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Biomedical subjects

S Maeda

Publications and source records attributed to S Maeda.

At least 469 records · Page 26Linked to original sources
PubMed1995

The growth and recovery of vibrotactile TTs caused by hand-transmitted repetitive shocks of various waveforms.

The effect of shock repetition rate on the temporary threshold shifts (TTSs) in vibrotactile perception at the fingers has been studied with shocks having exponential decays and hanning waveforms. The repetition rate of shocks delivered at the hand varied from 2 shocks per second up to 64 shocks per second. Subjects were exposed to vertical hand-transmitted repetitive shock vibration of equal energy contents. The magnitudes of the stimuli were adjusted to 2.8 ms-2 r.m.s. so that they were all equally severe according to current standards for assessing the severity of hand-transmitted vibration (e.g. International Standard 5349, 1986). It was found that the TTS in vibrotactile perception decreased with decreasing shock repetition rate for both waveforms. The relation between the TTS, the logarithm of exposure time, and the logarithm of the ratio between the frequency-weighted r.m.s. acceleration and the peak amplitude was described by the relation TTS = 16.1 + 3.9log10T + 17.9log10 (RMS/PEAK), where TTS is the temporary threshold shift (in decibels), T is the exposure time, and RMS is the frequency-weighted r.m.s. acceleration according to BS 6842 and ISO 5349, and PEAK is the peak amplitude of the frequency-weighted acceleration. This shows that current standards are not appropriate for the prediction of the changes in vibrotactile perception produced by shocks such as those on many hand-held percussive tools.

Acceleration↗
PubMed1994

Thyroid hormone metabolism in a transthyretin-null mouse strain.

Transthyretin (TTR) is the principal carrier of thyroid hormones in rodent plasma and the major protein synthesized by the choroid plexus. Mice lacking TTR generated by targeted disruption (Episkopou, V., Maeda, S., Nishiguchi, S., Shimada, K., Gaitanaris, G. A., Gottesman, M. E., and Robertson, E. J. (1993) Proc. Natl. Acad. Sci. U.S.A. 90, 2375-2379) had a 50% decrease in total thyroxine (T4) plasma levels but had normal free hormone levels as compared to wild-type mice. In the mutant serum there was increased T4 binding to thyroxine-binding globulin. Thyroxine-binding globulin mRNA levels were the same in mutant and wild-type animals. Wild-type serum depleted of TTR also presented increased T4 binding to thyroxine-binding globulin, suggesting that TTR competes with thyroxine-binding globulin for T4 binding. Total and free triiodothyronine and thyrotoropin-stimulating hormone levels were not affected by the absence of TTR. Liver deiodinase-I activity, mRNA levels, and brain deiodinase-II activity were normal in the mutant mice, suggesting that the absence of TTR does not affect tissue thyroid hormone content. The low T4 levels found in the mutant mice sera cannot be accounted for by increased glucuronidation because the liver activity of UDP-glucuronosyltransferase was not affected in the TTR-deficient mice. We concluded that transthyretin-deficient mice are euthyroid in the absence of the major plasma T4 carrier. We ascribed this to the normal free hormone levels in the serum of the mutant mice. Our data, therefore, strongly supported the free hormone hypothesis for thyroxine uptake (Mendel, C. M. (1989) Endocr. Rev. 10, 232-274).

Animals↗
PubMed1994

bcl-2 expression in epidermal keratinocytic diseases.

BACKGROUND: The bcl-2 protein has been shown to suppress apoptosis, and overexpression of the bcl-2 protein has been reported in several malignant tumors. Skin is one of the largest organs in the body, and the most common human malignancies arise from keratinocytes in the epidermis. In this paper, the authors analyzed immunohistochemically the expression of the bcl-2 protein in several keratinocytic (KC) tumors and inflammatory skin disorders to investigate the role of bcl-2 in the development of benign and malignant skin tumors. METHODS: Seventy-two frozen tissues from patients with inflammatory KC proliferation (chronic dermatitis [CD] and psoriasis vulgaris [PV]), seborrheic keratosis (SK), carcinoma in situ of KC tumors (actinic keratosis [AK] and Bowen's disease [BD]), basal cell carcinoma (BCC), and squamous cell carcinoma (SCC), 2 SCC cell lines, and 20 normal skin were immunostained with an anti-bcl-2 monoclonal antibody. RESULTS: Tissue with normal KC, CD, PV, and SK scarcely expressed the bcl-2 protein. Seventy-three percent of tissue with BD, 25% with AK, 67% with BCC, and 100% with SCC showed obvious bcl-2 protein expression. bcl-2 expression of BCC, BD, and SCC was restricted to the involved lesions, and surrounding normal tissue with KCs were bcl-2 negative. Interestingly, tissue with atrophic AK expressed no bcl-2 protein (none of five cases), whereas tissue with hypertrophic AK reacted weakly with the anti-bcl-2 antibody (two of three cases). CONCLUSIONS: bcl-2 protein expression in patients with KC may be related to tumorigenic proliferation possibly due to enhanced cell survival, but not when inflammatory proliferation of keratinocytes is present.

Bowen's Disease↗
PubMed1994

Crystallization and preliminary X-ray diffraction studies of curculin. A new type of sweet protein having taste-modifying action.

A taste-modifying protein, curculin, has been crystallized by the vapor diffusion method using polyethylene glycol 400 as a precipitant. The crystals belong to orthorhombic space group P2(1)2(1)2(1) with unit cell dimensions: a = 105 A, b = 271 A, c = 48.7 A. The crystals diffract X-rays to at least a resolution of 3.0 A and are suitable for X-ray crystallographic studies.

Crystallization↗
PubMed1994

Non-involvement of ras mutations in flat colorectal adenomas and carcinomas.

Ras gene mutations occur relatively early during colorectal tumor development and have been observed in 40-50% of malignant colorectal tumors. Advances in endoscopic techniques have made it possible to detect small, flat colorectal tumors that could not be detected by standard examinations. To determine whether ras gene mutations are also involved in the genesis of small, flat colorectal tumors, we examined ras point mutations in 34 cases of small polypoid or flat elevated colorectal tumors (32 adenomas, 2 carcinomas) and in 26 cases of small, flat colorectal tumors (13 adenomas, 13 carcinomas) by means of the polymerase chain reaction (PCR) and dot-blot hybridization. Ras gene point mutations were observed in 16 of the 34 tumors of the former type (47%), but in none of the 26 tumors of the latter type, even though the grade of dysplasia was severe in the flat tumors. Our results suggest that different genetic pathways for tumor progression may exist for polypoid and for flat colorectal carcinomas.

Adenoma↗
PubMed1994

Determination of clonidine in human plasma by gas chromatography-electron-impact mass spectrometry.

A new and sensitive gas chromatographic-mass spectrometric (GC-MS) assay for routine analysis of clonidine in human plasma is described. Quantification is carried out with simple electron-impact ionization mass spectrometry and solid-phase cartridges for preliminary extraction from plasma. The pentafluorobenzyl derivative of clonidine yields an intense ion fragment at m/z 354, and the lower limit of detection is 0.025 ng/ml for a 1-ml plasma sample. The practical applicability of this method is demonstrated by determining plasma concentrations of clonidine in a clinical study of a new transdermal delivery system for clonidine.

Administration, Cutaneous↗
PubMed1994

High-level expression of porcine muscle adenylate kinase in Escherichia coli: effects of the copy number of the gene and the translational initiation signals.

Porcine muscle adenylate kinase (ADK) was overproduced in Escherichia coli using the expression plasmid with double A-T-G codon at the translational starting site and the Shine-Dalgarno (SD) sequence 10 bp apart from the first A-T-G. We used the expression vectors pKK223-3 and pMK2. pMK2 is about 10-20 times larger in copy number than pK223-3. For both vectors, duplication of A-T-G was effective and the quantity of the expressed ADK from the double A-T-G plasmid was 2 approximately 4-fold more than that achieved when only one A-T-G was present. The amount of the produced ADK was maximum in the case of using pMK2 with double A-T-G. The overproduced ADK formed inclusion bodies in E. coli. It was solubilized in 6 M guanidine hydrochloride and refolded. Through two steps of column chromatography, ADK was purified. It has the same amino acid composition and grossly the same activity as that reported by Schirmer et al. (1970). Its amino acid sequence of the NH2-terminal region was identical with that deduced from the cDNA sequence including the NH2-terminal methionine.

Adenylate Kinase↗
PubMed1994

Establishment of human oral-cancer cell lines (KOSC-2 and -3) carrying p53 and c-myc abnormalities by geneticin treatment.

Two cultured cell lines derived from human squamous-cell carcinomas were established through xenografted tumors in nude mice by "Geneticin" treatment, which allows to eliminate contaminated mouse fibroblasts and obtain enriched tumor cells at the early stage of cultivation. Line KOSC-2 and KOSC-3 were each derived from a squamous-cell carcinoma of the oral floor and of the lower gingiva, respectively. Both lines grew in a cobblestone pattern, demonstrating their epithelial heritage. Giemsa-banding patterns by chromosome analysis confirmed that both lines are of human origin. Molecular analysis of cancer-related genes, including the Ha-ras, c-myc and p53 genes, was performed. KOSC-3 cells showed co-over-expression of p53 and c-myc mRNA, in addition to p53 point mutation at codon 248 with transition from CGG to TGG. However, loss of heterozygosity (LOH) on chromosome 17 was detected in both lines by Southern blotting. These cell lines provide a model for elucidating the mechanism involving p53 inactivation and c-myc-gene over-expression.

Aged↗
PubMed1994

p53 gene abnormalities are closely related to hepatoviral infections and occur at a late stage of hepatocarcinogenesis.

Hepatocellular carcinoma (HCC) accumulates a mutation of the p53 gene with a common substitution of nucleotide in a particular site. It is hypothesized that infection of hepatitis B virus (HBV) or exposure to aflatoxins could induce it. In Japan, the concentration of aflatoxins in the environment is low; however, infection of HBV and/or hepatitis C virus (HCV) is frequently seen in patients with HCC. The purpose of our studies was to determine whether these hepatoviral factors influence p53 alterations. In our results, p53 abnormalities, which were composed of loss of heterozygosity (LOH) and/or point mutation, were shown in 39% of patients. We postulated that they occurred at late stages in tumor growth based on the following two results. LOH analysis on p53 showed that most of the tumor nodule consisted of two phenotypes, LOH and non-LOH cancer cells. The p53 abnormalities correlated with the grade of cancer cell atypia which advanced with tumor growth. HBV and HCV infections were identified by polymerase chain reaction using DNA extracted from cancerous and noncancerous regions of the liver. By these methods, the patients who had been infected with either HBV or HCV showed an incidence of p53 abnormalities (45%) higher than those infected by neither (13%). However, the detection rate of these viruses was lower in the HCC region (33%) than that in the noncancerous region (56%) in cases with mutated p53. The low rate of HCV detection (22%) in the HCC region with altered p53 was attributable to these different viral detection rates. There was a difference in pattern of p53 mutational changes in patients depending upon whether they were infected by HBV or by HCV. Two of three HBV-infected patients had a transversional change of nucleotide at the G:C site to T:A. However, in cases with HCV, four of eight patients had a transitional change of nucleotide of p53. These results showed that HBV and HCV infections affect carcinogenic pathways causing p53 abnormalities independently.

Adolescent↗
PubMed1994

Expression of adhesion molecules on human hematopoietic progenitor cells at different maturational stages.

In this report we examined the expression of several adhesion molecules on human hematopoietic progenitor cells at different maturational stages. Human hematopoietic progenitor cell-enriched fractions were prepared from bone marrow cells by depleting lymphocytes and monocytes (CD2+, CD14+ and CD19+ cells). These cells were separated into adhesion molecule-positive and -negative cell populations by immunomagnetic separation methods and then assessed for their ability to form various colony forming cells (CFC). CD44 and CD49d were expressed on multipotent hematopoietic progenitor cells, or mixed colony forming units (CFU-Mix), erythroid burst forming units (BFU-E), granulocyte-macrophage CFU (CFU-GM) and erythroid CFU (CFU-E). Leu8 was expressed on CFU-Mix, BFU-E and some populations of CFU-GM, but not CFU-E. CD11a was expressed on some populations of CFU-Mix, CFU-GM and BFU-E. CD54 was expressed only on some populations of CFU-GM. These results suggest that Leu8, CD44, CD49d and CD11a appear to play important roles in the differentiation and proliferation of human hematopoietic progenitor cells at different maturational stages in the bone marrow microenvironment.

Antigens, CD↗
PubMed1994

p53 mutations in flat- and polypoid-type colorectal tumors detected by temperature-gradient gel electrophoresis.

Reports of cases of flat-type colorectal tumors are increasing in Japan, but almost nothing has been elucidated about the genetic abnormalities of these tumors. In this study, we have examined p53 mutations in six cases of colon cancer cell lines, 22 cases of flat-type colorectal tumors, and 27 cases of polypoid-type colorectal tumors using the polymerase chain reaction (PCR) and temperature-gradient gel electrophoresis (TGGE); the latter has recently been developed as a screening method for gene mutations. p53 mutations were observed in four colon cancer cell lines, six flat-type colorectal tumors, and three polypoid-type colorectal tumors, all of which were analyzed by direct sequencing. These mutations were observed only in adenomas with high-grade dysplasia and in colorectal cancers but not in adenomas with low-grade dysplasia. These observations suggest that p53 gene mutations are involved in flat-type as well as polypoid-type colorectal tumors at relatively later stages of carcinogenesis and that TGGE seems to be useful as one of the rapid screening methods.

Adenoma↗
PubMed1994

Lp(a): an acute-phase reactant?

The present study was designed to confirm the transient increases of plasma Lp(a) levels as an acute-phase reactant and to clarify the significance of these increases with the use of patients with acute myocardial infarction and patients subjected to surgical operations. Although interleukin 6, C-reactive protein and alpha 1 antitrypsin reached the maximal levels 1-2 days, 3 days and 4-5 days, respectively, after the episodes, the peak time of Lp(a) levels was delayed some extent in both patient groups. Studying the transient increases of Lp(a) levels as a function of apo(a) isoforms analyzed by density-gradient ultracentrifugation and SDS-PAGE, the higher-density Lp(a) particles preferentially containing high-molecular-weight apo(a) isoforms increased more than the lower-density Lp(a) particles containing low-molecular-weight apo(a) after the episodes. The immunohistochemical findings suggest that Lp(a) may play an important role as an acute-phase reactant in the repair of tissue injury, especially in the process of angiogenesis.

Acute-Phase Reaction↗
PubMed1994

Fully mechanized latex immunoassay for serum lipoprotein(a).

We have developed a fully automated system to quantify lipoprotein(a) (Lp(a)) in human serum, based on the latex-enhanced turbidimetric immunoassay by application of the Immuno Chemistry Analyzer 501X. This assay was carried out with undiluted serum and was able to detect at Lp(a) levels higher than 4.0 mg/l. When judged to be out of range of the calibration (> 600 mg/l), the sample was automatically re-tested after automatic 10-fold dilution. Within-run C.V.s ranged from 1.9 to 2.1% and between-run C.V.s from 2.7 to 3.9%. Results by the present method were in good agreement with those by the in-house ELISA (r = 0.978) and the commercial ELISA (r = 0.990). The distribution of Lp(a) levels in sera from 508 healthy donors was highly skewed; the mean and median were 158 mg/l and 105 mg/l, respectively.

Adolescent↗
PubMed1994

Cerebrospinal fluid (CSF) neuropeptide Y- and somatostatin-like immunoreactivities in man.

We have measured cerebrospinal fluid (CSF) neuropeptide Y-like immunoreactivity (NPY-LI) and somatostatin-like immunoreactivity (SLI) in control subjects and in patients with various neurologic disorders. We observed a significant reduction in CSF SLI in control subjects over 60 years of age, compared with the younger controls. CSF SLI was significantly decreased in multiple sclerosis (MS), or Guillain-Barre syndrome, compared with that of age-matched control subjects. A reduced concentration of NPY-LI was found in CSF of patients with MS. We have also examined the molecular heterogeneity of peptide-LI in CSF. Gel chromatography, not high performance liquid chromatography (HPLC), suggested two NPY immunoreactive materials in CSF. Gel chromatography and HPLC revealed three SLI components in CSF: somatostatin 14, somatostatin 28 and a higher molecular weight precursor. Our results suggest that 1) there may be more than one form of NPY in human CSF, and 2) somatostatin neurons might be more susceptible to alteration than NPY neurons in various pathological conditions and aging.

Adult↗
PubMed1994

A comparison of vibrotactile thresholds on the finger obtained with different equipment.

Vibrotactile thresholds on the finger have been compared using two alternative systems. One system prescribed the push force, the contact force, and the surround, while this was not defined for the other system. The experiment was performed with nine male subjects attending on three different days. It was found that the two systems yielded vibrotactile thresholds which were significantly different. The dependence of vibrotactile thresholds on the frequency of vibration, the area of contact with vibration, the conditions surrounding the contact area, the contact force, the push force, the finger temperature, and the distortion of waveform must be considered when quantifying vibrotactile thresholds.

Adult↗
PubMed1994

Prevention of autoimmune insulin-dependent diabetes in non-obese diabetic mice by anti-LFA-1 and anti-ICAM-1 mAb.

Diverse adhesion molecules participate in many important responses and thus would be implicated in the pathogenesis of various autoimmune diseases. However, there is little evidence for the role of these molecules in autoimmune insulin-dependent diabetes mellitus. Here we present several lines of evidence suggesting that leukocyte function-associated antigen-1 (LFA-1) and its counter-receptor intercellular adhesion molecules (ICAM-1), one of the most important pairs among these adhesion molecules, are involved in the development of autoimmune diabetes in the non-obese diabetic (NOD) mouse. Immunohistochemical study showed the hyperexpression of ICAM-1 on islet-infiltrating mononuclear cells and vascular endothelium in NOD pancreas. In vivo administration of anti-LFA-1 or anti-ICAM-1 mAb from 5 to 30 (or 12) weeks of age exerted a very strong preventative effect on the development of spontaneous diabetes with a marked reduction of insulitis, whereas both antibodies, even combined to use simultaneously, could not prevent cyclophosphamide-induced diabetes. Adoptive transfer of insulitis and diabetes to young NOD mice following the injection of islet-derived mononuclear cells from diabetic donors was completely blocked by administration of both antibodies to recipients. The present study, therefore, provides the first evidence that immunointervention to LFA-1-ICAM-1 interaction has a strong prophylactic effect on autoimmune diabetes in NOD mice.

Animals↗
PubMed1994

Structures of replacement vectors for efficient gene targeting.

The relationship between DNA structure of replacement vectors and gene targeting efficiency was studied using positive-negative selection. The vectors contained pBR322 DNA, a bacterial neomycin-resistance gene (neo) for positive selection, a herpes simplex virus (HSV) thymidine kinase gene (tk) for negative selection, and a mouse genomic fragment, including exons 1 to 3 of the transthyretin (ttr) gene. The neo gene that confers G418 resistance was inserted into the second ttr exon, and the HSV-tk gene that confers gancyclovir (GANC) sensitivity was added to the 3' end of the ttr fragment. The vectors were linearized by digesting with restriction enzyme(s) and transfected into mouse embryonal carcinoma F9 cells. In this system, the enrichment by GANC selection as well as the frequency of gene targeting was increased by placing the pBR322 DNA at the 3' end of the HSV-tk gene. Adding one more HSV-tk gene at the 5' end of the ttr fragment did not increase the enrichment by GANC selection. This enrichment factor was also increased by reducing the size of the ttr fragment present between the two selection markers. However, it decreased the frequency of gene targeting and, overall, it did not increase the efficiency of isolating targeted clones. When structures of the vector DNA fragments present in 20 G418-resistant and GANC-resistant non-targeted clones were examined by Southern blot analysis, the inefficiency of GANC selection proved to be mostly caused by exonucleolytic degradation of HSV-tk genes progressing from ends of the vectors.

Animals↗