scholarly journals Pharmacological studies of a lipase GA-56 produced by Pseudomonas sp. V. Teratogenic effect in mice and rats of GA-56.

1974 ◽  
Vol 70 (1) ◽  
pp. 107-118 ◽  
Author(s):  
Shunkichi TAMURA ◽  
Shoji TSUTSUMI ◽  
Shigeru NOZAKI
Keyword(s):  
Teratogenic Effect ◽  
Pseudomonas Sp ◽  
Pharmacological Studies

scholarly journals Pharmacological studies of a lipase GA-56 produced by Pseudomonas sp.

1973 ◽  
Vol 69 (1) ◽  
pp. 191-200 ◽  
Author(s):  
Shunkichi TAMURA ◽  
Shigeru NOZAKI
Keyword(s):  
Pseudomonas Sp ◽  
Pharmacological Studies

scholarly journals Pharmacological studies of a lipase GA-56 produced by Pseudomonas sp.

1973 ◽  
Vol 69 (1) ◽  
pp. 177-189
Author(s):  
Shunkichi TAMURA ◽  
Shoji TSUTSUMI ◽  
Shigeru NOZAKI
Keyword(s):  
Pseudomonas Sp ◽  
Pharmacological Studies

Teratogenic effect of meclizine, cyclizine, and chlorcyclizine

JAMA ◽  
1965 ◽  
Vol 194 (9) ◽  
pp. 987-989 ◽  
Author(s):  
J. F. Sadusk
Keyword(s):  
Teratogenic Effect

Phytochemical and pharmacological studies of Crotalaria madurensis leaves

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
SHM Hala ◽  
SAM Mohamed ◽  
TI Magada ◽  
SA El Batran ◽  
DE Omayma
Keyword(s):  
Pharmacological Studies

Phytochemical and pharmacological studies on commercial teas

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HC Rodda ◽  
FKE Rubra ◽  
B Ramya
Keyword(s):  
Pharmacological Studies

Mechanism of the Antiplatelet Action of Dipyridamole in Whole Blood: Modulation of Adenosine Concentration and Activity

1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Receptor ◽  
Whole Blood ◽  
Blood Cells ◽  
Inhibitory Action ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Adenosine Concentration ◽  
Pharmacological Studies

SummaryDipyridamole inhibits platelet aggregation in whole blood at lower concentrations than in plasma. The blood cells responsible for increased effectiveness in blood are the erythrocytes. Using the impedance aggregometer we have carried out a series of pharmacological studies in vitro to elucidate the mechanism of action of dipyridamole in whole blood. Adenosine deaminase, an enzyme breaking down adenosine, reverses the inhibitory action of dipyridamole. Two different adenosine receptor antagonists, 5’-deoxy-5’-methylthioadenosine and theophylline, also partially neutralize the activity of dipyridamole in blood. Enprofylline, a phosphodiesterase inhibitor with almost no adenosine receptor antagonistic properties, potentiates the inhibition of platelet aggregation by dipyridamole. An inhibitory effect similar to that of dipyridamole can be obtained combining a pure adenosine uptake inhibitor (RE 102 BS) with a pure phosphodiesterase inhibitor (MX-MB 82 or enprofylline). Mixing the blood during preincubation with dipyridamole increases the degree of inhibition. Lowering the haematocrit slightly reduces the effectiveness.Although we did not carry out direct measurements of adenosine levels, the results of our pharmacological studies clearly show that dipyridamole inhibits platelet aggregation in whole blood by blocking the reuptake of adenosine formed from precursors released by red blood cells following microtrauma. Its slight phosphodiesterase inhibitory action potentiates the effects of adenosine on platelets.

Therapy of post-stroke depression – a systematic review

2013 ◽  
Vol 10 (02) ◽  
pp. 108-129 ◽  
Author(s):  
W. Gaebel ◽  
W. Wannagat ◽  
J. Zielasek
Keyword(s):  
Systematic Review ◽  
Large Scale ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Placebo Control ◽  
Post Stroke ◽  
Pharmacological Studies ◽  
Post Stroke Depression ◽  
Control Procedures ◽  
Antidepressant Pharmacotherapy

SummaryWe performed a systematic review of randomized placebo-controlled pharmacological and non-pharmacological trials for the therapy and prevention of post-stroke depression that have been published between 1980 and 2011. We initially identified 2 260 records of which 28 studies were finally included into this review. A meta-analytic approach was hampered by considerable differences regarding the kinds of therapeutic regimens and the study durations. Modest effects favoring treatment of post-stroke depression could be found for pharmacological treatment as well as repetitive transcranial magnetic stimulation. For the prevention of post-stroke depression, antidepressant pharmacotherapy showed promising results. However, large-scale studies with better standardized study populations, optimized placebo control procedures in non-pharmacological studies, and replication in larger follow-up studies are still necessary to find the optimal therapeutic regimens to prevent and treat post-stroke depression.

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