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Biomedical subjects

M Ibe

Publications and source records attributed to M Ibe.

46 records · Page 3Linked to original sources
PubMed1994

[Effects of combined administration of prednisolone and mizoribine in the course of remission for SLE children with nephritis].

Since oral steroid therapy was introduced for SLE, the long-term prognosis of the patients has been significantly improved. Adverse effects of the drug, however, are inevitable for these patients. The characteristic of the adverse effects especially for the child case is the suppression of linear growth. In order to prevent these undesirable effects and to improve their quality of life (QOL), we had introduced the methylprednisolone pulse therapy for SLE in children as both an initial and a relapse therapy. Although this therapy improved QOL of the patients significantly, there was little benefit for the growth disturbance. Then, we have introduced Mizoribine in addition to prednisolone (PSL) therapy for more than 18 months in three SLE children with lupus nephritis. In this trial, the combination therapy was effective for the decrease of urinary protein in one case, and for the reduction of a dosage of oral PSL in one case. In other case, MZR showed only partial immunosuppression. Thus, we concluded that there was a limitation with this combination therapy, however, it is one of the worthy therapy to be tried in SLE children with nephritis.

Adolescent↗
PubMed1993

Presence in Kawasaki disease of antibodies to mycobacterial heat-shock protein HSP65 and autoantibodies to epitopes of human HSP65 cognate antigen.

The central features of Kawasaki disease are immune activation and cytokine-mediated generalized vasculitis. To identify the predisposing factors, we examined the antibody response to BCG antigens, since reactivation of a previous BCG inoculation site is an early, specific manifestation of this disease. BCG antigens were separated on SDS-PAGE, transferred to membrane, and incubated with acute- and convalescent-phase sera of 21 patients with Kawasaki disease. Sera were also examined for the presence of antibodies to mycobacterial 65-kDa heat-shock protein (HSP65), and to its human homolog P1 antigen using synthetic peptides of nonhomologous region. To demonstrate the HSP65-sensitized T cells, in vitro proliferation assay was performed. All convalescent, but not acute phase, sera showed a strong antibody reactivity against 65-kDa protein. The reactivity was directed to recombinant HSP65. Non-cross-reactive sequences between rHSP65 and human HSP65 cognate were synthesized. The sera recognized these peptides of rHSP65 and autologous P1 antigen. Peripheral lymphocytes proliferated following the addition of rHSP65 (stimulation indices, 2.16-7.82; mean, 4.54). These findings suggest that HSP65 may be the most potent factor predisposing to Kawasaki disease, and that an autoreactivity to the epitope of the human HSP65 homolog may be related to the susceptibility to the disease.

Amino Acid Sequence↗
PubMed1992

Immunoglobulin G (IgG), IgG1, and IgG2 determinations from endoscopic biopsy specimens in control, Crohn's disease, and ulcerative colitis subjects.

Acute exacerbations of chronic inflammatory bowel disease (ulcerative colitis and Crohn's disease) are characterised by an increase in immunoglobulin G (IgG) positive cells in the mucosa, whereas uninflamed mucosa of inflammatory bowel disease patients displays only moderately increased or normal numbers of these cells. Previous data suggest that acute exacerbations of ulcerative colitis and Crohn's disease can be distinguished by different IgG subclass expression of mucosal immunocytes and a different IgG subclass production pattern of lamina propria lymphocytes. A procedure to obtain enough intestinal mononuclear cells from biopsy specimens to measure in vitro IgG and IgG1 production in control subjects and various patient groups has been established. IgG2 could be measured in Crohn's disease and ulcerative colitis only, as the concentrations in control subjects were below the sensitivity of the ELISA method. We found that IgG and IgG1 production correlated with the degree of local inflammation in both diseases, even in slightly inflamed mucosa, compared with control subjects. The proportion of IgG1 subclass was significantly increased in severely inflamed mucosa of both ulcerative colitis and Crohn's disease patients. A major difference between Crohn's disease and ulcerative colitis mucosa is apparent in mild or no inflammation. In Crohn's disease mucosa in remission, the IgG1/IgG ratio is comparable with that in controls, yet ulcerative colitis mucosa still displays significantly increased proportions of IgG1. In addition, the IgG2/IgG ratio is 0.12 in ulcerative colitis and 0.19 in Crohn's disease patients. The results show the dependence of local IgG and IgG1 production on the degree of inflammation and that an increase in subclass IgG1 in ulcerative colitis is present at all stages, including remission. These findings support the hypothesis that different immunoregulatory mechanisms are involved in Crohn's disease and ulcerative colitis. Environmental stimuli or genetic background may be responsible for the observed differences.

Biopsy↗
PubMed1992

[Effect and limitation of intravenous methylprednisolone pulse therapy in the long-term follow-up of childhood systemic lupus erythematosus].

The course of 6 patients with childhood systemic lupus erythematosus was analysed with emphasis on the effect and limitation of intravenous methylprednisolone pulse therapy in the long-term follow-up. The present findings suggest that using pulse therapy within 2 months in the course of disease flares, probably before irreversible organ damage has occurred, may be more beneficial in suppressing the disease activity and maintaining long-term remission. The demonstration of low serum complement activity (CH 50), and in some cases, proteinuria, was useful to decide the time of pulse therapy. Complications of pulse methylprednisolone plus long-term oral prednisolone therapy included cushingoid appearance and low body height in addition to cataract and glaucoma, all of which were attributable not to methylprednisolone pulse therapy alone but to long-term accumulation of corticosteroids. The combination therapy including several immunosuppressants needs to be established in order to avoid these steroidal complications.

Administration, Oral↗
PubMed1990

[Hyper IgE syndrome--a disease of imbalanced activation of helper T-cell subsets?].

Hyper-IgE syndrome is a rare immunodeficient disorder characterized by recurrent severe staphylococcal infections of the skin and sinopulmonary tract, chronic eczematoid rashes, coarse facial features, mild eosinophilia, and markedly elevated serum IgE levels. Hyperimmunoglobulinemia D, depressed DTH, and varying degrees of pathogenesis of this syndrome is unknown. The clinical manifestations and the recent research findings indicated the followings: 1) increased production of IL-4: hyperimmunoglobulinemia E, increased number of Fc epsilon R(+)-cells in peripheral blood, 2) defective production of IFN-gamma: abnormal local inflammatory responses (formation of cold abscesses), chemotactic defect in the circulating neutrophils (abnormalities in IFN-gamma/IL-8 pathway), depressed DTH, 3) T-cell immunodeficiency?-chronic dermatitis? 4) genetic factors (frequent familial occurrence, characteristic facial appearance with broad nasal bridge). These observations led us to postulate that both the increased production of IL-4 and the defective production of IFN-gamma may be the immunopathological bases of this syndrome. Recently, these cytokines were demonstrated to be secreted by different subsets of helper T-cells, designated TH1 and TH2, in murine system, suggesting that the regulatory imbalances between IL-4 and IFN-gamma in this syndrome might be due to the differential activation or inactivation of these helper T-cell subsets.

Humans↗
PubMed1989

Demonstration of mother-to-infant transmission of hepatitis B virus by means of polymerase chain reaction.

To investigate the failure of vaccines to prevent mother-to-infant transmission of hepatitis B virus (HBV), serum, cord blood, and colostrum samples from eleven mothers, known to be carriers of hepatitis B surface antigen, and their infants were examined by means of a highly sensitive polymerase chain reaction (PCR) method. HBV-specific DNA was detected in ten maternal serum samples, eight samples of colostral whey, eight samples of colostral cells, and one cord blood sample. Four infants of mothers with HBV-DNA-positive colostrum showed low responsiveness to hepatitis B vaccine. The infant whose cord blood was positive for HBV DNA showed low responsiveness to hepatitis B vaccine and subsequently became an HBV carrier. These results suggest the need for further study to evaluate whether breastfeeding is advisable for HBV carriers.

Carrier State↗
PubMed1986

S100-protein-containing dendritic cells in fetal and newborn epidermis and thymus.

Skin and thymus were obtained from abortuses of varying ages and from neonatal autopsies to determine if S100-protein-containing dendritic cells were present. Using an unlabeled antibody peroxidase-antiperoxidase method, we could not detect these dendritic cells in epidermis prior to live birth, but did detect them at all fetal ages in thymus. Within 24 hours of live, full-term delivery, dendritic cells containing S100 protein were identified in epidermis.

Fetus↗