Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
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Volume 48, Issue 2
Displaying 1-21 of 21 articles from this issue
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Contents
  • Genome analysis of susceptibility genes in autoimmune disease
    -ultimate approach for clarification of the pathogenesis-
    TOSHIKAZU SHIRAI
    2002 Volume 48 Issue 2 Pages 136-143
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.136
    JOURNAL FREE ACCESS
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    Autoimmune disease is a complex multigenic disease. Variable combinations of susceptibility genes at multiple loci determine the diverse autoimmune disease phenotypes. Major genes predisposing to autoimmune diseases are no doubt related to key events in the pathogenesis, and may involve a variety of genes in the immune system. Recently, the application of the polymerase chain reaction and the availability of maps of microsatellites and single nucleotide polymorphisms (SNPs) have facilitated a genome-wide scan to define the number and locations of genes for complex traits. However, the large number of susceptibility loci and the extensive complexity of multi-factorial inheritance have delayed the completion of a genome-wide analysis of loci for human autoimmune diseases. Genetic studies of murine models of autoimmune disease have shed light on these obstacles evident in studies of human diseases. Major genetic loci and several potent candidate polymorphic genes have been identified, particularly in SLE-prone mouse strains. These candidate genes frequently show epistatic interaction in the expression of autoimmune phenotypes, and thus can explain the complexity of their inheritance patterns. Nevertheless, the final identification of the nature and function of the susceptibility genes and their roles in the pathogenesis of SLE need further investigation. The ultimate goal for the identification of susceptibility genes will largely depend on the generation of genetically manipulated mutant mice with homologous recombination of the potential target gene. Such knowledge will lead to elucidation of the genetic and cellular mechanisms involved in the dysregulation of self-reactive lymphocytes in the pathogenesis of autoimmune disease. Prophylactic and therapeutic clinical approaches can then be better designed.
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  • Surgery for portal hypertension and hepato-biliary-pancreatic carcinoma
    SHUNJI FUTAGAWA
    2002 Volume 48 Issue 2 Pages 144-152
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.144
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    [in Japanese]
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  • The research and treatment for corneal disorders
    ATSUSHI KANAI
    2002 Volume 48 Issue 2 Pages 153-164
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.153
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  • Influence of surgical stress on lymphocyte subsets of the Spleen in tumor bearing mice
    MAKO HINO
    2002 Volume 48 Issue 2 Pages 207-215
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.207
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    To investigate the influence of surgical stress, we studied the change of T-lymphocyte subsets, natural killer (NK) cells and NK activity of the spleen using tumor bearing mice. The tumor bearing mice were grouped on the 20th and 25th days after inoculation. Each group, including the control group, which was not inoculated with the tumor cells, were put under surgical stress by means of a laparotomy for 2 hours. The following results were obtained. 1. T-lymphocytes were remarkably reduced alongside tumor progression. 2. On the 20th day after tumor inoculation, surgical stress decreased the positive rate of T-lymphocytes. 3. On the 25th day after tumor inoculation, surgical stress reduced the T-lymphocytes. These results suggest that in the late phase after tumor inoculation, T-lymphocytes of the spleen cannot respond to surgical stress.
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  • Gene expression profile study of corneal endothelium
    NOBUHIKO TACHIBANA, TAKURO FUJIMAKI, SHINJI NAKAMURA, TOSHINARI FUNAKI ...
    2002 Volume 48 Issue 2 Pages 216-225
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.216
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    Objective: We evaluated the gene expression profile of the rabbit corneal endothelium to isolate candidate genes for corneal dystrophies. Materials and methods: We performed a random sequence and homology search analysis of 1,000 clones from the rabbit corneal endothelial cDNA library in the previous study. Forty-five genes, including six unknown genes, were listed as frequently observed cDNAs in the library. We re-analyzed these cDNAs by a similarity search of the latest database, including the human genome sequence. The newly identified genes were selected for further characterization. Results: Two cDNA sequences (C82954 and C83005) showed significant similarity to the newly identified human genes. 1. C82954 showed significant similarity to the human esophageal cancer related gene 4 protein (ECRG4), which was mapped to human chromosome 2. A rabbit cDNA clone, containing a 444 bp open reading frame, was isolated using the 5'rapid amplification of cDNA ends (5'RACE) method. We presumed that the cDNA is a rabbit homologue of ECRG4. The expression of ECRG4 was observed in all the tissues examined using RT-PCR. 2. The human homologue of C83005 was similar to part of the mouse polydomain protein gene (polydom), which was mapped to human chromosome 9. RT-PCR study indicated that the expression of this gene was detected in the corneal endothelium, conjunctiva, tunica mucosa oris, intestine, lung, spleen, and esophagus. In situ hybridization using C83005 as a probe showed the specific labeling of endothelial cells in the cornea and lymphocytes in the spleen. Conclusions: ECRG4 and polydom are possible genes which are highly expressed in the corneal endothelium.
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  • Clinical and histlological phenotype of a macular corneal dystrophy with carbohydrate sulfotransferase gene 6 Arg211Trp mutation.
    HIROO HAYATSU, NOBUKO IIDA, ATSUSHI FURUHATA, KEIKO FUJIKI, AKIRA MURA ...
    2002 Volume 48 Issue 2 Pages 226-232
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.226
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    Objective: Macular corneal dystrophy (MCD) is an autosomal recessive inheritance disorder which manifests bilateral corneal opacity. It has been reported that keratan sulfate side chains on keratan sulfate proteoglycans are not sulfated. Furthermore, a previous study showed decreased sulfotransferase activity in the cornea, which leads to the accumulation of low sulfated keratan sulfate in a MCD cornea. Recently, the corneal N-acetylglucosamine-6-sulfotransferase gene (C-G1cNAc6ST, CHST6) has been identified as the causative gene for MCD. To assess the genetic characteristics of a Japanese family with MCD, we looked for a mutation in the CHST6 gene in patients with MCD. Patients: A patient with MCD and her family were included in this study. Methods: DNA was isolated from peripheral blood cells of the patient and selected relatives. The CHST6 gene was amplified and directly sequenced. Results: Direct sequencing of the CHST6 gene revealed that the patient has a single base-pair substitution, resulting in an amino acid substitution at 211 arginine to tryptophane (Arg211Trp). Conclusion: The patient had no detectable keratan sulfate in the serum and accumulation in the cornea was positively stained with the 1/20-5D4 antibody as in a previous study. Arg211Trp may cause a new variant form of type I MCD.
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  • Dihydropyrimidine dehydrogenase gene expression in patients with hepatocellular carcinoma and metastatic liver cancer
    TAKAHISA SUZUKI, HIROYUKI SUGO, KUNIAKI KOJIMA, MASAKI FUKASAWA, TOMOE ...
    2002 Volume 48 Issue 2 Pages 233-242
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.233
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    Objective: We studied dihydropyrimidine dehydrogenase (DPD) mRNA expression in patients with hepatocellular carcinoma (HCC) and metastatic liver cancer (Meta), and investigated the correlation between DPD activity and mRNA expression. Patients: Sixteen patients with hepatocellular carcinoma and eight patients with metastatic liver cancer (7 colorectal cancers and one breast cancer) were enrolled in this study. Method: The DPDmRNA expression was measured by real time reverse transcription polymerase chain reaction (Real Time RT-PCR), while DPD activity was measured using a radio enzymatic assay. Results: We investigated the correlation between DPD activity and mRNA expression, and a significant linear correlation was observed in the cancerous region (p<0.0001) and the non-cancerous region (p<0.01), in spite of differences in the tumor type. When comparing the DPDmRNA expression between the cancerous region and the non-cancerous region, no significant differences were observed in patients with HCC. However, in patients with Meta, the DPDmRNA expression in the non-cancerous region was significantly higher than that in the cancerous region (p<0.01). The DPDmRNA expression in the cancerous region was significantly higher in HCC patients than in Meta patients (p<0.05). On the other hand, the expression in the non-cancerous region was significantly higher in the Meta patients than in the HCC patients (p<0.05). Regarding the relationship between the clinical-pathological factors and the DPDmRNA expression, a significant correlation was observed between the DPDmRNA expression in the noncancerous region and the preoperative ICG R15 value (r=-0.559, p<0.01). The DPDmRNA expression decreased in patients with liver cirrhosis. These findings indicate that the DPDmRNA expression was influenced by liver function. Conclusion: We consider that 5-FU treatment will not be effective for tumors with a high DPD mRNA expression. Furthermore, adverse effects will easily occur in patients with liver damage. The DPDmRNA expression is considered to be a useful indicator for determining the suitability of chemotherapy in patients with liver cancer.
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  • Problems associated with the emergency system at Juntendo University Urayasu Hospital
    AKIO KIDOKORO, JUN IGARI, TATUJI KANOU, KENJI TAKAMORI, TOSHIHIDE MARU ...
    2002 Volume 48 Issue 2 Pages 243-250
    Published: September 30, 2002
    Released on J-STAGE: November 12, 2014
    DOIhttps://doi.org/10.14789/pjmj.48.243
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    Over the past seventeen years, in the southern regions of Higashikatsushika Chiba and Edogawa-ku Tokyo, Juntendo University Urayasu Hospital has contributed to community medicine, nominally as a secondary emergency hospital, and in practice as a tertiary one. In September 1999, at the request of the communities and government offices in these areas, the hospital launched an emergency medical response system in which physicians work overtime as emergency staff. Intended to reinforce the region's advanced emergency system, the same system had previously been adopted at Juntendo University Hospital. Averaging 8,938 in the years before the introduction of the program, the number of patients treated in the emergency room increased dramatically to 15,264 during the year following the introduction of the emergency medical response system, and to 15,822 in the second year of the program. Similarly, the number of patients transferred to emergency room by ambulance had averaged 1,141 over the previous seven years, but leapt to 2,648 during the year following and to 2,703 in the second year. After averaging 1,225 during the previous seven years, the number of patients admitted to the hospital via the emergency room increased to 1,969 during the year following the introduction of the system, and to 1,978 in the second year. Among the five private university hospitals in Chiba prefecture, Juntendo University Urayasu Hospital had the highest rate of transfers by ambulance and the sharpest increase in emergency transfers after the introduction of this system. At this juncture, it is important that we continue discussions within the hospital on the future direction of the emergency system at Juntendo University Urayasu Hospital.
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