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Biomedical subjects

S Fukuhara

Publications and source records attributed to S Fukuhara.

262 records · Page 15Linked to original sources

[Electron microscopic investigation of the leishmaniasis cutanea. I. Leishmania tropica in the tissue (author's transl)].

On two patients suffering from Leishmaniasis cutanea from the old world florid and later a residual lesion could be removed for electron-mircroscopic examination, and the following was found: 1. A pseudocarcinomatous follicular epidermal proliferation in the florid lesion. 2. Macrophages with one to three Leishmania cells can be proved in histiocytes nests. The parasites are not always clearly surrounded by host cell membrane. 3. The endocellular Leishmania cells have a ciliary system which is open on the outside. It is, therefore, correct to speak of a cryptomastigotic shape of the flagellum. The kinetoplast shows direct transition to mitochondria. The number of periplast fibrillae or tubuli amounted to 95-97 which is less than in other types of Leishmania. Yet no further morphological distinctive feature between Leishmania tropica and the other types is discernible when a comparison with the pertinent literature is made. 4. No parasites to be considered virulent were found now in the late residual focus of previously secured cutaneous Leishmaniasis. The macrophages, on the other hand, contained big vacuoles with lamellar residual substances. These are regarded as rests of the parasites.

Adult↗

[Electron microscopical investigation of rhinoscleroma (author's transl)].

A boy from Togo with a resistent Rhinoscleroma was observed. The specific granuloma was examinated by histological and electron microscopic methods. The plasma cells form fibrillary material or guttate Russel bodies in the rough endoplasmatic reticulum. The morphology of Mikulicz-cells and Klebsiella rhinoscleromatis is described. The cells are supposed to be (histiocytic) macrophages. The surface of the germs is coated with a fimbria-like radiate substance which in the vacuoles of the cells is crosslinked. This material could be the eliciting antigen for the formation of Russel bodies. These bodies then may represent immune substances bound within the cell.

Adolescent↗

Measurement technique for the incident electron current in secondary electron detectors and its application in scanning electron microscopes.

A measurement technique for incident electron current in secondary electron (SE) detectors, especially the Everhart-Thornley (ET) detector, based on signal-to-noise ratio (SNR), which uses the histogram of a digital scanning electron microscope (SEM) image, is described. In this technique, primary electrons are directly incident on the ET detector. This technique for measuring the correlation between incident electron current and SNR is applicable to the other SE detectors. This correlation was applied to estimate the efficiency of the ET detector itself, to evaluate SEM image quality, and to measure the geometric SE collection efficiency and the SE yield. It was found that the geometric SE collection efficiency at each of the upper and lower detectors of a Hitachi S-4500 SEM was greater than 0.78 at all working distances.

Journal Article↗

Participation of alpha IIb beta 3 in platelet microparticle generation by collagen plus thrombin.

We investigated the role of alpha IIb beta 3 in microparticle generation by normal and thrombasthenic platelets stimulated with collagen plus thrombin. Microparticle generation by normal platelets was scarcely inhibited by monoclonal antibodies for glycoprotein Ib and glycoprotein IX. Although one monoclonal anti-alpha IIb beta 3 antibody (NNKY1-32) partly inhibited microparticle generation, 3 other monoclonal anti-alpha IIb beta 3 antibodies had little effect. However, the combination of 4 monoclonal anti-alpha IIb beta 3 antibodies or treatment with a polyclonal anti-alpha IIb beta 3 antibody significantly inhibited microparticle generation (p < 0.05). Microparticle generation by thrombasthenic platelets also occurred after stimulation with collagen plus thrombin, although at a significantly lower level compared with normal platelets. Monoclonal antibodies for resting alpha IIb beta 3, P-selectin, activated alpha IIb beta 3 and beta 2-glycoprotein I bound to microparticles from healthy platelets. In contrast, only a monoclonal antibody for beta2-glycoprotein I bound to thrombasthenic microparticles. These results suggest that microparticle generation by collagen plus thrombin occurs via two different mechanisms which are dependent and independent of alpha IIb beta 3, respectively. The alpha IIb beta 3-dependent mechanism appears to require activation of alpha IIb beta 3.

Amino Acid Sequence↗

Platelet-derived microparticles in alloxan-induced diabetes in rabbits.

To study platelet-derived microparticle generation in diabetes mellitus, we injected alloxan into male Japanese white rabbits. Injection of alloxan induced diabetes, but did not cause any significant change in various biochemical and hematological parameters. However, diabetic rabbits showed a significant elevation of platelet-derived microparticles from 8 weeks after alloxan injection (week 0: 0.45 +/- 0.24%; week 8: 1.12 +/- 0.61%, p < 0.005). These microparticles are known to have prothrombinase activity, suggesting that they may promote vascular complications in diabetes and may be used as a marker of vascular disease.

Alloxan↗

Annexin V expression and membrane vesiculation during activation of leukemic cell lines.

We investigated annexin V expression and membrane vesiculation during activation of four leukemic cell lines (U937, HL60, HEL, and CMK11-5) in order to determine whether annexin V had a role in the coagulation abnormalities related to malignancy. After stimulation by tissue plasminogen activator, binding of a monoclonal anti-annexin V antibody to U937 cells and HL60 cells increased in comparison with binding to control cells. Stimulation with thrombin or lipopolysaccharide also induced such an increase, but U46619 did not. Following activation of U937 and HL60 cells with thrombin and lipopolysaccharide, microparticle formation increased. Tissue plasminogen activator caused an increase of microparticles in U937 cells, but not HL60 cells. On the other hand, CMK11-5 and HEL cells did not show any increase of microparticles. These results suggest that some agonists can potently stimulate expression of prothrombinase

Annexin A5↗

Heterogeneity of acute myeloblastic leukemia without maturation: an ultrastructural study.

We demonstrated by ultrastructural examination that the leukemic blasts of 13 patients with acute myeloblastic leukemia (AML) without maturation (M1 in the French-American-British classification) showed heterogeneous features. In 7 patients, the leukemic blasts had a high level of light microscopic myeloperoxidase positivity (> 50%). Ultrastructurally, the cells were myeloblast-promyelocytes with 100% myeloperoxidase positivity, and these 7 patients appeared to have typical AML. In contrast, the remaining 6 patients had leukemic blasts with a low myeloperoxidase positivity (< 50%) and heterogeneous features. Three had ultrastructural features of myelomonocytic or monocytic lineage, 1 had myelomonocytic cells associated with megakaryoblasts, and 1 had undifferentiated blasts. The former group had a better prognosis than the latter, indicating that ultrastructural analysis of M1 leukemia may help predict the response to therapy.

Adolescent↗

Proteasome inhibitor 1 enhances paclitaxel-induced apoptosis in human lung adenocarcinoma cell line.

Paclitaxel is a chemotherapeutic drug that induces apoptosis in tumor cells by stabilizing microtubules, prevents normal mitosis, and blocks the cell cycle at the G2/M phase. We have previously reported that the activation of caspase-3 and caspase-8 plays a crucial role in paclitaxel-induced apoptosis. Anti-tumor reagents including paclitaxel, irradiation, and other stimuli activate the transcription factor NF-kappaB, which has the ability to suppress the apoptotic potential of those stimuli. Using a human lung adenocarcinoma cell line (LC-2-AD), we therefore examined whether the inhibition of NF-kappaB activity by proteasome inhibitor 1 (PS1) could become a new adjuvant therapy for cancer. A synergistic effect on apoptosis induction was observed with the combination of more than 0.1 microg/ml paclitaxel and 0.5 microM PS1. An increase in the cell number of apoptotic cells is correlated with the loss of Deltaphim and the activation of caspase-3 and caspase-8. Furthermore, augmented apoptosis is related to NF-kappaB activation. Based on these findings, we propose that the combination of paclitaxel with PS1 could be a new strategy for cancer treatment.

Adenocarcinoma↗