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The mechanisms by which Helicobacter pylori colonizes and persists within the gastric mucosa are poorly understood. The gastric immune response observed in vivo during H. pylori infection, is characterized by a polarization of Th1 cell type that seems to be responsible for gastric pathology. The purpose of this study was to test the direct effect of H. pylori cagA(+)/vacA(+ )(live and/or gentamicin-killed) on human peripheral blood mononuclear cells (PBMCs) in order to evaluate the production of regulated activation normal T cell expressed and secreted (RANTES) in vitro. We also evaluated the possible relationship between RANTES release and the presence of IL-12 and IFN-gamma in supernatants of the same cells. In the present study, we show for the first time that the low amount of RANTES in supernatants of PBMC incubated with killed H. pylori is linked, at least in part, to the inhibition of IL-12 and IFN-gamma release.

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Herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) are common human pathogens that in particular cases can also cause severe problems especially in immunodeficient patients. The present paper reports the antiviral and immunomodulatory properties of a methanolic extract of C. spinosa buds (CAP), rich in flavonoids, including several quercetin and kaempferol glycosides. In particular we have investigated whether the in vitro exposure of human peripheral blood mononuclear cells (PBMCs) to CAP might inhibit the replication of HSV-2 and modulate the induction kinetics of IL-12, TNF-alpha IFN-gamma. Our findings have shown that CAP treatment interferes with HSV-2 replication in PBMCs inhibiting the extracellular virus release upregulating their production of IL-12, IFN-gamma and TNF-alpha. One could speculate that CAP may contribute in improving immune surveillance of PBMCs toward virus infection by up-regulating expression of peculiar proinflammatory cytokines; it should thus be successfully employed for treatment of HSV-2 infections in immunocompromised hosts.

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Novel 9-fluoren-beta-O-glycosides, designed as DNA-intercalating agents in structural correlation with antiviral tilorone and anticancer anthracyclines, have been prepared with yields in beta-anomers ranging between 25 and 63%. They have been screened for antiproliferative, immunostimulating and antiviral properties against HSV-1 and HSV-2 viruses. Compounds displaying significant antiviral activity against HSV-2 are acetylated 1 and deprotected 6 9-fluorenyl-O-d-arabinopyranoses, whereas 9-fluorenyl-O-d-glucopyranose 3 is the most effective on HSV-1 replication, followed by 1 and 6. The conformational properties of these compounds have been evaluated by molecular modelling techniques.

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Bruxism is one of the most prevalent, complex, and destructive dental functional disorders. It is difficult to identify, especially in its early stages, because most patients are unaware of the habit. Although many factors contribute to the etiology of the disorder, there is little valid and reliable clinical research to assure a correct diagnosis. The effects of bruxism are multiple and diverse and include temporomandibular joint pain and dysfunction, head and neck pain, tooth wear, mobility, erosion, abrasion, loss of and damage to supporting structures, muscle pain and spasm, disturbance of esthetics, and interference and oral comfort. Treatment may be simple or complex, depending on the nature of the disorder. More severe disorders are difficult to treat, and the prognosis may be questionable. Because the diagnosis and treatment of bruxism is inadequately defined and poorly understood, carefully designed clinical research projects are encouraged.

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An individual, whose parents are third cousins, has been shown to be homozygous for the rare Mi.V. condition. The proposita's red blood cells type as M-, N+(weak), S-, s+(strong), U+, Mi(a-), Vw-, Hil+; Wr(a-b-). The cells react, albeit less strongly than most other samples, with anti-Ena. However, from studies on the red blood cells of the proposita and on those of another person of the En(a+), Wr(a-b-) phenotype, it is apparent that the term "anti-Ena" actually describes a number of antibodies of differing specificities. Inhibition studies with sialoglycoprotein (SGP) isolates, and tests on protease-modified red blood cells illustrate some of the differences in specificity. Biochemical analyses of the SGPs of the red blood cells of the MiV homozygote and those of her parents confirm that the Mi.V condition is associated with the absence of normal MN SGP (alpha) and normal Ss SGP (delta), the appearance of a hybrid SGP molecule comprised of a portion of the MN SGP at its NH2 terminal end, and a portion of the Ss SGP at its C terminal end.

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The serum of J.R. contains anti-Wrb and her red blood cells are of the phenotype Wr(a-b-). Evidence was obtained that suggested that her cells totally lack normal MN and Ss sialoglycoproteins (SGPs), and carry instead an abnormal SGP, which is likely to be a hybrid SGP resembling the MN SGP in its outer portion and the Ss SGP in its inner portion. Although the apparent hybrid SGPs of J.R. and the MiV homozygote are virtually indistinguishable in terms of their electrophoretic mobility (apparent molecular weight 40,000) and staining characteristics, they are not identical. That of J.R. is associated with a weak M and increased S antigen, while that of the MiV homozygote is associated with a very weak N, a greatly exalted s, and the rare antigen, Hil. Like the study on the blood of the MiV homozygote, serologic studies on the red blood cells of J.R. have revealed considerable heterogeneity of what have previously been called the Ena antigen and anti-Ena antibodies.

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An auto-anti-Ena, which reacts with trypsin, but not with ficin-treated red blood cells, and which can be totally inhibited with sialoglycoprotein (SGP) isolates from red blood cells, is described. From comparative studies on this antibody and on the four known examples of allo-anti-Ena, it is clear that the term "anti-Ena" describes a heterogeneous group of related but not identical specificities. The specificities contained within the auto-anti-Ena described are different from those within any of the sera containing allo-anti-Ena. Several of the specificities that have been included under the blanket term, anti-Ena, complex with the MN SGP of normal red blood cells, but recognize different portions of that polypeptide.

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Thirty-five examples of anti-dl, autoantibodies initially reacting with all red blood cells against which they were tested, were examined prior to, and following adsorption with Jk(a-b-) red blood cells. None of them was found to contain autoanti-Jk3. One example of autoanti-Jka was identified in an adsorbed eluate. The antibody had been produced by a pregnant Caucasian, in whom laboratory and clinical evaluation showed that the auto-antibody was benign in vivo.

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Two examples of an autoantibody that defines a hitherto unrecognized Rh system antigen are described. Both were produced by C-negative individuals and ostensibly resembled anti-C in specificity. However, adsorption studies showed that the antigen that the autoantibodies define is present on all red blood cells with a "normal" Rh phenotype and on D--/D-- and Dc--/Dc--samples. The antigen detected is not present on Rhnull red blood cells. Serologic studies have shown that the new antibody, that has been named anti-Rh39, has a different specificity from those that define the antigens C, Ce(rhi), G, Hro, Hr, CG, LW, Rh:29, Rh:34 and U. A possible relationship between auto-anti-Rh39 and allo-anti-C, in terms of the immune response, is discussed.

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A patient, previously studied by us, who had produced a benign autoantibody with a specificity that mimicked anti-C, has now produced allo-anti-C that is not of the mimicking type. She is no longer producing any serologically demonstrable autoantibody. It is highly probable that conversion from auto to alloantibody production in this patient was prompted by the introduction of additional foreign immunogen on fetal red blood cells during her third pregnancy.

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The hemagglutinating properties of a large proportion of anti-M and anti-N reagents, and sera containing antibodies to MN-related antigens, have been shown to be unaffected by treatment of red blood cells with neuraminidase. These antibodies, which define NANA-independent MN-system structures, provide further evidence that MN blood group specificity may also be determined by moieties other than N-acetylneuraminic acid.

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An antibody defining an antigen that is very similar in structure to M is described. The reactions of this antibody are considered in the light of what is now known of the biochemical structure of the M and N blood group antigens.

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Using two anti-Ena antibodies, from which anti-Wrb had been removed, and anti-U antibodies, the authors have failed to demonstrate any difference in the amounts of Ena and U antigens on the red blood cells of individuals with one and two functioning Ena(En.OP) genes. Two En(a--) samples, one from an individual who is En/En (En.op/En.op) and the other En/Mk (En.op/Mk), could not be distinguished from U-positive samples from individuals with two functioning U (U.OP) genes in dosage studies with anti-U.

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Sodium dodecylsulfate polyacrylamide gel electrophoretic methods were applied to S--s--and En(a--) red cells as well as to erythrocytes from individuals being heterozygous for these defects. The results demonstrate more conclusively than previous data, that the glycosylated part of the MN glycoprotein is lakcing in En(a--) red cell membranes. S--s--U--erythrocytes either lack the Ss glycoprotein completely or contain a defective molecule which is devoid of the glycosylated part. Conversely, S--s--U+ cells exhibit small amounts of Ss glycoprotein which could only be detected when large amounts of extracted glycoproteins were separated. It is shown that this molecule possesses the 'N' antigenic determinant.

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Many persons who are of a "deletion" or "null" phenotype with regard to a particular blood group system, form a complex specificity antibody or mixture of antibodies, when immunized. Recently, we demonstrated that M.E.P., the En(a-), Wr(a- b-) proposita in a family described by Darnborough has at least, anti-Ena and anti-Wrb in her serum. We suggested that the same two antibodies might be present in the serum of G.W., the En(a-), Wr(a- b-) propositus in the family reported by Furuhjelm et al. We have now been able to confirm that G.W.'s serum does contain antiEna and anti-Wrb and that the antibodies can be separated by adsorption. Because, at this time, it is not known if En(a-), Wr(a- b-) people lack other common antigens from their red blood cells, the possibility remains that the anti-Ena, separated from the anti-Wrb, might be a mixture of antibodies. These findings are important in that they show that reported typings for Ena were actually performed with mixtures of at least anti-Ena and anti-Wrb. Anti-Ena, lacking antiWrb, can be made only by adsorption of a serum containing the two antibodies, onto En(a+), Wr(a+b-) red blood cells, with recovery of the anti-Ena by elution.

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Forty-eight autoantibodies with apparent 'simple' anti-Rh specificity (anti-e, -E, -c, -D, -C, -Ce, -G), have been studied by means of multiple absorption tests. The finding that 34 (70.8%) of these antibodies could bind to red blood cells lacking the antigens that the antibodies appeared to define, indicated that the antibodies had different specificities than seemed to be the case in initial antibody identification tests. Those autoantibodies that at first appeared to be directed against the Rh antigens e, E or c, most often had anti-Hr or anti-Hro specificity. These data explain why some apparent anti-Rh autoantibodies can be eluted from the red blood cells of patients negative for the antigens that the antibodi:s appear to define. However, they also illustrate that the phenomenon of autoantibodies mimicking specificities that they do not possess is common in patients positive for the antigens against which their autoantibodies appear to be directed. An explanation for the mode of action of these autoantibodies in complexing with the Rh agglutinogen is proposed, and the significance of the antibodies in transfusion therapy is considered.

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A "normal" individual with a positive, direct antiglobulin test is described. In common with many other "normal" persons in whom a similar finding has been made, there was no evidence of an increased rate of in vivo red blood cell destruction in this patient. The patient successfully completed a pregnancy during the time that detailed serologic studies on her autoantibodies were being performed. Although the maternal autoantibodies were demonstrable in both an eluate made from the red blood cells of her newborn infant, and in the cord serum, there was no reason to believe that the antibodies caused red blood cell destruction in the infant. The case was of further interest because of the specificities of some of the autoantibodies. Although the mother and child were both C-negative, eluates from their red blood cells contained what ostensibly appeared to be anti-C. Studies that showed that the antibody could be totally adsorbed with C-negative, as well as C-positive red blood cells, proved that this was another example of an autoantibody mimicking an alloantibody. Although this autoantibody appeared initially to have anti-C specificity it was eventually shown to be more closely related to anti-Hr or anti-Rh34, than to anti-C.

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The finding that En(a-) red blood cells are Wr(a-b), and thus probably represent a "null" phenotype of the Wright system, has provided evidence of the independence of the Wright blood group system from many others. Detection of blood group antigens on "null" red blood cells almost certainly indicates that those antigens do not belong to the same blood group system as the "null" cells. In the case of Wright, lack of certainty that En(a-) is the "real", or only, null type slightly reduces the weight of the evidence.

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