913 resultados para Relatively Free Group
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Let ZG be the integral group ring of the finite nonabelian group G over the ring of integers Z, and let * be an involution of ZG that extends one of G. If x and y are elements of G, we investigate when pairs of the form (u(k,m)(x*), u(k,m)(x*)) or (u(k,m)(x), u(k,m)(y)), formed respectively by Bass cyclic and *-symmetric Bass cyclic units, generate a free noncyclic subgroup of the unit group of ZG.
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Let G be a group of odd order that contains a non-central element x whose order is either a prime p >= 5 or 3(l), with l >= 2. Then, in U(ZG), the group of units of ZG, we can find an alternating unit u based on x, and another unit v, which can be either a bicyclic or an alternating unit, such that for all sufficiently large integers m we have that < u(m), v(m)> = < u(m)> * < v(m)> congruent to Z * Z.
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Under p = c, we prove that it is possible to endow the free abelian group of cardinality c with a group topology that makes its square countably compact. This answers a question posed by Madariaga-Garcia and Tomita and by Tkachenko. We also prove that there exists a Wallace semigroup (i.e., a countably compact both-sided cancellative topological semigroup which is not a topological group) whose square is countably compact. This answers a question posed by Grant.
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If * : G -> G is an involution on the finite group G, then * extends to an involution on the integral group ring Z[G] . In this paper, we consider whether bicyclic units u is an element of Z[G] exist with the property that the group < u, u*> generated by u and u* is free on the two generators. If this occurs, we say that (u, u*)is a free bicyclic pair. It turns out that the existence of u depends strongly upon the structure of G and on the nature of the involution. One positive result here is that if G is a nonabelian group with all Sylow subgroups abelian, then for any involution *, Z[G] contains a free bicyclic pair.
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The effects of experimental infection with Giardia lamblia were studied in 30-day old conventional and germfree CFW mice (7 animals in each group) of both sexes. Cysts were observed in the feces of both groups 6 to 7 days after intragastric infection of each animal with about 2.5 x 10(5) G. lamblia trophozoites. Fecal cyst level was statistically higher in germfree mice (about 10(5) cysts/g feces) when compared with the conventional group (about 10(4) cysts/g feces). The peak of infection in the conventional group apparently occurred on the 10th day after infection as indicated by an increase of fecal weight and by histopathological examination. Intense infiltration of the lamina propria and high reactional hyperplasia of the lymphoid component were observed in the conventional group. There was no infiltration or hyperplasia in germfree infected mice and fecal weight was relatively constant throughout the experiment. These results suggest that, as is the case for other intestinal pathogenic protozoa, the intestinal microflora is indispensable for the expression of the pathogenicity but not for the multiplication of G. lamblia.
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The histo-blood group ABH antigens were first described in humans. These antigens are only present on erythrocytes from great apes and humans, while in more primitive animals they are found in tissues and body fluids. The ABH antigens are mainly distributed in tissues exposed to the external environment and potentially serve as ligands for pathogens or inhibitors of tissue connections. The objective of this paper was two-fold: (i) to determine the presence of Helicobacter sp. in the gastric mucosa of 16 captive and 24 free-living New World monkeys and (ii) to evaluate the presence of histopathological alterations related to bacterial infection and the associated expression of ABH antigens in the tissue. Stomach tissues from 13 species of monkey were assessed using haematoxylin-eosin and modified Gram staining (Hucker) methods. An immunohistochemical analysis of the tissue revealed the presence of infectious bacteria that were characteristic of the genus Helicobacter sp. The results demonstrate that various species of monkey might be naturally infected with the Helicobacter sp. and that there is an increased susceptibility to infection. This study serves as a comparative analysis of infection between human and non-human primates and indicates the presence of a new species of Helicobacter.
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The competitive regime faced by individuals is fundamental to modelling the evolution of social organization. In this paper, we assess the relative importance of contest and scramble food competition on the social dynamics of a provisioned semi-free-ranging Cebus apella group (n=18). Individuals competed directly for provisioned and clumped foods. Effects of indirect competition were apparent with individuals foraging in different areas and with increased group dispersion during periods of low food abundance. We suggest that both forms of competition can act simultaneously and to some extent synergistically in their influence on social dynamics; the combination of social and ecological opportunities for competition and how those opportunities are exploited both influence the nature of the relationships within social groups of primates and underlie the evolved social structure. Copyright (c) 2008 S. Karger AG, Basel
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We show that it is consistent with ZFC that the free Abelian group of cardinality c admits a topological group topology that makes it countably compact with a non-trivial convergent sequence. (C) 2011 Elsevier B.V. All rights reserved.
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Recombinant human group II phospholipase A2 (sPLA2) added to human platelets in the low microg/ml range induced platelet activation, as demonstrated by measurement of platelet aggregation, thromboxane A2 generation and influx of intracellular free Ca2+ concentration and by detection of time-dependent tyrosine phosphorylation of platelet proteins. The presence of Ca2+ at low millimolar concentrations is a prerequisite for the activation of platelets by sPLA2. Mg2+ cannot replace Ca2+. Mg2+, given in addition to the necessary Ca2+, inhibits sPLA2-induced platelet activation. Pre-exposure to sPLA2 completely blocked the aggregating effect of a second dose of sPLA2. Albumin or indomethacin inhibited sPLA2-induced aggregation, similarly to the inhibition of arachidonic acid-induced aggregation. Platelets pre-treated with heparitinase or phosphatidylinositol-specific phospholipase C lost their ability to aggregate in response to sPLA2, although they still responded to other agonists. This suggests that a glycophosphatidylinositol-anchored platelet-membrane heparan sulphate proteoglycan is the binding site for sPLA2 on platelets. Previous reports have stated that sPLA2 is unable to activate platelets. The inhibitory effect of albumin and Mg2+, frequently used in aggregation studies, and the fact that isolated platelets lose their responsiveness to sPLA2 relatively quickly, may explain why the platelet-activating effects of sPLA2 have not been reported earlier.
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TGN38 is one of the few known resident integral membrane proteins of the trans-Golgi network (TGN). Since it cycles constitutively between the TGN and the plasma membrane, TGN38 is ideally suited as a model protein for the identification of post-Golgi trafficking motifs. Several studies, employing chimeric constructs to detect such motifs within the cytosolic domain of TGN38, have identified the sequence 333YQRL336 as an autonomous signal capable of localizing reporter proteins to the TGN. In addition, one group has found that an upstream serine residue, S331, may also play a role in TGN38 localization. However, the nature and degree of participation of S331 in the localization of TGN38 remain uncertain, and the effect has been studied in chimeric constructs only. Here we investigate the role of S331 in the context of full-length TGN38. Mutations that abolish the hydroxyl moiety at position 331 (A, D, and E) lead to missorting of endocytosed TGN38 to the lysosome. Conversely, mutation of S331 to T has little effect on the endocytic trafficking of TGN38. Together, these findings indicate that the S331 hydroxyl group has a direct or indirect effect on the ability of the cytosolic tail of TGN38 to interact with trafficking and/or sorting machinery at the level of the early endosome. In addition, mutation of S331 to either A or D results in increased levels of TGN38 at the cell surface. The results confirm that S331 plays a critical role in the intracellular trafficking of TGN38 and further reveal that TGN38 undergoes a signal-mediated trafficking step at the level of the endosome.
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