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

1974 ◽  
Vol 70 (1) ◽  
pp. 71-88
Author(s):  
Shunkichi TAMURA ◽  
Shigeru NOZAKI
2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Hye-Sun Lim ◽  
Yun Soo Seo ◽  
Seung Mok Ryu ◽  
Byeong Cheol Moon ◽  
Goya Choi ◽  
...  

Background. Mantidis Ootheca (MO), described as the ootheca of Hierodula patellifera Serville, 1839, Tenodera angustipennis (Saussure, 1869), or Statilia maculate (Thunberg, 1784) in Korean Herbal Pharmacopoeia, is an important herbal material that has been traditionally used for treating several medical conditions including renal failure, spermatorrhea, and pediatric enuresis in Korea. Objective. The present study investigated the potential subacute toxicity of MO water extract during a 2-week repeated oral administration of doses of 0, 50, 150, or 450 mg/kg/day to C57BL/6 male mice by gavage. Methods. The following parameters were examined during the study period: mortality, clinical signs, body weight, hematology, serum biochemistry, gross findings, organ weight, and histopathology. All the mice were euthanized at the end of the treatment period. Results. No treatment-related changes in mortalities, clinical signs, body weight, gross finding, and organ weight change were detected after 14 days of oral MO extract administration. In addition, no meaningful MO extract treatment-related changes were observed in the hematological, serum biochemical, and histopathological parameters compared with the normal control group following treatment with doses of up to 450 mg/kg/day. Conclusion. Based on these findings, we concluded that treatment of mice with the water extract of MO did not result in significant toxicity and, therefore, it could be considered safe for further pharmacological studies.


1973 ◽  
Vol 69 (1) ◽  
pp. 191-200 ◽  
Author(s):  
Shunkichi TAMURA ◽  
Shigeru NOZAKI

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

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

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

1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen

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.


2013 ◽  
Vol 10 (02) ◽  
pp. 108-129 ◽  
Author(s):  
W. Gaebel ◽  
W. Wannagat ◽  
J. Zielasek

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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