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Biomedical subjects

F Takeuchi

Publications and source records attributed to F Takeuchi.

At least 109 records · Page 6Linked to original sources
PubMed1988

Growth inhibitor of calcium oxalate monohydrate crystal in vitamin B6-deficient rat urine and kidney.

Urinary and renal inhibitory activities of calcium oxalate monohydrate crystal growth in normal or vitamin B6-deficient rats were investigated. Renal inhibitory activity in vitamin B6-deficient rats was lower than that in normal rats. Renal inhibitory activity in vitamin B6-deficient rats was about 74% of normal level. Urinary inhibitory activity did not show a significant difference between normal and vitamin B6-deficient rats.

Animals↗
PubMed1988

[Intracranial physiological calcification on computed tomography (Part 1): Calcification of the pineal region].

Of intracranial physiological calcification, common calcification of pineal region, choroid plexus of lateral ventricles and of basal ganglia was examined based on the frequency of occurrence of age and sex and type of CT scanners. Consecutive cases of 2877 (1450 males and 1427 females) underwent plain CT scanning were studied. Pathological calcification was excluded from this study. Three types of CT scanners (SCN-200, Somatom 2 and TCT-10 A) were used. As a whole, calcification was shown in 67.7% in pineal region, 57.6% in choroid plexus of lateral ventricles and 7.5% in basal ganglia. First, we reported in detail the calcification of pineal region, in which calcification occurred most frequently. Calcification in pineal region had a close relation with age by increasing with aging. The youngest patient was 8 years old. There was a striking increase in number of patients aged from 10 to 39 years. There was a gradual increase in those aged over 40 years. Of patients aged from 70 to 79 years, calcification was found in 81.5%. The incidence was noted no changes in patients aged over 80 years. As for patients aged over 20 years, calcification was observed in 75.1% (82.6% males and 68.0% females). In patients aged from 20 to 79 years, the calcification was significantly higher in male than female. Although there was a different incidence of calcification examined by three types of CT scanners, it was not significant. There was no significant difference between thickness of 8 mm section and 10 mm.

Adolescent↗
PubMed1988

[Intracranial physiological calcification on computed tomography (Part 2): Calcification in the choroid plexus of the lateral ventricles].

In this paper, we describe calcification in the choroid plexus of lateral ventricles with a discussion of the frequency of occurrence in categories of age, sex, and laterality, and its correlation with pineal calcification. The study was conducted on 2877 consecutive cases (1450 males and 1427 females) that had plain CT scanning. Three types of CT scanners (SCN-200, Somatom 2 and TCT-10 A) were used. This series included only calcification of the choroid plexus in the trigone of the lateral ventricles (glomus). Calcification was found in none of the cases aged under 9 years, 5.9% aged from 10 to 14 years and 17.4% aged from 15 to 19 years. The calcification rate strikingly increased with increasing age of the cases. It was 51.5% of cases between 30 and 39 years of age. After that, the increasing rate of calcification gradually decreased, however calcification was found in 74.4% of cases aged over 80 years. The calcification rate was 64.7% in our total series of cases aged over 20 years, 66.5% aged over 30 years and 70.7% aged over 50 years. The calcification rate of male cases was greater than that of females in the age group of over 15 years. However, there was a significant difference only in the cases ranging from 60 to 79 years of age. The initial incidence of male cases was found at the age of 12 years and that of females at the age of 16 years. There was no difference in calcification on right and left sides.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Changes in chromatin structure during aging of human skin fibroblasts.

Human skin fibroblasts from embryo, 16-, 30- and 60-year-old adults were cultivated and passaged in vitro. Their chromatin structures were examined by the sensitivity to micrococcal nuclease and by electron microscopy. When the mode of DNA degradation by the nuclease was analysed during in vitro aging of the embryo skin fibroblasts, the discrete ladder of nucleosomal DNA became obscure in old cells. Analogous change of chromatin structure was also observed even in young cells as their donor ages increased. From the observation with electron microscopy, it became clear that chromatin of fibroblasts from 30-year-old adults does not have regularly spaced nucleosomes, compared with chromatin from embryo. These results suggest that the length of the linker DNA which connects core particles becomes to be heterogeneous by aging, both in vivo and in vitro in human skin fibroblasts.

Adolescent↗
PubMed1987

The longest-lived patient with homozygous familial hypercholesterolemia secondary to a defect in internalization of the LDL receptor.

The authors report the longest-lived patient with homozygous familial hypercholesterolemia, the seventh case of a defect in internalization of low-density lipoprotein (LDL). The patient is a 57-year-old man, whose plasma total cholesterol (TC) and LDL-cholesterol (LDL-C) concentrations were 465-660 mg/100 ml and 461 mg/100 ml, respectively, while his plasma high-density lipoprotein-cholesterol (HDL-C) was 13.6-16.9 mg/100 ml. He was the product of a consanguineous marriage, and his parents, brothers, and a sister had mild hypercholesterolemia. His coronary angiogram revealed diffuse coronary artery narrowing. Receptor studies revealed that his fibroblasts bound as much LDL as normal cells, but could not internalize or degrade LDL.

Apoproteins↗
PubMed1986

Differential composition of cytosol 5'-nucleotidases between T and B lymphoblasts.

WI-L2 cells (a B-lymphoblastoid cell line) were more resistant than CEM cells (a T-lymphoblastoid cell line) to deoxyadenosine, ara-A (9-beta-D-arabinofuranosyladenine), or ara-C (1-beta-D-arabinofuranosylcytosine) inhibition. This was caused by a difference in the composition of cytosol 5'-nucleotidases between WI-L2 and CEM cells. In intact cells, the endogenous production of deoxyadenosine from WI-L2 cells deficient in adenosine kinase (EC 2.7.1.20) and deoxycytidine kinase (EC 2.7.1.74) was consistently high, despite changes in endogenous adenosine production. Endogenous production of deoxyadenosine from CEM cells deficient in adenosine kinase and deoxycytidine kinase was, however, coordinated with endogenous adenosine production. In broken cells, cytosol dAMPase (2'-deoxyadenosine 5'-monophosphate 5'-nucleotidase) activity of WI-L2 cells was 3-5-fold higher than that of CEM cells. dAMPase activity could be separated from ATP-activated IMPase (inosine 5'-monophosphate 5'-nucleotidase) by gel filtration (molecular weight: dAMPase; 39,000-46,000; ATP-activated IMPase, greater than 150,000). Cytosol ATP-activated IMPase and dAMPase were isolated by phosphocellulose or DEAE-Bio-Gel A chromatography from non-specific phosphatases. The ATP-activated IMPase showed only marginal activity towards dAMP (2'-deoxyadenosine 5'-monophosphate), ara-AMP (9-beta-D-arabinofuranosyladenine 5'-monophosphate), or ara-CMP (cytosine-beta-D-arabinofuranoside 5'-monophosphate), even in the presence of ATP. The activity of ATP-activated IMPase was similar in WI-L2 and CEM cells. dAMPase was separated into two peaks by DEAE-Bio-Gel A chromatography; one of these peaks degraded ara-AMP and ara-CMP. The activities of both peaks from WI-L2 cells were higher than those from CEM cells. These results show that the degradation of dAMP, ara-AMP or ara-CMP was more specific and rapid in WI-L2 than in CEM cells.

5'-Nucleotidase↗
PubMed1986

Altered kinetic properties of a mutant adenine phosphoribosyltransferase.

Three siblings in a Japanese family experienced recurrent 2,8-dihydroxyadenine urolithiasis despite the presence of adenine phosphoribosyltransferase (APRT) activities in the hemolysates (19.9% to 28.2% of normal value). However, studies on viable T cells from these patients indicated that APRT was not functional in viable cells. Further analysis of the partially purified enzymes from hemolysates disclosed that patient's APRT had a reduced affinity to 5-phosphoribosyl-1-pyrophosphate (PRPP). Seven healthy members of this family whose APRT functioned normally in viable T cells had the erythrocyte enzyme levels between the patients and normal individuals (38.2% to 65.6%), suggesting that they are carriers of the defective gene. These results indicate that the defective gene code a unique mutant APRT with a reduced affinity to PRPP, and the patients are homozygotes. The mutant enzyme was also shown to be more heat-stable than normal enzyme. However, since mutant enzyme, unlike normal enzyme, was insensitive to the stabilization effect of PRPP, the latter became more heat-stable than the former when the heat treatment was performed in the presence of PRPP. This type of defect with alterations in the kinetic and physical properties of APRT as described here is likely to be a common type of APRT deficiency in Japan.

Adenine Phosphoribosyltransferase↗
PubMed1986

Normal thermostability of hypoxanthine guanine phosphoribosyltransferase in erythrocytes from Werner's syndrome patients.

The thermostability of erythrocyte hypoxanthine guanine phosphoribosyltransferase of 2 Werner's syndrome patients was compared with that of normal subjects of different ages. No significant difference was observed regarding the thermal stability of the enzyme among normal subjects and Werner's syndrome patients. The activities of other erythrocyte enzymes, phosphoribosylpyrophosphate synthetase, adenine phosphoribosyltransferase, adenosine deaminase and purine nucleoside phosphorylase, were similar between Werner's syndrome and normal subjects.

Adult↗
PubMed1985

Two separate tyrosine protein kinases in human platelets.

Tyrosine protein kinase activities were detected in the cytosolic fraction (PC-TPK) and the particulate fraction (PM-TPK) in human platelets using the synthetic peptide, E11G1 (Glu-Asp-Ala-Glu-Tyr-Ala-Ala-Arg-Arg-Arg-Gly) as a substrate. PC-TPK and PM-TPK were different in substrate specificities, divalent cation requirements and apparent Mr values. These results strongly suggest that in platelets there exist at least two separate tyrosine protein kinases; one is present in cytosol and the other might be associated with membranes.

Blood Platelets↗
PubMed1985

Effect of tryptophan metabolites on the activities of rat liver pyridoxal kinase and pyridoxamine 5-phosphate oxidase in vitro.

Pyridoxal kinase was purified 4760-fold from rat liver. The Km values for pyridoxine and pyridoxal were 120 and 190 microM respectively, and pyridoxine showed substrate inhibition at above 200 microM. Pyridoxamine 5-phosphate oxidase was also purified 2030-fold from rat liver, and its Km values for pyridoxine 5-phosphate and pyridoxamine 5-phosphate were 0.92 and 1.0 microM respectively. Pyridoxine 5-phosphate gave a maximum velocity that was 5.6-fold greater than with pyridoxamine 5-phosphate and showed strong substrate inhibition at above 6 microM. Among the tryptophan metabolites, picolinate, xanthurenate, quinolinate, tryptamine and 5-hydroxytryptamine inhibited pyridoxal kinase. However, pyridoxamine 5-phosphate oxidase could not be inhibited by tryptophan metabolites, and on the contrary it was activated by 3-hydroxykynurenine and 3-hydroxyanthranilate. Regarding the metabolism of vitamin B-6 in the liver, the effects of tryptophan metabolites that were accumulated in vitamin B-6-deficient rats after tryptophan injection were discussed.

Animals↗
PubMed1985

Clinical, demographic, and genetic aspects of the Werner syndrome in Japan.

A total of 196 typical patients with the Werner syndrome, a caricature of aging, was studied to define the details of the clinical manifestations, demography and genetic aspects in Japan. Most of the previously reported clinical characteristics and the autosomal recessive inheritance of this syndrome were confirmed, but no significant linkage was revealed between specific HLA type and the Werner syndrome. The frequency of the Werner syndrome in Japan was estimated using two methods which indicated approximately 300 cases among 100 million people.

Adult↗
PubMed1985

Autoradiographic studies of DNA replication in Werner's syndrome cells.

We have compared cultured fibroblasts of early passage derived from patients with the Werner syndrome and from normal subjects in several aspects of cell cycle time and DNA replication. The average cycle time was prolonged in Werner's syndrome cells compared with normal cells because of changes in the duration of S phase. The durations of G1 and G2 were unchanged. In addition, the labeling index was lower in Werner's syndrome cells, suggesting that there are two cell-cycle abnormalities in Werner's syndrome cells. The cause of the prolongation of S phase was investigated by DNA fiber autoradiography and alkaline sucrose density gradient sedimentation. The rate of DNA chain elongation was not different in Werner's syndrome cells from that in normal cells, but the frequency of replication initiation was decreased in Werner's syndrome cells.

Adult↗
PubMed1985

Rapid method for the diagnosis of partial adenine phosphoribosyltransferase deficiencies causing 2,8-dihydroxyadenine urolithiasis.

More than half of the Japanese patients with 2,8-dihydroxyadenine urolithiasis only partially lack adenine phosphoribosyltransferase (APRT), while all the Caucasian patients with the same disease completely lack the enzyme. APRT activities in healthy heterozygotes for the complete APRT deficiencies were at the same levels as the Japanese patients, and simple enzyme assay does not distinguish between these two conditions. We have previously shown, using viable T-cells, that the enzyme was non-functional in the cells from the Japanese patients although they contain considerable APRT activities in the cell extracts. In the present investigations, we devised a rapid method using erythrocytes for the diagnosis of partial APRT deficiencies accompanied by severe impairment in adenine metabolism causing 2,8-dihydroxyadenine lithiasis. Thus, erythrocytes from three different families with 2,8-dihydroxyadenine urolithiasis associated with partial APRT deficiencies incorporated only minimal amounts of radioactive adenine, while normal erythrocytes incorporated significant amounts. These data indicate that severe impairment in adenine metabolism is shown not only in viable T-cells but also in viable erythrocytes. The present procedures provide a rapid method suitable for routine clinical use for the diagnosis of partial APRT deficiencies causing 2,8-dihydroxyadenine lithiasis.

Adenine↗
PubMed1985

Severe impairment in adenine metabolism with a partial deficiency of adenine phosphoribosyltransferase.

Among three unrelated patients with recurrent 2,8-dihydroxyadenine urolithiasis, two completely lacked adenine phosphoribosyltransferase (APRT) in both erythrocytes and proliferative T cells. The third patient possessed significant enzyme activities in both hemolysates and T-cell extracts at levels comparable to heterozygotes for complete APRT deficiency. Despite significant APRT activities in cell extracts, cultured T cells from the third patient were at least 100-fold more resistant than normal T cells to an adenine analog, 6-methylpurine, whose cytotoxicity is dependent on APRT. These data indicate that APRT activity in T cells from the third patient is positive in cell extracts, but apparently not operating in viable cells. Although the cells from the patients with complete APRT deficiency were as resistant to 6-methylpurine as the cells from the third patient, the cells from the heterozygotes for complete APRT deficiency were almost as sensitive as normal T cells. Therefore, adenine metabolism in the third patient but not in the heterozygotes seems to be as severely impaired as in the patients with complete APRT deficiency, which is quite consistent with the clinical manifestations in these individuals.

Adenine↗