PubMed Health⌕ Search

Biomedical subjects

M Deguchi

Publications and source records attributed to M Deguchi.

At least 19 recordsLinked to original sources
PubMed1992

Generation of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor.

Antigen-presenting, major histocompatibility complex (MHC) class II-rich dendritic cells are known to arise from bone marrow. However, marrow lacks mature dendritic cells, and substantial numbers of proliferating less-mature cells have yet to be identified. The methodology for inducing dendritic cell growth that was recently described for mouse blood now has been modified to MHC class II-negative precursors in marrow. A key step is to remove the majority of nonadherent, newly formed granulocytes by gentle washes during the first 2-4 d of culture. This leaves behind proliferating clusters that are loosely attached to a more firmly adherent "stroma." At days 4-6 the clusters can be dislodged, isolated by 1-g sedimentation, and upon reculture, large numbers of dendritic cells are released. The latter are readily identified on the basis of their distinct cell shape, ultrastructure, and repertoire of antigens, as detected with a panel of monoclonal antibodies. The dendritic cells express high levels of MHC class II products and act as powerful accessory cells for initiating the mixed leukocyte reaction. Neither the clusters nor mature dendritic cells are generated if macrophage colony-stimulating factor rather than granulocyte/macrophage colony-stimulating factor (GM-CSF) is applied. Therefore, GM-CSF generates all three lineages of myeloid cells (granulocytes, macrophages, and dendritic cells). Since > 5 x 10(6) dendritic cells develop in 1 wk from precursors within the large hind limb bones of a single animal, marrow progenitors can act as a major source of dendritic cells. This feature should prove useful for future molecular and clinical studies of this otherwise trace cell type.

Animals↗
PubMed1992

[Inhibition of Cls activity by methylprednisolone].

From a clinical study it was found that serum ClINH activity increased 6 hours after methylprednisolone (MP) pulse therapy in all the patients we studied with connective tissue diseases. Furthermore plasma ClINH-Cls complex decreased after pulse therapy. These phenomena lead us to investigate the effect of MP on Cls. 1) When a constant amount of Cls (8 micrograms/ml) was incubated with several concentrations of MP (2-50 mg/ml), the Cls activity of consuming C4 hemolysis was inhibited by MP in a dose-dependent manner. 2) MP inhibited consumption of C2 as well as C4 by Cls in a dose-dependent manner, even when MP had been removed by dialysis following incubation with Cls. These experimental data suggested that the trace amounts of Cls generated by immune complexes could be inhibited by long circulation of MP even at low concentrations in vivo, and resulted in a decrease of ClINH consumption and ClINH-Cls complex formation. These results indicated that the inhibition of Cls activity is one of the most important mechanisms in the process of the anti-inflammatory effect of MP in vivo.

Complement C1 Inactivator Proteins↗
PubMed1991

[Kinetics of immune complex deposition and influence of decomplementation on their clearance in cationized antigen induced acute serum sickness].

Using a murine acute serum sickness model caused by cationized bovine gamma-globulin (CBGG), the histological findings, accumulation of CBGG in the organs and the effect of decomplementation for the clearance of immune complex (IC) were investigated. The accumulation of CBGG increased in the lungs in the presence of anti-CBGG antibody 1 hour after injection of CBGG, but did not change in the kidneys. This suggests that CBGG forms IC in situ in the kidneys, and that circulating IC accumulates in the lungs. Decomplementation did not influence the uptake of CBGG immediately after challenge but delayed the clearance of CBGG in the kidneys, lungs, liver and spleen. A beneficial role of the complement system in the clearance of IC even for those formed in situ was recognized. Histological changes, cellular infiltration and microvascular destruction, evoked in the lungs in this experimental model immediately after challenge, were not seen in the kidney, suggesting the different modes of complement activation in these organs.

Animals↗
PubMed1991

[The relationship between complement C3 receptors (CR1, CR3) on polymorphonuclear leukocytes and complement fragments during hemodialysis].

The expression of complement receptor type 1 (CR1) and type 3 (CR3) on polymorphonuclear leukocytes (PMNs) and generation of complement fragments, C3a, C5a, C4d, iC3b and Bb, were studied in patients during hemodialysis using cuprammonium rayon (Cu) membranes. Furthermore, the relation between the expression of CR1 and CR3 on PMNs from healthy donors and complement fragments was investigated. The expression of CR1 and CR3 on PMNs increased during hemodialysis. Plasma C3a, C5a and iC3b levels increased in the first 15 minutes and then decreased at 120 minutes of dialysis. But plasma Bb level remained high until the end of hemodialysis. Purified Bb had no effect on the expression of CR1 and CR3 on PMNs, but C5a augmented those expression in vitro. Nafamostat mesilate, an artificial proteinase inhibitor, inhibited augmentation of complement receptors on PMNs in concentration dependent fashion. C5a generated through the activation of complement was thought to take an important role in the increased expression of CR1 and CR3 on PMNs.

Aged↗
PubMed1991

[Complement fragments in patients with bronchial asthma].

In this study, we investigated the pharmacological reactions induced by ibudilast to the complement system with the aim of clarifying the functional relation of the complement system to allergic reactions and pathology in patients with bronchial asthma. Complement hemolytic activities (CH50 and ACH50), complement profile, anaphylatoxins (C3a and C5a) and complement fragments (Bb, iC3b and C4d) were measured in 20 patients with bronchial asthma. One of antiasthmatic activities induced by ibudilast was concluded to be brought about though inactivation of the alternative complement pathway working on type III allergic reaction. Ibudilast increased the complement fragment Bb in the patients' plasma with the fairly controlled bronchial asthma. This increase in circulating Bb was suspected to be a result of inactivation of intermediate complement complexes, for example C3b.Bb.P, because the amounts in plasma of C3 and C5 showed no changes, while those of factor, B, P, H and I were decreased by ibudilast administration in patients with fairly controlled bronchial asthma. This antiasthmatic ability of ibudilast was restrained in those patients whose peripheral leukocytopenia was advanced before ibudilast administration, and in those whom ibudilast did not provoke an increase in the plasma level of iC3b, or did not prevent the serum level of C5 from increasing. In those unfairly controlled cases, enough anaphylatoxins, especially C5a might be produced to make the margination of peripheral neutrophils to the lung and increase CR3 on neutrophils binding with iC3b.

Adult↗
PubMed1991

A comparative trial of the reactogenicity and immunogenicity of Takeda acellular pertussis vaccine combined with tetanus and diphtheria toxoids. Outcome in 3- to 8-month-old infants, 9- to 23-month-old infants and children, and 24- to 30-month-old children.

The reactogenicity and immunogenicity of the Takeda acellular pertussis vaccine combined with tetanus and diphtheria toxoids were compared in 139 infants aged 3 to 8 months, 60 infants and children aged 9 to 23 months, and 99 children aged 24 to 30 months. Good antibody responses to pertussis toxin (PT), filamentous hemagglutinin (FHA), and agglutinogens occurred in all age groups after both the third and fourth doses. After the fourth (booster) dose, the mean antibody values in initially seronegative infants vaccinated at 3 to 8 months of age were as follows: anti-PT, 67.8 enzyme-linked immunosorbent assay units (EU) per milliliter; anti-FHA, 149.5 EU/mL; the agglutinin titer was 125.6. The values in initially seronegative children vaccinated at 24 to 30 months of age were as follows: anti-PT, 92.9 EU/mL; anti-FHA, 251.7 EU/mL; the agglutinin titer was 275.8. Reactions following immunization were minimal. Except for drowsiness after the first dose in infants, there were no clinically significant differences in reactions between infants and older children. The findings in this study coupled with the recent demonstration of efficacy of this vaccine in 2-year-old children supports the recent Japanese recommendation to lower the age of immunization with acellular pertussis vaccine combined with tetanus and diphtheria toxoids to 3 months.

Anorexia↗
PubMed1990

[A simplified method for the assessment of C1 esterase inhibitor function].

From the result that the activated form of C1-s(C1-s) prolonged the kinetics of hemolysis via complement, this assay was applied to assess C1 esterase inhibitor (C1INH) function. In the kinetic assay, the complement hemolytic activity was evaluated by the time which required to cause 50% reduction of the initial turbidity of sensitized sheep erythrocytes, and was expressed as T1/2. (1) T1/2 of pooled normal human sera (p-NHS) showed dose-dependent prolongation by the addition of various amounts of C1-s. (2) Preincubation of various amounts of functionally pure C1INH with the constant amounts of C1-s inhibited dose-dependently the prolongation of T1/2 by C1-s. (3) The C1INH activity of NHS was 840 +/- 80 units/ml (n = 6) and that of the C1INH deficient serum was 80 units/ml, which were calculated from the standard curve established by the addition of various amounts of purified C1INH. This test requiring only C1-s and sensitized sheep erythrocytes is simple technically and high in sensitivity, and seems to be useful for the routine assay for C1INH function of human sera.

Animals↗
PubMed1990

[Plasma levels of complement fragments during hemodialysis in patients with chronic renal failure].

The kinetics of hemodialysis-induced leukopenia and generation of complement fragments including C3a, C5a, C4d, iC3b and Bb were investigated in 14 patients during hemodialysis using cellulose acetate (CA), cuprophan (Cu) and ethylenevinyl alcohol (EVA) membranes. A marked leukopenia in the first 15 minutes was observed in CA and Cu. Plasma C3a levels were higher in CA than in Cu and EVA. Plasma C5a levels were higher in CA and Cu than in EVA. There was a negative correlation between the white blood cell counts and plasma C5a levels at 15 minutes (gamma = -0.85, p less than 0.001). Plasma C4d levels showed no increase in all membranes. Plasma iC3b levels were higher significantly in Cu than in CA and EVA. Plasma Bb levels in the first 15 minutes increased significantly in all membranes, and furthermore continued to increase till the end of hemodialysis in CA and Cu. This study revealed that all the membranes tested activated the complement via the alternative pathway to produce Bb, iC3b, C3a and C5a. C5a was thought to take an important role in transient leukopenia. Furthermore, Bb was accumulated during hemodialysis in CA and Cu, and its biological effects on patients undergoing hemodialysis should be studied.

Adult↗
PubMed1989

[Pregnancy induced hypertension (PIH) and osteoporosis].

The authors have already reported that the bone density of normal pregnant women might be kept at the same density as in normal non-pregnant women. However, it might be decreased in women with pregnancy induced hypertension (PIH) by estimating serum calcium levels, serum levels of calcium regulating hormones and calcium secretion into the urine. In order to demonstrate this theory, the degree of bone density in the second metacarpal bone of normal or PIH pregnant women was measured by X-ray using microdensitometry method (MD method). In MD method, six indices, such as MCI, d, GSmin, GSmax, sigma GS/D and densitometric pattern, are calculated by computer analysis of the X-ray of the bilateral hands. By the evaluation of the degree of bone atrophy, scores such as 0 better than the regression line of healthy women, which were prepared according to each age, 1 until 1 delta to the aggravation, 2 until 2 delta, and 3 more than 2 delta were totaled and evaluated as normal, initial stage of bone atrophy, 1st degree of bone atrophy, 2nd degree of bone atrophy and 3rd degree of bone atrophy for 0-3 scores, 4-9 scores, 10-12 scores and 13-18 scores, respectively (delta = 1 S.D.). The metacarpal index (MCI) of normal pregnant women in 3rd trimester was more than the mean in all cases, while cases more than 2 delta of the mean were noted in 29.4% of mild PIH and 11.8% of severe PIH, and a decreasing tendency of width of bone cortex was considered in PIH women. On the other hand, width of bone marrow (d) increased significantly in mild and severe PIH women. In the index for the density of only bone cortex area (GSmax) in PIH women, cases less than mean -1 delta were noted in 29.3% of mild types and in 11.8% of severe types respectively, and a high incidence was noted even though it was insignificant compared with 7.4% of normal pregnant women. In the index of the densities of bone cortex and bone marrow (GSmin), cases less than mean -1 delta were noted more frequently in PIH women than normal pregnant women, but in the index of bone density per unit length (sigma GS/D) no differences were noted between PIH and normal pregnant women.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorptiometry, Photon↗
PubMed1989

Specific [125I]Bolton-Hunter substance P binding sites in human and rat skin.

[125I]Bolton-Hunter substance P [( 125I]BH-SP) binding sites in rat and human skin were investigated, using quantitative receptor autoradiographic and emulsion autoradiographic methods. [125I]BH-SP binding sites were discretely localized in skin areas anatomically corresponding to dermal papillae, sweat glands, and hair follicles. The highest density of the binding sites was in the dermal papilla of the finger, followed by the sweat gland. [125I]BH-SP binding to the dermal papillae of the human finger pad skin and rat paw pad skin was displaced by unlabeled SP, with a high affinity, and Kd values were calculated to be 744 pM and 297 pM, respectively. The existence of [125I]BH-SP binding sites supports the idea of the neurotransmitter role of substance P in skin dermal papilla.

Adult↗
PubMed1989

[Changes of complement in immune complex glomerulonephritis induced by cationized antigen].

Complement system takes an important role in the pathogenesis of immune complex glomerulonephritis. In this study the precise changes of serum complement and its deposition in the glomeruli were investigated in the mice models induced with cationized bovine gamma-globulin (CBGG). Balb/c mice preimmunized with CBGG were injected intravenously with CBGG three times every 24 hours. Proteinuria and hypoalbuminemia have developed from day 3 until the death on day 9-13 of progressed azotemia. This nephritis resembled to mesangial proliferative glomerulonephritis histopathologically. Immunofluorescent study revealed granular deposits of CBGG, IgG, A, M and C3 along the glomerular capillary loop. Serum C3 decreased to about 50% of normal controls within 1 hour after challenge of antigen and plasma C3 conversion evaluated by crossed-immunoelectrophoresis, occurred in accordance with C3 reduction and then decreased. Immunofluorescent study showed a big difference in the mode of deposition among IgG, CBGG and C3. The most intense deposits of C3 in the glomeruli were seen 12 hours after challenge of CBGG, and then gradually decreased until the next challenge. IgG and CBGG antigen deposited most intensely soon after the challenge of antigen, and gradually decreased. These results led us to conclude that there existed two phases of complement activation in this immune complex induced mice glomerulonephritis; an early phase activation of complement by antigen-antibody complexes in the circulation and later phase activation of complement by immune complexes after deposition of them in situ glomeruli.

Animals↗
PubMed1988

[A study on bone density in women during pregnancy and postpartum].

Although 25-30 grams of calcium is transported into the fetus during pregnancy, it is suggested that the maternal bone might be kept at the same density as in non-pregnant women by measuring serum or urinary calcium concentrations and calcium regulating hormones simultaneously (Ohara et al. Folia Endocrinol., 1986). In this study, the influence of pregnancy on the maternal bone was investigated by measuring the degree of bone density in the second metacarpal bone of pregnant or puerperal women in an X-ray picture using a microdensitometer and a computer (Microdensitometry method; MD method, Inoue et al., 1983). Among six indices provided by this method, d (bone marrow width) tended to increase, but MCI (Barnett's metacarpal index) tended to decrease toward late pregnancy. GSmin, GSmax and sigma GS/D were significantly lower in the third trimester of pregnancy than in the second trimester of pregnancy. The densitometric patterns were A in most of the pregnant and puerperal women, but one case with the pattern of AB and two cases with the pattern of B were found in the third trimester of pregnancy. The sum of the scores of the six indices, which were based on the severity of each index, was within 0-3 in pregnant or puerperal women though it tended to increase as pregnancy progressed. From these results, it was confirmed that maternal bone density was maintained within the normal limits throughout pregnancy and postpartum.

Absorptiometry, Photon↗
PubMed1987

[Studies on the dynamics of insulin secretion and the regulatory mechanism of insulin receptor in fetal rats].

In order to clarify the onset of insulin secretion and the regulatory mechanism of its receptor induction in fetus, blood glucose, serum insulin and its hepatic receptor in situ in fetal rats (D18-D21) were measured and the changes of the levels of insulin and its receptor after the direct injection of glucose (1g/kg) to fetal rats in utero were investigated. In fetal rats (D18-D21), both serum insulin and glucose levels increased as pregnancy progresses and specific binding of insulin in fetal liver microsomal membranes increased on D21 of gestation, mainly due to the increase in binding affinity rather than binding capacity. After the direct injection of glucose to the fetus in utero, the rapid increase in serum insulin and the rapid decrease in insulin specific binding to liver microsomal membranes were observed in a part of D20 and all of D21 fetal rats, which was mainly due to the decrease of binding capacity. This suggests that the acute elevation of endogenous insulin level followed by the decrease of insulin specific binding in fetal rat liver is based on the down regulation mechanism of insulin receptor, because the amounts of insulin separated from liver microsomal membranes were less than one twentieth of the insulin concentration which are enough to decrease the binding capacity of hepatic receptor theoretically. In addition, the dissociation of 125I-insulin from liver microsomal membranes of glucose-treated rats were indistinguishable from that of control. From these results, it can be concluded that the onset of glucose-stimulated insulin secretion appears in fetal rats on D20 of gestation and the elevation of endogeneous insulin rapidly down-regulates the number of hepatic insulin receptor in fetal rats.

Animals↗
PubMed1987

Mechanism of killing of Giardia lamblia trophozoites by complement.

Only antibodies of the IgM class support the lytic effect of complement on Giardia lamblia (GL). We sensitized GL trophozoites (SGL) at 4 degrees C with serum containing anti-GL antibodies or IgM purified from this serum, and either normal human serum (NHS), complement 2-deficient human serum (C2d-HS), or C4-deficient guinea pig serum was used as source of complement. SGL were killed by NHS (86%) and by the deficient sera (50 and 40%, respectively), suggesting activation of the alternative pathway. However, the reaction was inhibited by Mg-EGTA. These observations led to studies of the role of C1. The lytic effect of NHS and C2d-HS on SGL was abolished by immunochemically depleting C1 from these sera, and reconstituted by adding purified C1q plus C1r and C1s. Factor B-depleted C2d-HS also lost its capacity to mediate killing, but reconstitution with factor B led to a dose-dependent increase in the killing of SGL. We next investigated the participation of the membrane attack complex in this system. SGL carrying C5b to C7 were lysed when incubated with C8 alone (56%); the addition of C9 further increased killing (98%), while C9 in the absence of C8 had no effect. We concluded that although activation of the classical pathway produces lysis of SGL, lysis may also proceed through a unique pathway of complement activation that requires C1 and factor B, but is independent of C4 and C2. Lysis of SGL can be accomplished by C5b to C8 in the absence of C9.

Animals↗
PubMed1987

Anemia-inducing substance (AIS) in advanced cancer: inhibitory effect of AIS on the function of erythrocytes and immunocompetent cells.

The effects of anemia-inducing substance (AIS), found in the plasma of tumor-bearing subjects, on red blood cells (RBC) and cellular immunity were examined. The results obtained may be summarized as follows: 1) The osmotic resistance and the deformability of RBC were decreased in patients with terminal cancer. 2) Normal human RBC were made less deformable and their membrane was made fragile by treatment with cachectic plasma from those patients, and these changes in physical properties were irreversible. 3) Energy metabolism in RBC was affected by AIS, that is, ATP concentration and pyruvate kinase activity in RBC were lowered and transmembrane glucose influx was suppressed. 4) AIS was removed from cachectic plasma by repeated adsorption with normal RBC, and the inhibitory effect on cellular immunity was lessened as AIS was removed. 5) AIS was detected in cachectic RBC membrane, monocytes, and tumor tissue by indirect immunofluorescence assay using rabbit anti-AIS antibody prepared by us. These observations suggest strongly that tumor-derived AIS appears in the blood of patients with terminal cancer, shows cytotoxicity to RBC and immunologically competent cells, and plays a role in the pathogenesis of cancer cachexy.

Adenosine Triphosphate↗