Search PubMed⌕ Search

Biomedical subjects

N Tanaka

Publications and source records attributed to N Tanaka.

At least 505 records · Page 28Linked to original sources
PubMed1999

Chromosome-type aberrations induced in chromosome 9 after treatment of human peripheral blood lymphocytes with mitomycin C at the G(0) phase.

To determine the fate of chromosome aberrations induced primarily by clastogenic chemicals, aberrations of chromosome 9 in cultured human peripheral blood lymphocytes were analyzed after exposure to mitomycin C (MMC) at G(0) phase. Chromosome 9 painting by fluorescence in situ hybridization revealed that the translocation of 9p or 9q to another chromosome and the centric fragment representing the entire length of 9p were characteristically generated from chromatid-type aberrations involving the centromeric region of chromosome 9. These changes were not observed at 48 h after culture initiation, but persistently appeared at later stages (72-120 h postinitiation). Induction of centric fragments of 9p and micronuclei without the alpha satellite DNA of chromosome 9 suggested that most of the breaks were induced near the alpha satellite DNA locus on 9q. Modified patterns of chromosome 9 aberrations were also observed, being related to the copy number of the short or long arm of the chromosome. Such unbalanced karyotypes could remain in the lymphocyte genome over further cell divisions for at least 120 h after culture initiation, indicating that these aberrant cells can survive and that they could pose a health risk.

Adult↗
PubMed1999

Increase in thioredoxin activity of intestinal epithelial cells mediated by oxidative stress.

Hydrogen peroxide was cytotoxic to the small intestine epithelial cell line, IEC-6, as judged from an MTT assay and the release of lactate dehydrogenase. The glutathione S-transferase and thioredoxin reductase activities and SH content decreased dose-dependently with H2O2, but thioredoxin activity increased at low H2O2 concentrations. In addition, the increase in thioredoxin activity was time-dependent during the initial stages of oxidative stress. A reverse transcription-polymerase chain reaction (RT-PCR) amplification also showed that the mRNA content in IEC-6 cells increased time-dependently at 0.25 mM H2O2. These results indicate that cellular oxidative shock causes an increase in the activity of thioredoxin, which is involved in the defense mechanism against oxidative stress.

Animals↗
PubMed1999

Effects of nicorandil on aortic input impedance: a comparative study with nitroglycerin.

A study of aortic input impedance was performed to evaluate the effects of nicorandil on the systemic circulation, and the effects were compared with those of nitroglycerin. Sixteen patients with coronary artery disease were divided into 2 age-matched groups. Aortic input impedance was obtained from Fourier analysis of aortic pressure and flow signals at baseline conditions, after intravenous administration of either 4 mg (Group 1) or 8 mg (Group 2) nicorandil, and 20 min after 0.3 mg sublingual nitroglycerin. In Group 1, the first harmonic impedance modulus (Z1, 304+/-140 dyne x s x cm(-5)) and the average of the first to third harmonics (Z1-3, 207+/-99 dyne x s x cm(-5)), indices of wave reflection, significantly decreased (24.4% (p<0.05) and 24.7% (p<0.01), respectively) after nicorandil, and 41.3% (p<0.01) and 33.9% (p<0.01) after nitroglycerin. The effects between the 2 vasodilators were not significantly different. In Group 2, Z1 and Z1-3 (275+/-138 and 196+/-93 dyne x s x cm(-5), respectively) also decreased after administration of nicorandil (28.4% (p<0.01) and 35.9% (p<0.01), respectively), and after administration of nitroglycerin (23.9% (p<0.01) and 28.7% (p<0.01), respectively), without any significant difference between the 2 drugs. Characteristic impedance and total peripheral resistance (R) in both groups remained unchanged except for R after 8 mg nicorandil (from 1830+/-415 to 1433+/-428 dyne x s x cm(-5); p<0.01). Like nitroglycerin, both doses of nicorandil reduced wave reflection. The reduction in R after 8 mg nicorandil is related to decreased tone in the resistance arteries, probably due to potassium channel opener effects.

Aged↗
PubMed1999

Nystatin effects on vacuolar function in Saccharomyces cerevisiae.

The effects of nystatin, a polyene antibiotic, was studied in Saccharomyces cerevisiae by isolating and characterizing nystatin-sensitive mutants. We isolated a number of nystatin-sensitive mutants by ethylmethane sulfonate mutagenesis. One of these mutants, the nss1 mutant, was characterized in detail. The mutant was sensitive to stresses such as high temperature or high concentrations of monovalent and divalent cations. The nss1 mutants showed severe vacuolar protein sorting and vacuolar morphology defects. The nss1 mutant was demonstrated to have a mutational lesion in the known VPS16 gene, which is essential for vacuolar protein sorting in S. cerevisiae. All of the vacuolar deficient mutants (vps11, vps16, vps18, and vps33) were sensitive to nystatin. Nystatin was found to cause extensive enlargement of the vacuole in wild-type S. cerevisiae cells. These results are discussed with special reference to the vacuolar function of S. cerevisiae.

Alleles↗
PubMed1999

[The relationship between p53 protein and c-erb B-2 expression and apoptosis in colorectal cancer].

In order to elucidate the relationship between tumor growth and various kinds of gene expression and the occurrence of apoptosis in the front portion of neoplastic invasion, 57 advanced colorectal cancers were studied by immunohistochemical staining of p53, c-erb B-2, the TUNEL method and electron microscopy. Light microscopically, the columnar epithelial cells of adenocarcinoma frequently showed a decrease in high and a fall off into the lumen in tumor invasive forefront. Immunohistochemically the positive rate of p53 and c-erb B-2 in tumors with high vascular invasion were higher (p < 0.05) than in those with low vascular invasion. There was a close correlation between the vascular or lymphatic invasion and positive immunoreactivity of p53 and c-erb B-2. The apoptosis index was demonstrated to be related to vessel invasion, over expression of p53 and inflammatory cell infiltration around the front portion of the tumor invasion. These results suggested that p53. c-erb B-2 and the apoptosis index should be evaluated in conjunction with the prognostic factors in colorectal cancer. The infiltrative inflammatory cells may induce apoptosis of the tumor cells.

Adult↗
PubMed1999

Diabetic nephropathy accompanied by iodine-induced non-autoimmune primary hypothyroidism: two case reports.

We reported 2 diabetic patients with nephrotic syndrome due to advanced diabetic nephropathy complicated by non-autoimmune primary hypothyroidism. Hypothyroidism developed along with the anasarcous status. Histological examinations of the thyroid gland revealed almost normal thyroid follicles without lymphocytic infiltration. The amounts of thyroid hormone lost into the extravascular space such as in urine and ascites were not sufficient to cause hypothyroidism alone. Serum total iodine levels measured during the hypothyroidal state in both cases were definitely elevated, and the perchlorate discharge test of both cases showed positive discharge (24 and 34%, respectively). The thyroid functions normalized after iodine restriction in the first case and initiating hemodialysis in the second case, in parallel with normalization of serum total iodine levels. These findings suggest that impaired renal handling of iodine resulting in elevation of serum iodine levels, rather than an autoimmune mechanism or extravascular hormone loss, played a principal role in the development of primary hypothyroidism found in these 2 patients, probably through a prolonged Wolff-Chaikoff effect.

Aged↗
PubMed1999

Activation of the transcription factor ISGF3 by interferon-gamma.

The interferon-stimulated gene factor 3 (ISGF3) transcription factor has been extensively studied in the context of the type I interferon (IFN-alpha/beta)-mediated antiviral response; it consists of the major DNA-binding component p48, and the signal transducers and activators of transcription (Stat)1 and Stat2. We show here that type II IFN (IFN-gamma) can also invoke the activation of ISGF3 in mouse primary embryonic fibroblasts. In fact, the two Stat proteins were tyrosine phosphorylated in IFN-gamma stimulated cells. Our present findings reveal an additional mechanism by which these two distinct types of cytokines, IFN-alpha/beta and -gamma, can commonly elicit antiviral activities.

Animals↗
PubMed1999

Modulatory effect of a serine protease inhibitor on surgical stress: its clinical implications.

The relationship between endogenous cytokine antagonists and surgical stress is poorly understood. Surgical stress induces immunosuppression, and the reversed therapy of postoperative immunosuppression has been expected. The aim of the present study was to assess the effect of a serine protease inhibitor on postoperative immune reactivity. Twenty patients with colorectal cancer were randomly separated into experimental and control groups of 10 patients each. The experimental group received perioperative administration of a serine protease inhibitor while the control group did not. Plasma levels of cytokine antagonists, which suppress cell-mediated immunity, such as cortisol, interleukin-1 receptor antagonist, soluble interleukin-2 receptor (sIL-2R) and soluble tumor necrosis factors p55, p75 (sTNF-R55, -R75) were simultaneously measured. Significant reductions of plasma concentration of sIL-2R and sTNF-R55 were observed. Perioperative administration of a serine protease inhibitor may contribute to ameliorating immunosuppression after major surgery.

Adult↗
PubMed1999

Hydrocortisone sodium succinate suppressed production of interleukin-10 by human peripheral blood mononuclear cells: clinical significance.

Corticoids are well known for their immunosuppressive properties. Interleukin-10 (IL-10) is an intrinsic antiinflammatory peptide in immune diseases, originally identified as cytokine synthesis inhibitory factor. We examined the effect of hydrocortisone sodium succinate (HSS) on the production of IL-10 by human peripheral blood mononuclear cells (PBMCs). PBMCs from healthy volunteers and cancer-burden patients were preincubated separately with or without HSS for 1 h, then stimulated with 5 microg/ml lipopolysaccharide (LPS). Production of IL-10 by human PBMCs was detected with LPS stimulation and its production was higher in cancer-burden patients than in normal volunteers, although this was not statistically significant. HSS suppressed production of IL-10 by LPS-stimulated PBMCs in a dose-dependent manner both in normal volunteers and in cancer-burden patients. These results indicate that, in addition to their antiinflammatory properties, corticoids act to restore the immunosuppressive states even in cancer-burden states.

Adult↗
PubMed1999

Prediction of the development of hepato-cellular-carcinoma in patients with liver cirrhosis by the serial determinations of serum alpha-L-fucosidase activity.

OBJECTIVE: Evaluation of the usefulness of the serial determinations of serum alpha-L-fucosidase (AFU) activity for prediction of the development of hepatocellular carcinoma (HCC) was performed. METHODS AND PATIENTS: Serum AFU activity was determined monthly for 42 months in 73 patients with liver cirrhosis (LC). RESULTS: HCC was diagnosed in 27 patients by means of ultrasonography during this observation period. In 23 (85%) of the 27 patients, serum AFU activity was found to exceed 700 nmole/ml/h during the LC stage. HCC developed within a few years in 23 (82%) of 28 LC patients with AFU activity exceeding 700 nmole/ml/h, in contrast, it developed in only 4 (9%) of 45 LC patients with AFU activity below 700 nmole/ml/h. AFU activity was already elevated in 23 (85%) of 27 patients at least 6 months before the detection of HCC by ultrasonography. CONCLUSION: It is conceivable that the development of HCC can be predicted by means of serial determinations of serum AFU activity in patients with LC.

Carcinoma, Hepatocellular↗
PubMed1999

[Efficacy of middle ear surgery for patients with hearing aids and middle ear disease].

Of 356 cases that underwent middle ear surgery for hearing improvement, 30 (8.4%) with air conduction hearing aids and middle ear disease were evaluated pre- and postoperatively. All surgeries were performed by the same surgeon. Diagnoses included 22 chronic otitis media, 5 chronic otitis media with cholesteatoma, 1 otosclerosis and 2 ossicular anomaly. Chief complaints at the first visit to Fukui Medical University Hospital were otorrhea (17 cases), hard of hearing (28 cases), dizziness (2 cases) and tinnitus (2 cases). Nineteen patients underwent surgery on both ears and eleven on one ear including five ears that showed better hearing preoperatively. Surgical procedures were tympanoplasty type I (15 cases), modified type III (8 cases), modified type IV (3 cases), stapedotomy (2 cases) and implantable hearing device (2 cases). After surgery, 16 patients (group 1) did not need hearing aids, while 14 (group 2) still needed hearing aids. Preoperative hearing was 64.1dB (n = 30) on average and average hearing one year after surgery in group 1 (35.4 +/- 14.1dB) was significantly better than in group 2 (58.1 +/- 18.4dB). After surgery, otorrhea stopped in all cases (100%), subjective hearing loss improved in 82% of the patients, vertigo improved in 100% and tinnitus improved in 50%. These results emphasize the benefits of surgical therapy, and the reasons why it should be recommended to patients with hearing aids and middle ear disease, such as to improve hearing disorders, to stop otorrhea and to prevent progressive sensorineural hearing loss.

Adolescent↗
PubMed1999

[Liver abscess].

Explore the source record for details and available documents.

Diagnosis, Differential↗
PubMed1999

[A case of bronchogenic in situ carcinoma originating in fourth order bronchi].

A case of bronchogenic in situ carcinoma originating in forth order bronchi was reported. Sputum cytology showed class IV in lung cancer mass screening in a 69-year-old male, although X-ray was negative. Bronchofiber scopy was repeated twice, and fine granular change of spur between Blai and ii was found in the second time. Right upper lobectomy was underwent, and post-surgical histology was in situ squamous cell carcinoma. The literature on early lung cancer was reviewed, and implication for management of bronchofiberscopic early lung cancer in general rule for clinical and pathological record of lung cancer was discussed.

Aged↗
PubMed1999

Vascular endothelial growth factor acts as a pericyte mitogen under hypoxic conditions.

Angiogenesis is the process by which new vascular networks are formed from preexisting capillaries. The small vessels are composed of two types of cells, namely endothelial cells (EC) and pericytes, with the former being encircled by the latter. We previously showed that hypoxia, the principal cause of angiogenesis, can induce the proliferation of pericytes as well as EC. In this report we present evidence that the hypoxic induction of pericyte growth can be ascribed at least in part to vascular endothelial growth factor (VEGF) produced by this very cell type. First, the finding that hypoxia can stimulate the proliferation of pericytes was confirmed by cultivating bovine retinal pericytes in a controlled-atmosphere culture chamber containing various concentrations of oxygen and then assaying pericyte synthesis of DNA. Second, Northern blot analysis revealed that pericyte levels of mRNA encoding VEGF increased as the atmospheric oxygen tension was decreased; this was accompanied by an increase in de novo synthesis of VEGF proteins. Third, pericytes were able to respond to exogenously added VEGF, resulting in a dose-dependent increase in viable cell numbers. Fourth, polyclonal antibodies against VEGF efficiently blocked the hypoxic induction of pericyte growth. Fifth, pericytes expressed the gene for fms-like tyrosine kinase 1 (flt1) as the predominant form of VEGF receptor, and tyrosine phosphorylation of this receptor protein was enhanced when pericytes were exposed to hypoxia, as it was when cells were exposed to VEGF. Sixth, the antisense DNA complement of flt1 mRNA abolished the hypoxia-induced stimulation of pericyte growth. Finally, exogenous VEGF stimulated the migration of pericytes in a dose-dependent manner. The results thus suggest that VEGF, which has been thought to be a specific mitogen for EC, also acts on neighboring pericytes, probably in both autocrine and paracrine manners, and that the hypoxia-induced overproduction of VEGF could promote not only EC sprouting but also the recruitment of pericytes, thereby contributing to the maturation of newly formed microvessels.

Animals↗
PubMed1999

[Adult case of isolated noncompaction of left ventricular myocardium revealed at hospitalization for tuberculous pleuritis].

A 48-year-old man was diagnosed with isolated noncompaction of the left ventricular myocardium. He had been suffering from dyspnea during light exercise since early February 1997, which worsened with time. Eventually, he visited our hospital on February 14. He was admitted urgently because orthopnea was observed and chest radiogram showed massive left pleural effusion. The diagnoses were pulmonary tuberculosis and tuberculous pleuritis. Echocardiography at admission showed generalized hypokinesis of the left ventricle, so we suspected that his condition was complicated by myocarditis. However, virus antibody levels were not elevated, and no obvious findings compatible with myocarditis or cardiomyopathy were obtained by right ventricular myocardial biopsy. Left ventricular contractility remained low and a trabecular mesh structure was seen at the left ventricular apex. Thus, the diagnosis was isolated noncompaction of the left ventricular myocardium. This disorder has been highlighted in pediatric patients, but few adult cases have been reported.

Echocardiography↗
PubMed1999

A retrospective study using nail clippings of rheumatoid susceptible alleles of HLA-DRB1 as a prognostic factor in early rheumatoid arthritis.

OBJECTIVE: To evaluate whether the number of susceptible factors influences disease progression in Japanese patients diagnosed with early rheumatoid arthritis (RA). METHODS: Fifty-eight Japanese outpatients (46 female, 12 male; mean age 48.9 yrs) with early RA of less than one year after onset were enrolled in the study. The criteria for early RA (Japanese Ministry of Welfare) were used. DNA was extracted from fingernail clippings and the gene frequencies of HLA-DRB1 alleles were investigated. The degrees of progression of (1) clinical symptoms, (2) laboratory findings, (3) radiographic changes, and (4) magnetic resonance imaging score were analyzed by a comparison of the above at time of diagnosis and at final examination (an average of 14 months after the time of diagnosis). RESULTS: The frequencies of the susceptible factors (S: 0101, 0401, 0404, 0405, 1001, and 1402) were 17, 3.4, 0.9, 29, 0, and 0%, respectively. The progression of inflammatory autoimmune activity, erosion incidence, and synovial proliferation severity in the S/S group was significantly more rapid than that in the other groups. In the disease activity at each time, the difference between the S/S group and the S/N group was significant, as was that between the S/S group and the N/N group, but the difference between the S/N group and the N/N group was not significant. CONCLUSION: Haplotyping of HLA-DRB1 using the patient's nail clippings may be useful as a prognostic marker for disease progression in early RA.

Adult↗
PubMed1999

Recombinant adenovirus expressing wild-type p53 is antiangiogenic: a proposed mechanism for bystander effect.

Angiogenesis is required for the growth and progression of malignancies. Recent studies have demonstrated that genetic alterations may accompany acquisition of the angiogenic phenotype. The tumor suppressor gene p53 is most frequently mutated in human cancers and is also known to be a transcriptional regulator of a variety of genes. Here, we investigated the antiangiogenic effect of the wild-type p53 (wt-p53) gene transfer on a human non-small cell lung cancer cell line. Mutant p53-expressing H226Br non-small cell lung cancer cells were transduced with the wt-p53 gene using a recombinant adenoviral vector (Ad5CMVp53) and applied to semiquantitative reverse transcription-PCRs for the detection of altered mRNA expression of angiogenic and/or antiangiogenic factors. In vivo neovascularization assay of Ad5CMVp53-infected cells was then performed using a membrane-diffusion chamber system s.c. transplanted in nu/nu mice. We also evaluated the effect of Ad5CMVp53-infected H226Br cells on nontransduced tumor cells in vivo by s.c. inoculating mixture of cells into nu/nu mice. Ad5CMVp53 infection markedly inhibited the expression of an angiogenic factor, vascular endothelial growth factor, and increased the expression of a novel antiangiogenic factor, brain-specific angiogenesis inhibitor 1, resulting in reduced neovascularization in vivo. Mixing experiments showed that tumor cells transduced with the wt-p53 gene inhibited the in vivo tumor growth of adjacent nontransduced cells. Our data suggest that a recombinant adenovirus expressing the wt-p53 gene is antiangiogenic, which may explain, in part, the mechanism of the bystander effect induced by the wt-p53 gene transfer on adjacent tumor cells.

Adenoviruses, Human↗