Biomedical subjects
Publications and source records attributed to T Takeda.
We present a case report of a 73-yr-old woman with progressive systemic sclerosis who showed extensive pericardial uptake of 67Ga by scintigraphy. At autopsy, primary pericardial mesothelioma was found.
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Using a cell culture system, age-associated changes in immune activities were investigated in newly developed, short-lived mouse strains. These SAM-P strains of mice (H-2k), which have a remarkably short life span (around 9 months) under conventional breeding conditions, showed an age-associated early decline in several immune functions, as compared to ordinary strains of AKR/J (H-2k) and C3H/He (H-2k) mice. Their antibody-forming capacity to T-independent antigen, DNP-Ficoll, and natural killer (NK) cell activity showed a markedly early onset of regression and a sharp decline from the level of control mice at 2 months of age. SAM-P strains of mice have a profound defect in antibody response to a T-dependent (TD) antigen, such as sheep red blood cells (SRBC), thus there was only a feeble antibody response to SRBC as early as the age of 2 months, and a negligible response at a later age. In contrast, the allo-specific cytotoxic T lymphocyte (CTL) response of the mice was as high as that of control mouse strains at 2 months of age and declined little until at least 6 months of age. The early age-related functional decline in the immune system of SAM-P mice suggests that these new inbred strains are appropriate models for investigating the age-related appearance of immune dysfunctions.
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Seasonal variations in urinary levels of vanillylmandelic acid (VMA) and homovanillic acid (HVA) have been investigated over a two-year period, using 31,466 filter-paper specimens of urine from infants of 6 months of age who underwent Sapporo City's screening for neuroblastoma. Levels of both VMA and HVA (micrograms/mg creatinine) were significantly higher in summer (11.48 +/- 7.40, n = 7,569, and 18.70 +/- 8.18, n = 7,582, respectively) than in winter (10.72 +/- 5.76, n = 8,143, and 16.46 +/- 7.17, n = 8,148, respectively) throughout the two years (P less than 0.01, t-test). Although the cause of this difference could not be found, its actual clinical relevance was thought to be small since there was no significant relation between monthly rate of re-screened infants and monthly mean levels of VMA or HVA (P greater than 0.05, Spearman-Rank correlation).
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The establishment of cut off values in vanillylmandelic acid (VMA) and homovanillic acid (HVA) in 24-hr urine specimens for the purpose of separating true positive cases from normal infants has been discussed. The specimens were collected at the time when thorough examinations under a mass screening programme for neuroblastoma were taking place, and data from 17 infants with neuroblastoma (patients) and 50 healthy infants (controls) have been employed. The function square root VMA2 + HVA2 = 34 (micrograms/mg of creatinine) separated the two groups with no overlapping cases. This function represents the distance from the origin of the VMA-HVA co-ordinates, and is thought to be one of the most reasonable discriminant methods when considering the distribution pattern of the data for normal cases and patients.
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We describe a simple and rapid method for measuring catecholamine metabolites in urine collected on filter paper. By this method, "high-performance" liquid chromatography, urinary vanillylmandelic acid and homovanillic acid can be measured within 15 min after being eluted from filter paper treated with tartrate buffer. One hundred urine samples can be pretreated within 2 h and 100-120 samples analyzed at 18-min intervals overnight in two chromatographic systems. Moreover, urinary creatinine also can be measured rapidly because of the use of microtiter plates. We applied this method in a mass screening program for early detection of neuroblastoma in infants. Between April 1986 and March 1987, two patients with neuroblastoma were detected. In all, neuroblastoma has been detected in 17 of 88,887 infants so examined since April 1981.
Calcium-activated phospholipid dependent protein kinase (protein kinase C) activity in platelets was measured in 4, 12, and 20-week-old SHR and WKY. At age 4-weeks, there was no significant difference in protein kinase C activity and systolic blood pressure between SHR and WKY. In 12 and 20-week-old SHR, both protein kinase C activity and systolic blood pressure were significantly higher than in the age-matched WKY. These results suggest that protein kinase C may be involved in the control of blood pressure in SHR and WKY.
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The primary structure of murine apolipoprotein A-II (apo A-II) has been determined. Apo A-II consists of a single polypeptide chain of 78 amino acid residues, of which the amino-terminus is pyrrolidone carboxylic acid. Except for residues 5 and 38, the amino acid sequence is identical to that of murine senile amyloid protein (ASSAM), which has a common antigenicity with apo A-II. Substitution of glutamine (ASSAM) for proline (apo A-II) at position 5 is distinct and may possibly be related to murine senile amyloid-ogenesis.
Two putative serum precursors which cross-react with antiserum against murine senile amyloid protein (ASSAM) were isolated from the high density lipoprotein (HDL) of normal mouse serum. Apolipoproteins designated "apoSASSAM-1" and "apoSASSAM-2" have the same molecular weight as tissue amyloid fibril protein. ApoSASSAM-1 and apoSASSAM-2 migrate to an intermediate position between apoA-I and apoC on alkaline-urea polyacrylamide gel electrophoresis and are present mainly in HDL apoproteins and to a slight extent in very low density lipoprotein apoproteins when compared to apoC. ApoSASSAM-1 and apoSASSAM-2 are polymorphic; there are two apparent isoproteins of apoSASSAM-1 with isoelectric points of 4.72 and 4.79 and two major isoproteins of apo-SASSAM-2. Subunit bands of ASSAM separated by alkaline-urea polyacrylamide gel electrophoresis and that migrated to the same positions as apoSASSAM-1 and apoSASSAM-2 were labeled by anti-apoSASSAM-1 antiserum. The amino acid compositions of apoSASSAM-1 and apoSASSAM-2 were much the same and closely resembled those of ASSAM and mouse apoA-II. Sequence analysis of apoSASSAM and ASSAM revealed a blocked amino terminus. ApoSASSAM is considered to be a mouse apoA-II and probably transforms to amyloid fibril "ASSAM" in tissues through a process yet to be clarified.
The primary structure of a murine senile amyloid protein (ASSAM) was determined. The protein consists of a single polypeptide chain of 78 amino acid residues. The amino-terminus is blocked with pyrrolidone-carboxylic acid. The sequence differs from that of the known murine amyloid A protein and is highly homologous to human apolipoprotein (apo) A-II. The result indicates that the putative precursor of the senile amyloid protein is apo A-II in mice.
cDNA clones encoding the murine senile amyloid protein (ASSAM) have been isolated from animal models of accelerated senescence (SAM-P/1) and from normal aging (SAM-R/1). Immunochemical and protein sequence studies revealed that apolipoprotein (apo) A-II is a serum precursor of ASSAM. A 17-base synthetic oligonucleotide based on residues 39-44 of ASSAM was used as a hybridization probe for screening newly constructed SAM-P/1 and SAM-R/1 liver cDNA libraries. The structure of murine apo A-II cDNA is of interest because of the amino acid substitution found in ASSAM and serum apo A-II of SAM-P; in SAM-R or other random bred slc:ICR mice, amino acid residue 5 of mature apo A-II is proline but, in SAM-P, this amino acid is changed to glutamine. This amino acid replacement is caused by two nucleotide substitutions (CCA for proline codon to CAG for glutamine codon). The third base mutation may not be relevant to the substitution of amino acid. Attention is directed to the relation of this amino acid substitution to the specific deposition of apo A-II, as a tissue amyloid fibril.
We developed a solid-phase radioimmunoassay for complement (C)-fixing nuclear ribonucleoprotein (nRNP):anti-nRNP immune complexes (nRNP ICs). The assay was based on the ability of the C-fixing nRNP ICs to bind strongly to immobilized F(ab')2 anti-C3. The extent of binding was quantified by incubating the C-fixing nRNP ICs bound to anti-C3 with 125I-labeled anti-nRNP-specific IgG. The interaction between anti-C3 and C-fixing nRNP ICs was rapid, time- and concentration-dependent and sensitive over a broad range of nRNP IC concentrations in an antigen-antibody ratio of 8 : 1 (9.8-5000 ng of human aggregated IgG equivalent per ml). We found that the assay also detected an immunoreactive U1-RNP antigen in Sm : anti-Sm immune complexes but did not detect SSA : anti-SSA immune complexes. The assay was preliminary applied for serum samples obtained from patients with mixed connective tissue disease (MCTD), and elevated concentrations of nRNP immune complexes were found in 3 out of 5 patients with MCTD. This assay appears to be applicable to the detection and quantification of circulating nRNP ICs in patients with MCTD.