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Biomedical subjects

M Majima

Publications and source records attributed to M Majima.

At least 19 recordsLinked to original sources
PubMed1992

A useful and sensitive method for demonstration of the involvement of either kallikrein-kinin system in pathological states.

In rat carrageenin-induced pleurisy, bradykinin (BK) was hardly able to be detected (< 160 pg per rat) in the exudates. In contrast, des-Phe8-Arg9-BK (des-8,9-BK) level, determined by an enzyme immunoassay (EIA) newly developed, was larger in the exudate and the levels were kept throughout the entire course of this inflammation. Arg-Pro-Pro-Gly-Phe ([1-5] BK) level, measured by an EIA newly developed, was much higher than that of des-8,9-BK in the exudate. Intrapleural administration of soy bean trypsin inhibitor (0.3 mg per rat) reduced the levels of both des-8,9-BK and [1-5] BK in the exudates. Reduction in the residual levels of plasma prekallikrein (P-Kall) and high-molecular-weight-kininogen (HMW-K), not low-molecular-weight-kininogen (LMW-K), were accompanied with increase in these BK degradation products, indicating that plasma prekallikrein was activated in the pleural cavity. On the other hand, intravenous injection of acetaldehyde to rats pretreated with disulfiram resulted in the significant increase in the levels of [1-5] BK in the blood, which was accompanied with reduction in the residual levels of LMW-K, not of HMW-K and P-Kall in plasma. These results indicated that the detection of BK degradation products was a good marker for the kinin release in vivo and that the concomitant reduction of the precursor proteins allowed us to identify the type of kallikrein-kinin systems relevant to the kinin release.

Acetaldehyde↗
PubMed1992

Ion-spray mass spectrometric analysis of glycosaminoglycan oligosaccharides.

Oligosaccharides from hyaluronic acid and chondroitin 6-sulfate were prepared by digestion with testicular hyaluronidase and separated according to their degree of polymerization by gel-permeation chromatography. These materials were successively analyzed by negative-mode ion-spray mass spectrometry with an atmospheric-pressure ion source. An ion-spray interface was used to produce ions via the ion evaporation process, producing mass spectra containing a series of molecular species carrying multiple charges. Using two adjacent multiply charged molecular ions, the exact molecular weights up to the tetradecasaccharide were calculated with a precision of +/- 1 dalton. This type of mass spectrometry was also demonstrated to be feasible for the analysis of mixtures of oligosaccharides, including tetra-, hexa-, octa- and decasaccharides, from hyaluronic acid or chondroitin 6-sulfate without separation. Ion-spray mass spectrometry was thus shown to be applicable to the structural analysis of oligosaccharides from glycosaminoglycans.

Animals↗
PubMed1992

A unique case of cutaneous calcinosis with transepidermal elimination.

A case of cutaneous calcinosis with unique clinical and histological features which occurred on the cheek of a 14-year-old girl, is reported. Our case had no abnormal findings in laboratory data. Serum calcium and phosphate were normal, there was no underlying disease, and the possibility of self-inflicted dermatoses was denied. Transmission electron microscopy and X-ray microanalysis showed calcium and phosphate deposited around collagen fibers, which were eliminated from the epidermis.

Adolescent↗
PubMed1992

Increased secretion of glandular-kallikrein in the bronchial washings induced by intravenous injection of leukotriene C4 in guinea-pigs.

1. Intravenous administration of leukotriene C4 (LTC4) and LTD4 (1-10 nmol kg-1) caused a dose-dependent increase in secretion of glandular-kallikrein in the bronchial washings of guinea-pigs, as measured by cleavage of a synthetic substrate and the formation of kinin. LTC4 was more potent than LTD4 and pilocarpine was much less potent than peptide leukotrienes on a molecular basis. 2. The increases in levels of glandular-kallikrein in the bronchial washings that were induced by LTC4 (3 nmol kg-1, i.v.) were almost completely inhibited by pretreatment with an antagonist of leukotrienes (ONO-1078), with an antagonist of thromboxane (S-1452), with an inhibitor of thromboxane synthetase (OKY-046), with indomethacin, with atropine or with scopolamine. These results indicate that the LTC4-induced increase in levels of glandular-kallikrein may have been mediated by the formation of thromboxane and the release of acetylcholine. 3. The increases in levels of glandular-kallikrein in the bronchial washings induced by STA2 (20 pmol kg-1, i.v.), a stable analogue of thromboxane A2, were completely blocked by pretreatment with atropine, whereas increases induced by pilocarpine (41 mumol kg-1, i.v.) were not blocked by pretreatment with indomethacin, although such increases were inhibited by atropine. This result indicates that secretion of kallikrein stimulated by LTC4 may have been mediated by the successive formation of thromboxane A2 and release of acetylcholine. 4. Intravenous administration of bradykinin (3-30 nmol kg-1) caused a dose-dependent increase in levels of glandular-kallikrein in the bronchial washings. This increase was completely inhibited by pretreatment with atropine, with indomethacin or with an antagonist of thromboxane.5. The increases in levels of glandular-kallikrein in the bronchial washings induced by LTC4 (3 nmol kg'- , i.v.) and pilocarpine (41 flmol kg- 1, i.v.) were significantly inhibited by pretreatment with an antagonist of bradykinin. These results suggest that intravenous LTC4 may increase secretion of glandular-kallikrein via formation of thromboxane A2 and release of acetylcholine in that order, and kinin released by kallikrein may enhance the rate of secretion of glandular-kallikrein.

Acetylcholine↗
PubMed1992

A stable metabolite, Arg-Pro-Pro-Gly-Phe, of bradykinin in the degradation pathway in human plasma.

Degradation of bradykinin (BK) in human plasma was investigated by searching for a stable metabolite as a marker of kinin release in vivo. BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK). Des-9-BK was degraded to [1-5]BK without an increase in des-8,9-BK, and des-8,9-BK was also degraded to [1-5]BK. D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK. The half lives of BK, des-9-BK, des-8,9-BK and [1-5]BK under the present experimental conditions were 60 min, 90 min, 14 min and 4.2 hr, respectively. Among the metabolites, [1-5]BK was the most stable one and may be used as a marker for BK production in vivo.

Adult↗
PubMed1992

Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats.

Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in Brown Norway (BN) kininogen-deficient rats (BN-Ka) and normal rats from the same strain (BN-Ki) after nephrectomy. Systolic blood pressure, which was determined by the tail-cuff method, of BN-Ki increased gradually during this treatment. In contrast, the blood pressure of mutant BN-Ka increased rapidly 2 weeks after the onset of the treatment. Urinary excretion of active kallikrein and prokallikrein increased at the same degree in rats of both strains during this treatment. Significant increase in urinary sodium excretion was observed with a tendency to increase in urine volume during the treatment in normal BN-Ki rats, whereas both parameters were essentially not increased in mutant BN-Ka rats, which could not generate urinary kinin. Aprotinin infusion by osmotic minipump to normal BN-Ki rats during the DOCA-salt treatment resulted in significant further increase in the systolic blood pressure.

Animals↗
PubMed1992

Plasma exudation by activated plasma kallikrein after intraperitoneal injection of lambda-carrageenin or endotoxin in rats.

The experimental study was carried out to examine whether intraperitoneal injection of carrageenin or endotoxin activates plasma kallikrein-kinin system to induce plasma exudation in rats. Intraperitoneal injection of 2% lambda-carrageenin induced plasma exudation in the peritoneal cavity by activation of plasma prekallikrein. Intraperitoneal injection of endotoxin (3mg/kg) also resulted in intraperitoneal plasma exudation, but plasma kallikrein-kinin system did not seem to be involved.

Animals↗
PubMed1992

Increase in the kinin levels in the bronchial washings after intravenous injection of leukotriene C4 in guinea pigs.

In guinea pig plasma, bradykinin (BK) was degraded mainly to des-Arg1-BK by an aminopeptidase-like enzyme, which was inhibited by 2-mercaptoethanol. Besides this degradation, BK was also hydrolyzed by kininase I and kininase II from C-terminal end to des-Arg9-BK, des-Phe8-Arg9-BK and Arg-Pro-Pro-Gly-Phe ([1-5] BK). The formation of des-9-BK was strongly blocked by DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid (MGPA) and that of des-8,9-BK and [1-5] BK was inhibited by captopril. When guinea pigs were pretreated with a cocktail of 2-mercaptoethanol, MGPA and captopril, intravenous administration of leukotriene (LT) C4 (10 nmol/kg) caused an increase in the levels of free kinin in the bronchial washings of guinea pigs. This increase was accompanied with the increase in glandular-kallikrein activity, which could be inhibited by aprotinin. As BK is reported to induce both bronchoconstriction and bronchial secretion, the increased free BK induced by LTC4 might enhance the effect of LTC4.

3-Mercaptopropionic Acid↗
PubMed1991

Insulin-dependent diabetes mellitus in which glycemic control was improved during pregnancy but deteriorated after delivery with the occurrence of postpartum thyrotoxicosis: a case report.

We report a patient, a twin, with diabetes mellitus whose hyperglycemic state fluctuated during the course of the pregnancy and the subsequent delivery. She was diagnosed as having slowly progressive IDDM because of her clinical course and the findings of serum positive ICA/CF, positive HLA-DR4 and disconcordance of diabetes mellitus with her identical twin. Insulin therapy was not initially needed in the first two years because the endogenous insulin secretion was not completely reduced. After two years of insulin therapy the patient became pregnant. Her glycemic control was remarkably improved without changes in dietary intake and insulin dosage. After delivery glycemic control deteriorated after delivery with the occurrence of postpartum thyroiditis. Urinary excretion of CPR was increased during pregnancy but decreased after delivery. ICA/CF in serum were persistently detected in the whole observation period. It seems that the improved glycemic control during pregnancy was caused by the reduction in the autoimmune reaction and the deterioration in glycemic control during the postpartum period was induced by the acceleration of the autoimmune reaction by the same mechanism of postpartum autoimmune thyroiditis.

Adult↗
PubMed1991

Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system.

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.

Animals↗
PubMed1991

[Evaluation of urinary incontinence among the nursing home elderly].

We assessed the prevalence of urinary incontinence and contributory factors such as senile dementia, impaired mobility, medication, associated disorders and urinary tract infection in 98 elderly residents of a nursing home. The residents' mean age was 79 years, and 78% were women. Urinary incontinence was found in 47 (48%), of whom 21 had severe urinary incontinence for which they needed to wear diapers. Senile dementia and impaired mobility were observed in 53 (54%) and 45 (46%), respectively. We also found that those with both dementia and impaired mobility had significantly (p less than 0.01) precipitated urinary incontinence. However, no significant effects on urinary incontinence were observed for associated disorders, medication or urinary tract infection. A cystometrogram performed in 73 of the 98 residents revealed detrusor overactivity in 47%. In addition, there were significant correlations between the incidence of detrusor overactivity, and the prevalence of dementia or urinary incontinence. These results suggest that senile dementia and immobility are independent risk factors for urinary incontinence in the elderly, and that detrusor overactivity, which was found to be associated with senile dementia, is a possible cause of urinary incontinence.

Aged↗
PubMed1990

Hyaluronidase assay using fluorogenic hyaluronate as a substrate.

The reducing terminal of hyaluronate was labeled with a fluorogenic reagent, 2-aminopyridine. The pyridylaminohyaluronate was incubated with testicular hyaluronidase for 1 h. After incubation, 4 vol of ethanol was added to the incubation mixture, followed by centrifugation. The fluorescence of the supernatant containing the degradation products of hyaluronidase digestion was then determined by fluorospectrophotometry (excitation wavelength, 320 nm; emission wavelength, 400 nm). It was found that the increase of the pyridylamino products was linearly correlated with enzyme concentration (up to 0.1 national formulary unit), incubation time (up to 60 min), and substrate concentration (up to 2.5 microM). The fluorogenic substrate was also applicable for the determination of crude hyaluronidase. This simple, rapid, and sensitive hyaluronidase assay was made possible by the use of pyridylaminohyaluronate as a substrate.

Aminopyridines↗
PubMed1990

A new type of exo-beta-glucuronidase acting only on non-sulfated glycosaminoglycans.

Using chondroitin as a substrate, a new type of exo-beta-glucuronidase (EC 3.2.1.31) from rabbit liver was purified using a combination of ammonium sulfate fractionation, DEAE-cellulose chromatography, gel filtration on Sephracryl S-300, affinity chromatography through heparin-Sepharose CL-6B, and preparative polyacrylamide gel electrophoresis. This enzyme acts only on non-sulfated glycosaminoglycans and their oligosaccharides and was shown to be quite different from exo-beta-glucuronidase, which does act on p-nitro-phenyl-beta-D-glucuronide with regard to the following properties. 1) Neither sulfated glycosaminoglycanoligosaccharides nor p-nitrophenyl-beta-D-glucuronide were substrates for the enzyme. 2) The molecular weight was found to be about 130,000 by gel filtration, compared with a molecular weight of 280,000-300,000 for beta-glucuronidase, which acts on p-nitro-phenyl-beta-D-glucuronide. 3) The enzyme showed maximal activity at pH 5.0, compared with an optimum pH of 4.5 for beta-glucuronidase, which acts on p-nitro-phenyl-beta-D-glucuronide. 4) The enzyme showed maximal activity in 0.075 M NaCl but no activity above 0.25 M NaCl. 5) The enzyme was inhibited strongly by compounds bearing a sulfate group. 6) The enzyme did not react with an antibody against beta-glucuronidase acting on p-nitrophenyl-D-glucuronide. It is suggested that the enzyme may be involved in the catabolism of glycosaminoglycans, acting especially on chondroitin after the desulfation reaction and/or hyaluronic acid, but showing little involvement with the detoxification system.

Ammonium Sulfate↗
PubMed1989

Evidence for the involvement of a plasma kallikrein-kinin system in the immediate hypotension produced by endotoxin in anaesthetized rats.

1. In vitro incubation of normal rat plasma with endotoxin from E. coli (3-10 mg ml-1) in the incubation mixture) caused a dose-dependent increase in levels of free kinin and plasma kallikrein in the presence of o-phenanthroline, together with a mirror-image, dose-dependent decrease in the residual levels of the precursors, plasma prekallikrein and high-molecular-weight kininogen. Low-molecular-weight kininogen levels were not modified. 2. Intravenous injection of endotoxin (3-30 mg kg-1) into the femoral vein of anaesthetized rats resulted in dose-dependent hypotension. In blood collected up to 15 min after injection, the levels of prekallikrein and high-molecular-weight kininogen in plasma were decreased while levels of the active forms, plasma kallikrein and free kinin, showed a transient increase in the blood 1 min after administration of endotoxin. 3. A degradation product of bradykinin, des-Phe8-Arg9-bradykinin, as measured by a newly developed enzyme immunoassay, was detectable up to 5 min after administration of endotoxin. 4. Intravenous infusion of soybean trypsin inhibitor inhibited both the formation of bradykinin and des-Phe8-Arg9-bradykinin and the initial hypotension. 5. It can be concluded from our results that plasma prekallikrein is activated in the blood immediately after administration of endotoxin to rats and that bradykinin is a major cause of the immediate hypotension.

Anesthesia↗