Inhibitory effect of bone resorption and inflammation with etidronate therapy in patients with rheumatoid arthritis for 3 years and in vitro assay in arthritis models

2005 ◽  
Vol 26 (7) ◽  
pp. 627-632 ◽  
Author(s):  
Kaname Yamamoto ◽  
Shinichi Yoshino ◽  
Goukei Shue ◽  
Masakazu Nagashima
Author(s):  
Katsumi Nishikawa ◽  
Hitoshi Kawakubo ◽  
Kenji Matsumoto ◽  
Hisashi Yago ◽  
Yoshio Toyomaki ◽  
...  

2007 ◽  
Vol 82 (1) ◽  
pp. 588-592 ◽  
Author(s):  
Makoto Ujike ◽  
Hiroki Nishikawa ◽  
Akira Otaka ◽  
Naoki Yamamoto ◽  
Norio Yamamoto ◽  
...  

ABSTRACT The peptides derived from the heptad repeat (HRP) of severe acute respiratory syndrome coronavirus (SCoV) spike protein (sHRPs) are known to inhibit SCoV infection, yet their efficacies are fairly low. Recently our research showed that some proteases facilitated SCoV's direct entry from the cell surface, resulting in a more efficient infection than the previously known infection via endosomal entry. To compare the inhibitory effect of the sHRP in each pathway, we selected two sHRPs, which showed a strong inhibitory effect on the interaction of two heptad repeats in a rapid and virus-free in vitro assay system. We found that they efficiently inhibited SCoV infection of the protease-mediated cell surface pathway but had little effect on the endosomal pathway. This finding suggests that sHRPs may effectively prevent infection in the lungs, where SCoV infection could be enhanced by proteases produced in this organ. This is the first observation that HRP exhibits different effects on virus that takes the endosomal pathway and virus that enters directly from the cell surface.


1996 ◽  
Vol 102 (1-2) ◽  
pp. 223-226 ◽  
Author(s):  
Govind J. Kapadia ◽  
Shekhar C. Sharma ◽  
Harukuni Tokuda ◽  
Hoyoku Nishino ◽  
Shinichi Ueda

Bone ◽  
1993 ◽  
Vol 14 (6) ◽  
pp. 829-834 ◽  
Author(s):  
K. Kitamura ◽  
M. Katoh ◽  
O. Komiyama ◽  
H. Kitagawa ◽  
F. Matsubara ◽  
...  

1968 ◽  
Vol 20 (03/04) ◽  
pp. 384-396 ◽  
Author(s):  
G Zbinden ◽  
S Tomlin

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.


2009 ◽  
Vol 21 (2) ◽  
Author(s):  
Nadja Larsen ◽  
Kim F. Michaelsen ◽  
Anders Pærregaard ◽  
Finn K. Vogensen ◽  
Mogens Jakobsen

2021 ◽  
pp. 1-9
Author(s):  
Anita Virtanen ◽  
Outi Huttala ◽  
Kati Tihtonen ◽  
Tarja Toimela ◽  
Tuula Heinonen ◽  
...  

<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.


Sign in / Sign up

Export Citation Format

Share Document