53 research outputs found

    Daily Plasmodium yoelii infective mosquito bites do not generate protection or suppress previous immunity against the liver stage

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Human populations that are naturally subjected to <it>Plasmodium </it>infection do not acquire complete protection against the liver stage of this parasite despite prolonged and frequent exposure. However, sterile immunity against <it>Plasmodium </it>liver stage can be achieved after repeated exposure to radiation attenuated sporozoites. The reasons for this different response remain largely unknown, but a suppressive effect of blood stage <it>Plasmodium </it>infection has been proposed as a cause for the lack of liver stage protection.</p> <p>Methods</p> <p>Using <it>Plasmodium yoelii </it>17XNL, the response generated in mice subjected to daily infective bites from normal or irradiated mosquitoes was compared. The effect of daily-infected mosquito bites on mice that were previously immunized against <it>P. yoelii </it>liver stage was also studied.</p> <p>Results</p> <p>It was observed that while the bites of normal infected mosquitoes do not generate strong antibody responses and protection, the bites of irradiated mosquitoes result in high levels of anti-sporozoite antibodies and protection against liver stage <it>Plasmodium </it>infection. Exposure to daily infected mosquito bites did not eliminate the protection acquired previously with a experimental liver stage vaccine.</p> <p>Conclusions</p> <p>Liver stage immunity generated by irradiated versus normal <it>P. yoelii </it>infected mosquitoes is essentially different, probably because of the blood stage infection that follows normal mosquito bites, but not irradiated. While infective mosquito bites do not induce a protective liver stage response, they also do not interfere with previously acquired liver stage protective responses, even if they induce a complete blood stage infection. Considering that the recently generated anti-malaria vaccines induce only partial protection against infection, it is encouraging that, at least in mouse models, immunity is not negatively affected by subsequent exposure and infection with the parasite.</p

    Color Capable Sub-Pixel Resolving Optofluidic Microscope and Its Application to Blood Cell Imaging for Malaria Diagnosis

    Get PDF
    Miniaturization of imaging systems can significantly benefit clinical diagnosis in challenging environments, where access to physicians and good equipment can be limited. Sub-pixel resolving optofluidic microscope (SROFM) offers high-resolution imaging in the form of an on-chip device, with the combination of microfluidics and inexpensive CMOS image sensors. In this work, we report on the implementation of color SROFM prototypes with a demonstrated optical resolution of 0.66 ”m at their highest acuity. We applied the prototypes to perform color imaging of red blood cells (RBCs) infected with Plasmodium falciparum, a particularly harmful type of malaria parasites and one of the major causes of death in the developing world

    Produção de resinas ligno-fenol-formaldeĂ­do a partir do bagaço da cana-de-açĂșcar.

    Get PDF
    Este Comunicado TĂ©cnico visa apresentar recomendaçÔes para produção de resina ligno-fenol-formaldeĂ­do, em escala de laboratĂłrio, a partir da lignina extraĂ­da do bagaço da cana-de-açĂșcar e a prova de conceito de sua aplicação em placas de fibra de mĂ©dia densidade (MDF medium density fiberboard).bitstream/item/206193/1/CT-255.pd

    An extensive reef system at the Amazon River mouth

    Get PDF
    Large rivers create major gaps in reef distribution along tropical shelves. The Amazon River represents 20% of the global riverine discharge to the ocean, generating up to a 1.3 x 10(6)-km(2) plume, and extensive muddy bottoms in the equatorial margin of South America. As a result, a wide area of the tropical North Atlantic is heavily affected in terms of salinity, pH, light penetration, and sedimentation. Such unfavorable conditions were thought to imprint a major gap in Western Atlantic reefs. We present an extensive carbonate system off the Amazon mouth, underneath the river plume. Significant carbonate sedimentation occurred during lowstand sea level, and still occurs in the outer shelf, resulting in complex hard-bottom topography. A permanent near-bottom wedge of ocean water, together with the seasonal nature of the plume's eastward retroflection, conditions the existence of this extensive (similar to 9500 km(2)) hard-bottom mosaic. The Amazon reefs transition from accretive to erosional structures and encompass extensive rhodolith beds. Carbonate structures function as a connectivity corridor for wide depth-ranging reef-associated species, being heavily colonized by large sponges and other structure-forming filter feeders that dwell under low light and high levels of particulates. The oxycline between the plume and subplume is associated with chemoautotrophic and anaerobic microbial metabolisms. The system described here provides several insights about the responses of tropical reefs to suboptimal and marginal reef-building conditions, which are accelerating worldwide due to global changes.Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Coordenadoria de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERS)Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)BrasoilMCTIBrazilian NavyU.S. NSFGordon and Betty Moore Foundation (GBMF)Univ Fed Rio de Janeiro UFRJ, Inst Biol, BR-21941599 Rio De Janeiro, RJ, BrazilUniv Fed Rio de Janeiro, COPPE, Inst Alberto Luiz Coimbra Posgrad & Pesquisa Engn, Lab Sistemas Avancados Gestao Prod, BR-21941972 Rio de Janeiro, RJ, BrazilInst Pesquisas Jardim Bot Rio de Janeiro, BR-22460030 Rio De Janeiro, RJ, BrazilUniv Sao Paulo, Inst Oceanog, BR-05508120 Sao Paulo, SP, BrazilUniv Fed Espirito Santo, Dept Oceanog, BR-29199970 Vitoria, ES, BrazilUniv Estadual Norte Fluminense, Lab Ciencias Ambientais, Ctr Biociencias & Biotecnol, BR-28013602 Campos Dos Goytacazes, RJ, BrazilUniv Fed Fluminense, Inst Geociencias, BR-24210346 Niteroi, RJ, BrazilUniv Fed Fluminense, Inst Biol, BR-24210130 Niteroi, RJ, BrazilUniv Fed Rio de Janeiro, Museo Nacl, BR-20940040 Rio De Janeiro, RJ, BrazilFed Univ Para, Inst Estudos Costeiros, BR-68600000 Braganca, PA, BrazilUniv Fed Sao Paulo, Dept Ciencias Mar, BR-11070100 Santos, SP, BrazilUniv Fed Pernambuco, Dept Oceanog, BR-50670901 Recife, PE, BrazilUniv Georgia, Dept Marine Sci, Athens, GA 30602 USAUniv Fed Paraiba, BR-58297000 Rio Tinto, PB, BrazilUniv Estadual Santa Cruz, Dept Ciencias Biol, BR-45650000 Ilheus, BA, BrazilUniv Fed Sao Paulo, Dept Ciencias Mar, BR-11070100 Santos, SP, BrazilU.S. NSF: OCE-0934095GBMF: 2293GBMF: 2928Web of Scienc

    Adenylyl Cyclase α and cAMP Signaling Mediate Plasmodium Sporozoite Apical Regulated Exocytosis and Hepatocyte Infection

    Get PDF
    Malaria starts with the infection of the liver of the host by Plasmodium sporozoites, the parasite form transmitted by infected mosquitoes. Sporozoites migrate through several hepatocytes by breaching their plasma membranes before finally infecting one with the formation of an internalization vacuole. Migration through host cells induces apical regulated exocytosis in sporozoites. Here we show that apical regulated exocytosis is induced by increases in cAMP in sporozoites of rodent (P. yoelii and P. berghei) and human (P. falciparum) Plasmodium species. We have generated P. berghei parasites deficient in adenylyl cyclase α (ACα), a gene containing regions with high homology to adenylyl cyclases. PbACα-deficient sporozoites do not exocytose in response to migration through host cells and present more than 50% impaired hepatocyte infectivity in vivo. These effects are specific to ACα, as re-introduction of ACα in deficient parasites resulted in complete recovery of exocytosis and infection. Our findings indicate that ACα and increases in cAMP levels are required for sporozoite apical regulated exocytosis, which is involved in sporozoite infection of hepatocytes

    The duration of mitosis and daughter cell size are modulated by nutrients in budding yeast

    No full text
    It is virtually impossible to think of cell division without thinking of cellular growth. If cells would divide without growing an adult organism would be as big as the cells that it originated from. Growth must, therefore, be coupled with cellular division with a precision so great that all cells of a given tissue maintain, as we know, remarkably little variation in size.Maintaining cell size homeostasis is critical for life. Not only is cellular hypertrophy known as an adaptive mechanism in response to metabolic demand, loss of size control is also commonly associated with malignancy.Coordination of cell size and division is achieved via cell size checkpoints which ensure that a cell has grown enough before it progresses through the cell cycle. Cell size checkpoints are best known in yeast where a sole checkpoint is believed to regulate cell size. Such checkpoint has been described to occur at the G1/S transition. In this thesis I revisit old concepts at the light of new techniques and present results that support the hypothesis that significant cell size regulation occurs during mitosis. In addition I will provide evidence that suggest that mitotic cell size regulation is achieved through coordination of the phosphatase PP2A Rts1 and the kinase Gin4. Cooperatively they control Swe1 activity in response to nutrients, allowing for nutrient modulation of cell size
    • 

    corecore