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K Saionji

Publications and source records attributed to K Saionji.

At least 19 recordsLinked to original sources

[Plasma macrophage colony-stimulating factor level and changes of monocyte subpopulations in chronic renal failure patients treated with hemodialysis].

This study was carried out on 52 hemodialysis (HD) patients. The concentrations of macrophage colony-stimulating factor (M-CSF) in plasma and dialysate were measured by ELISA. Plasma M-CSF level increased in HD patients. M-CSF levels of dialysate were under the detection limit. The monocyte subpopulations were studied using double staining of CD14 and CD16 by flow cytometry. The percentage and absolute number of CD14+/CD16+ cells were much higher in HD patients (p < 0.001, respectively, Mann-Whitney U-test). A new subpopulation of blood monocyte, CD14+/CD16+, has been identified which possesses the features of tissue macrophage. The elevations of this subpopulation were also reported under some pathological conditions, and in subject treated with recombinant M-CSF. HD is the pathological condition which induces the increase in plasma M-CSF as well as change of monocyte subpopulation.

Female

[Homeostasis of antioxidant status in hemodialysis patients].

Oxidative stress, which occurs when there is excessive free-radical production or low antioxidant levels, makes significant contributions to pathogenesis in many human diseases. Cardiovascular disease is the major cause of mortality in patients receiving hemodialysis. For these patients, oxidative stress and increased lipid peroxidation may contribute to increased risk of atherosclerosis. The aim of this study was to determine if hemodialysis patients were associated with disturbance of homeostasis of antioxidant status. In this experiment, total antioxidant status of serum is measured by its ability to inhibit generation of free radicals from 2,2'-amino-di-[3-ethylbenzthiazole sulphonate] by metmyoglobin and hydrogen peroxide. Status of radical scavengers, such as serum total protein, albumin, uric acid and total bilirubin, was also measured. Blood were collected from three different episodes of hemodialysis. In the first group (n = 29), blood were collected before and after hemodialysis. In the second group (n = 29), blood were collected after dialysis and before next hemodialysis. In the third group (n = 8), blood were collected before hemodialysis. After last hemodialysis, patients started ingesting vitamin C and blood were collected before next hemodialysis. There was a marked reduction of total antioxidant status after hemodialysis in the first group. There was a marked increase in total antioxidant status before next hemodialysis in the second group. High doses of vitamin C caused increase in total antioxidant status in the third group. In conclusion, disturbance of homeostasis of total antioxidant status were observed in patients receiving hemodialysis. This may play a role in the pathogenesis in these groups.

Adult

Evaluation of the expression of human CAP18 gene during neutrophil maturation in the bone marrow.

To understand the gene expression of CAP18 (18-kDa cationic antibacterial protein), a member of cathelicidins, we evaluated mRNA and protein expression of CAP18 using human bone marrow cells and mature neutrophils. Northern blot analysis revealed that CAP18 mRNA was expressed more abundantly in bone marrow cells than mature neutrophils, whereas Western blot analysis indicated that CAP18 protein was more abundant in mature neutrophils than bone marrow cells. Consistent with this, in situ hybridization using bone marrow cells demonstrated that the expression of CAP18 mRNA was neutrophil lineage-specific and was observed primarily in myelocytes (>95%) with limited expression in more immature cells (promyelocytes) and mature cells (metamyelocytes, band cells, and segmented neutrophils). Furthermore, immunohistochemical study indicated that, coincident with the increase of CAP18 mRNA levels, CAP18-positive cells increased markedly at myelocyte stage, and the increased levels remained almost constant (>95%) in metamyelocytes, band cells, and segmented neutrophils, although the mRNA levels were remarkably reduced in these cells. Together these observations indicate that CAP18 gene transcription likely occurs lineage- and stage-specifically at the myelocyte stage of neutrophil maturation in the bone marrow and results in the synthesis and cytoplasmic accumulation of CAP18, which is present in the subsequent stages of neutrophil maturation.

Anti-Bacterial Agents

Granulocyte colony-stimulating factor administration increases serum concentrations of soluble selectins.

In order to explore the possible role of granulocyte colony-stimulating factor (G-CSF) in the inflammatory process, we examined the serum concentrations of soluble selectins (sL-selectin, sE-selectin and sP-selectin) following in vivo administration of G-CSF to five healthy volunteers and 12 neutropenic patients with haematological malignancies. The serum concentrations of both sL-selectin and sE-selectin were slightly but significantly increased after G-CSF administration in the healthy volunteers. The serum concentrations of all three selectins were significantly increased after G-CSF administration in the neutropenic patients concomitant with an increase in their neutrophil counts. These findings suggest that G-CSF may participate in the leucocyte-endothelial cell interactions in vivo.

Adult

[In vitro activities of faropenem against clarithromycin resistance Helicobacter pylori isolates].

Agar dilution and semi-solid agar dilution were used to determine the MIC of faropenem (FRPM) against 24 H. pylori isolates. FRPM was active against clarithromycin resistance H. pylori isolates. And, the MICs obtained by both methods were in agreement. The results suggest that FRPM was not affected by pH and is a clinically useful oral antibiotic for the eradication therapy of H. pylori infections.

Anti-Bacterial Agents

In vivo administration of granulocyte colony-stimulating factor increases the surface expression of sialyl-Lewis(x) on neutrophils in healthy volunteers.

We examined the in vivo effect of granulocyte colony-stimulating factor (G-CSF) on the surface expression of putative counterligands for endothelial selectins on neutrophils in healthy volunteers. G-CSF (50 microg/m2/day) was administered subcutaneously to 5 healthy volunteers for 4 days. The expression of surface antigens on neutrophils was determined by flow cytometry and monoclonal antibodies. G-CSF administration increased the number of leukocytes, mainly of neutrophils, which was associated with an increase in the expression of the high-affinity Fc receptor for IgG (FcRI, CD64) and CD14 on neutrophils. G-CSF administration decreased the surface expression of L-selectin on neutrophils, whereas it increased the expression of sialyl-Lewisx but not Lewisx on neutrophils. These findings suggest that G-CSF participates in the neutrophil-endothelial cell interactions in vivo by modulating the expression of adhesion molecules and ligands for endothelial selectins on neutrophils.

Gangliosides

Altered surface expression of effector cell molecules on neutrophils in myelodysplastic syndromes.

The surface expression of effector cell molecules on neutrophils was examined in 18 patients with myelodysplastic syndromes (MDS) and 20 healthy control subjects. The MDS patients were further classified as low clinical risk (L-MDS, n=7) and high clinical risk (H-MDS, n=11). The expression of Fc receptors for IgG (FcR), complement receptors (CR) and cellular adhesion molecules on neutrophils was determined by flow cytometry and monoclonal antibodies. The effect of granulocyte colony-stimulating factor (G-CSF) and tumour necrosis factor-alpha (TNF) on L-selectin shedding and CR up-regulation on neutrophils was also examined. The percentage of FcRI-positive neutrophils and CD11b/CR3 expression on neutrophils were significantly increased in the H-MDS patients when compared to the controls. In contrast, the expression of FcRII, FcRIII, L-selectin, LFA-1 and CD18 on neutrophils was significantly reduced in the H-MDS patients compared with the controls. The L-MDS neutrophils exhibited lower expressions of CR1, L-selectin, LFA-1 and CD18 than those of the controls. Neutrophils from some H-MDS patients showed impaired L-selectin shedding and CR up-regulation after stimulation with G-CSF or TNF, although these were not significantly different when assessed in the whole H-MDS group. These findings suggest that an altered surface expression of effector cell molecules and an impaired modulation of cellular adhesion molecules on neutrophils may contribute to the increased susceptibility to bacterial infections in MDS patients.

Aged

[Plasma macrophage colony-stimulating factor, granulocyte macrophage colony-stimulating factor and granulocyte colony-stimulating factor levels in continuous ambulatory peritoneal dialysis patients].

From a pathophysiological perspective, several studies have been performed on cytokines in chronic renal failure patients treated with continuous ambulatory peritoneal dialysis (CAPD). Because the peritoneal macrophages in CAPD patients produce some cytokines and the urinary secretion route for cytokines lost in those patients, CAPD patients are considered to have different plasma cytokine levels. Among the various cytokines, research on certain inflammatory cytokine levels has been reported. In studies of CAPD patients, peripheral blood and dialysate can be used as specimens. There are two methods of research. One involves determining the cytokine concentration in specimens and culture supernatant, while the other is to determine the mRNA expression of mononuclear cells in specimens and cultured mononuclear cells. The plasma levels of macrophage colony stimulating factor (M-CSF), granulocyte macrophage colony stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) were measured in CAPD patients without peritonitis. Plasma M CSF, GM CSF and G-CSF levels in CAPD patients were higher than those in healthy volunteers (p < 0.0001).

Adult

[The influence of local anesthetics on human leukocyte functions studied by micro whole blood collection and flowcytometry].

The influence of local anesthetics (pure bupivacaine and lidocaine with no preservative) on human leukocyte functions was examined. (a) The effect of bupivacaine on the phagocytosis of granulocyte was studied by bioassay. (b) The effect of lidocaine on the appearance of iC3b receptor (CR3) of granulocyte and monocyte (which is an important cell-adhesion-factor) was examined using flowcytometry. (c) The influence of lidocaine on phagocytosis of granulocyte and monocyte and on respiratory burst of granulocyte was examined using flowcytometry. (d) The influence of lidocaine on phagocytosis and that on respiratory burst were compared. These studies revealed that both phagocytosis and respiratory burst were inhibited by lidocaine, and the inhibition of respiratory burst was stronger than the inhibition of phagocytosis by local anesthetics' immunosuppressive effects. It was concluded that the balance of immunosuppressive action due to antimicrobial action and bactericidal ability of local anesthetics determined the occurrence of local bacterial infection.

Anesthetics, Local

Increased expression of the high-affinity receptor for IgG (FcRI, CD64) on neutrophils in multiple myeloma.

The surface expression of effector cell molecules on neutrophils was examined in 19 patients with multiple myeloma (MM), 6 patients with monoclonal gammopathy of undetermined significance (MGUS) and 22 healthy control subjects. The expression of Fc receptors for IgG (FcR), complement receptors (CR), and cellular adhesion molecules on neutrophils was determined by flow cytometry and monoclonal antibodies. MM neutrophils exhibited higher expression of FcRI, CR3, and CR4 and lower expression of FcRII and L-selectin than that in MGUS and controls. Granulocyte colony-stimulating factor (G-CSF, 50 micrograms/m2/d) was administered subcutaneously to 8 patients with MM and to 4 healthy volunteers. G-CSF administration increased the expression of FcRI, FcRII, and CR1 on neutrophils and decreased the expression of FcRIII on neutrophils in both groups. The application of G-CSF also resulted in increase of CR3 and CR4 expression and in decrease of L-selectin expression on neutrophils in healthy volunteers but not in MM patients. These findings suggest that MM neutrophils may be activate in vivo and that effector cell molecular expression on MM neutrophils is further modulated by G-CSF application.

Adult

[TDM and sampling].

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Blood Specimen Collection

Alterations of effector cell molecule expression on neutrophils in granulocyte colony-stimulating factor-producing tumour.

A 68-year-old man was diagnosed as having a granulocyte colony-stimulating factor (G-CSF)-producing mediastinal tumour. Mediastinotomy was performed, and thereafter the elevated leucocyte count and serum G-CSF concentration returned to the normal range. The surface expression of effector cell molecules on neutrophils was serially examined. Before operation, the expression of FcRI and CR1 was increased but the expression of FcRIII and L-selectin was reduced in the patient. The altered expression of these molecules returned to the normal levels after operation. These findings suggest that G-CSF produced by the tumour modulated neutrophil effector cell molecule expression in the patient.

Aged

Granulocyte colony-stimulating factor administration modulates the surface expression of effector cell molecules on human monocytes.

Granulocyte colony-stimulating factor (G-CSF) has been shown to stimulate human neutrophil functions, both in vitro and in vivo. We examined the effects of G-CSF administration on the surface expression of effector cell molecules on human neutrophils and monocytes. G-CSF (50 micrograms/m2/d) was administered subcutaneously to five healthy volunteers once a day for 7 d. Venous blood was obtained immediately before and after the completion of G-CSF administration and 1 week after the last G-CSF administration. The surface expression of complement receptors (CR), Fc receptors for IgG(FcR) and cellular adhesion molecules on human neutrophils and monocytes were determined by indirect immunofluorescence using flow cytometry and monoclonal antibodies. The expression of CR1, CR3, FcRI and FcRII on neutrophils increased significantly after G-CSF administration and then decreased after the last G-CSF administration. The expression of human leucocyte adhesion molecule-1 (LAM-1) on neutrophils reflected the above expression. On the other hand, the administration of G-CSF increased the expression of CR1, CR3, FcRI and FcRIII on monocytes. The expression of CR1, CR3 and FcRI on monocytes then decreased after the last G-CSF administration, whereas the expression of FcRIII remained at an increased level. These findings indicate that G-CSF administration modulates the expression of effector cell molecules on circulating monocytes as well as on neutrophils, resulting in enhanced defence against selected infections or in potentiation of the tumouricidal capacity of phagocytes in cancer patients.

Adult

[A novel method for detection of anti-neutrophil cytoplasmic antibody (ANCA) using flow cytometry].

UNLABELLED: It has been reported that anti-neutrophil cytoplasmic antibody (ANCA) is a specific serological marker for systemic necrotizing vasculitis, such as Wegener's granulomatosis, microscopic polyarteritis and idiopathic crescentic glomerulonephritis. Although the standard method for ANCA detection enplays an indirect immunofluorescence technique (IIF), the method is not objective. We attempted to detect ANCA by a more objective method using flow cytometry. MATERIALS AND METHOD: Thirty ANCA positive sera (cytoplasmic in 4, perinuclear in 26) and 20 ANCA negative sera including 2 sera with anti-nuclear antibody (ANA) detected by standard IIF were used for this study. For flow cytometric analysis, heparinized blood was taken from normal healthy volunteers. Neutrophils in the heparinized blood was incubated with human recombinant tumor necrosis factor alpha (rTNF alpha) in order to facilitate reaction between the antigens of ANCA and ANCA. Primed neutrophils were incubated with sera. After washing with phosphate buffered saline, immunofluorescence-labeled antibody against human IgG was added and incubated. The mean intensity of fluorescence (MIF) of the neutrophils was measured by flow cytometry (FACS, Becton-Dickinson CO., U.S.A.) for each sample. ANCA was considered positive by flow cytometric analysis if MIF of the sample was over the mean +2SD for normal human sera. RESULTS: By flow cytometric analysis, ANCA was detected in all ANCA positive samples by IIF and in 3 ANCA negative samples by IIF, of which 2 had ANA. However, it was possible to discriminate serum with positive ANCA from serum with positive ANA by flow cytograms because ANA reacted with the nuclei of both lymphocytes and neutrophils showing two peaks on the histogram.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antineutrophil Cytoplasmic

Complement receptor type 1 (CR1) deficiency on neutrophils in myelodysplastic syndrome.

We present a patient with myelodysplastic syndromes (MDS) whose neutrophils exhibited defective expression of complement receptor type 1 (CR1). A 73-year-old man was admitted with an evolution of MDS from RA into RAEBT according to the FAB classification of MDS. The neutrophil alkaline phosphatase (NAP) score was zero. The surface expression of membrane effector molecules on neutrophils was determined by indirect immunofluorescence using flow cytometry and monoclonal antibodies. The expression of CR1 on neutrophils as identified by staining with CD35 was defective in the patient, and the expression of other complement receptors (CR3 and CR4), Fc receptors and adhesion molecules was normal. CR1 deficiency and defective NAP score on neutrophils in the patient might account for impairment of common storage pool, presumably novel intracellular secretory vesicles.

Aged

Local anesthetic lidocaine inhibits the effect of granulocyte colony-stimulating factor on human neutrophil functions.

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) enhanced superoxide (O2-) release in human neutrophils stimulated by the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) and inversely regulated the surface expression of cellular adhesion molecules, leukocyte adhesion molecule-1 (LAM-1) and CD11b/CD18 leukocyte integrin, on human neutrophils; that is, rhG-CSF downregulated the expression of LAM-1 and upregulated the expression of CD11b on neutrophils. The cationic local anesthetic lidocaine inhibited not only FMLP-induced O2- release in neutrophils but also FMLP-induced CD11b upregulation and LAM-1 downregulation on neutrophils in a dose-dependent manner. Lidocaine also abolished the priming effect of rhG-CSF for enhanced release of O2- in neutrophils and inhibited rhG-CSF-induced CD11b upregulation and LAM-1 downregulation on neutrophils in a dose-dependent manner. These findings suggest that lidocaine inhibits human neutrophil functions, such as adherence to endothelial cells, by interfering with the expression of cellular adhesion molecules on neutrophils, and that lidocaine might have anti-inflammatory properties by inhibiting the effect of inflammatory cytokines.

Anesthesia, Local

[G-CSF and G-CSF receptor].

Relationship between leucocytosis and G-CSF blood concentration were examined. Increase in blood concentration of G-CSF of surgical patient and dialysis patient with leucocytosis were noticed. Determination of G-CSF receptor on leucocyte was performed by the flow cytometry using biotinylated G-CSF. Modulation of G-CSF receptor on leucocyte at surgery and dialysis was identified in vivo. Studies of G-CSF blood concentration and modulation of G-CSF receptor are useful in analysis of dynamics of leucocyte and analysis of infectious disease.

Granulocyte Colony-Stimulating Factor

Granulocyte colony-stimulating factor down-regulates the surface expression of the human leucocyte adhesion molecule-1 on human neutrophils in vitro and in vivo.

The leucocyte adhesion molecule-1 (LAM-1) is the human homologue of the murine peripheral lymph node homing receptor, MEL-14, and might play a crucial role in neutrophil localization at inflammatory sites. We have reported previously that recombinant human granulocyte colony-stimulating factor (rhG-CSF) stimulates or enhances several neutrophil functions in vivo, as well as in vitro. To further explore the possible role of G-CSF in inflammation we studied the effect of rhG-CSF on the surface expression of LAM-1 on human neutrophils, both in vitro and in vivo. The expression of LAM-1 by human neutrophils was investigated by indirect immunofluorescence using flow cytometry and monoclonal antibodies anti-Leu-8 and TQ1. A whole blood analysis was performed to minimize in vitro manipulation. Most circulating human neutrophils expressed LAM-1 on the cell surface. Brief exposure of neutrophils to rhG-CSF in vitro decreased the surface expression of LAM-1. rhG-CSF down-regulated neutrophil LAM-1 expression in a time- and dose-dependent manner. Neutrophils from healthy volunteers and from patients who were receiving rhG-CSF exhibited a decreased expression of LAM-1 after rhG-CSF administration, and the expression thereafter returned or overshot the pretreatment level after stopping rhG-CSF administration. These findings indicate that rhG-CSF down-regulates the surface expression of LAM-1 on human neutrophils in vivo, as well as in vitro, and G-CSF might participate in neutrophil-endothelial cell interaction in inflamed tissue.

Antigens, CD