5 resultados para Fusões
Resumo:
An MBA Thesis, presented as part of the requirements for the degree of Masters in Business Administration from the NOVA - School of Business and Economics
Resumo:
Dissertao apresentada na Faculdade de Cincias e Tecnologia da Universidade Nova de Lisboa para a obteno do grau de Mestre em Engenharia do Ambiente, perfil Gesto e Sistemas Ambientais
Resumo:
RESUMO - Perante o actual contexto de conteno de gastos no sector da sade e consequente preocupao com a eficincia do sistema, temse assistido a mudanas vrias no modelo de gesto e organizacional do sistema de sade. Destacase a alterao da estrutura hospitalar, com vista racionalizao dos seus recursos internos, onde as fusões hospitalares tm assumido um papel determinante. Em Portugal, nos ltimos 10 anos, assistiuse a uma significativa reduo do nmero de hospitais (de sensivelmente 90 para 50 unidades), exclusivamente atravs das fusões e sem quaisquer alteraes no nmero de estruturas fsicas existentes. No obstante os argumentos justificativos desta reforma, a avaliao dos objectivos implcitos insuficiente. Neste mbito, pretendeuse com este estudo contribuir para a anlise do impacte da criao de centros hospitalares na reduo de gastos, isto , verificar se a consolidao e consequente reengenharia dos processos produtivos teve consequencias ao nvel da obteno de economias de escala. Para esta anlise usouse uma base de dados em painel, onde se consideraram 75 hospitais durante 7 anos (20032009), nmero que foi reduzindo ao longo do perodo em anlise devido s inmeras fusões j referidas. Para avaliar os ganhos relativos s fusões hospitalares, ao nvel da eficincia tcnica e das economias de escala, recorreuse fronteira estocstica especificada funo custo translog. Estimada a fronteira, foi possvel analisar trs centros hospitalares especficos, onde se comparou o perodo prfuso (20052006) com o perodo aps a fuso (20082009). Como variveis explicativas, relativas produo hospitalar, considerouse o nmero de casos tratados e os dias de internamento (Vita, 1990; Schuffham et al., 1996), o nmero de consultas e o nmero de urgncias, sendo estas variveis as mais comuns na literatura (Vita, 1990; Fournier e Mitchell, 1992; Carreira, 1999). Quanto varivel dependente usouse o custo varivel total, que compreende o total de custos anuais dos hospitais excepto de imobilizado. Como principais concluses da investigao, em consequncia da criao dos centros hospitalares, so de referir os ganhos de escala na fuso de hospitais de reduzida dimenso e com mais servios complementares. --------ABSTRACT - Driven by the current pressure on resources induced by budgetary cuts, the Portuguese Ministry of Health is imposing changes in the management model and organization of NHS hospitals. The most recent change is based on the creation of Hospital Centres that are a result of administrative mergers of existing hospitals. In less than 10 years the number of hospitals passed from around 90 to around 50, only due to the mergers and without any change in the existing number of physical institutions. According to the political discourse, one of the main goals expected from this measure is the creation of synergies and more efficiency in the use of available resources. However, the merger of the hospitals has been a political decision without support or evaluation of the first experiments. The aim of this study is to measure the results of this policy by looking at economies of scale namely through reductions in the expenditures, as expected and sought by the MoH. Data used covers 7 years (20032009) and 75 hospitals, number that has been reduced my the enoumerous mergers during the last decade. This work uses a stochastic frontier analysis through the translog cost function to examine the gains from mergers, which were decomposed into technical efficiency and economies of scale. It was analised these effects by the creation of three specific hospital centers, using a longitudinal approach to compare the period premerger (20032006) with the postmerger period (200709). To measure changes in inpatient hospital production volume and length of stay are going to be considered as done by Vita (1990) and Schuffham et al. (1996). For outpatient services the number of consultations and emergencies are going to be considered (Vita, 1990; Fournier e Mitchell, 1992; Carreira, 1999). Total variable cost is considered as the dependent variable explained the aforementioned ones. After a review of the literature results expected point to benefits from the mergers, namely a reduction in total expenditures and in the number of duplicated services. Results extracted from our data point in the same direction, and thus for the existence of some economies of scale only for small hospitals.
Resumo:
RESUMO: A Malria causada por parasitas do gnero Plasmodium, sendo a doena parasitria mais fatal para o ser humano. Apesar de, durante o sculo passado, o desenvolvimento econmico e a implementao de diversas medidas de controlo, tenham permitido erradicar a doena em muitos pases, a Malria continua a ser um problema de sade grave, em particular nos pases em desenvolvimento. A Malria transmitida atravs da picada de uma fmea de mosquito do gnero Anopheles. Durante a picada, os esporozotos so injetados na pele do hospedeiro, seguindo-se a fase heptica e obrigatria do ciclo de vida. No fgado, os esporozotos infetam os hepatcitos onde se replicam, dentro de um vacolo parasitrio (VP) e de uma forma imunitria silenciosa, em centenas de merozoitos. Estas novas formas do parasita so as responsveis por infetar os eritrcitos, iniciando a fase sangunea da doena, onde se os primeiros sintomas se manifestam, tais como a caracterstica febre cclica. A fase heptica da doena a menos estudada e compreendida. Mais ainda, as interaes entre o VP e os organelos da clulas hospedeira esto ainda pouco caracterizados. Assim, neste estudo, as interaes entre os organelos endocticos e autofgicos da clula hospedeira e o VP foram dissecados, observando-se que os anfisomas, que so organelos resultantes da interseco do dois processos de trfego intracelular, interagem com o parasita. Descobrimos que a autofagia tem tambm uma importante funo imunitria durante a fase heptica inicial, ao passo, que durante o desenvolvimento do parasita, j numa fase mais tardia, o parasita depende da interao com os endossomas tardios e anfisomas para crescer. Vesiculas de BSA, EGF e LC3, foram, tambm, observadas dentro do VP, sugerindo que os parasitas so capazes de internalizar material endoctico e autofgico do hospedeiro. Mais ainda, mostramos que esta interao depende da cinase PIKfyve, responsvel pela converso do fosfoinositidio-3-fosfato no fosfoinositidio-3,5-bifosfato, uma vez que inibindo esta cinase o parasita no capaz de crescer normalmente. Finalmente, mostramos que a protena TRPML1, uma protena efetora do fosfoinositidio-3,5-bifosfato, e envolvida no processo de fuso das membranas dos organelos endocticos e autofgicos, tambm necessria para o crescimento do parasita. Desta forma, o nosso estudo sugere que a membrana do VP funde com vesiculas endocticas e autofgicas tardias, de uma forma dependente do fositidio-3,5-bifosfato e do seu effetor TRPML1, permitindo a troca de material com a clula hospedeira. Concluindo, os nossos resultados evidenciam que o processo autofgico que ocorre na clula hospedeira tem um papel duplo durante a fase heptica da malaria. Enquanto numa fase inicial os hepatcitos usam o processo autofgico como forma de defesa contra o parasita, j durante a fase de replicao o VP funde com vesiculas autofgicas e endocticas de forma a obter os nutrientes necessrios ao seu desenvolvimento.--------- ABSTRACT: Malaria, which is caused by parasites of the genus Plasmodium, is the most deadly parasitic infection in humans. Although economic development and the implementation of control measures during the last century have erradicated the disease from many areas of the world, it remains a serious human health issue, particularly in developing countries. Malaria is transmitted by female mosquitoes of the genus Anopheles. During the mosquito blood meal, Plasmodium spp. sporozoites are injected into the skin dermis of the vertebrate host, followed by an obligatory liver stage. Upon entering the liver, Plasmodium parasites infect hepatocytes and silently replicate inside a host cell-derived parasitophorous vacuole (PV) into thousands of merozoites. These new parasite forms can infect red blood cells initiating the the blood stage of the disease which shows the characteristic febrile malaria episodes. The liver stage is the least characterized step of the malaria infection. Moreover, the interactions between the Plasmodium spp. PV and the host cell trafficking pathways are poorly understood. We dissected the interaction between Plasmodium parasites and the host cell endocytic and autophagic pathways and we found that both pathways intersect and interconnect in the close vicinity of the parasite PV, where amphisomes are formed and accumulate. Interestingly, we observed a clearance function for autophagy in hepatocytes infected with Plasmodium berghei parasites at early infection times, whereas during late liver stage development late endosomes and amphisomes are required for parasite growth. Moreover, we found the presence of internalized BSA, EGF and LC3 inside parasite vacuoles, suggesting that the parasites uptake endocytic and autophagic cargo. Furthermore, we showed that the interaction between the PV and host traffic pathways is dependent on the kinase PIKfyve, which converts the phosphoinositide PI(3)P into PI(3,5)P2, since PIKfyve inhibition caused a reduction in parasite growth. Finally, we showed that the PI(3,5)P2 effector protein TRPML1, which is involved in late endocytic and autophagic membrane fusion, is also required for parasite development. Thus, our studies suggest that the parasite parasitophorous vacuole membrane (PVM) is able to fuse with late endocytic and autophagic vesicles in a PI(3,5)P2- and TRPML1-dependent manner, allowing the exchange of material between the host cell and the parasites, necessary for the rapid development of the latter that is seen during the liver stage of infection. In conclusion, we present evidence supporting a specific and essential dual role of host autophagy during the course of Plasmodium liver infection. Whereas in the initial hours of infection the host cell uses autophagy as a cell survival mechanism to fight the infection, during the replicative phase the PV fuses with host autophagic and endocytic vesicles to obtain nutrients required for parasite growth.
