903 resultados para Transporting Atpase


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Some organisms disperse energy, associated with the transportation of resource, which is not necessarily food. Stingless bees of Central Amazonia (Melipona flavolineata and M. lateralis) collect clay in banks along streams for nest building. The moisture of the clay varies along the bank, and bees collect clay from specific location, indicating that there is some sort of preference regarding their selection. This study aims at identifying: if larger bees carry more clay; if there is a preference for moisture of substrates; and if bees are less efficient accumulating and transporting clay when it is wet. In order to do so, I measured the size of the bees and of the pellets of clay found in the corbicula. I set up a field experiment to test substrate preferences. The amount of clay transported, increased exponentially in accordance to the size of the bee, and the preferred substrate was the driest clay. The amount and the efficiency of removal of clay were not affected by the moisture of the substrate. Despite the wet clay being denser, it does not reduce the efficiency of exploitation of the resource, but suggests that bees spend more energy to carry the same quantity of wet clay, which may be the underlying mechanism explaining their preference for removing drier clay.

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The extraocular muscle fibres of the South-American opossum were determined according to their metabolic profiles using NADH-diaforase, and myofibrilar ATPase after pre-incubation in both acid (pH 4.3) and alkaline (pH 10.4) media. Three muscles were selected to study the arrangement of the fibres (obliquous dorsalis, rectus dorsalis and rectus lateralis muscles). It was demonstrated that they are organized in two layers: the orbital layer composed by small diameter fibres and the global layer with three-times thicker fibres than the former. The global layer has three fibre types: white, red and intermediate; while the orbital layer presents two fibre types, which react differently to the ATPase.

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The dendrimers of poly (amidoamine) (PAMAM) are nanoparticles which have proven succeed in transporting drugs due to high solubility, low toxicity and ability to control drugs release. Studies have explored the biological potential of dendrimers such as to transport genes, development of vaccines, antiviral, antibacterial and anticancer therapies. This review of literature on the PAMAM dendrimers discusses the architecture and general construction of dendrimers and intrinsic properties of the PAMAM. This study also describes how the PAMAM interact with many drugs and the potential of these macromolecules as well as drug nanocarriers in transdermal routes of administration, ocular, respiratory, oral and intravenous administration. Dendrimers promises good future prospects for the biomedicine.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Abstract Background: Several mechanisms have been proposed to contribute to cardiac dysfunction in obesity models, such as alterations in calcium (Ca2+) handling proteins and β-adrenergic receptors. Nevertheless, the role of these factors in the development of myocardial dysfunction induced by obesity is still not clear. Objective: The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca2+ handling and the β-adrenoceptor system. Methods: Male 30-day-old Wistar rats were fed with standard food (C) and a cycle of five hypercaloric diets (Ob) for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers. Results: Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca2+ were compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation. Conclusion: Obesity promotes cardiac dysfunction related to changes in intracellular Ca2+ handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca2+ ATPase (SERCA2) activation via Ca2+ calmodulin kinase. (Arq Bras Cardiol 2011; 97(3) : 232-240).

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Pós-graduação em Engenharia Elétrica - FEIS

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O alumínio (Al) em solos ácidos encontra-se na forma Al3+, sendo considerado tóxico às plantas de interesse agronômico, como o limoeiro Cravo (Citrus limonia), afetando principalmente seu crescimento radicular . O presente estudo avaliou como o Al influencia as raízes de C. limonia, visando correlacionar a concentração endógenea de IAA, a expressão dos genes SAUR X10A e SAUR 15A e a inibição do crescimento radicular. As plantas foram submetidas à hidroponia em diferentes concentrações de Al na solução nutritiva (0, 370 μM, 740 μM, 1110 μM, e 1480), tendo seu crescimento avaliado semanalmente em um período de dois meses. Além disso, as soluções contrastantes tiveram a expressão gênica e a concentração endógenea de IAA avaliados utilizando qRT-PCR e GC-MS, respectivamente. O tratamento com Al inibiu o crescimento radicular das plantas, além de alterar a concentração de IAA nas raízes (apresentou-se algumas vezes maior nas primeiras semanas em relação ao controle, havendo um decaimento e igualação na concentração hormonal de ambos os tratamentos) e inibir a expressão dos genes SAUR. A inibição do crescimento radicular pode ser atribuida à uma mudança de padrão e acumulação do ácido indol-acético (IAA) no ápice da raiz, provocada pela alteração na distribuição das proteínas de transporte. Concomitantemente, proteínas da família SAUR (small auxin-up RNA) têm suas expressões gênicas induzidas em presença de IAA e estão relacionadas à acidificação do apoplasto: a queda na atividade da H+-ATPase provoca a altereção do pH nesta região prejudicando a alongação da célula via crescimento ácido. Embora haja uma mesma quantidade de IAA na raiz, os genes SAUR são reprimidos na condição de estresse pelo Al, indicando que a inibição do crescimento radicular em C. limonia deve ocorrer em resposta a um conjunto de fatores

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O alumínio (Al) em solos ácidos encontra-se na forma Al3+, sendo considerado tóxico às plantas de interesse agronômico, como o limoeiro Cravo (Citrus limonia), afetando principalmente seu crescimento radicular . O presente estudo avaliou como o Al influencia as raízes de C. limonia, visando correlacionar a concentração endógenea de IAA, a expressão dos genes SAUR X10A e SAUR 15A e a inibição do crescimento radicular. As plantas foram submetidas à hidroponia em diferentes concentrações de Al na solução nutritiva (0, 370 μM, 740 μM, 1110 μM, e 1480), tendo seu crescimento avaliado semanalmente em um período de dois meses. Além disso, as soluções contrastantes tiveram a expressão gênica e a concentração endógenea de IAA avaliados utilizando qRT-PCR e GC-MS, respectivamente. O tratamento com Al inibiu o crescimento radicular das plantas, além de alterar a concentração de IAA nas raízes (apresentou-se algumas vezes maior nas primeiras semanas em relação ao controle, havendo um decaimento e igualação na concentração hormonal de ambos os tratamentos) e inibir a expressão dos genes SAUR. A inibição do crescimento radicular pode ser atribuida à uma mudança de padrão e acumulação do ácido indol-acético (IAA) no ápice da raiz, provocada pela alteração na distribuição das proteínas de transporte. Concomitantemente, proteínas da família SAUR (small auxin-up RNA) têm suas expressões gênicas induzidas em presença de IAA e estão relacionadas à acidificação do apoplasto: a queda na atividade da H+-ATPase provoca a altereção do pH nesta região prejudicando a alongação da célula via crescimento ácido. Embora haja uma mesma quantidade de IAA na raiz, os genes SAUR são reprimidos na condição de estresse pelo Al, indicando que a inibição do crescimento radicular em C. limonia deve ocorrer em resposta a um conjunto de fatores

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The Na+/H+ exchanger isoform 3 (NHE3) is essential for HCO3- reabsorption in renal proximal tubules. The expression and function of NHE3 must adapt to acid-base conditions. The goal of this study was to elucidate the mechanisms responsible for higher proton secretion in proximal tubules during acidosis and to evaluate whether there are differences between metabolic and respiratory acidosis with regard to NHE3 modulation and, if so, to identify the relevant parameters that may trigger these distinct adaptive responses. We achieved metabolic acidosis by lowering HCO3- concentration in the cell culture medium and respiratory acidosis by increasing CO2 tension in the incubator chamber. We found that cell-surface NHE3 expression was increased in response to both forms of acidosis. Mild (pH 7.21 +/- 0.02) and severe (6.95 +/- 0.07) metabolic acidosis increased mRNA levels, at least in part due to up-regulation of transcription, whilst mild (7.11 +/- 0.03) and severe (6.86 +/- 0.01) respiratory acidosis did not up-regulate NHE3 expression. Analyses of the Nhe3 promoter region suggested that the regulatory elements sensitive to metabolic acidosis are located between -466 and -153 bp, where two consensus binding sites for SP1, a transcription factor up-regulated in metabolic acidosis, were localised. We conclude that metabolic acidosis induces Nhe3 promoter activation, which results in higher mRNA and total protein level. At the plasma membrane surface, NHE3 expression was increased in metabolic and respiratory acidosis alike, suggesting that low pH is responsible for NHE3 displacement to the cell surface.

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Floating-Harbor syndrome (FHS) is a rare condition characterized by short stature, delayed osseous maturation, expressive-language deficits, and a distinctive facial appearance. Occurrence is generally sporadic, although parent-to-child transmission has been reported on occasion. Employing whole-exome sequencing, we identified heterozygous truncating mutations in SRCAP in five unrelated individuals with sporadic MS. Sanger sequencing identified mutations in SRCAP in eight more affected persons. Mutations were de novo in all six instances in which parental DNA was available. SRCAP is an SNF2-related chromatin-remodeling factor that serves as a coactivator for CREB-binding protein (CREBBP, better known as CBP, the major cause of Rubinstein-Taybi syndrome [RTS]). Five SRCAP mutations, two of which are recurrent, were identified; all are tightly clustered within a small (111 codon) region of the final exon. These mutations are predicted to abolish three C-terminal AT-hook DNA-binding motifs while leaving the CBP-binding and ATPase domains intact. Our findings show that SRCAP mutations are the major cause of FHS and offer an explanation for the clinical overlap between FHS and RTS.

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It has been shown that ouabain (OUA) can activate the Na,K-ATPase complex and mediate intracellular signaling in the central nervous system (CNS). Inflammatory stimulus increases glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptors, which are usually coupled to the activation of nitric oxide synthase (NOS). Nuclear factor-kappa B (NF-kappa B) activation modulates the expression of genes involved in development, plasticity, and inflammation. The present work investigated the effects of OUA on NF-kappa B binding activity in rat hippocampus and the influence of this OUA-Na,K-ATPase signaling cascade in NMDA-mediated NF-kappa B activation. The findings presented here are the first report indicating that intrahippocampal administration of OUA, in a concentration that did not alter Na,K-ATPase or NOS activity, induced an activation of NF-kappa B, leading to increases in brain-derived neurotrophic factor (Bdnf), inducible NOS (iNos), tumor necrosis factor-alpha (Tnf-alpha), and B-cell leukemia/lymphoma 2 (Bcl2) mRNA levels. This response was not linked to any significant signs of neurodegeneration as showed via Fluoro-Jade B and Nissl stain. Intrahippocampal administration of NMDA induced NF alpha B activation and increased NOS and alpha 2/3-Na,K-ATPase activities. NMDA treatment further increased OUA-induced NF-kappa B activation, which was partially blocked by MK-801, an antagonist of NMDA receptor. These results suggest that OUA-induced NF-kappa B activation is at least in part dependent on Na,K-ATPase modulatory action of NMDA receptor in hippocampus. The interaction of these signaling pathways could be associated with biological mechanisms that may underlie the basal homeostatic state linked to the inflammatory signaling cascade in the brain. (c) 2011 Wiley Periodicals, Inc.

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Background/Aims: Hypomagnesemia may induce hypercholesterolemia, but the contrary has not been described yet. Thus, magnesium homeostasis was evaluated in rats fed a cholesterol-enriched diet for 8 days. This study has a relevant clinical application if hypomagnesemia, due to hypercholesterolemia, is confirmed in patients with long-term hypercholesterolemia. Methods: Both hypercholesterolemic (HC) and normocholesterolemic rats (NC) were divided into sets of experiments to measure hemodynamic parameters, physiological data, maximum capacity to dilute urine (C-H2O), variations (Delta) in [Ca2+](i) and the expression of transporter proteins. Results: HC developed hypomagnesemia and showed high magnesuria in the absence of hemodynamic abnormalities. However, the urinary sodium excretion and C-H2O in HC was similar to NC. On the other hand, the responses to angiotensin II by measuring Delta [Ca2+](i) were higher in the thick ascending limb of Henle's loop (TAL) of HC than NC. Moreover, high expression of the cotransporter NKCC2 was found in renal outer medulla fractions of HC. Taken together, the hypothesis of impairment in TAL was excluded. Actually, the expression of the epithelial Mg2+ channel in renal cortical membrane fractions was reduced in HC. Conclusion: Impairment in distal convoluted tubule induced by hypercholesterolemia explains high magnesuria and hypomagnesemia observed in HC. Copyright (C) 2011 S. Karger AG, Basel

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The Hsp70 is an essential molecular chaperone in protein metabolism since it acts as a pivot with other molecular chaperone families. Several co-chaperones act as regulators of the Hsp70 action cycle, as for instance Hip (Hsp70-interacting protein). Hip is a tetratricopeptide repeat protein (TPR) that interacts with the ATPase domain in the Hsp70-ADP state, stabilizing it and preventing substrate dissociation. Molecular chaperones from protozoans, which can cause some neglected diseases, are poorly studied in terms of structure and function. Here, we investigated the structural features of Hip from the protozoa Leishmania braziliensis (LbHip), one of the causative agents of the leishmaniasis disease. LbHip was heterologously expressed and purified in the folded state, as attested by circular dichroism and intrinsic fluorescence emission techniques. LbHip forms an elongated dimer, as observed by analytical gel filtration chromatography, analytical ultracentrifugation and small angle X-ray scattering (SAXS). With the SAXS data a low resolution model was reconstructed, which shed light on the structure of this protein, emphasizing its elongated shape and suggesting its domain organization. We also investigated the chemical-induced unfolding behavior of LbHip and two transitions were observed. The first transition was related to the unfolding of the TPR domain of each protomer and the second transition of the dimer dissociation. Altogether. LbHip presents a similar structure to mammalian Hip, despite their low level of conservation, suggesting that this class of eukaryotic protein may use a similar mechanism of action. (C) 2012 Elsevier Inc. All rights reserved.