An analysis was performed of 2,168 consecutive stroke patients who were examined by computed tomography and entered into a hospital-based stroke registry in Akita Prefecture, Japan. The occurrence of cerebral hemorrhage, cerebral infarction, and subarachnoid hemorrhage was 30, 55, and 14%, respectively. Age-specific rates of subarachnoid hemorrhage were higher in women than men; other types of stroke showed a preponderance in men. Total strokes increased in the winter; this seasonal difference was confined to cerebral hemorrhage. Putaminal hemorrhages predominated in the younger age groups; thalamic hemorrhage and cerebellar hemorrhage were predominant in the older age groups. The increased accuracy of the diagnosis of stroke subtypes by the use of computed tomography in this study is in contrast to other community-based epldemiologic studies that have relied solely on clinical diagnosis. This increased accuracy is seen to be the reason that new ratios of stroke subtype incidence have been identified. (Stroke 1987;18:402-406) T HE World Health Organization coordinated a collaborative study of stroke incidence in 17 centers from developing and developed countries between 1971 and 1974.' The Japanese centers participating were found to have the highest age-adjusted stroke incidence rates of the 17 centers in the study. Among all these centers, Akita, Japan showed the highest incidence rate for stroke. In epidemiologic studies, diagnosis of stroke is usually based on clinical judgment. The accuracy of clinical diagnoses is known to be rather high, 23 but misdiagnosis can reach 20-30% 4 in pathologic subtypes of stroke (i.e., cerebral hemorrhage, cerebral infarction, and subarachnoid hemorrhage, SAH). Because misdiagnosis of subtypes distorts the results in epidemiologic studies of stroke and because computed tomography (CT) provides highly accurate diagnoses, 5 the Akita medical community has confirmed most stroke patients in recent years by CT, and since 1983 has set up a hospitalbased stroke registry of patients confirmed by CT. This paper analyzes the diagnoses in the stroke registry in Akita and compares them with the results of previous community-based epidemiologic studies of the subtypes of stroke. Subjects and MethodsAll strokes diagnosed by CT from November 1, 1983 to May 31, 1985 were included in the present study. Twenty-four hospitals, encompassing all instiFrom the doctors group of clinico-epidemiological study for stroke, Akita.Address for reprints: Kazuo Suzuki, MD, Department of Epidemiology, Research Institute of Brain and Blood Vessels-Akita, 6-10, Senshu-Kubota-Machi, Akita 010, Japan.Received May 15, 1986; accepted November 5, 1986. tutes using CT in Akita Prefecture, participated. Stroke was defined as the onset of rapidly developing clinical signs of focal or global disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than a vascular origin. Recurring attacks were included. All cases were examined using CT within 3 weeks of the onset...

Alizarin-phenylboronic acid interactions were used in a new design strategy for self-organized fluorescent sensors of metal ions and anions. First, Alizarin Red S (ARS), which binds effectively to phenylboronic acid (PBA) at neutral conditions in water, proved to be an excellent fluorescent indicator for the selective detection of metal ions; the fluorescent-active ARS-PBA ensemble causes an efficient and selective quenching in the fluorescence by adding metal ions. It was also found that anion-induced phenylboronates can bind effectively to alizarin and greatly enhance the fluorescence in MeOH. The observation makes it possible to design new self-organized anion sensory systems composed of alizarin (as reporter) and phenylboronic acids (PBAs, as receptor), such as PBA or 3-nitrophenylboronic acid (NPBA). By combining spectroscopic studies (UV-vis and fluorescence) and 11 B NMR measurements, a ternary complex (F 2 -alizarin-PBAs) has been determined. The resulting self-organized sensory system is applicable even to the detection of anions dissolved in water, when liquid [alizarin, PBA, 18-crown-6 in CH 2 ClCH 2 Cl]-liquid [KX (X 5 halogen, OAc, H 2 PO 4 ) in water at pH 5.5] two-phase extraction is employed.

Selective anion-induced organization of phenylboronic acids and alizarin results in a new TURN-ON fluorescent sensor for anions in MeOH.

No abstract

Paclitaxel, an anti-mitotic anti-cancer agent, is active against solid tumors. The inhibition of depolymerization and promotion of microtubular assembly are essential for the anti-tumor activity of paclitaxel. Microtubule-associated proteins (MAPs) co-polymerize with tubulin and play some roles in microtubular dynamics. We examined the effect of paclitaxel on the interaction between tubulin and MAPs. Human lung-cancer cells, PC-14, were synchronized to G1/S border by the thymidine-double-block technique. After release from exposure to thymidine, the cells were treated briefly with 2 nM paclitaxel and the levels of alpha and beta tubulins and MAPs were examined after various times. Immunoblot analysis of paclitaxel-treated cells showed no changes in the overall expression of alpha and beta tubulins, microtubule-associated protein 2 (MAP2) or MAPs in comparison with controls. The samples were immunoprecipitated with anti-alpha- and anti-beta-tubulin antibodies and reblotted with an anti-MAP2 antibody, which showed that the amount of co-immuno-precipitated MAP2 in the synchronized cells, were increased by the brief paclitaxel treatment. These results suggest that paclitaxel treatment enhances the interaction between alpha and beta tubulins and MAP2. Since the phosphorylation state of MAP2 regulates the affinity of MAP2 for tubulins, and mitogen-activated protein (MAP) kinase is considered to be one of the kinases responsible for MAP2 phosphorylation, the effect of paclitaxel treatment on the MAP-kinase activity of synchronized PC-14 cells was examined. Two bands with molecular masses of 42 and 44 kDa were detected by an "intra-gel" MAP-kinase assay using myelin basic protein as the substrate. Paclitaxel treatment inhibited the MAP-kinase activity of PC-14 cells and inhibition was maximal at the G2/M phase of the cell cycle. Similar, concentration-dependent inhibition by paclitaxel of cellular MAP kinase of human synchronized small-cell lung carcinoma, H69, was observed. No inhibition of the MAP kinase of the paclitaxel-resistant sub-line H69/Txl by paclitaxel was observed, suggesting that some change of the MAP-kinase cascade had occurred in these cells. No direct inhibition of MAP-kinase activity by paclitaxel was observed in the cell-free assay (in vitro), suggesting that paclitaxel did not inhibit MAP kinase directly. Since it has been speculated that p34cdc2 kinase is also a kinase that phosphorylates MAP2, the effect of paclitaxel treatment on the p34cdc2-kinase activity of synchronized PC-14 and PC-9 cells was examined. Paclitaxel inhibited p34cdc2-kinase activation at the G2/M phase. These results suggest that paclitaxel inhibited MAP kinase and p34cdc2 kinase in vivo indirectly. These actions of paclitaxel may be responsible for the increased affinity between MAP2 and tubulins that it induces.