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Biomedical subjects

M Yamaguchi

Publications and source records attributed to M Yamaguchi.

At least 1,027 records · Page 57Linked to original sources
PubMed1993

Interleukin-1 beta stimulates prostaglandin E2 and F2 alpha synthesis in human ovarian granulosa cells in culture.

To evaluate the roles of interleukin-1 (IL-1) in regulation of ovarian prostaglandin (PG) synthesis, we examined the effects of IL-1 beta on PGE2, PGE2 alpha, 6-keto-PGF 1 alpha and thromboxane (TX) B2 synthesis in cultures of human ovarian granulosa cells. Granulosa cells were obtained from hyperstimulated follicles in patients undergoing oocyte retrieval for in vitro fertilization-embryo transfer (IVF-ET). IL-1 beta increased immunoreactive concentrations of PGE2 and PGF2 alpha in culture medium in time- and dose-dependent manners. Concentration of PGE2 was significantly higher after 24 h incubation with 5 or more units/ml of IL-1 beta, when compared to the control value obtained without IL-1 beta (P < 0.05). Concentration of PGF2 alpha was significantly higher after 8 h incubation with more than 2 units/ml of IL-1 beta (P < 0.05). The increase in PGE2 was observed even in the presence of human chorionic gonadotropin (hCG), and blocked by indomethacin, an inhibitor of cyclooxygenase. During a 10 day incubation period, stimulatory effects of IL-1 beta on PG synthesis were observed only on the first 2 days incubations. Concentrations of 6-keto-PGF 1 alpha and TXB2 were below our measurement limits. This study demonstrated that IL-1 beta stimulates PG synthesis in human ovarian granulosa cells in vitro. IL-1 seems to play an important role in regulating ovarian functions.

Cells, Cultured↗
PubMed1993

High-performance liquid chromatographic determination of 5-hydroxyindoles by post-column fluorescence derivatization.

A selective and sensitive high-performance liquid chromatographic method with post-column fluorescence detection has been developed for the determination of 5-hydroxyindoles. Five biogenic 5-hydroxyindoles (5-hydroxytryptophan, 5-hydroxytryptamine, 5-hydroxyindol-3-ylacetic acid, 5-hydroxytryptophol and N-acetyl-5-hydroxytryptamine) were separated by isocratic elution on a reversed-phase column, TSKgel ODS-80Tm, and then converted into fluorescent derivatives by post-column reaction with benzylamine and potassium hexacyanoferrate(III) reagents. The detection limits (signal-to-noise ratio = 3) for the indoles were in the range 140-470 fmol per injection volume (100 microliters). The method was applied to the determination of 5-hydroxyindol-3-ylacetic acid in human urine, with direct sample injection.

Adult↗
PubMed1993

Proliferation and differentiation of myelodysplastic CD34+ cells in serum-free medium: response to individual colony-stimulating factors.

The presence of serum or contaminant cells may alter clonal development of haematopoietic progenitor cells in vitro. To investigate the pathogenesis of myelodysplastic syndromes (MDS), marrow progenitor cells from 13 MDS patients were highly purified using monoclonal antibodies including CD34 and immunomagnetic microspheres. The cells positive for CD34 in the purified cells were in the range from 87% to 98%. These purified cells were cultured in serum-free medium with individual colony stimulating factors (CSFs) to investigate whether CD34+ cells from MDS patients have abnormal responses to individual CSFs. Dose response experiments with the purified CD34+ cells and recombinant human macrophage-CSF (rM-CSF), granulocyte-CSF (rG-CSF), granulocyte/macrophage-CSF (rGM-CSF), interleukin-3 (rIL-3) or erythropoietin (rEP) were performed in serum-free fibrin clots in 11 patients. Five patients showed a diminished response to rG-CSF and one patient to rEP. In the remaining six patients the purified CD34+ cells did not respond to a stimulation of any individual CSFs. The results indicate that the progenitor cell growth abnormalities in these disorders involve a defect in the capacity of progenitor cells to respond to stimulation with G-CSF, and present direct evidence for the manner in which myelodysplastic CD34+ cells are impaired.

Adult↗
PubMed1993

Elevated levels of soluble ICAM-1 in sera from patients with bronchial asthma.

We measured the levels of soluble intercellular adhesion molecule-1 (sICAM-1) in sera from patients with bronchial asthma. sICAM-1 levels in sera from atopic asthmatic patients in stable conditions were higher than in normal control subjects. Furthermore, the sICAM-1 levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These results suggest that higher levels of sICAM-1 in sera reflect the upregulation of ICAM-1 expression in allergic inflammation.

Adult↗
PubMed1993

Segmental glomerular necrosis as an active index of IgA nephropathy: a study with 100 serial sections of 128 cases.

One hundred serial sections from each of 128 cases with immunoglobulin A (IgA) nephropathy were examined by light microscopy to clarify the relationship between segmental glomerular necrosis (SGN) and progression of glomerular injury. The cases were divided into five groups according to the percentage of glomeruli with cellular/fibrocellular (C/F) crescents, fibrous adhesion and/or sclerosis: grade I, 0%; grade II, < 20%; grade III, 20-50%; grade IV, 50-80%; and grade V, 80% or more. The serial sections revealed unequivocally focal occurrence of SGN in 39 cases (30%). Segmental glomerular necrosis was never found in the cases of grade I (0%, 0/28), while it appeared in those of grade II (33%, 12/36), grade III (46%, 13/28), grade IV (48%, 13/27) and grade V (11%, 1/9). The incidence of the cases with C/F crescents showed a similar tendency among the groups. In addition, focal C/F crescents were more frequent in cases with SGN (82%) than in those without SGN (24%). In particular, cellular crescents in 26 cases were formed in close proximity to SGN. These results suggested that SGN in IgA nephropathy was a more common finding than formerly evaluated and that it potentially participated in the progression of glomerular injuries closely associated with crescent formation. Unequivocally, focal occurrence of SGN corresponded well with the slowly progressive course of the glomerular disease.

Adolescent↗
PubMed1993

Endothelin-3-induced relaxation of rat thoracic aorta: a role for nitric oxide formation.

1. Endothelin-3 (ET-3) at concentrations below those which caused contraction (30 nM) elicited endothelium-dependent relaxation followed by rebound contraction in rat isolated thoracic aorta. 2. Endothelin-1 also relaxed the rat aorta with a similar potency. 3. The nitric oxide (NO) synthase inhibitor, NG-nitro L-arginine, the radical scavenger, haemoglobin and the soluble guanylate cyclase inhibitor, methylene blue, each inhibited the ET-3-induced relaxation. 4. The calmodulin inhibitor, calmidazolium, considerably attenuated the relaxation caused by ET-3 without affecting that to nitroprusside. 5. Concentrations of ET-3 that were necessary to induce the relaxation also caused concentration-dependent elevation of guanosine 3':5'-cyclic monophosphate (cyclic GMP) levels. 6. NG-nitro L-arginine, haemoglobin, methylene blue, calmidazolium and removal of the endothelium completely abolished ET-3-stimulated cyclic GMP production. 7. These results suggest that ET-3 triggers NO formation possibly via ETB receptors on the endothelium to activate soluble guanylate cyclase, which in turn stimulates cyclic GMP production and smooth muscle relaxation. The enzyme contributing to the NO formation may be of the calcium/calmodulin-dependent, constitutive type.

Acetylcholine↗
PubMed1993

Muscle contraction and inward current induced by silver and effect of Ca2+ channel blockers.

Single fibers from toe or anterior tibialis muscle contracted transiently and then tonically in the presence of 1.8 mM Ca2+ on addition of 10 microM Ag+. Exposure of fibers to Cd2+ completely inhibited tonic contraction and modified phasic contraction to some extent. Nifedipine at 10 microM initially potentiated and then completely inhibited twitch tension; subsequently, fibers no longer contracted phasically in response to 20 microM Ag+, whereas slight tonic contraction still occurred. Fibers with membrane potential clamped at -90 mV produced maintained inward current on application of Ag+. Simultaneous administration of 1 mM Cd2+ and 10 microM Ag+ to fibers voltage clamped with the double mannitol gap technique almost completely blocked the inward current. Removal of Cd2+ elicited a rapid and large inward current. Ag(+)-induced inward current was inhibited when 1 mM Cd2+ was applied to fibers during development of the inward current. In fibers paralyzed with 10 microM nifedipine, the inward current induced by 10 microM Ag+ was partially inhibited. These results suggest that phasic contraction induced by Ag+ is controlled by L-type Ca2+ channels (probably voltage sensors) located in the T-tubular membrane, whereas tonic contraction involves Ca2+ channels sensitive and/or insensitive to dihydropyridine in the surface and T-tubular membranes.

Animals↗
PubMed1993

Effect of vagotomy on ornithine decarboxylase activity in rat duodenal mucosa.

The aim of this study was to determine whether the circadian rhythm of ornithine decarboxylase (ODC) activity in rat small intestine is controlled by factors other than luminal nutrients. ODC activity in duodenal and jejunal mucosa of rats fed ad libitum was measured at four time points (0500, 1100, 1700, 2300 h; light period: 0800-2000 h). ODC activity in the jejunum increased in the dark period, which is when rats normally eat. In contrast, ODC activity in the duodenum began to increase at 1700 h, which is when rats do not normally eat, as indicated by the recorded feeding pattern. The increase in ODC activity in the duodenum at 1700 h, but not at other time points, was abolished by subdiaphragmatic vagotomy, whereas vagotomy had no effect on the feeding pattern of rats. Subdiaphragmatic vagotomy had no effect on ODC activity in the jejunum. ODC activity in the duodenum increased following glycoprivation of the central nervous system induced by infusion of 2-deoxyglucose into the third cerebroventricle. These results indicate that the increase in duodenal ODC activity at 1700 h is due to a signal from the upper brain structure through the vagal nerve and not to luminal nutrient factors.

Animals↗
PubMed1993

Beta-alanyl-L-histidinato zinc enhances various bone-regulating factors' effects on bone alkaline phosphatase activity in tissue culture.

The present investigation was undertaken to clarify the interaction of beta-alanyl-L-histidinato zinc (AHZ) and other bone-regulating factors on bone alkaline phosphatase in tissue culture. Calvariae were removed from weanling rats (3-week-old males) and cultured for periods up to 48 h in Dulbecco's modified Eagle medium. The experimental cultures contained 10(-5) mol/l AHZ which reveals in maximum effect on bone formation. Bone alkaline phosphatase activity was significantly increased by the presence of AHZ (10(-5) mol/l), insulin (10(-8) mol/l), sodium fluoride (10(-2) mol/l), aluminium sulfate (2 x 10(-3) mol/l), while the enzyme activity was not altered by estradiol (10(-9) mol/l), calcitonin (3 x 10(-8) mol/l), hydrocortisone (10(-8) mol/l), indomethacin (10(-6) mol/l) and imidazole (10(-3) mol/l). The presence of AHZ (10(-5) mol/l) clearly enhanced the calcitonin-, sodium fluoride- or diltiazem-increased bone alkaline phosphatase activity. Meanwhile, AHZ did not interact for the effects of other hormones and reagents. Moreover, the presence of cycloheximide (10(-6) mol/l), an inhibitor of protein synthesis, completely blocked the enhancement of bone alkaline phosphatase activity by AHZ. These findings suggest that AHZ has an effect different from bone cellular response for other bone-regulating factors, and that bone protein synthesis was a necessary component for AHZ action.

Alkaline Phosphatase↗
PubMed1993

Difference between renal failure associated with methylprednisolone pulse therapy and deterioration of renal function unrelated to methylprednisolone therapy.

In this study, we attempted to analyze the differences between renal failure associated with methylprednisolone (MP) pulse therapy and natural deterioration of renal function that was unrelated to MP administration. Of 80 patients with renal or collagen disease who received MP pulse therapy at our hospitals, 13 were selected for the study whose serum creatinine levels increased more than 0.5 mg/dl from baseline values following therapy. Somewhat arbitrarily, 7 patients were placed in an MP-associated renal deterioration group (group 1) in which serum creatinine levels returned naturally, or following induced diuresis, to baseline levels, and 6 patients in an MP-independent natural deterioration group (group 2) in which renal function progressively deteriorated. Renal function similarly deteriorated in the two groups following pulse therapy, irrespective of the degree of crescent formation. Our data suggested that hypoproteinemia is the most important index for differentiating MP-associated renal failure from natural deterioration of renal function unrelated to MP pulse therapy. In patients that are nephrotic and have impaired renal function, worsening of renal function following pulse therapy may partly be due to transient MP-associated renal failure. On the other hand, in patients without hypoproteinemia, worsening of renal function is most likely due to active primary disease and is probably not associated with MP pulse therapy.

Aged↗
PubMed1993

Cardiotoxicity of human recombinant interleukin-2 in rats. A morphological study.

BACKGROUND: One of the side effects of interleukin 2 (IL-2) cancer immunotherapy in humans is the vascular leak syndrome, which is frequently associated with depression of myocardial function, myocarditis, and myocardial necrosis. METHODS AND RESULTS: To investigate this cardiotoxicity, IL-2 (three doses of 5 x 10(5) Cetus units/day i.p.) was given to rats for 2, 3, or 5 days. Heart, lung, liver, spleen, and kidney tissues were studied by light and electron microscopy and with immunoperoxidase techniques. Cardiac changes consisted of focal lymphocytic and eosinophilic infiltration, myocyte vacuolization, myofibrillar loss, and necrosis. Ultrastructural alterations included swelling of endothelial cells, with dissociation of intercellular junctions, migration of lymphocytes into the interstitium, and interstitial hemorrhage and edema. Close contact between infiltrating lymphocytes, particularly large granular lymphocytes, and cardiac myocytes was often observed in areas of tissue damage. All lesions were more severe on day 5 than on days 2 and 3. Immunoperoxidase stains demonstrated asialo GM1 ganglioside antibody-positive, granular lymphocytes to be much more frequent in myocardium of IL-2-treated rats than in that of control rats. CONCLUSIONS: Although we cannot exclude the possibility of a direct toxic effect of IL-2 on myocytes, our observations suggest that the myocardial damage produced by this agent is triggered by IL-2-activated lymphocytes that exert cytolytic effects, first on endothelial cells and then on cardiac myocytes, thus producing lesions that involve both the cardiac microcirculation and the muscle cells.

Animals↗
PubMed1993

Mast cells are essential for the full development of silica-induced pulmonary inflammation: a study with mast cell-deficient mice.

Silicosis provides a good model for chronic interstitial pulmonary inflammation. In order to clarify the role of mast cells in the development of interstitial lung diseases, silica suspension was transnasally administered to mast cell-deficient mice (WBB6F1-W/Wv) and their mast cell-intact littermates (WBB6F1(-)+/+) as well as to normal mice (C57BL/6). Histologic examinations and analyses of bronchoalveolar lavage fluid (BALF) components indicated that silica instillation induces less severe lung lesions in mast cell-deficient mice than in mast cell-intact mice. BALF neutrophilia was prominent in mast cell-intact mice, but mast cell-deficient mice developed significantly milder BALF neutrophilia. An increase in the number of lung mast cells was observed in mast cell-intact mice. To further prove the involvement of mast cells, bone marrow-derived cultured mast cells from +/+ mice were adoptively transferred to mast cell-deficient mice. These mast cell-reconstituted mice developed more severe pulmonary lesions than did the mast cell-deficient mice; the severity of the lesions was similar to that in mast cell-intact mice. In addition, BALF neutrophilia was elicited by mast cell reconstitution. A significant number of mast cells was found in the lungs of mast cell-reconstituted mice when silica was administered. These results suggest the involvement of mast cells in the development of silicosis and implicate interactions between mast cells and neutrophils in the pathogenesis of this disorder.

Animals↗
PubMed1993

Effect of insulin administration on bone formation is impaired in rats with skeletal unloading.

The effect of insulin administration on bone formation was investigated in the femoral diaphysis of rats with skeletal unloading. When the femoral-diaphyseal tissues from normal rats were cultured in the presence of insulin (10(-9) and 10(-8) M) for 48 h, the hormone produced a significant increase of alkaline phosphatase activity, collagen, deoxyribonucleic acid (DNA) and calcium contents in the bone tissues, indicating that it has a direct stimulatory effect on bone formation. Moreover, when normal rats received a subcutaneous administration of insulin (5.0 IU/100 g body weight) 5 times at 24-h intervals, the hormone caused a significant increase of alkaline phosphatase activity, DNA and calcium contents in the femoral diaphysis. Those increases were not seen by insulin administration to the skeletal-unloading rats with hindlimb hang for 4 d. The present results indicate that the stimulatory effect of insulin on bone formation is lost by skeletal unloading. The finding further supports the view that insulin impairment plays an important role in the deterioration of bone formation by microgravity.

Alkaline Phosphatase↗
PubMed1993

Preventive effect of beta-alanyl-L-histidinato zinc on the deterioration of bone metabolism in ovariectomized rats.

The preventive effect of beta-alanyl-L-histidinato zinc (AHZ) on the deterioration of bone metabolism was investigated in the femoral diaphysis of ovariectomized rats. AHZ (10, 30 and 100 mg/kg body weight/d) was orally administered to ovariectomized rats for 6 weeks. Ovariectomy produced a significant decrease in estradiol, calcitonin, calcium and inorganic phosphorus concentrations in the serum as compared with those from sham-operated rats. The dose of 30 and 100 mg AHZ/kg prevented any decrease in serum inorganic phosphorus concentration caused by ovariectomy. Alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium contents in the femoral diaphysis of ovariectomized rats significantly decreased in comparison with those from sham-operated rats. These decreases were completely prevented by the dose of AHZ (10, 30 and 100 mg/kg). Electron microscopical analysis showed a rough alteration of bone matrix in the femoral diaphysis of ovariectomized rats. This alteration was clearly modified by the doses of AHZ (10, 30 and 100 mg/kg). Also, dosages of AHZ (30 and 100 mg/kg) restored the atrophy of osteoblasts and cartilage cells caused by ovariectomy. The present study suggests that oral administration of AHZ can prevent the deterioration of bone metabolism by ovariectomy. AHZ may have a therapeutic role in the treatment of osteoporosis.

Alkaline Phosphatase↗
PubMed1993

Effect of beta-alanyl-L-histidinato zinc on bone metabolism in rats with adjuvant arthritis.

The effect of a new zinc compound, beta-alanyl-L-histidinato zinc (AHZ), on osteopenia was investigated in rats with adjuvant arthritis. Arthritis was induced in female rats by administering 1% Mycobacterium butyricum (MB) into the subplantar surface of the right hind paw. AHZ (10, 30 and 100 mg/kg body weight) was orally administered to MB-treated rats 28 times at 24-h intervals, and the rats were bled 24 h after the last administration. Treatment with MB caused a remarkable increase in paw volume and a corresponding decrease in the ratio of albumin per globulin in serum, indicating that the treatment induces inflammation. These alterations were not significantly changed by the administration of AHZ (10, 30 and 100 mg/kg). Serum calcium and zinc concentrations are significantly decreased in rats with adjuvant arthritis. These decreases were completely restored by the administration of AHZ (30 and 100 mg/kg). Furthermore, the inflammation-induced decreases in alkaline phosphatase activity and calcium content in the femoral diaphysis were clearly blocked by the administration of AHZ (30 and 100 mg/kg). Also, the larger doses of AHZ (30 and 100 mg/kg) produced a significant increase in femoral-diaphyseal deoxyribonucleic acid and in the zinc content in rats with adjuvant arthritis. These results suggest that AHZ has a stimulating effect on bone formation in the femoral diaphysis of rats with adjuvant arthritis, although the compound did not have an anti-arthritic effect.

Alkaline Phosphatase↗
PubMed1993

Absorption of recombinant human granulocyte colony-stimulating factor (rhG-CSF) and blood leukocyte dynamics following intranasal administration in rabbits.

Absorption of recombinant human granulocyte colony-stimulating factors (rhG-CSF) following intranasal administration of aqueous preparations containing rhG-CSF with or without dimethyl-beta-cyclodextrin was investigated. It was found that rhG-CSF was absorbed and the total leukocyte numbers in peripheral blood markedly increased after intranasal instillation of rhG-CSF solution (pH 4) without excipients. Simultaneously administered dimethyl-beta-cyclodextrin enhanced nasal absorption of rhG-CSF. Consequently, serum rhG-CSF concentrations and total leukocyte numbers were greatly increased.

Administration, Intranasal↗
PubMed1993

[Effects of terguride, an ergot alkaloid derivative, on the central nervous system: biochemical and behavioral studies].

Effects of terguride, a 9,10-dihydrogenated derivative of lisuride, on the central nervous system were investigated in rodents in comparison with those of lisuride. In vitro binding studies in rat brains showed that terguride, similar to lisuride, had a high affinity for D2-, 5-HT1A-, 5-HT2-, alpha 1- and alpha 2-receptors. Terguride, as does lisuride, induced hypomotility and yawning at low doses in rats, suggesting its presynaptic D2-agonist action. Terguride, unlike the postsynaptic D2-agonist lisuride, induced neither hypermotility nor stereotypy in rats and guinea pigs, but suppressed the hypermotility and stereotypy induced by apomorphine. Terguride suppressed haloperidol-induced catalepsy in rats and induced contralateral rotations in unilaterally 6-OHDA-lesioned rats, as does lisuride. These effects may be due to the postsynaptic D2 partial agonist action. Terguride, unlike lisuride, neither induced the serotonin syndrome nor generalized to the discriminative stimuli of the 5-HT1A- agonist 8-OH-DPAT in rats. Terguride did not induce head twitch in mice. Terguride blocked noradrenaline-induced lethality and clonidine-induced hypothermia at high doses in mice. Repeated administration of terguride did not affect the behavioral actions in rats. Thus, the effects of terguride on the central nervous system seems to be produced by mediation of the agonist and partial agonist actions at presynaptic and postsynaptic D2- receptors, respectively.

Animals↗