PubMed Health⌕ Search

Biomedical subjects

S Takasugi

Publications and source records attributed to S Takasugi.

At least 37 records · Page 2Linked to original sources
PubMed1984

Isolation of urinary trypsin inhibitor-like inhibitor from human lung cancer tissue.

In the present study, a trypsin inhibitor was first extracted from lung cancer tissue and purified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A final yield of 20 to 60 micrograms of inhibitor with a specific activity of 2040 units/mg of protein was obtained from 1 g of original lung cancer tissue. This inhibitor inhibited trypsin strongly, plasma kallikrein weakly, and plasmin more weakly, and its molecular weight was approximately 43,000 to 45,000 as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Its antigenicity was confirmed to be quite the same as that of human urinary trypsin inhibitor by double immunodiffusion, immunoelectrophoresis, and neutralization with anti-urinary trypsin inhibitor rabbit immunoglobulin.

Aged↗
PubMed1984

[Three cases of intracranial chordoma. Typical chordoma and chondroid chordoma].

Three cases of intracranial chordoma: 2 cases of typical chordoma and a case of chondroid chordoma, were reported and the clinico-pathological difference between these two types of chordoma was discussed. It is well known that typical chordoma is composed of physaliferous cells containing various quantities of intracytoplasmic mucin histologically, whereas chondroid chordoma as Heffelfinger reported in 1973 is composed of cellular area with scanty myxoid matrix and Chondroid matrix. Clinical course of the typical chordoma shows recurrence of the tumor within 2 years after surgical removal and radiation therapy in the majority of the cases, and the average survival range is said to be about 4.1 years, while chondroid chordoma takes benign course with average survival of 24.1 years after surgery and radiation therapy. One of our two patients with typical chordoma died from the recurrence two years after surgery and radiation therapy. However, the patients with chondroid chordoma showed no sign of recurrence over 2 years after subtotal removal and radiation. Surgical approach for the removal of the tumor was discussed as well. When the tumor is rather small and located at the upper clival region, transsphenoidal approach may be preferable, otherwise other approach should be chosen. When tumor has forward extension over the clivus, subtemporal approach will be most favorable with wider operative field. Identification of vessels and nerves around the tumor will be readily obtained by this approach.

Adult↗
PubMed1983

Multiple molecular forms of acid-stable plasmin inhibitor derived from human urinary trypsin inhibitor.

It was found that cyanogen bromide (BrCN) treatment of the highly purified human urinary trypsin inhibitors (H-UTI; specific activity 1,897 U/mg protein, and L-UTI; specific activity 1,850 U/mg protein) readily produced new plasmin inhibitors with almost no loss of UTI activity. Five multiple forms of chemically cleaved inhibitors (UTIB-I, UTIB-II, UTIB-III, UTIB-IV and UTIB-V) could be isolated from BrCN-treated L-UTI by isoelectric focusing and gel filtration. These inhibitors were very acid-stable and their isoelectric points (pI) were 4.5, 4.6, 4.9, 5.1 and 6.4, respectively. The molecular weights by SDS-polyacrylamide gel electrophoresis were almost the same at about 23,000 +/- 3,000. Although these inhibitors showed both anti-plasmin and anti-trypsin activities, much higher anti-plasmin/anti-trypsin activities were observed in the cleaved inhibitors than in the parent UTI. They competitively inhibited human plasmin with Ki values of 3.0-4.1 X 10(-8) mol/l (H-D-Val-Leu-Lys-pNA substrate).

Antifibrinolytic Agents↗
PubMed1983

[Effect of 1-[3-[4-(diphenylmethyl)-1-priperazinyl]-propyl]-1,3-dihydro-2H-benzimidazol-2- one (oxatomide) on contraction of canine bronchial muscle].

Effect of oxatomide on contraction of canine bronchial smooth muscle caused by administration of histamine and by challenge of ascaris-antigen were investigated and compared against the effects of histamine H1-receptor antagonist (CPM) and inhibitor of histamine release from mast cells (DSCG). Oxatomide in concentrations of 0.05 microgram/ml to 2.0 microgram/ml inhibited, dose-responsively, contraction of bronchial smooth muscle strip by administration of histamine (10 micrograms/ml). When this concentration was less than 0.3 microgram/ml, CPM inhibited the contraction significantly stronger than oxatomide. However, in concentration over 0.5 microgram/ml, no difference in inhibitory effect could be demonstrated. On the other hand, DSCG could not inhibit the contraction. Oxatomide in concentrations of 0.05 microgram/ml to 1.0 micrograms/ml inhibited, dose-responsively, contraction of the muscle strip sensitized spontaneously by ascaris antigen challenges. There was no difference in inhibitory effect between oxatomide and DSCG at the same level of concentration. Oxatomide (0.5 microgram/ml) and CPM (0.5 microgram/ml) both inhibited completely the constriction response of bronchus caused by histamine stimulation (10 micrograms/ml). Although constriction response by ascaris antigen challenge was inhibited completely by oxatomide (0.5 microgram/ml), it could not be inhibited completely by CPM (0.5 microgram/ml). Oxatomide inhibited even the residual constriction response which could not accomplished by CPM. These results suggest that oxatomide might have not only an effect as a histamine H1-receptor antagonist and anti-histamine releasing agent from mast cell, but also anti-SRS-A.

Animals↗
PubMed1983

Metabolic deterioration in shock state and its modulation.

The initial cellular reaction against the deleterious effects of shock-inducing stimuli apparently elevates the energy-producing capacity so that the cell is able to sustain its normal function. Several endocrine events are fundamentally important as triggering factors for this kind of reaction. As the shock state advances, cellular metabolism deteriorates progressively and cellular energy is exhausted. Depression of intracellular cAMP may induce cellular metabolic unresponsiveness to hormonal stimuli. Consistent degradation of high-energy substances, extreme deviation of the redox state in the NAD+-NADH system, and decrease of endogenous key substances such as L-carnitine ultimately may lead to a standstill of cellular enzymatic reactions (Fig. 13). Methods intended to sustain cellular membrane and enzymatic systems may offer the best contribution to the improvement of shock therapy.

Adenine Nucleotides↗
PubMed1982

Studies on the activation mechanism of fibrinolytic enzyme system in plasma by human pancreatic elastase.

In the present study, the activation mechanism of fibrinolytic enzyme system in plasma by human pancreatic elastase was investigated. It was confirmed that human pancreatic elastase not only converted the co-existing plasminogen to low molecular weight-plasminogen which could be easily activated by the activator, but also inhibited alpha 2-macroglobulin and alpha 2-plasmin inhibitor which are antiactivators or fast reacting antiplasmins, and consequently, induced the activation of the fibrinolytic enzyme system in plasma.

Chromatography, Affinity↗
PubMed1982

Low molecular weight trypsin-plasmin inhibitors isolated from papain treated urinary trypsin inhibitor.

Papain treatment of human urinary trypsin inhibitor (UTI67; mol. wt. 43,000 by SDS-polyacrylamide gel electrophoresis, specific activity 1,897 U/mg protein) produced four new protease inhibitors, which were highly purified by gel chromatography on Sephadex G-100 and isoelectric focusing. The purified inhibitors (UTI26, UTI9-I, UTI9-II, and UTI9-III) were shown to be homogeneous by polyacrylamide disc gel electrophoresis, and had apparent molecular weights of 26,000, 9,000, 9,000, and 9,800, respectively, by sodium dodecyl sulfate gel electrophoresis. During enzymatic degradation of UTI67, the amino acid compositions changed to more basic, and the isoelectric point increased from pH 2.0 (UTI67) to pHs 4.4, 5.2, 6.6, and 8.3 (UTI26, UTI9-I, UTI9-II, UTI9-III), respectively. Both the parent and degraded inhibitors had anti-plasmin activity as well as antitrypsin and anti-chrymotrypsin activities. Much higher anti-plasmin/anti-trypsin and anti-plasmin/anti-chymotryspin activities were observed in the degraded inhibitors than in the parent UTI67. They competitively inhibited human plasmin with Ki values of 1.13 X 10(-7) - 2.12 X 10(-6) M (H-D-Val-Leu-Lys-pNA substrate). The reactions were very fast and the active site of the inhibitors of plasmin was thought to be different from that to trypsin or chymotrypsin.

Amino Acids↗
PubMed1982

Neural and humoral factors influence gastric receptive relaxation in dogs.

To clarify the neural and humoral factors which control gastric receptive relaxation, the effects of various types of vagotomy or splanchnicotomy on receptive relaxation of the canine innervated corpus pouch were investigated. The influence of gastrin, histamine H1-receptor antagonist, and anti-histamine releasing agents on receptive relaxation were also examined. Selective proximal vagotomy or splanchnicotomy resulted in a slight disturbance in receptive relaxation. Truncal vagotomy produced a marked disturbance in receptive relaxation. Administration of tetragastrin potently inhibited receptive relaxation, however, recovery occurred by injecting a histamine H1-receptor antagonist. Increased serum gastrin induced by perfusion of the antrum with liver extract solution disturbed receptive relaxation and this response was inhibited by pretreatment with transamine, an inhibitor of histamine release from histamine secreting cells. These results indicate that receptive relaxation in the canine stomach is controlled not only by vagal and splanchnic nerves, but also by gastrin and histamine.

Animals↗
PubMed1982

Isolation and characterization of a pancreatic elastase from plasma of patients with acute pancreatitis.

1. An elastase-like enzyme in plasma of patients with acute pancreatitis was purified by DEAE-cellulose column chromatography and polyacrylamide-gel disc electrophoresis. 2. In this way 0.24 mg of purified enzyme with a specific activity of 3.94 succinyl-L-alanyl-L-alanyl-L-alanyl-p-nitroanilide units/mg of protein was obtained from 10 ml of plasma. 3. The purified material was homogeneous as ascertained by sodium dodecyl sulphate/polyacrylamide-gel disc electrophoresis and had an apparent molecular weight of 24 000 as measured by gel filtration on Sephadex G-100. 4. This enzyme hydrolysed denatured casein and Congo Red-elastin as well as succinyl-L-alanyl-L-alanyl-L-alanyl-p-nitroanilide. Its amidolytic activity was inhibited by soya bean trypsin inhibitor, but not by aprotinin. 5. Although the enzyme was immunologically similar to elastase 2, its kinetic properties and substrate specificity were apparently different. 6. We propose that an elastase-like enzyme, probably different from elastase 1 or elastase 2, is liberated from the pancreas into blood during acute pancreatitis and becomes combined with alpha 2-macroglobulin.

Acute Disease↗
PubMed1981

Purification and characterization of kallikrein from plasma of patients with acute pancreatitis.

1. A kallikrein-like enzyme in plasma of patients with acute pancreatitis was further purified by successive hydroxyapatite/cellulose and Sepharose-4B column chromatography. 2. By these procedures 0.26 mg of purified enzyme with a specific activity of 215 S-2266 chromozyme units/mg of protein was obtained from 10 ml of original plasma. 3. The purified material was homogeneous as ascertained by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis and had an apparent molecular weight of 31 000 as measured by gel filtration on Sephadex G-200. 4. It was confirmed immunologically that this enzyme was pancreatic kallikrein, which is distinct from plasma kallikrein, and that it could combine with alpha 2-macroglobulin only in the presence of trypsin.

Acute Disease↗