Marketing e a Evolução do Serviço Móvel em Cabo Verde

O Presente trabalho intitulado “Marketing e a Evolução do Serviço Móvel em Cabo Verde”, enquadra-se no âmbito do curso de licenciatura em Economia e Gestão, Vertente Administração e Controlo Financeiro ministrado pela Universidade Jean Piaget de Cabo Verde. No contexto actual onde a concorrência é cada vez mais forte e a busca pela competitividade é uma necessidade constante, as empresas necessitam estar cada vez mais bem preparadas para poderem dar respostas às necessidades dos clientes. Através de uma boa política de marketing a empresa consegue identificar as necessidades dos clientes, e tentar satisfaze-los da melhor forma possível. Pretende com este trabalho, responder a seguinte pergunta de partida: Qual é o contributo dado pelo marketing na evolução do serviço móvel em Cabo Verde, para isto, o objectivo geral é analisar o contributo do marketing na sua evolução, e os especificos são: Caracterizar o serviço em estudo, relacionar a evolução do serviço móvel em Cabo Verde com esforço do marketing, comparar as campanhas do marketing com a aderência dos clientes, entender como o marketing influencia os clientes nas suas decisões, compreender como é que o marketing pode contribuir para evolução do sector das telecomunicações móveis no país, propor sugestões para uma maior evolução de serviço em estudo com boas práticas do marketing. A pesquisa é de natureza qualitativa e quantitativa, sendo a recolha dos dados e das informações feita por meio de estudo documental e de entrevistas às entidades prestadora do serviço móvel em Cabo Verde. Com a realização deste trabalho conclui-se que, com base nas informações das entrevistas aplicadas aos sujeitos de pesquisa, que temos um serviço móvel muito evoluído, e que o marketing tem contribuído bastante na evolução da mesma.

Relatório de Jogos de Marketing - Evolutec-Computer

A Evolutec-Computer é uma empresa especializada em engenharia eletrônica, que recebeu um financiamento de uma firma internacional de acionistas, que decidiu entrar no mercado de produção de microcomputador. Por conseguinte, foi criada uma nova divisão de PC Marketing para prosseguir nesta oportunidade de negócio. A fim de iniciar essa divisão, a Cooporate Headquarters forneceu o capital inicial (dinheiro do investimento). O montante concedido seria usado para abrir escritórios de vendas, design das marcas e realizar atividades de pesquisas R&D para as novas tecnologias. A nossa empresa recebeu 500.000 USD nos primeiros quatro semestres e 5.000.000 USD no quinto semestre, somando um total de 7.000.000 USD. A Evolutec-Computer terá o controlo da divisão de PC para os próximos dois anos (8 semestres/períodos de decisão). Dentro desse prazo, a Coorporate Headquarters espera ver a criação de uma divisão autossuficiente. A equipa criada pela Evolutec terá que ser capaz de gerar proveito das operações e contribuir para o lucro da corporação como um todo. Dentro dos 8 semestres, espera-se obter lucro suficiente para cobrir os investimentos iniciais...The Evolutec-Computer is a company specialized in electronic engineering, which has received funding from an international firm shareholder, who decided to enter the PC production market. Therefore, a new PC Marketing Division was created to pursue this business opportunity. In order to start this division, the Corporate Headquarters provided the initial capital (investment money). The sum would be used to open sales offices, design brands and carry out R & D research activities for new technologies. Our company received $ 500,000 in the first four semesters and $ 5,000,000 in the fifth semester, for a total of $ 7,000,000. The Evolutec-Computer will control the PC division for the next two years (eight semesters/decision periods). Within that period, the Coorporate Headquarters hopes to see the creation of a selfsufficient division. The team set up by Evolutec will have to be able to generate profit from operations and contribute to the profit of the corporation as a whole. Within 8 semesters, is expected to make enough profit to cover the initial investment. The performance of our company will be measured by Headquarter through the Balanced Scorecard, which will be based on financial performance, effectiveness of the marketing plan, market performance, investments in the company's future and wealth creation.

Relatório Final Jogos-Simulação De Marketing – Power Computer

This school in the course of Marketing Business Management and specifically Entrepr This school in the course of Marketing Business Management and specifically Entrepreneurship in the discipline of Simulation - Games Marketing year was accordingly for the creation of a company in the computer business in business online simulator called Marketplace, in order to put into practice all the theoretical knowledge acquired during all previous semesters. This platform we were confronted with decisions in eight quarters corresponding 4 every year , in order to encourage learning in a practical way, a virtual and dynamic environment. Every quarter acareados with well organized tasks taking as a reference point defined strategies such as market research analysis, branding , store management after its creation , development of the policy of the 4Ps , identifying opportunities , monitoring of finances and invest heavily . All quarters were subjected decisions and are then given the results , such as: market performance , financial performance, investments in the future , the "health" of the company 's marketing efficiency then analyzed by our company , teaching and also by competition Balanced Scorecard ie , semi-annual and cumulative . For the start of activities it was awarded the 1st year a total of 2,000,000, corresponding to 500,000 out of 4 first quarter , and 5,000,000 in the fifth quarter in a total of 7,000,000 . The capital invested was used to buy market research, opening sales offices , create brands , contract sales force , advertise products created and perform activity R & D in order to make a profit and become self- sufficient to guarantee the payment of principal invested to headquarters ( Corporate Headquarters ) .

Molecular determinants of desensitization in an ENaC/degenerin channel.

Epithelial Na(+) channel (ENaC)/degenerin family members are involved in mechanosensation, blood pressure control, pain sensation, and the expression of fear. Several of these channel types display a form of desensitization that allows the channel to limit Na(+) influx during prolonged stimulation. We used site-directed mutagenesis and chemical modification, functional analysis, and molecular dynamics simulations to investigate the role of the lower palm domain of the acid-sensing ion channel 1, a member of the ENaC/degenerin family. The lower palm domains of this trimeric channel are arranged around a central vestibule, at ∼20 Å above the plasma membrane and are covalently linked to the transmembrane channel parts. We show that the lower palm domains approach one another during desensitization. Residues in the palm co-determine the pH dependence of desensitization, its kinetics, and the stability of the desensitized state. Mutations of palm residues impair desensitization by preventing the closing movement of the palm. Overexpression of desensitization-impaired channel mutants in central neurons allowed--in contrast to overexpression of wild type--a sustained signaling response to rapid pH fluctuations. We identify and describe here the function of an important regulatory domain that most likely has a conserved role in ENaC/degenerin channels.

Audit report on the Iowa Turkey Marketing Council for the years ended December 31, 2008 and 2007

Audit report on the Iowa Turkey Marketing Council for the years ended December 31, 2008 and 2007

The 19th Ion Channel Meeting. September 2008, France.

The annual meeting of the French Ion Channels Society, held on the Mediterranean coast of France, is aimed at gathering the international scientific community working on various aspects of ion channels. In this report of the 19th edition of the meeting, held in September 2008, we summarize selected symposia on aspects of the ion channel field from fundamental to clinical research. The meeting is an opportunity for leading investigators as well as young researchers to present and discuss their recent advances and future challenges in the ion channel field.

Iowa Fisheries Research Technical Series No. 75-1 Variations in the abundance of channel catfish year classes in the upper Mississippi River and causative factors Don R. Helms, Fishery Research Biologist Fisheries Section Jerry M. Conley, Superintendent of Fisheries December, 1975

study of channel catfish in the Mississippi River to determine differences in year class abundance and causative factors

A novel dominant mutation of the Nav1.4 alpha-subunit domain I leading to sodium channel myotonia.

BACKGROUND: Mutations in SCN4A may lead to myotonia. METHODS: Presentation of a large family with myotonia, including molecular studies and patch clamp experiments using human embryonic kidney 293 cells expressing wild-type and mutated channels. RESULTS: In a large family with historic data on seven generations and a clear phenotype, including myotonia at movement onset, with worsening by cold temperature, pregnancy, mental stress, and especially after rest after intense physical activity, but without weakness, the phenotype was linked with the muscle sodium channel gene (SCN4A) locus, in which a novel p.I141V mutation was found. This modification is located within the first transmembrane segment of domain I of the Na(v)1.4 alpha subunit, a region where no mutation has been reported so far. Patch clamp experiments revealed a mutation-induced hyperpolarizing shift (-12.9 mV) of the voltage dependence of activation, leading to a significant increase (approximately twofold) of the window current amplitude. In addition, the mutation shifted the voltage dependence of slow inactivation by -8.7 mV and accelerated the entry to this state. CONCLUSIONS: We propose that the gain-of-function alteration in activation leads to the observed myotonic phenotype, whereas the enhanced slow inactivation may prevent depolarization-induced paralysis.

Simultaneous Optical Recording in Multiple Cells by Digital Holographic Microscopy of Chloride Current Associated to Activation of the Ligand-Gated Chloride Channel GABA(A) Receptor.

Chloride channels represent a group of targets for major clinical indications. However, molecular screening for chloride channel modulators has proven to be difficult and time-consuming as approaches essentially rely on the use of fluorescent dyes or invasive patch-clamp techniques which do not lend themselves to the screening of large sets of compounds. To address this problem, we have developed a non-invasive optical method, based on digital holographic microcopy (DHM), allowing monitoring of ion channel activity without using any electrode or fluorescent dye. To illustrate this approach, GABA(A) mediated chloride currents have been monitored with DHM. Practically, we show that DHM can non-invasively provide the quantitative determination of transmembrane chloride fluxes mediated by the activation of chloride channels associated with GABA(A) receptors. Indeed through an original algorithm, chloride currents elicited by application of appropriate agonists of the GABA(A) receptor can be derived from the quantitative phase signal recorded with DHM. Finally, chloride currents can be determined and pharmacologically characterized non-invasively simultaneously on a large cellular sampling by DHM.

Audit report on the Iowa Turkey Marketing Council for the years ended December 31, 2009 and 2008

Audit report on the Iowa Turkey Marketing Council for the years ended December 31, 2009 and 2008

Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis

Background Multiple Sclerosis (MS) is an acquired inflammatory demyelinating disorder of the central nervous system (CNS) and is the leading cause of nontraumatic disability among young adults. Activated microglial cells are important effectors of demyelination and neurodegeneration, by secreting cytokines and others neurotoxic agents. Previous studies have demonstrated that microglia expresses ATP-sensitive potassium (KATP) channels and its pharmacological activation can provide neuroprotective and anti-inflammatory effects. In this study, we have examined the effect of oral administration of KATP channel opener diazoxide on induced experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Methods Anti-inflammatory effects of diazoxide were studied on lipopolysaccharide (LPS) and interferon gamma (IFNy)-activated microglial cells. EAE was induced in C57BL/6J mice by immunization with myelin oligodendrocyte glycoprotein peptide (MOG35-55). Mice were orally treated daily with diazoxide or vehicle for 15 days from the day of EAE symptom onset. Treatment starting at the same time as immunization was also assayed. Clinical signs of EAE were monitored and histological studies were performed to analyze tissue damage, demyelination, glial reactivity, axonal loss, neuronal preservation and lymphocyte infiltration. Results Diazoxide inhibited in vitro nitric oxide (NO), tumor necrosis factor alpha (TNF-¿) and interleukin-6 (IL-6) production and inducible nitric oxide synthase (iNOS) expression by activated microglia without affecting cyclooxygenase-2 (COX-2) expression and phagocytosis. Oral treatment of mice with diazoxide ameliorated EAE clinical signs but did not prevent disease. Histological analysis demonstrated that diazoxide elicited a significant reduction in myelin and axonal loss accompanied by a decrease in glial activation and neuronal damage. Diazoxide did not affect the number of infiltrating lymphocytes positive for CD3 and CD20 in the spinal cord. Conclusion Taken together, these results demonstrate novel actions of diazoxide as an anti-inflammatory agent, which might contribute to its beneficial effects on EAE through neuroprotection. Treatment with this widely used and well-tolerated drug may be a useful therapeutic intervention in ameliorating MS disease.

Identification of amino acid residues in the alpha, beta, and gamma subunits of the epithelial sodium channel (ENaC) involved in amiloride block and ion permeation.

The amiloride-sensitive epithelial Na channel (ENaC) is a heteromultimeric channel made of three alpha beta gamma subunits. The structures involved in the ion permeation pathway have only been partially identified, and the respective contributions of each subunit in the formation of the conduction pore has not yet been established. Using a site-directed mutagenesis approach, we have identified in a short segment preceding the second membrane-spanning domain (the pre-M2 segment) amino acid residues involved in ion permeation and critical for channel block by amiloride. Cys substitutions of Gly residues in beta and gamma subunits at position beta G525 and gamma G537 increased the apparent inhibitory constant (Ki) for amiloride by > 1,000-fold and decreased channel unitary current without affecting ion selectivity. The corresponding mutation S583 to C in the alpha subunit increased amiloride Ki by 20-fold, without changing channel conducting properties. Coexpression of these mutated alpha beta gamma subunits resulted in a non-conducting channel expressed at the cell surface. Finally, these Cys substitutions increased channel affinity for block by external Zn2+ ions, in particular the alpha S583C mutant showing a Ki for Zn2+ of 29 microM. Mutations of residues alpha W582L, or beta G522D also increased amiloride Ki, the later mutation generating a Ca2+ blocking site located 15% within the membrane electric field. These experiments provide strong evidence that alpha beta gamma ENaCs are pore-forming subunits involved in ion permeation through the channel. The pre-M2 segment of alpha beta gamma subunits may form a pore loop structure at the extracellular face of the channel, where amiloride binds within the channel lumen. We propose that amiloride interacts with Na+ ions at an external Na+ binding site preventing ion permeation through the channel pore.

Voltage-gated sodium channel expression in mouse DRG after SNI leads to re-evaluation of projections of injured fibers.

BACKGROUND: Dysregulation of voltage-gated sodium channels (Na(v)s) is believed to play a major role in nerve fiber hyperexcitability associated with neuropathic pain. A complete transcriptional characterization of the different isoforms of Na(v)s under normal and pathological conditions had never been performed on mice, despite their widespread use in pain research. Na(v)s mRNA levels in mouse dorsal root ganglia (DRG) were studied in the spared nerve injury (SNI) and spinal nerve ligation (SNL) models of neuropathic pain. In the SNI model, injured and non-injured neurons were intermingled in lumbar DRG, which were pooled to increase the tissue available for experiments. RESULTS: A strong downregulation was observed for every Na(v)s isoform expressed except for Na(v)1.2; even Na(v)1.3, known to be upregulated in rat neuropathic pain models, was lower in the SNI mouse model. This suggests differences between these two species. In the SNL model, where the cell bodies of injured and non-injured fibers are anatomically separated between different DRG, most Na(v)s were observed to be downregulated in the L5 DRG receiving axotomized fibers. Transcription was then investigated independently in the L3, L4 and L5 DRG in the SNI model, and an important downregulation of many Na(v)s isoforms was observed in the L3 DRG, suggesting the presence of numerous injured neurons there after SNI. Consequently, the proportion of axotomized neurons in the L3, L4 and L5 DRG after SNI was characterized by studying the expression of activating transcription factor 3 (ATF3). Using this marker of nerve injury confirmed that most injured fibers find their cell bodies in the L3 and L4 DRG after SNI in C57BL/6 J mice; this contrasts with their L4 and L5 DRG localization in rats. The spared sural nerve, through which pain hypersensitivity is measured in behavioral studies, mostly projects into the L4 and L5 DRG. CONCLUSIONS: The complex regulation of Na(v)s, together with the anatomical rostral shift of the DRG harboring injured fibers in C57BL/6 J mice, emphasize that caution is necessary and preliminary anatomical experiments should be carried out for gene and protein expression studies after SNI in mouse strains.