Assessment of the conservation status of natural and semi-natural patches associated with urban areas through habitat suitability indices

Urban environments rely on the surrounding natural ecosystems remnants as providers of ecosystem functions, therefore these areas not only support a unique biodiversity but also have a social value for maintaining public health and wellbeing. For this reason, urbanization is considered to be one the biggest threats to ecosystems, leading to native biodiversity simplification and, thus, to a detriment of the provided ecosystem services. Moreover, this change in land use results in high levels of landscape fragmentation and modification in areas surrounding the habitat remnants which, in consequence, become inadequate for many native species. In this context, it is important that urban planners have the information to assess the possible consequences of future changes in land use in order to increase the landscape chances of supporting both, native biodiversity and the needs of a growing human population. The objective of the present work is to evaluate the ecological integrity of natural and semi-natural vegetation patches immersed in an urban area in order to generate a conceptual framework for landscape assessment that allows urban planners to envision the best choice for city development at a given place. To do so, we developed a quantitative integral environmental evaluation index that includes ecological characterization, geological characterization, and environmental characterization (presence of anthropic disturbance) of the assessed area. We conclude that the index we have generated in this work is suitable to be used as a management tool to allow an unbiased valuation and to identify managing situations that require a short term response.Fil: Natale, Evangelina Sandra. Fundación Conservación y Desarrollo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Villalba, G.. Fundación Conservación y Desarrollo; ArgentinaFil: Junquera, J. E.. Fundación Conservación y Desarrollo; ArgentinaFil: Zalba, Sergio Martín. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Grupo de Estudios en Conservación y Manejo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

A hybrid double-dot in silicon

We report electrical measurements of a single arsenic dopant atom in the tunnel-barrier of a silicon SET. As well as performing electrical characterization of the individual dopant, we study series electrical transport through the dopant and SET. We measure the triple points of this hybrid double dot, using simulations to support our results, and show that we can tune the electrostatic coupling between the two sub-systems.Comment: 11 pages, 6 figure

Beyond-adiabatic Quantum Admittance of a Semiconductor Quantum Dot at High Frequencies: Rethinking Reflectometry as Polaron Dynamics

Semiconductor quantum dots operated dynamically are the basis of many quantum technologies such as quantum sensors and computers. Hence, modelling their electrical properties at microwave frequencies becomes essential to simulate their performance in larger electronic circuits. Here, we develop a self-consistent quantum master equation formalism to obtain the admittance of a quantum dot tunnel-coupled to a charge reservoir under the effect of a coherent photon bath. We find a general expression for the admittance that captures the well-known semiclassical (thermal) limit, along with the transition to lifetime and power broadening regimes due to the increased coupling to the reservoir and amplitude of the photonic drive, respectively. Furthermore, we describe two new photon-mediated regimes Floquet broadening, determined by the dressing of the QD states, and broadening determined by photon loss in the system. Our results provide a method to simulate the high-frequency behaviour of QDs in a wide range of limits, describe past experiments, and propose novel explorations of QD-photon interactions

The inhibitory effect of leptin on angiotensin II-induced vasoconstriction in vascular smooth muscle cells is mediated via a nitric oxide-dependent mechanism

Leptin inhibits the contractile response induced by angiotensin (Ang) II in vascular smooth muscle cells (VSMCs) of the aorta. We studied in vitro and ex vivo the role of nitric oxide (NO) in the effect of leptin on the Ang II-induced vasoconstriction of the aorta of 10-wk-old Wistar rats. NO and nitric oxide synthase (NOS) activity were assessed by the Griess and (3)H-arginine/citrulline conversion assays, respectively. Stimulation of inducible NOS (iNOS) as well as Janus kinases/signal transducers and activators of transcription (JAK/STAT) and phosphoinositide 3-kinase (PI3K)/Akt signaling pathways were determined by Western blot. The contractile responses to Ang II were evaluated in endothelium-denuded aortic rings using the organ bath system. Changes in intracellular Ca(2+) were measured in VSMCs using fura-2 fluorescence. Leptin significantly (P < or = 0.01) stimulated NO release and NOS activity in VSMCs. Leptin's effect on NO was abolished by the NOS inhibitor, N(G)-monomethyl l-arginine, or the iNOS selective inhibitor L-N(6)-(1-iminoethyl)-lysine. Accordingly, leptin increased iNOS protein expression, with a comparable time course with that of NO production and NOS activity. Leptin also significantly increased STAT3 (P < or = 0.01) and Akt (P < or = 0.001) phosphorylation. Moreover, either the JAK2 inhibitor, AG490, or the PI3K inhibitor, wortmannin, significantly (P < or = 0.05) abrogated the leptin-induced increase in iNOS protein. Finally, both N(G)-monomethyl L-arginine and L-N(6)-(1-iminoethyl)-lysine inhibitors completely blunted (P < or = 0.001) the leptin-mediated inhibition of the Ang II-induced VSMC activation and vasoconstriction. These findings suggest that the endothelium-independent depressor action of leptin is mediated by an increase of NO bioavailability in VSMCs. This process requires the up-regulation of iNOS through mechanisms involving JAK2/STAT3 and PI3K/Akt pathways

NADPH Oxidase–Dependent Superoxide Production Is Associated With Carotid Intima-Media Thickness in Subjects Free of Clinical Atherosclerotic Disease

Objective—Oxidative stress plays a critical role in the pathogenesis of atherosclerosis. The NADPH oxidase constitutes the main source of superoxide in phagocytic and vascular cells. This study aimed to investigate the levels of NADPH oxidase–mediated superoxide production in phagocytic cells and the association between phagocytic superoxide production and carotid intima-media thickness (IMT), a surrogate marker of asymptomatic atherosclerosis. Methods and Results—NADPH oxidase–mediated superoxide production was determined by a chemiluminescence assay using lucigenin and associated with IMT for 184 asymptomatic subjects free of overt clinical atherosclerotic disease. Compared with individuals in the lowest tertile of superoxide production, those in the upper tertile ( 20 counts/sec) showed significantly higher IMT (P 0.05). In correlation analysis, a positive relationship was found between superoxide production and carotid IMT. Superoxide production also correlated positively (P 0.05) with body mass index (BMI). In multivariate analysis, the association of superoxide production with carotid IMT remained significant after adjustment for age, sex, systolic blood pressure, BMI, triglycerides, glucose, and smoking. Conclusions—In a population sample of adults without clinically overt atherosclerotic disease, increased NADPH oxidase activity was associated with enhanced carotid IMT, suggesting a relationship between phagocytic NADPH oxidase– mediated oxidative stress and the development of atherosclerosis

Increased phagocytic nicotinamide adenine dinucleotide phosphate oxidase–dependent superoxide production in patients with early chronic kidney disease

Background. Oxidative stress has been implicated in the pathogenesis of atherosclerosis that develops in patients with advanced chronic kidney disease (CKD). This study was designed to investigate whether a relationship exists between phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase–dependent superoxide anion (•O2 −) production and subclinical atherosclerosis in patients with early CKD. Methods. Superoxide production was assayed by chemiluminescence under baseline and stimulated conditions on mononuclear cells obtained from asymptomatic patients with stage 1 to 2 CKD (N = 22) and healthy controls (N = 21). Ultrasonographic determination of carotid intima-media thickness (IMT) was used to assess the presence of atherosclerosis. Results. Although there were no differences in baseline •O2 − production between controls and patients, the •O2 − production in phorbol myristate acetate–stimulated mononuclear cells was increased (P < 0.05) in patients compared with controls. The phorbol myristate acetate–induced •O2 − production was completely abolished by apocynin, a specific inhibitor of NADPH oxidase. A direct correlation (r = 0.441, P < 0.05) was found between plasma insulin levels and NADPH oxidase–mediated •O2 − production in patients. Carotid IMT was higher (P < 0.005) in patients than in controls. CarotidIMTvalues above the upper normal limit in controls were found in 70% and 40% of patients with increased or normal NADPH oxidase–mediated •O2 − production, respectively. Conclusion. Generation of •O2 − that is mainly dependent on NADPH oxidase is abnormally enhanced in patients with early CKD. It is suggested that this alteration could be related to the development of subclinical atherosclerosis in these patients

Polymorphisms and promoter overactivity of the p22(phox) gene in vascular smooth muscle cells from spontaneously hypertensive rats

In a previous study, we found that the p22(phox) subunit of the NADH/NADPH oxidase is overexpressed in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHRs) with enhanced vascular production of superoxide anion ((.)O(2)(-)). Thus, we have investigated whether changes in the sequence or activity of the promoter region of p22(phox) gene are present in SHRs. To carry out this analysis, first of all, we characterized the rat gene structure and promoter region for the p22(phox) subunit. The p22(phox) gene spans approximately 10 kb and contains 6 exons and 5 introns. Primer extension analysis indicated the transcriptional start site 100 bp upstream from the translational start site. The immediate promoter region of the p22(phox) gene does not contain a TATA box, but there are a CCAC box and putative recognition sites for nuclear factors, such as SP1, gamma-interferon, and nuclear factor-kappaB. Using reporter-gene transfection analysis, we found that this promoter was functional in VSMCs. Furthermore, we observed that p22(phox) promoter activity was significantly higher in VSMCs from SHRs than from normotensive Wistar-Kyoto rats. In addition, we found that there were 5 polymorphisms in the sequence of p22(phox) promoter between Wistar-Kyoto rats and SHRs and that they were functional. The results obtained in this study provide a tool to explore the mechanisms that regulate the expression of p22(phox) gene in rat VSMCs. Furthermore, our findings show that changes in the sequence of p22(phox) gene promoter and in the degree of activation of VSMCs are responsible for upregulated expression of p22(phox) in SHRs

Relación entre las fases precoces de la enfermedad renal y el síndrome metabólico

Advanced kidney disease is a major health problem due to its association with high cardiovascular morbidity and mortality. Early recognition of advanced kidney disease is the mainstay to avoid its progression. Since metabolic syndrome and insulin resistance are risk factors for both cardiovascular and advanced kidney disease, we investigated the relationship of early kidney disease (EKD) with metabolic syndrome and insulin resistance, and their association with surrogate markers of arteriosclerosis. METHODS: We studied 1498 subjects. Insulin resistance was defined as HOMA >/=3.7 mmol (muU)/L(2) and EKD as stages 1 and 2 of the NKF-KDOQI. Carotid intima-media thickness was used as a surrogate marker of arteriosclerosis. RESULTS: The presence of one trait of metabolic syndrome was associated with an odds ratio (OR) for EKD of 2.3 (95% confidence interval [CI], 1.18-4.48) that increased to 6.72 (95% CI, 3.56-13.69) in subjects with the syndrome. All the traits of the syndrome except low level of high-density lipoproteins showed an increased OR for EKD. Increasing HOMA was also directly correlated with higher OR for EKD, being as high as 3.89 (95% CI, 1.99-7.59) for subjects in the fourth quartile. Subjects with the syndrome plus EKD showed an increased intima-media thickness compared with those without kidney disease. CONCLUSIONS: Insulin resistance and all metabolic syndrome traits except low level of high-density lipoproteins were significantly associated with an increased OR for EKD. Both metabolic syndrome and EKD were independently and additively related to the presence of surrogate markers of arteriosclerosis

Functional Effect of the p22phox -930A/G Polymorphism on p22phox Expression and NADPH Oxidase Activity in Hypertension

Oxidative stress induced by superoxide is implicated in hypertension. NADPH oxidase is the main source of superoxide in phagocytic and vascular cells, and the p22phox subunit is involved in NADPH oxidase activation. Recently we reported an association of 930A/G polymorphism in the human p22phox gene promoter with hypertension. This study was designed to investigate the functional role of this polymorphism in hypertension. We thus investigated the relationships between the 930A/G polymorphism and p22phox expression and NADPH oxidase–mediated superoxide production in phagocytic cells from 70 patients with essential hypertension and 70 normotensive controls. Genotyping of the polymorphism was performed by restriction fragment length polymorphism. NADPH oxidase activity was determined by chemiluminescence assays, and p22phox mRNA and protein expression was measured by Northern and Western blotting, respectively. Compared with hypertensive subjects with the AA/AG genotype, hypertensive subjects with the GG genotype exhibited increased (P 0.05) phagocytic p22phox mRNA (1.26 0.06 arbitrary unit [AU] versus 0.99 0.03 AU) and protein levels (0.58 0.05 AU versus 0.34 0.04 AU) and enhanced NADPH oxidase activity (1998 181 counts/s versus 1322 112 counts/s). No differences in these parameters were observed among genotypes in normotensive cells. Transfection experiments on vascular smooth muscle cells showed that the A-to-G substitution of this polymorphism produced an increased reporter gene expression in hypertensive cells. Nitric oxide production, as assessed by measurement of serum nitric oxide metabolites, was lower in GG hypertensive subjects than in AA/AG hypertensive subjects. In conclusion, these results suggest that hypertensive subjects carrying the GG genotype of the p22phox 930A/G polymorphism are highly exposed to NADPH oxidase-mediated oxidative stress