{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:07:48Z","timestamp":1777792068966,"version":"3.51.4"},"reference-count":33,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[1993,5,1]],"date-time":"1993-05-01T00:00:00Z","timestamp":736214400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[1993,5]]},"abstract":"<jats:p>\n                    Changes in protein kinase C (PKC) activity, membrane lipid metabolism, and the extent of 20-kDa myosin light chain (MLC) phosphorylation in spastic cerebral basilar arteries were examined by using the beagle \u201ctwo-hemorrhage\u201d model of subarachnoid hemorrhage. In spastic arteries at days 4 and 7, cytosolic PKC activity showed a decrease of 40\u201345% with no significant changes in membrane PKC activity as compared with nonspastic control arteries. Cytosolic PKC activity of the day 14 arteries returned toward the normal control level with the remission of vasospasm. Western blot analysis of the PKC isoforms revealed that the amounts of PKC\u03b1 and PKC\u03b5 but not PKC\u03b6 were decreased in spastic arteries. As compared with nonspastic arteries, spastic arteries showed higher rates of incorporation of [\n                    <jats:sup>3<\/jats:sup>\n                    H]choline into phosphatidylcholine (PC) and [\n                    <jats:sup>14<\/jats:sup>\n                    C]ethanolamine into phosphatidylethanolamine (PE), but not of [\n                    <jats:sup>3<\/jats:sup>\n                    H]myoinositol into phosphoinositides, suggesting the stimulated turnover of PC and PE. The extent of 20-kDa MLC phosphorylation was not increased in the spastic arteries at days 4 or 7 as compared with that in the nonspastic control arteries. These results demonstrate that PKC activity and related membrane lipid metabolism are altered in spastic basilar arteries after subarachnoid hemorrhage.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1993.55","type":"journal-article","created":{"date-parts":[[2011,5,19]],"date-time":"2011-05-19T05:50:29Z","timestamp":1305784229000},"page":"409-415","source":"Crossref","is-referenced-by-count":48,"title":["Alterations in Protein Kinase C Activity and Membrane Lipid Metabolism in Cerebral Vasospasm after Subarachnoid Hemorrhage"],"prefix":"10.1177","volume":"13","author":[{"given":"Yoh","family":"Takuwa","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toru","family":"Matsui","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Saitama Medical School, Saitama, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoichiro","family":"Abe","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshiaki","family":"Nagafuji","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Saitama Medical School, Saitama, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kamejiro","family":"Yamashita","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takao","family":"Asano","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Saitama Medical School, Saitama, 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