13 research outputs found
Indian War Bonds
46-3Indian AffairsIndian War Bonds. [1948] Issued by California in 1852 for expenses incurred in suppressing Indian hostilities.1881-4
鹿児島県における学校ソーシャルワーク事業(令和4年度報告)
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2023(令和 5)年度事業計画
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2022(令和4)年度事業報告
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lanceolata
Claytonia lanceolata Purshwestern spring beautyclaytonie lancéoléeS.E. slope, grassy damp water shed6000 feetwhit
discoidea
Matricaria discoidea de CandolleMatricaria matricarioidesalong Mo. #7, about 4 miles southeast of Garden CityRoadsid
China's Enterprises Management Tequnic & Production System : A Case of Carpet Factory
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Nitric oxide modulates tissue plasminogen activator release in normotensive subjects and hypertensive patients.
We evaluated the possible role of NO in modulating tissue plasminogen activator (t-PA) release in the forearm microcirculation of normotensive subjects and hypertensive patients. Essential hypertensive patients are characterized by endothelial dysfunction because of a reduced NO availability and also show an impaired t-PA release. In healthy volunteers and essential hypertensive patients, we studied local t-PA release and forearm blood flow changes (strain-gauge plethysmography) induced by intrabrachial administration of acetylcholine (0.45 and 1.5 microg/100 mL/min) and of sodium nitroprusside (0.5 and 1.0 microg/100 mL/min), an endothelium-dependent and -independent agonist, respectively. Acetylcholine was also repeated in the presence of intra-arterial infusion of the NO synthase inhibitor N(G)-monomethyl-l-arginine (100 microg/100 mL/min). In normotensive subjects, vasodilation to acetylcholine was blunted by N(G)-monomethyl-l-arginine. In these subjects, acetylcholine infusion induced a significant, dose-dependent increase in net forearm t-PA release. N(G)-monomethyl-l-arginine significantly reduced basal t-PA release, as well as acetylcholine-induced t-PA release. In essential hypertensive patients, vasodilation to acetylcholine was reduced as compared with controls and resistant to N(G)-monomethyl-l-arginine. In contrast to what was observed in healthy control subjects, in hypertensive patients, acetylcholine had no effect on t-PA release. Similarly, N(G)-monomethyl-l-arginine failed to modify either the tonic or the agonist-induced t-PA release. Both tonic and agonist-induced release of NO are directly involved in t-PA release by endothelial cells. Essential hypertension, characterized by a reduction in tonic and stimulated NO availability, is also associated with impaired capacity of t-PA release, suggesting a major role of impaired NO availability in worsening both vasodilation and t-PA release