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Biomedical subjects

M Majima

Publications and source records attributed to M Majima.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1989

Modulation of plasma exudation by PGE2 and that of leukocyte migration by LTB4 in inflammatory models.

Des-Phe8-Arg9-BK could be detected in the entire course of rat carrageenin pleurisy up to 24 h, together with a reduction of the residual levels of high molecular weight kininogen and prekallikrein. On the basis of this continuous release of bradikinin, prostaglandin E2 was released up to 5 h in the pleural exudate and enhanced the plasma leakage. In rat cardiac infarction, the initial increase in the number of polymorphonuclear leukocytes in the cardiac tissue was accompanied by leukotriene B4 in the tissue and this was followed by the second increase and activation of the complement system.

Animals↗
PubMed1989

Impaired regulation of skin temperature in patients with diabetes mellitus evaluated by the cold exposure test.

This study aimed at evaluating vasomotor response of the hand in patients with diabetes mellitus. A skin temperature of the hand was measured before and after exposure to ice water, and the recovery rates of the skin temperature were determined at 3, 5, and 10 min after the cold exposure. Ninety-two diabetics ranging in age from 25 to 59 years and 43 normal subjects ranging from 23 to 69 years old participated in this study. Since the recovery rate was delayed in normal subjects over the age of 60, comparison was made between the diabetics and the normals under 60 years old. The skin temperature was significantly lower in 26 diabetics with severe peripheral neuropathy (PN) than 40 diabetics without PN. The recovery rate were markedly delayed in the patients with PN, and also delayed in diabetics with severe retinopathy. The recovery rate was not different between the patients with and without ischemic changes in electrocardiogram. The delayed recovery rate was most prominent in the diabetics who had both abnormal heart rate variation (HRV) and orthostatic hypotension, followed by those with abnormal HRV but without orthostatic hypotension. Recovery rates in the diabetics with abnormal HRV alone were within the normal range. Our data suggest that the dysfunction of the regulation of skin temperature in the patients with diabetes mellitus was due to peripheral sympathetic nerve abnormality. The cold exposure test would be useful in the estimation of the sympathetic nerve activity of the diabetics.

Adult↗
PubMed1988

Demonstration of N-acetylchondrosine-degrading beta-glucuronidase in rabbit liver.

N-Acetylchondrosine was incubated at pH 4.0 with a rabbit-liver crude enzyme extract. Gel filtration of the reaction products on Sephadex G-15 revealed the presence of monosaccharide liberated from the disaccharide. The monosaccharide fraction was analyzed by gas-liquid chromatography, and identified as a mixture of glucuronic acid and N-acetylgalactosamine. These results indicate the presence of beta-glucuronidase, which degrades N-acetylchondrosine, in rabbit liver. The discovery of the presence of this enzyme may help to establish the complete degradation process of chondroitin sulfates.

Animals↗
PubMed1988

Isolation and characterization of a chondroitin sulfate-degrading endo-beta-glucuronidase from rabbit liver.

An endo-beta-glucuronidase acting on chondroitin sulfate was isolated from rabbit liver and purified about 550-fold, using a combination of ammonium sulfate fractionation, DEAE-cellulose chromatography, gel filtration on Sephacryl S-300, affinity chromatography through heparin-Sepharose CL-6B and preparative polyacrylamide gel electrophoresis. The pH optimum of this enzyme was 4.0 and the Km value 7 X 10(-3) M for chondroitin sulfate (Mr 40,000). The isoelectric point of the enzyme was found to be at pH 5.4. The molecular weight, estimated by gel filtration through Sephacryl S-200 and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was 35,000. This enzyme, which was found in the liver, kidney, spleen, and lung, hydrolyzed the glucuronyl galactose linkage of the linkage region of chondroitin sulfate possessing a very small peptide segment. The enzyme did not hydrolyze proteoglycan. It was concluded that an endo-beta-glucuronidase is involved in the catabolism of proteoglycan chondroitin sulfates.

Animals↗
PubMed1988

[Serum thyrotropin concentrations in patients with Sheehan's syndrome: reevaluation of the usefulness in the diagnosis].

Serum concentrations of thyroid-stimulating hormone (TSH) were determined, using a highly sensitive immunoradiometric assay (IRMA), in 10 patients with Sheehan's syndrome. Serum TSH levels in these patients were from 2.3 to 9.0 microU/ml, with the mean of 6.4 +/- 2.3(SD) microU/ml, and the data were similar to those measured by a conventional RIA method. The levels of serum TSH in these patients were normal or even higher than those of healthy women (1.8 +/- 1.3 microU/ml). After supplement therapy by cortisol, serum TSH levels decreased, but remained within the detectable range that was greater than 0.15 microU/ml. After supplement therapy by 1-thyroxine (T4), serum TSH levels moderately decreased in all patients, and excessive 1-T4 administration resulted in a fall of serum TSH levels to lower than the detectable limit. Thyroidal 123 I uptake was low in 3 out of 6 patients examined, which supports a recent hypothesis of reduced biological activity of the patient's TSH. While, the remaining 3 patients had normal thyroidal 123 I uptake, and administration of perchlorate had no effects on thyroidal radioactivity. Thus, it may be possible that in the former group of patients the TSH has a reduced biological activity, and in the latter group of patients, iodine trapping is intact but further synthesis and secretion of thyroid hormone from the gland are impaired. When the response of serum TSH to TRH was examined, the peak serum TSH levels increased in all patients. The peak TSH levels were 4.8 to 10.2 microU/ml with the mean of 7.5 microU/ml, but the data overlapped with those of normal subjects (peak level ranging 5.9 approximately 27.7 microU/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Development of hyperthyroidism following primary hypothyroidism: a case report with changes in thyroid-related antibodies.

We report a 48-year-old woman who developed hyperthyroidism following primary hypothyroidism. The serum T4 level was initially low and serum TSH level was high with clinical signs of hypothyroidism. The thyroid gland was not enlarged. Therapy with L-T4 was started. Three years later she developed hyperthyroidism; serum free T4 increased to 29.1 pmol/l after cessation of L-T4 therapy. The 123I thyroid uptake was increased with no suppression by exogenous T3. When she was hypothyroid, the activity of thyroid stimulating antibodies (TSAb) in serum measured by cyclic AMP production in cultured porcine thyroid cells were negative at 93.4% (normal less than 140%), while thyroid stimulation-blocking antibodies (TSBAb) determined by inhibition of TSH-induced cyclic AMP increase were positive at 96.1% (normal less than 40%). When hyperthyroidism subsequently occurred, TSBAb became negative (30.9%), while TSBAb became positive (163.3%). The findings indicate that hypothyroidism due to the potent TSBAb activity is not always persistent, but can be changed when various types of thyroid-relating antibodies change in the course of the disease.

Antibodies↗