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Biomedical subjects

K Tanoue

Publications and source records attributed to K Tanoue.

At least 127 records · Page 7Linked to original sources
PubMed1985

Endocytosis by platelets during cationized ferritin-induced aggregation.

Localization of cationized ferritin (CF) particles in the process of CF-induced aggregation of rabbit platelets was investigated by electron microscopy. CF particles attached to the surface membrane of discoidal platelets immediately after the addition of CF. Some platelets were connected to each other through the CF particles located on their surfaces. At 30 s after the addition of CF, aggregation of platelets in round form was observed. During the time course of aggregation, CF particles moved to the interplatelet spaces. Also CF particles were found in the open canalicular system, the membrane component of which was stained with ruthenium red. On the other hand, CF particles were also found in ruthenium-red-negative vesicles in platelets. At 180 s after, CF particles containing vacuoles, which showed acid phosphatase activity, were observed in the aggregates. These results suggest that part of CF particles may be incorporated into the cytoplasma by endocytosis.

Animals↗
PubMed1984

Appearance of platelet-clumping activity in heparinized plasma after acidification--it's mainly due to aggregation of fibrinogen.

Platelet-clumping activity was found after acidifying heparinized rabbit plasma to pH 5.5 in the presence of calcium ions. We tried to isolate the activity from plasma by gel filtration under low salt and high salt condition, and we found that the activity was related to the formation of plasma protein aggregates. Immunological examination and the results of fibrin monomer affinity chromatography indicated that fibrinogen was the main component of the plasma aggregates. This phenomenon was not related to the activation of blood coagulation. The binding of fibrinogen in the presence of heparin or calcium ions at low ionic strength may induce the appearance of platelet-clumping activity.

Animals↗
PubMed1984

Neutralization of the local negative charge carried by glycoprotein (GP)-Ib in ristocetin-induced platelet agglutination.

Pretreatment of platelets with chymotrypsin dose-dependently decreased glycoprotein (GP)-Ib amounts as measured by SDS-PAGE, ristocetin-induced agglutination and platelet electrophoretic mobility (EPM). Decrease in platelet EPM in response to 0.75 mg/ml ristocetin alone were 7.0 +/- 2.3 and 6.8 +/- 4.3% (M +/- S.E., n = 6) for control and chymotrypsin-treated platelets, respectively (p greater than 0.2). Von Willebrand factor (vWF) alone had no effect on platelet EPM. However, in the presence of 0.75 mg/ml ristocetin, added vWF (2.9 micrograms/ml) caused a further 6.3 +/- 3.8% decrease in control platelet EPM, but caused no significant decrease in the enzyme-treated platelets (p less than 0.05). In the presence of 0.3 mg/ml ristocetin, added vWF (2.9-14.5 micrograms/ml) caused a small but significant decrease in control platelet EPM, but caused no significant decrease in the enzyme-treated platelets. These findings suggested that the GP-Ib carrying negative charge decreased by binding of vWF might facilitate a mutual approach of the GP-Ib molecules and bridge formation by vWF between different platelets.

Adult↗
PubMed1984

Electron microscopic observations on platelet aggregation induced by cationized ferritin.

Washed and gel-filtered human platelets were dose-dependently aggregated by the addition of cationized ferritin (CF). Ca++ and plasma factors were not necessary to induce the aggregation. Immediately after the addition of CF, CF particles were attached to the surface of platelets that showed discoid form, as observed electron microscopically. Some platelets were connected to each other through the CF particles located on their membranes. After the addition of CF, the following was observed: at 15 sec after, platelets showed a round form and were aggregated to each other; at 3 min after, centralization of granules was clearly seen and the aggregates increased their size during the time course; at 3-5 min after, the CF-connected aggregates were found locally. Around the aggregates, other platelets were aggregated, though not through the membrane-located CF. Observing with a lumiaggregometer, the aggregation showed a biphasic curve associated with adenosine triphosphate (ATP) release. The second part of aggregation curve was inhibited by PGI2, PGE1, aspirin, N-ethylmaleimide, and apyrase. The first part of the aggregation curve was inhibited only by heparin. Neuraminidase treatment also inhibited the aggregation dose-dependently. These findings suggest that neutralization of the platelet surface negative charge by a positively charged macromolecule can trigger platelet aggregation, which is followed by the release reaction.

Adenosine Triphosphate↗
PubMed1983

Activation of platelets in cancer, especially with reference to genesis of disseminated intravascular coagulation.

Seventy-five cancer patients were evaluated on a scale of coagulation abnormalities related to DIC, one point given for each of the following criteria fulfilled and the score (0 to 4) being used. 1. Platelet count less than 150 x 10(3)/mu 1. 2. PT prolonged more than 1 sec over control or APTT prolonged more than 10 sec over control. 3. Fibrinogen less than 250 mg/dl (mean fibrinogen value of the cancer patients minus 1SD). 4. FDP greater than or equal to 20 micrograms/ml. The patients were distributed with 27% for score 0, 38% for 1, 20% for 2, 7% for 3 and 8% for 4. Platelet mode volume in score 4 was smaller than that of the other groups. Platelet aggregation by epinephrine was decreased in score 3 and 4 (P less than 0.01), while it was increased in score 0 (P less than 0.05). ADP-induced aggregation was increased in score 0 and 1 (P less than 0.01 - 0.05). The mean value of beta-thromboglobulin in cancer patients (44 +/- 24 ng/ml) was significantly higher than that of control (22 +/- 13 ng/ml) (P less than 0.01). These results suggest the existence of hyperfunction of platelets in cancer patients and possibility of a triggering mechanism of such activated platelets in the genesis of DIC in cancer.

Adult↗
PubMed1983

Sudden death induced by intracoronary platelet aggregation.

Sodium arachidonate (AA, 1.5 mg/kg) was injected into the coronary arteries in 16 rabbits. Arrhythmia, marked ST-T depression and apnea appeared in all cases, and 7 cases died within 10 min after the AA. Before the injection, the thromboxane B2 (TXB2) value was 1.2 +/- 0.2 ng/ml (mean +/- SE) and the 6-keto-PGF1 alpha value was 2.1 +/- 0.4 ng/ml. Three minutes after the AA, TXB2 values were 5.0 +/- 1.1 in the surviving cases and 17.9 +/- 6.5 ng/ml in the cases which died. 6-keto-PGF1 alpha values were 47.7 +/- 4.6 in the surviving cases and 248.5 +/- 69.3 ng/ml in the cases which died. There occurred no deaths in 7 cases pretreated with aspirin (ASA) and in 11 cases pretreated with OKY-046 and 1581, which are specific inhibitors of TXA2 synthetase. TXB2 values did not change in the ASA and OKY groups after the AA injection. 6-keto-PGF1 alpha values did not change in the ASA group and increased in the OKY group after the AA injection. Histological findings of the heart showed more remarkable ischemic changes in the non-pretreated group than in the ASA and OKY groups. These results suggest a role for TXA2 in sudden death. PGI2 production was extremely enhanced, suggesting the presence of a protective mechanism against thrombogenesis in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Role of surface negative charge in platelet function related to the hyperreactive state in estrogen-treated prostatic carcinoma.

The relationship between platelet surface negative charge and hyperfunction was examined by determining electrophoretic mobility (EPM), aggregability, and sialic acid of platelets in prostatic cancer, prostatic cancer with estrogen, prostatic cancer with estrogen and aspirin, prostatic hypertrophy, and healthy aged males. Estrogen treated prostatic cancer patients had significantly higher platelet EPM. A good linear correlation was found between sialic acid and EPM (r = 0.97, p less than 0.001). EPM was negatively correlated with primary aggregations by adrenaline and ADP but not with secondary or maximum aggregations, suggesting increased surface negative charge may inhibit primary aggregation. Estrogen and platelet population changes influenced surface negative charge. Neuraminidase removal of platelet surface sialic acid resulted in dose-dependent decreases of EPM which paralleled decreases in sialic acid. Aspirin treated patients and platelets incubated with aspirin in vitro both showed increased platelet EPM. These results suggest that platelet surface negative charge may directly affect platelet function.

Aged↗
PubMed1981

Platelet aggregation in patients with Moyamoya disease.

Platelet aggregation was studied by giving ADP or adrenalin to 28 patients with Moyamoya disease. There were 7 males and 21 females, and 27 normal controls, 11 males and 16 females. We found that 2 muM of ADP, and 9.1 and 22.7 muM of adrenalin induced statistically significant increases in nondissociative patterns of platelet aggregation in the patient group. Maximum aggregation was significantly increased in the patient group compared with the controls by the addition of ADP (2 and 4 muM) or adrenalin (9.1 and 22.7 muM). When patients were divided into two groups under and over 20 years of age, there was no discernible difference of platelet aggregation in either group.

Adenosine Diphosphate↗