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V Amato Neto A A Moreira G M Ferreira S A do Nascimento L Matsubara R Campos P L Pinto 《Revista do Instituto de Medicina Tropical de S?o Paulo》1990,32(3):185-188
With the objective of knowing adequately the spectrum of activity of albendazole against intestinal helminthiases, we made observations regarding hymenolepiasis caused by Hymenolepis nana. Two series of investigations were carried out: a) treatment of mice with single doses of either 25 or 50 mg/kg, repeated after ten days, using as controls animals treated with 25 mg/kg of praziquantel or not treated with any antiparasitic drugs; b) treatment of adults and children with 400 mg daily for three consecutive days, repeated after ten days. 相似文献
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Katherine R. Amato Marie-Claire Arrieta Meghan B. Azad Michael T. Bailey Josiane L. Broussard Carlijn E. Bruggeling Erika C. Claud Elizabeth K. Costello Emily R. Davenport Bas E. Dutilh Holly A. Swain Ewald Paul Ewald Erin C. Hanlon Wrenetha Julion Ali Keshavarzian Corinne F. Maurice Gregory E. Miller Geoffrey A. Preidis Laure Segurel Burton Singer Sathish Subramanian Liping Zhao Christopher W. Kuzawa 《Proceedings of the National Academy of Sciences of the United States of America》2021,118(25)
Individuals who are minoritized as a result of race, sexual identity, gender, or socioeconomic status experience a higher prevalence of many diseases. Understanding the biological processes that cause and maintain these socially driven health inequities is essential for addressing them. The gut microbiome is strongly shaped by host environments and affects host metabolic, immune, and neuroendocrine functions, making it an important pathway by which differences in experiences caused by social, political, and economic forces could contribute to health inequities. Nevertheless, few studies have directly integrated the gut microbiome into investigations of health inequities. Here, we argue that accounting for host–gut microbe interactions will improve understanding and management of health inequities, and that health policy must begin to consider the microbiome as an important pathway linking environments to population health. 相似文献
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Liu SC; Palek J; Yi SJ; Nichols PE; Derick LH; Chiou SS; Amato D; Corbett JD; Cho MR; Golan DE 《Blood》1995,86(1):349-358
Southeast Asian ovalocytosis (SAO) is an asymptomatic trait characterized by rigid, poorly deformable red cells that resist invasion by several strains of malaria parasites. The underlying molecular genetic defect involves simple heterozygous state for a mutant band 3 protein, which contains a deletion of amino acids 400 through 408, linked with a Lys 56-to-Glu substitution (band 3-Memphis polymorphism). To elucidate the contribution of the mutant SAO band 3 protein to increased SAO red blood cell (RBC) rigidity, we examined the participation of the mutant SAO band 3 protein in increased band 3 attachment to the skeleton and band 3 oligomerization. We found first that SAO RBC skeletons retained more band 3 than normal cells and that this increased retention preferentially involved the mutant SAO band 3 protein. Second, SAO RBCs contained a higher percentage of band 3 oligomer-ankyrin complexes than normal cells, and these oligomers were preferentially enriched by the mutant SAO protein. At the ultrastructural level, the increased oligomer formation of SAO RBCs was reflected by stacking of band 3-containing intramembrane particles (IMP) into longitudinal strands. The IMP stacking was not reversed by treating SAO RBCs in alkaline pH (pH 11), which is known to weaken ankyrin-band 3 interactions, or by removing the cytoplasmic domain of band 3 from SAO membranes with trypsin. Finally, we found that band 3 protein in intact SAO RBCs exhibited a markedly decreased rotational mobility, presumably reflecting the increased oligomerization and the membrane skeletal association of the SAO band 3 protein. We propose that the mutant SAO band 3 has an increased propensity to form oligomers, which appear as longitudinal strands of IMP and exhibit increased association with membrane skeleton. This band 3 oligomerization underlies the increase in membrane rigidity by precluding membrane skeletal extension, which is necessary for membrane deformation. 相似文献
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