Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
Search
Advanced search
OR
Browse
Search
Volume 40, Issue 1
Displaying 1-21 of 21 articles from this issue
Show all abstracts
    • |<
    • <
    • 1
    • >
    • >|
Contents
  • Chloride currents are necessary for sustained ATP-induced intracellular calcium increase in human aortic endothelial cells
    KAZUHIKO YUMOTO
    1994 Volume 40 Issue 1 Pages 43-51
    Published: May 23, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.43
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    Extracellular ATP causes a biphasic increase in cytosolic free Ca2+ concentration ([Ca2+] i) in endothelial cells. In cultured human aortic endothelial cells [Ca2+] i was measured using fura-2AM.Ten μM ATP rapidly increased in [Ca2+] i from 60±7nM to 309±30nM (n=17) by releasing Ca2+ from internal stores (phasic phase).After the phasic phase, [Ca2+] i remained elevated, 200±35nM and 170±29nM at 3 and 5 min, respectively (tonic phase). Increasing the extracellular potassium ([K+] o) to 140mM suppressed the tonic phase without affecting the phasic phase. When [Cl- o was reduced during the tonic phase from 146mM to 20mM by substituting aspartate for chloride, [Ca2+] i rapidly returned to the basal level. Superfusion with 20mM [Cl-] o markedly suppressed the ATP-induced response in the tonic phase with little change in the basal and phasic levels (basal level 65±6nM n.s., phasic level 308±40uM n.s., 3 min 89±14nMp<0.01, 5min later 85±10nM p<0.01, n=8).Superfusion with 20mM [Cl-] o also inhibited the phasic increase in [Ca2+] i after the second application of ATP. Three hundred μM niflumic acid, a chloride channel blocker, completely suppressed the tonic phase (basal level 63±7nM n.s., peak level 350±64nM n.s., 3min 66±10nM p<0.01, 5min 69±14nM p<0.01 n=8). These results suggest that the chloride currents are necessary to maintain agonistinduced influx of Ca2+ which produces the tonic increase in [Ca2+] i.
    View full abstract
    Download PDF (1152K)
  • Effect of cytokine on chick osteoclast activity stimulated by lipopolysaccharide and heparin
    CHIEKO HAMADA, MINORU KUBOTA, YASUHIKO TOMINO, HIKARU KOIDE
    1994 Volume 40 Issue 1 Pages 52-60
    Published: May 23, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.52
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    We examined whether osteoblasts and bone marrow stromal cells mediate the effect of LPS (10μg/ml) and heparin (5μg/ml) in chick osteoclast activity in vitro, using disaggregated osteoclast resorption assay. LPS stimulated osteoclasts to excavate bone in culture without serum. The stimulation was blocked by cyclosporin A (0.1μ8/ml), but not indomethacin (10-5M). Although heparin elicited osteoclastic bone resorption with or without serum, cyclosporin A and indomethacin suppressed these stimulatory effects. Using the antibodies against : interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and tumor necrosis factor-beta (TNF-β), TNF-α antibody blunted the effect of LPS or heparin to chick osteoclastic bone resorption, whereas the antibodies against IL-1, IL-6 and TNF-β had no effect on LPS or heparin stimulation. Moreover, the osteoclasts cocultured bone marrowderived stromal cells (ST2) or clonal osteogenic cells (MC3T3-E1) and pretreated with LPS for 24hrs, showed increased activity, which was inhibited by TNF-α antibody. These results suggest that LPS and heparin cause an increase in bone resorption in vitro by releasing TNF-α from osteoblasts and bone marrow stromal cells.
    View full abstract
    Download PDF (1214K)
  • Morphological features of coronary lesions responsible for sudden onset type of acute myocardial infarction.
    -A possible mechanism of atheroma rupture-
    HIROMASA SUZUKI
    1994 Volume 40 Issue 1 Pages 61-70
    Published: May 23, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.61
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    Stenosis of an infarct-related coronary artery, which was successfully recanalized after thrombotic therapy, is frequently not as severe as expected in patients with acute myocardial infarction (AMI) without preceding angina pectoris (AP). To clarify the mechanism of the sudden onset type of AMI, we conducted a morphological study of 40 autopsied patients (35men/5 women with a mean age of 68 years), who died within one week after the first episode of AMI. Among these 40 patients, the coronary lesions in 21 cases (group A) that dies of AMI without preceding AP were histopathologically compared with those of 19 AMI cases (group B) that did have preceding chronic stable AP. There was no significant difference in the clinical profiles between the two groups, including age, gender distribution, coronary risk factors, or location of infarct-related coronary arteries. In group A compared with group B, the grade of luminal narrowing at the coronary lesion was significantly lower (A : 81% vs B : 93%), the incidence of plaque rupture was higher (A : 86% vs B : 53%), and the mean percent area of lipid deposition was much higher (A : 79% vs B : 58%) (p<0.01). The characteristic morphological feature of coronary lesion in group A was an eccentric lipid-rich plaque with rupture showing mild stenosis and presence of occlusive thrombosis superimposed on the location of intramural hemorrhage. Local thinning of the fibrous cap with abundant macrophages and foam cell invasion, rich cholesterol deposition causing a large necrotic core within the intima, and a reduction of muco-polysaccharides in the extracellular matrix of the intima were also frequently observed. The risk of rupture is much higher in developing lipid-rich plaque than in organized collagen-rich plaque and despite a small size compatible with low grade angiographic narrowing, this type of coronary lesion can be responsible for sudden onset type of acute myocardial infarction.
    View full abstract
    Download PDF (3332K)
  • Expression of LHRH in the olfactory system in the human embryo
    SATORU AKUTSU
    1994 Volume 40 Issue 1 Pages 71-77
    Published: May 23, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.71
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    The development of neurons expressing luteinizing hormone-releasing hormone (LHRH) has been studied immunohistochemically in human embryos obtained by legal artificial interruption during six weeks to nine weeks of gestation. In a 14mm embryo, LHRH-immunoreactive (-ir) neurons were not detected in the olfactory-forebrain axis. In 19mm embryos, LHRH-ir cells were detected in the epithelium of the anlage of the vomeronasal organ and along the olfactory-terminal nerve complex. Many ir cells were also recognized in the ventrolateral forebrain. A few ir cells reached the preoptic area. In these embryos, LHRH-ir cells in the terminal and olfactory nerves had a strongly positive reaction to a highly polysialylated form of neural cell adhesion molecule (NCAM-H). In 23mm embryos, large clusters of LHRH-ir cells were found along the terminal nerve and the olfactory nerve. These cells were distributed broadly from the ventrolateral forebrain to the lateral hypothalamus, whereas LHRH-ir cells were rarely detected in the olfactory epithelium. These results suggest that LHRH neurons originate from the olfactory epithelium of the anlage of the vemeronasal organ. As development progresses they migrate through the nasal septum, and enter the forebrain with the terminal nerve and the olfactory nerve. The close association of NCAM-H with the developing LHRH neurons raises the possibility that NCAM-H plays some role in guiding the migrating LHRH neurons from the olfactory epithelium to the forebrain in the human embryo.
    View full abstract
    Download PDF (2267K)
  • Origin of LHRH neurons in the chick embryo : effect of the olfactory placode ablation
    SATORU AKUTSU
    1994 Volume 40 Issue 1 Pages 78-82
    Published: May 23, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.78
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    There is considerable evidence suggesting that luteinizing hormone-releasing hormone (LHRH) neurons do not originate in the brain, but rather migrate from the nasal region to the forebrain during embryonic development. To elucidate the origin of LHRH neurons in the chick brain and investigate the migration phenomenon of these neurons, the olfactory placodes a possible site containing precursor cells of the LHRH neurons was surgically removed from chick embryos during an early stage of development. A unilateral olfactory placodectomy resulted in the absence of LHRH-immunoreactive (LHRH-ir) cells in the olfactory-forebrain axis of the surgically-altered side, whereas the development of LHRH neuronal system was not disturbed on the untreated side. In the embryos in which a fragment of the medial olfactory epithelium was spared, a small number of LHRH-ir cells were detected in the nasal region of the treated side. Where the lack of the central projection of the olfactory nerve caused stagnation of LHRH-ir cells, no ir cells were found in the brain area. These results suggest that LHRH neurons originate in the olfactory placode, then migrate to the forebrain along the olfactory nerve.
    View full abstract
    Download PDF (1335K)
    • |<
    • <
    • 1
    • >
    • >|
feedback
 Top