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Biomedical subjects

S Akizuki

Publications and source records attributed to S Akizuki.

At least 73 records · Page 4Linked to original sources

Parainfluenza virus pneumonitis in an adult.

Parainfluenza virus uncommonly causes fatal giant cell pneumonia in immunocompromised infants and children. To our knowledge, this is the first adult case of parainfluenza virus pneumonia. A 77-year-old woman who was diagnosed as having small-cell carcinoma of the lung underwent chemotherapy. She died of lung edema. Analysis of her serum showed antibodies to parainfluenza virus types 2 and 3 at titers of 1:64 and 1:128, respectively. The postmortem examination revealed giant cell pneumonia, in which giant cells and detached alveolar lining cells had intracytoplasmic inclusions. On electron microscopic examination, the intracytoplasmic inclusions contained fuzzy-form nucleocapsids.

Aged↗

[A case of systemic lupus erythematosus complicated with pulmonary hypertension and massive pericardial effusion].

A 22 year-old-female had suffered from polyarthralgia and Raynaud's phenomenon since 1984. In 1986, she was diagnosed as systemic lupus erythematosus (SLE). In April 1988, she was admitted to Kawasaki Municipal Hospital because of fever and dyspnea on exertion (DOE). Physical examination showed high fever, butterfly rash, oral ulcer and elevation of heart sound IIp on auscultation. Laboratory findings revealed that erythrocyte sedimentation rate was elevated to 105 mm/hr. The following values were observed, anti DNA antibody 391 IU/ml, serum IgA 5mg/dl, anti IgA antibody weakly positive. Chest X ray showed CTR 65%. Echo cardiogram showed massive pericardial effusion. 201T1 myocardial SPECT revealed right ventricular pressure over loading. PSL 40 mg/day was started to administer for the massive pericardial effusion due to SLE activities. On 6th of June, right heart catheterization confirmed the pulmonary hypertension (PPA 22 mmHg, Pulmonary artery resistance (PAR) 1163 dyne/sec/cm-5/mm2). By the treatment with PSL, massive pericardial effusion was gradually improved but DOE clinically unchanged. Second right heart catheterization was done on 8th of August. PAR was improved to 895 dyne/sec/cm-5/mm2 but PPA was elevated to 26 mmHg. It is very interesting that PPA was elevated although PAR was improved by PSL therapy. It is considered that the increase in venous return which was caused by improvement of massive pericardial effusion induced conversely the elevation of PPA. Additionally she was complicated with IgA deficiency. It may occur not only by the immunogenetical disorder such as HLA or IgG subclass alteration but also by anti IgA antibody or lymphocytes dysfunction complicated with SLE.

Adult↗

The mouse osteopontin gene. Expression in monocytic lineages and complete nucleotide sequence.

Murine macrophage cell lines and resident macrophages showed various levels of expression of the murine osteopontin (OP) gene, and macrophage stimulating agents were found to enhance transcription of the gene with kinetics which are unique for each stimulator. The organization of the murine OP gene was determined. The gene comprises six exons and five introns and spans approximately 4.8 kilobases. Exon 1 contains the 16 amino acids of the leader sequence. Exons 2, 3, 4, 5, and 6 encode 12, 27, 14, 94, and 129 amino acid residues, respectively. Exon 5 encodes regions containing 10 consecutive Asp amino acid residues and a Gly-Arg-Gly-Asp-Ser peptide. Exon 6 encodes the C-terminal half of OP and contains no 15- and 54-base pair nucleotide sequences which are deleted in murine OP cDNA compared to that of rat OP cDNA. Since Southern blot analysis indicated that the OP gene is a single copy, it is obvious that the murine OP cDNA has the sequence previously determined (Miyazaki, Y., Setoguchi, M., Yoshida, S., Higuchi, Y., Akizuki, S., and Yamamoto, S. (1989) Nucleic Acids Res. 17, 3298). A comparison with the cDNA sequences reported previously suggested the presence of nucleotide sequence polymorphisms. The 5' end of the murine OP gene was defined by primer extension and S1 nuclease mapping. Sequence analysis of the 5'-flanking DNA revealed the presence of many potential regulatory motifs.

Amino Acid Sequence↗

Molecular cloning of cDNA encoding MS2 antigen, a novel cell surface antigen strongly expressed in murine monocytic lineage.

cDNA clones which strongly hybridized with a 3.1 kb mRNA from mouse macrophages and macrophage cell lines and weakly with mRNA from P815 but not from a variety of other cell lines and tissues were isolated from cDNA libraries constructed using mRNA from murine macrophage cell lines and peritoneal macrophages. Treatment of a macrophage cell line with macrophage stimulators significantly enhanced transcription of the mRNA. Sequencing analysis of these clones demonstrated that the cDNA consisted of 3036 bp insert containing a 2478 bp open reading frame followed by a 538 bp 3' untranslated region. The amino acid sequence, deduced from the nucleotide sequence of the cDNA, predicted a protein containing a signal peptide, an extracellular region, a transmembrane domain, and a cytoplasmic tail. The extracellular region had five putative N-glycosylation sites and a cysteine-rich domain, whereas the cytoplasmic region consisted of a proline-rich amino acid sequence significantly similar to CD2. SDS-PAGE and NEPHGE SDS-PAGE analysis of the immunoprecipitated membrane of the macrophage cell lines prepared by using rabbit anti-MS2 peptide antibody raised against a synthetic peptide preparation relative to a hydrophilic region of the MS2 amino acid sequence confirmed that MS2 protein is a cross-linked protein having approximate molecular sizes of 89 kd and pl 6.5-7.0. These results show that MS2 protein is a novel cell surface antigen expressed mainly in monocytic lineages.

ADAM Proteins↗

Mouse and human CD14 (myeloid cell-specific leucine-rich glycoprotein) primary structure deduced from cDNA clones.

cDNA clones complementary to MS7-4 (Setoguchi et al. (1988) Somat. Cell Mol. Genet. 14, 427-438) from a mouse macrophage cDNA library were separated. Sequence analysis of these clones demonstrated that the longest cDNA clone, MS7X, had a 1366 bp insert and high homology with that of the human CD14 gene (Ferrero and Goyert (1988) Nucleic Acids Res. 16, 4173). Using the MS7X cDNA probe, cDNA clones were separated from cDNA libraries constructed from a human macrophage cell line and macrophages. The total cDNA sequence was 1364 bp in length, with an open reading frame of 1125 nucleotides matching that of the human CD14 gene except for one nucleotide difference. The amino-acid sequence (mouse CD14), deduced from the nucleotide sequence of the MS7X insert consisted of 351 amino-acid residues with a high leucine content (17.66%) and five putative N-glycosylation sites, and in vitro translation predicted a protein of molecular mass of 37.5 kDa. Human CD14 had 356 amino-acid residues, with high leucine content (15.5%), and contained four putative N-glycosylation sites. Mouse CD14 showed 13 building blocks, of which internal nine blocks have a conserved leucine motif and significant homology with human leucine-rich alpha 2-glycoprotein.

Amino Acid Sequence↗

Insertional activation of N-myc by endogenous Moloney-like murine retrovirus sequences in macrophage cell lines derived from myeloma cell line-macrophage hybrids.

Hybrids formed from a myeloma cell line, NS1, and macrophages initially show myeloma properties but later, after loss of the parental macrophage genome and consequent loss of myeloma characteristics, express macrophage properties. Molecular studies demonstrated that macrophage properties in the hybridomas originate from the NS1 parental cells (M. Setoguchi, S. Yoshida, Y. Higuchi, S. Akizuki, and S. Yamamoto, Somatic Cell Mol. Genet. 14:427-438, 1988). In such hybrids, N-myc was activated by insertion of endogenous Moloney-like retrovirus sequences into mouse N-myc exon 3 when the hybrids gained macrophage properties. Interestingly, expression of N-myc took place in all aged hybrids. These results suggest that such unique insertional mutagenesis occurs in a regionally specific manner and that expression of N-myc may play a role in hematopoietic lineage conversion.

Amino Acid Sequence↗

[Quantitative assessment of arterial capacitance in human by noninvasive method].

The purpose of this study was to determine the magnitude of arterial capacitance in human by noninvasive method. In 60 patients (Age: 62.1 +/- 13.4 years) without cardiovascular disease first-pass radionuclide angiography was performed using a digital gamma camera to calculate cardiac output and stroke volume (SV). Systolic interval (ts), diastolic interval (td) and arterial blood pressure were measured using ECG, phonocardiography and sphygmomanometer. We assumed a simple model in which all capacitance (C) lumped into one site with a resistance (R) in parallel to the C. C was calculated by the following basic equations. (Formula; see text) arterial diastolic pressure, E: left ventricular external work. Our results showed: 1) Arterial capacitance ranged from 0.38 ml/mmHg to 2.10 ml/mmHg and more than 60% of stroke volume was pooled in the arterial capacitor during systole. 2) Arterial capacitance fell linearly with age (C = 2.37-0.02 x Age, r = -0.680, p less than 0.001). It is concluded that the capacitor played an important role in arterial circulation.

Adult↗

[An autopsy case of HTLV-I associated myelopathy (HAM)].

An autopsy case of HTLV-I associated myelopathy (HAM) was reported. The patient was a 55-year-old man from Kagoshima, who had no history of blood transfusion. He was admitted to our hospital because of muscle weakness of legs and dysuria, which having since one month ago. On admission, he was able to walk with assistance, but his legs were severely spastic, and Babinski's sign was positive bilaterally. Superficial sensation was normal, but vibration sense was mildly decreased in his legs. CSF showed mild mononuclear pleocytosis with elevated protein. Myelogram and CT were normal. Serum and CSF antibodies to HTLV-I were positive at titers of X4,096 and X128, respectively by immunofluorescent assay, and specific IgG bands (p19, p24, p28 and p53 in serum and p19, p24, p53 in CSF) were detected by western blot analysis. His paraparesis continued to worsen. He became bed-ridden within 2 months. He was received corticosteroid medication. He regained the ability to walk with assistance, and continued taking corticosteroid. In July 4, 1986, macrohematuria appeared and inoperable transitional cell carcinoma of rt. kidney was found by further examination. Chemotherapy were not effective against the carcinoma and he died on July 21, 1987. Neuropathological findings were summarized as follows: cerebral hemisphere was normal except for mild cellular infiltration in the leptomeninges; lesions consisted in unilateral pyramidal tract of pons & medulla and in partial anterior, posterior and lateral columns of the spinal cord; demyelination with axonal degeneration, marked gliosis, numerous lipid-laden macrophages and mild perivascular infiltration of mononuclear cells in these areas.(ABSTRACT TRUNCATED AT 250 WORDS)

HTLV-I Antibodies↗

Molecular analysis of expression of parental cell properties in hybrids between monocytes and a myeloma cell line.

Interspecific hybrid cell lines (HINS lines) between human monocytes and a mouse (H-2d) myeloma cell line, NS1, initially showed myeloma properties, but later expressed macrophage properties, while losing myeloma cell characteristics and undergoing a marked reduction in the number of chromosomes. The aged HINS cells showed mouse but not human phenotypes. Molecular genetic analysis demonstrated loss of BLUR8 genes, expression of mouse macrophage specific genes, and enhanced transcription of H-2d and mouse beta 2-microglobulin genes in the aged cells, confirming that the hybrids' macrophage properties were attributable to NS1 genes. Transcription of kappa light chain genes was not detectable in aged HINS cells, although the genes were retained. Since some rearrangements of the genes were suggested and cycloheximide treatment induced no transcription of the genes, cis mechanisms might be involved in the loss of expression of the genes.

Animals↗

An autopsy case of human T-lymphotropic virus type I-associated myelopathy.

This report describes the first autopsy case of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM). The disease mainly affected the spinal cord, particularly the lateral and anterior columns, where loss of myelin and axon was observed. The changes were bilateral and occurred mainly along the tract. Perivascular and parenchymal infiltration with lymphocytes and macrophages, as well as astrocytosis, were observed in the white and grey matters of the spinal cord. Blood vessels in the spinal cord and in the subarachnoid space of the spinal cord showed hyalinoid thickening of media and adventitia associated with infiltration of lymphocytes. These findings are similar to those of tropical spastic paraparesis (TSP).

Autopsy↗

Enhancement of c-fos expression is associated with activated macrophages.

Unique hybrids (HINS and CANS lines) between macrophages and a myeloma cell line, NS1 initially expressed myeloma functions but later expressed active macrophage functions together with constitutive expression of c-fos gene. Enhancement of c-fos transcription was also observed in activated mouse peritoneal macrophages, and a range of macrophage-stimulating substance was found to induce c-fos transcription kinetic unique to each stimulator including immediate, delayed and prolonged responses in aged HINS-B3 cells, which displayed low levels of steady-state c-fos transcription. It was also found that a significant enhancement of c-fos transcription followed restimulation with either interferon gamma (IFN gamma) or lipopolysaccharide (LPS) after an initial IFN gamma stimulation. Thus it appeared that enhanced c-fos expression was closely connected with macrophage activation. On the other hand, macrophage stimulators suppressed [3H]thymidine incorporation into aged HINS-B3 cells. These results may simply suggest that c-fos expression contributes to macrophase activation but not to cell proliferation. However, it is also possible to speculate that c-fos expression contributes to cell proliferation as a salvage system operating to overcome the suppression during the macrophage activation.

Animals↗