Hirosaki Medical Journal
Online ISSN : 2434-4656
Print ISSN : 0439-1721
Volume 55 , Issue 3-4
Showing 1-4 articles out of 4 articles from the selected issue
Original Article
  • Noriko Ishizaki, Rika Kanezaki, Tsutomu Toki, Etsuro Ito
    2004 Volume 55 Issue 3-4 Pages 83-94
    Published: 2004
    Released: October 19, 2021
    JOURNAL FREE ACCESS
        Transient abnormal myelopoiesis (TAM) is a leukemoid reaction which is found in about 10% of cases with Down's syndrome during the neonatal period. While in most of the cases, it resolves spontaneously without any antileukemic therapy, 20-30% of cases develop acute megakaryoblastic leukemia (AMKL) after the remission. It is important to isolate the responsible gene for TAM, because it may lead to elucidation of the process of oncogenesis in hematopoietic cells. Possible candidate location has been reported to be in the pericentric region of 21q. In this report, we tried to identify novel genes in the region of 21q11-21 and isolated 13 independent clones by the screening of cDNA library of CMK11-5 cells, derived from AMKL in Down's syndrome. Analysis of the clones revealed that the 9 clones of them were derived from the same transcript coded in 21q11-21. The clone #64, one of the 9 clones was the full length of the gene and we could indicate the exon-intron structure of the novel gene. The predictive amino acid sequences from the gene had no homology to known proteins.
    Download PDF (833K)
  • Atsushi Ishiguro, Tomoko Komatsu, Kazufumi Yamagata, Yoshiko Tamai, Hi ...
    2004 Volume 55 Issue 3-4 Pages 95-100
    Published: 2004
    Released: October 19, 2021
    JOURNAL FREE ACCESS
        Eleven patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) have been treated with imatinib mesylate, which is a molecular targeted therapeutic agent. The patients were evaluated for hematological responses, cytogenetic responses, and toxic effects. The median age was 54 years (range, 21-73 years) and the clinical stage was 8 in chronic, 2 in accelerated, and 1 in blastic phase. After a median follow-up of 11 months, all patients have obtained hematological responses, including 9 of complete hematological response (CHR). Two patients in chronic phase and 1 in accelerated phase who had no prior therapy achieved complete cytogenetic response (Complete CR), and 5 in chronic phase achieved Major partial CR. Toxic effects of Grade 3 to 4 appeared in 5 patients, including the eruption, the muscle pain, and the hematological toxicity. The other patients without severe toxic effects could continue the treatment with imatinib, and patients in chronic phase who were able to maintain the initial dose with less toxic effects had superior cytogenetic responses.
    Download PDF (476K)
  • Hiroshi Murakami, Naoki Tamasawa, Kazumi Yamato, Jutaro Tanabe, Nobuhi ...
    2004 Volume 55 Issue 3-4 Pages 101-107
    Published: 2004
    Released: October 19, 2021
    JOURNAL FREE ACCESS
        The effect of fenofibrate in type 2 diabetic patients with dyslipidemia was examined. Thirteen patients with type 2 diabetes mellitus and mixed hyperlipidemia; serum total cholesterol (TC) > 220 mg/dl and/or triglyceride (TG) > 150 mg/dl, were included in the study. Fenofibrate was administered at daily dose from 200 to 300 mg, and following items were implemented just prior to, at 3 months after, and at 6 months after the administration: amount of serum lipid, electrophoresis of lipoprotein by the method of polyacrylamide gel electrophoresis (PAGE), quantification of cholesterol (RLP-C) and triglyceride (RLP-TG) in remnant-like particle. TC significantly decreased at 6 months after administration (p<0.05), while TG at 3 and 6 months after administration was significantly lowered (p<0.05). Concentration of RLP-C that was 16.3 mg/dl before administration of fenofibrate decreased with statistical significance to attain 6.2 mg/dl and 7.2 mg/dl in 3 and 6 months after administration, respectively (p<0.01). In the case of RLP-TG, the concentration of 92.2 mg/dl before administration was observed to be lowered with time with statistical significance to reach 28.7 mg/dl and 32.7 mg/dl in 3 and 6 months, respectively (p<0.01). The low-density lipoprotein (LDL) particle size significantly increased at 6 months after administration (p<0.05). In all cases the remnant lipoprotein was observed on PAGE before administration, the bands disappeared or decreased in 8 cases by the treatment with fenofibrate. It was suggested that fenofibrate lowered RLP-C and RLP-TG, and improved the LDL particle size in type 2 diabetics with dyslipidemia.
    Download PDF (478K)
  • Kazuhisa Mamiya, Mitsuru Nakazawa
    2004 Volume 55 Issue 3-4 Pages 108-114
    Published: 2004
    Released: October 19, 2021
    JOURNAL FREE ACCESS
        Keratan sulfate proteoglycans, such as lumican and keratocan, play an important role in corneal morphogenesis by modulating collagen fibrillogenesis during embryonic development. We examined the role of a highly conserved 37-CX₃CXCX₉C-53 domain adjacent to the N-terminus of lumican in collagen fibrillogenesis, using site-specific mutagenesis to prepare plasmid DNA encoding for wild type (CX₃CXCX₉C) and C/S mutant (Cx₃SXCX₉C) lumican. cDNAs were cloned into a expression vector. Cultures of MK/T-1 cells, an immortalized cell line from mouse keratocytes expressing human telomerase reverse transcriptase were transfected with the cDNAs. Stable transfectants were selected and cloned in the presence of zeocin. The stable transfectants maintain a dendritic morphology similar to the parental MK/T-1 cells. Western blot analysis with antibodies against c-Myc-­tag and lumican detected a 42 kDa lumican protein from the culture medium of the wild type and C/S mutant transfectants. Ultrastructural analyses by transmission electron microscopy (TEM) showed that both cell lines generated a multi-layered stroma in vitro. However, the matrix assembled by the two cell lines differed. Compared to the mutant cell line, the wild type cells assembled a more organized matrix with regions containing orthogonal collagen fibrils. In addition, the fibrils in the extracellular matrix formed by the mutant cell line showed apparent alterations in fibril packing and structure. The results indicate that the lumican C/S mutant may interfere with collagen fibrillogenesis and stromal matrix assembly, potentially due to an alteration in lumican folding.
    Download PDF (652K)
feedback
Top