To understand the development of the trabecular meshwork of the eye, floating cellular aggregates (multicellular spheroids) were formed from human trabecular cells in a non-adherent environment of culture and incubated for up to one month. Dissociated trabecular cells formed multicellular spheroids within one day in the non-adherent environment, and apoptosis continued to occur in the spheroids which had been initially filled with cells. The final structure after one month appeared as a meshwork of cells with large extracellular spaces. Epidermal and basic fibroblast growth factor (EGF and bFGF) protected trabecular cells in the spheroids from apoptosis and, as a result, kept the spheroids filled with cells even after one month. In the absence of excess EGF or bFGF, the multicellular spheroids grown in vitro from human trabecular cells mimicked the mesh-like structure of normal trabecular tissue. In constrast, under an excess of these growth factors, spheroids of high cellularity, resembling the abnormal trabecular tissues of patients with congenital glaucoma, were formed.
en-copyright= kn-copyright= en-aut-name=MatsuoToshihiko en-aut-sei=Matsuo en-aut-mei=Toshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsuoNobuhiko en-aut-sei=Matsuo en-aut-mei=Nobuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University en-keyword=human trabecular cells kn-keyword=human trabecular cells en-keyword=multicellular spheroids kn-keyword=multicellular spheroids en-keyword=basic fibroblast growth factor kn-keyword=basic fibroblast growth factor en-keyword=epidermal growth factor kn-keyword=epidermal growth factor en-keyword=histology kn-keyword=histology END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=233 end-page=236 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Cancer cachexia and depressive states: a neuro-endocrine-immunological disease? en-subtitle= kn-subtitle= en-abstract= kn-abstract=Plasma 5-hydroxytryptamine (serotonin), tryptophan, neopterin and cortisol levels were measured in patients with depressive cancer cachexia and in healthy controls during the same time period. Patients with advanced cancers had significantly raised neopterin, a marker of endogenous gamma-interferon (IFN-γ) production, and cortisol values, but decreased serotonin and tryptophan levels. Much work has been done to elucidate the possible role of serotonin in depressive states. IFN-γ induces a high level of indoleamine dioxygenase (IDO), a tryptophan degrading enzyme, and high cortisol levels induce high tryptophan oxygenase activity, which in turn increases metabolism along the tryptophannicotinic acid pathway. These results suggest that persistent immune activation and intense adrenal activity occur in patients with cancer cachexia, resulting in disorders involving tryptophan metabolism followed by depression in cancer cahexia.
en-copyright= kn-copyright= en-aut-name=IwagakiHiromi en-aut-sei=Iwagaki en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HizutaAkio en-aut-sei=Hizuta en-aut-mei=Akio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UomotoMasashi en-aut-sei=Uomoto en-aut-mei=Masashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakeuchiYoshiaki en-aut-sei=Takeuchi en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SaitoShinya en-aut-sei=Saito en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University en-keyword=cancer cachexia kn-keyword=cancer cachexia en-keyword=neuro-endocrine-immune interactio kn-keyword=neuro-endocrine-immune interactio en-keyword=serotonin kn-keyword=serotonin en-keyword=neopterin kn-keyword=neopterin en-keyword=cortisol kn-keyword=cortisol END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=173 end-page=178 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Mental deterioration in childhood epilepsy en-subtitle= kn-subtitle= en-abstract= kn-abstract=Mental retardation is detected in 20-30% of children with epilepsy at hospitals specializing in treatment of childhood epilepsy. However, the incidence of mental deterioration in childhood epilepsy is not high. In this study, mental deterioration was found in 52 (1.8%) of the 2,880 children with epilepsy at Okayama University Hospital. The patients showing mental deterioration mostly suffered from specific epileptic syndromes, such as West syndrome, Lennox-Gastaut syndrome, severe myoclonic epilepsy in infancy and epilepsy with continuous spike-waves during slow wave sleep. These types of epilepsy show generalized electroencephalographic (EEG) abnormalities. It is presumed that mental deterioration is caused by the total effects of prolonged diffuse EEG abnormalities and the age of the patients. Antiepileptic drugs exert a relatively minor effect on mental deterioration.
en-copyright= kn-copyright= en-aut-name=OkaEiji en-aut-sei=Oka en-aut-mei=Eiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SanadaSatoshi en-aut-sei=Sanada en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AsanoTakashi en-aut-sei=Asano en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IshidaTakashi en-aut-sei=Ishida en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=National Hospital of Fukuyama en-keyword=mental deterioration kn-keyword=mental deterioration en-keyword=mental retardation kn-keyword=mental retardation en-keyword=epilepsy kn-keyword=epilepsy en-keyword=EFG kn-keyword=EFG en-keyword=children kn-keyword=children END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=207 end-page=212 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Analysis of the genome of an Epstein-Barr-virus (EBV)-related herpesvirus in a cynomolgus monkey cell line (Si-IIA) en-subtitle= kn-subtitle= en-abstract= kn-abstract=A simian cell line, Si-IIA, harboring Epstein-Barr-virus (EBV) -related herpesvirus (Si-IIA-EBV), produces malignant lymphoma in rabbits when administered by intravenous inoculation. In this study, we analyzed the Si-IIA-EBV genome and compared it with human EBV and herpesvirus macaca fascicularis 1 (HVMF 1 ), which is associated with B-cell lymphoma developing in SIV-infected immunosuppressed monkeys. DNA from Si-IIA-EBV was amplified by the polymerase chain reaction using three different primer pairs complementary to human EBV (B95-8) DNA; two of the primer pairs covered part of the long internal repeat 1 region (IR 1) and the third covered part of the BRRF 1 region. Direct sequencing of the three PCR products revealed that Si-IIA-EBV DNA had about 82% nucleotide homology to the human EBV DNA in all three regions and 92.4% homology to HVMF1 in the IR1 region. The blotting pattern by Southern blot analysis was different between Si-IIA-EBV and human EBV.
en-copyright= kn-copyright= en-aut-name=InoHideo en-aut-sei=Ino en-aut-mei=Hideo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKazuhiko en-aut-sei=Hayashi en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YanaiHiroyuki en-aut-sei=Yanai en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TeramotoNorihiro en-aut-sei=Teramoto en-aut-mei=Norihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KoiralaTirtha Raj en-aut-sei=Koirala en-aut-mei=Tirtha Raj kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChenHong-Li en-aut-sei=Chen en-aut-mei=Hong-Li kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TakahashiKiyoshi en-aut-sei=Takahashi en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=AkagiTadaastu en-aut-sei=Akagi en-aut-mei=Tadaastu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University en-keyword=Epstein-Barr virus kn-keyword=Epstein-Barr virus en-keyword=HVMF 1 kn-keyword=HVMF 1 en-keyword=lymphoma kn-keyword=lymphoma en-keyword=?monkey cell line kn-keyword=?monkey cell line en-keyword=PCR kn-keyword=PCR END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=195 end-page=206 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=cDNA cloning, sequence analysis and expression of a mouse 44-kDa nuclear protein copurified with DNA repair factors for acid-depurinated DNA en-subtitle= kn-subtitle= en-abstract= kn-abstract=We purified a 44-kDa nuclear protein from salt-extract of permeable mouse ascites sarcoma cells in an effort to isolate factors involved in the repair of acid-depurinated DNA. It was copurified with a major AP endonuclease (APEX nuclease) by sequential column chromatography then further purified by sodium dodecyl sulphate-poly-acrylamide gel electrophoresis as a possible DNA repair support factor. Its partial amino acid sequences were determined, and a cDNA clone for the protein was isolated from a mouse T-cell cDNA library using long degenerate oligonucleotide probes deduced from the amino acid sequence. The complete nucleotide sequence of the cDNA (1.7 kilobases) was determined. Northern hybridization using this cDNA detected two transcripts: 1.8kb being the major one and 2.6 kb being the minor one. The complete amino acid sequence for the protein predicted from the nucleotide sequence of the cDNA indicates that the 44-kDa protein consists of 394 amino acids with a calculated molecular weight of 43,698. In tests performed thus far, the recombinant 44-kDa protein expressed in Escherichia coli has not expressed any repair-support activity. It remains to be analyzed whether the protein attains this activity after appropriate posttranslational modifications. Most parts of the 44-kDa protein cDNA and the deduced amino acid sequence were found to be identical to those of the protein p38 -2G4, recently reported as a cell cycle-specifically modulated nuclear protein of 38kDa. The p38-2G4 may be a truncated form of the present 44-kDa protein.
en-copyright= kn-copyright= en-aut-name=NakagawaYuko en-aut-sei=Nakagawa en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=WatanabeSekiko en-aut-sei=Watanabe en-aut-mei=Sekiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AkiyamaKosuke en-aut-sei=Akiyama en-aut-mei=Kosuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SarkerAltaf H en-aut-sei=Sarker en-aut-mei=Altaf H kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TsutsuiKen en-aut-sei=Tsutsui en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=InoueHajime en-aut-sei=Inoue en-aut-mei=Hajime kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SekiShuji en-aut-sei=Seki en-aut-mei=Shuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University en-keyword=44-kDa protein kn-keyword=44-kDa protein en-keyword=nuclear protein kn-keyword=nuclear protein en-keyword=cDNA cloning kn-keyword=cDNA cloning en-keyword=cDNA sequencing kn-keyword=cDNA sequencing en-keyword=recombinant protein kn-keyword=recombinant protein END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=179 end-page=194 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Evaluation of exposure to mixed solvents by analysis of urinary metabolites and solvents: content ranges en-subtitle= kn-subtitle= en-abstract= kn-abstract=To evaluate worker's exposure to mixed solvents, equations for the calculation of the biological hazard index, which is defined as biological levels tolerable for exposure to mixture, were developed. When biological levels of exposure indicators were not affected by coexposure, rules similar to those for airborne monitoring could be applied. Namely, when the components had additive effects, the biological hazard index was calculated from the concentration of urinary metabolites or parent solvents, by an equation which was essentially similar to the equation for the calculation of the hazard index. In the present study, the confidence limits of the biological hazard index and predictive limits for individual specimens were calculated. These equations could be used under the condition that the uptake, metabolism and elimination of solvents were practically unaffected by coexposure. When urinary metabolites or solvents of some components of a mixed solvent alone were determined and those of the remaining components were not determined, the concentration of urinary metabolites or solvents of remaining components were estimated from the airborne concentration of the other components.
en-copyright= kn-copyright= en-aut-name=OgataMasana en-aut-sei=Ogata en-aut-mei=Masana kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=Okayama University en-keyword=evaluation kn-keyword=evaluation en-keyword=coexposure kn-keyword=coexposure en-keyword=organic solvents kn-keyword=organic solvents en-keyword=urinary metabolites kn-keyword=urinary metabolites en-keyword=content ranges kn-keyword=content ranges END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=227 end-page=232 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Establishment of a new myeloid cell line with i(17q) as the sole chromosomal anomaly from the bone marrow of a patient with myelodysplastic syndrome en-subtitle= kn-subtitle= en-abstract= kn-abstract=A new myeloid cell line, MTO-94, was established from the bone marrow of a patient with myelodysplastic syndrome (MDS). MTO-94 cells matured in culture medium without the addition of growth factors, and yielded neutrophils with pseudo-Pelger Huët anomaly or hypersegmentation until 6 months. Ten months after the start of cell cultivation, MTO-94 consisted of myeloblasts. Surface phenotypes were as follows: CD7 90.3%, CD13 99.6%, CD33 75.6%, HLA-DR 96.3% and CD34 0.9%. The karyotype was 46, XY, i(17q). The proliferation of MTO-94 cells was enhanced by rhlL-3, G-CSF, rhGM-CSF and rhSCF but not by rhlL-6 and erythropoietin. MTO-94 cells with i(17q) might be useful in the study of biological aspects of not only MDS, but also hematological malignancies with i(17q) as the sole chromosomal anomaly.
en-copyright= kn-copyright= en-aut-name=MizobuchiNoriko en-aut-sei=Mizobuchi en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakahashiIsao en-aut-sei=Takahashi en-aut-mei=Isao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HorimiTadashi en-aut-sei=Horimi en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamamotoMegumi en-aut-sei=Yamamoto en-aut-mei=Megumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HamadaKyoko en-aut-sei=Hamada en-aut-mei=Kyoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YorimitsuSeiichi en-aut-sei=Yorimitsu en-aut-mei=Seiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KubonishiIchiro en-aut-sei=Kubonishi en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Kochi Municipal Central Hospital affil-num=2 en-affil= kn-affil=Kochi Municipal Central Hospital affil-num=3 en-affil= kn-affil=Kochi Municipal Central Hospital affil-num=4 en-affil= kn-affil=Kochi Municipal Central Hospital affil-num=5 en-affil= kn-affil=Kochi Municipal Central Hospital affil-num=6 en-affil= kn-affil=Kochi Municipal Central Hospital affil-num=7 en-affil= kn-affil=Kochi Medical School en-keyword=isochromosome 17q kn-keyword=isochromosome 17q en-keyword=myeloid cell line kn-keyword=myeloid cell line en-keyword=myelodysplastic syndrome kn-keyword=myelodysplastic syndrome END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=4 article-no= start-page=219 end-page=225 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199708 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The role of three-dimensional computed tomography in the management of maxillofacial bone fractures en-subtitle= kn-subtitle= en-abstract= kn-abstract=The findings of three-dimensional computed tomography (3DCT) and two-dimensional computed tomography (2DCT) with helical CT scanning were compared for 21 patients with maxillofacial bone fractures. The results of this study suggest that the 3DCT evaluation can be divided into 3 groups. The first group, in which 3DCT is superior to 2DCT, includes severe complicated midface fractures, for example, tripod fractures and complicated maxillary bone fractures. The second group, in which 3DCT is equal to 2DCT, includes simple fractures, for example, nasal bone fractures and isolated zygomatic fractures. In this group, patients and their families could easily understand the nature of the fracture and clinical course shown by 3DCT as compared with conventional X-ray and 2DCT. The third group, in which 3DCT is inferior to 2DCT, includes blowout fractures. Although 3DCT does not provide additional information in blowout fractures, helical scanning permits clear observation of multiplanar images without artifacts arising from metal prostheses by excluding lower slices during image reconstruction. We conclude that 3DCT provides useful information, especially in regard to the extent of complex fracture lines, as in tripod fractures.
en-copyright= kn-copyright= en-aut-name=OhkawaMotoomi en-aut-sei=Ohkawa en-aut-mei=Motoomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TanabeMasatada en-aut-sei=Tanabe en-aut-mei=Masatada kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ToyamaYoshihiro en-aut-sei=Toyama en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KimuraNaruhide en-aut-sei=Kimura en-aut-mei=Naruhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=UematsuKoji en-aut-sei=Uematsu en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SatohGen en-aut-sei=Satoh en-aut-mei=Gen kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Kagawa Medical University affil-num=2 en-affil= kn-affil=Kagawa Medical University affil-num=3 en-affil= kn-affil=Social Health Insurance Ritsurin Hospital affil-num=4 en-affil= kn-affil=Social Health Insurance Ritsurin Hospital affil-num=5 en-affil= kn-affil=Social Health Insurance Ritsurin Hospital affil-num=6 en-affil= kn-affil=Social Health Insurance Ritsurin Hospital en-keyword=3DCT kn-keyword=3DCT en-keyword=helical CT kn-keyword=helical CT en-keyword=maxillofacial bone fractures kn-keyword=maxillofacial bone fractures en-keyword=facial bone fractures kn-keyword=facial bone fractures END