PubMed Health⌕ Search

Biomedical subjects

Masako Yamazaki

Publications and source records attributed to Masako Yamazaki.

8 recordsLinked to original sources
PubMed2006

Synergistic effect of cilostazol and dipyridamole mediated by adenosine on shear-induced platelet aggregation.

INTRODUCTION: The Cilostazol Stroke Prevention Study found that cilostazol, a phosphodiesterase 3 inhibitor, can reduce the risk of subsequent stroke in Japanese patients with cerebral infarction. Here, we measured the effects of cilostazol in vitro on shear-induced platelet aggregation, an important mechanism of thrombosis at arterial bifurcations or stenotic lesions. We also evaluated the influences of intrinsic adenosine on the ability of cilostazol to inhibit shear-induced platelet aggregation by investigating the effect of dipyridamole, an inhibitor of cellular adenosine reuptake, in combination with cilostazol in vitro. MATERIALS AND METHODS: We measured platelet aggregation induced by a shear rate of 10,800 s(-1) in whole blood and in platelet-rich plasma from healthy volunteers using a cone-plate streaming chamber. RESULTS: Both cilostazol and adenosine dose-dependently inhibited shear-induced platelet aggregation in platelet-rich plasma samples. Adding a low concentration of adenosine (0.3 microM) did not inhibit shear-induced platelet aggregation, but significantly enhanced the inhibitory effect of cilostazol in platelet-rich plasma. Dipyridamole dose-dependently inhibited shear-induced platelet aggregation in whole blood and significantly enhanced the inhibitory effect of cilostazol on shear-induced platelet aggregation, but did not affect shear-induced platelet aggregation in platelet-rich plasma. The inhibitory effects of cilostazol combined with dipyridamole in whole blood were almost completely reversed by adenosine deaminase. CONCLUSIONS: Dipyridamole appears to synergistically enhance the inhibitory effect of cilostazol on shear-induced platelet aggregation by maintaining high plasma levels of adenosine.

Adenosine↗
PubMed2006

New modalities and aspects of antiplatelet therapy for stroke prevention.

Antiplatelet therapy is indicated for secondary prevention of ischaemic stroke. The first-line antiplatelet agent is aspirin. The effect of aspirin is, however, very limited, and this limited effect of aspirin is argued with termed 'aspirin resistance'. Strategies against aspirin resistance may include alternative use of other antiplatelet agents, combination of aspirin with other antiplatelet agents and investigation into molecular targets to develop novel antiplatelet agents. Progress in antiplatelet therapy should be directed at further reducing the risk of ischaemic events including ischaemic stroke without increasing the risk of haemorrhagic events including haemorrhagic stroke.

Aspirin↗
PubMed2005

Clinical characteristics of stroke patients with antiphospholipid antibodies.

BACKGROUND: Antiphospholipid syndrome is important as a cause of ischemic stroke, although clinical characteristics of the syndrome are not well documented. METHODS: We analyzed differences in clinical characteristics between 40 antiphospholipid-antibody (aPL)-positive and 40 aPL-negative stroke patients. RESULTS: Stroke patients with aPL were significantly younger and were more likely to be women in comparison with stroke patients without aPL. Valvular heart disease, neurological complications and hematological disorders were more frequent in the aPL-positive group. The mean value of thrombin-antithrombin III complex was significantly lower in the aPL-positive group. Cerebral infarctions in the carotid system were less and large-artery lesions more frequent in the aPL-positive patients. CONCLUSIONS: Stroke patients with aPL have clinical characteristics distinct from stroke patients without aPL.

Acute Disease↗
PubMed2005

Effect of remnant-like particle on shear-induced platelet activation and its inhibition by antiplatelet agents.

Remnant-like particles (RLPs) have been reported to promote atherosclerosis and to have effects on platelet function. We studied the effects of RLP on shear-induced platelet activation and their inhibition by antiplatelet agents in vitro. RLP were separated using two monoclonal antibodies, anti apo B-100 and anti apo A-I. These RLP fractions were added to whole blood (WB) or platelet-rich plasma (PRP) in serial dilution of 1, 10 or 100 microg RLP triglyceride (TG) per ml of total sample volume. These samples were incubated, and then stimulated with a high shear stress of 108 dyn/cm(2). Shear-induced platelet aggregation (SIPA) was calculated from the percentage of single platelet loss. P-selectin expression on platelet surface and platelet-derived microparticle (PMP) generation were measured before and after stimulation with shear stress using flow cytometer. SIPA was significantly enhanced by RLP in WB but not in PRP. This enhancing effect was not dose-dependent and was greatest at 10 microg TG/ml. P-selectin expression induced by shear stress was only enhanced by RLP at a concentration of 100 microg TG/ml in both WB and PRP, while generation of PMP induced by shear stress was only enhanced by RLP at a concentration of 100 microg TG/ml in WB. Aspirin inhibited only the enhancement of SIPA by RLPs, while cilostazol inhibited the enhancement of not only SIPA but also p-selectin expression and PMP generation by RLPs.

Antibodies, Monoclonal↗
PubMed2004

A pre-senile case of limbic encephalitis and cerebellar degeneration, with subacute onset of progressive dementia.

In case a pre-senile patient presented subacutely progressive dementia, secondary dementia, such as paraneoplastic neurological syndrome (PNS), hypothyroidism, confusion, early phase of primary degenerative dementia and prion diseases are to be considered. It is a case of pathologically confirmed, and clinico-pathologically assessed limbic encephalitis with cerebellar degeneration. The patient was a 63-year old male, with a well followed up medical history of gastric cancer 8 years earlier. Four weeks after he presented himself at our hospital his memory and disorientation progressively declined. A neurological examination revealed gaze nystagmus, with potential secondary dementia. However, no abnormal findings were detected from systemic radiological examination, or from chemical analyses. Two months later, after the onset of the disease, he presented additional symptoms, including seizure, gait disturbance, and insomnia. On admission, neurological examinations revealed gaze nystagmus and progression of dementia; however, his thought process was relatively preserved. No paroxysmal synchronized discharge was seen on electroencephalogram. Chest X-rays showed an inflammatory infiltration. In spite of anti-biotic medication, he died due to respiratory failure. The autopsy was limited to the brain. Histologically, limited lymphocytic infiltration into the hippocampus through the entorhinal cortex, with marked neuronal loss and gliosis was observed. Neuronophagia, microglial nodules, and perivascular lymphocytic infiltration were also seen. Additionally, most of the Purkinje cells in the cerebellum were lost, with Bergmann's gliosis and sparse lymphocytic infiltration. No tumor was observed in the brain. Pathological findings of the brain were compatible with paraneoplastic limbic encephalitis and cerebellar degeneration, though no neoplasm, clinically or pathologically, was detected in this patient. Consequently, it is suggested that when a senile patient presents sub-acute onset of progressive dementia, with a variety of neurological symptoms, paraneoplastic syndrome is to be taken into consideration, even if a tumor or an auto-antibody is not detected since the resection of the tumor is still the best therapeutic means. Otherwise immuno-suppressive and steroid therapies should be used.

Alzheimer Disease↗
PubMed2002

Flow cytometric analysis of reticulated platelets in patients with ischemic stroke.

Reticulated platelets are newly formed platelets containing a residual amount of RNA, and percentage of reticulated platelets (%RP) has been shown to reflect platelet turnover. Recently, a new flow cytometric approach for analyzing %RP in patients with thrombocytopenic disorders has been reported. We measured %RP by flow cytometry using the fluorescent dye thiazole orange (TO) to evaluate platelet kinetics in patients with different clinical categories of ischemic stroke. Patients with ischemic stroke were categorized into lacunar (n=25), atherothrombotic (n=26) and cardioembolic stroke (n=17). %RP was significantly higher in patients with cardioembolic stroke than in controls (n=140). Stepwise multiple regression analysis also showed cardioembolic stroke (R(2)=0.14) to be significant independent predictors of %RP among stroke patients even after adjustment for other factors. We concluded that %RP is increased in patients with cardioembolic stroke, which may reflect increased platelet turnover as a consequence of platelet consumption during thrombogenesis.

Aged↗