Efficacy of different antifouling treatments for seawater cooling systems

In an industrial seawater cooling system, the effects of three different antifouling treatments, viz. sodium hypochlorite (NaClO), aliphatic amines (Mexel1432) and UV radiation, on the characteristics of the fouling formed were evaluated. For this study a portable pilot plant, as a side-stream monitoring system and seawater cooling system, was employed. The pilot plant simulated a power plant steam condenser, having four titanium tubes under different treatment patterns, where fouling progression could be monitored. The nature of the fouling obtained was chiefly inorganic, showing a clear dependence on the antifouling treatment employed. After 72 days the tubes under treatment showed a reduction in the heat transfer resistance (R) of around 70% for NaClO, 48% for aliphatic amines and 55% for UV, with respect to the untreated tube. The use of a logistic model was very useful for predicting the fouling progression and the maximum asymptotic value of the increment in the heat transfer resistance (DRmax). The apparent thermal conductivity (l) of the fouling layer showed a direct relationship with the percentage of organic matter in the collected fouling. The characteristics and mode of action of the different treatments used led to fouling with diverse physicochemical properties

Management of alliance portfolios and the role of the board of directors

The objective of the present work consists in testing whether the strategic involvement of boards of directors has a positive influence on the development of alliance portfolio management capability and on the value that the alliance portfolio generates. A variance-based structural equation modelling (Partial Least Squares) has been applied to a sample constituted by 139 top Spanish companies. Our analysis shows that the strategic involvement of the board of directors has a positive and influence on the management of alliance portfolios, thereby influencing the value of that portfolio in an indirect way. Unlike previous literature, this study links the functions of the board of directors to organizational capabilities, connecting the literature on corporate governance and on management of alliance portfolios

Niche-Associated Activation of Rac Promotes the Asymmetric Division of <i>Drosophila</i> Female Germline Stem Cells

Background: Drosophila female germline stem cells (GSCs) reside adjacent to a cellular niche that secretes Bone Morphogenetic Protein (BMP) ligands and anchors the GSCs through adherens junctions. The GSCs divide asymmetrically such that one daughter remains in the niche as a GSC, while the other is born away from the niche and differentiates. However, given that the BMP signal can be diffusible, it remains unclear how a local extracellular asymmetry is sufficient to result in a robust pattern of asymmetric division. Methods and Findings: Here we show that GSCs are polarized with respect to the cellular niche. We first use a modified biosensor to demonstrate that the small GTPase Rac is asymmetrically activated within the GSC at the niche-GSC interface. Experiments using loss-of-function and gain-of-function mutations in Rac indicate that asymmetric Rac activity both localizes the microtubule binding protein Apc2 to orient one GSC centrosome at the niche-GSC interface during interphase and activates the Jun N-terminal kinase pathway to increase the ability of the GSC to respond to BMP ligands. Other processes act in concert with each function of Rac. Specifically, we demonstrate that the GSC cell cycle arrests at prometaphase if centrosomes are misoriented. Conclusions: Thus, the GSCs, an adult stem cell present in a cellular niche, have a niche-associated polarity that couples control of the division plane with increased response to an extracellular maintenance signal. Other processes work in parallel with the Rac-mediated polarity to ensure a robust pattern of asymmetric division. We suggest that all adult stem cells likely employ multiple, independently acting mechanisms to ensure asymmetric division to maintain tissue homeostasis.</p

Analysis of platelets from a diet-induced obesity rat model: elucidating platelet dysfunction in obesity

Obesity is one of the main health problems in industrialized countries. The contribution of multiple factors developed in obesity can hardly be modeled in vitro. In this context, the development of animal models mimicking human obesity could be essential. The aim of the present study was to compare platelets from a diet-induced obesity (DIO) rat model with their lean control group in order to elucidate platelet dysfunction mechanisms in obesity and correlate the results with previous data from morbid obese patients. In parallel, we also established a blood collection and platelet isolation methodology to study the DIO rat model at biochemical and functional level. Optimal blood collection was obtained from vena cava and platelet isolation was based on a serial of centrifugations avoiding platelet activation. Our results show that the DIO rat model simulate obesity pathologically since weight gain, fasting glucose and platelet counts are increased in obese rats. Interestingly, platelet levels of the active form of Src (pTyr(419)) showed a tendency to increase in DIO rats pointing towards a potential dysfunction in Src family kinases-related signalling pathways in obesity. Moreover, platelets from DIO rats adhere more to collagen compared with the control group, pointing towards Glycoprotein VI (GPVI) as one of the dysregulated receptors in obesity, in agreement with our recent studies in humans. These results confirm that obesity, in line with human studies, present a platelet dysregulation, and highlight the relevance of considering novel antithrombotic drug targets in these patients, such as GPVI

The action of obestatin in skeletal muscle repair: stem cell expansion, muscle growth, and microenvironment remodeling

The development of therapeutic strategies for skeletal muscle diseases, such as physical injuries and myopathies, depends on the knowledge of regulatory signals that control the myogenic process. The obestatin/GPR39 system operates as an autocrine signal in the regulation of skeletal myogenesis. Using a mouse model of skeletal muscle regeneration after injury and several cellular strategies, we explored the potential use of obestatin as a therapeutic agent for the treatment of trauma-induced muscle injuries. Our results evidenced that the overexpression of the preproghrelin, and thus obestatin, and GPR39 in skeletal muscle increased regeneration after muscle injury. More importantly, the intramuscular injection of obestatin significantly enhanced muscle regeneration by simulating satellite stem cell expansion as well as myofiber hypertrophy through a kinase hierarchy. Added to the myogenic action, the obestatin administration resulted in an increased expression of VEGF/VEGFR2 and the consequent microvascularization, with no effect on collagen deposition in skeletal muscle. Furthermore, the potential inhibition of myostatin during obestatin treatment might contribute to its myogenic action improving muscle growth and regeneration. Taken together, our data demonstrate successful improvement of muscle regeneration, indicating obestatin is a potential therapeutic agent for skeletal muscle injury and would benefit other myopathies related to muscle regeneration

Nutrición y secreción gástrica: un nuevo enfoque proteómico

Comunicación a congreso

Caracterización por Proteómica del tejido muscular esquelético como órgano endocrino

Comunicaciones a congreso

Rat adipose tissue secretome differential analysis from different anatomical locations

Comunicaciones a congreso