A Rapid in vitro Assay of the Histamine H3-receptor: Inhibition of Electrically Evoked Contractions of Guinea-pig Ileum Preparations

1991 ◽  
pp. 37-38
Author(s):  
G.J. Menkveld ◽  
H. Timmerman
Keyword(s):  
Guinea Pig ◽  
In Vitro Assay ◽  
Guinea Pig Ileum ◽  
Vitro Assay ◽  
Histamine H3 Receptor ◽  
Receptor Inhibition ◽  
Electrically Evoked Contractions ◽  
Evoked Contractions ◽  
Histamine H3

Histamine H3 receptor desensitization in the guinea-pig ileum

1998 ◽  
Vol 341 (2-3) ◽  
pp. 253-256 ◽  
Author(s):  
Carmen Pérez-Garcı́a ◽  
Lydia Morales ◽  
Luis F Alguacil
Keyword(s):  
Guinea Pig ◽  
Receptor Desensitization ◽  
Guinea Pig Ileum ◽  
Histamine H3 Receptor ◽  
H3 Receptor ◽  
Histamine H3

Intrinsic factor-like activity in extracts of guinea pig intestine

1965 ◽  
Vol 208 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Shigeo Ukyo ◽  
Bernard A. Cooper
Keyword(s):  
Guinea Pig ◽  
Intrinsic Factor ◽  
In Vitro Assay ◽  
Factor Activity ◽  
Vitro Assay ◽  
Factor B ◽  
Saline Extract ◽  
Human Gastric Juice ◽  
Normal Human

Co57-labeled B12 tube fed to guinea pigs with normal human gastric juice has been found in both the supernatant and sediment of a saline extract of intestinal mucosa. The Co57-labeled material in the supernatant was excluded from Sephadex G-25, was not ultrafiltrable, and functioned as an intrinsic factor-B12-Co57 complex in an in vitro assay for intrinsic factor activity.

In Vitro Assay of Platelet Adhesiveness with Washed and Tanned Human Red Cells

1968 ◽  
Vol 20 (03/04) ◽  
pp. 384-396 ◽  
Author(s):  
G Zbinden ◽  
S Tomlin
Keyword(s):  
Platelet Adhesion ◽  
Sodium Citrate ◽  
Blood Platelets ◽  
In Vitro Assay ◽  
Red Cells ◽  
Platelet Adhesiveness ◽  
Vitro Assay ◽  
In Vitro System ◽  
Human Red Cells

SummaryAn in vitro system is described in which adhesion of blood platelets to washed and tannic acid-treated red cells was assayed quantitatively by microscopic observation. ADP, epinephrine and TAME produced a reversible increase in platelet adhesiveness which was antagonized by AMP. With Evans blue, polyanetholsulfonate, phthalanilide NSC 38280, thrombin and heparin at concentrations above 1-4 u/ml the increase was irreversible. The ADP-induced increase in adhesiveness was inhibited by sodium citrate, EDTA, AMP, ATP and N-ethylmaleimide. EDTA, AMP and the SH-blocker N-ethylmaleimide also reduced spontaneous platelet adhesion to red cells. No significant effects were observed with adenosine, phenprocoumon, 5-HT, phthalanilide NSC 57155, various estrogens, progestogens and fatty acids, acetylsalicylic acid and similarly acting agents, hydroxylamine, glucose and KCN. The method may be useful for the screening of thrombogenic and antithrombotic properties of drugs.

Angiogenic Effect of Pravastatin Alone and with Sera from Healthy and Complicated Pregnancies Studied by in vitro Vasculogenesis/Angiogenesis Assay

2021 ◽  
pp. 1-9
Author(s):  
Anita Virtanen ◽  
Outi Huttala ◽  
Kati Tihtonen ◽  
Tarja Toimela ◽  
Tuula Heinonen ◽  
...  
Keyword(s):  
Direct Effect ◽  
Late Onset ◽  
Maternal Serum ◽  
In Vitro Assay ◽  
Serum Samples ◽  
Therapeutic Concentration ◽  
Tubule Formation ◽  
Vitro Assay ◽  
Angiogenesis Assay

<b><i>Objective:</i></b> To determine the direct effect of pravastatin on angiogenesis and to study the interaction between pravastatin and maternal sera from women with early- or late-onset pre-eclampsia (PE), intrauterine growth restriction, or healthy pregnancy. <b><i>Methods:</i></b> We collected 5 maternal serum samples from each group. The effect of pravastatin on angiogenesis was assessed with and without maternal sera by quantifying tubule formation in a human-based in vitro assay. Pravastatin was added at 20, 1,000, and 8,000 ng/mL concentrations. Concentrations of angiogenic and inflammatory biomarkers in serum and in test medium after supplementation of serum alone and with pravastatin (1,000 ng/mL) were measured. <b><i>Results:</i></b> Therapeutic concentration of pravastatin (20 ng/mL) did not have significant direct effect on angiogenesis, but the highest concentrations inhibited angiogenesis. Pravastatin did not change the levels of biomarkers in the test media. There were no changes in angiogenesis when therapeutic dose of pravastatin was added with maternal sera, but there was a trend to wide individual variation towards enhanced angiogenesis, particularly in the early-onset PE group. <b><i>Conclusions:</i></b> At therapeutic concentration, pravastatin alone or with maternal sera has no significant effect on angiogenesis, but at high concentrations the effect seems to be anti-angiogenic estimated by in vitro assay.

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