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Biomedical subjects

K Ishiguro

Publications and source records attributed to K Ishiguro.

At least 127 records · Page 7Linked to original sources
PubMed1994

Fluoride distribution in dentine and cementum in human permanent teeth with vital and non-vital pulps.

Twenty-two selected permanent teeth [11 with vital pulps and 11 with non-vital (necrotic) pulps] were obtained from patients aged from 20 to 73 yr in Nagoya, Japan. Fluoride (F) profiles in tooth samples were examined by using an abrasive micro-sampling technique. F levels in the pulpal dentine were significantly higher in vital than non-vital teeth for each age group, although there were observed increases of F with age. In the cementum the F levels were strongly related to age and there were few differences in profiles and levels of F between vital and non-vital teeth. It was concluded that vital pulp is an important factor for the pulpal dentine to absorb fluoride.

Adult↗
PubMed1994

Identification of tissue inhibitor of metalloproteinases-1 (TIMP-1) in human teeth and its distribution in cementum and dentine.

An inhibitory activity toward matrix metalloproteinases such as interstitial collagenase, 72-kDa gelatinase/type IV collagenase, and stromelysin-1 was detected in an EDTA extract of pulverized roots of human teeth, and identified as TIMP-1 by sodium dodecyl sulphate-polyacrylamide gel electrophoresis and immunoblotting. Distribution of TIMP-1 in human cementum and dentine was investigated by a sandwich enzyme immunoassay in combination with an abrasive microsampling technique. TIMP-1 could not be detected in cementum from some teeth but in others decreased from a fairly low value at the surface towards the cementodentinal junction. TIMP-1 concentrations in the dentine increased consistently from the cementodentinal junction toward the predentine. The average TIMP-1 concentration in the dentine (54.1 +/- 18.5 pg/mg +/- SE) was significantly (P < 0.05) higher than that (9.6 +/- 6.0 pg/mg +/- SE) in the cementum.

Adolescent↗
PubMed1994

The specific inhibition of crystal growth of monohydrogen potassium L-tartrate by d-catechin.

Crystal growth of monohydrogen potassium L-tartrate in an ethanolic aqueous solution was specifically inhibited by d-catechin, but not by either its epimeric isomer at C3, l-epicatechin or by gallic acid and caffeic acid. 3D-Structure similarity search of d-catechin with two molecules of the tartrate and docking study of d-catechin with the crystal model of the tartrate suggested that d-catechin mimics a structure consisting of the two tartrate molecules in the inhibition. Differences in the conformation of the catechol moieties of d-catechin and l-epicatechin may explain the distinct inhibitory effects of the epimeric isomers.

Catechin↗
PubMed1994

Microfluorocytometric detection of nuclear DNA damage to cancer cells in squamous cell carcinoma after hyperthermia.

An 84-year-old woman had a squamous cell carcinoma on her left thigh. Before operation, half of the tumor mass was irradiated with a microwave at 43 degrees C for an hour. After the hyperthermia, the tumor mass was removed, and the DNA instability was investigated by microfluorocytometric measurement of the cells stained with pararosaniline-Feulgen after hydrolysis with 2N HCl at 30 degrees C. The kinetic parameters k1, which is the rate constant for the generation of an apurinic acid, k2, which is the rate constant for the depolymerization of the apurinic acid and which reflects the degree of DNA instability for acid hydrolysis, and y0, which is the theoretical value of the single-stranded DNA present initially and reflects the degree of DNA damage, were determined by a computer fitting of the Bateman function to the hydrolysis curve plotting of the fluorescence intensity of the pararosaniline-Feulgen staining the apurinic acid against the different hydrolysis times. The parameter values y0 and k2 of the cells treated by hyperthermia were much higher than those of the cells treated without hyperthermia. It is our conclusion that this microfluorometric detection would be valuable as an evaluation method for a cancer therapy, although more data from other cancers and treatments will be needed.

Aged↗
PubMed1994

[Prolonged exposure to intravesical foreign body induces a giant calculus with attendant renal dysfunction].

A 31-year-old man came to our hospital complaining of severe voiding pain. He had inserted a fishing line made of nylon into his urethra at the age of eighteen, which was unable to be taken out and had been left there for 13 years. Preoperative ultrasonogram showed severe bilateral hydronephrosis and the serum BUN and creatinine level were as high as 45.2 mg/dl and 4.8 mg/dl, respectively. A huge bladder stone was demonstrated in X-ray film, the patient was admitted and vesicolithotomy was performed. The size of the stone was 10.5 x 7.5 x 7.5 cm and the weight was 360 grams. The fishing line was found inside the stone and the length was over 3 meters. The serum BUN and creatinine level after the operation were still high as 28.4 mg/dl and 4.1 mg/dl, respectively, and they did not improve even after six months following.

Adult↗
PubMed1993

A cdc2-related kinase PSSALRE/cdk5 is homologous with the 30 kDa subunit of tau protein kinase II, a proline-directed protein kinase associated with microtubule.

We previously reported that tau protein kinase II (TPKII) from bovine brain was composed of 30 kDa and 23 kDa subunits. The 30 kDa subunit of TPKII can be regarded as a catalytic subunit because of its ATP-binding activity. Antibodies directed against TPKII-phosphorylated tau also reacted with tau phosphorylated by cdc2 kinase obtained from starfish oocytes, indicating that TPKII and cdc2 kinase phosphorylate the same sites. We determined the amino acid sequence of the 30 kDa subunit and found it to be homologous with a cdc2-related kinase, PSSALRE/cdk5. Moreover, an antibody against PSSALRE/cdk5 reacted with the 30 kDa subunit. These results indicate that the 30 kDa subunit of TPKII is bovine homologue of PSSALRE/cdk5. Expression of the 30 kDa subunit mRNA was enhanced in juvenile rat brain. This result supports our previous hypothesis that the kinase works actively in juvenile brain.

Amino Acid Sequence↗
PubMed1993

Interaction of the tail domain of high molecular weight subunits of neurofilaments with the COOH-terminal region of tubulin and its regulation by tau protein kinase II.

We previously showed that neurofilaments interact with microtubules (MTs) via their high molecular weight subunits (NF-H) after alkaline phosphatase treatment. Here we studied the effects of phosphorylation of NF-H on this interaction. tau protein kinase II, Ser/Thr protein kinase, phosphorylated NF-H in the tail domain, decreased its electrophoretic mobility to a native level, and also restored its property to be less interactive with MTs. Phosphorylation by cAMP-dependent protein kinase caused no shift of electrophoretic mobility or dissociation from MTs. We conclude that the tail domain of NF-H directly interacts with the MT surface, and the interaction is regulated via phosphorylation of the tail domain of NF-H by Ser/Thr protein kinase like tau protein kinase II. To characterize the binding domain of NF-H on MTs, subtilisin digestion of MTs and competition analysis with the MT binding fragment of tau protein were performed. The dissociation constant of NF-H to subtilisin MTs was higher than that to intact MTs. The maximum binding of NF-H was reduced when tau fragments existed. These results revealed that the COOH-terminal region of tubulin is involved in the binding to NF-H, and the NF-H and microtubule-associated protein binding domains are closely apposed on the surface of MTs.

Animals↗
PubMed1993

Tau protein kinase II has a similar characteristic to cdc2 kinase for phosphorylating neurofilament proteins.

Tau protein kinase II purified from a bovine brain tau protein fraction (Ishiguro, K., Takamatsu, M., Tomizawa, K., Omori, A., Takahashi, M., Arioka, M., Uchida, T., and Imahori, K. (1992) J. Biol. Chem. 267, 10897-10901) was shown to have a similar substrate specificity to cdc2 kinase in that both phosphorylate neurofilament (NF) proteins. Tau protein kinase II recognized the dephosphorylated form of the heavy subunit of NF (NF-H) as a predominant substrate. The substrate was phosphorylated to the same extent with tau protein kinase II as with cdc2 kinase. Upon phosphorylation, the electrophoretic mobility of the NF-H on SDS-polyacrylamide gel electrophoresis changed to the position of the phosphorylated form. A synthetic peptide containing a KSPXK sequence was by far a better substrate for tau protein kinase II than that containing a KSPXX sequence, as was also observed with cdc2 kinase. NF-H lost its microtubule-associating ability upon phosphorylation with tau protein kinase II as well as with cdc2 kinase. Although anti-PSTAIR antibody (PSTAIR is an amino acid sequence commonly found in cdc2 and several cdc2-related kinases) failed to react with tau protein kinase II, tau protein kinase II bound to p13suc1-Sepharose beads (p13suc1 is a yeast protein known to bind to cdc2 kinase).

Amino Acid Sequence↗
PubMed1993

Glycogen synthase kinase 3 beta is identical to tau protein kinase I generating several epitopes of paired helical filaments.

We previously reported that tau protein kinase I (TPKI) induced normal tau protein into a state of paired helical filaments (PHF); this is further confirmed here by immunoblot analysis using several antibodies. We also present the amino acid sequence of TPKI, which is identical to glycogen synthase kinase 3 beta (GSK3 beta). Moreover, we found that TPKI activity was inseparable from GSK3 activity throughout the purification procedure. These results indicate that TPKI is identical to GSK3 beta.

Amino Acid Sequence↗
PubMed1993

Amyloid beta protein precursor accumulates in swollen neurites throughout rat brain with aging.

We immunocytochemically studied the expression of amyloid beta protein precursor (APP) in the brains of normal aged rats, and found APP accumulation in swollen neurites, most of which were axons. These swollen neurites appeared throughout the central nervous system of aged rats; most of them were negative for neurofilament, ubiquitin, and tau. Such widely distributed APP accumulation in swollen neurites may reflect impaired fast axonal transport due to aging. APP immunostaining may be a good method to detect widely distributed age-related changes.

Aging↗
PubMed1993

Diagnostic significance of skin immunolabelling with antibody against native cerebral amyloid in Alzheimer's disease.

Skin taken from patients with Alzheimer's disease (AD) and control patient groups were immunolabelled using antisera against either purified native cerebral beta protein or synthetic beta peptide. Native amyloid antiserum frequently labelled vascular walls in AD skin but rarely in control skin. Semi-quantitative analysis of the positive vessels showed a significant difference between the two groups. Sweat glands and dermal nerves were labelled in both groups. However, synthetic beta peptide antiserum showed no significant difference. Vascular wall labelling in skin with native amyloid antiserum is useful in the differential diagnosis of AD.

Aged↗
PubMed1993

Distribution of fluoride in cortical bone of human rib.

We describe a detailed study of fluoride distribution with age in the human cortical rib bone. Human ribs were obtained from 110 subjects (M:68, F;42) aged 20-93 years. The fluoride distribution from the periosteal to endosteal surfaces of the ribs was determined by sampling each specimen using an abrasive micro-sampling technique, and the samples were analyzed using the fluoride electrode, as described by Weatherell et al. [1]. The concentration of fluoride was highest in the periosteal region, decreased gradually towards the interior of the tissue where the concentration of fluoride tended toward the plateau, and then rose again towards the endosteal surface. Patterns of fluoride distribution changed with age, and the difference between periosteal and endosteal fluoride levels increased with age. Although average fluoride concentrations increased with age in both sexes, there was a significant difference between males and females at the age of about 55 years (P < 0.05).

Adult↗
PubMed1993

Hypertension in rats does not potentiate hypercholesterolemia and aortic cholesterol deposition induced by a hypercholesterolemic diet.

The effect of a hypercholesterolemic diet (HCD) on hyperlipemia and atherogenesis was investigated using normotensive Wistar/Kyoto rats (WKY), spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP), with systolic blood pressures increasing in that order. Feeding an HCD diet containing cholesterol, cholate and suet induced hypercholesterolemia in all the strains examined as compared with a normal diet. The plasma cholesterol levels were significantly higher in WKY than in SHR and SHRSP fed the HCD diet. The HCD diet also induced hepatic fat deposition, particularly deposition of cholesteryl esters, a slight increase in aortic cholesterol deposition, and elevation of both monoenoic/saturated fatty acid ratios and linoleate/arachidonate ratios in tissue lipids. The changes induced in the three strains by the HCD diet were not positively correlated with blood pressures. The HCD diet affected hepatic acyl-CoA:cholesterol acyltransferase and plasma lecithin:cholesterol acyltransferase activities differently in WKY and SHR which, in addition to the induction of delta 9 desaturase, may partly account for the difference in the diet-induced changes in the fatty acid compositions of plasma cholesteryl esters. The results indicate that hypertension per se does not stimulate the development of hypercholesterolemia and arterial cholesterol deposition induced by an HCD diet, suggesting that other factors are involved.

Animals↗
PubMed1993

Differential expression of alpha 1-antichymotrypsin in the aged human brain.

The localization of alpha 1-antichymotrypsin (ACT) mRNA and ACT immunoreactivity (ACT-IR) were examined in 12 brains obtained at post-mortem from elderly patients, four of whom had Alzheimer's disease. A biotinylated oligonucleotide probe was used for in situ hybridization histochemistry and the relationship between the expression of both ACT mRNA and ACT-IR and the extent of beta protein or tau deposition were investigated. The extent of beta-plaques, tau-tangles, and ACT-IR were rated from (-) to (++). In brains without plaques and tangles, there were no detectable ACT mRNA signals in the gray matter, and those in the white matter were weak; in these brains, ACT-IR was generally weak. The brains with beta-plaques but no tangles showed weak ACT mRNA expression in astrocytes of both the gray and white matter; they also showed weak ACT-IR in the astrocytes. In the brains from patients with Alzheimer's disease with both plaques and tangles, ACT mRNA was expressed intensely in a majority of the astrocytes in the white and gray matter. Some senile plaques-associated astrocytes expressed ACT mRNA and ACT-IR was strong in the white matter astrocytes. ACT-IR and ACT mRNA expression in astrocytes was correlated with the extent of beta and tau depositions.

Aged↗
PubMed1993

Tau protein kinase II is involved in the regulation of the normal phosphorylation state of tau protein.

To study the phosphorylation state of tau in vivo, we have prepared antisera by immunizing rabbits with synthetic phosphopeptides containing phosphoamino acids at specific sites that are potential targets for tau protein kinase II. Immunoblot experiments using these antisera demonstrated that tau in microtubule-associated proteins is phosphorylated at Ser144 and at Ser315. Almost all tau variants separated on two-dimensional gel electrophoresis were phosphorylated at Ser144 and nearly one-half of them at Ser315. Phosphorylation at Ser144 and at Thr147 of tau isolated from heat-stable brain extracts was shown to be developmentally regulated, with the highest level of phosphorylation found at postnatal week 1. In vitro phosphorylation of tau by tau protein kinase I, a kinase responsible for abnormal phosphorylation of tau found in paired helical filaments of patients with Alzheimer's disease, was enhanced by prior phosphorylation of tau by tau protein kinase II. Thus, we suggest that tau protein kinase II is indirectly involved, at least in part, in the regulation of the phosphorylation state of tau in neuronal cells.

Aging↗