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Biomedical subjects

N Watanabe

Publications and source records attributed to N Watanabe.

At least 595 records · Page 33Linked to original sources
PubMed1995

Brain SPECT with neuro-Behçet disease.

A patient with neuro-Behcet disease is described. SPECT using Tc-99m HMPAO was performed to evaluate brain perfusion. The brain SPECT revealed decreased perfusion in the right frontal, parietal, temporal, and occipital lobes. MRI showed high intensity lesions in the white matter in the right periventricular centrum semiovale and frontal region on T2 weighted images. Gray matter abnormalities were evident on brain SPECT, but not on MRI. Brain SPECT using Tc-99m HMPAO may provide useful clinical information on regional cerebral cortical abnormalities associated with neuro-Behcet disease.

Behcet Syndrome↗
PubMed1995

Discordant findings between krypton-81m gas and Tc-99m labeled ultrafine aerosol lung ventilation SPECT in two patients with idiopathic pulmonary fibrosis.

Technegas, a newly developed ultra-fine dry dispersion of Tc-99m labeled carbon with a particle size of approximately 5 nm to 20 nm, possesses the properties for lung ventilation imaging using SPECT. The authors observed a discrepancy between krypton-81m gas and technegas lung ventilation SPECT in two patients with idiopathic pulmonary fibrosis who demonstrated heterogeneously decreased distribution of technegas without regions of high count density (focal hot spots) of tracer in their lungs in spite of the almost homogenous distribution of krypton-81m gas. This finding could be explained by the duration of radioactive gas inhalation. Technegas lung ventilation SPECT images reflected lung ventilation with tidal breathing. Conversely, Kr-81m gas lung ventilation SPECT images reflected not only lung ventilation, but also lung volumes. These two radioactive agents for lung ventilation SPECT show different findings.

Administration, Inhalation↗
PubMed1995

I-123 MIBG imaging of metastatic carcinoid tumor from the rectum.

I-131 MIBG, a specific radiopharmaceutical agent for scintigraphic imaging and treatment of pheochromocytoma and neuroblastoma may be useful for detection of apudomas. Scintigraphy with I-123 radiolabeled MIBG was performed in a patient with metastatic carcinoid tumor from the rectum. I-123 MIBG scintigraphic findings showed multiple areas of abnormal tumor uptake of hepatic and bone metastases from the rectal carcinoid. Bone scintigraphy demonstrated multiple metastatic lesions. Computed tomography revealed multiple solid tumors of the liver. This report describes accumulation of I-123 MIBG in the liver and bone metastases from the rectal carcinoid. Radioiodine MIBG scintigraphy may be useful for detecting metastatic lesions, for evaluating postoperative recurrence, and also for the treatment of the carcinoid tumor.

3-Iodobenzylguanidine↗
PubMed1995

Increased pulmonary clearance of aerosolized 99Tcm-DTPA in patients with a subset of stage I sarcoidosis.

Measurement of the pulmonary clearance of aerosolized 99Tcm-diethylenetriamine pentaacetate (99Tcm-DTPA) as a marker of pulmonary parenchymal damage was performed in 10 non-smokers with sarcoidosis, none of whom was on medication, and the results compared with 12 normal controls. Posterior images were obtained using a single-headed gamma camera, with the subjects in a supine position, for 30 min after inhalation of aerosolized 99Tcm-DTPA had ceased. The pulmonary clearance of 99Tcm-DTPA was significantly increased in the sarcoidosis patients (57.6 +/- 22.1 min in the right lung, 62.2 +/- 22.7 min in the left lung) compared with the controls (79.3 +/- 10.2 and 78.4 +/- 7.7 min in the right and left lungs, respectively) (P < 0.05). Six of the 10 patients with sarcoidosis showed levels of pulmonary clearance, in both the right and left lungs, below the 95.5% confidence limit (mean +/- 2 S.D.) for the controls. Increased pulmonary clearance of 99Tcm-DTPA was also found in 2 of 4 patients with stage I sarcoidosis. No relationship was found between the pulmonary clearance of 99Tcm-DPTA and inflammatory markers (ACE, lysozyme) in the serum.

Adult↗
PubMed1995

Whole-body 201Tl scintigraphy during one-leg exercise and at rest in normal subjects: estimation of regional blood flow changes.

To determine the effect of exercise intensity on regional blood flow in exercising and resting leg muscles and organs, we assessed relative changes in the regional distribution of 201Tl during one-leg ergometer exercise and at rest by whole-body scintigraphy as an estimate of regional blood flow changes in 10 healthy males. The regional 201Tl activity was expressed as a percentage of the whole-body activity, and relative changes in each region were compared to those at the anaerobic threshold (AT) and at peak exercise. In the legs, the distribution of 201Tl in the exercising thigh and calf increased significantly at the AT to 390.7 and 219.2% respectively of resting levels (both P < 0.01), but remained unchanged the resting thigh from rest to peak exercise. Conversely its distribution in the resting calf decreased significantly at the AT to 60.0% of the resting level (P < 0.01). However, there were no significant differences between AT and peak exercise. In the organs, the distribution of 201Tl in the lung, liver, spleen and kidneys decreased significantly at the AT to 88.4 +/- 10.4%, 67.0 +/- 11.5%, 62.4 +/- 11.8% and 67.0 +/- 8.6% respectively of resting levels (all P < 0.01). Redistribution of blood flow to the exercising leg occurs predominantly during mild to moderate exercise. Therefore, blood flow in the leg during strenuous exercise depends primarily upon an increase in cardiac output. The splanchnic organs are the major sources of redistribution.

Adult↗
PubMed1995

Sequence analyses of human parainfluenza virus type 4A and type 4B fusion proteins.

cDNAs encoding human parainfluenza virus type 4A and type 4B (hPIV-4A and -4B) fusion (F) proteins were cloned and sequenced. The predicted amino acid sequences of the F proteins had similar characteristic traits to those reported for the F proteins of other paramyxoviruses. They were more closely related to the F proteins of simian virus 5 (SV5), mumps virus (MuV), hPIV-2 and Newcastle disease virus (NDV) than to the F proteins of hPIV-1, hPIV-3, Sendai virus (SV) and measles virus (MV). In addition, hPIV-4A, hPIV-4B, SV5 and MuV shared a common feature of genomic organization: there was a small ORF between the F and haemagglutinin-neuraminidase (HN)-coding sequences, implying a common ancestry.

Amino Acid Sequence↗
PubMed1995

Characterization of a novel human tumor necrosis factor-alpha mutant with increased cytotoxic activity.

Various novel recombinant human tumor necrosis factor-alpha (TNF) mutants were prepared using protein engineering techniques, and their cytotoxic activity was compared with that of the intact form of TNF (intact TNF). Mutant 471 (a TNF mutant molecule with the deletion of 7 amino acids at the amino-terminal and the substitution of Pro8Ser9Asp10 by ArgLysArg) had a 6-fold higher cytotoxic activity against murine L929 cells. The mutant TNF had an increased ability to bind to TNF receptor on murine L929 fibroblasts cells. A cross-linking study revealed that mutant 471 had an increased ability to form an active trimer. Mutant 471 also showed higher cytotoxic activity against human KYM myosarcoma cells and human MIA PaCa-2 pancreatic carcinoma cells. The possible cachectin activity of the mutant was almost the same as that of intact TNF. These results suggest that mutant 471 might be a more promising candidate as an anticancer agent than intact TNF.

Amino Acid Sequence↗
PubMed1995

Reversal of tumor necrosis factor resistance in tumor cells by adriamycin via suppression of intracellular resistance factors.

Tumor necrosis factor (TNF) and various chemotherapeutic drugs show synergistic antitumor effects in vitro and in vivo, though the mechanism is not clear. Based on our previous finding that endogenous TNF (enTNF) acts as an intracellular resistance factor against exogenous TNF by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD), we examined the suppression of these resistance factors by chemotherapeutic drugs and the resulting increase in TNF cytotoxicity. Pretreatment of HeLa cells, which produce an appreciable amount of enTNF and show apparent TNF resistance, with TNF followed by adriamycin (ADM) resulted in an additive effect, whereas pretreatment with ADM followed by TNF resulted in a synergistic effect. After treatment of HeLa cells with ADM, the expression of enTNF was remarkably suppressed and MnSOD activity was decreased by one-half. These results indicate that suppression of the intracellular resistance factors, i.e., enTNF and MnSOD, by ADM plays an important role in the mechanism of the synergistic antitumor effect of TNF in combination with ADM.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

CMV viraemia demonstrated in the serum of a patient with cytomegalovirus pneumonia.

We attempted to demonstrate the expression of cytomegalovirus (CMV) particles in the serum of an acute lymphocytic leukaemia patient with CMV pneumonia. The serum sample was applied to an affinity column coupled with human monoclonal antibody C23 which recognizes the envelope glycoproteins of CMV virus and neutralizes the viral activity. The DNA obtained from each fraction was amplified by double polymerase chain reaction (PCR) and analysed by gel electrophoresis. Bands were clearly observed in the eluted fraction. These results strongly suggest that CMV particles exist in the sera of patients with CMV pneumonia.

Base Sequence↗
PubMed1995

Localization of T cell receptor (TCR)-gamma delta + T cells into human colorectal cancer: flow cytometric analysis of TCR-gamma delta expression in tumour-infiltrating lymphocytes.

We analysed TCR-gamma delta expression in tumour-infiltrating lymphocytes (TIL) obtained from 13 patients with colorectal cancer and simultaneously isolated the T lymphocytes from normal intestinal tissue (IL) to compare the frequencies of TCR-gamma delta expression in TIL, IL, and peripheral blood lymphocytes (PBL) in the same patient. Flow cytometric analysis showed that the frequency of TCR-gamma delta expression in TIL (2.75 +/- 1.84%) was significantly lower than that in IL (15.28 +/- 9.45%, P < 0.01). However, a larger quantity of TIL was separated than IL per unit weight of specimen, so the total number of gamma delta T cells obtained per unit weight was not different between tumour tissue and normal intestine. In addition, phenotypic analysis revealed that about half of the TCR-gamma delta + TIL were CD8+ (CD4+, 3.0 +/- 3.1%; CD8+, 54.7 +/- 19.9%, mean +/- s.d. of five patients), and a very similar result was obtained in TCR-gamma delta + IL (CD4+, 2.7 +/- 2.4%; CD8+, 53.1 +/- 17.4%). In contrast, most TCR-gamma delta + PBL were double-negative (CD4+, 3.2 +/- 3.0%; CD8+, 20.6 +/- 7.4%). These results indicated that TCR-gamma delta + CD8+ T cells selectively and consistently localized in colorectal tumour tissue, similarly to normal intestinal epithelium.

Aged↗
PubMed1995

[A case of toxic shock-like syndrome due to Streptococcus pyogenes].

A case of toxic-shock syndrome due to Streptococcus pyogenes is reported. A 76-year-old female was admitted with complaints of fevers and chills. She had been suffering from cellulitis on her right dorsum pedis for 7 months. Laboratory data on admission showed elevated values of WBC, CRP, and dysfunction of the liver and kidney. She was diagnosed as sepsis due to the cellulitis, and was treated with PIPC and FMOX. However, several hours after admission, her blood pressure decreased and oliguria appeared. Bacteriological examinations from the blood and the cellulitis revealed group A beta-hemolytic Streptococcus which gave streptococcal pyrogenic exotoxin (T-28, SPE.B + C). She died 23 hours after her admission in spite of changing antibiotics to a high-dose of PC-G therapy. This is one of the rare cases of toxic shock-like syndrome due to Streptococcus pyogenes from the cellulitis of the dorsum pedis.

Aged↗
PubMed1995

In vitro antimycobacterial activities of pyrazinamide analogs.

We synthesized various pyrazine derivatives and pyrazinamide analogs and assayed their antimycobacterial activities in vitro in order to find new drugs which are more active against Mycobacterium tuberculosis than pyrazinamide and also active against Mycobacterium avium and Mycobacterium intracellulare. Of the drugs synthesized, four drugs, namely, pyrazine thiocarboxamide, N-hydroxymethyl pyrazine thiocarboxamide, pyrazinoic acid n-octyl ester, and pyrazinoic acid pivaloyloxymethyl ester, were not only bacteriostatic but also bacteriocidal against these three species of mycobacteria in vitro under conditions in which pyrazinamide showed no or little activity. In conclusion, these four drugs are possible candidates for new antimycobacterial agents, and animal experiments are now under way.

Antitubercular Agents↗
PubMed1995

Both the changes of six amino acids and the C-terminal truncation caused by a one-base insertion in the defective env gene of Friend spleen focus-forming virus significantly affect the pathogenic activity of the encoded leukemogenic membrane glycoprotein (gp55).

Friend spleen focus-forming virus (F-SFFV) causes acute erythroleukemia in mice and encodes in its defective env gene an Env-like membrane glycoprotein (gp55). The F-SFFV env gene has three characteristic structures compared with that of ecotropic murine leukemia viruses (MuLVs): substitution by the polytropic MuLV env sequence, a 585-bp deletion, and a 1-bp insertion. All of these characteristic structures are essential for the leukemogenic potential of gp55 of polycythemia-inducing isolates of F-SFFV (F-SFFVp). The 1-bp insertion causes changes of six amino acids and truncation by 34 amino acids at the C terminus. In this study, we constructed 12 mutant F-SFFV genomes starting from the wild-type F-SFFVp and examined the effect of the C-terminal truncation and the six altered amino acids on the pathogenic activity of gp55. The results indicated that at least 18 to 24 amino acids must be deleted from the C terminus for the env product to be pathogenically active. We also found that the six altered amino acids contributed significantly to the pathogenic activity of gp55. Analyses of the cellular processing of these mutant gp55s supported a correlation between the pathogenic activity of gp55 and its efficiency in overall cellular processing.

3T3 Cells↗
PubMed1995

Loss of E-cadherin-dependent cell-cell adhesion due to mutation of the beta-catenin gene in a human cancer cell line, HSC-39.

Detachment of cell-cell adhesion is indispensable for the first step of invasion and metastasis of cancer. This mechanism is frequently associated with the impairment of either E-cadherin expression or function. However, mechanisms of such abnormalities have not been fully elucidated. In this study, we demonstrated that the function of E-cadherin was completely abolished in the human gastric cancer cell line HSC-39, despite the high expression of E-cadherin, because of mutations in one of the E-cadherin-associated cytoplasmic proteins, beta-catenin. Although immunofluorescence staining of HSC-39 cells by using an anti-E-cadherin antibody (HECD-1) revealed the strong and uniform expression of E-cadherin on the cell surface, cell compaction and cell aggregation were not observed in this cell. Western blotting (immunoblotting) using HECD-1 exhibited a 120-kDa band which is equivalent to normal E-cadherin. Northern (RNA) blotting demonstrated a 4.7-kb band, the same as mature E-cadherin mRNA. Immunoprecipitation of metabolically labeled proteins with HECD-1 revealed three bands corresponding to E-cadherin, alpha-catenin, and gamma-catenin and a 79-kDa band which was apparently smaller than that of normal beta-catenin, indicating truncated beta-catenin. The 79-kDa band was immunologically identified as beta-catenin by using immunoblotting with anti-beta-catenin antibodies. Examination of beta-catenin mRNA by the reverse transcriptase-PCR method revealed a transcript which was shorter than that of normal beta-catenin. The sequencing of PCR product for beta-catenin confirmed deletion in 321 bases from nucleotides +82 to +402. Southern blotting of beta-catenin DNA disclosed mutation at the genomic level. Expression vectors of Beta-catenin were introduced into HSC-39 cells by transfection. In the obtained transfectants, E-cadherin-dependent cell-cell adhesiveness was recovered, as revealed by cell compaction, cell aggregation, and immunoflourescence staining. From these results, it was concluded that in HSC-39 cells, impaired cell-cell adhesion is due to mutations in beta-catenin which results in the dysfunction of E-cadherin.

Antibodies, Monoclonal↗