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Biomedical subjects

B Dupont

Publications and source records attributed to B Dupont.

At least 343 records · Page 19Linked to original sources
PubMed1983

Laboratory and clinical assessment of ketoconazole in deep-seated mycoses.

Forty-eight cases of deep mycoses were studied and treated with ketoconazole, each with in vitro evaluation of the minimum inhibitory concentrations (MIC) of the causative fungi, in vivo pharmacokinetic, clinical, and mycologic evaluations, several months to two years after the treatment was stopped. Excellent results were obtained in six cases of chronic mucocutaneous candidiasis, with restoration of immunologic disturbances; 23 cases of systemic candidiasis, including new aspects of heroin addicts with cutaneous, ocular, or osteoarticular manifestations; eight cases of histoplasmosis, five due to Histoplasma capsulatum and three to Histoplasma duboisii, with cure in seven and remission in one; one case of African blastomycosis (Blastomyces dermatitidis); three cases of mycetoma, two due to Monosporium apiospermum, one due to a dematiacious fungus; three cases of entomophthoromycosis with cure; one case of fungal arthritis, due to new hyphomycete similar to M. apiospermum, pathogenic for laboratory animals; one case of Drechslera longirostrata causing vertebral arthritis, following a fungal endocarditis and cured by combination of ketoconazole with amphotericin B, each agent alone being ineffective; and other deep mycoses.

Adolescent↗
PubMed1983

Allocytotoxic T cell clones: both Leu 2+3- and Leu 2-3+ T cells recognize class I histocompatibility antigens.

T cell clones were selected which were cytotoxic for human class I major histocompatibility target antigens. Specificity was based on target cell panel studies and inhibition by monoclonal antibodies to class I determinants. Eight clones were Leu 2+3-. The cytotoxicity of these clones was inhibited by antibody to the Leu 2 antigen. Two clones expressed the Leu 2-3+ phenotype and were not inhibited by anti-Leu 2a or anti-Leu 3a antibodies. These studies indicate that class I-specific cytotoxic T cells are distributed in both T cell subsets, though predominantly in the Leu 2+3- group. In addition, these studies suggest that the Leu 3 molecule may not function in identical fashion in Leu 3+ cytotoxic T cells, which recognize class I target antigens, as in those which recognize class II targets.

Antibodies, Monoclonal↗
PubMed1983

Mixed lymphocyte reactions for individuals with phenotypic identity for specific HLA-B,DR determinants: the role of linkage disequilibrium and of specific DR and other class II determinants.

Although many patients who might benefit from therapeutic bone marrow transplantation lack HLA identical sibling donors, results from many centers now indicate that transplants involving donors other than identical siblings have been successful in a substantial number of cases. Most of these cases were selected because cells from the patient and donor were compatible in mixed lymphocyte culture. We have previously shown that the prediction of mixed lymphocyte culture nonreactivity by HLA-B,DR matching is far more successful if the matched donors shared antigen combinations known to possess significant positive linkage disequilibrium. We now also show that cells from donors with unrelated haplotypes having the specific DR determinants DR1, DR2, and DR3 are more likely than cells from donors with other haplotypes to be mutually compatible in mixed lymphocyte culture. However, even cells from donors with haplotypes with the highest levels of positive linkage disequilibrium frequently show significant mutual stimulation which can, in selected family studies, be attributed to determinants like SB that map between HLA-D/DR and GLO.

Bone Marrow Transplantation↗
PubMed1983

Ferritin secretion by human mononuclear cells: association with HLA phenotype.

A number of different observations indicate that cells of the immune system can participate in the prevention of potential tissue toxicity from iron accumulation and that, in turn, iron and iron binding proteins have important effects on immune responses. The current studies were undertaken to examine a specific aspect of the interaction of iron with human peripheral blood mononuclear cells. A modified hemolytic plaque-forming assay was used to measure ferritin secretion in vitro by phytohemagglutinin activated or nonactivated mononuclear cells in response to stimulation by ferric citrate. Cells from 55 unrelated healthy subjects collectively representing all well-defined HLA-A, B, C, and DR antigens were studied. There were large reproducible differences in the numbers of plaques formed by different individuals, and there was a statistically significant increase in the frequency of the HLA determinant A3 among the "low" responders. Ferritin secretion measured with an antibody specific for acidic ferritin also showed a distinction between A3 and non-A3 donors. In preliminary cell mixing studies, ferritin secretion by mononuclear cells was shown to require the presence of monocytes and to be influenced by the secretion characteristics of both the monocyte and the T-cell donor. These results may provide a clue to the mechanism of development of idiopathic hemochromatosis which is an HLA-A-linked autosomal recessive disease associated with the specific HLA antigen HLA-A3.

Cell Adhesion↗
PubMed1983

Association of HLA-DR5 with mycosis fungoides.

Mycosis fungoides (MF) and Sézary syndrome (SS) are uncommon neoplasms of the lymphoreticular system with distinct clinical, histologic, and immunologic features. Based on the thymus-derived nature of the neoplastic cells, MF and SS are both classified as cutaneous T-cell lymphoma. While substantially greater understanding of MF and SS has been made possible, the exact mechanism for the initiation of either disease is still unknown. The possible involvement of environmental factors as well as viral etiology, i.e., retroviruses, has been suggested. In order to investigate the possible role of HLA-associated variations in genetic susceptibility, 74 patients with histologically documented MF were typed for HLA-A, -B, and -C antigens. Half of these patients were also typed for HLA-DR antigens. An increase in DR5 was the only statistically significant deviation in HLA antigen frequencies in these patients (53% in MF as compared with 20% in controls). An increased frequency of HLA-DR5 has also been associated with scleroderma and juvenile rheumatoid arthritis both of which have immunologic alterations. Also HLA-DR5 has been associated with renal cell carcinoma and Kaposi's sarcoma. The association of MF with DR5 suggests that some individuals with the DR5 antigen may be at higher risk for virally initiated and/or neoplastic diseases possibly through an HLA-linked defect in the immune system.

Adenocarcinoma↗
PubMed1983

Frequencies of HLA and Gm immunogenetic markers in Kaposi's sarcoma.

An outbreak of Kaposi's sarcoma in homosexual men has recently been observed in New York and California which differs from the "classic" North American disease with regard to younger age of onset and clinical prognosis. Although the exact mechanism for initiation of either disease is still unknown, a viral mechanism has been suggested in both cases. In order to investigate the possible role of HLA-associated variations in genetic susceptibility, 39 patients with histologically documented Kaposi's sarcoma were typed for HLA-A,B,C antigens. Most of these patients were also typed for HLA-DR antigens and for Gm allotypes. A significant increase in DR5 occurred in both groups. Decreases in B8 and DR3 and an increase in homozygosity for the Gm haplotype 3;5,13 were also noted. These results suggest that HLA and Gm linked immune response factors may play a role in the induction of both these forms of the disease.

HLA Antigens↗
PubMed1983

Nonsalt-losing congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency with normal glomerulosa function.

In studies of a 6-yr-old boy and his non-HLA identical 8-yr-old sister, we demonstrated 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency in the biosynthetic pathways of glucocorticoids and androgens, but not mineralocorticoids. The sister did not manifest abnormal genital development at birth, but developed premature adrenarche at the age of 4 yr, with clitoromegaly and advanced bone age. The brother had perineal hypospadias at birth and developed premature adrenarche at the age of 6 yr. In both siblings, baseline and ACTH-stimulated delta 5 steroids were markedly elevated. The baseline and ACTH-stimulated ratios of delta 5 to delta 4 steroids remained extremely high, and all steroids promptly suppressed with dexamethasone (DEX). Normal baseline PRA and serum and urinary aldosterone (Aldo) levels increased after stimulation with a low Na+ diet. Renal Na+ conservation was normal after dietary Na+ deprivation with and without DEX administration. The PRA to pH 1 Aldo ratio remained normal with normal and low Na+ diets, regardless of DEX administration, indicating normal glomerulosa function with renin stimulation. In both siblings, ACTH increased PRA and Aldo levels, maintaining the PRA to pH 1 Aldo ratio unchanged from the baseline value. In contrast, in control children, PRA was suppressed, while Aldo increased, resulting in a fall of the PRA to pH 1 Aldo ratio. The increase in PRA with exogenous ACTH in these siblings suggests there may be an ACTH-stimulable mineralocorticoid antagonist. During prolonged DEX administration, hCG administration caused a slight increase in 17-hydroxypregnenolone and dehydroepiandrosterone in both the siblings, while testosterone (T) rose poorly in the brother, and estradiol did not rise at all in the sister. These results suggest the possibility of a deficiency of 3 beta-HSD in the gonads as well as the adrenals. After [3H]dehydroepiandrosterone iv infusion, there was normal conversion to [3H]-conjugated testosterone glucuronide, suggesting the presence of normal peripheral 3 beta-HSD activity. We propose that in these siblings, there is a deficiency of 3 beta-HSD in the adrenal zona fasciculata and zona reticularis, whereas 3 beta-HSD activity is intact in the zona glomerulosa. In addition, in these siblings, 3 beta-HSD deficiency was present in the gonads, while peripheral 3 beta-HSD activity appeared to be intact. These cases demonstrate further the heterogeneity of congenital adrenal hyperplasia due to 3 beta-HSD deficiency.

3-Hydroxysteroid Dehydrogenases↗
PubMed1983

HLA genotyping in family members and patients with familial polycystic ovarian disease.

To determine whether the familial occurrence of polycystic ovarian disease (PCO) is related to the major histocompatibility complex (HLA), four families in whom at least two siblings had clinical evidence of disease were examined. The diagnosis of PCO was confirmed by increased serum testosterone, androstenedione, and LH levels compared to those in normal women. Elevated concentrations of dehydroepiandrosterone sulfate indicated excess adrenal androgen secretion. The result of HLA genotyping in the families studied demonstrate that PCO does not exhibit linkage to the HLA system.

Androgens↗
PubMed1983

Genotyping steroid 21-hydroxylase deficiency: hormonal reference data.

Hormonal reference data, in the form of nomograms relating baseline and stimulated levels of adrenal hormones, provide a means of genotyping steroid 21-hydroxylase (21-OH) deficiency in congenital adrenal hyperplasia. Data from both 360- and 60-min ACTH stimulation tests are given. The serum hormone concentrations that have proven most useful in classifying 21-OH deficiency are 17-hydroxyprogesterone and delta 4-androstenedione. These nomograms clearly distinguish the patient with classical 21-OH deficiency from those with the milder symptomatic and asymptomatic nonclassical forms of 21-OH deficiency (previously referred to as late onset and cryptic forms) as well as heterozygotes for all of the forms and those subjects predicted by HLA genotyping to be unaffected. The nomograms also can identify individuals heterozygous for 21-OH deficiency in the general population who have a characteristic heterozygote response. These nomograms provide a powerful tool by which to assign the 21-OH deficiency genotype. Patients whose hormonal values fall on the regression line within a defined group are assigned to that group. In view of the strong correlation between the 60- and 360-min ACTH stimulation tests, the less cumbersome and shorter 60-min test can be used with the same confidence as the longer test.

Adrenal Hyperplasia, Congenital↗
PubMed1983

Transplantation for severe combined immunodeficiency with HLA-A,B,D,DR incompatible parental marrow cells fractionated by soybean agglutinin and sheep red blood cells.

Three patients with severe combined immunodeficiency (SCID) received transplants of HLA haplotype-mismatched parental bone marrow depleted of T lymphocytes by differential agglutination with soybean agglutinin (SBA) and subsequent E-rosette depletion. Two patients achieved durable engraftment with reconstitution of both humoral and cell-mediated immunity. Neither of these patients developed graft versus host disease (GVHD). The third patient achieved only a transient engraftment with concomitant development of mitogen-responsive lymphocytes of paternal origin. Our experience indicates that depletion of T lymphocytes by this technique can abrogate the potential of histoincompatible marrow grafts to induce lethal GVHD without limiting immunologic reconstitution. It also provides further evidence of nonimmune mechanisms of graft resistance that may necessitate preparative treatment of patients with SCID before transplantation with HLA-mismatched marrow cells.

Bone Marrow Transplantation↗
PubMed1983

Interleukin 2-dependent natural killer (NK) cell lines from patients with primary T cell immunodeficiencies.

Bulk cultured cell lines with natural killer (NK) activity were derived by in vitro culture with interleukin 2-containing conditioned medium (IL 2-CM) of peripheral blood mononuclear leukocytes (PBL) from patients with primary T cell deficiencies. Lines were developed from three patients with severe combined immunodeficiency (SCID) and one patient with Nezelof's syndrome and contained several populations of cells with distinct phenotypes. All lines contained a cell population expressing the Leu-5 (50K) (sheep red blood cell receptor), 3A1 (40K), and OKT10 antigens, but lacking the pan T cell antigens Leu-1 (67K) and Leu-4 (19K) as well as the markers of T cell subsets Leu-2a (32K) and Leu-3a (56K). These cells failed to express the Leu-7 antigen and only weakly expressed OKM1. In addition, one line contained a population of Leu-5+, 3A1+, OKT10+, Leu-2a+, Leu 1-, and Leu 4- cells. Three of the lines also contained populations with classic T cell (Leu-1 and-Leu 4+) phenotypes. The lines were enriched in NK activity compared with the PBL from which they were derived. Their growth was strictly dependent on IL 2-CM. Highly purified IL 2, lacking any other detectable protein contaminants or lymphokine activities, was capable of supporting the growth of the Leu-5+, 3A1+ "null" cell populations from these lines without alteration in their functional activity or phenotype. Thus, studies of in vitro expanded cell lines from patients with severe disorders of T cell function and thymic involution indicate that this "null" cell population does not require thymic maturation to develop its effector function. This "null" cell population can be maintained in vitro in the presence of IL 2. This finding is analogous to the data obtained from study of NK cells in athymic (nude) mice.

Animals↗
PubMed1983

Immunologic effects of interleukin 2 in primary immunodeficiency diseases.

Five children with primary deficiencies of T cell function were studied to assess the effects of highly purified exogenous Interleukin 2 (IL 2) on their in vitro T cell responses. The lymphocytes from one child with Nezelof's T cell deficiency demonstrated absence of endogenous IL 2 production and improved proliferative responses to mitogen or alloantigen in the presence of exogenous IL 2. Moreover, during in vitro mixed lymphocyte culture in the presence of exogenous IL 2, his lymphocytes were able to develop into cytotoxic effector cells. A second child with Nezelof's syndrome demonstrated a different type of defect. The lymphocytes from this child had less impairment of endogenous IL 2 production. Although IL 2 increased the proliferation of his cells in response to PHA, similar augmentation was not seen after stimulation with OKT3 or alloantigen. In cell-mediated cytotoxicity assays, after mixed lymphocyte culture, natural killer-like activity was strongly boosted in the cultures that contained IL 2, but T cell-mediated cytotoxicity was not. The lymphocytes from three patients with severe combined immunodeficiency did not show improved proliferative responses in the presence of IL 2. Thus, only one of the five patients demonstrated the combination of defective endogenous IL 2 production, but preservation of the ability to respond appropriately to exogenous IL 2. This child may therefore have suffered from a T cell defect pathophysiologically similar to that seen in nude or aged mice.

Antibodies, Monoclonal↗
PubMed1983

[Fungal osteoarthritis of the knee with joint destruction treated with ketoconazole].

The authors report a case of acute fungal arthritis following traumatic inoculation (bramble prick) in a 9 year-old boy. The implicated fungus was an highly pathogenic atypical strain of Scedosporium (monosporium) apiospermum. Two surgical operations (synovectomy and arthrodesis) and antifungal treatment with ketoconazole led to recovery. The pathogenic role of this fungus and especially the importance of toxic phenomena are discussed. This case is compared with other in the literature. The part of ketoconazole in the recovery of this patient is emphasized.

Antifungal Agents↗
PubMed1983

[Medical aspects of urinary tract infections].

The authors undertake a general review of recent advances in the field of urinary tract infections. Attention is drawn to the fact that bacteria can proliferate only if they adhere to the wall of the urinary tract before penetrating the epithelial cells. This adhesion is dependent upon adhesins which, in the urinary tract, can fix only upon specific receptors. It can therefore be understood that a mucosa bearing many receptors can easily by reinfected with organisms with the intestinal flora as their point of departure, via perineal and peri-urethral meatal infestation in the woman. A recent therapeutic advance is based upon the use of beta-lactamase inhibitors. A beta-lactamine neutralises the beta-lactamase produced by the organism and the other beta-lactamine acts as an antibiotic and kills the organism. This combination of two lactamines will probably be increasingly widely used in dealing with organisms. It is important to note that bacteriologists draw attention to the need to detect congenital abnormalities or foreign bodies or neighbouring infections, before incriminating only problems of bacterial virulence and the abnormally abundant presence of receptors on the urethrovesical mucosa. In the absence of urological disease, the treatment of lower urinary tract infections in the woman is not based upon any particular rules since short-term treatment seems just as effective as long-term treatment. The problem is completely different in the treatment of acute pyelonephritis which requires a minimum of three weeks using an antibiotic with powerful tissue diffusion.

Humans↗
PubMed1983

Analysis of two new leukemia-associated antigens detected on human T-cell acute lymphoblastic leukemia using monoclonal antibodies.

Two monoclonal antibodies (anti-3-3 and anti-3-40) were produced, which identify two new leukemia-associated antigens. Both antibodies reacted with most cell lines derived from patients with T lymphoblastic leukemia (T-ALL), but were not detected on suspensions of normal hematopoietic cells (including thymocytes) by cytotoxicity, absorption, or indirect immunofluorescence assays. Analysis of fresh leukemic cells indicated that anti-3-3 only reacted with T-ALL cells, while anti-3-40 also reacted with some non-T, non-B ALL cells and a few acute myelocytic leukemia (AML) cells. The 3-40 antigen was also found histopathologically in frozen sections of several normal tissues, including the epithelial cells and a few lymphoid cells of the thymus, and some malignant tissues. The 3-3 antigen was not found in any tissue studied. A "double absorption"assay provided additional serologic evidence that the two antibodies identify different antigenic determinants. Biochemical analysis indicated that the molecules immunoprecipitated by anti-3-3 and anti-3-40 have molecular weights of 35,000-40,000 daltons. This study demonstrated that the 3-3 and 3-40 antigens are markers for human T-ALL and can be used along with the normal T-lymphocyte antigen, 3A1, to discriminate T-ALL from cutaneous T-cell lymphoma (CTCL), adult T-cell leukemia (ATL), and T-cell chronic lymphocytic leukemia (T-CLL).

Adult↗