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Biomedical subjects

M Takaoka

Publications and source records attributed to M Takaoka.

At least 145 records · Page 8Linked to original sources
PubMed1990

Epidemiological study of mites and guanine in house dust.

The total number of mites, and the amount of guanine contained in house dust was determined in samples obtained from homes with and without asthmatic patients in Yokohama City. The data were quantified and their possible association with various factors within the home was examined. The largest number of mites and the greatest amount of guanine were most strongly associated with carpet floor coverings, followed by tatami mats, and then by wooden flooring. A multi-variate analysis revealed that the major factors influencing the number of mites and the amount of guanine in homes were the living room flooring, and the age of the house. Correlation to such living factors ranged from 60 to 70 percent. In the families with asthmatics the frequency of cleaning was an important additional factor. This likely was a result of the strict instructions given by doctors to asthmatic patients. It was shown that the amount of guanine contained in house dust is an indicator of not only the number of mites but also of the amount of allergens contained in home dust.

Animals↗
PubMed1990

Conversion of rat urinary prokallikrein to its active form.

A peptide derived from rat urinary prokallikrein by trypsin treatment comprised 7 amino acids, the sequence (Ala-Pro-Pro-Val-Gln-Ser-Arg) of which was identical with that of the N-terminal region in prokallikrein. Thus, with trypsin treatment, rat urinary prokallikrein is converted to the active form with the release of the N-terminal propeptide consisting of 7 amino acids. An Arg-1-Val+1 bond in the prokallikrein was found to be the site of proteolytic cleavage of the propeptide.

Amino Acid Sequence↗
PubMed1990

[Results of patch test using mite components in atopic dermatitis (AD) patients. 1st report. "As is patch test" using crushed mites].

UNLABELLED: As is patch test using crushed live mites and crushed dried dead mites of Dermatophagoides pteronyssinus (D.p.), Dermatophagoides farinae (D.f.), & Tryophagus ptrescentiae (T.p.) was performed on 49 AD patients and 18 control patients suffering from dermatitis other than AD. RESULTS: 1) with crushed dried dead mites all patients showed negative reactions but with live mites 11 among 49 AD patients were positive (22.4%); 2) female mites were more positive than males at the rate 8:1; 3) with cases positive to mites, (a) D.p. was positive in all 11 positive cases (100%), (b) D.f. was negative in 5 cases (0%), and (c) T.p. was positive in 2 cases among 4 (50%); 4) because of the pathological manifestations of spongiosis and the infiltration of histiocytes and lymphocytes, the possibility of contact allergy to mite elements was suggested, as a mechanism of atopic dermatitis.

Adolescent↗
PubMed1990

[Result of "as is patch test" using mite elements in atopic dermatitis (AD) patient. 2nd report, "Mite lipid"].

The antigenicity of mite lipid was studied, taking atopic dermatitis as an allergic disease. Lipid was extracted from Dermatophagoides pteronyssinus (Dp) and D. farinae (Df). It was tentatively designated a mite lipid antigen (Dp-L, Df-L), and then a patch test was performed. An extract from animal food (LC) and acetone were used as the controls. With only Dp-L, a positive reaction of more than one plus (+) of the ICDRG standard was noted in 3 out of 21 cases of AD. Histology of the above-mentioned positive cases revealed spongiosis and infiltration of small round cells in the upper dermis along with scattered eosinophiles. Leu 6 positive cells were noted frequently in the epidermis and dermis. The lipid components of Dp-L were made up mostly of phospholipid and triglycerides+, and lipoprotein was not contained. Judging from the findings above it appears necessary to study not only protein but also lipid in connection with the mite antigenicity++ in AD in the future.

Adolescent↗
PubMed1989

Purification and partial characterization of a thiol proteinase activating prokallikrein from the rat kidney cortex.

The rat kidney cortex contains at least three kinds of prokallikrein-activating proteinase, and among these the one with the highest molecular weight was purified by a procedure including chromatography on CM-cellulose, concanavalin A-Sepharose, organomercurial-Sepharose 4B and Sephadex G-100. The resulting preparation was apparently homogeneous, as assessed by SDS-polyacrylamide gel electrophoresis. The molecular weight was estimated to be 57,000. The optimal pH for the activation of prokallikrein by the preparation, termed activator I, was around 4.5. Activator I was inhibited by E-64, iodoacetate and leupeptin, but not by PMSF and phosphoramidon. In immunodiffusion analysis, the antiserum to activator I formed an immunoprecipitin arc with the extract from the kidney cortex or submandibular gland, but not with that from the pancreas. These results indicate that activator I is a thiol proteinase with a molecular weight of 57,000. A proteinase immunologically identical with activator I appears to be present in the submandibular gland.

Amino Acids↗
PubMed1989

Activation of inactive kallikrein in the rat kidney during low sodium intake.

A method was developed to measure the protease responsible for activation of inactive kallikrein in the rat kidney. The renal protease was evaluated by incubating the purified rat urinary inactive kallikrein with the renal cortical extract in the presence of cysteine at pH 5.0. The renal cortical extract produced a dose- and time-dependent activation of the inactive kallikrein. Levels of the renal protease responsible for activation of inactive kallikrein remained unchanged with dietary sodium restriction. On the other hand, urinary excretion of total, active, and inactive kallikrein increased significantly during low sodium intake, with no change in the ratio of active to total kallikrein. These results suggest that low sodium intake stimulates the biosynthesis of inactive kallikrein but not the activation of this kallikrein precursor in the kidney.

Animals↗
PubMed1989

[A case of nephrotic syndrome associated with pulmonary infarction and renal vein thrombosis. (A review of literature)].

A case of nephrotic syndrome found by pulmonary infarction associated with renal vein thrombosis was reported. The renal biopsy showed the presence of membranous glomerulonephritis. The patient had the increase of serum level of the coagulation factor II, V, fibrinogen and FDP, and the level of urine FDP. These laboratory data suggested that the hyper coagulation state of his blood caused by nephrotic state, induced his multiple thromboembolism. We surveyed 47 case report abstracts of nephrotic syndrome patients having thromboembolism on the Japanese Journal of Nephrology published from 1974 to 1986. The histopathology of their renal biopsies showed the high incidence of membranous glomerulonephritis, followed by minimal change nephrotic syndrome and focal glomerular sclerosis. Renal vein thrombosis was the most common thromboembolism in the reports, followed by thrombosis of cerebral vessels, peripheral vessels and pulmonary artery. Some patients died of pulmonary infarction or myocardial infarction. These data showed that we must keep in mind of the possibility of thromboembolism in the treatment of nephrotic syndrome.

Glomerulonephritis, Membranous↗
PubMed1988

The effects of H1- and H2-receptor blocking agents on postsynaptic potentials recorded from the bull-frog sympathetic ganglion.

The effects of H1-blockers (pyrilamine, diphenhydramine and promethazine) and H2-blockers (cimetidine, ranitidine) on the postsynaptic potentials of the bull-frog sympathetic ganglion were studied by means of the sucrose gap method. All the H1-blockers tested, at concentrations of 10(-6)-10(-4) M, depressed the amplitudes of both action and slow postsynaptic potentials in positive and negative directions in a concentration-dependent manner; these drugs had more potent inhibitory effects on postsynaptic potentials. In the case of H2-blockers, action and postsynaptic potentials were slightly depressed as perfusion continued at 10(-4) M. From the present experiments, it was concluded that H1-blockers directly inhibit postsynaptic potentials of the sympathetic ganglions, and that this inhibition may be responsible for various autonomic disturbances attributed to H1-blockers.

Action Potentials↗
PubMed1988

Mechanism of hematuria. II. A scanning electron microscopic demonstration of the passage of blood cells through a glomerular capillary wall in rabbit Masugi nephritis.

A model of hematuria was established in rabbits. An accelerated form of unilateral Masugi nephritis was induced in 10 New Zealand white rabbits by an intravenous injection of duck antirabbit kidney serum and by ligating the left renal artery immediately after the injection of the antibody. All 10 rabbits became hematuric 1-2 weeks after the injection of the antibody and red blood cell (RBC) casts were found in the urinary sediment of all these animals. An ultrastructural examination of renal glomeruli by transmission electron microscopy revealed the transcapillary passage of polymorphonuclear leukocytes through the gaps of the glomerular basement membrane (GBM). RBC were found in the urinary space in 50% of the glomeruli observed by scanning electron microscopy (SEM) and the passage of leukocytes and RBCs through the glomerular capillary wall was also observed. Gaps in the GBM became clearer after the removal of cellular components by detergents. In control rabbits, no RBCs could be observed in the urinary space, and isolated GBM were intact by SEM. These data further support the hypothesis that in rabbit Masugi nephritis hematuria is a result of the passage of RBCs through gaps in the GBM.

Animals↗
PubMed1988

Effect of sodium intake on urinary renin excretion in rats.

The present study was carried out to investigate the effect of sodium intake on urinary renin excretion in rats. Renin activity was measured before and after acidification, by radioimmunoassay of angiotensin I generated by incubation with partially purified homologous renin substrate. The molecular weight of renin was determined by gel filtration. Low sodium intake for 4 weeks resulted in a 16-fold increase in urinary renin excretion and led to a 15-fold increase in plasma renin activity. A 2.5-fold increase in renal renin content was simultaneously observed. In contrast, high sodium intake for 4 weeks decreased urinary renin excretion, plasma renin activity and renal renin content to about 20%, 25% and 35% of the control level, respectively. No significant change in renin activity after acidification was observed in all the urine samples. The molecular weight of renin in the urine from rats on low or high sodium intake was 40,000, the value being identical with that from control rats. These results indicate that urinary renin excretion is well correlated with plasma renin activity, and that only active renin with a molecular weight of 40,000 is excreted in the urine of rats, even under conditions of altered sodium intake.

Animals↗
PubMed1988

Occurrence of spontaneous diabetes mellitus in a cynomolgus monkey (Macaca fascicularis) and impaired glucose tolerance in its descendants.

Spontaneous diabetes mellitus was diagnosed in a cynomolgus monkey. Clinical and pathological features, such as abnormal glucose tolerance, loss of insulin response, or degeneration of pancreatic beta-cells, resemble human noninsulin-dependent diabetes mellitus. Two descendants of the monkey have developed impaired glucose tolerance and insulin response. Genetic factors seem involved in the appearance of carbohydrate intolerance in this family group of monkeys.

Animals↗
PubMed1988

Immunological identification of rat urinary inactive kallikrein as a proform of tissue kallikrein.

Antibody was raised against a synthetic undecapeptide (PS 11) which corresponds to the prosegment of the rat tissue kallikrein precursor. The potential to recognize rat urinary active or inactive kallikrein was assessed by an enzyme immunoassay method for PS 11, using beta-D-galactosidase as the labeling enzyme. The active kallikrein failed to compete with the enzyme-labeled PS 11 in binding to the antibody. The inactive kallikrein displaced the enzyme-labeled PS 11 in this enzyme immunoassay, and the displacement curve was in parallel with that of PS 11. These results indicate that rat urinary inactive kallikrein contains a prosequence recognized by the antibody to PS 11. This inactive kallikrein is probably a proform of tissue kallikrein.

Animals↗
PubMed1987

Fibrillar ultrastructure of the glomerular basement membrane of the rat kidney as revealed by digestive treatment.

Rat kidney glomerular basement membrane (GBM) was isolated and digested with alpha-amylase and elastase. Electron microscopy revealed a meshwork structure composed of fibrils 3 nm in width. They appeared to be type IV collagen fibrils. We succeeded in clarifying a significant ultrastructural aspect of the GBM which had been unclear until now. The findings are consistent with our previously proposed GBM molecular sieve theory.

Animals↗