Search PubMed⌕ Search

Biomedical subjects

Y Matsuo

Publications and source records attributed to Y Matsuo.

At least 55 records · Page 3Linked to original sources
PubMed2001

[A case of spinal dural AVF treated by endovascular embolization].

Here we report a case of spinal dural arteriovenous fistula(AVF) treated by endovascular embolization. A 58-year-old female presented with progressive intermittent claudication and numbness of the lower extremities. MRI showed swelling of the spinal cord with intramedullary high signal intensity on T2-weighted image and intramedullary enhancement, suggested spinal cord myelopathy. Myelography demonstrated the dilated serpentine vessels in the subarachnoid space and focal filling defect. Angiography showed spinal dural AVF fed by bilateral lateral sacral artery. The draining vein was posterior spinal vein. Endovascular embolization using liquid material was performed under general anesthesia. The injection of glue included the distal feeding artery, the shunt itself and the initial part of draining vein. A complete cure was achieved, with a normal postoperative angiogram. MRI returned to normal with complete disappearance of T2 high signal, cord enlargement and enhancement by contrast medium. It was suggested that venous congestion induced the transient spinal ischemia, manifested as intermittent claudication. Endovascular embolization using liquid material was safe and quite effective for spinal dural AVF.

Central Nervous System Vascular Malformations↗
PubMed2001

Clinicopathological and molecular evidence indicating the independence of bronchioloalveolar components from other subtypes of human peripheral lung adenocarcinoma.

Although human lung adenocarcinoma has diverse histological subtypes, the correlation between histological subtypes and occurrence of the p53 gene mutation has been given less attention. We investigated 145 surgically resected lung adenocarcinomas to search for the incidence of p53 mutations and for record data on survival in each histological subtype, according to the new WHO criteria (1999). The frequency of p53 mutation in bronchioloalveolar carcinoma (BAC; 0% in 17 cases) and BAC with invasive growth component (BAC-invasive; 11% in 27 cases), which is conventionally categorized as the mixed subtype in WHO typing, were apparently significantly lower than in other types (non-BAC including acinar, papillary, solid, or mixed histology with these subtypes; 48% in 101 cases; P < 0.01). Multivariate analysis revealed that the histological subtype including BAC-invasive was a strong, independent, and significant prognostic factor (P < 0.03), as were tumor size and pathological stage (P < 0.001 and 0.002, respectively) for overall survival. However, the occurrence of p53 mutation itself was seen to be significant only in case of the univariate analysis. Therefore, histological subtyping may be a better prognostic indicator than is p53 mutation. These findings suggest that the WHO classification with the BAC and BAC-invasive from other histological subtypes may prove useful to predict the outcome for surgically treated patients with lung adenocarcinoma.

Adenocarcinoma↗
PubMed2000

Structure, expression, and chromosomal localization of the human gene encoding a germinal center-associated nuclear protein (GANP) that associates with MCM3 involved in the initiation of DNA replication.

A 210kDa protein named GANP is upregulated in germinal center (GC)-B cells in the spleen of antigen-immunized mouse. We studied a human ganp gene (hganp) encoding a putative polypeptide of 1980 amino acids. The carboxyl-terminal 721-amino-acid sequence of hGANP is identical to Map80, that is presumably generated by alternative splicing of hganp/Map80 gene. The genomic segment carrying hganp and Map80 genes was isolated, and the chromosomal location was determined on 21q22.3. Northern blot analysis with RNAs from various organs demonstrated a single band of 7kb hganp mRNA, which suggests a preferential transcription of hganp gene from the hganp/Map80 locus. The hGANP expression was upregulated in GCs of the tonsil, as demonstrated by in-situ RNA hybridization and immunohistochemical analyses. The hGANP, with the domain (Map-box) capable of binding to MCM3 in B cells, might be involved in regulation of cell-cycle progression and DNA replication of GC-B cells.

Acetyltransferases↗
PubMed2000

A Di-leucine signal in the ubiquitin moiety. Possible involvement in ubiquitination-mediated endocytosis.

Some plasma membrane receptors in yeast are known to be internalized and degraded in lysosomes upon ligand-dependent ubiquitination. However, the role of ubiquitination in endocytosis and lysosomal degradation in higher eukaryotes has been controversial. In order to directly assess this question, we investigated the fate of chimeric molecules in which ubiquitin moiety was fused in-frame to the cytoplasmic region of membrane proteins. The chimeric proteins with the wild-type ubiquitin were endocytosed and delivered to lysosomes efficiently. Mutant ubiquitin with lysine-to-arginine substitution could still mediate endocytosis, suggesting that polyubiquitination is not required for the endocytosis. We next searched for the existence of an endocytosis signal(s) in the ubiquitin moiety, and identified a di-leucine signal, Leu(43)-Ile(44). The Leu(43)-Ile(44) sequence mediated endocytosis and lysosomal sorting in a Leu(43)-dependent manner. These results suggest that the di-leucine signal in ubiquitin can be involved in ubiquitination-mediated endocytosis and lysosomal targeting of membrane proteins.

Amino Acid Sequence↗
PubMed2000

Cigarette smoking and risk for impaired fasting glucose and type 2 diabetes in middle-aged Japanese men.

BACKGROUND: The contribution of cigarette smoking to development of impaired fasting glucose and type 2 diabetes remains unclear. OBJECTIVE: To investigate the association of cigarette smoking with development of impaired fasting glucose and type 2 diabetes. DESIGN: Prospective cohort study. SETTING: Work site in Osaka, Japan. PARTICIPANTS: 1,266 Japanese male office workers 35 to 59 years of age who did not have impaired fasting glucose or type 2 diabetes and were not taking medication for hypertension at study entry. MEASUREMENTS: Fasting plasma glucose levels were measured at annual health examinations from May 1994 through May 1999. Impaired fasting glucose was defined as a fasting glucose level of at least 6.1 mmol/L (110 mg/dL) but less than 7.0 mmol/L (126 mg/dL). Type 2 diabetes was defined as a fasting glucose level of 7.0 mmol/L or more or current receipt of hypoglycemic medication. RESULTS: 87 and 54 men developed impaired fasting glucose and type 2 diabetes during 5,817 and 5,937 person-years follow-up, respectively. After controlling for potential predictors of diabetes, the relative risk for impaired fasting glucose compared with never-smokers was 1.62 (95% CI, 0.85 to 3.10) for ever-smokers, 1.14 (CI, 0.58 to 2.25) for persons who smoked 1 to 20 cigarettes/d, 1.33 (CI, 0.63 to 2.80) for those who smoked 21 to 30 cigarettes/d, and 2.56 (CI, 1.32 to 4.95) for those who smoked 31 or more cigarettes/d (P for trend for current smokers only = 0.013). The respective multivariate-adjusted relative risks for type 2 diabetes compared with never-smokers were 1.08 (CI, 0.34 to 3.42), 1.88 (CI, 0.71 to 5.00), 3.02 (CI, 1.15 to 7.94), and 4.09 (CI, 1.62 to 1,029) (P for trend for current smokers only < 0.001). The number of pack-years of exposure was also positively related to development of impaired fasting glucose and type 2 diabetes (P for trend = 0.039 and 0.002, respectively). The relative risk for impaired fasting glucose and type 2 diabetes in current smokers versus never-smokers was stronger among men with a body mass index less than 242 kg/m2 than among men with a body mass index of 24.2 kg/m2 or more, although the absolute risk was greater in more obese men. CONCLUSION: The number of cigarettes smoked daily and the number of pack-years of exposure seem to be associated with development of impaired fasting glucose and type 2 diabetes in middle-aged Japanese men.

Adult↗
PubMed2000

omega-agatoxin IVA-sensitive Ca(2+) channel blocker, alpha-eudesmol, protects against brain injury after focal ischemia in rats.

omega-Agatoxin IVA-sensitive Ca(2+) channels have been thought to be involved in physiological excitatory amino acid glutamate release and these channels may also contribute to the development of ischemic brain injury. Recently, we demonstrated that alpha-eudesmol from Juniperus virginiana Linn. (Cupressaceae) inhibits potently the presynaptic omega-agatoxin IVA-sensitive Ca(2+) channels. In the present study, we investigated the effects of alpha-eudesmol on brain edema formation and infarct size determined after 24 h of reperfusion following 1 h of middle cerebral artery occlusion in rats. We first found that alpha-eudesmol concentration-dependently inhibited glutamate release from rat brain synaptosomes and that its inhibitory effect was Ca(2+)-dependent. In the middle cerebral artery occlusion study, intracerebroventricular (i.c.v.) treatment with alpha-eudesmol significantly attenuated the post-ischemic increase in brain water content. alpha-Eudesmol also significantly reduced the size of the infarct area determined by triphenyltetrazolium chloride staining after 24 h of reperfusion. Using a microdialysis technique, we further demonstrated that alpha-eudesmol inhibits the elevation of the extracellular concentration of glutamate during ischemia. From these results, we suggest that alpha-eudesmol displays an ability to inhibit exocytotic glutamate release and to attenuate post-ischemic brain injury.

Animals↗
PubMed2000

Evolutionary change of codon usage for the histone gene family in Drosophila melanogaster and Drosophila hydei.

The nucleotide divergence in the protein-coding region for replication-dependent and replication-independent histone 3 and 4 genes of Drosophila melanogaster and Drosophila hydei occurred mostly at the synonymous site. Therefore, the pattern of codon usage was analyzed in the two species, considering the genomic codon bias, which is proposed for estimating the genomic composition pressure in the protein-coding regions. The results indicated that the codon usage in the histone gene family could be explained mostly by the genomic codon bias. However, biases for Ala and Arg were commonly observed for the histone 3 and histone 4 gene families, and biases for Ser, Leu, and Glu were observed in a gene-specific manner. This suggests that both genomic codon bias and gene- or codon-specific bias are responsible for the nucleotide differentiation in the protein-coding region of the histone genes.

Animals↗
PubMed2000

Molecular evolution of the histone 3 multigene family in the Drosophila melanogaster species subgroup.

Molecular evolution of the histone multigene family was studied by cloning and sequencing regions of the histone 3 gene in the Drosophila melanogaster species subgroup. Analysis of the nucleotide substitution pattern showed that in the coding region synonymous changes occurred more frequently to A or T in contrast to the GC-rich base composition, while in the 3' region the nucleotide substitutions were most likely in equilibrium. These results suggested that the base composition at the third codon position of the H3 gene, i.e., codon usage, has been changing to A or T in the Drosophila melanogaster species subgroup.

Animals↗
PubMed2000

Angiosarcoma associated with chronic lymphedema (Stewart-Treves syndrome) of the leg: MR imaging.

Magnetic resonance (MR) imaging findings of two patients with Stewart-Treves syndrome are presented. MR imaging showed edematous changes in the subcutaneous fat and skin masses that proved to be angiosarcomas. MR signal intensity of the tumor was low compared with fat on T1-weighted images and intermediate and heterogeneous on T2-weighted images. In one patient, administration of intravenous Gd-DTPA showed marked enhancement in the early phase, which persisted until the delayed phase. These finding on dynamic MR imaging may reflect the abundant vascular spaces seen in these tumors.

Aged↗
PubMed2000

Internal hernia with triple hiatus of congenital origin: report of a case.

We report herein the case of a 65-year-old woman who was referred to our department with prolonged ileus symptoms despite conservative therapy. A plain abdominal radiograph showed intestinal gas shadows with an air-fluid level in the lesser curvature of the stomach. As no improvement was achieved by the insertion of a short tube, a long tube was inserted. A loop formation of the long tube in the subphrenic region was detected on an abdominal radiograph, and an enterogram showed an interruption in the ileum in the lower abdomen. The patient was diagnosed as having an adhesional ileus and a strangulated ileus due to a lesser sac hernia. A laparotomy was performed which revealed that the small intestine had herniated into the lesser sac space through a hiatus of Treitz' fossa and a hiatus in the transverse mesocolon. Furthermore, part of the small intestine had herniated through an omental hiatus. The herniated intestine was manually reduced and the hiatus was closed. However, as the right ovary was found to have adhered to the ileum and stenosis was seen, we were forced to perform partial resection of the ileum. Considering that this patient had no history of laparotomy in the upper abdomen, abdominal injury, or acute abdomen, it was surmised that the three abnormal hiatuses were congenital.

Aged↗
PubMed2000

Malignant hematopoietic cell lines: in vitro models for the study of multiple myeloma and plasma cell leukemia.

Multiple myeloma (MM) is a neoplasm of a terminally differentiated B-cell. The disease is progressive and always lethal characterized by the slow proliferation of malignant plasma cells in the bone marrow. Much of our current understanding of the biology of MM has been obtained by studying MM-derived cell lines. Human myeloma cell lines were shown to be suitable model systems for use in various fields of the biological sciences. However, it has proved very difficult to establish cell lines from plasma cell dyscrasias. Most reported MM cell lines have been derived from patients with advanced disease and from extramedullary sites. Nevertheless, within the last 20 years more than 100 cell lines have been established. A significant portion of this panel is partially or well characterized with regard to their cell culture, clinical, immunophenotypic, cytogenetic and functional features. Distinct immunoprofiles could be assigned to MM cell lines. All MM cell lines display chromosomal aberrations; in more than 80% of the cell lines analyzed, chromosome 14 band q32 (immunoglobulin heavy chain locus) is affected; the various types of 14q+ chromosomes showed different distributions among the MM cell lines. A large percentage of MM cell lines is constitutively interleukin-6-dependent or responsive to various cytokines. It is important to realize that not every cell line established from a patient with myeloma is a neoplastic cell line. So-called 'myeloma cell lines' have been previously reported and are still widely used which are in reality Epstein-Barr virus (EBV)-positive B-lymphoblastoid cell lines. The presence of the EBV-genome in residual normal B-cells provides them with a selective growth advantage after explantation. In summary, a significant number of authentic and well-characterized MM cell lines has been established and described. The availability of these bona fide MM cell lines is of great importance for the study of the biology, etiology and treatment of the disease.

Hematopoiesis↗
PubMed2000

Antimicrobial susceptibilities and serotypes of Streptococcus pneumoniae in southwestern Japan and correlation of penicillin-binding protein 2b and 2x mutations in susceptibilities of penicillin G and cefotaxime.

MICs of penicillin G and other drugs and serotypes were determined for 218 strains of Streptococcus pneumoniae isolated from children in southwestern Japan. Twenty-one (9.6%) and 81 (37.2%) isolates were penicillin-resistant (MIC >/=2.0 microg/ml) and intermediate (MIC 0.13-1.0 microg/ml), respectively. Panipenem was most active parenteral agent against penicillin-intermediate (MIC(90) 0.125 microg/ml) and -resistant strains (MIC(90) 0.25 microg/ml). Among oral beta-lactam agents, cefditoren had good activity against penicillin-intermediate and resistant strains (MIC(90) 0.5/1.0 microg/ml). Serogroup 6 was the most prevalent (65/218) among all strains and 19F (44 strains) was the most prevalent among penicillin-intermediate and -resistant strains. Both pbp2b resistant and susceptible genes were found in penicillin-intermediate strains. Pbp2x resistant genes were found in 33 of 80 (41.3%) cefotaxime-susceptible strains. These results suggest that possible resistance mechanisms may occur even in drug susceptible strains and that drug susceptibility survey should be updated carefully in Japan.

Aminoacyltransferases↗
PubMed2000

Structural genomics projects in Japan.

Two major structural genomics projects exist in Japan. The oldest, the RIKEN Structural Genomics Initiative, has two major goals: to determine bacterial, mammalian, and plant protein structures by X-ray crystallography and NMR spectroscopy and to perform functional analyses with the target proteins. The newest, the structural genomics project at the Biological Information Research Center, focuses on human membrane proteins.

Animals↗
PubMed2000

p53 alterations in human leukemia-lymphoma cell lines: in vitroartifact or prerequisite for cell immortalization?

Alteration of the p53 gene is one of the most frequent events in human tumorigenesis. The inactivation of p53 tumor suppressor function can be caused by chromosome deletion, gene deletion, or mainly by point mutations. p53 mutations occur moderately often in hematopoietic malignancies. A significantly higher frequency of p53 alterations in cell lines vs primary samples has been observed for all types of malignant hematopoietic cell lines. It has been postulated that p53 gene abnormalities arise in cell lines during in vitro establishment of the culture or prolonged culture; but it is also conceivable that those cases that carry p53 mutations may be more suitable for in vitro establishment as permanent cell lines. We analyzed data on the p53 gene status in a panel of matched primary hematopoietic tumor cells and the respective cell lines derived from this original material. In 85% (53/62) of the pairs of matched primary cells and cell lines, the in vivo and in vitro data were identical (both with p53 wild-type or both with the same p53 mutation). In some instances, serial clinical samples (eg at presentation and relapse) and serial sister cell lines were available. These cases showed that a clinical sample at presentation often had a p53 wild-type configuration whereas the derived cell line and a relapse specimen carried an identical p53 point mutation. These findings suggest that a minor clone, at first undetectable by standard analysis, represents a reservoir for the outgrowth of resistant cells in vivo and also a pool of cells with a growth advantage in vitro, providing a significantly higher chance of immortalization in culture. This was further supported by studies employing mutant allele-specific gene amplifications, a technique which is significantly more sensitive (100- to 1000-fold) than the commonly applied SSCP assay with a sensitivity threshold of about 10% mutated cells within a pool of wild-type cells. Taken together, this analysis confirms the usefulness of human hematopoietic cell lines as in vitro model systems for the study of the biology of hematopoietic malignancies. It further underlines the notion that p53 gene alterations confer a survival advantage to, at least some, malignant cells in vitro and presumably also in vivo; however, it is highly unlikely that a p53 mutation alone would suffice for the immortalization of a cell line in vitro or tumor development in vivo. Leukemia (2000) 14, 198-206.

Adolescent↗
PubMed2000

A novel natural killer cell line (KHYG-1) from a patient with aggressive natural killer cell leukemia carrying a p53 point mutation.

We present the establishment of a natural killer (NK) leukemia cell line, designated KHYG-1, from the blood of a patient with aggressive NK leukemia, which both possessed the same p53 point mutation. The immunophenotype of the primary leukemia cells was CD2+, surface CD3-, cytoplasmic CD3epsilon+, CD7+, CD8alphaalpha+, CD16+, CD56+, CD57+ and HLA-DR+. A new cell line (KHYG-1) was established by culturing peripheral leukemia cells with 100 units of recombinant interleukin (IL)-2. The KHYG-1 cells showed LGL morphology with a large nucleus, coarse chromatin, conspicuous nucleoli, and abundant basophilic cytoplasm with many azurophilic granules. The immunophenotype of KHYG-1 cells was CD1-, CD2+, surface CD3-, cytoplasmic CD3epsilon+, CD7+, CD8alphaalpha+, CD16-, CD25-, CD33+, CD34-, CD56+, CD57-, CD122+, CD132+, and TdT-. Southern blot analysis of these cells revealed a normal germline configuration for the beta, delta, and gamma chains of the T cell receptor and the immunoglobulin heavy-chain genes. Moreover, the KHYG-1 cells displayed NK cell activity and IL-2-dependent proliferation in vitro, suggesting that they are of NK cell origin. Epstein-Barr virus (EBV) DNA was not detected in KHYG-1 cells by Southern blot analysis with a terminal repeat probe from an EBV genome. A point mutation in exon 7 of the p53 gene was detected in the KHYG-1 cells by PCR/SSCP analysis, and direct sequencing revealed the conversion of C to T at nucleotide 877 in codon 248. The primary leukemia cells also carried the same point mutation. Although the precise role of the p53 point mutation in leukemogenesis remains to be clarified, the establishment of an NK leukemia cell line with a p53 point mutation could be valuable in the study of leukemogenesis.

Antigens, CD↗
PubMed2000

Malignant hematopoietic cell lines: in vitro models for the study of natural killer cell leukemia-lymphoma.

Malignancies involving natural killer (NK) cells are rare disorders. The complexity of NK cell-involving disorders has only recently been appreciated. Modern classifications discern immature (precursor) from mature NK cell leukemias-lymphomas. Continuous NK leukemia-lymphoma cell lines represent important model systems to study these neoplasms. While there are a number of putative NK cell lines which are, however, either not characterized, not immortalized, non-malignant, non-NK, or plain false cell lines, six bona fide malignant NK cell lines have been established and are sufficiently well characterized: HANK1, KHYG-1, NK-92, NKL, NK-YS and YT. Except for YT which was derived from a not further defined acute lymphoblastic lymphoma, these cell lines were established from patients with various NK cell malignancies. Five of the six cell lines are constitutively interleukin-2-dependent. Their immunoprofile is remarkably similar: CD1-, CD2+, surface CD3 (but cytoplasmic CD3epsilon+), CD4-, CD5-, CD7+, CD8-, CD16-, CD56+, CD57-, TCRalphabeta-, TCRgammadelta-, negative for B cell and myelomonocytic markers. The immunoglobulin heavy chain and T cell receptor genes are all in germline configuration. All six lines show complex chromosomal alterations, with both numerical and structural aberrations, attesting to their malignant and monoclonal nature. Functionally, these cells which contain azurophilic granules in their cytoplasm are nearly universally positive in NK activity assays. Three of five cell lines are Epstein-Barr virus-positive (type II latency). The composite data on these six cell lines allow for the operational definition of a typical malignant NK cell line profile. NK leukemia-lymphoma cell lines will prove invaluable for studies of normal and malignant NK cell biology.

Antigens, CD↗