Biomedical subjects

A Masuda

Publications and source records attributed to A Masuda.

At least 307 records · Page 17Linked to original sources

PubMed1986

Synthetic peptides as antigens for the detection of humoral immunity to Plasmodium falciparum sporozoites.

The presence of antibodies against P. falciparum sporozoites in humans living in malaria-endemic areas was measured using as antigen the synthetic peptide (NANP)3, which represents the immunodominant region of the circumsporozoite (CS) protein. By using a competitive binding assay it was determined that antibodies which recognize (NANP)3 do not react with a 22-Mer synthetic peptide representing a cross-reacting epitope present in an antigen (5.1) from the blood stages of the parasite. Antibodies present in human sera which react with the 5.1 peptide did not react with (NANP)3. This strongly suggests that antibodies to (NANP)3 found in sera of individuals living in endemic areas are a reflection of exposure to P. falciparum sporozoites. These results validate the use of (NANP)3 for epidemiological studies to detect and measure humoral immunity to P. falciparum sporozoites.

Amino Acid Sequence↗

PubMed1986

The antagonistic effect of corticotropin-releasing factor on pentobarbital in rats.

The effects of corticotropin-releasing factor (CRF) on pentobarbital-induced sleeping time and hypothermia in rats were studied. Intraventricular administration of CRF significantly shortened the sleeping time induced by pentobarbital injection (50 mg/kg b.wt.) in a dose-dependent manner. CRF also attenuated the hypothermic effect of pentobarbital. However, peripheral administration of CRF did not affect the action of pentobarbital. alpha-Helical CRF9-41, CRF antagonist, reversed the effects of CRF. These results suggest that CRF antagonizes the effects of pentobarbital within the central nervous system.

Animals↗

PubMed1986

Atrial natriuretic factor is released from rat hypothalamus in vitro.

In vitro release of atrial natriuretic factor (ANF) from rat hypothalamic fragment during 60 min incubation was studied using a specific and sensitive radioimmunoassay (RIA). The Sephadex G-75 gel filtration profiles of the incubation medium revealed that the majority of released ANF-like immunoreactivity (LI) had a molecular weight same as alpha-atrial natriuretic polypeptide and a small amount of ANF-LI of larger molecular size was also released. The release of ANF was increased by addition of 50 mM KCl and the release by 50 mM KCl was completely suppressed in the presence of 2 mM EGTA, a chelating agent of Ca2+. A23187, a Ca2+ ionophore, at a concentration of 2 X 10(-4) M augmented the release of ANF-LI. These results indicate that hypothalamic ANF is released in a Ca2+-dependent manner like other hypothalamic peptides. This suggests that hypothalamic ANF acts as a neurotransmitter and/or neuromodulator in the hypothalamus and possesses some role in the regulation of pituitary hormone secretion.

Animals↗

PubMed1986

Rat atrial natriuretic factor suppresses proopiomelanocortin-derived peptides secretion from both anterior and intermediate lobe cells and growth hormone release from anterior lobe cells of rat pituitary in vitro.

Synthetic rat atrial natriuretic factor (ANF) was found to attenuate, in a dose-dependent manner, basal and corticotropin-releasing factor-induced secretion of proopiomelanocortin-derived peptides from cultured anterior and intermediate lobe cells of rat pituitary. ANF was also found to suppress basal and growth hormone-releasing factor-stimulated secretion of growth hormone from anterior lobe cells of rat pituitary. These results, together with reports of the existence of ANF-positive neurons in the hypothalamus and ANF-positive fibers in the median eminence, suggest that hypothalamic ANF is probably involved in the regulation of pituitary hormone secretion, especially that of proopiomelanocortin-derived peptides and growth hormone.

Adrenocorticotropic Hormone↗

PubMed1986

The method of urinary total kallikrein and prekallikrein measurement, and their urinary excretions in the patients with essential hypertension.

The method of measurement for urinary total kallikrein (KAL) and preKAL in human was developed, and daily excretions of urinary total KAL, KAL and preKAL were investigated in patients with essential hypertension. Forty microliter of urine samples were incubated with or without 120 micrograms of chymotrypsin-free trypsin for total KAL or KAL, respectively. KAL was measured with direct radioimmunoassay and kininogenase assay. PreKAL was calculated by the subtraction of KAL from total KAL. The subjects of this study included 7 normotensives (NT) and 8 essential hypertensives (EHT). Daily excretions of total KAL, KAL and preKAL were significantly lower in EHT than those in NT. KAL/total KAL ratio, which reflects the conversion rate from preKAL to KAL in the kidney, was not significantly different between EHT and NT. From these results, it is suggested that decreased urinary KAL excretion in EHT is mainly caused by reduced preKAL production rather than the impaired conversion from preKAL to KAL in the kidney. It is emphasized that this method of measurement for urinary total KAL and preKAL may be a very useful tool for research of the renal kallikrein-kinin system.

Adult↗

PubMed1986

Pulmonary function after lobectomy in children under ten years of age.

A long-term follow-up study on pulmonary function in twelve lobectomized children under ten years of age at the time of surgery was performed to determine the patterns of compensation. In the patients over ten years old at the time of the test performed over two years postoperatively, there was neither compensatory regeneration nor compensatory overdistension of the remaining lung tissue. However, there appeared to be an increase in the vital capacity, probably due to the growth of surrounding tissue such as thorax, respiratory muscles, and diaphragm. In contrast, the children tested under the age of eight years showed evidence of mild overdistension during the early postoperative period, but not at two years. There was no sign of overdistension in the patients over ten years of age at the time of testing.

Age Factors↗

PubMed1986

Insulin autoimmune syndrome with insulin-resistant diabetes at the incipient stage prior to hypoglycemic attacks.

Insulin autoimmune syndrome is characterized by spontaneous hypoglycemia, glucose intolerance, hyperinsulinemia and insulin-binding antibodies in serum without previous immunization. A 31-year-old man with Graves' disease developed insulin autoantibodies after therapy with methimazole. The patient was unique in that persistent hyperglycemia with polyuria and polydipsia had continued for several days before frequent hypoglycemic attacks appeared. We were able to extract a huge amount of immunoreactive insulin (116,000 microU/ml) with acid-ethanol from his serum obtained in the diabetic stage, and serum C-peptide immunoreactivity was as high as 268 ng/ml. The insulin-binding activity of his serum was quite potent, and when 1:5,000 diluted serum was incubated with 125I-porcine insulin, 71.2% of the label could be precipitated by polyethylene glycol. The insulin-binding protein was identified as mainly IgG with kappa light chains. Insulin-binding activity was not detected in serum obtained before methimazole therapy, suggesting that the drug was responsible for the induction of antibodies in this patient. The antibodies recognized porcine, sheep, bovine and horse insulins as well as human insulin. The mechanisms by which the antibodies produced hyper- and hypoglycemia have also been discussed.

Adult↗

PubMed1986

Monoclonal anti-gametocyte antibodies identify an antigen present in all blood stages of Plasmodium falciparum.

Two polypeptides of 150 and 130 kDa present in all asexual and sexual blood stages of Plasmodium falciparum have been identified with anti-gametocyte monoclonal antibodies. The apparent molecular mass of these antigens is identical in different developmental stages of the parasite and in different isolates. These antigens are released in the culture supernatant during the process of schizogony and are also detected in the sera of patients undergoing a primary P. falciparum infection. Antibodies against these antigens occur in sera of a large percentage of children and most adults living in malaria-endemic areas, suggesting that they are highly immunogenic. The anti-gametocyte monoclonal antibodies react with a synthetic peptide (Glu-Glu-Asn-Val)4, present in antigen Pf155 [Perlmann, H. et al. (1984) J. Exp. Med. 159, 1686-1704] and in the ring-infected erythrocyte surface antigen [Coppel, R.L. et al. (1984) Nature 310, 789-792], indicating that these polypeptides are closely related. In contrast, two glycophorin-binding proteins of similar molecular mass [Perkins, M.E. (1984) J. Exp. Med. 160, 788-798] appear to be entirely distinct from the presently described antigens. We failed to observe any in vitro inhibitory activity of the monoclonal antibodies on merozoite invasion and on gametocyte infectivity.

Animals↗

PubMed1986

In vitro release of growth hormone-releasing factor from rat hypothalamus: effect of insulin-like growth factor-1.

The release of growth hormone-releasing factor (GHRF) from rat hypothalamus was investigated in vitro. After 60 min preincubation the released GHRF from sliced rat hypothalamic fragments during 60 min incubation was detected by a highly specific and sensitive radioimmunoassay for rat GHRF. The release of GHRF was Ca2+-dependent and enhanced by high concentration of K+. Insulin-like growth factor-1 (IGF-1) significantly decreased GHRF release to 65% and 84% of the control at concentrations of 10(-8) M and 10(-7) M, respectively. These results suggest that this in vitro system is useful for the investigation of the mechanism of GHRF release from the hypothalamus and that IGF-1 is probably involved in the feedback inhibition of growth hormone secretion by attenuating GHRF release from the hypothalamus besides countering the effect of GHRF on the pituitary.

Animals↗

PubMed1986

Effect of timing of partial hepatectomy on the induction of preneoplastic liver foci in rats given hepatocarcinogens.

Beginning 2 weeks after an intraperitoneal injection of diethylnitrosamine (DEN), rats were fed diet containing either 2-acetylaminofluorene (2-AAF), 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), alpha-isomer of 1,2,3,4,5,6-hexachlorocyclohexane (alpha-HCH), or phenobarbital (PB) for 6 weeks and subjected to partial hepatectomy (PH) after various periods of chemical administration. The effect of timing of PH was most apparent in rats fed 2-AAF. The size of gamma-glutamyl transpeptidase positive foci was largest when PH was performed 1-3 weeks after the start of chemical feeding. Similar tendency was slightly observed with 3'-Me-DAB or alpha-HCH administration, but not with PB or basal diet feeding. Thus, the enhancing effect of PH on the induction of the preneoplastic liver foci was affected by the type of chemical and the timing of the operation.

2-Acetylaminofluorene↗

PubMed1986

Modification by antioxidants and p,p'-diaminodiphenylmethane of 7,12-dimethylbenz[a]anthracene-induced carcinogenesis of the mammary gland and ear duct in CD rats.

The effects of antioxidants on mammary gland carcinogenesis pretreated with 7,12-dimethylbenz[a]anthracene (DMBA) in female Sprague-Dawley rats were examined. The antioxidants used were butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), sodium L-ascorbate, alpha-tocopherol, ethoxyquin and p,p'-diaminodiphenylmethane (DDPM), which is an inhibitor of carcinogenesis in the liver, kidney and urinary bladder. Female Sprague-Dawley rats of 50 days old were treated with 2.5 mg/100 g body weight of DMBA, and from 1 week later were given diet supplemented with 1% BHA, 0.7% BHT, 5% sodium L-ascorbate, 1.5% alpha-tocopherol, 0.5% ethoxyquin or 0.1% DDPM for 33 weeks and then killed. The incidences of mammary tumors, carcinomas and fibroadenomas in DMBA-treated animals were reduced by diet containing BHA or ethoxyquin. Diet containing BHT or DDPM inhibited the induction of only fibroadenomas. The incidence of ear duct tumors in DMBA-treated animals was reduced by diet containing BHT, alpha-tocopherol or ethoxyquin.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1986

Immunocytochemical study on the immune complex and germinal center of synovial tissue of rheumatoid arthritis with special regard to complement and follicular dendritic cells.

To analyze the immunological role of lymphoid germinal centers and follicular dendritic cells (FDC) in synovial tissue of rheumatoid arthritis (RA), we tried to detect the immune complex in germinal centers by light and electron microscopic immunocytochemistry with special emphasis on immunoglobulin, complement components, RA factor, and DRC-1 antigen. Immunoglobulins mainly distributed intercellularly in the germinal center in a lacy network pattern, and show partial intracytoplasmic localization in some germinal center lymphoid cells. Early complement components of classical pathway (C1q, C4, C3c, and C3d) and RA factor distributed lacily similarily to immunoglobulin, but intracytoplasmic positivity is never observed. These coexistent positive sites are identical to DRC-1 positive sites which are the surface of extended processes of FDC membrane. A similar finding is observed in primary follicles or lymphoid aggregates less often than germinal centers. These results indicate that some germinal centers trap the immune complex, including RA factor at least closely related with FDCs, and also RA factor is one of the triggers of antigen as well as developing germinal centers.

Antibodies, Monoclonal↗

PubMed1986

The effect of glucose and free fatty acids on growth hormone (GH)-releasing factor-mediated GH secretion in rats.

We have examined the effect of glucose and FFA on GH-releasing factor (GHRF)-mediated GH secretion in rats under pentobarbital anesthesia. Hyperglycemia did not affect GH secretion induced by administration of 20, 100, and 200 ng GHRF/100 g body weight. In contrast, GH response to 50 ng GHRF/100 g body weight in lipid heparin-treated rats, which showed high plasma FFA levels, was significantly suppressed compared with the control group (plasma peak GH: control, 1526 +/- 263 ng/ml; lipid-heparin group, 377 +/- 69 ng/ml P less than 0.05, mean +/- SEM). This suppressive effect of FFA on GH secretion was abolished by pretreatment with antisomatostatin serum (ASS) (GH level at 4 min after GHRF administration: ASS-saline group, 1606 +/- 210 ng/ml; ASS-lipid-heparin group, 1531 +/- 174 ng/ml; mean +/- SEM). These results suggest that hyperglycemia does not change the GH response to GHRF and that elevation of plasma FFA suppresses GHRF-induced GH secretion by the stimulation of somatostatin secretion in rats.

Animals↗

PubMed1986

The responses of plasma adrenocorticotropin and cortisol to corticotropin-releasing hormone (CRH) and cerebrospinal fluid immunoreactive CRH in anorexia nervosa patients.

Pituitary-adrenocortical responses to the iv injection of 100 micrograms synthetic ovine corticotropin-releasing hormone (CRH) were studied in 13 patients with anorexia nervosa, and the concentrations of immunoreactive CRH in cerebrospinal fluid were measured in 7 of them. Mean basal levels of plasma ACTH and cortisol were 32 +/- 5 pg/ml (+/- SEM) and 21.1 +/- 1.5 micrograms/dl, respectively. The latter value was significantly higher than that in age-matched normal women (P less than 0.005). The mean increments of plasma ACTH and cortisol in response to CRH injection in those 13 patients were 21 +/- 5 pg/ml and 5.3 +/- 1.7 micrograms/dl, respectively, significantly lower than those in normal women (58 +/- 6 pg/ml and 15.3 +/- 7.7 micrograms/dl, respectively; P less than 0.005). When 4 patients were reexamined after weight gains of between 3 and 22 kg, their responses to the CRH injection increased. The mean concentration of immunoreactive CRH in the cerebrospinal fluid of seven patients was 30.8 +/- 3.9 pg/ml (+/- SEM), which was higher than the value of 18.4 +/- 1.1 pg/ml (P less than 0.005) in control subjects with cervical spondylosis. These findings suggest the possibility that hypersecretion of CRH may occur in patients with anorexia nervosa.

Adolescent↗

PubMed1986

Studies on the response of growth hormone (GH) secretion to GH-releasing hormone, thyrotropin-releasing hormone, gonadotropin-releasing hormone, and somatostatin in acromegaly.

The plasma GH response to GH-releasing hormone (GHRH), TRH, or GnRH administration was examined in 25 acromegalic patients. Plasma GH levels increased in 21 patients after GHRH, in 19 after TRH, and in 4 after GnRH. The four GHRH nonresponders had had acromegaly longer than had the GHRH responders. No specific combination of GH responsiveness to these 3 releasing hormones was found among the patients. Infusion of 1 mg GHRH for 150 min gradually increased plasma GH levels, with some fluctuations, from the beginning to the end of infusion in normal subjects and in 7 patients who were GHRH responders, but a bolus injection of 100 micrograms GHRH at the end of the infusion did not further elevate plasma GH levels. These results suggest that desensitization to GHRH occurred in the normal subjects and acromegalic patients. However, in 5 acromegalic patients who responded to both GHRH and TRH, a bolus injection of 500 micrograms TRH given at the end of the 150-min infusion of 1 mg GHRH evoked a further plasma GH rise. In 5 normal subjects and 2 patients who were responders to GHRH but not TRH, a bolus injection of 500 micrograms TRH did not cause plasma GH elevation at the end of 150-min infusion of 1 mg GHRH. These results imply that TRH and GnRH stimulate GH secretion from the adenoma cells in vivo through receptors different from those for GHRH. In vitro studies using cultured pituitary adenoma cells from 2 patients revealed that the responses of GH secretion to GHRH were similar to those in vivo. These data, therefore, suggest that the responsiveness of GH secretion to stimuli is determined by the specificity of the receptors on adenoma cells. The action of somatostatin-28 was more potent than that of somatostatin-14 in the suppression of GH secretion from adenoma cells.

Acromegaly↗

PubMed1986

Effect of a single administration of somatostatin analogue (SMS 201-995) on GH, TSH and insulin secretion in patients with acromegaly.

The effect of a long-acting somatostatin analogue SMS 201-995 on GH secretion was investigated. Eleven acromegalic patients received a single dose of 50 micrograms SMS 201-995 administered subcutaneously, and plasma GH, IGF-I, GRF, TSH, IRI and blood glucose were determined at regular intervals. Nine of 11 patients had elevated basal plasma GH levels above 5 ng/ml. In all patients, plasma GH levels fell immediately from 39.5 +/- 17.3 ng/ml (mean +/- SEM) to 4.3 +/- 1.6 ng/ml (P less than 0.05) with a maximal inhibition of 82.9 +/- 3.3% of the basal levels and the suppression persisted for about 6 h of the observation period. IGF-I and GRF levels were not apparently altered. TSH and IRI levels also rapidly fell. Blood glucose levels fell slightly by 0.5 h. Ten of 11 patients had pain at injection sites. Except for this, no side effects were observed. Our results show that the new somatostatin analogue SMS 201-995 may inhibit GH hypersecretion in acromegalic patients for significant periods, suggesting that this agent can be a useful clinical tool for the treatment of acromegaly.

Acromegaly↗

PubMed1986

The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems.

In order to clarify the mechanism of the hypotensive action of captopril, the acute and chronic effects of this drug on the kallikrein-kinin and renin-angiotensin systems were investigated respectively in 14 and 19 patients with hypertension. To determine the acute effect, a dose of 50 mg of captopril was administered once orally. For the chronic effect, 75-300 mg of the drug was administered daily for 14 days. In observations of the acute effect, blood pressure decreased significantly at 30 min. and maximally at 60-180 min. after administration with no change in heart rate. Significant increases in blood kinin levels and plasma renin activity (PRA), and a decrease in plasma angiotensin II levels were also observed. A marked augmentation was also found in urinary kinin excretion, but not in urinary kallikrein excretion. Moreover, the changes in blood pressure significantly correlated negatively with basal PRA, basal plasma angiotensin II and the changes in blood kinin levels, and positively with the changes in plasma angiotensin II. In our study of the chronic effect of captopril, similar changes in blood kinin levels, PRA, plasma angiotensin II levels, blood pressure and heart rate to the acute effect study were observed. Significant correlations of the changes in blood pressure were found negatively with basal PRA, basal plasma angiotensin II levels and the changes in blood kinin levels and positively with the changes in plasma angiotensin II levels. In addition, significant increases in urine volume and urinary sodium excretion occurred following administration of captopril for 14 days, and both increases negatively correlated with the changes in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Localization of renal kallikrein-kinin system components in the kidney.

In a study using a stop-flow technique in dog kidney, the existence of kallikrein and kinin was recognized in distal tubules. The presence of kininase I was seen in both distal and proximal tubules, and also partly in the distal tubules. The presence of kininase II in the distal tubules was again confirmed by pretreatment with SQ14225. No evidence of kinin formation, however, was obtained in the proximal nephrons in stop-flow method. From these results, it was suggested that kininase I and II localized in proximal tubules may destroy the kinin filtered from glomeruli at the proximal level, while kallikrein and kininogen and also kininase I and II in the distal tubules may regulate the activity of the renal kallikrein-kinin system in the distal nephrons.

Animals↗