diet in apolipoprotein E-knockout mice or in VSMCs cultured in the presence of low serum. CONCLUSION: Sp1 is a key factor in maintaining basal Mfn2 transcription in VSMCs. Given the anti-proliferative actions of Mfn2, Sp1-induced Mfn2 transcription may represent a mechanism for prevention of VSMC proliferation and neointimal lesion and development.

The promoter activity of human Mfn2 depends on Sp1 in vascular smooth muscle cells

AIMS: Mitofusin-2 (Mfn2) expression is dysregulated in vascular proliferative disorders and its overexpression attenuates the proliferation of vascular smooth muscle cells (VSMCs) and neointimal lesion development after balloon angioplasty. We sought to gain insight into the mechanisms that control Mfn2 expression in VSMCs. METHODS AND RESULTS: We cloned and characterized 2 kb of the 5'-flanking region of the human Mfn2 gene. Its TATA-less promoter contains a CpG island. In keeping with this, 5'-rapid amplification of cDNA ends revealed six transcriptional start sites (TSSs), of which TSS2 and TSS5 were the most frequently used. The strong CpG island was found to be non-methylated under conditions characterized by large differences in Mfn2 gene expression. The proximal Mfn2 promoter contains six putative Sp1 motifs. Sp1 binds to the Mfn2 promoter and its overexpression activates the Mfn2 promoter in VSMCs. Chemical inhibition of Sp1 reduced Mfn2 expression, and Sp1 silencing reduced transcriptional activity of the Mfn2 promoter. In keeping with this view, Sp1 and Mfn2 mRNA levels were down-regulated in the aorta early after an atherogenic diet in apolipoprotein E-knockout mice or in VSMCs cultured in the presence of low serum. CONCLUSION: Sp1 is a key factor in maintaining basal Mfn2 transcription in VSMCs. Given the anti-proliferative actions of Mfn2, Sp1-induced Mfn2 transcription may represent a mechanism for prevention of VSMC proliferation and neointimal lesion and development.

Notes breus (flora). Addicions i anotacions a la flora vascular de les illes Medes

Nota breu de flora relacionada amb la localització a les Illes Medes, d'una sèrie de tàxons que no figuren en el catàleg florístic de Bolòs & Vigo (1984)

DWI and complex brain network analysis predicts vascular cognitive impairment in spontaneous hypertensive rats undergoing executive function tests

The identification of biomarkers of vascular cognitive impairment is urgent for its early diagnosis. The aim of this study was to detect and monitor changes in brain structure and connectivity, and to correlate them with the decline in executive function. We examined the feasibility of early diagnostic magnetic resonance imaging (MRI) to predict cognitive impairment before onset in an animal model of chronic hypertension: Spontaneously Hypertensive Rats. Cognitive performance was tested in an operant conditioning paradigm that evaluated learning, memory, and behavioral flexibility skills. Behavioral tests were coupled with longitudinal diffusion weighted imaging acquired with 126 diffusion gradient directions and 0.3 mm(3) isometric resolution at 10, 14, 18, 22, 26, and 40 weeks after birth. Diffusion weighted imaging was analyzed in two different ways, by regional characterization of diffusion tensor imaging (DTI) indices, and by assessing changes in structural brain network organization based on Q-Ball tractography. Already at the first evaluated times, DTI scalar maps revealed significant differences in many regions, suggesting loss of integrity in white and gray matter of spontaneously hypertensive rats when compared to normotensive control rats. In addition, graph theory analysis of the structural brain network demonstrated a significant decrease of hierarchical modularity, global and local efficacy, with predictive value as shown by regional three-fold cross validation study. Moreover, these decreases were significantly correlated with the behavioral performance deficits observed at subsequent time points, suggesting that the diffusion weighted imaging and connectivity studies can unravel neuroimaging alterations even overt signs of cognitive impairment become apparent.

Corologia de la flora vascular d'interès de conservació al Parc Natural del Montseny

Presentem els resultats dels estudis realitzats des del 2009 al 2012, amb la finalitat de millorar la informació corològica disponibled'espècies de flora vascular considerades d'interès de conservació al Parc Natural del Montseny. S'han tingut en compte un total de 125tàxons. D'aquests, 3 corresponen a tàxons nous per la flora del massís (Aconitum vulparia, Botrychium matricariifolium i Polystichumlonchitis), 7 han estat retrobats i 13 corresponen a novetats per algun dels quadrats UTM 10 × 10 prospectats. Tot i les troballes, moltesespècies no han sigut localitzades durant el treball de camp. En alguns casos, atribuïm aquest fet a la reducció de les poblacions o fins i tota la desaparició, fet que afecta principalment a aquelles espècies vinculades majoritàriament a ambients oberts, que han patit una recessióimportant durant les darreres dècades. Aquest fenomen ha estat especialment rellevant al massís del turó de l'Home, sobretot a la vall deSanta Fe

Imaging of the Vulnerable Atherosclerotic Plaque. Pre-Clinical Evaluation of PET Tracers for Vascular Inflammation

Atherosclerosis is a vascular inflammatory disease causing coronary artery disease, myocardial infarct and stroke, the leading causes of death in Finland and in many other countries. The development of atherosclerotic plaques starts already in childhood and is an ongoing process throughout life. Rupture of a plaque and the following occlusion of the vessel is the main reason for myocardial infarct and stroke, but despite extensive research, the prediction of rupture remains a major clinical problem. Inflammation is considered a key factor in the vulnerability of plaques to rupture. Measuring the inflammation in plaques non-invasively is one potential approach for identification of vulnerable plaques. The aim of this study was to evaluate tracers for positron emission tomography (PET) imaging of vascular inflammation. The studies were performed with a mouse model of atherosclerosis by using ex vivo biodistribution, autoradiography and in vivo PET and computed tomography (CT). Several tracers for inflammation activity were tested and compared with the morphology of the plaques. Inflammation in the atherosclerotic plaques was evaluated as expression of active macrophages. Systematic analysis revealed that the uptake of 18F-FDG and 11C-choline, tracers for metabolic activity in inflammatory cells, was more prominent in the atherosclerotic plaques than in the surrounding healthy vessel wall. The tracer for αvβ3 integrin, 18Fgalacto- RGD, was also found to have high potential for imaging inflammation in the plaques. While 11C-PK11195, a tracer targeted to receptors in active macrophages, was shown to accumulate in active plaques, the target-to-background ratio was not found to be ideal for in vivo imaging purposes. In conclusion, tracers for the imaging of inflammation in atherosclerotic plaques can be tested in experimental pre-clinical settings to select potential imaging agents for further clinical testing. 18F-FDG, 18F-galacto-RGD and 11C-choline choline have good properties, and further studies to clarify their applicability for atherosclerosis imaging in humans are warranted.

Caracterización de la respuesta morfológica de variedades susceptibles y resistentes de yuca (Manihot esculenta Crantz) a la bacteriosis vascular causada por Xanthomonas axonopodis pv. manihotis

Xanthomonas axonopodis pv. manihotis es una de las principales limitaciones del cultivo de yuca. En esta investigación, mediante microscopía óptica, se realizó un análisis comparativo de los cambios morfológicos e histoquímicos en tallos de una variedad de yuca susceptible (TMS60444) y una resistente (CM6438-14), 7 y 14 días después de ser inoculadas con la cepa patogénica CIO151. Se pudo detectar que la variedad resistente genera barreras de calosa en las paredes celulares del parénquima cortical y del floema, manteniendo funcional este tejido. En tanto que los tejidos vasculares de la variedad susceptible colapsan, el floema por obstrucción total con tapones de calosa y por formación de compuestos fenólicos, y el xilema por formación de tílides y/o acumulación de compuestos fenólicos, sin poder frenar el avance sistémico de la enfermedad.

Vascular Function in Chronic Kidney Disease and in Renovascular Disease

Cardiovascular mortality is 15 to 30 times higher in patients with chronic kidney disease than in the age-adjusted general population. Even minor renal dysfunction predicts cardiovascular events and death in the general population. In patients with atherosclerotic renovascular disease the annual cardiovascular event and death rate is even higher. The abnormalities in coronary and peripheral artery function in the different stages of chronic kidney disease and in renovascular disease are still poorly understood, nor have the cardiac effects of renal artery revascularization been well characterized, although considered to be beneficial. This study was conducted to characterize myocardial perfusion and peripheral endothelial function in patients with chronic kidney disease and in patients with atherosclerotic renovascular disease. Myocardial perfusion was measured with positron emission tomography (PET) and peripheral endothelial function with brachial artery flow-mediated dilatation. It has been suggested that the poor renal outcomes after the renal artery revascularization could be due to damage in the stenotic kidney parenchyma; especially the reduction in the microvascular density, changes mainly evident at the cortical level which controls almost 80% of the total renal blood flow. This study was also performed to measure the effect of renal artery stenosis revascularization on renal perfusion in patients with renovascular disease. In order to do that a PET-based method for quantification of renal perfusion was developed. The coronary flow reserve of patients with chronic kidney disease was similar to the coronary flow reserve of healthy controls. In renovascular disease the coronary flow reserve was, however, markedly reduced. Flow-mediated dilatation of brachial artery was decreased in patients with chronic kidney disease compared to healthy controls, and even more so in patients with renovascular disease. After renal artery stenosis revascularization, coronary vascular function and renal perfusion did not improve in patients with atherosclerotic renovascular disease, but in patients with bilateral renal artery stenosis, flow-mediated dilatation improved. Chronic kidney disease does not significantly affect coronary vascular function. On the contrary, coronary vascular function was severely deteriorated in patients with atherosclerotic renovascular disease, possibly because of diffuse coronary artery disease and/or diffuse microvascular disease. The peripheral endothelial function was disturbed in patients with chronic kidney disease and even more so in patient with atherosclerotic renovascular disease. Renal artery stenosis dilatation does not seem to offer any benefits over medical treatment in patients with renovascular disease, since revascularization does not improve coronary vascular function or renal perfusion.