Search PubMed⌕ Search

Biomedical subjects

S Sakata

Publications and source records attributed to S Sakata.

At least 217 records · Page 12Linked to original sources
PubMed1988

Adrenomedullary origin of the hindquarter vasodilation during the transposition response of the rat.

Transposing a rat from the home cage to a new cage produces a cardiovascular response (transposition response) characterized by an increase in hindquarter blood flow with unchanged systemic arterial pressure. Arterial blood samples were collected from rats before and during this response for radioenzymatic assay of catecholamines. During the transposition response, the concentration of adrenaline and noradrenaline in plasma increased about six- and two-fold, respectively. Ablation of the adrenal medulla prevented these changes in plasma catecholamine concentration. Constant i.v. infusion of adrenaline, at rates producing a hindquarter flow approximately matching that observed during the transposition response, evoked an increase in plasma adrenaline concentration also approximately matching the increase observed during the transposition response. It is concluded that the increase in plasma adrenaline secreted from the adrenal medulla is the main cause of the increase in hindquarter blood flow in the transposition response.

Adrenal Medulla↗
PubMed1988

Characterization of serum platelet-activating factor (PAF) acetylhydrolase. Correlation between deficiency of serum PAF acetylhydrolase and respiratory symptoms in asthmatic children.

Platelet-activating factor (PAF) acetylhydrolase has been recognized as an enzyme that inactivates PAF. We developed a convenient and reproducible method for determining human serum PAF acetylhydrolase activity. The assay was based on measurement of [14C]acetate produced from 1-O-alkyl-2-[14C]-acetyl-sn-glycero-3-phosphocholine upon precipitation of the complex of radioactive substrate and albumin with TCA. The apparent Km value of PAF acetylhydrolase (near the physiological concentration of serum protein) was 1.5 X 10(-4) M PAF. 32 subjects with serum PAF acetylhydrolase deficiency were found among 816 healthy Japanese adults. The low PAF acetylhydrolase activity in the deficient serum might not be due to the presence of enzyme inhibitor. Both the sensitivity to PAF and the metabolism of PAF in platelets from PAF acetylhydrolase-deficient subjects were almost the same as those of normal subjects. Deficiency in serum PAF acetylhydrolase appeared to be transmitted by autosomal recessive heredity among five Japanese families. Among healthy adults, healthy children, and asthmatic children, who were grouped into five classes on the basis of respiratory symptoms (remission, wheezy, mild, moderate, and severe groups), the probability of PAF acetylhydrolase deficiency was significantly higher in groups with severe symptoms (moderate and severe) (P less than 0.01). These results suggest that deficiency of serum PAF acetylhydrolase might be one of the factors leading to severe respiratory symptoms in asthmatic children.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1988

A case of silent thyroiditis associated with idiopathic thrombocytopenic purpura.

A 51-year-old woman had symptoms of thyrotoxicosis which disappeared spontaneously within two months. She was diagnosed as a case of silent thyroiditis on the basis of both the clinical course and the laboratory data such as low uptake of radioactive iodine and technesium. She also had petechiae in her arms which were diagnosed as an idiopathic thrombocytopenic purpura (I.T.P.). This case would seem to expand the spectrum of the coexistence of autoimmune thyroid diseases and I.T.P. which is believed to be an autoimmune disease.

Autoantibodies↗
PubMed1988

Molecular recognition of human insulin receptor by autoantibodies in a human serum.

Immune IgG was obtained from a patient's serum with autoantibodies against human insulin receptor (HIR). The binding activity of these autoantibodies to seven synthetic peptides of the alpha-subunit of HIR was examined by radioimmuno-adsorbent titrations. Autoantibodies were bound by two of these peptides, namely alpha 277-299 and alpha 705-731, and this binding was not inhibited by a very large (1,000 x) molar excess of normal human IgG. Furthermore, none of the peptides exhibited any binding activity towards 125I-labelled normal human IgG. Therefore, it was concluded that the regions alpha 277-299 and alpha 705-731 contain autoantigenic sites of HIR. In addition, region alpha 655-670 might constitute a minor antigenic site of HIR. Localization of these autoantigenic sites will permit the molecular investigation of the insulin-like activity of anti-HIR autoantibodies.

Amino Acid Sequence↗
PubMed1988

Effects of cadmium on in vitro and in vivo erythropoiesis: erythroid progenitor cells (CFU-E), iron, and erythropoietin in cadmium-induced iron deficiency anemia.

Effects of cadmium (Cd) on in vitro and in vivo erythropoiesis in rats were studied by methylcellulose colony assay. Cd suppressed the in vitro growth of late erythroid progenitors (CFU-E) in a dose-dependent fashion and did not lose its inhibitory potency with increasing doses of erythropoietin (EPO). In addition, in marrow suspension cultures, Cd did not significantly influence 59Fe incorporation into both the cells and heme, and the Cd dose-responsive inhibition curve of the number of living cells was similar to that of CFU-E. These results suggest that the suppression of CFU-E colony formation by Cd is not due to the blocking of either EPO action to stimulate the growth of CFU-E or the iron incorporation into the cells ahd heme, but due to its direct cytotoxic effect. The colony suppression by Cd could be prevented by adding metallothionein to the cultures. On the other hand, oral administration of Cd to animals (100 mg/liter in drinking water) induced an iron deficiency anemia characterized by microcytic hypochromic red cells, decreased plasma iron, and increased total iron binding capacity. Marrow CFU-E density steadily increased as plasma iron decreased due to Cd administration and reached a plateau after 50 days. Plasma EPO titers were also found to be elevated in such a Cd-induced anemia. Parenteral iron administration during the Cd drinking period could completely prevent the development of iron deficiency anemia and the increase of both CFU-E and plasma EPO. There was a hyperbolic correlation between CFU-E and plasma iron or transferrin saturation. These results demonstrate that oral CD administration produces bone marrow hyperplasia at the CFU-E level due to iron deficiency.

Anemia, Hypochromic↗
PubMed1987

[Preparation of an immunoadsorbent interacting specifically with cortisol-binding globulin (CBG) and its application to the interaction between CBG and cortisol--evaluation of the association constant (Ka) between CBG and cortisol in normal subjects].

We have developed a simple method for the evaluation of the association constant (Ka) between cortisol binding globulin (CBG) and cortisol using immunoadsorbent and a small amount of serum. Immunoadsorbent was prepared as follows; gamma-globulin fraction was obtained from goat anti-human CBG antiserum by salting out using 50% ammonium sulfate, followed by coupling to CNBr-activated Sepharose 4B. Immunoadsorbent thus prepared was used for the evaluation of Ka value between cortisol and CBG. Sera obtained from 5 healthy subjects (3 males and 2 females) were treated with charcoal (Norit A) to remove endogenous cortisol. Each of 10 microliter of serum was incubated with a constant amount of 125I-cortisol and different concentrations of unlabelled cortisol for 12 hours at 25 degrees C, pH 7.4. Then, 50 microliter of anti-CBG-Sepharose 4B (immunoadsorbent) was added to each incubation mixture, followed by incubation for another 4 hours at 25 degrees C. After centrifugation, radioactivity of the precipitate was counted and the results were analyzed using Scatchard plot. The Ka value between serum CBG and cortisol in 5 healthy subjects was 1.70 X 10(8)M-1 (SD = 0.24), which is comparable with that of a previously reported value using purified CBG from a large amount of serum. Interassay variation of this method was satisfactory with CV value of 10.1%. Our present method is considered to be clinically relevant, since it does not require purification of CBG from serum, and a relatively small amount (total amount, less than 200 microliter) of serum is enough to evaluate Ka value between CBG and cortisol.

Adult↗
PubMed1987

A case of diabetes mellitus associated with anti-insulin autoantibodies without previous insulin injection.

A case of diabetes mellitus who had high levels of fasting immunoreactive insulin (IRI) and low levels of immunoreactive C-peptide (CPR) is reported. Examination of her serum disclosed the presence of IgG class k + lambda type anti-insulin autoantibodies. She has never been treated with insulin, nor had drugs which have been reported to be responsible for inducing insulin autoimmune syndrome. Despite the presence of autoantibodies against insulin, she has never experienced hypoglycemia. Significance of the production of autoantibodies against insulin and physicochemical parameters of anti-insulin antibodies in her serum are discussed.

Autoantigens↗
PubMed1987

Response of pancreatic tumor to intraoperative radiotherapy: medical imaging and pathologic system approach.

For analyzing the local reaction of pancreatic carcinoma to electron intraoperative radiotherapy, successive computed tomography scanning for tumor volumetry was employed, together with surgical clip localization for tumor area using orthogonal x-rays. Soon after radiotherapy the tumor volume and clipped tumor region began to decrease. After a certain interval, computed tomography volumetry revealed that the irradiated tumor had started to increase in size again, whereas the clipped area had not. Autopsies demonstrated that the increase related chiefly to cancer regrowth outside the primary radiation field.

Aged↗
PubMed1987

Serum thyroglobulin concentration in patients with diabetes mellitus.

The serum thyroglobulin (Tg) concentration was measured in 97 patients with diabetes mellitus (39 males, 58 females). Hyper Tg-nemia which exceeds the normal range (1.0-26.6 ng/ml) was observed in 10 patients (3 out of 21 cases treated with diet alone, 3 out of 50 cases treated with oral hypoglycemic agents, 4 out of 26 cases treated with insulin). There was no significant correlation between concentrations of serum Tg and triiodothyronine (T3), thyroxine (T4), fasting plasma glucose (FPG), and hemoglobin A1c (HbA1c). However, a positive correlation was observed between serum concentrations of Tg and thyroid stimulating hormone (TSH). Patients with diabetes were divided into three groups according to the mode of treatment (Group I; diet alone, n = 21, Group II; oral hypoglycemic agents, n = 50, Group III; insulin, n = 26). No significant difference in the serum Tg concentration was observed among the three groups. They were also divided into two groups; normal Tg-nemia (Group A, n = 87) and hyper Tg-nemia (Group B, n = 10). There was no difference between levels of T3, T4, FPG, and HbA1c in the two groups. The serum TSH concentration measured by double antibody RIA and two site immunoradiometric assay in Group B was significantly higher than that in Group A. These results suggest that hyper Tg-nemia in patients with diabetes could be due to the increased TSH concentration which reflects latent subclinical primary hypothyroidism in them.

Administration, Oral↗