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Biomedical subjects

J Merino

Publications and source records attributed to J Merino.

At least 127 records · Page 7Linked to original sources
PubMed1991

[Extrinsic compression of the right atrium due to a mediastinal germ-cell tumor].

A patient with a mediastinal mass detected by plain chest roentgenogram is presented. The echocardiographic-Doppler examination and the computed tomography precise the gross nature and extent of the tumour and its anatomical location producing obstruction of the right atrium and modifying the blood flow pattern in this chamber. The serum tumour markers and the transthoracic biopsy confirm the diagnosis of primary mediastinal germ cell tumour.

Adult↗
PubMed1991

[Cardiovascular risk factors in the working population of Alicante].

The aim of the present study was to evaluate the prevalence of certain cardiovascular risk factors in the population of Asepeyo-Elche. The study sample was a working population of 697 persons (71.8% males and 28.2% females) with ages ranging from 15 to 65 years (mean age 34.7 +/- 13.2 years), seen during the first 6 months of 1990 in the health care center of Asepeyo-Elche. The evaluated cardiovascular risk factors and their prevalence rates were: hypertension (14.2%), hypercholesterolemia (18.5%), smoking (52.5%), hyperglycemia (3.5%), obesity (28.2%) and sedentariness (80.3%). We conclude that in our working population the prevalence rates of some cardiovascular risk factors are high and that intervention programs to modify the diet and lifestyle are mandatory to prevent the pathogenetic consequences of these factors.

Age Factors↗
PubMed1990

In vivo effects of anti-IL-4 monoclonal antibody on neonatal induction of tolerance and on an associated autoimmune syndrome.

The role of IL-4 in the cellular interactions leading to the induction of CTL tolerance to H-2b alloantigens and to the development of a lupus-like autoimmune disease in BALB/c mice after neonatal injection with (C57BL/6 x BALB/c)F1 cells was investigated in vivo by using an anti-IL-4 mAb. Treatment of F1 cell-injected BALB/c mice with 15 mg of anti-IL-4 mAb was shown to interfere with tolerance induction, as assessed by the high percentages of H-2b target cell lysis and the very low or undetectable levels of B cell chimerism markers observed in these mice. Treatment with 4.5 mg of anti-IL-4 mAb interfered with tolerance induction only in one-third of F1 cell-injected BALB/c mice, but that dose induces specific modulations of the autoimmune manifestations in all mice, leading to the nearly complete prevention of the disease. In particular, the production of anti-ssDNA IgG1 and of total IgG1 and IgE antibodies was seriously affected by the treatment, as well as the proliferation and membrane Ia and K expression of F1 donor splenic cells and thymic APC. Treatment of F1 cell-injected BALB/c mice between 24 and 48 h of life with 0.5 mg of anti-IL-4 mAb did not interfere with tolerance induction, but had similar effects on the autoimmune syndrome as treatment with 4.5 mg. These results suggest that, after F1 cell injection of newborn mice, IL-4 plays an important role in the cellular interactions leading to the induction of tolerance to the corresponding alloantigens and to the development of the associated autoimmune syndrome.

Animals↗
PubMed1990

Autoimmune syndrome after induction of neonatal tolerance to alloantigens: analysis of the role of donor T cells in the induction of autoimmunity.

The injection of (C57BL/6 x BALB/c) F1 spleen cells into BALB/c newborn mice leads to activation of persisting F1 donor B cells and development of a lupus-like syndrome in tolerized BALB/c mice. This syndrome is characterized by hypergammaglobulinaemia, high levels of anti-DNA and anti-Sm antibodies, circulating immune complexes and deposits of immunoglobulin in renal glomeruli. The role of donor T cells in this model was investigated by injecting the newborn mice with F1 cells depleted in different T cell subsets by using specific monoclonal antibodies (MoAbs). Tolerance, as shown by an absence of H-2b-specific CTL alloreactivity and persistence of immunoglobulin bearing the donor allotype were observed in mice injected with F1 cells previously depleted in the CD4+ and/or CD8+ T cell subsets as well as in those which received Thy-1+-depleted F1 spleen cells. In these mice, a typical autoimmune syndrome was found, including splenomegaly and lymphadenopathy, anti-ssDNA and anti-aortic myosin IgG antibodies and renal deposition of immunoglobulin. However, some quantitative changes were seen: the levels of anti-aortic myosin antibodies were lower in mice tolerized with CD4+-depleted F1 cells than in those receiving untreated F1 cells. Conversely, higher levels of these autoantibodies were observed in mice tolerized with CD8+-depleted F1 cells. These results suggest that mature donor T cells are not necessary neither for the establishment of neonatal tolerance to alloantigens nor for the activation of F1 donor B cells in the production of the autoimmune syndrome in tolerant mice, but they may contribute in the regulation of the expression of autoreactive B cell clones.

Animals↗
PubMed1990

CD4+ T cells play a major role for IgM and IgG anti-DNA production in mice infected with Plasmodium yoelii.

The infection by a non-lethal strain of Plasmodium yoelii induces the formation of autoantibodies such as anti-DNA and anti-Sm antibodies in mice. The extent of the relative increase in serum levels of IgM and IgG anti-DNA and anti-Sm antibodies and their kinetics were found to be similar to those of anti-hapten antibodies and of total IgM and IgG levels. This strongly suggested that anti-DNA and anti-Sm autoantibody responses observed in malaria-infected mice are a result of polyclonal activation of B cells. The analysis of the IgG subclasses reacting with DNA antigen showed significant levels of the T cell-dependent isotypes, IgG1 and IgG2. The role of T cells in the activation of autoreactive B cells was confirmed by using athymic nude mice. Indeed, BALB/c-nu/nu and C57BL/6-nu/nu mice failed to produce IgG anti-DNA antibodies after infection with P. yoelii. Moreover, the reconstitution of BALB/c nude mice with lymph node cells from congenic euthymic BALB-Igb mice showed the activation of autoreactive B cells in nude mice by T cells from euthymic mice. Studies in mice depleted of CD4+ T cells strongly suggested that malaria-induced anti-DNA antibodies were almost entirely dependent on the presence of CD4+ T cells, as this depletion significantly decreased IgM anti-DNA antibodies and completely abolished the IgG anti-DNA production, including the IgG3 subclass in infected mice. In contrast, depletion of the CD8+ T cell subset had no effect on the production of autoantibody in malaria-infected mice. Our results indicate that CD4+ T cells play a major role for both IgM and IgG anti-DNA production during the course of malaria infection.

Animals↗
PubMed1989

Autoimmune syndrome after induction of neonatal tolerance to alloantigens. CD4+ T cells from the tolerant host activate autoreactive F1 B cells.

The induction of transplantation tolerance to H-2b alloantigens in BALB/c (H-2d) mice by neonatal injection of (C57BL/6 x BALB/c)F1 spleen cells, produces an autoimmune lupus-like syndrome due to an activation of persisting F1 donor B cells. This syndrome is characterized by hypergammaglobulinaemia, high levels of anti-DNA antibodies, as well as by circulating immune complexes and glomerular deposits of Ig. The role of host T cells in this model was investigated by using athymic BALB/c nu/nu mice as recipients of normal (C57BL/6 x BALB.Igb)F1 spleen cells. In these "tolerized" BALB/c nu/nu mice, there was a persistence of F1 donor B cells but none of the autoimmune features were expressed, conversely to tolerized BALB/c nu/+ littermates. The injection of CD4+CD8- T lymphocytes from adult normal BALB/c mice in 3-wk-old tolerized BALB/c nu/nu mice triggered the appearance of all the autoimmune findings observed in euthymic tolerant mice. The autoantibodies were produced by persisting F1 donor B cells as shown by allotype analysis. More strikingly, a similar triggering of the autoimmune syndrome, including high titers of anti-DNA IgG antibodies and circulating immune complexes, was observed after injection of CD4+CD8- T cells from 2-wk-old tolerant BALB/c mice into "tolerized" BALB/c nu/nu mice. The anti-ssDNA antibodies were shown to bear only the Ighb allotype, indicating their exclusive origin from F1 donor B cells. These results imply that CD4+ T cells from the tolerant mice are necessary for the activation of autoreactive F1 B cells and for the development of the autoimmune syndrome occurring in this model. They also suggest that, although there is a marked depletion of H-2b-specific alloreactive CTL precursors in those neonatally tolerized mice, this state of tolerance can be associated with the persistence of H-2b-specific alloreactive CD4+ cells.

Animals↗
PubMed1989

Thrombocytopenia associated with the induction of neonatal tolerance to alloantigens: immunopathogenic mechanisms.

BALB/c mice rendered tolerant to alloantigens by neonatal injection of semi-allogeneic (C57BL/6 x BALB/c)F1 spleen cells develop a thrombocytopenia in association with an autoimmune lupus-like syndrome. The possible mechanisms involved in the thrombocytopenia were investigated. The development of thrombocytopenia was first detected at 3 weeks of age coinciding with the start of the other autoimmune manifestations and was always related to a state of tolerance and B cell chimerism. There was a significant increase of megakaryocytes in bone marrow and spleens from thrombocytopenic tolerant mice and radiolabeled platelets from these mice were more rapidly eliminated from the bloodstream than normal platelets when injected into normal recipients. A significant correlation between the spleen weight and the decrease of the circulating platelets was observed, although some mice with severe thrombocytopenia had only a moderate spleen enlargement. Thrombocytopenia significantly correlates with the levels of platelet-associated IgG (PAIgG) but not with anti-single-stranded DNA antibodies or circulating immune complexes. Platelets from mice with high levels of PAIgG had a shorter life-span when injected into normal mice than those from mice with low or normal PAIgG. The possibility that PAIgG are partially due to antibodies reacting specifically with platelet membrane components was analyzed. First, F(ab')2 Ig fragments from tolerant mice were shown to bind to normal platelets, in contrast to F(ab')2 Ig fragments from normal mice. Second, some monoclonal antibodies produced by hybridomas derived from tolerant mice reacted in vitro with platelets and induced a transient thrombocytopenia after i.v. injection into normal mice. These data suggest that the thrombocytopenia observed in tolerant mice is the result of a peripheral hyperdestruction of platelets associated with (a) hypersplenism, (b) nonspecific fixation of immunoglobulins, probably as immune complexes and (c) with autoantibodies reacting specifically with platelets. It may represent an interesting model for human chronic idiopathic thrombocytopenia.

Animals↗
PubMed1988

Igh-C allotype-linked control of anti-DNA production and clonotype expression in mice infected with Plasmodium yoelii.

The infection of nonlethal strain of Plasmodium yoelii induces the formation of IgG anti-DNA antibodies as a result of polyclonal B cell activation. By using various nonautoimmune strains of mice including H-2 or Igh congenic or recombinant mice, the levels and clonotypes of anti-DNA antibodies elicited by the malaria infection were analyzed in relation to the expression of the MHC or Igh gene. Our results showed there were little, if any, differences in serum anti-DNA levels and their clonotypes among B10 and B6 H-2 congenic mice. In contrast, malaria-induced IgG anti-DNA responses markedly differed quantitatively and clonotypically between murine strains bearing the Ighb allotype and those bearing the Igha, Ighj, Ighd, or Ighn allotype. The latter group of mice produced approximately 5 to 10 times more IgG anti-DNA antibodies than the former group of mice. Clonotypically, mice bearing the Ighb allotype developed high alkaline anti-DNA antibodies of pH 8.0 to 8.5, whereas non-Ighb mice failed to express such alkaline anti-DNA spectrotypes, and exhibited more neutral spectrotypes (pH 7.0 to 8.0). Studies on the Igh recombinant mice indicated that the observed quantitative and clonotypical differences in IgG anti-DNA production was not associated with the variable region, but with the constant region of the Igh gene complex. Our results have suggested that IgG anti-DNA responses occurring as a result of polyclonal B cell activation during the course of malaria infection markedly differs quantitatively and clonotypically among murine strains and appear to be controlled at least in part by the Igh-C gene or gene(s) closely linked to it.

Animals↗
PubMed1988

Hereditary articular chondrocalcinosis. Clinical and genetic features in 13 pedigrees.

Thirteen pedigrees with familial articular chondrocalcinosis were identified through a systematic radiologic survey of the first-degree blood relatives of 76 patients with chondrocalcinosis. Forty-one persons, 30 women and 11 men, distributed in 25 sibships were affected. Their mean age at the time of study was 65.09 +/- 11.36 years. The disease was of early onset only in four pedigrees. The clinical manifestations in these four pedigrees were similar to those found in the kindred with a late onset. In 15 persons, the process was asymptomatic. In the 26 symptomatic patients, the arthropathy was mild, with clinical and radiologic features similar to those observed in sporadic chondrocalcinosis. There was no linkage of chondrocalcinosis to the HLA-A and HLA-B antigens in the 11 pedigrees in which tissue typing was performed. The pattern of involvement in these 13 pedigrees supports an autosomal dominant mode of inheritance. These data suggest that hereditary chondrocalcinosis is not infrequent and very often is clinically indistinguishable from the sporadic form of the disease.

Aged↗
PubMed1988

Long-term evaluation of the Ionescu-Shiley pericardial xenograft bioprosthesis in the aortic position.

From August 1977 through October 1984, 241 patients underwent aortic valve replacement with the Ionescu-Shiley pericardial valve. There were 130 males and 11 females in this series with an average age of 50.8 years (range 15 to 78 years). Isolated aortic valve replacement was performed in 121 patients (50.2%) and associated cardiac surgery in 120 (49.8%). Valve size was 21 mm or smaller in 107 cases (50.2%). Cumulative duration of follow-up was 1,260 patient-years with a mean follow-up of 5.16 years per patient. Five patients were lost to follow-up. Maximum follow-up was 10.5 years. There were 26 hospital deaths and 15 late deaths (1.19% per pt-yr). The expected 10.5 year actuarial survival rate is 82% +/- 2.9%. Twelve thromboembolic episodes occurred in seven patients--seven central and five peripheral events. The thromboembolic rate was 0.95% per patient-year--32% for patients with isolated aortic valve replacement and 0.63% for patients with concomitant surgery. Freedom from thromboembolic episodes at 10.5 years is 73% +/- 12%. Structural valve deterioration was found in 24 patients (1.9% per pt-yr) with an actuarial freedom from primary tissue failure of 77.5% +/- 5.4% at 10.5 years. Reoperation was required in 39 cases (3.09% per pt-yr)--primary tissue failure (n = 24), paravalvular leak (n = 7), infective endocarditis (n = 6), and valve thrombosis (n = 2).

Adolescent↗
PubMed1988

Expression of anti-DNA clonotypes and the role of helper T-lymphocytes during the autoimmune response in mice tolerant to alloantigens.

BALB/c mice neonatally injected with semiallogeneic (C57BL/6 x BALB/c) F1 spleen cells become tolerant to C57BL/6 alloantigens and exhibit chimaerism due to persistence of F1 lymphocytes. Such mouse chimaeras develop an autoimmune (lupus-like) disease characterised by hypergammaglobulinaemia with production of autoantibodies against DNA, Sm antigen and other self-antigens characteristic of SLE in addition to circulating immune complexes and glomerular deposition of immunoglobulins. We have studied the autoimmune response by analysing the isoelectric focusing (IEF)+ patterns (spectrotypes) of anti-ss and anti-dsDNA antibodies produced by these animals. The results show that the anti-DNA response is remarkably restricted, only a very small number of lymphoid cell clones responding in the majority of animals. The behaviour of these clones has been followed during the development of the autoimmune response by analysis of their individual IEF patterns (clonotypes). The first appearance of clones secreting anti-DNA autoantibodies was observed in 3-4 week old mice. Changes in spectrotype occurred during the course of the response but they remained restricted to a very small number of clones in almost all the animals studied. Changes in clonotype consistent with somatic mutation in committed, anti-DNA-secreting clones were also observed. Helper T-lymphocytes of host origin are shown to be required for the development of an autoimmune response.

Animals↗
PubMed1987

Autoimmune syndrome after induction of neonatal tolerance to alloantigens: effects of in vivo treatment with anti-T cell subset monoclonal antibodies.

BALB/c (H-2d) mice rendered tolerant to h-2b alloantigens by neonatal injection of semiallogeneic (C57BL/6 X BALB/c)F1 spleen cells develop autoimmune features due to an abnormal activation of persisting F1 donor B cells. The role of T cells in this autoimmune syndrome was studied by in vivo treatment of tolerant mice with anti-L3T4(GK-1.5) or anti-Ly-2 (H-35-17.2) monoclonal antibodies. The treatment of tolerant mice from day 2 to day 21 of life with anti-L3T4 MAb completely prevented the occurrence of circulating immune complexes of anti-ssDNA anti-Sm and anti-hapten (FITC) IgG antibodies as well as the glomerular deposition of Ig that were usually seen in untreated tolerant mice. This effect persisted for at least 6 wk after stopping this treatment. When the injections of anti-L3T4 MAb were delayed until day 15 of life, a very significant decrease of the autoimmune manifestations was still observed. Treatment of tolerant mice with anti-Ly-2 MAb during the same period had no effects on the autoimmune disease as compared with untreated tolerant mice. No effects on the maintenance of tolerance vs H-2b alloantigens were observed after treatment with anti-L3T4 MAb, as followed by the decrease of CTL and CTL-p alloreactivity and by the persistence of F1 donor B cells, indicated by the presence of Ig bearing the Ighb donor allotype. These results suggest the existence of interactions between L3T4+ T cells and persisting autoreactive B cells from F1 donor origin in the development of the autoimmune syndrome after neonatal induction of transplantation tolerance.

Animals↗