Reposicionamento da marca Portugal

RESUMO: A Marca de um País também vende. A imagem de um País é nos dias de hoje um activo muito importante para a sua economia. Uma marca é uma promessa feita ao consumidor, é o ponto de referência de todas as impressões, positivas e negativas adquiridas ao longo do tempo. O Marketing é a ferramenta que deverá percepcionar, estudar e apresentar factores de diferenciação, mostrar e convencer os consumidores das qualidades de um produto ou serviço. A realidade impõe uma atenção especial ao tema e a Marca Portugal teve um boom de programas de desenvolvimento e de promoção a partir dos anos 90 do séc. XX. O responsável pela gestão da Marca Portugal é o Governo, através da AICEP, Agência para o Investimento e Comércio Externo de Portugal, que tem como missão aumentar a notoriedade de Portugal, dinamizando o investimento estruturante e a internacionalização das empresas, criando condições competitivas e estimulando a exportação no Mercado Global, diversificando a oferta dos produtos e os Países de Destino. A falta de estratégia e os planos mal sucedidos, são alguns dos erros apontados à gestão da Marca Portugal, mas é determinante assumir claramente que a assumpção da Marca e o seu Reposicionamento é um vector estratégico para o desenvolvimento do País. Portugal tem boas referências, na indústria, nos serviços, tem produto, que podem ajudar a promover a imagem global de Portugal e contribuir para o aumento das receitas, seja das exportações, do Turismo ou do Investimento Estrangeiro. Portugal precisa de um Plano de Marketing e de uma entidade gestora de Marca, que garanta uma gestão eficaz da Marca Portugal, integrada e articulada com todos os produtos e serviços estratégicos para a exportação ou para o consumo interno. Esta dissertação apresenta um Modelo de Reposicionamento da Marca Portugal que agrega todos os pontos positivos que Portugal possui, como, a sua capacidade de vendas, o seu potencial para se investir, o que há para ser visitado, e desenvolve um programa sério e transversal que promova Portugal no estrangeiro e que atraia investidores e visitantes. ABSTRACT: The Brand of a Nation also sells. The image of a country is, nowadays, an important asset for its economy. A brand is a promise made to the consumer; it is the reference point for all impressions, positive and negative acquired over time. Marketing is the tool that must perceive, study and present differentiation factors, must show and convince consumers about the qualities of a product or service. Reality demands a special attention to this topic and the Portugal Brand experienced a development and promotion program boom since the 20th Century 90’s. Currently, the figure in charge of the management of the Portugal Brand is the Government, through AICEP, whose mission is to increase the notoriety of Portugal, captivating structural investment and the internationalization of enterprises, mainly small and medium businesses, creating competitive conditions and stimulating exports to the Global Market, diversifying product offer and Destination Countries. Some errors have been pointed out in the management of the Portugal Brand, such as lack of strategy and unsuccessful plans, but it is imperative to irrevocably understand that Brand assumption and its Repositioning is a strategic vector for the development of the Country. Portugal has good references, either in industry, or services, has product, that help promoting Portugal’s global image and contributing to an increase in revenues, either in exports, Tourism or Direct Investment. Portugal needs a Marketing Plan and a Brand management entity, such as a Brand strategic executive council, to ensure an effective management of the Portugal Brand, integrated and articulated with all the products and services flagged as strategic assets for exportation or domestic use. This thesis presents a Repositioning Model of the Portugal Brand that aggregates all positive aspects that Portugal has, such as sale capacity, potential for investment, lots of places to visit, and develops a serious and transversal program to promote Portugal abroad and to attract investors and visitors alike.

Intracellular signalling pathways regulating the adaptation of skeletal muscle to exercise and nutritional changes

The focus of the present review is to assimilate current knowledge concerning the differing signalling transduction cascades that control muscle mass development and affect skeletal muscle phenotype following exercise or nutritional uptake. Effects of mechanical loading on protein synthesis are discussed. Muscle growth control is regulated by the interplay of growth promoting and growth suppressing factors, which act in concert. Much emphasis has been placed on understanding how increases in the rate of protein synthesis are induced in skeletal muscle during the adaptive process. One key point to emerge is that protein synthesis following resistance exercise or increased nutrient availability is mediated through changes in signal transduction involving the phosphorylation of mTOR and sequential activation of downstream targets. On the other hand, AMPK activation plays an important role in the inhibition of protein synthesis by suppressing the function of multiple translation regulators of the mTOR signalling pathway in response to cellular energy depletion and low metabolic conditions. The effects of exercise and/or nutritional uptake on the activation of signalling molecules that regulate protein synthesis are highlighted, providing a better understanding of the molecular changes in the cell.

A dual role for integrin-linked kinase in platelets: regulating integrin function and alpha-granule secretion

Integrin-linked kinase (ILK) has been implicated in the regulation of a range of fundamental biological processes such as cell survival, growth, differentiation, and adhesion. In platelets ILK associates with beta 1- and beta 3-containing integrins, which are of paramount importance for the function of platelets. Upon stimulation of platelets this association with the integrins is increased and ILK kinase activity is up-regulated, suggesting that ILK may be important for the coordination of platelet responses. In this study a conditional knockout mouse model was developed to examine the role of ILK in platelets. The ILK-deficient mice showed an increased bleeding time and volume, and despite normal ultrastructure the function of ILK-deficient platelets was decreased significantly. This included reduced aggregation, fibrinogen binding, and thrombus formation under arterial flow conditions. Furthermore, although early collagen stimulated signaling such as PLC gamma 2 phosphorylation and calcium mobilization were unaffected in ILK-deficient platelets, a selective defect in alpha-granule, but not dense-granule, secretion was observed. These results indicate that as well as involvement in the control of integrin affinity, ILK is required for alpha-granule secretion and therefore may play a central role in the regulation of platelet function. (Blood. 2008; 112: 4523-4531)

Local roles of TGF-beta superfamily members in the control of ovarian follicle development

Members of the transforming growth factor-beta (TGF-beta) superfamily have wide-ranging influences on many tissue and organ systems including the ovary. Two recently discovered TGF-beta superfamily members, growth/differentiation factor-9 (GDF-9) and bone morphogenetic protein-15 (BMP-15; also designated as GDF-9B) are expressed in an oocyte-specific manner from a very early stage and play a key role in promoting follicle growth beyond the primary stage. Follicle growth to the small antral stage does not require gonadotrophins but appears to be driven by local autocrine/paracrine signals from both somatic cell types (granulosa and theca) and from the oocyte. TGF-beta superfamily members expressed by follicular cells and implicated in this phase of follicle development include TGF-beta, activin, GDF-9/9B and several BMPs. Acquisition of follicle-stimulating hormone (FSH) responsiveness is a pre-requisite for growth beyond the small antral stage and evidence indicates an autocrine role for granulosa-derived activin in promoting granulosa cell proliferation, FSH receptor expression and aromatase activity. Indeed, some of the effects of FSH on granulosa cells may be mediated by endogenous activin. At the same time, activin may act on theca cells to attenuate luteinizing hormone (LH)-dependent androgen production in small to medium-size antral follicles. Dominant follicle selection appears to depend on differential FSH sensitivity amongst a growing cohort of small antral follicles. Activin may contribute to this selection process by sensitizing those follicles with the highest "activin tone" to FSH. Production of inhibin, like oestradiol, increases in selected dominant follicles, in an FSH- and insulin-like growth factor-dependent manner and may exert a paracrine action on theca cells to upregulate LH-induced secretion of androgen, an essential requirement for further oestradiol secretion by the pre-ovulatory follicle. Like activin, BMP-4 and -7 (mostly from theca), and BMP-6 (mostly from oocyte), can enhance oestradiol and inhibin secretion by bovine granulosa cells while suppressing progesterone secretion; this suggests a functional role in delaying follicle luteinization and/or atresia. Follistatin, on the other hand, may favor luteinization and/or atresia by bio-neutralizing intrafollicular activin and BMPs. Activin receptors are expressed by the oocyte and activin may have a further intrafollicular role in the terminal stages of follicle differentiation to promote oocyte maturation and developmental competence. In a reciprocal manner, oocyte-derived GDF-9/9B may act on the surrounding cumulus granulosa cells to attenuate oestradiol output and promote progesterone and hyaluronic acid production, mucification and cumulus expansion.(C) 2003 Elsevier Science B.V. All rights reserved.

Endosomes: a legitimate platform for the signaling train

Although long regarded as a conduit for the degradation or recycling of cell surface receptors, the endosomal system is also an essential site of signal transduction. Activated receptors accumulate in endosomes, and certain signaling components are exclusively localized to endosomes. Receptors can continue to transmit signals from endosomes that are different from those that arise from the plasma membrane, resulting in distinct physiological responses. Endosomal signaling is widespread in metazoans and plants, where it transmits signals for diverse receptor families that regulate essential processes including growth, differentiation and survival. Receptor signaling at endosomal membranes is tightly regulated by mechanisms that control agonist availability, receptor coupling to signaling machinery, and the subcellular localization of signaling components. Drugs that target mechanisms that initiate and terminate receptor signaling at the plasma membrane are widespread and effective treatments for disease. Selective disruption of receptor signaling in endosomes, which can be accomplished by targeting endosomal-specific signaling pathways or by selective delivery of drugs to the endosomal network, may provide novel therapies for disease.

The proliferative effect of synthetic N-POMC(1-28) peptides in rat adrenal cortex: A possible role for cyclin E

Modified synthetic N-POMC(1-28) without disulfide bridges has been shown to act as an adrenal mitogen. Cyclins and their inhibitors are the major cell cycle controls, but in the adrenal cortex the effect of ACTH and N-POMC on the expression of these proteins remains unclear. In this work, we evaluate the effect of different synthetic N-POMC peptides on the S-phase of the cell cycle. In addition, we examine the cyclin E expression in rat adrenal cortex. Rats treated with dexamethasone were injected with ACTH and/or synthetic modified N-POMC and/or synthetic N-POMC with disulfide bridges. DNA synthesis was determined by BrdU incorporation and protein expression was analyzed by immunoblotting and immunohistochemistry. The results showed that similarly to modified N-POMC without disulfide bridges, administration of synthetic N-POMC with disulfide bridges and the combination of ACTH and N-POMC promoted an increase of BrdU-positive nuclei in adrenal cortex. However, the proliferative effect of N-POMC was comparable to that of ACTH only in the zona glomerulosa. An increase in cyclin E expression was observed 6 h after N-POMC treatment in the outer fraction of the adrenal cortex, in agreement with immunohistochemical findings in the zona glomerulosa. In summary, the effect of synthetic N-POMC with disulfide bridges was similar to modified synthetic N-POMC, increasing proliferation in the adrenal cortex, confirming previous evidence that disulfide bridges are not essential to the N-POMC mitogenic effect. Moreover, cyclin E appears to be involved in the N-POMC- and ACTH-stimulated proliferation in the zona glomerulosa of the adrenal cortex. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

Metallopeptidase inhibitors arrest vital biological processes in the fungal pathogen Scedosporium apiospermum

P>Scedosporium apiospermum is an emerging agent of opportunistic mycoses in humans. Previously, we showed that mycelia of S. apiospermum secreted metallopeptidases which were directly linked to the destruction of key host proteins. In this study, we analysed the effect of metallopeptidase inhibitors on S. apiospermum development. As germination of inhaled conidia is a crucial event in the infectious process of S. apiospermum, we studied the morphological transformation induced by the incubation of conidia in Sabouraud-dextrose medium at 37 degrees C. After 6 h, some conidia presented a small projection resembling a germ-tube. A significant increase, around sixfold, in the germ-tube length was found after 12 h, and hyphae were exclusively observed after 24 h. Three distinct metallopeptidase inhibitors were able to arrest the transformation of conidia into hyphae in different ways; for instance, 1,10-phenanthroline (PHEN) completely blocked this process at 10 mu mol l-1, while ethylenediamine tetraacetic acid (EDTA) and ethylene glycol-bis (beta-aminoethyl ether; EGTA) only partially inhibited the differentiation at up to 10 mmol l-1. EGTA did not promote any significant reduction in the conidial growth, while PHEN and EDTA, both at 10 mmol l-1, inhibited the proliferation around 100% and 65%, respectively. The secretion of polypeptides into the extracellular environment and the metallopeptidase activity secreted by mycelia were completely inhibited by PHEN. These findings suggest that metallo-type enzymes could be potential targets for future therapeutic interventions against S. apiospermum.

Immobilization of primary cultures of insulin-releasing human pancreatic cells

Transplantation of pancreatic islets isolated from organ donors constitutes a promising alternative treatment for type 1 diabetes, however, it is severely limited by the shortage of organ donors. Ex vivo islet cell cultures appear as an attractive but still elusive approach for curing type 1 diabetes. It has recently been shown that, even in the absence of fibrotic over-growth, several factors, such as insufficient nutrition of the islet core, represent a major barrier for long-term survival of islets grafts. The use of immobilized dispersed cells may contribute to solve this problem due to conceivably easier nutritional and oxygen support to the cells. Therefore, we set out to establish an immobilization method for primary cultures of human pancreatic cells by adsorption onto microcarriers (MCs). Dispersed human islets cells were seeded onto Cytodex1 microcarriers and cultured in bioreactors for up to eight days. The cell number increased and islet cells maintained their insulin secretion levels throughout the time period studied. Moreover, the cells also presented a tendency to cluster upon five days culturing. Therefore, this procedure represents a useful tool for controlled studies on islet cells physiology and, also, for biotechnological applications.

Targeted Nucleotide Exchange in Bovine Myostatin Gene

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Myostatin (GDF8) single nucleotide polymorphisms in Nellore cattle

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Effect of superstimulatory treatments on the expression of genes related to ovulatory capacity, oocyte competence and embryo development in cattle.

Multiple ovulation (superovulation) and embryo transfer has been used extensively in cattle. In the past decade, superstimulatory treatment protocols that synchronise follicle growth and ovulation, allowing for improved donor management and fixed-time AI (FTAI), have been developed for zebu (Bos indicus) and European (Bos taurus) breeds of cattle. There is evidence that additional stimulus with LH (through the administration of exogenous LH or equine chorionic gonadotrophin (eCG)) on the last day of the superstimulatory treatment protocol, called the 'P-36 protocol' for FTAI, can increase embryo yield compared with conventional protocols that are based on the detection of oestrus. However, inconsistent results with the use of hormones that stimulate LH receptors (LHR) have prompted further studies on the roles of LH and its receptors in ovulatory capacity (acquisition of LHR in granulosa cells), oocyte competence and embryo quality in superstimulated cattle. Recent experiments have shown that superstimulation with FSH increases mRNA expression of LHR and angiotensin AT(2) receptors in granulosa cells of follicles >8 mm in diameter. In addition, FSH decreases mRNA expression of growth differentiation factor 9 (GDF9) and bone morphogenetic protein 15 (BMP15) in oocytes, but increases the expression of both in cumulus cells, without diminishing the capacity of cumulus-oocyte complexes to generate blastocysts. Although these results indicate that superstimulation with FSH is not detrimental to oocyte competence, supplementary studies are warranted to investigate the effects of superstimulation on embryo quality and viability. In addition, experiments comparing the cellular and/or molecular effects of adding eCG to the P-36 treatment protocol are being conducted to elucidate the effects of superstimulatory protocols on the yield of viable embryos.

Cultivo e caracterização de células-tronco embrionárias de bovinos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Single-cell expression analysis of BMP15 and GDF9 in mature oocytes and BMPR2 in cumulus cells of women with polycystic ovary syndrome undergoing controlled ovarian hyperstimulation

To detect expression of bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9) in oocytes, and their receptor type 2 receptor for BMPs (BMPR2) in cumulus cells in women with polycystic ovary syndrome (PCOS) undergoing in vitro fertilization (IVF), and determine if BMPR2, BMP15, and GDF9 expression correlate with hyperandrogenism in FF of PCOS patients. Prospective case-control study. Eighteen MII-oocytes and their respective cumulus cells were obtained from 18 patients with PCOS, and 48 MII-oocytes and cumulus cells (CCs) from 35 controls, both subjected to controlled ovarian hyperstimulation (COH), and follicular fluid (FF) was collected from small (10-14 mm) and large (> 18 mm) follicles. RNeasy Micro Kit (Qiagen(A (R))) was used for RNA extraction and gene expression was quantified in each oocyte individually and in microdissected cumulus cells from cumulus-oocyte complexes retrieved from preovulatory follicles using qRT-PCR. Chemiluminescence and RIA assays were used for hormone assays. BMP15 and GDF9 expression per oocyte was higher among women with PCOS than the control group. A positive correlation was found between BMPR2 transcripts and hyperandrogenism in FF of PCOS patients. Progesterone values in FF were lower in the PCOS group. We inferred that BMP15 and GDF9 transcript levels increase in mature PCOS oocytes after COH, and might inhibit the progesterone secretion by follicular cells in PCOS follicles, preventing premature luteinization in cumulus cells. BMPR2 expression in PCOS cumulus cells might be regulated by androgens.

Strategies to identify and further characterize novel and known genes involved in regulation of skeletogenesis

372 osteochondrodysplasias and genetically determined dysostoses were reported in 2007 [Superti-Furga and Unger, 2007]. For 215 of these conditions, an association with one or more genes can be stated, while the molecular changes for the remaining syndromes remain illusive to date. Thus, the present dissertation aims at the identification of novel genes involved in processes regarding cartilage/ bone formation, growth, differentiation and homeostasis, which may serve as candidate genes for the above mentioned conditions. Two different approaches were undertaken. Firstly, a high throughput EST sequencing project from a human fetal cartilage library was performed to identify novel genes in early skeletal development (20th week of gestation until 2nd year of life) that could be investigated as potential candidate genes. 5000 EST sequences were generated and analyzed representing 1573 individual transcripts, corresponding to known (1400) and to novel, yet uncharacterized genes (173). About 7% of the proteins were already described in cartilage/ bone development or homeostasis, showing that the generated library is tissue specific. The remaining profile of this library was compared to previously published libraries from different time points (8th–12th, 18th–20th week and adult human cartilage) that also showed a similar distribution, reflecting the quality of the presented library analyzed. Furthermore, three potential candidate genes (LRRC59, CRELD2, ZNF577) were further investigated and their potential involvement in skeletogenesis was discussed. Secondly, a disease-orientated approach was undertaken to identify downstream targets of LMX1B, the gene causing Nail-Patella syndrome (NPS), and to investigate similar conditions. Like NPS, Genitopatellar syndrome (GPS) is characterized by aplasia or hypoplasia of the patella and renal anomalies. Therefore, six GPS patients were enrolled in a study to investigate the molecular changes responsible for this relatively rare disease. A 3.07 Mb deletion including LMX1B and NR5A1 (SF1) was found in one female patient that showed features of both NPS and GPS and investigations revealed a 46,XY karyotype and ovotestes indicating true hermaphroditism. The microdeletion was not seen in any of the five other patients with GPS features only, but a potential regulatory element between the two genes cannot be ruled out yet. Since Lmx1b is expressed in the dorsal limb bud and in podocytes, proteomic approaches and expression profiling were performed with murine material of the limbs and the kidneys to identify its downstream targets. After 2D-gel electrophoresis with protein extracts from E13.5 fore limb buds and newborn kidneys of Lmx1b wild type and knock-out mice and mass spectrometry analysis, only two proteins, agrin and carbonic anhydrase 2, remained of interest, but further analysis of the two genes did not show a transcriptional down regulation by Lmx1b. The focus was switched to expression profiles and RNA from newborn Lmx1b wild type and knock-out kidneys was compared by microarray analysis. Potential Lmx1b targets were almost impossible to study, because of the early death of Lmx1b deficient mice, when the glomeruli, containing podocytes, are still immature. Because Lmx1b is also expressed during limb development, RNA from wild type and knock-out Lmx1b E11.5 fore limb buds was investigated by microarray, revealing four potential Lmx1b downstream targets: neuropilin 2, single-stranded DNA binding protein 2, peroxisome proliferative activated receptor, gamma, co-activator 1 alpha, and short stature homeobox 2. Whole mount in situ hybridization strengthened a potential down regulation of neuropilin 2 by Lmx1b, but further investigations including in situ hybridization and protein-protein interaction studies will be needed.