910 research outputs found

    The effect of atmospheric aerosol particles and clouds on net ecosystem exchange in the Amazon

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    Carbon cycling in the Amazon is closely linked to atmospheric processes and climate in the region as a consequence of the strong coupling between the atmosphere and biosphere. This work examines the effects of changes in net radiation due to atmospheric aerosol particles and clouds on the net ecosystem exchange (NEE) of CO<sub>2</sub> in the Amazon region. Some of the major environmental factors affecting the photosynthetic activity of plants, such as air temperature and relative humidity, were also examined. An algorithm for clear-sky irradiance was developed and used to determine the relative irradiance, <i>f</i>, which quantifies the percentage of solar radiation absorbed and scattered due to atmospheric aerosol particles and clouds. Aerosol optical depth (AOD) was calculated from irradiances measured with the MODIS (Moderate Resolution Imaging Spectroradiometer) sensor, onboard the Terra and Aqua satellites, and was validated with ground-based AOD measurements from AERONET (Aerosol Robotic Network) sun photometers. Carbon fluxes were measured using eddy covariance technique at the Large-Scale Biosphere-Atmosphere Experiment in Amazonia (LBA) flux towers. Two sites were studied: the Jaru Biological Reserve (RBJ), located in Rondonia, and the Cuieiras Biological Reserve at the K34 LBA tower (located in a preserved region in the central Amazon). Analysis was performed continuously from 1999 to 2009 at K34 and from 1999 to 2002 at RBJ, and includes wet, dry and transition seasons. In the Jaru Biological Reserve, a 29% increase in carbon uptake (NEE) was observed when the AOD ranged from 0.10 to 1.5 at 550 nm. In the Cuieiras Biological Reserve, the aerosol effect on NEE was smaller, accounting for an approximate 20% increase in NEE. High aerosol loading (AOD above 3 at 550 nm) or high cloud cover leads to reductions in solar flux and strong decreases in photosynthesis up to the point where NEE approaches zero. The observed increase in NEE is attributed to an enhancement (~50%) in the diffuse fraction of photosynthetic active radiation (PAR). The enhancement in diffuse PAR can be done through increases in aerosols and/or clouds. In the present study, it was not possible to separate these two components. Significant changes in air temperature and relative humidity resulting from changes in solar radiation fluxes under high aerosol loading were also observed at both sites. Considering the long-range transport of aerosols in the Amazon, the observed changes in NEE for these two sites may occur over large areas in the Amazon, significantly altering the carbon balance in the largest rainforest in the world

    Subtle reproductive impairment through nitric oxide-mediated mechanisms in sea urchins from an area affected by harmful algal blooms

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    The health of the sea urchin Paracentrotus lividus, a key species in the Mediterranean Sea, is menaced by several pressures in coastal environments. Here, we aimed at assessing the reproductive ability of apparently healthy P. lividus population in a marine protected area affected by toxic blooms of Ostreospsis cf. ovata. Wide-ranging analyses were performed in animals collected prior to and during the bloom, as well as at several times thereafter, during the reproductive season. Adults showed a low fertilization rate, along with high nitric oxide (NO) levels in the gonads and the nitration of the major yolk protein toposome, which is an important player in sea urchin development. Serious developmental anomalies were observed in the progeny, which persist several months after the bloom. NO levels were high in the different developmental stages, which also showed variations in the transcription of several genes that were found to be directly or indirectly modulated by NO. These results highlight subtle but important reproductive flaws transmitted from the female gonads to the offspring with the NO involvement. Despite a recovery along time after the bloom, insidious damages can be envisaged in the local sea urchin population, with possible reverberation on the whole benthic system

    Diffractive phase-shift lithography photomask operating in proximity printing mode

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    Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)A phase shift proximity printing lithographic mask is designed, manufactured and tested. Its design is based on a Fresnel computer-generated hologram, employing the scalar diffraction theory. The obtained amplitude and phase distributions were mapped into discrete levels. In addition, a coding scheme using sub-cells structure was employed in order to increase the number of discrete levels, thus increasing the degree of freedom in the resulting mask. The mask is fabricated on a fused silica substrate and an amorphous hydrogenated carbon (a:C-H) thin film which act as amplitude modulation agent. The lithographic image is projected onto a resist coated silicon wafer, placed at a distance of 50 mu m behind the mask. The results show a improvement of the achieved resolution - linewidth as good as 1.5 mu m - what is impossible to obtain with traditional binary masks in proximity printing mode. Such achieved dimensions can be used in the fabrication of MEMS and MOEMS devices. These results are obtained with a UV laser but also with a small arc lamp light source exploring the partial coherence of this source. (C) 2010 Optical Society of America18161638716405Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)FAPESP_BrasilCNPq_Brasi

    The protective role of the 3-mercaptopyruvate sulfurtransferase (3-MST)-hydrogen sulfide (H<sub>2</sub>S) pathway against experimental osteoarthritis.

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    Osteoarthritis (OA) is characterized by the formation and deposition of calcium-containing crystals in joint tissues, but the underlying mechanisms are poorly understood. The gasotransmitter hydrogen sulfide (H &lt;sub&gt;2&lt;/sub&gt; S) has been implicated in mineralization but has never been studied in OA. Here, we investigated the role of the H &lt;sub&gt;2&lt;/sub&gt; S-producing enzyme 3-mercaptopyruvate sulfurtransferase (3-MST) in cartilage calcification and OA development. 3-MST expression was analyzed in cartilage from patients with different OA degrees, and in cartilage stimulated with hydroxyapatite (HA) crystals. The modulation of 3-MST expression in vivo was studied in the meniscectomy (MNX) model of murine OA, by comparing sham-operated to MNX knee cartilage. The role of 3-MST was investigated by quantifying joint calcification and cartilage degradation in WT and 3-MST &lt;sup&gt;-/-&lt;/sup&gt; meniscectomized knees. Chondrocyte mineralization in vitro was measured in WT and 3-MST &lt;sup&gt;-/-&lt;/sup&gt; cells. Finally, the effect of oxidative stress on 3-MST expression and chondrocyte mineralization was investigated. 3-MST expression in human cartilage negatively correlated with calcification and OA severity, and diminished upon HA stimulation. In accordance, cartilage from menisectomized OA knees revealed decreased 3-MST if compared to sham-operated healthy knees. Moreover, 3-MST &lt;sup&gt;-/-&lt;/sup&gt; mice showed exacerbated joint calcification and OA severity if compared to WT mice. In vitro, genetic or pharmacologic inhibition of 3-MST in chondrocytes resulted in enhanced mineralization and IL-6 secretion. Finally, oxidative stress decreased 3-MST expression and increased chondrocyte mineralization, maybe via induction of pro-mineralizing genes. 3-MST-generated H &lt;sub&gt;2&lt;/sub&gt; S protects against joint calcification and experimental OA. Enhancing H &lt;sub&gt;2&lt;/sub&gt; S production in chondrocytes may represent a potential disease modifier to treat OA

    ACE-inhibition ameliorates vascular reactivity and delays diabetes outcome in NODmice.

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    Recently, we have demonstrated a direct correlation among hyperglycaemia, vascular dysfunction and eNOS post-translational regulation in non non-obese diabetic mice (NOD). Here, we evaluate the impact of two ACE-inhibitors therapy, zofenopril and enalapril in NOD mice. Insulin-dependent diabetes mellitus (IDDM) development was monitored weekly through glycosuria measurement. Zofenopril and enalapril were dosed at 0.5 mg/kg/die orally. Animals were sacrificed at different points and aortas used for western blotting or for tissue bath experiments. Bovine aortic endothelial cells in high glucose medium are treated with zofenoprilat or enalaprilat. Cells and supernatant were utilised for western blot analysis and for nitrite/nitrate determination, respectively. In ex-vivo experiments chronic administration of both drugs restored PE-induced contraction but not Isop-induced vasodilatation, however only zofenopril reduced caveolin-1 expression. In vitro, both drugs inhibited caveolin-1 expression and increased NOx production. However, zofenopril caused inhibition of both parameters at a concentration 200 fold lower than enalalpril. In vivo, zofenopril delays the onset of diabetic conditions of about 50%, and ameliorates polyuria. In conclusion our data suggest that ACE-inhibitor therapy may be useful in IDDM, in particular sulphydrylated inhibitor would display a better efficacy especially if administered early on the development of diabetes

    Comparative study between wet and dry etching of silicon for microchannels fabrication

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    FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOIn this work we present a comparative study of two processes for the fabrication of an array of microchannels for microfluidics applications, based on integrated-circuit technology process steps, such as lithography and dry etching. Two different methods were investigated in order to study the resulting microstructures: wet and dry deep etching of silicon substrate. The typical etching depth necessary to the target application is 50 mu m.1093015FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO2016/09509-112. Conference on Advanced Fabrication Technologies for Micro/Nano Optics and Photonics3 a 5 de Fevereiro de 2019San Francisco, CA, Estados UnidosSPIE; Nanoscribe Gmb

    Compared clinical efficacy and bone metabolic effects of low-dose deflazacort and methyl prednisolone in male inflammatory arthropathies: a 12-month open randomized pilot study.

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    Objective. To evaluate: (i) a correct equivalence ratio of clinical efficacy between low-dose deflazacort (DFZ) and methyl prednisolone (MP); and (ii) bone metabolic effects of low-dose DFZ and MP in the treatment of male RA and PsA. Methods. A total of 21 male patients with active RA or PsA, naive to steroid treatment were chosen for the study. Group I: 10 patients treated for 6 months with DFZ 7.5 mg, calcium, cholecalciferol and a DMARD; for the following 6 months with MP 4 mg, calcium, cholecalciferol and a DMARD. Group II: 11 patients treated for 6 months with MP 4 mg, calcium, cholecalciferol and a DMARD; for the following 6 months with DFZ 7.5 mg, calcium, cholecalciferol and a DMARD. At day 0, 90, 180, 240 and 360 evaluation of ACR improvement criteria; a blood sample for total and bone-specific ALP, calcium, phosphorus, PTH, SHBG, estradiol, ACTH, osteocalcin, LH, OPG; a sample of urine for calcium, phosphorus, creatinine and DPD. Results. 13/21 patients (6/10 Group I; 7/11 Group II) reached ACR 20 at 6 months; 14/21 (7/10 Group I, 7/10 Group II) at 12 months. Only at the third month we observed in Group II vs Group I a reduction of OPG (24% vs 6%, P= n.s.); ALP (P < 0.001) and osteocalcin (P = 0.006) decreased in both groups from the third month; DPD decreased in both groups only from the sixth month (P = 0.002). Conclusions. The correct equivalence ratio of DFZ to MP is 1.875:1, and of DFZ to prednisolone 1.5:1. We found a relative prevalence of bone resorption compared to bone formation in the first 6 months of treatment. The trend of OPG requires further investigation

    Duchenne's muscular dystrophy involves a defective transsulfuration pathway activity

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    Duchenne muscular dystrophy (DMD) is the most frequent X chromosome-linked disease caused by mutations in the gene encoding for dystrophin, leading to progressive and unstoppable degeneration of skeletal muscle tissues. Despite recent advances in the understanding of the molecular processes involved in the pathogenesis of DMD, there is still no cure. In this study, we aim at investigating the potential involvement of the transsulfuration pathway (TSP), and its by-end product namely hydrogen sulfide (H2S), in primary human myoblasts isolated from DMD donors and skeletal muscles of dystrophic (mdx) mice. In myoblasts of DMD donors, we demonstrate that the expression of key genes regulating the H2S production and TSP activity, including cystathionine γ lyase (CSE), cystathionine beta-synthase (CBS), 3 mercaptopyruvate sulfurtransferase (3-MST), cysteine dioxygenase (CDO), cysteine sulfonic acid decarboxylase (CSAD), glutathione synthase (GS) and γ -glutamylcysteine synthetase (γ-GCS) is reduced. Starting from these findings, using Nuclear Magnetic Resonance (NMR) and quantitative Polymerase Chain Reaction (qPCR) we show that the levels of TSP-related metabolites such as methionine, glycine, glutathione, glutamate and taurine, as well as the expression levels of the aforementioned TSP related genes, are significantly reduced in skeletal muscles of mdx mice compared to healthy controls, at both an early (7 weeks) and overt (17 weeks) stage of the disease. Importantly, the treatment with sodium hydrosulfide (NaHS), a commonly used H2S donor, fully recovers the impaired locomotor activity in both 7 and 17 old mdx mice. This is an effect attributable to the reduced expression of pro-inflammatory markers and restoration of autophagy in skeletal muscle tissues. In conclusion, our study uncovers a defective TSP pathway activity in DMD and highlights the role of H2S-donors for novel and safe adjuvant therapy to treat symptoms of DMD
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