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M Murai

Publications and source records attributed to M Murai.

At least 199 records · Page 11Linked to original sources
PubMed1993

[A case of cutaneous squamous cell carcinoma after renal allotransplantation].

We describe herein a renal transplant recipient who developed cutaneous squamous cell carcinoma 15 years after the first transplantation. A 41-year-old Japanese man received a renal transplant from his mother for end-stage glomerulonephritis in December 1975 when he was 25 years old. Unfortunately, he suffered irreversible chronic rejection and returned to hemodialysis in March 1986. In December 1986 he received the second renal transplant from his father. In November 1990, the patient developed a nodule just lateral to his right lateral eye angle. He was treated with cryosurgery by a nearby dermatologist four times. However, the lesion did not improve, and he came to our hospital. Cutaneous biopsy specimen showed squamous cell carcinoma. The nodule was resected without decreasing the dose of cyclosporine and azathioprine. He has remained asymptomatic with out evidence of recurrent cutaneous lesions for two years of followup. This patient seems to represent the 3rd case of cutaneous cancer after renal transplantation in Japan.

Adult↗
PubMed1993

[High Molecular Weight Urokinase Reference Standard (Control 901) of National Institute of Health Sciences].

A candidate for "High Molecular Weight Urokinase Reference Standard (HMW-UK RS, Control 901)" of the National Institute of Health Sciences (NIHS) was examined for evaluating the fibrinolytic activity. The urokinase activity of the candidate HMW-UK RS was determined by "two-stage method" as 800 Unit/Amp. against the present Urokinase Reference Standard (Control 881), through the collaborative study involving five laboratories. According to the gel-permeation chromatography of the candidate for the molecular determination, it was confirmed that more than 97% of the total urokinase activity was attributed to the higher molecular fraction, named HMW-UK. Thus it was authorized as the High Molecular Weight Urokinase Reference Standard of the NIHS.

Government Agencies↗
PubMed1993

The contribution of a serum component(s) modified by B cells to the mechanism for macrophage activation by liposomes.

The effects of liposomes on the activation of mouse peritoneal macrophages were investigated in vitro by measuring the phagocytosis of opsonized sheep red blood cells (SRBC) via Fc receptors on the surface of macrophages. The addition of liposomes to mouse peritoneal exudate cells in RPMI-1640 medium with 10% fetal calf serum (FCS) caused an increase in the ingestion activity. In the absence of FCS, this increase was not observed, suggesting that some component(s) present in FCS is the causative factor(s) for this activation. When liposomes were added to the macrophage monolayer, the ingestion activity did not increase, showing that liposomes did not activate peritoneal macrophages directly, and that non-adherent cells may be involved. Following addition of the culture medium (conditioned medium), which was prepared by incubation of FCS with liposome-treated non-adherent cells or cell ghosts, to the macrophage monolayer, the ingestion activity of macrophages increased in either case. When the conditioned medium prepared with liposome-treated B cells was used for cultivation of liposome-untreated macrophages, a markedly enhanced ingestion activity was observed. However, the conditioned medium prepared with liposome-treated T cells did not affect the ingestion activity. These findings demonstrate that liposome-activated B cells modify some component(s) in FCS, and that the modified component(s) subsequently activates the phagocytosis of opsonized SRBC via Fc receptors on macrophages.

Animals↗
PubMed1993

[Activity of Lansoprazole (new proton pump inhibitor) against Helicobacter pylori and its therapeutic efficacy].

Lansoprazole, one of PPIs, is a strong antacid and it cures stomach and duodenal ulcers at early stages as well as having antibiotic action towards HP. The in vitro MIC of the product is between 3.13 and 12.5 micrograms/ml and it was 12.5 micrograms/ml, which was the same as MIC of colloidal bismuth citrate, in our study. Sterilizing effect of Lansoprazole is reported to be the direct attack on HP bacteria from electron microscopic findings. Our study revealed that Lansoprazole would preserve the epithelial cells on the edge of a stomach ulcer and would protect PAS-positive substance within them. Lansoprazole is said to cure many H2-Blocker resistant ulcers and to suppress the rate of recurrence of stomach and duodenal ulcers. These effects are considered to be attributable to maintenance of mucous barrier and maintenance of cytoprotection of the gastric mucosa by Lansoprazole as well as its sterilizing action mainly on HP.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1993

Contribution of N-acetyl-beta-D-galactosamine-specific lectin to Fc receptor-mediated phagocytosis by mouse peritoneal macrophages.

The contribution of lectin-like receptors on the cell surface of mouse peritoneal macrophages to the process of phagocytosis of IgG-coated sheep red blood cells (SRBC) through Fc receptors has been investigated. Phagocytosis was activated by conditioned medium containing modified vitamin D3-binding protein (DBP) prepared by the incubation of foetal calf serum (FCS) with lysophosphatidyl-choline-treated splenic non-adherent cells. Fc receptor-mediated phagocytosis of opsonized SRBC was specifically inhibited by the addition of N-acetyl-beta-D-galactosamine. The binding of modified Gc globulin, human DBP, to peritoneal macrophage was only inhibited by the addition of N-acetyl-beta-D-galactosamine, and was dependent on N-acetyl-beta-D-galactosamine concentration. In the presence of cycloheximide, activated phagocytosis was reduced to control levels. By Scatchard plot analysis of binding studies, the number of Fc receptors of macrophages which were activated by conditioned medium increased 3.6-fold in comparison to that of control macrophages. These findings suggest that lectin-like receptors having a specificity to N-acetyl-beta-D-galactosamine are involved in activating the process of Fc receptor-mediated phagocytosis of opsonized SRBC by macrophages, and that modified DBP promotes the synthesis of Fc receptors through the N-acetyl-beta-D-galactosamine-specific lectin on macrophage surface.

Acetylgalactosamine↗
PubMed1992

Studies on neurokinin antagonists. 2. Design and structure-activity relationships of novel tripeptide substance P antagonists, N alpha-[N alpha-(N alpha-acetyl-L-threonyl)-N1-formyl-D-tryptophyl]-N- methyl-N-(phenylmethyl)-L-phenylalaninamide and its related compounds.

Continuing studies on the chemical modification of the previously reported novel tripeptide SP antagonist, N alpha-[N alpha-[N alpha- (tert-butyloxycarbonyl)glutaminyl]-N1-formyl-D-tryptophyl]phenylalanine benzyl ester [Boc-Gln-D-Trp-(CHO)-Phe-OBzl (1)], are described herein. We initially investigated the stability of 1 in guinea pig plasma and liver homogenate to elucidate the most labile part in the structure. It was consequently revealed that the benzyl ester part was easily hydrolyzed to produce the inactive acid analog. Thus we searched for a benzyl ester surrogate that would be more resistant to hydrolytic enzymes. This approach found an isosteric amide structure, N-methyl-N-(phenylmethyl)amide, suitable in terms of potency and stability. Subsequent modification of the amino terminal into N alpha-acetyl-L-threonine led to the most potent compound, N alpha-[N alpha-(N alpha-acetyl-L-threonyl)-N1-formyl-D-tryptophyl]-N- methyl-N-(phenylmethyl)-L-phenylalaninamide [Ac-Thr-D-Trp(CHO)-Phe-NMeBzl (5a, FR113680)]. This compound 5a potently blocked 3H-SP binding to guinea pig lung membranes with IC50 of (5.8 +/- 0.78) x 10(-9) M. In vitro, 5a inhibited SP-induced contraction of isolated guinea pig trachea strips with IC50 of 2.3 x 10(-6) M and caused no contraction when used alone in this preparation up to 3.2 x 10(-5) M. In addition 5a exhibited no effect on the contraction induced by histamine or acetylcholine. Intriguingly, it was demonstrated in vivo that 5a suppressed the SP-induced bronchoconstriction and airway edema in guinea pigs with ED50 of 0.42 mg/kg and 0.66 mg/kg, respectively, when administered intravenously.

Acetylcholine↗
PubMed1992

Effects of the tripeptide substance P antagonist, FR113680, on airway constriction and airway edema induced by neurokinins in guinea-pigs.

FR113680 is a newly developed tripeptide substance P (SP) receptor antagonist. The effects of FR113680 on airway constriction and airway edema induced by neurokinins were investigated in guinea-pigs. In in vitro experiments, FR113680 inhibited the contraction of isolated guinea-pig trachea induced by SP and neurokinin A (NKA) in a dose-dependent manner with IC50 values of 2.3 x 10(-6) and 1.5 x 10(-5) M, respectively. The tracheal contraction induced by histamine and acetylcholine was not affected by FR113680. FR113680 (5 x 10(-5) M) also significantly inhibited the atropine-resistant contraction of isolated guinea-pig bronchi induced by electrical field stimulation. In in vivo experiments, FR113680 given i.v. inhibited SP-induced airway constriction in guinea-pigs at doses of 1 and 10 mg kg-1. However, FR113680 only inhibited NKA- and capsaicin-induced airway constriction by 40-50% even at a dose of 10 mg kg-1. FR113680 also inhibited SP-induced airway edema in guinea-pigs with the same potency as it inhibited SP-induced airway constriction. Histamine-induced airway constriction and airway edema were not affected at a dose of 10 mg kg-1. These results suggest that FR113680 preferentially inhibits responses induced by NK1 receptor activation (SP-induced airway constriction and airway edema), but is less effective on a NK2 receptor-induced response (airway constriction by NKA and neurogenic stimulation).

Amino Acid Sequence↗
PubMed1992

Studies on neurokinin antagonists. 1. The design of novel tripeptides possessing the glutaminyl-D-tryptophylphenylalanine sequence as substance P antagonists.

To discover a novel and low molecular weight substance P (SP) antagonist we postulated that the essential binding domain of peptide ligands was only a small portion in the whole structure. On the basis of this assumption, we selected the known octapeptide SP antagonist D-Pro-Gln-Gln-D-Trp-Phe-D-Trp-D-Trp-Phe-NH2 (1) as a lead and synthesized its fragment tripeptides which were evaluated for their activity to block 3H-SP binding on guinea pig lung membranes. The protected tripeptide N alpha-[N alpha-[N alpha-(tert-butyloxycarbonyl)-L-glutaminyl]-N1-formyl-D-tryptophyl]- L-phenylalanine benzyl ester [Boc-Gln-D-Trp(CHO)-Phe-OBzl (4a)], corresponding to the Gln-D-Trp-Phe part of 1, exhibited 7-fold potent inhibitory activity in comparison with 1. Studies on structure-activity relationships revealed that the D-tryptophan, L-phenylalanine, and benzyl ester were quite important to maintain the high binding affinity. It was also indicated that 4a antagonized the SP-induced contraction of isolated guinea pig trachea strips (IC50 = 4.7 x 10(-6) M).

Amino Acid Sequence↗
PubMed1992

Intracellular localization of Staphylococcus aureus within primary cultured mouse kidney cells.

Staphylococcus aureus Cowan I was incubated with monolayers of cells derived from several portions of mouse kidney, and found to be ingested by all types of the renal cells. Intracellular localization of S. aureus was determined by resistance of intracellular cocci against lysostaphin digestion and confirmed by electron microscopy. From renal medulla, three morphological variants of the hyperosmolarity-tolerant (HOT) cells were obtained. The rate of cocci-ingesting cells varied from 16.9% to 93.4% among these of the HOT cells at the end of 3-hr incubation. From renal cortex, three morphological variants of epithelial cells grew in medium RK-1. Among them, only the cells on the edge of colony ingested Cowan I, while the epithelial cells on the center of colony ingested few cocci. Transferred from medium RK-1 to MEM supplemented with 10% FBS, part of the cortical cells changed into fibroblast-like appearance and obtained the capacity to ingest Cowan I. This result may indicate the correlation between ingesting capacity and cellular morphology. From a glomerulus, epithelial (GE) cells and fibroblast-like (GF) cells were obtained. The GE cells ingested not only S. aureus Cowan I but Staphylococcus epidermidis and Staphylococcus saprophyticus after 30-min incubation, while the GF cells, like both of the HOT cells and the cortical cells, ingested only S. aureus. These results suggest a possibility that S. aureus is located within nonprofessional phagocytes during its infection and intracellular coccus plays an important role in its pathogenicity.

Animals↗
PubMed1992

Conspicuous ingestion of Staphylococcus aureus organisms by murine fibroblasts in vitro.

A conspicuous adhesion of Staphylococcus aureus organisms to murine cutaneous fibroblasts and NIH/3T3 cells cultured in vitro and subsequent ingestion of S. aureus organisms by these fibroblasts are described. In the present experimental system, only fibroblasts-adhering S. aureus organisms were efficiently ingested by fibroblasts unlike S. epidermidis and S. saprophyticus. These findings might suggest a correlation between the pathogenesis of S. aureus and its intracellular localization in non-professional phagocytes such as fibroblasts in a special reference to its higher pathogenicity than those of coagulase negative counterparts.

3T3 Cells↗
PubMed1992

FR 113680: a novel tripeptide substance P antagonist with NK1 receptor selectivity.

1. We have discovered a novel tripeptide substance P (SP) antagonist, FR 113680 [N alpha-[N alpha-(N alpha-acetyl-L-threonyl)-N'-formyl-D- tryptophyl]-N-methyl-N-phenylmethyl-L-phenylalaninamide]. In binding experiments, FR 113680 inhibited [3H]-SP binding to guinea-pig lung membranes (NK1) in a competitive manner but had not effect on [3H]-SP binding to rat cerebral cortical membranes (NK1), [3H]-neurokinin A ([3H]-NKA) binding to rat duodenum smooth muscle membranes (NK2) and [3H]-eledoisin (Ele) binding to rat cerebral cortical membranes (NK3). 2. In bioassay experiments, FR 113680 dose-dependently inhibited SP-induced guinea-pig ileum contraction (NK1), but did not inhibit either NKA-induced rat vas deferens contraction (NK2) or neurokinin B (NKB)-induced contraction of rat portal vein (NK3). According to Schild plot analysis, the inhibitory effect of FR 113680 on SP-induced guinea-pig ileum contraction is competitive and the pA2 value is 7.53. 3. The inactivity of FR 113680 on NK1 receptors in rat compared to guinea-pig may represent species-specific forms of the NK1 receptor. 4. These findings suggest that FR 113680 interacts selectively with the NK1 neurokinin receptor.

Animals↗
PubMed1992

Pharmacological profile of a high affinity dipeptide NK1 receptor antagonist, FK888.

1. In our search for compounds that inhibit the binding of [3H]-substance P (SP) to guinea-pig lung membranes, the dipeptide SP antagonist, FK888, was developed by chemical modification of the parent compound, (D-Pro4, D-Trp7,9,10, Phe11)SP4-11. 2. In a [3H]-SP binding assay using guinea-pig lung membranes and rat brain cortical synaptic membranes, FK888 displaced [3H]-SP binding with a Ki value of 0.69 +/- 0.13 nM and 0.45 +/- 0.17 microM, respectively, in a competitive manner. 3. FK888 inhibited the contraction of guinea-pig isolated ileum induced by SP in the presence of atropine and indomethacin (a NK1 receptor bioassay) with a pA2 value of 9.29 (8.60-9.98). 4. FK888 inhibited contractions of rat vas deferens by NKA (a NK2 receptor bioassay) and of rat portal vein by NKB (a NK3 receptor bioassay) at concentrations at least 10,000 times greater than that required to inhibit contractions of guinea-pig ileum. 5. FK888 also inhibited SP-induced airway oedema in guinea-pig after both intravenous and oral administration. 6. These data demonstrate that FK888 is a potent and selective NK1 antagonist which is active both in vitro and in vivo.

Administration, Oral↗
PubMed1992

Guide-wire-directed detachable balloon: clinical application in treatment of varicoceles.

Wire-directed detachable balloons were used in embolization treatment of varicoceles in six patients. Advancement of the balloon over a guide wire allowed easy embolization of the internal spermatic vein at the level of the inguinal ring. Additional detachable balloons were used to occlude the collateral vessels to the varicocele. This method proved highly effective in embolization of tortuous veins and in placement of multiple balloons.

Adolescent↗
PubMed1992

A case of asymptomatic cortisol producing adrenal adenoma.

We describe a man without the clinical findings of Cushing's syndrome, but who harbored an incidentally found cortisol-producing adrenal adenoma. On adrenal 131I-adsterol imaging, there was good uptake to the nodule, but no visualization of the contralateral adrenal. No abnormalities were found in the basal plasma cortisol, ACTH, urinary free cortisol and 17OHCS. However, dynamic hormone assessment revealed the existence of abnormal cortisol secretion: no suppression to dexamethasone, incomplete response to human corticotropin-releasing hormone, and lack of diurnal variation in plasma cortisol. Left adrenalectomy was performed with the diagnosis of cortisol-producing adrenal tumor. The pathological finding was an adrenal adenoma, and the perifusion of the excised tissues revealed a negligible response of the tumor tissue to ACTH though the residual normal cortex responded. Postoperative course was uneventful without replacement therapy with cortisol. It is suggested that the tumor autonomously produced a small amount of cortisol not only insufficient to provide clinical Cushing's syndrome, but also to provide typical suppression of hypothalamo-pituitary corticotroph-adrenal system.

Adenoma↗
PubMed1992

WS9326A, a novel tachykinin antagonist isolated from Streptomyces violaceusniger no. 9326. II. Biological and pharmacological properties of WS9326A and tetrahydro-WS9326A (FK224)

WS9326A binds competitively to [3H]substance P (NK-1 receptor) binding sites on guinea-pig lung membranes (IC50 = 3.6 x 10(-6) M), and acts as a tachykinin antagonist in various functional assays. WS9326A inhibited tracheal constrictions produced by exogenously added substance P and neurokinin A, with IC50 values of 9.7 x 10(-6) M and 3.5 x 10(-6) M, respectively. WS9326A inhibited neurokinin A-induced bronchoconstriction in a dose dependent manner when administered to guinea-pigs intravenously together with neurokinin A, and was also effective in preventing capsaicin-induced bronchoconstriction, which is known to be caused by release of endogenous tachykinins (substance P and neurokinin A). FK224 (tetrahydro-WS9326A; catalytic hydrogenation of WS9326A gave FK224) was more potent than WS9326A in the [3H]substance P receptor binding assay using guinea-pig lung membrane (IC50 = 1.0 x 10(-7) M).

Animals↗
PubMed1992

[Immunological study of interferon-gamma therapy for advanced renal cell carcinoma].

Immunologic and anti-tumor effects of interferon-gamma were studied in six patients with advanced renal cell carcinoma. A daily dose of 10 x 10(6) JRU/m2 of interferon-gamma (IFN-gamma) was given consecutively for five days and the treatment reiterated nine days later. Then the same dose was given every two days for three times and this regimen was also reiterated nine days later. Peripheral blood lymphocytes were analyzed before and one, three, five and eight weeks after the initial administration of IFN-gamma. Although the total number of lymphocytes and monocytes were not changed, CD8 (23.4 to 31.2%, p < 0.05), CD16 (12.4 to 19.3%, p < 0.01) and LeuHLA-DR (29.0 to 39.5%, p < 0.01) positive lymphocytes were significantly increased after the therapy. Non-induced LAK activity (0.6 to 10.8%, p < 0.05) and serum neopterin (3.5 to 10.8 nmol/L, p < 0.01) were also increased. These immunological parameters drastically changed during the consecutive administration of IFN-gamma, and tended to return to the previous value after this period. However, tumor regression was not clinically obtained. Our findings indicate that interferon-gamma stimulated the anti-tumor activity of the host, and administration of IFN-gamma is thought to be of immunological significance even in the advanced high stage cases.

Aged↗